Economic Zoology

ECONOMIC ZOOLOGY
Economic zoology deals with the application of zoological knowledge for the benefit of mankind. It includes culturing
animals for mass production for human use and to control or eradicate animals that are injurious to man directly or
indirectly.

The following chapters are included here

 Beneficial and harmful insects

 Sugarcane pest – Pyrilla perpusilla
 Castor pest – Achaea janata
 Rice grain pest – Sitophilus oryzae
 Apiculture (Bee-keeping)
 Honey bee
 Sericulture (Silk worm)
 Lac culture (Lac insect)
 Carp culture
 Pearl culture and mollusc culture
 Prawn culture
 Venomous animals – Centipedes, wasps, honey bee
 Diseases of man
 Cattle and livestock diseases
 Arthropod vectors of diseases
 Non-poisonous and poisonous snakes of India
 Model organisms used in research
 Vermiculture
ECONOMIC IMPORTANCE OF INSECTS
(Dr. Girish Chandra)
 The estimated annual value of the ecological services provided by insects in the
United States alone is at least $57 billion, an amount that justifies greater investment in the
conservation of these services. Without the activities of insects, human life on earth would
eventually be extinguished. Over one lakh currently living species of insects have been
identified, but the true number is surely much larger, about a million.

BENEFICIAL INSECTS

Pollinators of crops (Bees, wasps, butterflies, moths, hoverflies, beetles)

Many plants depend on insects to transfer pollen as they forage. Plants attract insects
in various ways, by offering pollen or nectar meals and by guiding them to the flower using
scent and visual cues. This has resulted in strong relationships between plants and
insects. Value of crop production from pollination by native insects is estimated to be about
$3 billion in US alone. When we talk about pollinators the ones that come to mind are honey
bees and butterflies, but there are also many other insects that perform this job for flowering
plants, as well. There are flies, wasps, beetles and even some other insects that most people
know nothing about, such as Hemiptera and thrips. There are many important pollinating
insect species in the orders: Hymenoptera (bees, wasps, and ants), Lepidoptera (butterflies
and moths), Diptera (flies) and Coleoptera (beetles).

As adults these insects feed on pollen and nectar from flowers. They forage from plant
to plant and may initiate pollination by transferring pollen from an anther to a stigma. Female
bees and pollen wasps provision their nests with pollen and nectar that they actively collect
onto their bodies. Their larvae then feed on the collected pollen and nectar. Yucca moth
larvae do not feed on pollen or nectar but on the seeds of yucca plants. The adults pollinate
the yucca plant by actively collecting pollen onto their palps and then placing the collected
pollen on a receptive stigma to ensure proper seed set for their offspring.

Economic value of insect pollination worldwide is estimated at U.S. $217 billion

(Science Daily, Sept. 15, 2008). German scientist found that the worldwide economic value of
the pollination service provided by insect pollinators, bees mainly was dollar153 billion in 2005
for the main crops that feed the world. This figure amounted to 9.5% of the total value of the
world agricultural food production. The study also determined that pollinator disappearance
would translate into a consumer loss of food estimated between dollar 190 to 310 billion.

Predators of pests (Dragonflies, beetles, bugs, lacewings, wasps)

The arthropod predators of insects and mites include beetles, true bugs, lacewings,
flies, midges, spiders, wasps, and predatory mites. Insect predators can be found throughout
plants, including the parts below ground, as well as in nearby shrubs and trees. Some
predators are specialized in their choice of prey, others are generalists. Some are extremely
useful natural enemies of insect pests. Unfortunately, some prey on other beneficial insects as
well as pests.
Major characteristics of arthropod predators:

 Adults and immature stages are often generalists rather than specialists.
 They generally are larger than their prey.
 They kill or consume many preys.
 Males, females, immature stages and adults may be predatory.
 They attack immature and adult prey.

Important insect predators include lady beetles, ground beetles, rove beetles, flower
bugs and other predatory true bugs, lacewings and hover flies. Spiders and some families of
mites are also predators of insects and mite pests. Natural enemies play an important role in
limiting potential pest populations. We have seen what happens when pesticides devastate
the natural enemies of potential pests. Surveys of agricultural systems give an indication of
the potential number and diversity of predators in a crop. For example, over 600 species of
predators in 45 families of insects and 23 families of spiders and mites have been recorded in
cotton. Eighteen species of predatory insects (not including spiders and mites) have been
found in potatoes in the northeastern United States.

Parasites of pests (Hymenoptera and Diptera)

Parasitoids are insects with an immature stage that develops on or in an insect host,
and ultimately kills the host. Adults are typically free-living, and may be predators. They may
also feed on other resources, such as honeydew, plant nectar or pollen. Because parasitoids
must be adapted to the life cycle, physiology and defenses of their hosts, many are limited to
one or a few closely related host species. Crop losses averted by beneficial insects from
predators or parasites of agricultural pests are estimated to be $4.5 billion. The most valuable
insect parasites belong to the following groups:

 Tachinid Flies (Diptera)

 Ichneumonid Wasps (Hymenoptera)
  Braconid Wasps (Hymenoptera)
 Chalcid Wasps (Hymenoptera)

These parasites live in or on one host insect pest which is killed after the parasite
completes its development. Parasite (also called parasitoid) adults are free-living; the
immature stage lives on or inside a host and kills the host before the host completes its
development. Parasites lay one or more eggs on the outside of the host body or they insert
the eggs inside their host. The immature parasite feeds on the host and requires only a single
individual prey to complete its development. Free-living adults may feed on nectar from
flowering plants or obtain nutrients by piercing the body of host insects and withdrawing fluids
(host-feeding). Parasites are often considered more effective natural enemies than predators
because many have a narrower host range, require only one host to complete development,
have an excellent ability to locate and kill their host and can respond rapidly to increases in
host populations.

Productive insects (Silkworm, Honey bees, Lac insects)

Sericulture is an agro-based industry. It involves rearing of silkworms for the
production of raw silk, which is the yarn obtained out of cocoons spun by certain species of
insects. The major activities of sericulture comprises of food-plant cultivation to feed the
silkworms which spin silk cocoons and reeling the cocoons for unwinding the silk filament for
value added benefits such as processing and weaving. Five varieties of silk worms are
reared in India for producing this natural fibre. Bombyx mori, the silk worm, feeds on the
leaves of mulbery to produce the best quality of fibre among the different varieties of silk
produced in the country. Antherea assama is confined to only Brahmaputra Valley of India in
the world. It produces the famous muga silk. Tasar silk is a product of Antherea mylitta, which
feeds on Terminalia tomentosa grown in the thick jungles of Bihar, Madhya Pradesh and
Orissa. The recent introduction of Antherea royeli and Antherea perniyi has enabled the
country to produce the oak tasar silk, Phylosamia ricini, the eri silkworm, which feeds
on Ricinus communis, is raised in Assam and Orissa commercially. Of the total production of
2,969 tonnes of silk in India, as much as 2,445 tonnes is produced by the mulberry
silkworms, Bombyx mori.

Lac Insect any of the species of Metatachardia, Laccifer,

Tachordiella, Austrotacharidia, Afrotachardina,and Tachardina of the superfamly Coccoidea,
order Homoptera that are noted for resinous exudation from the bodies of females. Members
of two of the families viz. Lacciferidae and Tachardinidae appear to be more concerned with
lac secretion. There are several lac insects, some of which secrete highly pigmented wax. The
Indian lac insect Laccifer lacca is important commercially. It is found in tropical or subtropical
regions on banyan and other plants. The females are globular in form and live on twigs in cells
of resin created by exudations of lac. Of the many species of lac insect, Laccifer lacca,
(=Tachardia lacca) is the commercially cultured lac insect. It is mainly cultured in India and
Bangladesh on the host plant, Zizyphus mauritiana and Z. jujuba. The insect starts its life as a
larva or nymph which is about 0.6 mm long and 0.25 mm wide across the thorax. The young
settles down on a suitable place of the host plant gregariously. On the average some 150 of
such larvae may be present per square inch of the twig.

Apiculture or beekeeping is the maintenance of honey bee colonies, commonly in

hives by a beekeeper in apiary in order to collect honey and beeswax, and for the purpose of
pollinating crops. The genus Apis is comprised of a comparatively small number of species
including the western honeybee Apis mellifera, the eastern honeybee Apis cerana, the
giant bee Apis dorsata, and the small honeybee Apis florea.
Nectar is a sugar solution produced by flowers containing about 80% water and 20% sugars.
Foraging bees store the nectar in the ‘honey sac’ where the enzyme invertase will change
complex sugars into simple sugars called mono-saccharides. Upon return to the hive, the
foraging bee will disgorge the partially converted nectar solution and offer it to other bees.
Housekeeping bees will complete the enzymatic conversion, further removing water until the
honey solution contains between 14 – 20% water.

Human food value

There are 1,462 recorded species of edible insects. Doubtless there are thousands
more that simply have not been tasted yet. 100 grams of cricket contains: 121 calories, 12.9
grams of protein, 5.5 g of fat, 5.1 g of carbohydrates, 75.8 mg calcium, 185.3 mg of
phosphorous, 9.5 mg of iron, 0.36 mg of thiamin, 1.09 mg of riboflavin, and 3.10 mg of niacin.
Compare this with ground beef, which, although it contains more protein (23.5 g.), also has
288.2 calories and a whooping 21.2 grams of fat. Usually crickets, grasshoppers, beetle and
moth larvae and termites are eaten. Australian aborigines regularly ate honey pot ants, adult
bogong moths and the larvae of wood moths. Being rich source of protein, grasshoppers have
been eaten in nearly all regions of the world. They are a common food in parts of Asia and
Africa—fried, roasted or ground to be mixed with flour. The grasshoppers eat green plants,
however, by far outweighs their value as food. Insects are an important food for many
vertebrates, including birds, amphibians, reptiles, fish and mammals. These “insectivorous”
vertebrates usually feed on many insect species, and rarely focus on specific pests, unless
they are very abundant.

Scavangers

Ants, beetles, apterygotes, cockroaches, crickets and a large number of other insects
thrive on dead carcasses, left over organic matter or excreta and in the process clean the
environment. Economic losses avoided every year by the burial of livestock waste by dung
beetles only are estimated to be over $3.8 billion.
NEUTRAL INSECTS

Majority of insects, almost 98% of all insect species, live in low populations in different
ecosystems, without causing appreciable damage. But they form an important component of
the food web and work unnoticed. Conservation of such fauna is important since we do not
know the interactions of such insects with the animal and plant species.

INJURIOUS INSECTS

Less than 1% of insects are regarded as pests. They can be classified into the
following categories.

Pests of agriculture and forestry (Locusts, caterpillars, bugs, hoppers, aphids etc.)

Locusts are among the most destructive of all insect pests. Swarms of desert locusts
were among the plagues of the Biblical Egyptians, and they still plague farmers throughout
Asia and Africa. Their threat is so great that regional and international organizations monitor
desert locust populations and launch control measures when necessary.

Locusts are particularly destructive in hot, dry regions when a sudden increase in their
numbers, combined with food shortage, forces them to migrate. They migrate in huge swarms,
devouring virtually every green plant in their path.

Pests of stored grains

The most common insect pests of stored cereal grains are:

Rice Weevil (Sitophilus oryzae); Lesser Grain Borer (Rhyzopertha dominica);
Rust Red Flour Beetle: (Tribolium spp.); Sawtooth Grain
Beetle: (Oryzaephilus surinamensis); Flat Grain Beetle:(Cryptolestes spp.); Indian Meal
Moth (Plodia interpunctella); Angoumois Grain Moth (Sitotroga cerealella);Khapra
beetle (Trogoderma granarium); Rice moth (Corcyra cephalonica).

Insect management for stored grain depends upon good sanitation and grain storage
practices. Clean storage areas to reduce the potential for insect migration into the new grain.
Once the grain is dried to 13 percent moisture or less, cool it as soon as possible by running
aeration fans. Reducing the grain temperature to less than 60ºF stops insect reproduction,
and lowering it to less than 50ºF stops insect feeding activity. Infested grains should be
fumigated by Aluminum phosphide (Phostoxin, Fumitoxin), which is best in most
circumstances. Methyl bromide may also be used.

Household pests (carpet beetles, furniture beetles, cloth moth, termites and silverfish)
 Common household pests include ants, termites, bed bugs, carpet beetles, furniture
beetles, book lice, house flies, fleas, cockroaches, silver fish, clothes moths and spiders – the
list seems almost endless. Common household pests enter our homes for shelter and food,
and also to nest and breed. Common household pests can cause damage to our homes
especially clothes, eatables and furniture. Household pests can also be a threat to health of
our families by spreading bacteria, diseases or allergens in our homes. Household pests can
be irritating, annoying or irritating and annoying. They can be controlled by spraying
insecticides or by fumigants and by maintaining hygiene.

Insects of medical and veterinary importance (Mosquitos, flea, beetles, flies)

Mosquitoes can spread diseases such as malaria, yellow fever, dengue fever. Tsetse
flies spread sleeping sickness. Lice suck human blood and can cause sores, which if left
untreated can become infected which may lead to blood
poisoning.
Screw worm flies lay their eggs in the wounds of farm animals and pets. Horseflies and black
flies suck blood and have painful bites, which can become infected. Houseflies spread germs
and spoil meat by laying eggs in it. Bubonic Plague (or Black Death) was the worst disease
epidemic in human history. It took 14 million lives–nearly 1 out of 4 people–in 14th-century
Europe. The plague is passed to humans by the bite of the Oriental rat flea (Xenopsylla
cheopis), which picks up the disease-causing bacteria from rats.

Pyrilla perpusilla
The Sugarcane Leafhopper
(Hemiptera: Lophopidae)

Host: This insect is a serious pest of sugarcane in northern India where it also
ccasionally feeds on maize, millets, rice, barley, oats, sorghum, bajra and wild
grasses.

Damage: The pest is found gregariously on the under surface of the leaves where
they suck up plant sap that causes yellowing and eventually drying of leaves. Under
low infestation yellow patches appear on the leaves. Photosynthesis is reduced
resulting in the reduction of sucrose content of the juice by up to 30%. Hoppers
secrete a sweet substance called honey dew that coats the leaves and attracts a
blackish fungus, which reduces photosynthesis resulting in yield loss.

Life cycle: Adult hoppers are straw coloured to brownish, 7-8 mm long, with a
pointed snout bearing piercing and sucking mouthparts. They are found gregariously
and jump off readily when disturbed. Adults are active fliers, migrating from one
crop to another and breed throughout the year. Eggs are light yellowish in colour,
oval, one mm long and laid on the lower surface of the leaf, near the midrib in
groups of about 20 eggs, which hatch in 6-15 days depending on temperature.
Nymphs are initially greenish, later turn pale brownish, wingless and with a pair of
anal filaments covered with whitish fluffy waxy material. There are 5 nymphal
instars which take 40-60 days to complete development. Multiplication of the pest is
favoured by high humidity and luxuriant plant growth as in heavily manured and
irrigated field or in rainy season.

Distribution: The pest is found throughout the Indian subcontinent

from Afghanistan to Burma and Thailand.

Control: The pest can be controlled by spraying 0.05% of parathion, malathion,

thiodon, fenitrothion or rogor. Dusting the plants with 10% Aldrin or dieldrin also
helps.

Conservation of the following natural enemies helps in containing the pest:

Egg parasitoids: Tetrastichus pyrillae, Cheiloneurus pyrillae, Ooencyrtus pyrillae,
O. pipilionus, Agoniaspis pyrillae.
Nymphal parasitoid: Lestodryinus pyrillae, Pyrilloxenos ompactus, Chlorodryinus
pallidus.
Predators: Coccinella septempunctata, C. undecimpunctata, Chilomenes
sexmaculata, Brumus suturalis.
Egg-predators: Nimboa basipunctata, Goniopteryx pusana.
The Castor Semilooper
(Achaea janata)
(Lepidoptera: Noctuidae)

Host: This is a pest of castor, pomegranate, rose, Zizyphus, Euphorbia, Tridax,

Cardiospermum, Ficus, Bauhinia, Citrus, mango etc.

Damage: Larvae defoliate plants quickly by feeding gregariously and voraciously.

Midribs and veins are left intact and other parts of the leaves eaten up. Being larger
in size, their capacity to cause damage is enormous. Young plants cannot sustain
damage and die. Adults are fruit-sucking moths that prefer to suck juice from mango
and citrus and fruits.

Life cycle: Adult moths are grayish-

brown in colour with wavy lines on the
fore wings. Hind wings are black in
colour and have one large median and
three marginal white spots. They are
medium sized robust moths. Eggs are
round, bluish green in color, ridged and
are laid singly on tender shoots, usually
on the undersurface of the leaves.
Fecundity of a female is 450 eggs.
Incubation period varies between 2-5
days after which a tiny larva hatches out
which is slender and yellowish-green in
colour. Young larvae are usually
gregarious but as they grown they get
scattered on leaves. A full grown larva
is a typical semilooper, has a bluish-
black body with a black head and reddish spots on the back and a reddish anal
tubercle. Legs are missing on the median segments which makes it walk with
looping action. Sometimes there are faint reddish-brown or whitish stripes on the
body. Full grown larva measures about 7 cms. There are 5-6 instar and the whole
larval period is about 15-20 days. Pupation takes place in soil or among fallen
leaves. Pupal period is 10-15 days but may be prolonged to few months under winter
conditions.

Distribution: The pest is distributed in the whole of Indian

subcontinent. Thailand, Malaysia, Philippines andIndonesia.

Control: As the larvae are large and prominent on the leaves, destroying them by
handpicking is quite easy. They are also eaten by birds in large numbers.
Chemical control can be achieved by spraying endrin 0.02%, parathion 0.025% or
by spraying 0.02% of diazinon, toxaphen, carbaryl, endosulfan and methyl
parathion.
Biological control involves conservation of the following parasitoids:
Egg parasites: Trichogramma evanescens. Larval parasite: Apanteles sundanus, A.
ruidus, Microplitis maculipennis, M. ensirus, M. similes, Euplectus leucostomus,
 Paniscus ocellaris, Zamesochorus orientalis, Tetrastichus ophiusae, Rogas
percurrens and Enicospilus sp.
Sitophilus oryzae
The Rice Weevil
(Coleoptera: Curculionidae)

Synonym: Calandra oryzae.

Host: This is primarily a pest of rice but occasionally attacks wheat, corn, jowar,
flour, beans, dry fruits and biscuits.

Damage: Larva as well as the adult cause damage to grains. Larvae feed inside the
seed and make in hollow and exit by making a circular hole on the surface. Adults
can damage several seeds by cutting an irregularly lined circular hole, through which
they feed on the kernel.

Life cycle: Adults are 2-3 mm long dark brown weevils, with four faint yellow spots
on the elytra. Body is punctured with minute pits. Sitophilus granarium is slightly
larger in size and is found in more temperate climate. Adults do not fly but try to
crawl away when disturbed. Their longevity can be up to 5 months. Eggs are
whitish, oval, 0.7 mm long. Females chew a small depression on the surface of rice
grain, lay an egg in it and seal it with a gelatinous fluid for protection. Grubs make
their way into seed to feed on kernel. They are plump,3-4 mm long, legless, dirty
white in colour with a brownish head. Pupation takes place inside the grain. Pupa is
light yellowish but later turns dark brown. Adult emerges by cutting a hole in the
grain.

Distribution: This pest is found quite abundantly throughout the warmer parts of
the world, extending up toBaluchistan in Europe and Japan in the east. In Palaearctic
region the species is replaced by Sitophilus granarium, which is wingless with
punctuate prothorax and elytra but without four yellow spots on elytra.
APICULTURE
Honeybees are indigenous to the Eurasian and African continents and were introduced to the
Americas and Australia by European settlers. In India the genus Apis has the following species: the
western honey bee, Apis mellifera, the eastern honey bee, Apis cerana indica, the rock bee, Apis
dorsata and the small bush bee Apis florea.

The Dwarf Honeybee or Bush Bee (Apis florea)

 This species is considered the most primitive honey bee species and is also the smallest. Apis
florea is brownish and the basal part of abdomen is always red. There is another species, A.
andreniformis which is darker in colour and the first abdominal segment is totally black.

The Rock Bee (Apis dorsata)

This is a large wild honey bee found in southern Asia, mainly in the forested areas. The
workers are over 2 cm long and possess ferocious temperament. Hives are built in exposed places far
above the ground, on the branches of trees or under the cliffs of rocks and also on the ceilings of ruins
and abandoned buildings. The hive is made of a single vertical comb, sometimes more than a metre in
length. During breeding season in March-April they swarm and migrate to different places in the
forests looking for nesting sites.

The Asiatic honey bee (Apis cerana indica)

This is a medium sized honey bee found in southern Asia and all countries in the Himalayan
Range, viz, Afghanistan to Indonesia and also in Japan, Malaysia and Thailand. Apis cerana indica is
the subspecies still found in the wild in India, particularly in the Himalayan belt where it nests in tree
holes and crevices of rocks. The species can be domesticated by farmers for honey production as it has
gentle temperament and makes hive in enclosed spaces. Apis cerana is medium sized and has
transverse stripes on abdomen. It is commonly found in Himalaya where temperate fruits bloom and
provide abundant source of nectar. It can survive temperatures as low as 0ºC in winter.

The Western honey bee or the European bee (Apis mellifera)

This species is not indigenous to India but is introduced from USA and European countries in
order to increase honey production in apiaries. The species is slightly larger in size and lighter in color
and higher capacity to produce honey and hence is preferred by apiarists.

However, the species is also amenable to diseases such as the American foulbrood which sometimes
destroys large number of colonies.

LIFE CYCLE

Queen is the largest caste that has pupal period of 16 days. Queens are reared in enlarged cells
in which their larvae are fed exclusively on royal jelly. New queens can be raised by the worker bees
anytime if the main queen dies. The virgin queen takes to nuptial flights for mating and then settles in
the hive for laying eggs. The sterile worker bees clean the hive and feed the larvae during the first 10
days of their lives, after which they build comb cells in the hive. On 16 to 20th day, the worker makes
honey out of the nectar brought by forager. After the 20th day, the worker leaves the hive and spends
the rest of life as a forager and eventually dies as a water carrier.
 Workers, drones and queen larvae are fed on royal jelly during the first 3 days of life, after
which the worker larvae are fed on pollen and diluted honey, while those destined to develop into
queens are fed on protein rich royal jelly.

Queens are reared in specialized large queen cells which are specially constructed for queen
larvae and have a vertical orientation. When the old queen dies or becomes weak, the workers will
construct emergency cells known as supersedure queen cells, which are larger and project from the
comb.

Drones are genetically haploid males, which possess weak mouthparts and hence they cannot
forage for nectar or pollen themselves and have to be fed by the workers. Drones fertilize the queen by
mating in nuptial flight, after which drone dies. The drones are generally expelled from the hive and
die of cold and starvation. The queen stores sperms in small sac-like organ called
the spermatheca located in the queen’s abdomen.

HONEY MAKING

Honey making by bees is a specialized job in which they collect nectar from flowers. Nectar
is a clear liquid containing 80% water and sugars. The worker bees collect nectar in crop and pollen on
hind leg and then return to hive and unload it into the cell. The workers in hive then digest the raw
nectar for about 30 minutes and regurgitate it into the cell. This is done several times to add enzymes
and other materials into it. This honey is placed in empty cells of honeycomb to bring the water
content to less than 20%. They fan the honey with their wings to bring down the water contents. Once
ripe, the cells of the honeycomb are sealed with a wax cap.

Supersedure is a phenomenon in which old and ailing queen is replaced by a new one. As the
queen ages or ails the output of queen substance pheromone is not produced. This signals workers to
rear a new queen. The workers quickly detect the ailing queen or its inability to lay eggs and will then
rear a new queen.

PHEROMONES

Chemical secretions or pheromones produced by the queen bind the colony together. Workers
secrete pheromones from Nasanov gland which are inside the tip of abdomen. This helps the workers
to identify the members of their colony when they group together or collect nectar or water. The colony
pheromone is quickly recognized by the bees of the same colony because of its unique chemical
composition.

When a queen flies to mate, her pheromones attract all the drones. Another pheromone,
called queen substance is licked by workers from the queen’s body and passed to others. Queen
substance also inhibits the ovaries of workers and renders them sterile.
 The mandibular glands of workers also produce an alarm pheromone, which alerts the colony
when it is threatened or attacked by a predator. Workers leave the sting on the body of victim which
also produces a sting odor, which serves to attract other bees to the area for stinging,

BEE BREAD

Bed bread is a mixture of pollens collected by bees mixed with saliva and honey and contains
most of the necessary nutrients required by the colony. Bee pollen contains about 25% proteins that
carry about 18 amino acids. It also contains all essential vitamins, minerals, several enzymes, all
essential fatty acids and carbohydrates. Bee pollen is low in calories and proves to be quite useful for
activity enhancement. Bee bread provides energy to bees and enhances their performance.

Beeswax

Wax is secreted from the glands on abdominal segments 4-7. Beeswax is used by the honey
bees to build honey comb. There are sternal wax plates on abdominal segments 4-7, which are located
on the ventral side, from where it is removed as flakes and chewed with mandibles. Wax is softened
with the secretion of mandibular glands to make it into a paste.

Propolis

This is a glue-like substance collected by bees from trees. The sticky resin is mixed with wax
to make it into sticky glue which is used to construct the foundation of the comb strong. The bees also
use propolis to seal cracks in their hive.

Royal Jelly

The royal jelly is a milky substance that is made of digested pollens and honey mixed with the
secretion of pharyngeal gland of nursing bee. It is loaded with proteins, fats and all of the B vitamins.

Bee Venom

Honey bee venom contains Melittin, which is a potent anti-inflammatory agent. Adolapin is
another strong anti-inflammatory substance. Apamin found in venom inhibits calcium-dependent
potassium channels. Hyaluronidase, Phospholipase and Histamine are involved in the inflammatory
response of venom. Venom also contains small amounts of the neurotransmitters such as Dopamine,
Norepinephrine and Seratonin.

Bee venom is hemorrhagic in action. Apamine, melittin, phospholipase, hyaluronidase, inhibit

the nervous system and stimulate heart and adrenal glands. Also present in venom are certain
antibiotics.
Composition of honey
Carbohydrates
Unsurprisingly, these comprise the major portion of honey – about 82%. The carbohydrates
present are the monosaccharidesfructose (38.2%) and glucose (31%);
and disaccharides (~9%) sucrose, maltose, isomaltose, maltulose, turanose and kojibiose.
There are also some oligosaccharides present (4.2%), including erlose, theanderose and
panose, formed from incomplete breakdown of the higher saccharides present in nectar and
honeydew.
Proteins and Amino Acids
Honey contains a number of enzymes, including invertase, which converts sucrose to glucose
and fructose; amylase, which breaks starch down into smaller units; glucose oxidase, which
converts glucose to gluconolactone, which in turn yields gluconic acid and hydrogen
peroxide; catalase, which breaks down the peroxide formed by glucose oxidase to water and
oxygen; and acid phosphorylase, which removes inorganic phosphate from organic
phosphates.
Vitamins, Minerals and Antioxidants
Honey contains trace amounts of the B vitamins riboflavin, niacin, folic acid, pantothenic
acid and vitamin B6. It also contains ascorbic acid (vitamin C), and the minerals calcium,
iron, zinc, potassium, phosphorous, magnesium, selenium, chromium and manganese.
Other compounds
Honey also contains organic acids such as acetic, butanoic, formic, citric, succinic, lactic,
malic, pyroglutamic and gluconic acids, and a number of aromatic acids. The main acid
present is gluconic acid, formed in the breakdown of glucose by glucose oxidase. Honey also
contains hydroxymethylfurfural, a natural product of the breakdown of simple sugars below
pH 5.
Components of Royal Jelly
Most of the components of royal jelly seem to be designed to provide a balance of
nutrients for the larvae. However, the lipids present are unusual, in that they are unlike the
lipids of typical insect fats, which consist of 14-20 carbon fatty acids. Royal jelly lipids are
composed mainly of 8-10 carbon acids, hydroxy acids and diacids, which may be saturated,
unsaturated, linear or branched. They include hexanoic acid, octanoic acid, (E)-oct-2-enoic
acid, 8-hydroxyoctanoic acid, 3- and 10-hydroxydecanoic acid, and 3,10-dihydroxyoctanoic
acid. 10-hydroxydecanoic acid levels rise dramatically in summer. Royal jelly also contains
-9 sterols, 4 phospholipids, 5 glycolipids, and a variety of 16-33 carbon hydrocarbons.
The unusual lipids of royal jelly make it highly acidic, and give it good antimicrobial
properties. This seems to be the main role of the lipids. However, these properties disappear
above pH 6, so while royal jelly may be used as an effective skin-care product, its
antimicrobial properties are negligible within the body, where the pH is maintained at
about 7.4 by buffering systems. Because of this, there does not seem to be any
pharmaceutical use for royal jelly. However, its good balance of nutrients and high
nutrient levels mean that it has become a highly touted specialized health food.
 SERICULTURE
Sericulture was first introduced into China by Hoshomin, the Queen of China. For a long time sericulture was
considered to be a national secret by the Chinese and its industrial technique was not known in other countries.
Later, it was introduced into Europe and Japan by smuggling the secrets from China through travelling monks.
According to some sources, sericulture was introduced in India about 400 years ago and the industry flourished
as an agro-industry till 1857, with an annual production of a million kg of silk fibre.

According to Chinese legend, the technique of silk production using Bombyx mori was invented at
around 2,700 BC when prince Hoang-ti directed his wife Si -ling-chi to study the silkworm and explore the
practicability of using its thread for textile. Si -ling-chi devised not only the technique of culturing silkworm but
also the method of reeling the silk and making garments out of it. She was later crowned as “The Goddess of Silk
Worm”. Subsequently sericulture spread from China to other countries and silk became a precious commodity,
highly sought after in all countries. In 139 BC the world’s longest highway that stretched from Eastern China to
the Mediterranean Sea was opened, which was called “Silk Route” due to trade in silk.

Five species of silk worms are reared in India:

1. Bombyx mori meridionalis, the Mulberry silk worm (Lepidoptera: Bombycidae), feeds on the leaves of
mulberry (Morus alba) to produce the best quality silk fibre.

2. Antherea paphia or Antherea mylitta, the Tasar silk worm (Lepidoptera: Saturnidae), feeds on Terminalia
tomentosathat occurs in the jungles of Bihar, Madhya Pradesh, UP and Orissa.

3. Antherea royeli and Antherea perniyi, the Oak tasar silk worms (Lepidoptera: Saturnidae), feed on oak
trees and were introduced from foreign countries.

4. Antherea assama, the Muga silk worm (Lepidoptera: Saturnidae), is confined to the Brahmaputra Valley
of India and produces the famous muga silk.

5. Phylosamia ricini, the Eri silkworm (Lepidoptera: Saturnidae), which feeds on castor (Ricinus communis) is
raised inAssam, Madhya Pradesh, Rajasthan and Orissa commercially.

MULBERRY SILKWORM

Mulberry plantation

Four Indian species of mulberry, namely, Morus alba, M. indica, M. serrata & M. laevigata, are cultivated
as main food plants of silkworm. Different systems of plantations for mulberry are practiced in India. In India
where the temperature ranges from 16 oC to 31 oC, mulberry silkworm can be reared throughout the year.
Karnataka, where the temperature ranges from 16-31 degree centigrade, provides ideal climatic conditions for
rearing mulberry silkworm throughout the year, whereas in West Bengal, the multivoltine silk -worm rearing is
practised even under adverse temperature conditions. In Jammu & Kashmir univoltine variety of silkworm is
cultured only once a year during May-June.

LIFE CYCLE

Eggs of Bombyx mori are small and hard, about the size of a pin head and resembling poppy seeds. The
egg stage lasts 10 days; the larval stage lasts the longest, 25-30 days and the pupal stage takes 10 days. The
larvae are white, 4-5 cm long and moult four times during their growth. At the end of the larval duration, the
silkworm produces silk from its mouth to constructs a cocoon in some hidden and secure place. Healthy moths
are allowed to copulate for 4 hrs, after which the female is consigned to a dark plastic ‘cellule’ for egg laying.
She lays about 400 eggs in 24 hours.

Considering the various factors, such as the place of origin, voltinism (number of generations in a year),
the colour of cocoons, the larval markings, the colour, shape and size of cocoons, the silkworms are classified
into different breeds. The multivoltine races are reared in West Bengal and Karnataka due to optimum
temperature conditions. Bivoltine races diapause in winter and hence can have only two generations in a year.
Univoltine and bivoltine races require more leaves than the multivoltine ones. However, the yield and quality of
cocoons of the bivoltines are superior to those of multivoltines. The average a nnual yield of cocoons in India is
as low as 150 kg under rain fed conditions and 400 kg under irrigated conditions The cocoons after cooking are
reeled in hot water in different types of reeling machines. In India, 61 percent of the silk amounting to 1,3 20
tonnes is reeled on the country-type charkha.

NON-MULBERRY SILK WORMS

TASAR SILK WORM

Three species of Antherea are used for the extraction of tasar silk in India. They are Antherea mylitta, A.
perniyiand A. royeli. Out of the total non-mulberry silk produced in India, about 400 tonnes is produced
from Antherea mylitta in Madhya Pradesh, Orissa and Bihar. This silkworm feeds on Terminalia
tomentosa and Terminalia arjuna found in the forests of central and north-eastern parts of India. The tasar
silkworms is a wild species and hence cocoons are also collected by the tribal people from forests and silk is
obtained. The first crop, usually called the seed crop is raised during May to July, whereas the commercial crop
is raised during October-November.

The larvae are usually green in colour and moults four times before they complete their larval duration.
However, yellow, blue and white larvae are also reported. At the end of the larval period, they spin a ring like
structure around the twig and a long stalk from which the cocoon hangs. The cocoons are large and brown or
yellow in colour. Moths emerge from the cocoons in June. To obtain silk, the cocoons are cooked in caustic
potash and reeled to extract fibre and then spun to manufacture coarse thread.

The recent introduction of Antherea perniyi and A. royeli on oak trees in Manipur has opened up new
opportunities for the production of superior quality tasar silk in India. The cocoons of Antherea perniyi can be
easily reeled and fibre of superior quality can be obtained. Antherea royeli occurs in oak jungles of the sub-
Himalayan region.

MUGA SILK WORM

The golden-yellow silk produced by Antherea assama is found only in the Brahmaputra Valley of India.
This species of silkworm is semi -domesticated as the larvae which crawl down of trees at the end of their larval
period are collected and allowed to spin cocoons in captivity. Antherea assama produces golden yellow silk that
is of high quality which is expens ive. The worms feed on Som (Marchilus bombycina) and Soalu (Litsaea
polyantha) trees. At the end of the larval period, when the worms are ready to spin cocoons, they crawl down
the tree in search of suitable places for making cocoons. To obtain silk, the cocoons are boiled in soap and soda
solution and are reeled on a machine. The total production of muga silk in India is about 50 tonnes but there is
plenty of scope for expansion of this industry.

A single Muga female moth lays 150-200 eggs after copulating with the male for 6-8 hrs. The larvae are
yellowish with black markings on the body and have the habit of crawling down the trees in groups when all
leaves are consumed on the trees and larvae have matured. If larvae have not matured and the leaves on the
trees exhausted, they can be transferred to another tree. At the end of the larval period, when the worms are
ready to spin the cocoons, they crawl down the tree in search of a suitable place for the construction of
cocoons.

Spinning of Cocoons

The mature silkworms will come down from the trees to the base on ground in search of proper place for
spinning of Cocoons. Therefore, bundles of semidried twigs are collected and the worms are placed on these
twigs so that they make their cocoons.

ERI SILK WORM

The silk produced by Philosamia ricini is called Eri silk. It is grown in Assam and in the eastern parts of
India. The heavy rainfall & humid atmosphere in these parts are conducive to eri culture. The food plants
for Philosamia ricini is castor. This silk worm is multivoltine and reared indoors.

The eggs are white and hatch in ten days. The hatched larvae are mounted on castor leaves in the
rearing-houses and are allowed to grow by feeding on leaves. The worms moult four times during the larval
period of 30-32 days. Eri silkworm is generally hardy and not easily susceptible to diseases. At the end of larval
period, the larvae crawl in search of suitable places to spin cocoons.

The cocoons of the eri silkworm cannot be reeled, as they are made up of several small fibres and
hence the emergence of moths is allowed and the cocoons are spun like cotton to produce yarn. Approximately
ninety tonnes of eri silk is produced in the country annually.
 Recent efforts to rear tasar silkworms on oak plants in the sub-Himalayan range and in Manipur have
contributed to the production of a significant quantity of quality tasar silk. It has also opened up new avenues
for improving sericulture and also enhanced the employment potential in the tribal hilly areas.

LAC CULTURE
INTRODUCTION

Members of two families of Hemiptera, namely, Lacciferidae and Tachardinidae secrete lac over their
bodies for protection. Lac Insect belongs Laccifer of superfamily Coccoidea of order Hemiptera. In all 22 species
have been recorded under the genus Laccifer in Indian subcontinent.
India is still being regarded as the principal lac producing country of the world. Burma went into lac
trading since sixteenth century. Lac culture in China probably dates back to 4000 years and they use lac for
dyeing silk and leather goods. India produces about 65% of the world’s total output. Bihar and Jharkhand
account for 40% of India’s total production of lac.

HOSTS
Plants such as, Zizyphus mauritiana, Z. jujuba, Butea monosperma, Schleichera oleosa, Acacia arabica, A
catechu, Cajanus cajan, Ficus benghalensis, F. cunia, and F. religiosa are common hosts of the lac
insectLaccifer (=Tachardia) lacca.
BIOLOGY
Laccifer lacca, (=Tachardia lacca) is the commercially cultured lac insect. It is mainly cultured in India
and Bangladesh on the host plants such as ber, Zizyphus mauritiana, palas, Butea monosperma and
kusum,Schleichera oleosa.
Female insect is viviparous, producing about 1000 nymphs, deep red in colour with black eyes. The larvae
settle down on a suitable place of the host plant gregariously. A day or two after settlement, the larvae start
secreting lac all around the body except on the rostrum, spiracles and on the tip of abdomen. Thus it gets encased
in a cell of lac which gradually increases in size along with the increase in size of the insect. The insect moults
twice before reaching maturity. The male larvae produce elongated lac cells while the females produce oval cells
After the first moult larvae lose their legs, antennae and eyes and become bag -like. After the 3rd moult,
the larvae pass on to a pseudo-pupal stage. Males emerge and copulate with the females and die. The female
larvae never regain appendages and continue to remain under the lac cell, become adults and reproduce. As the
lac insects remain close together, lac secretion from adjacent cells coalesces with each other and forms a
continuous encrustation on the tree branch.

LAC CULTIVATION
Lac culture involves two important steps: (i) inoculation, and (ii) cropping. Inoculation can be carried
out through artificial infection of tender branches by brood lac stick obtained form mature lac trees immediately
after harvesting. In this process, the brood lac sticks are tied in bundles of 2 or 3 sticks on the branches of the host
tree, allowing maximu m contact with the branches.
 There are four seasons of lac cultivation and according to the Hindi calendar, they have been named
asKartiki, Aghani, Baisakhi, and Jethwi. The crop period, from inoculation to harvesting, for Kartiki, ranges
from July to November, for Aghani, from July to February, Baisakhi, from November to July, and Jethwi, from
February to July.
When young shoots come up on branches, the brood sticks are tied adjacent to the growing tender
branches in a way so that maximu m contact between shoots takes place. Within a week or two the larvae emerge
and settle down on tender shoots.

PROCESSING OF LAC
Lac encrustations are removed from the twigs of host plants by scraping. The raw lac thus obtained is
known as scraped lac or stick lac. Stick lac is crushed into small grains, sieved, washed with mild alkaline water
and dried. This semi-refined product, called seed lac or grain lac or Chowrie, which is further refined by a
system of hot melting, filtration and stretching into thin sheets which are subsequently broken into brittle flakes
called shellac. Alternatively the purified lac resin can be in the form of circular discs called button lac. If a
solvent process is used to purify the raw lac, de-waxed, decolorized lac can be obtained as the end product. The
normally amber coloured resin can also be bleached with sodium hypochlorite to obtain bleached lac, which is
white in colour. Bleached lac has specialised demand for coating medicinal tablets, confectioneries etc.
India is the principal lac producing country of the world, producing approximately 18,000 metric tonnes
of raw lac annually. About 85% of the country’s production is exported to various countries. The USA, Germany
and Egypt are some of the major lac importing countries of the world.

USES OF LAC
The various applications of lac can be summarized as follows:
Lac resin is used in food processing industry; cosmetics and toiletries industry; varnish and printing
industry; coating of fruits and vegetables; electrical industry; leather industry; adhesiv e industry; pharmaceutical
industry; perfumery industry; miscellaneous applications.
Lac dye (erythrolaccin) has been used in India as a skin cosmetic and dye for wool and silk. In China it
is a traditional dye for leather goods. The use of lac for dye has been supplanted by synthetic dyes. It is used in
medicine to protect liver and to fight obesity.
Lac is used in food, confectionery and beverages industry and textile industry.
Lac wax is used in polishes for shoe, floor, car polishes etc. It is used in electric insulations, lamination of
papers, hat proofing and coating of pictures and fossils.
Lac is used for manufacture of tailors chalks, crayons, bottle sealers, lipsticks, enamels, printing inks,
gramophone records and in fireworks.

NATURAL ENEMIES OF LAC

Predators:
Two moth predators cause a lot of damage to lac.
1. Eublemma amabilis. The larva is dirty white in colour and tunnels through the lac encrustation and feeds
on larvae and adults. It pupates within the tunnel and adults after emerging lay their eggs near the lac
encrustation.
 2. Holcocera pulverea. The damage by the brownish larva is similar to the above species. Pupa is slightly
bigger and yellowish-brown.
Parasites:
The following insects are parasitic on lac insect.
Paraecthrodryinus clavicornis; Erencyrtus dewitzi; Tachardiaephagus tachardiae; Eupelmus tachardiae;
Tetrasticus purpurens.
The above natural enemies can be controlled by maintaining healthy cultures and by enclosing the brood
lac sticks in wire mesh before inoculation so that natural enemies are not able to emerge and cause re -infestation.

INDIAN CARP CULTURE

Indian aquaculture has been growing at a fast pace over the last two decades, with
freshwater aquaculture contributing over 95% of the production. The three Indian major carps,
namely catla (Catla catla),rohu (Labeo rohita) and mrigal (Cirrhinusmrigala) contribute to the
bulk of production amounting to about two million tonnes annually (FAO, 2003). Silver carp,
grass carp and common carp formthe second important groupfor fish production. Average
national production from pondfisheries has increased from 0.6 tonnes/ha/year in 1974 to 2.2
tonnes/ha/year in 2002 (Tripathi, 2003).

COMPOSITE FISH CULTURE

The three major carps cultured in India, namely, catla(Catla catla),rohu(Labeo rohita)
andmrigal(Cirrhinus mrigala), contribute as much as 87 percent of the total Indian aquaculture
production. Three exotic carps were also introduced, namely, silver carp (Hypophthalmichthys
molitrix); grass carp(Ctenopharyngodon idellus) and common carp (Cyprinus carpio). There
are also several other medium and minor carp species, namely,Labeo calbasu, L. fimbriatus,
L. gonius, L. bata, L. ariza,Cirrhinus mrigala, Puntius sarana, Hypselobarbus pulchellus, H.
kolus and Amblypharyngodon mola, which are important in aquaculture. Among catfishes,
magur(Clariasbatrachus) is the only species that is widely cultured, while the catfish,
‘Singhi’(Heteropneustes fossilis) is cultured to some extent in the eastern states. Attempts
have also been made toculture the other catfishes like Pangasius pangasius, Wallago attu,
Sperata seenghala, S. aor and Ompokpabda. The finfish species of importance include
climbing perch (Anabastestudineus), murrels (Channa striata and C. marulius) and
tilapia (Oreochromismossambicus and Oreochromis niloticus).

PREPARATION OF PONDS
Pond preparation involves making the ponds weed and predator-free and generating
adequate natural food for the survival and growth of fishes. Control of aquatic weeds, removal
of undesirable flora and fauna and improvement of soil and water quality are important
aspects of fish management.Weeds have to be removed from the ponds first, after which the
tank is fertilized with both organic and inorganic fertilizers, such as Oil Cake and raw Cow
Dung @ 5,000 kg/acre. The PH of pond water should be 7.5 – 8.00, for which lime is added in
the tanks @ 200 kg/acre per annum. The lime increases pH and also helps in eradicating fish
parasites.The organic fertilizer in the form of raw cow dung is added in the tank @ 500
kg/acre per annum. This is followed by theapplication of inorganic fertilizers like Super
Phosphate @ 120 kg/acre and Ammonium Sulphate @ 200 kg/acre, in spaced intervals.

SPAWNING
Because of constant temperature and favourable weather conditions, carps
spawn all the year roundin India. Spawning takes place early in the morning when the water
surface cools down to about18 degrees. The female carp swims near the water surface
followed by the male carp in nuptial swimming and rubbing each other’s bodies. Female lays
egg and male releases its milt and eggs are fertilised.
Three days after fertilization, the eggs begin to hatch. The newly hatched larva is
about 5.5 mm long,delicate and transparent, with a yolk sac attached to the belly. It rarely
swims but settles on the bottom or on some floating object. On the second day, the larva
starts swimming and on the third day swims actively from surface to bottom. During these
stages, the larva or fry gets its nourishment from the yolk sac, which disappears on the third
day and the fry now must search for food and eat. Supplementary fry-feed in the form of hard-
boiled egg yolk or powdered milk can be applied on the water surface at this time.
Carpscan feed on almost anything like insects, shells and worms and can also eat
aquatic plants, bread crumbs, rice bran and fish meal made from corn, copra and soybean.

CHOOSING BROODERS
Both female and male brood fish should be carefully tended for 2-3 months before
induced spawning operations are carried out and males and females should
be segregated and kept in separate ponds.
To be good brooders the fish must be more than one year old and 150 gm in weight.
Sex can be determined by the shape of the genital papilla which is pointed in male and oval in
female. When the female is ready for induced spawning operations, It should have a bulging
abdomen that is soft to touch. The cloaca is reddish and prominent, and the contour of the
enlarged ovaries can be seen on both sides of the abdomen. The head should be small and
the snout pointed.
Nursery ponds are constructed to rear carp fry or larvae. A normal sized nursery
pond measures 5 x 10 m, with a depth of 0.5 m. Before filling up water the pond should
be cleaned thoroughly to get rid of predators and parasites that may be destructive the
larvae.About 1,500 to 3,000 fries can be stocked in the nursery pond andfed with milk, wheat
flour or boiled egg yolk by spreading it on the water surface. This feed can be
supplemented with rice bran, bread crumbs or fish meal, which can be given twice a day, in
the morning and in the afternoon.
Rearing ponds, where adult carpsare cultured until they reach marketable size, are
needed, which have dimensions of 15 x 50 m and depth of 1.5 to 2 m. Rearing
ponds should also be thoroughly cleaned before fillingthem with water. This is done
by exposing the bottom and letting it dry thoroughly.Next step involves application of
fertilizers, which encourages growth of aquatic plants, moss and algae, which are important
natural food andalso lead to growth of micro fauna. Manure in the form of chicken dropping is
the most commonly used being cheaper and more readily available in large quantities. When
carp fry reaches the length of about 5 to 7 cm, they are transferred from the nursery pond to
the rearing pond and allowed to grow to adult stage.

STOCKING OF PONDS
Ponds are stocked with fish fries of appropriate size. Fingerlings of over 10 cm in size
are recommended for stocking in culture ponds. Stocking of smaller fishes may result in
higher mortalities and slow growth duringthe initial months. In fish polyculture a fingerling size
of 50-100 g is preferred for stocking to ensure higher survival and better growth. Generally, a
density of 5,000 fingerlings is kept as a standard stocking rate per ha for carp polyculture,
which will give a yield of 3-5 ton/ha/yr.Prior to stocking, the fish fries should be dippedin 3-5%
potassium permanganate solution for 15 seconds to kill parasites. In composite fish farming, a
combination of six species are cultured, namely, Catla, Rohu, Mrigal and exotic Carps like
Silver Carps, bass and common Carp.Supplementary feeds like Groundnut Oil cake and Rice
Bran are fed to fishes during culture. At the end of the culture period of say 12 months, the
fish will reach marketable size and fetch attractive prices.

POST-STOCKING POND MANAGEMENT

While fertilizing the carp ponds, 20-25% of the total amount of organic manures
is applied a fortnight before stocking and the remaining amount is applied in equal instalments
on a bimonthly basis. Other commonly used organic manures include poultry manure, pig
dung, duck droppings, cow dung, domestic sewage, etc. Azolla, a nitrogen-fixing fern is used
as a bio-fertilizer for aquaculture at the rate of 40 tonnes/ha/yr, which supplements nutrients
required for intensive carp culture. The bio-processed organic manure, biogas slurry has also
been used as manure in carp culture.
The supplementary feed in carp polyculture is usually restricted to a mixture of
groundnut/mustard oil-cake and rice bran. Grass carps are fed with aquatic vegetation such
asHydrilla, Najas, Ceratophylum, duck weeds, etc. which can be kept in special enclosures
in corners of the pond. Feeding preferably twice-a-day is advocated @ 5% of the initial
biomass of stocking material for first month and then gradually reducing it.
Aeration may be done mechanically to increase the concentration of dissolved oxygen
in ponds, by paddle wheel aerators, aspirator aerators and submersible pond aerators. It is
also necessary to replace certain amount of water at regular intervals.

HARVESTING
Harvesting of fishes is usually done after a culture period of 10 months to one year.
However, fishes attaining the marketable size can be harvested periodically depending on
several factors, which also reduces the pressure of density in the ponds and thereby providing
sufficient space for the growth of fishes.
INDUCED REPRODUCTION IN FISH
Inducedfish farming has allowed farmers to breed and raise species that do not
naturally reproduce in captivity, to manipulate the timing of reproduction to suit production
cycles, getting fish to spawn on a predetermined date and fertilise and incubate eggs under
hatchery conditions. There are two main strategies used to induce reproduction. The first is to
provide an environment similar to that in which spawning occurs in nature. Catfish, for
example, likes to spawn in enclosed spaces and goldfish in vegetation and at high
temperatures.
The second strategy is to inject the fish with one or more naturally occurring
reproductive hormones or their synthetic analogs to manipulate maturation of gonads and
ovulation. The hormones injected include, Gonadotropin Releasing
Hormone(GnRH)analogs, dopamine antagonists and gonadotropins.Leutinizing Hormone
Releasing Hormone (LHRH) is a mammalian hormone that has been employed successfully
to induce reproduction in fishes. Dopamine inhibits the action of LHRH and hence a
dopamine antagonists are given for induced breeding.
Two types of gonadotropin extracts have been used to induce ovulation in
fishes, namely,Human Chorionic Gonadotropin (HCG) and fish pituitary extract. Pituitary
extracts are made by removing the pituitary from a fish and extracting the hormones, which
may then be injected into another fish. HCG offers three major advantages over the pituitary
extract, namely,1) it is much less expensive, 2) it is more stable and 3)it comes in a purified
form. An intraperitonial injection is given through the ventral part of the fish behind the pelvic
or pectoral fin. Intramuscular injections are commonly given on the dorsal part of the fish
above the lateral line and below the dorsal fin.Two doses with a time gap of 12 to 24 hours
are given.

OBTAINING PITUITARY EXTRACT (HYPOPHYSATION)

Pituitary gland contains gonadotropin hormone, which stimulates the production of
sex steroids in the gonads and induce maturation of gametes. Gonadotropin is composed
of follicle stimulating hormone (FSH)and luteinizing hormone (LH), which are responsible
for the egg development and egg ovulation.The skullof the fish from which,hypophysis is to
be collected, is cut open with a knife to remove the bone and meninges. The pituitary gland
can be seen after the mid-brain has been folded back by using forceps.The gland is taken out
and ground in the homogenizer and then distilled water is added and the gland is again
ground. The solution is taken in a syringe for injection. The female can be injected with two
doses with the time interval of 6 hours. The intramuscular injection is given in the area
between the base of the dorsal fin and lateral line.

OVULATION & FERTILISATION

 Stripping the fish is done by holding the female around the caudal fin with one hand,
while applying slight pressure to the abdomen with the other hand. A stream of eggs will eject
through the genital opening. The abdomen should be messaged from front to back to strip out
all the eggs.Ovulation occurs about ten hours after the second injection of
hormone. The eggs are collected in a dry plastic container. At the same time, the miltfrom a
male fish is made to drip on the eggs by pressing the testes with fingers and pouring the water
through the fine mesh cloth. Eggs and sperm are mixed and stirred gently. After about two
minutes, water is added two or three times to cleanse the fertilized eggs and then they are
transferred to the hatching happas, where most of the fertilized eggs hatch out within 24
hours. The
The yolk sac is absorbed in the body of fry in about 2 days, and then the larvae are
transferred from happas to the nursery tanks, where the fries feed and grow. Food has to be
given during the first 3 weeks and when the fries reach the size of 2–3 cm, they are distributed
in the rearing tanks where they are cultured further to adult marketable stage.

PEARL CULTURE,Mollusc culture

Pearl is produced by black lip pearl oyster or pearl oyster, Pinctada margaritifera ( var.
cumingii) and P. vulgaris, which grow to a size of 12-15 cm after 3 years of culture. Pearl
oysters occur throughout the Indo-Pacific Region. They have been fished for almost two
centuries for the mother-of-pearl industry and fine pearls were occasionally harvested from the
sea. To overcome the decimation of wild populations, spat collection tests were undertaken at
the beginning of the 20th century but the technique was only developed in the late 1950s.
There was a renewal of interest in pearls in the 1960s and the first grafts were carried out by
the French Fisheries Service, and the first grafted pearls were harvested in 1965. In the 1970s,
through private initiatives, this oyster began being cultured for pearl production and a market
was developed for Polynesian black pearls.

CULTURE TECHNIQUES

Hatchery rearing of spat is not yet fully controlled. Pearl oyster rearing chains are
suspended from a long line. Spat for culturing is collected in the natural environment by setting
artificial substrates. After 12-24 months without any intervention, the oysters grow to 5-10 cm
and are then set on oyster-rearing chains suspended from the subsurface long lines at 6 to 10 m
depth. 4,000 to 10,000 oysters are set on each of these 200 m oyster-rearing chains, which are
spaced 10 m apart. After 3-12 months, the oysters reach a size of around 10 cm and weigh
about 120 g, and at this stage they are ready to be grafted. After grafting, the oysters are again
set on long lines until the pearl grows, which is generally around 18 months. The regulations
stipulate a maximum density of 2,400 oysters per 200 m oyster-rearing chain. Only 25-30% of
these oysters form a marketable pearl, rest are rejected, die or produce poor quality pearls.
 The kechi pearl is formed by inserting pieces of the mantle of one mollusc into the
gonad of another. The result will be small, less than 7 mm, odd-shaped pearl but no nucleus is
required and as many as 20 pearls may be produced. When a nucleus is used, larger than 7 mm
pearls are formed, which are called "baroque".Mabe pearls are grown extensively by the
American pearl companies because they are relatively easy to implant. A semi-spherical core
(plastic in the case of Cross and Peach, and mother-of-pearl in the case of Latendresse type) is
inserted under the mantle, which is gradually covered by nacre resulting in a half pearl.
Different shapes such as rounds, kechis, baroques and mabes can be produced from the same
oyster by inserting nuclei of various shapes.

HISTORY

Harvesting natural pearls from the sea was expensive and difficult process that
produced very few pearls. Hence pearls were extremely rare and extremely valuable. It wasn’t
until the Japanese discovered how to nucleate molluscs to produce cultured pearls, that pearls
became available to people other than the very wealthy.
Kokichi Mikimoto, the son of a noodle maker, worked with his dedicated
wife Ume to develop a strategy that stimulated oysters to produce pearls on demand. It was this
discovery that brought about the beginning of oyster farming and pearl culture. At the same
time a government biologist, Tokichi Nishikawa, and a carpenter Tatsuhei Mise had also
each discovered the cause of pearl formation independently.
With these discoveries, and Mise’s patent in 1907 for a grafting needle, cultured pearls
became quite an important and competitive science. They didn’t even know about each other’s
efforts until Nishikawa applied for a nucleating patent and found out that Mise had
discovered exactly similar thing. They then collaborated and established the Mise-Nishikawa
method, which still forms the base of cultured pearls today. Mikimotofurther altered the Mise-
Nishikawa method and created a technique to culture round pearls. This patent was granted in
1916 and then Mikimoto overshadowed the works of all others. For example, Mikimoto’s
efforts were directly responsible for the development of the Akoya pearl.
South Sea pearls grow in the waters off the coasts of Australia,
the Philippines, Indonesia, Myanmar,Japan, and Thailand. In the 16th and 17th centuries when
the European explorers arrived, the global demand for South Sea pearls increased and by the
18th and 19th centuries, the South Sea pearl producing oysters were brought to the brink of
extinction. Culturing of pearls saved these oysters, and brought South Sea pearls to the level of
10% of the entire pearl market.
Tahitian pearls were originally believed to belong to God Oro who used rainbows to
visit earth. When the French arrived, the pearls were cultivated in the French Polynesian
waters. By the 1700, the number oftraders and explorers increased so much that the pearl-
producing molluscs quickly depleted and France was forced to take strict action and
placed severe regulations on the pearl fishing off these islands. It wasn’t until the Japanese
began the process of nucleation that Tahitian pearls could again be marketed.

PRAWN CULTURE
The prawn production in India accounts for about 15% of the total world production of prawn
and shrimps. For marine prawns, the percentage of Indian production to the world production
is about 20%. The major commercial prawn species reared in India are Macrobrachium.
rosenbergii and M. malcolmsonii.

BIOLOGY
Macrobrachium rosenbergii, also known as the giant river prawn or
the giant freshwater prawn, is native to the Indo-Pacific and northern Australian Regions.
The adult is found in freshwater, while its larval stages live in brackish water after the juvenile
stage. During mating, the male attaches its spermatophore on the ventral side of the abdomen
of female’s body and the eggs coming out of female genital opening are fertilised by the
sperms derived from spermatophores. The fertilised eggs are held in the brood chamber or
egg basket,which is made by the interlocking appendix interna of the pleopods
and are aerated by vigorous movements of the swimmerets for 2-3 weeks. This is in contrast
to shrimps, whose fertilized eggs are released into the sea. Females can lay 80,000-100,000
eggs during one spawning and eggs take an average of 20 days at 28°C to hatch into larvae.

After hatching, larvae are dispersed by the rapid movements of the abdominal
appendages of the female.Larvae are planktonic and swim upside down actively with tail
first posture and feed on small planktons. Larvaecomplete development in 15-
20 days and metamorphose into post larvae, which resemble miniature adults and generally
feed near bottom and then begin to migrate upstream into freshwater rivers within one or two
weeks after metamorphosis and are soon able to swim against the rapidly flowing
currents (contranatant behaviour) andcan also crawl over the stones in shallow waters.

HATCHERIES AND NURSERIES

Freshwater prawn hatcheries need supplies for both freshwater and sea water; the
latter can be drawn from areas where the salinity is 30 to 35 ppt. The brackish water derived
from the mixture of seawater, brine or artificial sea salts mixed with freshwater should have
salinity of 12-16 ppt, pH of 7.0 to 8.5 and dissolved oxygen level of 5 ppm.

The prawn farm site should also have the following facilities:
  A secure power supply to ensure that the components of hatchery, e.g. aeration, water
flow etc. can continue to function uninterrupted.
 An uninterrupted access for incoming and outgoing materials by road.
 Access to the uninterrupted seawater and freshwater supplies.
 Farm should not be close to cities, mines and industrial centres or to other activities that
may pollute the water supply.
 Farm should be situated in a climate where the temperature range of 28-31°C can be
easily maintained.
 Food supplies for larvae should be easily procured when required.
 Should have access to biological and veterinary assistance whenever required.
 Should be close to other nursery facilities feed sites.
 Should be close to the market for quick selling after harvesting.

OBTAINING BERRIED FEMALE PRAWNS

Berried females are those that carry fertilised eggs in their egg basket. They
can be obtained from rivers, canals, lakes and estuaries, where they are most abundant in the
beginning of rainy season. In the tropics, berried females can be obtained all the year round
from farm ponds containing adult animals. Selecting fast-growing, berried females from
ponds has a positive effect on the weight of prawns at harvest.

In the tropics, where berried females are readily available, special brood holding
facilities are not required but in temperate areas, indoor brood stocking facilities are
essential. Brood stock is disinfected by placing into freshwater containing 0.2-0.5 ppm
of copper sulphate or 15-20 ppm of formalin for about 30 minutes. Prawns should be
fed daily at the rate of 1-3% of total biomass.

Berried females can be collected from the holding system and placed in tanks where
the eggs will hatch into first instar larvae, which are collected by netting. The hatching
tanks should be covered to prevent bright sunlight to reach larvae for which the inner side of
the tanks should also be painted with black epoxy-resin paint.

LARVAL REARING TANKS

Different designs of containers can be used to grow freshwater prawn larvae, which
may be circular flat-bottom tanks, circular conical-bottomed plastic tanks, plastic-lined wooden
tanks, rectangular concrete tanks, concrete-faced brick tanks and earthen water
jars. Good drainage system is essential as water has to be removed from tanks at harvesting
time. Mixing tanks are also required for preparing the brackish water to be used in the
hatchery as well as storage tanks. Aeration of water is also essential which can be
done through PVC pipes, with holes cut at one foot intervals.
 Larvae should not be exposed to direct sunlight, for which 90% of the tan area should
be covered and shady. Some natural light is essential for good larval survival, which can
be provided through transparent roofs over the hatcheries. Physical filters that include sand
filters, drum screen filters, and medium filters should be easy to clean and designed to
minimize water loss.

Water needs to be chemically treated before it can be used in rearing tanks and also
should be physicallyfiltered by passing through the sand bed before transferring it to another
tank for treatment. Mix the seawater or brine with freshwater to form 12 ppt of brackish
water. The optimum temperature range for M. rosenbergii is 28-31°C. Below 24-26°C the
larvae will not grow well and the time taken for them to reach metamorphosis will be longer.

LARVAL FEEDING
A wide range of feeding material is used by different
hatcheries, which includes nauplius larvae ofshrimps, freshwater cladocerans, fish eggs, squid
flesh, frozen adult Artemia, rotifers, fish flesh, egg custard, worms and commercial
feeds available in the market. The quantity of food to be given depends on the utilization
of feed by larvae that vary from place to place. The quantity of feed consumed will increase as
the larvae grow.

HARVESTING POST LARVAE

When post larvae are about 7-8 mm long, they can withstand transfer from 12 ppt
water into freshwater.However, they should not be harvested from the larval tanks and
transferred directly into holding tanks containing freshwater but should be acclimatized to
fresh water in the larval tanks itself. When majority of larvae have metamorphosed, water
level in tanks should be reduced to about 35 cm. Then gradually the tank should be
flushed with freshwater over a period of 12 hours. The post larvae can then be collected and
transferred or the larval tanks can be refilled to 70 cm with fresh water and the animals
temporarily held in them. The best way to harvest post larvae from the larval tanks is to
reduce the water level and then remove them by nets.

HOLDING POST LARVAE BEFORE SALE

Post larvae cannot be held in holding tanks for more than a week or two prior
to stocking in nurseries. When the post larvae are in the holding tanks, the rearing water
should be changed every 2-3 days) toprovide aeration. Post larvae can be stocked at
densities of about 5,000/m2 for one week, although survivalincreases by reducing the density.

REARING PONDS
Pond size should be such that can be managed easily. Generally most farms
have ponds of around 0.2-0.6 ha size. Large ponds are normally wider than 30 m and often
drained for harvesting. The average depth of water in freshwater prawn ponds in tropical
areas should be about one meter; with a minimum of 0.75 m and a maximum of 1.2 m.
Deeper ponds are used in colder areas to maintain more stable water temperatures. The
banks of the ponds or embankments or bunds must be high enough for the highest water level
expected in the pond, which generally should be 1-2 feet higher than water level. The flow of
water into each pond must be controlled by valves, stop-logs or plugs. Paddle wheels are the
most efficient method of increasing dissolved oxygen levels in the pond water.

STOCKING
Stocking the ponds quickly reduces competitors and predators, which have less time
to become established. Often post larvae that are a week or two old after metamorphosis are
used to stock ponds, where they remain until harvesting. A stocking density of
about 40,000/ha is recommended for the monoculture
ofMacrobrachium rosenbergii. Using larger juveniles for stocking increases the survival rate
as well as the average weight of the animals by as much as about 30%.

FEED TYPE
Natural productivity of the ponds generally gives small production from the ponds.
Therefore, intensive farming must involve supplementary feeding to increase
productivity. Some farms claim to rely on fertilizers, rather than feeding at the beginning of
the rearing period, which stimulates algal bloom and lot of micro flora and fauna in the
ponds. Others find that providing feed from the beginning of the rearing period improves
performance and is cost-effective. Commercial feeds are the most productive and reliable to
use but they are expensive and unaffordable to small farmers.

HARVESTING MARKETABLE PRAWNS

Basically there are two methods of harvesting: culling and draining. The time
of harvesting depends partly on the growth rate and partly on the size of animals for market
requirements. Culling is used to harvest market-sized animals from the ponds to
remove faster growing prawns which increase density quickly. In tropics culling usually starts
5-7 months after post larvae have been stocked to take out the market-sized animals for
selling and keeping the smaller ones and soft-shelled animals in the pond for further growth.
After about 8-11 months ponds are drained and all animals are sold. In cull harvesting, a
seine net is pulled through the pond to remove market-sized animals, while in drain
harvesting, a harvesting sump is installed in front of the gate or outside the pond, in which
prawns will accumulate while water is being drained.

DISEASE CONTROL
Several diseases affect freshwater prawn larvae as well as adults. Some hatcheries
use formalin at the rate of 200 ppm daily as an effective remedy for protozoan and hydrozoan
parasites and fungal diseases. Formalin can also be used at a lower level of about 30 ppm
for longer periods, followed by water change after 24 hours. Larvae can also be transferred to
disinfecting tanks every 5-10 days to get rid of diseases and parasites. Daily dip of larvae
in Malachite green (0.2 ppm) for 30 min has also been used for treatment. Also, dipping in
copper sulphate 0.4 ppm solution for 6 hours is recommended. Antibiotics and sulfa drugs are
sometimes used to control filamentous bacteria and some hatcheries use lime (CaO) as a
prophylactic measure.
CENTIPEDES
Centipedes (Latin: hundred, legs) belong to Phylum Arthropoda, Subphylum Myriapoda,
ClassChilopoda. They are elongated, dorsoventrally flattened, metameric animals with one
pair of laterally attached legs in each body segment. They have a pair of venomous
claws which are modified maxillipedes that are used for defence as well as for hunting small
insects and worms. Their bites may have effects ranging from mild discomfort to life
threatening to man. Their narrow extended body is made up of anything between 15 to 150 or
more segments, depending on the species and individual, with each segment bearing a pair of
legs. The head carries a pair of long, sensitive antennae and, in addition to small chewing
mouthparts, a pair of large, strong claw-like structures which close together like tongs just
below the head and are equiped with poison glands. Centipedes are carnivorous and use their
poisonous head-claws to seize and paralyse their prey. They hunt, mostly at night, for
arthropods and other invertebrates such as insects, spiders and worms, although some of the
very large tropical species (the so called Giant Centipedes, in some cases up to 25 cm long)
also attack small vertebrates. Many of the larger centipedes have an unpleasant bite and the
poison of some giant species can be dangerous to humans, especially children.

Centipedes normally have a drab coloration combining shades of brown and red.
Scolopendromorphs have bright aposematic colors. Size can range from a few millimeters in
the smaller Lithobiomorphs and Geophilomorphs to about 30 cm in the largest
Scolopendromorphs. Scolopendra gigantea, found in Amazonian forests is the largest existing
species of centipede in the world, reaching over 30 cm in length. It is known to eat bats,
rodents and spiders.

Worldwide there are about 3,000 described species. Centipedes are found in an array of
terrestrial habitats from tropical rainforests to deserts. Accordingly, they are found in soil and
leaf litter, under stones and in deadwood logs. In addition, centipedes are among the largest
terrestrial invertebrate predators and often they contribute a significant proportion to
invertebrate predatory biomass in terrestrial ecosystems.

There are five orders of centipede: Craterostigmomorpha, Geophilomorpha,

Lithobiomorpha, Scolopendromorpha, and Scutigeromorpha.
 Males deposit a spermatophore for the female to pick it in her genital chamber. They
lay their eggs singly in holes in the soil, which is filled with soil and leaves. In some species,15
to 60 eggs are laid in a nest in the soil or in rotten wood and the female stays with the eggs,
guarding and licking them to protect them from fungi and predators. In anamorphic
development, as in Scutigera, nymph hatches from egg with only 4 pairs of legs and in
successive moults grows additional 5, 7, 9, 11, 15 pairs of legs. In orders Geophilomorpha and
Scolopendromorpha, development is epimorphic, in which all legs are fully formed when the
larvae hatch from eggs and offspring do not develop more legs between moults.

Scutigera, which habitually lives inside houses and other buildings, usually in slightly
damp places such as cellars and basements, is called House Centipedes, which generally grows
to about 3 cm long and differs from other centipedes in having very long, delicate legs,usually
15 pairs, with the hind pair extremely long and thin. They also have very long antennae and
compound eyes. In warm climates they can survive outside, living in caves and rocky places.
They are very fast runners and prey on flies, cockroaches and other insects. House Centipedes
can inflict a painful bite.

CONTROL

Controlling centipedes and millipedes outdoors includes removing objects that provide
harborage such as trash piles, rocks, boards, leaf piles, compost piles and similar materials.
Spraying or dusting diazinon, malathion, carbaryl, propoxur (Baygon), pyrethrin may provide
some control. Inside houses cracks, crevices or other hiding places such as under clothes
washers and dryers may be sprayed with the above-mentioned insecticides. Contact pesticides,
such as propoxur or pyrethrins may be sprayed directly on centipedes for quick control.
Carbaryl or diazinon granules may be used on turf.

WASPS
Insects known as wasps include the parasitic wasps and the stinging wasps of family Vespidae.
About 75,000 species of wasps are known, most of them parasitic or predators. Almost every
pest insect species has at least one wasp species that is a predator or parasite upon it and hence
wasps are increasingly used in biological pest control.

Wasps are characterized by two pairs of membranous wings, three pairs of legs and an
ovipositor (tube for laying eggs) that may be modified as sting in sterile females. The abdomen
is narrowly attached to the thorax by a petiole. In addition to their compound eyes, wasps also
have three simple eyes known as ocelli, arranged in a triangle on the top of the head. Males do
not have a sting. Females have diploid (2n) number of chromosomes and develop from
fertilized eggs. Males are haploid (n) and develop from unfertilized eggs.
 Yellow jackets and paper wasps prey on caterpillars and other larvae that can destroy
crops. Wasps feed on flower nectar and play a role in pollination. Wasps can be solitary or
colonial and social insects. Adult solitary wasps generally live and operate alone and may or
may not construct nests, whereas social wasps exist in colonies numbering up to several
thousand strong and build nests.

The type of nest produced by wasps can depend on the species and location. Many
social wasps produce paper pulp nests on trees, holes in the ground or in other such sheltered
areas. By contrast solitary wasps are generally parasitic or predatory and do not build nests at
all. Unlike honey bees, wasps have no wax producing glands. Many instead create a paper-like
substance primarily from wood pulp, which is gathered locally from weathered wood that is
softened by chewing and mixing with saliva. The pulp is then used to make combs with cells
for brood rearing. Mud daubers and pollen wasps construct mud cells in sheltered places
typically on the side of walls. Potter wasps similarly build vase-like nests from mud, often with
multiple cells, attached to the twigs of trees or against walls

Wasp sting

The sting is essentially a hollow tube through which the venom is squirted once the
tube has inserted into the skin of victim. The sting has evolved from the ovipositor of the
female. The sting of a wasp is rather like two swords lying parallel to one another in a sheath.
Each sword has backward-pointing barbs like a fish hook. The wasp thrusts one of the swords
into the victim's flesh, and uses it as an anchor to drive the second sword past it and in deeper.
The second sword is anchored in turn to push the first sword further in. It all happens within a
second, and once the sting is embedded well into the victim, venom is pumped into the
puncture wound. A wasp sting will normally deliver 3 to 15 mg of venom. The venom is
stored in a venom sac in the abdomen, which when squeezed by curling up the abdomen
delivers its load through the sting very rapidly in less than 0.3 seconds.

In contrast to the bee, the wasps and hornets can insert and withdraw their sting with
ease. The single wasp is therefore able to deliver multiple stings with ease. The volume of
venom delivered by a wasp sting is much less than that delivered by a bee. Depending on the
type of wasp the volume can range from as little as 2 micrograms to as much as 15
micrograms.
It should be remembered that the sting apparatus itself consists of a venom sac, which
contains the venom, and a redundant egg laying tube which acts rather like the needle on a
hypodermic syringe. This needle allows the wasp to curl up its abdomen, squeeze the venom
from the sac into the sting apparatus, and inject the venom into the poor victim. Another
feature unique to the wasp and hornet is that the venom contains a pheromone which alarms all
other wasps in the area and invites them to join the attack on the victim.
Wasp venom

Wasp venom is alkaline and so its effects can be neutralized by vinegar or acid to
reduce pain. Bee sting venom, on the other hand, is acidic containing formic acid (also known
as methanoic acid) and so its effects can be neutralised with bicarbonate of soda or alkali to
reduce pain. The principal component of venom is a protein — it is the protein that may cause
an allergic reaction in some people. Several different proteins have been demonstrated in wasp
venom, which vary among the different genera. Other components of venom include an
acetylcholine- like substances, histamine, serotonin, and kinins. Kinins are peptides that cause
slow contractions of smooth muscles, lower arterial blood pressure, and increase capillary
permeability.

Allergic reactions to stinging

Severe allergic reactions commence rapidly after the wasp stings. The whole body is
involved and a person may feel dizzy, nauseated and weak with swelling on the face. There
may be stomach cramps and diarrhoea. There can be itching around the eyes, a warm feeling or
coughing, hives breaking out, followed by vomiting and swelling. There can be wheezing,
shortness of breath or swallowing difficulty, hoarse speech and drop in blood pressure, shock,
unconsciousness and darkened skin. Reactions may begin in a few minutes and death may
occur within 30 minutes in case of multiple stinging.

Precautions from wasps

 If surrounded by a swarm of bees or wasps, move out of the way slowly. Do not try to
wave the insects away. Violent movements will only excite them and make them more
aggressive and likely to attack.
 Insect repellents are effective.
 Never aim a blow at a wasps' or bees' nest or attempt to throw them because the insects
will immediately attack.
 Stay away from things that attract insects, such as flowers, trees, bushes and piles of
wood.
 Be extra careful if you are eating or drinking (especially sweet things) outside.
 Smells and bright colours attract insects. Avoid scented creams and strong perfumes if
you are going to spend time outside.
 Long sleeves, long trousers, socks, shoes and gloves help protect you from stings.
 Close the windows in the house and the car to keep the insects out.
 Look out for insects' nests in your home or garden and have them removed immediately.
 Protective gear such as mesh covers for the face can be very effective against the
nuisance of the highland midge in summer for example.
 If you destroy the nests (aerial and ground) yourself, use a commercially available
stinging insect control aerosol containing Baygon, pyrethrin, permethrin or resmethrin which
can shoot a high-volume spray stream 15 to 20 feet, giving excellent quick knockdown and kill
of wasps and bees hit. After dark or in the evening, most have returned from foraging to the
nest. Thoroughly saturate the nest with spray, contacting as many insects as possible. Do not
stand directly under an overhead nest, since some insects receiving some of the spray may fall
but retain their ability to sting for some time. Repeat treatment if reinfestation occurs. Spray
the patio, picnic and garbage areas with permethrin (Astro, Dragnet, Flee, Permanone, Prelude,
Torpedo) or pyrethrins (Kicker, Microcare, Pyrenone, Pyrethrum, Synerol). Some formulations
are restricted use. A licensed pesticide applicator or pest control operator can apply restricted
use pesticides such as bendiocarb + pyrethrins (Ficam Plus), bifenthrin (Biflex), cyfluthrin
(Tempo), cypermethrin (Cynoff, Cyper-Active, Demon, Vikor), deltamethrin (Suspend) and
tralomethrin (Saga). Other labelled pesticides include acephate (Orthene), amorphous silica gel
(Drione), bendiocarb (Ficam), carbaryl (Sevin), chlorpyrifos (Dursban, Empire, Tenure),
diazinon, propoxur (Baygon) and resmethrin (Vectrin).

Sting Treatment

For stings causing itch, irritation, redness and swelling at the sting site, the following
may be useful: Applying Ice pack and Baking Soda or Meat Tenderizer. Make a paste with a
few drops of water to a teaspoon of meat tenderizer and quickly apply to the sting to reduce
pain and inflammation. Ammonia solution 1 to 2.5%, 3-4 times daily. Oral Antihistamines:
Chlortrimeton, Dimetane, Teldrin. Epinephrine Inhaler, Bronkaid mist, Primatene, Medihaler.
Topical Steroids: Cortaid, Dermolate, Lanacort, etc. Local Anaesthetics: Benzocaine,
Americaine, Dermoplast, Bactine, Foille, Lanacaine, Solarcaine. Oral Steroids can be given on
prescription only.

HONEY BEE
A bee colony has about 20,000 workers, one queen and about two dozen drones. Queen can lay up
to 3000 eggs per day but normal fecundity is about 600 eggs per day. Queen can produce male or
female offspring by choice; unfertilized eggs develop into males and fertilized ones into females.
Growing larvae can also be developed into queens or workers by choice, both of which are genetically
females. Males are called drones, which are darker, robust and hairy and larger than workers. There
are about two dozen of them in a hive and one of them manages to mate with queen during flight and
dies in the process.

A worker has a lifespan of 6 weeks, the first half of which is spent in the hive attending to
household chores, secreting wax and building hive, producing a highly nutritious royal -jelly and
converting nectar into honey. The latter part of life is spent in outdoor duties. Workers possess
morphological adaptations to carry out their duties. Their mandiblular glands secrete wax softening
substance, pharyngeal glands secrete a gelatinous highly nutritious substance called Royal Jelly a nd
stomach contains several glands that help in converting nectar into honey. There are wax glands on
abdominal segments 4-7 which open by several ducts on to the sternites 4-7. Hind legs have tibia and
basitarus modified to form a pollen basket and pollen press. Workers are sterile females and hence
their ovipositors are modified to form sting and accessory reproductive glands get modified to form
poison glands.

Bee Venom

Honey bee venom is hemorrhagic and contains at least 18 active substances. Melittin, the
most prevalent substance, is one of the most potent anti-inflammatory agents known. Adolapin is
another strong anti-inflammatory substance that has analgesic activity as well. Apamin enhances
nerve transmission. Other substances, such asHyaluronidase, Phospholipase, Histamine, and Mast
Cell Degranulating Protein (MSDP), are involved in the inflammatory response of venom, with the
softening of tissue and the facilitation of flow of the other substances. Finally, there are measurable
amounts of the neurotransmitters Dopamine, Norepinephrine and Seratonin.

The bee venom is easily soluble in water and acid, but almost insoluble in alcohol. The
three toxic effects of bee venom are: paralysis of the nervous system, increase in the permeability of
the blood capillaries and destruction of red blood cells. Melittin in high concentrations causes hemolysis
of red blood cells. Hyaluronidase is believed to be the "spreading" factor that allows the toxic bee
venom to infiltrate into the tissues. Phospholipase A through indirect action on the unsaturated fatty
acids causes hemolysis of red blood cells. The pain experienced after being stung may well be the
result of these actions.

HUMAN DISEASES
Diseases that affect humans need to be diagnosed accurately before they can be treated. In this
section, diagnosis, pathogenesis, identification of causative organism, prevention including
vaccination wherever available, treatment and drugs commonly prescribed are given.

Dengue

Japanese Encephalitis

Rabies

Epidemic Typhus

Tuberculosis

Amoebiasis
Yellow fever

Kala Azar

Filariasis

Small pox

Plague

Malaria

Cholera

AIDS

Dengue Fever
Dengue fever is an infectious disease carried by mosquitoes and caused by any of four related
dengue viruses. This disease used to be called break-bone fever because it sometimes causes
severe joint and muscle pain that feels like bones are breaking, hence the name. Health experts
have known about dengue fever for more than 200 years. Dengue fever is found mostly during
and shortly after the rainy season in tropical and subtropical areas of Africa, Southeast
Asia and China, India, Middle East, Caribbean and Central and South America, Australia and
the South and Central Pacific.

The World Health Organization estimates 50 to 100 million cases of dengue infection
occur each year. This includes 100 to 200 cases reported annually to the Centres for Disease
Control and Prevention (CDC), mostly in people who have recently travelled abroad. Many
more cases likely go unreported because some doctors do not recognize the disease. During the
last part of the 20th century, cases of dengue began increasing in many tropical regions of the
world. Epidemics also began occurring more frequently and with more severity. In addition to
typical dengue, dengue hemorrhagic fever and dengue shock syndrome also have increased in
many parts of the world.
Dengue fever is a benign acute febrile syndrome occurring in tropical regions. In some
cases the virus causes increased vascular permeability that leads to a bleeding diathesis or
disseminated intravascular coagulation (DIC) known as dengue hemorrhagic fever (DHF).
Secondary infection by a different dengue virus serotype has been confirmed as an important
risk factor for the development of DHF. In 20-30% of DHF cases, the patient develops shock,
known as the dengue shock syndrome (DSS). Worldwide, children younger than 15 years
comprise 90% of DHF subjects. Dengue is a homonym for the African word, ki denga
pepo, which appeared in English literature during an 1827-28 Caribbean outbreak. The first
definite clinical report of dengue is attributed to Benjamin Rush in 1789, but the viral aetiology
and its mode of transmission via mosquitoes were not established until the early 20th century.

DENGUE VIRUS
Dengue fever can be caused by any one of four types of dengue virus: DEN-1, DEN-2,
DEN-3, and DEN-4. A person can be infected by at least two, if not all four types at different
times during a life span, but only once by the same type.

TRANSMISSION
Mosquitoes become infected when they bite infected humans, and later transmit
infection to other people they bite. The two main species of mosquito, Aedes aegypti and Aedes
albopictus, have been responsible for all cases of dengue transmitted in this country. Dengue is
not contagious from person to person.

SYMPTOMS
Dengue fever usually starts suddenly with a high fever, rash, severe headache, pain
behind the eyes, and muscle and joint pain. The severity of the joint pain has given dengue the
name "break bone fever." Nausea, vomiting, and loss of appetite are common. A rash usually
appears 3 to 4 days after the start of the fever. The illness can last up to 10 days, but complete
recovery can take as long as a month. Most dengue infections result in relatively mild illness,
but some can progress to dengue hemorrhagic fever. With dengue hemorrhagic fever, the blood
vessels start to leak and cause bleeding from the nose, mouth, and gums. Bruising can be a sign
of bleeding inside the body. Without prompt treatment, the blood vessels can collapse, causing
shock which is called dengue shock syndrome. Dengue hemorrhagic fever is fatal in about 5
percent of cases, mostly among children.

Symptoms of typical uncomplicated classic dengue usually start with fever within 5 to
6 days after you have been bitten by an infected mosquito and include—
 High fever, up to 105 degrees Fahrenheit.
 Severe headache.
 Retro-orbital (behind the eye) pain.
 Severe joint and muscle pain.
 Nausea and vomiting.
 Rashes.
The rash may appear over most of your body 3 to 4 days after the fever begins. A
second rash may appear later in the disease.
Symptoms of dengue hemorrhagic fever include all of the symptoms of classic
dengue plus the following additional symptoms:
 Marked damage to blood and lymph vessels.
  Bleeding from the nose, gums, or under the skin, causing purplish bruises.
This form of dengue disease causes some deaths.
Symptoms of dengue shock syndrome—the most severe form of dengue disease—
include all of the symptoms of classic dengue and dengue hemorrhagic fever, plus the
following:
 Fluids leaking outside of blood vessels.
 Massive bleeding.
 Shock.
This form of the disease usually occurs in children (but sometimes adults too)
experiencing their second dengue infection. The fatality rate is 5 to 15 percent.

DIAGNOSIS
The health care provider can diagnose dengue fever by doing two blood tests, 2 to 3
weeks apart. The tests can show whether a sample of your blood contains antibodies to the
virus. In epidemics, a health care provider often can diagnose dengue by typical signs and
symptoms.

TREATMENT

There is no specific treatment for classic dengue fever, and like most people you will
recover completely within 2 weeks. To help with recovery, health care experts recommend the
following:
 Getting plenty of bed rest.
 Drinking lots of fluids such as fruit juices, soups and water with electrolytes.
 Taking medicine to reduce fever.
It is advised that people with dengue fever do not to take aspirin as it dilutes blood
which may complicate haemorrhage but Acetaminophen or other over-the-counter pain-
reducing medicines are safe for most people. For severe dengue symptoms, including shock
and coma, early emergency treatment with fluids and electrolytes can be lifesaving.

PREVENTION
The best way to prevent dengue fever is to take special precautions to avoid contact
with mosquitoes. Several dengue vaccines are being developed but none is likely to be
available in the next few years. When outdoors in an area where dengue fever has been found
use a mosquito repellent and dress in protective clothing such as long-sleeved shirts, long
pants, socks, and shoes. Because Aedes mosquitoes usually bite during the day, be sure to use
precautions especially during early morning hours before day break and in the late afternoon
before dark.
Other precautions include:
 Keeping unscreened windows and doors closed.
 Keeping window and door screens repaired.
  Getting rid of areas where mosquitoes breed, such as standing water in flower pots,
containers, birdbaths, discarded tires, etc.

Japanese Encephalitis
Japanese encephalitis is a potentially severe viral disease that is spread by infected
mosquitoes in the agricultural regions of Asia. It is one of several mosquito-borne virus
diseases that can affect the central nervous system and cause severe complications and death. It
can be a risk to travellers to rural areas where the disease is common. There is no specific
treatment for Japanese encephalitis but a vaccine is recommended for travellers whose
itineraries might put them at risk for Japanese encephalitis. All travellers should take
precautions to avoid mosquito bites to prevent Japanese encephalitis and other mosquito-borne
diseases.

Japanese encephalitis is a disease that is spread to humans by infected mosquitoes

in Asia. It is one of a group of mosquito-borne virus diseases that can affect the central nervous
system and cause severe complications and even death.

Infectious agent
Japanese encephalitis is caused by the Japanese encephalitis virus,
an arbovirus, which is anarthropod-borne virus. Arboviruses are a large group of viruses that
are spread by certain arthropods, most commonly blood-sucking insects. Japanese encephalitis
is spread by infected mosquitoes.

Distribution
Japanese encephalitis is found throughout rural areas in Asia and can also occur near
urban areas in some developing Asian countries. This is a seasonal disease that usually occurs
in the summer and fall in the temperate regions of China, Japan, and Korea. Countries which
have had major epidemics in the past, but which have controlled the disease primarily by
vaccination, include China, Korea, Japan, Taiwan and Thailand. Other countries that still have
periodic epidemics are Vietnam, Cambodia, Myanmar, India, Nepal, andMalaysia.

Mode of infection
Japanese encephalitis virus has a complex life cycle involving domestic pigs, birds and
a specific type of mosquito, Culex tritaeniorhynchus that lives in rural rice-growing and pig-
farming regions. The mosquito breeds in flooded rice fields, marshes, and standing water
around planted fields. The virus can infect humans, most domestic animals, birds, bats, snakes,
and frogs. After infection, the virus invades the central nervous system, including the brain and
spinal cord. Mosquitoes become infected by sucking blood from domestic pigs and wild birds
infected with the Japanese encephalitis virus. Infected mosquitoes then transmit the virus to
humans and animals during the feeding process. The virus multiplies in the blood systems of
domestic pigs and wild birds. Among persons who are infected by a mosquito bite, only 1 in 50
will develop an illness. Japanese encephalitis is the leading cause of viral encephalitis in Asia,
where 30,000 to 50,000 cases are reported each year.

Symptoms
Most infected persons develop mild symptoms or no symptoms at all. In people who
develop a more severe disease, it starts as a flu-like illness, with fever, chills, tiredness,
headache, nausea, and vomiting. Confusion and agitation can also occur in the early stage. The
illness can progress to a serious infection of the brain (encephalitis) and can be fatal in 30% of
cases. Among the survivors, another 30% will have serious brain damage, including paralysis.
Mild infections may occur without apparent symptoms other than fever with headache but in
the case of more severe infections there is headache, high fever, neck stiffness, stupor,
disorientation, coma, tremors, occasional convulsions and spastic paralysis.

Symptoms usually appear 6-8 days after the bite of an infected mosquito, incubation
period being 5-15 days.

Diagnosis
Diagnosis is based on tests of blood or spinal fluid.

Treatment
There is no specific treatment for Japanese encephalitis. Antibiotics are not effective
against viruses, and no effective anti-viral drugs have been developed. Care of patients centres
on treatment of symptoms and complications.

Prevention
Vaccination is recommended only for persons who plan to travel in the infection prone
areas for 4 weeks or more and in special circumstances such as an ongoing outbreak of disease.

Because of the potential for other mosquito-borne diseases in Asia, all travellers should
take steps to avoid mosquito bites. The mosquitoes that transmit Japanese encephalitis feed
mainly outside during the cooler hours at dusk and dawn. Travellers should minimize outdoor
activities at these times, use mosquito repellent on exposed skin and stay in well-screened
rooms. Travellers to rural areas should use a bed-net and aerosol room with insecticides.

Rabies is a serious viral disease that affects central nervous system. It is an

RABIES
infectious disease of animals caused by a bullet-shaped, enveloped RNA virus, 180 x 75 nm.
 Man is occasionally infected and once infection is established in the central nervous system,
the outcome is almost invariably fatal. Typically rabies spreads by way of the saliva of infected
animals, usually a rabid dog, that comes in contact with blood through a bite. Once infected,
the virus spreads from muscles to peripheral nerves to spinal cord and brain. From initial flu-
like symptoms, the illness progresses to convulsions, hallucinations, paralysis or breathing
failure and almost always to death. The severity of the bite determines the risk of infection.
The disease does not usually spread from man to man.
Incubation
After inoculation, the virus enters small nerve endings at the site of the bite. The virus
slowly travels up the nerve to reach the central nervous system, where it replicates and then
travels down the nerves to salivary glands where there is further replication. The time it takes
to do this depends upon the length of the nerves. A bite on the foot will have a much longer
incubation period than a bite on the face. The incubation period may last from two weeks to
six months. Very often the primary wound is healed and forgotten by the time of clinical
symptoms appear.
Clinical Symptoms

Furious Rabies
When the virus reaches the central nervous system, the patient suffers from headache,
fever, irritability, restlessness and anxiety. This may progress to muscle pains, salivation and
vomiting. After a few days to a week the patient may experience a stage of excitement and
painful muscle spasms, triggered sometimes by swallowing of saliva or water. Hence they fear
water (Hydrophobia). The patients are also excessively sensitive to air blown on the face. The
stage of excitement lasts only a few days before the patient lapses intocoma and death.
Once clinical disease manifests, there is a rapid, relentless progression to invariable
death, despite all treatment. The symptoms may include: Fever, headache, malaise, insomnia,
anxiety and confusion, slight or partial paralysis, excitation, hallucinations, agitation,
salivation, difficulty swallowing, convulsions and fear of water (hydrophobia) because of the
difficulty in swallowing
Dumb Rabies
Starts in the same way, but instead of progressing into excitement, the subject retreats
steadily and quietly downhill, with some paralysis, to death. Rabies diagnosis may easily be
missed.
ANIMAL RABIES

It is very similar to human rabies. In the stage of excitement the animal may bite
vigorously and viciously at anything: sticks, stones, grass, other animals and humans, without
provocation. Wild animals may be abnormally tame or appear sick – beware of approaching or
picking up such animals.
An animal infected with rabies carries the virus in its saliva, so if it bites a person, the
virus enters into the person’s body. It’s possible to get rabies from an animal scratch, too.
People sometimes describe animals that have rabies as "foaming at the mouth." This happens
because the animal’s nerves no longer work properly and it can’t swallow its own saliva.
Disease transmission
Most often rabies transmission occurs through the bite of a rabid animal. Rarely,
people contract rabies when saliva from an infected animal comes in contact with their eyes,
nose, mouth or a wound. This may occur if you’re licked by an infected animal. Inhaling the
rabies virus is another potential route of exposure, but one likely to affect only laboratory
workers.
The disease is endemic in wild animals in most parts of the world although some
countries (UK,Australia) have become rabies-free through vigorous control measures and
campaign. The wild animal cycle constitutes the natural reservoir. Wild animals may bite and
infect domestic animals (cattle, horses, pigs, dogs and cats) which in turn may infect man.
Occasionally wild animals may infect man directly. In recent decades, a separate form of dog
rabies spread from dog to dog has been recognized as spreading from West Africaeastwards
and southwards in Africa and Asia.
You’re at greatest risk of contracting rabies if your activities bring you into contact
with the rabies virus or a potentially rabid mammals. People at risk can include veterinarians,
animal caretakers, laboratory workers, hunters, forest rangers and people visiting bat-inhabited
caves.
ANIMAL RESERVOIRS
Mongoose (main reservoir in RSA in the wild), jackals, bats(some evidence to suggest
carrier status and droplet infection), foxes (in Europe), skunks, raccoons (in USA) and semi-
wild dogs.

DIAGNOSIS

If you’ve been bitten or have had contact with an animal that may have rabies, certain
information may help your doctor determine your risk of contracting rabies and how to treat
you. Take note of the following:

Where the incident occurred, a description of the animal and the vaccination status of
the domesticated animal should be found out. If the animal can be safely captured to be tested
for rabies, then if it survives for 8 days it would not be rabid. Another option is for health
professionals to conduct tests on the animal’s brain tissue to determine whether it has rabies.
Testing can be done quickly, but only after the animal is dead.

If you have the signs and symptoms of rabies, a number of tests using blood, saliva,
spinal fluid, brain tissue or skin tissue taken from the nape of your neck may be required to
identify or rule out rabies infection.
Prevention

Ways to help prevent exposure to rabies include: Keep your pets and other
domesticated animals up-to-date with regular animal rabies shots. Avoid contact with wild or
unfamiliar animals, whether they’re alive or dead. Seal or close any openings where animals
might find entry into your home. Report stray animals or any that act strangely or sick to your
local animal control authorities. Teach your children to never handle unfamiliar animals. If
your work or activities might bring you into contact with the rabies virus or a potentially rabid
mammal, consider getting a preventive vaccination. This vaccination — called pre-exposure
prophylaxis — involves three injections over three or four weeks. A booster shot can maintain
the vaccination’s effectiveness

TREATMENT

If bitten by an animal with rabies, thoroughly wash the wound or area of exposure with
soap and water. Quick action is important. Once the earliest signs and symptoms appear, death
almost always follows. Promptly contacting the doctor after a potential rabies exposure greatly
increases chance of survival.

The treatment — called post-exposure prophylaxis — consists of one dose of rabies

immunoglobulin and five doses of rabies vaccine over a 28-day period. Rabies
immunoglobulin and the first dose of rabies vaccine are administered as soon as possible after
the patient has been exposed. The immunoglobulin is given by injection around the site of bite
and into the upper arm muscle.

Immunoglobulins are disease-fighting proteins that provide you with temporary

antibodies. The rabies vaccine helps the body to start producing its own antibodies. Antibody
production takes time, but the antibodies produced by the body provide longer lasting
protection than do the ones contained in rabies immune globulin.

Although the vaccine isn’t painful, there might be mild physical reactions. Watch for
reactions such as swelling or redness where the injection was given. Headache, fever, nausea,
muscle aches and dizziness are other possible side effects. Contact your doctor if side effects
produce discomfort.

RABIES VACCINE

A good but expensive killed virus vaccine (Human Diploid Cell Vaccine,
HDCV) grown in human fibroblasts is available for safe use in man. The unusually long
incubation period of the virus permits the effective use of active immunization with
vaccine post–exposure. When used, vaccine has dramatically cut the rabies death rate. (Older
killed virus vaccines, made from infected neural tissues, were poorly immunogenic and had
allergic encephalitic side effects, but are still used in developing countries.)
Prophylaxis
High-risk persons, e.g. veterinarians, may be immunized before exposure, and then
merely require one or two booster doses if they should be exposed to rabies.
Animal Vaccines
A range of live and killed virus vaccines are available for domestic animals (farm
animals, cats and dogs).

Epidemic Typhus

Several rickettsia species cause the disease known as epidemic typhus in humans. The disease is

spread by ticks, mites, fleas, or lice, each agent having a distinct epidemiology, but all causing a disease

with signs similar to a bad cold with fever lasting form one to several weeks, chills, headache, and

muscle pains, as well as a body rash. There is often a large painful sore at the site of the bite and near by

lymph nodes are swollen and painful.

The four main types of typhus are:

 epidemic typhus
 Brill-Zinsser disease
 endemic or murine typhus
 scrub typhus

EPIDEMIC TYPHUS (European, Classic, Louse-borne)

Epidemic typhus is prevalent worldwide. It is an acute disease passed from human to human by the
body louse. Endemic epidemic typhus exists in highland populations in Africa and South America but
tourists are at minimal risk of acquiring lice and disease. Since World War II, large outbreaks of typhus
have occurred mainly in Africa, with reported cases coming predominantly from three
countries: Burundi, Ethiopia and Rwanda.
Epidemic typhus is caused by Rickettsia prowazekii, which is carried by the body
louse, Pediculus humanus corporis. When the lice feed on a human, they may simultaneously
defecate. When the person scratches the bite, the faeces, which carry the bacteria, are scratched into
the wound. Body lice are common in areas in which people live in overcrowded, dirty cond itions, with
few opportunities to wash themselves or their clothing. Because of this fact, this form of typhus
occurs simultaneously in large numbers of individuals living within the same community.
 Epidemic typhus causes fever, headache, weakness, and muscle aches. It also causes a rash
composed of both spots and bumps. The rash starts on the back, chest, and abdomen, then spreads to
the arms and legs. The worst types of complications involve swelling in the heart muscle or brain
(encephalitis). Without treatment, this type of typhus can be fatal. The disease is characterized by
high fever, intractable headache, and rash. Temperature reaches 104° F in several days and remains
high. Headache is generalized and intense. A macular eruption (dark spot on the skin) appears on
the fifth to sixth day, initially on the upper trunk, which then spreads to the entire body excepting,
usually, the face, palms and soles of the feet. The case-fatality rate is between 1% and 20%.
Prostration is due to low blood pressure, may be followed by vascular collapse. Fatalities are rare in
children; mortality increases with age.

Brill-Zinsser disease is a reactivation of an earlier infection with epidemic typhus. It affects

people years after they have completely recovered from epidemic typhus due to weakening of their
immune system. The bacteria can then gain hold again, causing illness, which tends to be extremely
mild. Brill-Zinsser disease is quite mild, resulting in about a week-long fever, and a light rash similar to
that of the original illness.

TICK TYPHUS (Spotted fever)

Tick typhus, actually a form of spotted fever, is not uncommon in travellers who spend time trekking
or on safari in Africa or the Indian subcontinent. Trekkers in southern Africa may be at risk from cattle or
wild-animal ticks.

Seek local advice on areas where ticks pose a danger and always check your skin carefully for ticks
after walking in a danger area such as a tropical forest. A strong insect repellent can help, and serious
walkers in tick areas should consider having their boots and trousers impregnated with benzyl benzoate
and dibutylphthalate.

SCRUB TYPHUS (Mite-borne typhus)

Scrub typhus is spread by mites that feed on infected rodents and exists mainly on Pacific islands and
in southeast and east Asia. Incidence is highest during the spring and summer when the activity of humans
brings them in contact with mites seeking animal hosts.
Scrub typhus is caused by Rickettsia tsutsugamushi. This bacterium is carried by mites or
chiggers. As the mites feed on humans, they deposit the bacteria. Scrub typhus occurs commonly in
the southwest Pacific,Southeast Asia, and Japan. It is a very common cause of illness in people living in
or visiting these areas. It occurs more commonly during the wet season.

Scrub typhus causes a wide variety of effects. The main symptoms include fever, headache,
muscle aches and pains, cough, abdominal pain, nausea and vomiting, and diarrhea. Some patients
experience only these symptoms. Some patients develop a rash, which can be flat or bumpy. The
individual spots eventually develop crusty black scabs. Other patients go on to develop a more serious
disease, in which encephalitis,pneumonia, and swelling of the liver and spleen (hepatosplenomegaly)
occur. Onset is sudden with fever, chills, headache, and generalized swelling of lymph nodes. At onset
of fever, a red lesion develops at the site of the bite. High fever to 104 °F develops during the first
week as well as a severe headache. A cough is present during the first week of fever and pneumonia
may develop. A rash also develops on the torso often extending to the arms and legs.

MURINE TYPHUS (Rat / flea typhus)

Murine typhus is relatively common throughout the world and is transmitted by fleas. It is clinically
similar to epidemic typhus, but milder. Highest incidence of cases occurs during the summer months when
rats and their fleas are most active and abundant.
Also called endemic typhus, it is carried by fleas. When a flea lands on a human, it may
defecate as it feeds. When the person scratches the itchy spot where the flea was feeding, the
bacteria-laden faeces are scratched into the skin, thus causing infection. The causative bacterium is
called Rickettsia typhi. Endemic typhus occurs most commonly in warm, coastal regions. In the United
States, southern Texas and southernCalifornia have the largest number of cases.

Symptoms of the disease include chills, headache and fever, lasting about 12 days. Rash and other
manifestations are similar to epidemic typhus.
DIAGNOSIS

A number of tests exist that can determine the reactions of a patient’s antibodies (immune
cells in the blood) to the presence of certain viral and bacterial markers. When the antibodies react in
a particular way, it suggests the presence of a rickettsial infection. Many tests require a fair amount of
time for processing, so thepractitioners will frequently begin treatment without completing tests,
simply on the basis of a patient’s symptoms.

PREVENTION,

Prompt removal of attached ticks and use of repellents to prevent tick attachment provide the best
preventions against tick typhus. Laundering of louse-infested clothing is the most effective means to avoid
person-to-person spread of lice and prevent epidemic typhus. Precautions taken when walking in rural
areas and the use of insect repellents will help prevent tick and mite-borne typhus.Prevention for each of
these forms of typhus includes avoidance of the insects that carry the causative bacteria. Other preventive
measures include good hygiene and the use of insect repellents.

VACCINATION

Vaccination against typhus is not required by any country as a condition for entry. Treatment of all
forms of typhus is similar. Production of typhus vaccine in the United States has been discontinued and
there are no plans for commercial production of a new vaccine.
TREATMENT

The antibiotics tetracycline or chloramphenicol is used for treatment of each of the forms of
typhus. Chloramphenicol, doxycycline or other forms of tetracycline result in rapid resolution of fever and
relapses are infrequent. A single dose of 200 mg of doxycycline (two tablets), irrespective of the patient’s
age can be given.
Cleanliness is important in preventing body louse infestations. The easiest control method for
o
occasional infestations is to expose infested clothing to a minimum temperature of 70 C for at least
one hour. In general, chemical control is required, which involves dusting technique to apply
insecticides and treating clothing. Suitable insecticidal dusts for body louse control are permethrin
(0.5%), temephos (2%), propoxur (1%) and carbaryl (5%). One thorough treatment of infested clothing
with insecticide should be sufficient. Dusting is not recommended for people with dermatological
problems or exposed wounds. Where infestation is known to be widespread, systematic application of
insecticide to all persons in the community is recommended.

TUBERCULOSIS
Tuberculosis (TB) is an infectious disease caused by the
bacterium, Mycobacterium tuberculosi. TB most commonly affects the lungs but can involve
almost any organ of the body. There is also a group of organisms referred to as atypical
tuberculosis. These involve other types of bacteria of Mycobacterium family. At times, these
bacteria can cause an infection that sometimes appears as typical tuberculosis. These "atypical"
mycobacteria are: M. kansasii that may produce similar clinical and pathologic symptoms of
disease. M. avium-intracellulare (MAI) seen in persons with AIDS and is not primarily a
pulmonary pathogen but occurs mostly in organs of the mononuclear phagocyte system.

Tuberculosis outside the lungs can appear in the following kinds:

Skeletal Tuberculosis : Tuberculous osteomyelitis, known as Pott’s disease, involves mainly

the thoracic and lumbar vertebrae followed by knee and hip. There is extensive necrosis and
bony destruction with compressed fractures with kyphosis and extension to soft tissues.

Genital Tract Tuberculosis : Tuberculous salpingitis and endometritis result from infection of
the fallopian tube that leads to granulomatous salpingitis, which can drain into the endometrial
cavity and cause agranulomatous endometritis with irregular menstrual bleeding and infertility.
In the male, tuberculosis involves prostate and epididymis leading to infertility.

Urinary Tract Tuberculosis: WBC’s appear in urine but a negative routine bacterial culture
may suggest the diagnosis of renal tuberculosis. Progressive destruction of renal parenchyma
occurs if not treated. Drainage to the ureters can lead to inflammation and ureteral stricture.

CNS Tuberculosis : A meningeal spread can occur and the cerebrospinal fluid typically shows
a high protein, low glucose, and lymphocytosis. The base of the brain is often involved, so that
various cranial nerves may be affected. Rarely, a solitary granuloma, or "tuberculoma", may
form and manifest with seizures.

Gastrointestinal Tuberculosis : This is uncommon today because routine pasteurization of

milk has eliminatedMycobacterium bovis infections. However, M. tuberculosi coughed up in
sputum may be swallowed through contamination. The classic lesions are circumferential
ulcerations with stricture of the small intestine, with ileo-caecal involvement.
Adrenal Tuberculosis : Spread of tuberculosis to adrenals is usually bilateral, so that both
adrenals are markedly enlarged. Destruction of cortex leads to Addison’s disease.

Scrofula: Tuberculous lymphadenitis of the cervical nodes is caused

by Mycobacterium scrofulaceum and may produce a mass of firm, matted nodes just under the
mandible.
There can be chronic draining fistulous tracts to overlying skin. This complication may appear
in children.

Cardiac Tuberculosis: The pericardium is the usual site for tubercular infection of heart. The
result is agranulomatous pericarditis that can be hemorrhagic. There can be fibrosis with
calcification, leading to a constrictive pericarditis.

HISTORY

Robert Koch isolated the tubercular bacillus in 1882 and established TB as an

infectious disease. In the 19th century, due to the absence of antibiotics, patients were isolated
in sanatoria and given treatment. Attempts were made to remove the infectious tissue by
surgery called thoracoplasty. Till the first half of 20th century, no effective treatment was
available. Streptomycin, the first antibiotic to fight TB, was introduced in 1946,
andisoniazid (Laniazid, Nydrazid) became available in 1952.
M. tuberculosis is a rod-shaped, slow-growing bacterium. Its cell wall has high acidic
content, which makes it hydrophobic, resistant to oral fluids. The cell wall absorbs a certain
dye and maintains a red color, hence the name acid-fast bacilli.

MODE OF INFECTION

A person can become infected with tuberculosis bacteria through inhalation of droplets
containing bacillus from the air. The bacteria get into the air when someone with tuberculosis
lung infection coughs, sneezes or spits. TB is not transmitted by just touching the clothes or
shaking the hands of someone who is infected. Tuberculosis is spread primarily from person to
person by breathing infected air especially in closed rooms. TB caused by Mycobacterium
bovis, however, is transmitted by drinking unpasteurized milk. Earlier this bacterium was a
major cause of TB in children, but rarely causes TB now since most milk is pasteurized.

PATHOLOGY

When the inhaled tuberculosis bacteria enter the lungs, they can multiply and cause
pneumonia. The local lymph nodes associated with the lungs may also become involved with
the infection and usually become enlarged. The infection can also spread to other parts of the
body. The body’s immune system in healthy people can fight the infection and stop the
bacteria from spreading. If the body is able to form scar tissue (fibrosis) around the TB
bacteria, then the infection is contained in an inactive state. Such an individual typically has no
symptoms and cannot spread TB to other people. The scar tissue and lymph nodes may
eventually harden due to the process of calcification of the scars. However, if the body’s
immune system is weakened, the TB bacteria can break through the scar tissue. The
breakthrough of bacteria can result in recurrence of the pneumonia and a spread of TB to other
parts of the body. It may take many months from the time the infection initially gets into the
lungs until symptoms develop. The usual symptoms that occur with an active TB infection are
a generalized tiredness or weakness, weight loss, fever, and night sweats. If the infection in the
lung worsens, then further symptoms can include coughing, chest pain, coughing up of sputum
or blood, and shortness of breath. If the infection spreads beyond the lungs, the symptoms will
depend upon the organs involved.

DIAGNOSIS

TB can be diagnosed in several different ways, including chest X-rays, analysis of

sputum, and skin tests. The chest x-rays can reveal evidence of active tuberculosis pneumonia
or scarring (fibrosis) or hardening (calcification) in the lungs. Examination of the sputum on a
slide (smear) under the microscope can show the presence of the tuberculosis bacteria. A
sample of the sputum can also be cultured in special incubators so that the tuberculosis bacteria
can subsequently be identified.

Several types of skin tests are used to screen for TB, e.g. tuberculin skin tests that
include the Mantouxtest, the Tine test, and the PPD (Purified Protein Derivative) test. In each
of these tests, a small amount of purified extract from dead tuberculosis bacteria is injected
under the skin. If a person is not infected with TB, then no reaction will occur at the site of the
injection. If a person is infected with tuberculosis, however, a raised and reddened area will
appear around the site of the test injection within 48 to 72 hours after the injection.

If the infection with tuberculosis has occurred recently, the skin test may be negative,
because usually it takes 2 to 10 weeks after infection for the skin to test positive. The skin test
can also be falsely negative if a person’s immune system is weakened due to another illness
such as AIDS or cancer or he is on medication that can suppress the immune response such as
cortisone or anti-cancer drugs.

TREATMENT

Treatment with antibiotics is recommended to treat as well as to prevent the TB from

turning into an active infection in those where it is dormant. The antibiotic used for this
purpose is called isoniazid (INH). If taken for 6 to 12 months, it will prevent the TB from
becoming active in the future. In fact, if a person with a positive skin test does not take INH,
there is a 5 to 10% lifelong risk that the TB will become active. Takingisoniazid is not
advisable (contraindicated) during pregnancy or for those suffering from alcoholism or liver
disease. Also, isoniazid can have side effects such as rashes, tiredness or irritableness. Liver
damage from isoniazid is rare and typically reverses once the drug is stopped. Very rarely,
however, in older people, the liver damage (INH hepatitis) can even be fatal. It is important
therefore, for the doctor to monitor a patient’s liver by periodically carrying out liver function
tests during the course of INH therapy.

Active TB is treated with a combination of medications

with isoniazid, Rifampicin (Rifadin),ethambutol (Myambutol) and pyrazinamide. Drugs are
often taken for the first two months of therapy to help kill any potentially resistant strains of
bacteria. Then the number is usually reduced to two drugs for the remainder of the treatment
based on drug sensitivity testing. Streptomycin, a drug that is given by injection, may be used
as well, particularly when the disease is extensive. Treatment usually lasts for many months
and sometimes for years. Successful treatment of TB is dependent largely on the compliance of
the patient.
Drug-resistant TB has become a very serious problem in recent years in certain
populations. For example, INH-resistant TB is seen among patients in Southeast Asia. Even
more serious problem is the multi-drug resistant TB that has been seen in prison populations.
Poor compliance by the inmates is thought to be the main reason for the development of multi-
drug resistance.

Surgery on the lungs may be indicated to help cure TB when medication has failed, but
in most cases is not required. Treatment with appropriate antibiotics will usually cure the
disease. Without treatment, however, tuberculosis can be lethal and hence early diagnosis is
important.

SUMMARY

Tuberculosis (TB) is an infection primarily of lungs (a pneumonia), caused by bacteria

calledMycobacterium tuberculosis. It is spread usually from person to person by breathing
infected air during close contacts.
TB can remain in an inactive (dormant) state for years without causing symptoms or
spreading to other people.
When the immune system of a patient with dormant TB is weakened, the TB can
become active and cause infections in the lungs or other parts of the body.
The risk factors for acquiring TB include close-contact situations, alcohol and IV drug
abuse, and certain diseases (e.g., diabetes, cancer, and HIV) and occupations (e.g., health care
workers).
 The most common symptoms of TB are fatigue, fever, weight loss, coughing, and night
sweats.
The diagnosis of TB involves skin tests, chest x-rays, sputum analysis (smear and
culture), and PCR tests to detect the genetic material of the causative bacteria.
Inactive tuberculosis may be treated with an antibiotic, isoniazid (INH), to prevent the
TB infection from becoming active.
Active TB is treated, usually successfully, with INH in combination with one or more
of several drugs, including rifampicin, ethambutol, pyrazinamide, and streptomycin.
Drug-resistant TB is a serious, as yet unsolved, public health problem, especially
in Southeast Asia and in prison populations.
The occurrence of HIV has been responsible for an increased frequency of tuberculosis.
Control of HIV in the future, however, should substantially decrease the frequency of TB.
AMOEBIASIS
Amoebiasis is an infection caused by the protozoan, Entamoeba histolytica, which is usually
contracted by drinking water or eating food contaminated with amoebic cysts. Most of the
infected people are asymptomatic but the disease has the potential to be chronic and it is
estimated by WHO that about 70,000 people die annually worldwide.

Symptoms that appear within 2-4 weeks of infection, can sometimes last for years,
which can range from mild diarrhoea to dysentery with blood and mucus. The blood comes
from the damaged lining of the intestine. In about 10% of invasive cases the amoebae enter the
bloodstream and may travel to other organs in the body, such as liver where blood from the
intestine reaches first but they can end up almost anywhere.

In asymptomatic infections the amoeba lives by eating and digesting bacteria and food
particles in the gut because it does not come in contact with the intestine due to the protective
mucus layer lining the gut. Disease occurs when amoeba comes in contact with the intestinal
lining, when it secretes enzymes that destroy cell membranes and proteins resulting in flask-
shaped ulcers in the intestine. Entamoeba histolytica ingests the destroyed cells by
phagocytosis and is often seen with red blood cells inside. A granulomatous mass known as an
amoeboma may form in the wall of the colon due to persistant cellular response, which may be
confused with cancer.

Symptom of Amoebiasis

Gastroenteritis, diarrhea or dysentery with abdominal pain and exhaustion is the main
symptom of amoebiasis. Poor appetite or fear of food due to abdominal bloating and cramps
and loose stools can occur. Later, with increased intensity of infection, fever, nausea and
bloody stools with slimy mucous occurs and complicates the condition. In due course, the
patient loses weight and stamina. Sometimes allergic reactions can occur throughout the body
due to the release of toxic substances or dead parasites inside the intestines. Dehydration and
gas formation and foul-smelling stools commonly occurs and diarrhea comes and goes. Mucus
and blood appears in the stool.

Diagnosis
Asymptomatic human infections are usually diagnosed by finding cysts shed with the
stool. Various flotation or sedimentation procedures have been developed to recover the cysts
from fecal matter and stains help to visualize the isolated cysts for microscopic examination.
Since cysts are not shed constantly, a minimum of 3 stools should be examined. In
symptomatic infections, the motile form (the trophozoite) can often be seen in fresh feces.
Serological tests exist and most individuals (whether with symptoms or not) will test positive
for the presence of antibodies. The levels of antibody are much higher in individuals with liver
abscesses. Serology only becomes positive about two weeks after infection. More recent
developments include a kit that detects the presence of ameba proteins in the feces and another
that detects ameba DNA in feces. These tests are not in widespread use due to their expense.

Colon biopsy is still by far the most widespread method of diagnosis of amoebic
dysenteri around the world. However it is not as sensitive or accurate in diagnosis as the other
tests available. It is important to distinguish the E. histolytica cyst from the cysts of
nonpathogenic intestinal protozoa such as Entamoeba coliby its appearance.
E. histolytica cysts have a maximum of four nuclei, while the commensal Entamoeba colihas
up to 8 nuclei. Additionally, in E. histolytica, the endosome is centrally located in the nucleus,
while it is off-center in Entamoeba coli. Finally, chromatoidal bodies in E. histolytica are
rounded, while they are jagged in Entamoeba coli. However, other species, Entamoeba
dispar and E. moshkovskii, are also a commensal and cannot be distinguished from E.
histolytica under the microscope. As E. dispar is much more common than E.histolytica in
most parts of the world this means that there is a lot of incorrect diagnosis of E.
histolyticainfection taking place. The WHO recommends that infections diagnosed by
microscopy alone should not be treated if they are asymptomatic and there is no other reason to
suspect that the infection is actually E. histolytica.

Prevention
To help prevent the spread of amoebiasis around the home:

Wash hands thoroughly with soap and hot running water for at least 10 seconds after
using the toilet or changing a baby's diaper, and before handling food
Clean bathrooms and toilets often. Pay particular attention to toilet seats and taps.
Avoid sharing towels or face washers.
Avoid raw vegetables when in endemic areas as they may have been fertilized using
human feces.
Boil water or treat with iodine tablets.
Treatment
E. histolytica infections occur in both the intestine and (in people with symptoms) in
tissue of the intestine and/or liver. As a result two different sorts of drugs are needed to rid the
body of the infection, one for each location. Metronidazole, or related drugs such
a tinidazole or ornidazole are used to destroy amebae that have invaded tissue. It is rapidly
absorbed into the bloodstream and transported to the site of infection. Because it is rapidly
absorbed there is almost none remaining in the intestine. Since most of the amoebae remain in
the intestine when tissue invasion occurs, it is important to get rid of those also or the patient
will be at risk of developing another case of invasive disease. Several drugs are available for
treating intestinal infections, the most effective of which has been shown to
be Paromomycin (also known as Humatin); Diloxanide furoate is used in the US. Both types
of drug must be used to treat infections, with metronidazole usually being given first, followed
by paromomycin or diloxanide. E. dispar does not require treatment, but many laboratories
(even in the developed world) do not have the facilities to distinguish this from E. histolytica.

For amoebic dysentery a multi-prong approach must be used, starting with one of :

Metronidazole, 500-750 mg, three times a day for 5-10 days.

Tinidazole, 2g once a day for 3 days is an alternative to metronidazole.
Ornidazole, 500 mg, twice a day for 5 days.
In addition to the above, one of the following luminal amebicides should be prescribed
as an adjunctive treatment, either concurrently or sequentially, to destroy E. histolytica in the
colon:
Paromomycin, 500mg three times a day for 10 days.
Diloxanide Furoate, 500mg three times a day for 10 days.
Iodoquinol, 650mg three times a day for 20 days.

For amoebic liver abscesses the following drugs are prescribed:

Metronidazole, 400mg three times a day for 10 days.
Tinidazole, 2g once a day for 6 days is an alternative to metronidazole.
Diloxanide furoate, 500mg three times a day for 10 days must always be given afterwards.
Doses for children are calculated on the basis of body weight and a pharmacist should
be consulted for help.
 Yellow FEVER

Yellow fever is a tropical disease that is spread to humans by

infected mosquitoes and is caused by the yellow fever virus. The
disease is found in urban and rural areas of tropical zone countries
in Africa and South America. Yellow fever has not been reported in Asia.
Yellow fever is a viral disease of short duration and varying severity that is transmitted
primarily by mosquitoes. The infection is so named because of the yellow skin colour
(jaundice) observed in people with serious illness. Symptoms of infection can be mild but often
increase in severity with the sudden onset of fever, muscle pain, nausea, vomiting, headache
and prostration. The disease may progress to visible haemorrhage, jaundice, kidney and liver
failure. The death rate in unvaccinated people may be as high as 50 per cent.

Yellow fever virus belongs to the Flaviviridae family, other members of which cause
dengue fever. The virus is introduced into the bloodstream via the saliva of the mosquito as it
bites. The virus can then be transported around the body and reproduce itself in a variety of the
body’s cells, usually the liver, kidneys and blood vessels. In serious cases, these cells may
become damaged themselves. In addition, the cells of the immune system are affected and
release large quantities of signalling substances. These substances are the cause of the normal
disease symptoms, such as muscular pain and fever.

Jungle yellow fever is mainly a disease of monkeys. It is spread from infected

mosquitoes to monkeys in the tropical rain forest. People get jungle yellow fever when they
put themselves in the middle of this natural cycle and are bitten by mosquitoes that have been
infected by monkeys. Jungle yellow fever is rare and occurs mainly in persons who work in
tropical rain forests.

Urban yellow fever is a disease of humans. It is spread by mosquitoes that have been
infected by other people. Aedes aegypti is the type of mosquito that usually carries yellow
fever from human to human. These mosquitoes have adapted to living among humans in cities,
towns, and villages. They breed in discarded tyres, flower pots, oil drums, and water storage
containers close to human dwellings. Urban yellow fever is the cause of most yellow fever
outbreaks and epidemics. People get yellow fever from the bite of an infected female mosquito.
The mosquito injects the yellow fever virus into the bite.

Yellow fever is common in West and Central Africa and in parts of South America.
Periodic epidemics in Africa lead to hundreds of thousands of cases. In total, yellow fever
occurs in 33 countries and 468 million people are at risk of catching the disease.
SYMPTOMS

Many yellow fever infections are mild, but the disease can cause severe, life-
threatening illness. Symptoms of severe infection are high fever, chills, headache, muscle
aches, vomiting, and backache. After a brief recovery period, the infection can lead to shock,
bleeding, and kidney and liver failure. Liver failure causes jaundice which is revealed by the
yellowing of skin and the whites of the eyes, which gives yellow fever its name. Symptoms
start 3 to 6 days after being bitten by an infected mosquito. Severe yellow fever infections can
be fatal.

DIAGNOSIS

Yellow fever is diagnosed by a blood test in the laboratory, where specific yellow fever
virus antibodies are detected in the blood.

PREVENTION

Yellow fever can be prevented by vaccination. Travellers should also take precautions
against mosquito bites when in areas with yellow fever transmission. If necessary, get
vaccinated for yellow fever before travel.

 Travellers should get vaccinated for yellow fever before visiting areas where yellow fever is
found.
 International regulations require proof of yellow fever vaccination for travel to and from certain
countries. People who get vaccinated should be given an International Certificate of Vaccination.
 Avoid mosquito bites when travelling in tropical areas. Mosquitoes that spread yellow fever
usually bite during the day. Travellers should take steps to reduce contact with mosquitoes
when outdoors and inside.
 Wear long-sleeved clothing and long pants. For extra protection, treat clothing with the
insecticide permethrin or any other suitable insecticide.
 Use insect repellent on exposed skin. The most effective repellents contain 20% to 35% DEET (N,
N-diethylmethyltoluamide).
 Spray living and sleeping areas with insecticide.
 Use a mosquito net when sleeping in a room that is not screened or air conditioned. For extra
protection, treat the bed net with the insecticide permethrin.
TREATMENT

There is no specific treatment for yellow fever. Persons with yellow fever should rest and drink
plenty of fluids. There are no medicines that are effective against this virus.
Serious cases of yellow fever always need hospital treatment. As there are no medicines that combat
the virus itself and the doctor can only treat the symptoms. If there is lack of fluid in the body leading
to disturbances in the electrolyte balance, this can be remedied by administration of fluids by
intravenous drip. In mild cases, the pain may be relieved with simple painkillers. High temperatures
can be treated by cooling the patient and giving appropriate medicines to lower the temperature.

VACCINATION REQUIREMENT

Many countries, particularly those in Asia, will refuse permission to enter to any person
who has recently been in a yellow fever infected country and who does not possess a valid
yellow fever vaccination certificate. Some countries will only allow unvaccinated persons to
enter if they agree to be vaccinated at their border. In this situation, you may not be able to
ensure the sterility of the items used to administer the vaccine.

To obtain a valid international yellow fever vaccination certificate you must be given a yellow
fever vaccine that has been approved by the WHO from a vaccination provider who has been
approved by a national health authority. The certificate must be in a form that has been approved by
the WHO and be completed according to WHO requirements. The disease is covered by the
International Quarantine Regulations, which are taken very seriously by authorities everywhere.
Vaccination provides protection for 10 years.

If a traveller is unvaccinated and contracts yellow fever the consequences can be

serious and may result in death.

KALA-AZAR
Leishmaniasis is a disease caused by the flagellate protozoan that belongs to the
genus Leishmania and is transmitted by the bite of sand flies of the genus Lutzomyia in
the New World and Phlebotomus in the Old World. The disease was named in 1901 after the
Scottish pathologist William Boog Leishman. This disease is also known as Leishmaniasis,
Orient Boils, Baghdad Boil, kala azar, black fever, sand fly disease, Dum-Dum fever or
espundia. Human infection is caused by about 21 species of Leishmania that include L.
donovani-complex with three species (L. donovani, L. infantum, and L. chagasi); the L.
mexicana-complex with 3 main species (L. mexicana, L. amazonensis,
and L. venezuelensis); L. tropica; L. major; L. aethiopica and the subgenus Viannia with four
main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L.
(V.)peruviana). The different species are morphologically indistinguishable, but they can be
differentiated by isoenzyme analysis, DNA sequence analysis, or by monoclonal antibodies.

Leishmaniasis is commonly found in Mexico, Central America, and South America—

from northern Argentina to southern Texas (not in Uruguay, Chile, or Canada), southern
Europe, Asia (not Southeast Asia), the Middle East, and Africa (particularly East and North
Africa). The disease is not found in Australia orOceania.

There are four main forms of leishmaniasis:

Visceral leishmaniasis – the most serious form and potentially fatal if untreated.
Cutaneous leishmaniasis – the most common form which causes a sore at the bite site, which
heal in a few months to a year, leaving an unpleasant looking scar. This form can progress to
any of the other three forms.
Diffused cutaneous leishmaniasis – this form produces widespread skin lesions which
resemble leprosy and is particularly difficult to treat.
Mucocutaneous leishmaniasis – commences with skin ulcers which spread causing tissue
damage to nose and mouth

LIFE CYCLE

Leishmaniasis is transmitted by the bite of female phlebotomine sand flies. The sand
flies inject into human blood the infective stage, metacyclic promastigotes, during blood meals.
Metacyclic promastigotes that reach the puncture wound are phagocytized by macrophages but
are not digested and transform into amastigote form. Amastigotes multiply in infected cells and
affect different tissues, depending upon the part on whichLeishmania species is involved.
These differing tissue specificities cause the differing clinical manifestations of the various
forms of leishmaniasis. Sand flies become infected when blood meals are sucked from the
infected host when they ingest macrophages infected with amastigote forms. In the sandfly's
midgut, the parasites change into promastigote forms, which multiply, differentiate into
metacyclic promastigotes and migrate to the proboscis from where they can be easily
transferred into human blood while sand fly feeds.

SYMPTOMS

A nodule appears in the area of the sand fly bite or rash or ulceration may be formed.
Four to six months after the bite, the following symptoms appear: Fevers twice a day with
chills and sweats, cough, weakness, diarrhoea, weight loss, gums and nose may bleed and skin
or eyes may turn yellow.

DIAGNOSIS

The spleen becomes extremely enlarged and hard. Liver becomes enlarged. The skin
turns darker in colour and warty eruptions appear on skin or ulcers may occur. Rashes of small,
red colour appear or raised lesions are found.
LABORATORY TESTS

Leishmania donovani infection is identified on the following tests:

 Buffy coat preparation of the blood is a special technique of preparing blood

film on slides, bone marrow, liver, lymph nodes, or the spleen for identification
of the causative organism. The organism may also be cultured and then
identified.

 IgM (an antibody reaction to the organism) agglutination testing is positive in

infected persons.

 White blood cell count is usually low in patients.

 The total protein in the blood becomes elevated (10g/dL or more), while
albumin level is low (3g/dL).

TREATMENT

The most common treatment for visceral leishmaniasis was developed in1930s, using
derivatives of antimony. Sodium stibogluconate (SSG) is taken as an intramuscular injection
over 30 or more days. It is available under the brand name Pentostam. Another antimonial
drug is Meglumine antimoniate available under the brand name Glucantime. It is not
completely understood how these drugs act against the parasite. They may be disrupting its
energy production or trypanothione metabolism. Unfortunately, in many parts of the world, the
parasite for visceral or muco–cutaneous leishmaniasis has become resistant to antimony drugs
but the level of resistance varies according to species.
Amphotericin is now the treatment of choice. AmBisome is an amphotericin B
liposome formulation that is given as an intravenous infusion. AmBisome was registered for
VL in the USA and Europe in the 1990s and has shown remarkable efficacy even after a single
dose in India.
Miltefosine (Impavido) is a new drug for visceral and cutaneous
leishmaniasis. Oral miltefosine was registered in India in 2002 and is now in Phase IV trials.
Currently, two drugs are under development, a drug to treat Chagas disease in Latin
America and a drug, Paromomycin to cure visceral leishmaniasis
in India. Paromomycin (aminosidine) is a low-cost intramuscular formulation that was
registered in late 2006 in India and is currently in Phase III trials in East Africa.
FILARIASIS

Filariasis is an infectious tropical disease caused by three thread-like parasitic filarial

worms,Wuchereria bancrofti, Brugia malayi, and Brugia timori, all transmitted by mosquitoes.
Lymphatic Filariasis, known as Elephantiasis puts at risk more than a billion people in more
than 80 countries. Over 120 million are already affected by and over 40 million of them are
seriously incapacitated and disfigured by the disease. One-third of the infected people live
in India, one third in Africa and the rest are in South Asia, the Pacific and theAmericas.

PATHOGENS

Pathogenic filarial parasites affect the lives of millions of people, especially those
living in tropical countries. The filarial parasites that pose the most serious public health
threats are Wuchereria bancrofti, Brugia malayi, Brugia timori, Onchocerca volvulus, and Loa
loa. All of these cause cutaneous manifestations. One filarial nematode, Mansonella
streptocerca, also causes cutaneous changes but is not a significant public health threat.

Human Filarial Parasites and Their Vectors

Disease Parasite Vector

Onchocerciasis O. volvulus Blackflies: Simulium species
Bancroftian Mosquitoes: Anopheles, Aedes,
W. bancrofti
filariasis Culex, and Mansoniaspecies
Malayan B. malayi and B. Mosquitoes: Anopheles, Aedes,
filariasis timori Culex, and Mansoniaspecies
Loiasis Loa loa Red flies: Chrysops species
Mansonelliasis M. streptocerca Midges: Culicoides species
Dirofilariasis Dirofilaria species Mosquitoes: Culex species

LIFE CYCLE

The thread-like, parasitic filarial worms Wuchereria bancrofti and Brugia malayi that
cause lymphatic filariasis live almost exclusively in humans. These worms are lodged in the
lymphatic system, the network of nodes and vessels that maintain the delicate fluid balance
between the tissues and blood and are an essential component for the body’s immune system.
They live for 4-6 years, producing millions of immature microfilariae (minute larvae) that
circulate in the blood. The disease is transmitted by mosquitoes that bite infected humans and
pick up the microfilariae that develop, inside the mosquito, into the infective stage in a process
that usually takes 7-21 days. The larvae then migrate to the mosquitoes’ mouth-parts, ready to
enter the punctured skin following the mosquito bite and completing the cycle.

SYMPTOMS
 Patients suffer from hydrocoel (fluid- filled balloon- like enlargement of scrotal sacs)
and elephantiasis of the legs and penis. Elephantiasis of the entire leg, the entire arm, the vulva
or the breast (swelling up to several times normal size) can take place.
Elephantiasis affects mainly the lower extremities and is caused when the parasites are lodged
in the lymphatic systemand block lymph flow. W. bancrofti can affect the legs, arms, vulva,
breasts, while Brugia timori rarely affects the genitals. Infection by Onchocerca volvulus and
the migration of its microfilariae through the cornea of eye is a major cause of blindness.

DIAGNOSIS

Until very recently, diagnosing lymphatic filariasis had been extremely difficult, since
parasites had to be detected microscopically in the blood, and in most parts of the world, the
parasites have a "nocturnal periodicity" that restricts their appearance in the blood to only the
hours around midnight. The diagnosis is made by identifying microfilariae on a stained blood
film. Blood must be drawn at night, since the microfilariae circulate at night when their vector,
the mosquito, is most likely to bite.

The new development of a very sensitive, very specific simple "card test" to detect
circulating parasite antigens without the need for laboratory facilities and using only finger-
prick blood droplets taken anytime of the day has completely transformed the approach to
diagnosis.

TREATMENT

Vector control, use of mosquito nets, and improved living conditions are still vital for
the control of these infections.

The drugs of choice for killing adult worms are Albendazole and Ivermectin.
Ivermectin (dihydroavermectin) is the drug of choice for the treatment of onchocerciasis. It is
a macrocyclic lactone derived from the actinomycete, Streptomyces avermitilis found in soil. It
functions as a single dose and is effective microfilaricide for O. volvulus.
Unlike diethylcarbamazine (DEC), ivermectin does not produce reaction in onchocerciasis
because it acts by paralyzing the microfilariae in the skin tissue spaces and lymphatics. They
are then swept away into the local lymph nodes, which may swell up and only cause some
local limb edema. On the other hand, DEC "unmasks" the microfilariae in the tissue spaces
where they are attacked by the various protective cells which cause reaction in the skin.

The addition of oral doxycycline (100 mg/d) given for 6 weeks from the start of
ivermectin to kill offWolbachia organisms enhanced the effects of ivermectin.
 Diethylcarbamazine or DEC (Hetrazan) is a microfilaricide with no effect on the adult
worm. It produces Mazzotti reactions that become severe in heavily infected persons. A low
dose of dexamethasone (3 mg/d) after onset of Mazzotti reaction controls the progression of
reaction without interfering with the macrofilaricidal efficacy of DEC.

Suramin is a microfilaricide given intravenously, starting with a test dose of 100 mg of

fresh 10% solution over 2 minutes. If no hypersensitivity develops, weekly dosages of 0.2 g,
0.4 g, 0.6 g, 0.8 g, and 1 g are given to adult patients. Rarely, patients experience eye lesions,
dermatitis, kidney damage, a Mazzotti- like reaction and/or death. Thus, the use of suramin
requires great caution and hence is generally not recommended.

Amocarzine is a new oral macrofilaricidal compound that has promising effects on

onchocerciasis inLatin America.

Doramectin (Dectomax, Pfizer) is a new drug related to ivermectin. Its efficacy and
safety in onchocerciasis are untested.

NODULECTOMY

A useful adjunct to chemotherapy popular in South America is removal of the palpable

nodules. InAfrica, nodulectomy has never been practiced widely because the nodules tend to
be deeper and located near delicate joint spaces. Alternatively, chloroquine can be injected
into young nodules that kill the worms.

Wolbachia organisms appear to play a critical role in the biology and metabolism of
filarial worms. The use of tetracycline to kill Wolbachia appears to be lethal to the adult O.
ochengi and recent evidences suggest that it is also effective against O. volvulus and perhaps
other filarial worms.

SMALLPOX
Smallpox, which is believed to have originated over 3,000 years ago in India or Egypt, is one
of the most devastating diseases known to mankind. Smallpox killed Queen Mary II
of England, Emperor Joseph I ofAustria, King Luis I of Spain, Tsar Peter II of Russia, Queen
Ulrika Elenora of Sweden and King Louis XV ofFrance.

The causative agent, Variola virus is a member of the genus Orthopoxvirus,

subfamilyChordopoxvirinae of family Poxviridae. Other members of the genus include
cowpox, camelpox, and monkeypox, the last one has caused the most serious recent human
poxvirus infections.
 The Variola virus measures 260 by 150 nanometers and contains a molecule of double-
stranded DNA, coding for some 200 different proteins. It is one of the largest viral genomes
known and this large size of the genome makes it especially difficult to create a synthetic copy
of the virus.

There are two forms of smallpox virus out of which Variola major causes the severe
and most common form of smallpox, with a more extensive rash and higher fever. There are
four strains of Variola major, namely,ordinary type that accounts for 90% or more of
cases; modified type which is mild and occurs in previously vaccinated persons; flat
type and haemorrhagic type, the last two of which are rare but very severe and fatal.
Historically, Variola major has an overall fatality rate of about 30%. Variola minor causes a
less common form of smallpox that is much less severe disease, with death rates of less than
1%.

The smallpox disease has now been eradicated after a successful worldwide vaccination
program. The last case of smallpox in the United States was in 1949. The last naturally
occurring case in the world was in Somalia in 1977.

TRANSMISSION

Smallpox can be spread through direct contact with infected body fluids or contaminated
objects such as bedding or clothing. Exposure to the virus is followed by an incubation period
during which people do not have any symptoms and may feel fine. This averages about 12 to
14 days but can range from 7 to 17 days. During this time, people are not contagious.

SYMPTOMS

The first symptoms of smallpox include fever, malaise, head and body aches and
sometimes vomiting. The fever is usually high, in the range of 101 to 104 degrees Fahrenheit.
At this time, people are usually too sick to carry on their normal activities. This is called
the prodrome phase and may last for 2 to 4 days. Rashesemerge first as small red spots on the
tongue and mouth. Later, red spots change into sores that break open and spread large amounts
of virus into the mouth and throat. At this time, the person becomes most contagious. Then
rashes appear on the skin, starting on the face and then spreading to the arms and legs and then
to the hands and feet. Usually the rashes spread to all parts of the body within 24 hours. As the
rashes appear, fever usually falls and the person may start to feel better. By the third day, the
rashes become raised into bumps. By the fourth day, the bumps fill with a thick, opaque fluid
and often have a button-like depression in the center. Fever often will rise again at this time
and remain high until scabs form over the bumps. The bumps becomepustules which
are sharply raised, usually round and firm to the touch. The pustules begin to form a crust and
then turn into scabs. By the end of the second week after the rashes appear, most of the sores
are scabbed over. Then the scabs begin to fall off, leaving marks on the skin that eventually
turns into pitted scars. Most scabs fall off by the fourth week after the rashes appear. The
disease is contagious to others until all of the scabs have fallen off.
There is no animal reservoir of the disease and insects do not play any role in
transmission.

In the past, smallpox was sometimes confused with chickenpox, a worldwide infection
of children that is seldom lethal. Chickenpox can be distinguished from smallpox by its much
more superficial lesions, their appearance more on the trunk than on face and extremities, and
by the development of successive crops of lesions in the same area.
TREATMENT

The disease, for which no effective treatment is known, killed as many as 30% of
infected persons. Between 65–80% of the survivors were left with deep pitted scars or
pockmarks, most of which are prominent on the face.

Edward Jenner (1798) demonstrated that inoculation with cowpox could protect against
smallpox, which brought the first hope that the disease could be controlled.
Through the success of global eradication campaign smallpox was finally restricted back
to Africa and then to a single last natural case that occurred in Somalia in 1977. A fatal
laboratory-acquired case occurred in theUnited Kingdom in 1978. The global eradication of
smallpox was certified, based on intense verification activities in several countries by a
commission of eminent scientists in December 1979 and subsequently endorsed by the World
Health Assembly in 1980. The vaccination administered up to 4 days after exposure to the
virus and before the rashes appear, provides protective immunity and prevents severity of the
disease.

No effective treatment, other than the management of symptoms, is currently

available. A number of compounds are under investigation as chemotherapic agents. One of
these, Cidofovir, has produced promising results in laboratory studies.

Due to the success of an intense worldwide public health campaign, no naturally

occurring case of this deadly disease has occurred since October 26, 1977, when an
unvaccinated hospital cook in Somalia became the last person to have naturally contracted the
smallpox virus.

The World Health Organization (WHO) officially declared smallpox eradicated in

1980.
VACCINES

In 1796, Edward Jenner tested his theory of disease protection by inoculating a young
boy with material obtained from a milkmaid who was infected with the milder cowpox virus.
The success of that experiment led to the development of a vaccine ( name from vacca, the
Latin word for cow) against smallpox.

Smallpox vaccine contains live Vaccinia virus of the orthopoxvirus family and closely
related to Variolavirus, the agent that causes smallpox. Immunity resulting from immunization
with Vaccinia virus protects against smallpox. Vaccination usually prevents smallpox infection
for at least ten years. Most existing vaccine stocks and the vaccine used in the WHO
eradication campaign consist of pulp scraped from Vaccinia-infected animal skin, mainly calf
or sheep, with phenol added to a concentration sufficient to kill bacteria but not so high as to
inactivate the Vaccinia virus. The vaccine is then freeze dried and sealed in ampules for later
re-suspension in sterile buffer and subsequent intradermal inoculation by multiple puncture
with a bifurcated needle.

CURRENT LOCATIONS OF SMALLPOX VIRUS

Only two laboratories in the world are known to house smallpox virus, namely,
the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, and the State
Research Center of Virology and Biotechnology in Koltsovo, Russia. The seed virus
(Vaccinia virus strain Lister Elstree) used for producing vaccine is being held for WHO by
the WHO Collaborating Centre for Smallpox Vaccine in Bilthoven, theNetherlands.

PLAGUE
Bubonic plague is mainly a disease of rats and rat fleas (Xenopsylla cheopis). Infection in
a human occurs when a person is bitten by an infected flea. The bacteria multiply inside the
stomach of flea by forming a mucilaginous plug at the entry to gizzard that blocks its passage
and causes the flea to starve. The ever-hungry flea then bites again and again to feed as it
cannot satisfy its hunger. In 1894, two bacteriologists, Alexandre
Yersin of France and Shibasaburo Kitasato of Japan working in Hong Kong isolated the
bacterium responsible for plague. Though both investigators reported their findings, a series of
confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin
as the primary discoverer of the organism. Yersin named it Pasteurella pestis in honor of the
Pasteur Institute, Paris, where he worked. In 1967 it was renamed as Yersinia pestis in honor
of AlexandreYersin.

In 1898, the French scientist, Paul-Louis Simond, who was working in China to battle
the epidemic, established that rat-flea was vector of the disease.

PATHOLOGY
An infected flea bites man and contaminates the wound with regurgitated blood that contains
the plague bacteria. Yersinia pestis can reproduce inside cells, so even if phagocytised, they
can still survive inside macrophage. Once inside body, bacteria enter lymphatic system.
Plague bacteria secrete several toxins, one of which is known to cause dangerous beta-
adrenergic blockade. Y. pestis spreads through the lymphatics of the infected person until it
reaches a lymph node, where it stimulates severe hemorrhagic inflammation causing the lymph
nodes to swell, the condition is called the characteristic "bubo" that is associated with the
disease.

Lymphatics ultimately drain into the bloodstream, so the plague bacteria enter blood
and travel to any part of body. In septicemic plague, there is rupture of blood capillaries of the
skin and other organs which creates black patches on the skin. There are red bite-like bumps on
the skin. Untreated, septicemic plague is universally fatal, but early treatment with antibiotics
reduces the mortality rate to between 4 and 15 percent. People who die from this form of
plague often die on the same day symptoms first appear.

The pneumonic plague infects the lungs and infection spreads from person-to-person
transmitted through respiratory droplets released by coughing. The incubation period for
pneumonic plague is usually between two and four days, but sometimes can be as little as a
few hours. The initial symptoms, of headache, weakness, and coughing with hemoptysis are
indistinguishable from other respiratory illnesses. Without diagnosis and treatment, the
infection can be fatal in one to six days and mortality in untreated cases is 50–90%.

SYMPTOMS

Infected persons usually start with flu-like symptoms after an incubation period of 3-7
days. Patients typically experience the sudden onset of fever, chills, head and body-aches and
weakness, vomiting and nausea. Clinical plague infection manifests itself in three forms
depending on the route of infection: bubonic, septicaemic and pneumonic.

Bubonic plague is the most common form of plague resulting from the bite of an
infective flea. Plague bacillus enters the skin from the site of the bite and travels through the
lymphatic system to the nearest lymph node. The lymph node then becomes inflamed because
the plague bacteria replicate there in large numbers. The swollen lymph node is called a
"bubo" which is very painful and can become suppurated as an open sore in advanced stage of
infection. Symptoms of bubonic plague generally appear within two to eight days after the
flea-bite. The bubo is usually 1 to 10 centimeters in diameter, in groin, armpit or neck,
swollen, painful and warm to touch. It can cause so much pain that you can’t move the affected
part of body. More than one bubo can develop, but typically buboes affect only one area of
your body.
 Septicaemic plague occurs when infection spreads directly through the bloodstream
without evidence of a "bubo". Septicaemic plague may result from flea bites and from direct
contact with infective materials through cracks in the skin.

Pneumonic plague is the most severe and least common form of plague that occurs
due to a secondary spread from the advanced infection of an initial bubonic form. Primary
pneumonic plague results from inhalation of infective droplets released into the air by
coughing patients and can be transmitted from human to human without involvement of fleas.
Untreated pneumonic plague has a very high fatality ratio.

PREVENTION
People who live and work in areas with active plague infection should take these
precautions:

 Eliminate food and shelter for rodents around homes, work places, and certain recreation
areas, such as picnic sites or camp-grounds where people congregate. Remove brush,
rock piles, junk, and food sources, including pet food.
 Health authorities should use appropriate and licensed insecticides to kill fleas during the
plague outbreaks in wild animals.
 Treat pets such as cats and dogs for flea control regularly.
 Avoid sick or dead animals and report such animals to the health department. Hunters
and trappers should wear rubber gloves when skinning animals.
 Use insect repellents when outdoors in areas where there is a risk of flea exposure.
Preventive treatment with antibiotics is recommended for:

 People who are bitten by fleas or who are exposed to tissues or fluids from a plague-
infected animal.

 People living in a household with a bubonic plague patient, since they may also be
exposed to infected fleas.

 People in close contact with a person or pet with suspected plague pneumonia.

People who travel to countries where plague occurs should take these additional
precautions:

 Avoid exposure to fleas from diseased rats. The risk of being bitten by infected fleas is
especially high after large numbers of plague-infected rats have died. Therefore, avoid
places that are infested with rats.
 If travel to such areas is essential, apply insect repellents to legs and ankles. Also apply
repellents and insecticides to clothes and outer bedding.
 Take preventive antibiotics if the risk of exposure is high.
TREATMENT

Vladimir Havkin, a doctor of Russian-Jewish origin who worked in India, was the first
to invent and test a plague antibiotic. The traditional treatments are:

Streptomycin 30 mg/kg of body weight, twice daily for 7 days

Chloramphe nicol 25–30 mg/kg of body weight, single dose, followed by 12.5–15 mg/kg of
body weight, 4 times daily
Tetracycline 2 g single dose, followed by 500 mg, 4 times daily for 7–10 days. The drug is
not suitable for children).
Gentamicin 2.5 mg/kg of body weight, twice daily for 7 days.
Doxycycline 100 mg (adults) or 2.2 mg/kg of body weight for children, orally twice daily have
also been shown to be effective.

VACCINATION

Plague vaccines at one time were widely used but have not proven to be successful in
preventing plague effectively. Vaccines are not recommended for protection in outbreak
situations. Vaccination is only recommended as a prophylactic measure for high-risk groups
such as laboratory personnel who are constantly exposed to the risk of contamination.
A formalin- inactivated vaccine is available for adults of high risk group but severe
inflammatory reactions frequently appear. Primary intramuscular injection is given, followed
by boosters at 3-5 months and another booster at 5-6 months. Then 3 more booster shots are
given at 6 months interval, followed by doses at 1-2 year interval.

MALARIA
Malaria is one of the most common infectious diseases and an enormous public
health problem. The disease is caused by a protozoan parasites of the
genus Plasmodium, which is usually referred to as malaria parasites.
The term malaria originated from the medieval Italian term, mala
aria meaning “bad air” and the disease was formerly called marsh fever due to its
association with swamps.
In 1880, a French army doctor working at the military hospital in Algeria
named Charles Louis Alphonse Laveran observed malarial parasites for the first
time inside the red blood cells of people suffering from malaria. For this and later
discoveries, he was awarded the 1907 Nobel Prize for Physiology or Medicine. The
protozoan was named Plasmodium by the Italian scientists Ettore
Marchiafava and Angelo Celli. A year later, Carlos Finlay, a Cuban doctor
treating patients with yellow fever in Havana, first suggested that mosquitoes were
transmitting disease to humans. However, it was Sir Ronald Ross working in India
who finally proved in 1898 that malaria was transmitted by mosquitoes to birds. He
isolated malarial parasites from the salivary glands of mosquitoes that had fed on
infected birds. For this work Ross received the 1902 Nobel Prize in Medicine. The
findings of Finlay and Ross were confirmed by a medical board headed by Walter
Reed in 1900.
MALARIA PARASITES
Malaria is caused by protozoan parasites of the genus Plasmodium (Phylum
Apicomplexa). In humans malaria is caused by P. falciparum, P. malariae, P.
ovale, and P. vivax, the last one is the most common one responsible for about 80 %
of all malaria cases. However, P. falciparum is the most deadly one, responsible for
about 15% of infections but 90% of deaths. Parasitic Plasmodium species also infect
birds, reptiles, monkeys, chimpanzees and rodents. There have been documented
human infections with several simian species of malaria, namely P. knowlesi, P.
inui, P. cynomolgi, P. simiovale, P. brazilianum, P. schwetzi and P. simium.
LIFE CYCLE
The parasite’s primary (definitive) hosts and vectors are female mosquitoes
of the Anopheles genus. A mosquito becomes infected when it takes a blood meal
from an infected human. Once ingested, the parasite’sgametocytes, taken up along
with the blood differentiate into male or female gametes, which fuse to
formzygote in the mosquito gut. The zygote is also called ookinete that penetrates
the gut lining and produces anoocyst outside the stomach wall. The diploid zygote
first undergoes reduction division and then divides by multiple fission to produce
haploid sporozoites inside the oocyst. When the oocyst ruptures, sporozoites are
released that migrate through the mosquito’s body to reach salivary glands, where
they are ready to infect a new human host when the mosquito bites a healthy man.
This type of transmission is occasionally referred to as anterior station transfer. Only
female mosquitoes feed on blood, thus males do not transmit the disease..
Malaria in humans develops via two phases: an exoerythrocytic (hepatic)
and an erythrocytic phase. When an infected mosquito pierces a person’s skin to
take a blood meal, sporozoites in the mosquito’s saliva enter the bloodstream and
migrate to the liver. Within 30 minutes of being introduced into the human host,
they infect hepatocytes, multiplying asexually to form schizont for a period of 6–15
days. Once in the liver they produce thousands of cryptozoites and
secondary metacryptozoites, which, following rupture of their host cells escape into
the blood and infect red blood cells, thus beginning the erythrocytic stage of the life
cycle. The parasites escape from the liver undetected by wrapping themselves in the
cell membrane of the host liver cell. Within red blood cells the parasites multiply
further asexually producing schizont that burst to release about two dozens
of merozoites that invade fresh red blood cells. Such cycles continue to occur every
48 hours causing chill and fever at the release of merozoites from RBCs.
Some P. vivax and P. ovale sporozoites do not immediately develop into
exoerythrocytic merozoites but instead produce hypnozoites that remain dormant
for periods ranging 6–12 months to as long as three years. After a period of
dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for
long incubation and late relapses in these two species of malaria.
The parasite is protected from attack by the body’s immune system because
for most of its life it resides within the liver and blood cells and is hidden from
immune surveillance. However, circulating infected blood cells are destroyed in the
spleen. To avoid this, P. falciparum produces adhesive proteins on the surface of the
infected blood cells, causing the blood cells to stick to the walls of smaller blood
vessels, thereby sequestering the parasite from the passage through the general
circulation and spleen. This stickiness of RBCs is the main factor that gives rise to
hemorrhagic complications associated with falciparum malaria. The smallest
branches of the circulatory system can be blocked by the attachment of masses of
these infected red blood cells. In cerebral malaria the sequestrated red blood cells
can breach the blood brain barrier, leading to coma.
Although the red blood cell surface adhesive proteins
(called PfEMP1 for Plasmodium falciparumerythrocyte membrane protein 1) are
exposed to the immune system, they do not serve as good immune targets because of
their extreme diversity. There are at least 60 types of these proteins within a single
parasite and perhaps limitless types in general parasite populations. Also, the
parasite switches between a broad repertoire ofPfEMP1 surface proteins thus
staying one step ahead of the pursuing immune system.
TREATMENT
The first effective treatment for malaria was the bark of cinchona tree,
which contains quinine. This tree grows on the slopes of the Andes, mainly in Peru.
Treatment with Chloroquine

Day 1 4 tablets (600mg base) or 10 mg/kg first dose.

2 tablets (300mg base) or 5 mg/kg 6-8 hours later.

Day 2 2 tablets (300mg base) or 5 mg/kg.

Day 3 2 tablets (300mg base) or 5 mg/kg

Next 14 Primaquine, 2 tablets (each tablet contains 7.5 mg base

days daily with food).

Most drugs used in treatment of malaria are active against the parasite stages
in blood and include the following:
Chloroquine
Sulfadoxine-pyrimethamine combination
Mefloquine
Atovaquone-proguanil combination
Quinine
Doxycycline
Artemisinin derivatives
In addition, primaquine is active against the dormant parasite in liver
called hypnozoites and hence prevents relapses. Primaquine should not be taken by
pregnant women or by people who are deficient in G6PD (glucose-6-phosphate
dehydrogenase).
Mefloquine is an antimalarial agent that acts as a blood schizonticide. It is
effective against all species of malaria (P. falciparum, P. vivax, P. malariae and P.
ovale). Its exact mechanism of action is not known. Mefloquine is active against the
erythrocytic stages of Plasmodium species. However, the drug has no effect against
the exoerythrocytic (hepatic) stages of the parasite and mature
gametocytes. Mefloquine is effective against malaria parasites resistant to
chloroquine and other 4-aminoquinoline derivatives, proguanil, pyrimethamine and
pyrimethamine-sulphonamide combinations.
Malarone (Atovaquone 250 mg plus Proguanil 100 mg), 4 tablets daily for
three consecutive days. This combination therapy is relatively new and appears to
be very effective but it is also very expensive.
For over 1,500 years Chinese have used leaves from Artemisia annua shrub
(sweet wormwood) to treat malaria. However, it is only in the late 1960s that its
anti-malarial ingredient, artemisinin was identified and extracted.
Today, artemisinin is considered the treatment of choice for
uncomplicated falciparum malaria, as prescribed by the World Health Organization
in 2001.
BENEFICIAL EFFECTS OF MALARIA
Sickle-cell disease
Distribution of malaria.The best-studied influence of the malaria parasite
upon the human genome is the blood disease, sickle-cell disease. In sickle-cell
disease, there is a mutation in the HBB gene, which encodes the beta globin subunit
of haemoglobin. The normal allele encodes a glutamate at position six of the beta
globin protein, while the sickle-cell allele encodes a valine. This change from a
hydrophilic to a hydrophobic amino acid encourages binding between haemoglobin
molecules, with polymerization of haemoglobin deforming red blood cells into a
“sickle” shape. Such deformed cells are cleared rapidly from the blood, mainly in
the spleen, for destruction and recycling.
In the merozoite stage of its life cycle the malaria parasite lives inside red
blood cells, and its metabolism changes the internal chemistry of the red blood cell.
Infected cells normally survive until the parasite reproduces, but if the red cell
contains a mixture of sickle and normal haemoglobin, it is likely to become
deformed and be destroyed before the daughter parasites emerge. Thus, individuals
heterozygous for the mutated allele, known as sickle-cell trait, may have a low and
usually unimportant level of anaemia, but also have a greatly reduced chance of
serious malaria infection. This is a classic example of heterozygote advantage.
Individuals homozygous for the mutation have full sickle-cell disease and in
traditional societies rarely live beyond adolescence. However, in populations where
malaria is endemic, the frequency of sickle-cell genes is around 10%. The existence
of four haplotypes of sickle-type hemoglobin suggests that this mutation has
emerged independently at least four times in malaria-endemic areas, further
demonstrating its evolutionary advantage in such affected regions. There are also
other mutations of the HBB gene that produce haemoglobin molecules capable of
conferring similar resistance to malaria infection. These mutations produce
haemoglobin types HbE and HbC which are common in Southeast Asia and Western
Africa, respectively.
Thalassaemias
Another set of mutations found in the human genome associated with
malaria are those causing blood disorders known as thalassaemias. Studies in
Sardinia and Papua New Guinea have revealed that the gene frequency of ?-
thalassaemias is related to the level of malarial endemicity in a populations. A
study on more than 500 children in Liberia revealed that those suffering with ?-
thalassaemia had a 50% decreased chance of getting clinical malaria. Similar studies
have found links between gene frequency and malaria endemicity in the?+ form
of ?-thalassaemia. Presumably these genes have also been selected in the course of
human evolution with malaria epidemic.
Duffy antigens
The Duffy antigens are antigens expressed on red blood cells and other
cells in the body acting as a chemokine receptors. The expression of Duffy antigens
on blood cells is encoded by Fy genes (Fya, Fyb, Fyc etc.). Plasmodium
vivax malaria uses the Duffy antigen to enter blood cells. However, it is possible to
express no Duffy antigen on red blood cells owing to the absence of Fy genes (Fy-
/Fy-). This genotype confers complete resistance to P. vivax infection. The genotype
is very rare in European, Asian and American populations, but is found in almost all
indigenous population of West and Central Africa. This is thought to be due to high
exposure of populations to P. vivax in Africa in the last few thousand years.
G6PD
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme which normally
protects from the effects of oxidative stress in red blood cells. However, a genetic
deficiency in this enzyme results in increased protection against severe malaria.
HLA and interleukin-4
 HLA-B53 is associated with low risk of severe malaria. This MHC class I
molecule presents liver stage and sporozoite antigens to T-Cells. Interleukin-4 is
produced by activated T-cells and promotes proliferation and differentiation of
antibody-producing B-cells. A study of the Fulani of Burkina Faso found that
the IL4-524T allele was associated with elevated antibody levels against malaria
antigens, which raises the possibility that this might be a factor in increased
resistance to malaria.
CHOLERA
Cholera is an acute intestinal infection caused by ingestion of food or water contaminated
with the bacterium Vibrio cholerae. It has a short incubation period of one to five days and
produces a toxin that causes painless, watery diarrhoea and vomiting that can quickly lead to
severe dehydration and death. The genusVibrio consists of Gram-negative straight or curved
rod-like bacteria, with a single polar flagellum. Vibrios are capable of both respiratory and
fermentative metabolism. Most species are oxidase-positive. V. cholerae and V.
parahaemolyticus are pathogens of humans. V. parahaemolyticus is an invasive organism
affecting primarily the colon, while V. Another species, Vibrio vulnificus is another emerging
pathogen of humans that causescholerae is noninvasive affecting the small intestine by
producing an enterotoxin. wound infections, gastroenteritis or a syndrome known as "primary
septicaemia."

HISTORY

During the 19th century cholera spread repeatedly from the Ganges delta in India to the
rest of the world before receding to South Asia. Six epidemics were recorded that killed
millions of people across Europe,Africa and the Americas. Cholera is mainly transmitted
through contaminated water and food and is closely related to unhygienic conditions of
surrounding environment. The absence or shortage of safe drinking water and insufficient
sanitation, combined with an unhygienic environmental status are the main causes of spread of
the disease. Cholera still remains a global threat to public health and one of the key indicators
of social development. While the disease is no longer an issue in countries where minimum
hygiene standards are met, it remains a threat in almost every developing country where
populations are large. The number of cholera cases reported to WHO during 2006 rose
dramatically, reaching the level of the late 1990s. A total of 236 896 cases were notified from
52 countries, including 6311 deaths, an overall increase of 79% compared with the number of
cases reported in 2005.

CHOLERA TOXIN

Cholera toxin activates the adenylate cyclase enzyme in cells of the intestinal mucosa
+ + –
leading to increased levels of intracellular cAMP, and the secretion of H 0, Na , K , Cl , and
2
 –
HCO into the lumen of the small intestine. The effect is dependent on a specific
3

receptor, monosialosyl ganglioside (GM1 ganglioside) present on the surface of intestinal

mucosal cells. The bacterium produces invasin, neuraminidase, during the colonization stage
which has the interesting property of degrading gangliosides to the monosialosyl form, which
is the specific receptor for the toxin. Once it has entered the cell, the A1 subunit enzymatically
transfers ADP ribose from NAD to a protein (called Gs or Ns), that regulates the adenylate
cyclase system which is located on the inside of the plasma membrane of mammalian cells.
Enzymatically, fragment A1 catalyzes the transfer of the ADP-ribosyl moiety of NAD to a
component of the adenylate cyclase system. Adenylate cyclase (AC) is activated normally by a
regulatory protein (GS) and GTP.

TRANSMISSION

The highly liquid diarrhea during cholera infection is loaded with bacteria that can
spread under unsanitary conditions to infect water used by other people. Cholera is transmitted
from person to person through ingestion of faeces–contaminated water.The sources of
contamination are typically other cholera patients whose diarrhoeal discharge is allowed to get
into waterways or into groundwater or drinking water supply. Any infected water or food
washed in such water and fish and shellfish living in the affected waterways can
cause infection. Cholera is rarely spread directly from person to person. V. cholerae occurs
naturally in the planktons of fresh, brackish, and salt water, attached primarily to
copepods. Both toxic and non-toxic strains exist. Coastal cholera outbreaks typically follow
zooplankton blooms.

COLONIZATION OF INTESTINE

There are several characteristics of pathogenic V. cholerae that help it in the

colonization process, namely, adhesins, neuraminidase, intestinal motility, chemotaxis and
toxin production. V. cholerae is resistant to bile salts and can penetrate the mucus layer of
small intestine, possibly aided by secretion of neuraminidase and proteases (mucinases).
They also withstand the propulsive gut motility by their own swimming ability and chemotaxis
directed against the gut mucosa. Two other possible adhesins in V. cholerae are a surface
protein that agglutinates red blood cells (hemagglutinin) and a group of outer membrane
proteins which are products of the acf (accessory colonization factor) genes. acf mutants have
been shown to have reduced ability to colonize the intestinal tract. It has been suggested that V.
cholerae might use these nonfimbrial adhesins to mediate a tighter binding to host cells than is
attainable with fimbriae alone

VACCINES
The oral vaccines are made from a live attenuated strain of V. cholerae. The ideal properties
of such a vaccine of the bacterium would be to possess all the pathogenicity factors required
for colonization of the small intestine but not to produce toxin molecules. Ideally it should
produce only the B subunit of the toxin which would stimulate formation of antibodies that
could neutralize the binding of the native toxin molecule to epithelial cells.

A new vaccine has been developed to combat the Bengal strain of Vibrio cholerae that
has started spreading in epidemic fashion in the Indian subcontinent and Southeast Asia.
The Bengal strain differs from previously isolated epidemic strains in that it is
sero group is 0139 rather than 01, and it expresses a distinct polysaccharide capsule. Since
previous exposure to 01 Vibrio cholerae does not provide immunity against 0139, populations
suffer from the Bengal form of cholera.

The noncellular vaccine is relatively nontoxic and contains little or no LPS and other
impurities. The vaccine will be used for active immunization against Vibrio cholerae O139 and
other bacterial species expressing similar surface polysaccharides. In addition, human or other
antibodies induced by this vaccine could be used to identify Vibrio cholerae Bengal for the
diagnosis of the infection and for environmental monitoring of the bacterium.

TREATMENT

Cholera can be simply and successfully treated by immediate replacement of body

fluids and salts lost through diarrhoea and vomiting. Patients can be treated with Oral
Rehydration Solution, a mixture of sugar and salts to be mixed with water and taken in large
amounts but patients who become severely dehydrated must be given intravenous fluids. With
prompt rehydration, less than 1% of cholera patients die.

In severe cases, an effective antibiotic can reduce the volume and duration of diarrhoea
and the period of Vibrio excretion. Tetracycline is the usual antibiotic of choice, but resistance
to it is increasing. Other antibiotics that are effective include, cotrimoxazole, erythromycin,
doxycycline, chloramphenicol and furazolidone.

Antibiotics used to treat cholera

Doxycycline, a single dose of 300 mg tablet

Tetracycline, 12.5 mg/kg or 500 mg tablet, 4 times per day
for 3 days.
Trimethoprim/sulfamethoxazole (TMP/SMX), TMP 5 mg/kg and
SMX 25 mg/kgc TMP 160 mg and SMX 800 mg twice a day for 3 days.
Furazolidone, 1.25 mg/kg or 100 mg tablet, 4 times per day for 3 days.

Erythromycin or chloramphe nicol may be used when the antibiotics recommended above are
not available, or where Vibrio cholerae O1 is resistant to them.
Doxycycline is the antibiotic of choice for adults but not for pregnant women.
TMP-SMX is the antibiotic of choice for children.
Tetracycline is equally effective in all age groups.
Furazolidone is the antibiotic of choice for pregnant women.

AIDS
AIDS stands for Acquired Immunodeficiency Syndrome. It is the most advanced stage
of infection with the Human Immunodeficiency Virus (HIV) which kills or damages
cells of the body’s immune system. HIV most often spreads through unprotected sex
with an infected person, by sharing drug needles or through contact with the blood of
an infected person. Women can give it to their babies during pregnancy or childbirth.

The first signs of HIV infection may appear as swollen glands and flu-like
symptoms which may come and go a month or two after infection. Severe symptoms
may not appear until months or years later. The CD4 count indicates how far the HIV
disease has advanced. CD4 counts in adults range from 500 to 1,500 cells per cubic
millimeter of blood. In general, the CD4 count goes down as HIV disease progresses,
to below 200, regardless of whether the persons are sick or not.

MODE OF INFECTION

Once HIV enters the human body, it attaches itself to a White Blood Cell (WBC)
called CD4, also called T4 cell, which are the main disease fighters of the body.
Whenever there is an infection, CD4 cells lead the infection-fighting army of the body
to protect it from falling sick. Hence damage of these cells can affect a person’s disease -
fighting capability and general health. After making a foothold on the CD4 cell, the
virus injects its RNA into the cell. The RNA then produces its DNA by using enzyme
reverse transcriptase. The viral DNA then gets attached to the DNA of the host cell
and thus becomes part of the cell’s genetic material. It is a virtual takeover of the cell.
Using the cell’s division mechanism, the virus now replicates and churns out hundreds
of thousands of its own copies. These cells then enter the blood stream, get attached to
other CD4 cells and continue to replicate. As a result the number of virus in the blood
rises and CD4 cell count declines.

There are several common ways that HIV can be passed from person to person
that include:

 Having unprotected sex with someone who is infected

 Using needles or syringes that have been used by people who are infected
 Receiving infected blood products or transplanted organs.
  Transmission from mother to child – An infected mother may pass the virus to
her developing fetus during pregnancy, birth or through breastfeeding.

SYMPTOMS

Many people do not develop any symptoms when they first become infected with
HIV. Some people, however, get flu-like illness within three to six weeks after exposure
to the virus. This illness, called Acute HIV Syndrome may include fever, headache,
tiredness, nausea, diarrhea and enlarged lymph nodes. These symptoms usually
disappear within a week to a month and are often mistaken for another viral infection.
During this period, virus in the body abounds and spreads to different parts,
particularly to lymphoid tissue. At this stage, the infected person is more likely to pass
the infection to others.

More severe symptoms may not surface for several years, even a decade or more
after the first entry of the virus or within two years in children born with the virus.
Some people may begin to have symptoms as soon as a few months while others may
be symptom-free for more than 10 years. During the “asymptomatic” period, the virus
will be actively multiplying, infecting, and killing cells of the immune system. The
following symptoms may appear in the infected person:

 Lack of energy.
 Weight loss.
 Frequent fevers and sweats.
 A thick, whitish coating on the tongue or mouth that is caused by a yeast infection
and sometimes accompanied by a sore throat.
 Severe or recurring vaginal yeast infections.
 Chronic pelvic inflammatory disease or severe and frequent infections like Herpes
zoster.
 Periods of extreme and unexplained fatigue that may be combined with
headaches, lightheadedness or dizziness.
 Rapid loss of weight that is not due to increased physical exercise or dieting.
 Bruising more easily than normal.
 Long-lasting bouts of diarrhea.
 Swelling or hardening of glands located in the throat, armpit or groin.
 Periods of continued, deep and dry coughing.
 Increasing shortness of breath.
 The appearance of discolored or purplish growths on the skin or inside the
mouth.
 Unexplained bleeding from skin mucous membranes or from any opening in the
body.
  Recurring and unusual skin rashes.
 Severe numbness or pain in the hands or feet, loss of muscle control and reflex
and paralysis or loss of muscular strength.
 An altered state of consciousness, personality change or mental deterioration.
 Children’s growth may be slow or they may fall sick frequently. HIV positive
persons are also found to be more vulnerable to cancers.

SYMPTOMS IN FEMALES

Although most of the symptoms of HIV infection are similar in men and
women, some are more typical of females. For example: Vaginal yeast infections may be
chronic, more severe and difficult to treat in women with HIV infection than in healthy
women.
Pelvic inflammatory disease, an infection of the female reproductive organs, may also
be more frequent and severe in women with HIV infection. Human papillomavirus
(HPV) infection, which causes genital warts may occur more frequently in HIV-infected
women and can lead to pre-cancerous lesions of the cervix or cancer of the cervix.

OPPORTUNISTIC INFECTIONS

The number of CD4 cells per ml of blood which ranges from 500 to 1,500 in a
healthy individual falls below 200 in AIDS infected people. The Viral Load will be very
high at this stage. Opportunistic infections are caused by bacteria, virus, fungi and
parasites. Some of the common opportunistic infections that affect HIV positive
persons are: Mycobacterium avium, Tuberculosis, Salmonellosis, Bacillary
Angiomatosis, Cytomegalovirus, Viral hepatitis, Herpes, Human papillomavirus,
Progressive multifocal leukoencephalopathy; Candidiasis, Cryptococcal meningitis and
Pneumocystis Carinii pneumonia, Toxoplasmosis, Cryptosporidiosis. HIV positive
persons are also prone to cancers like Kaposi’s sarcoma and lymphoma.

DIAGNOSIS

In the early stages of infection, HIV often produces no symptoms and the
infection can be diagnosed only by testing a person’s blood. Two tests are available to
diagnose HIV infection — one that looks for the presence of antibodies produced by
the body in response to HIV and the other that looks for the virus itself. If antibodies
are present, the test gives a positive result. A positive test has to be confirmed by
another test called Western Blot orImmunoflouroscent Assay (IFA). All positive
tests by ELISA need not be accurate and hence Western Blot and other tests are
necessary to confirm a person’s HIV status. ELISA requires specialized equipment and
blood samples need to be sent to a laboratory. To cut short this waiting period, Rapid
Tests that give results in 5 to 30 minutes are increasingly being used the world over.

The HIV antibodies generally do not reach detectable levels in the blood till
about three months after infection. This period, from the time of infection till the
blood is tested positive for antibodies is called theWindow Period. Sometimes, the
antibodies might take even six months to show up. Even if the tests are negative
during the Window Period, the amount of virus may be very high in an infected
person.

PREVENTION

Because there is no effective vaccine and no cure for HIV, the only way to
protect one is by taking preventive measures.
People should either abstain from having sex or use latex condoms
during sex. People who are allergic to latex can use polyurethane condoms.
Although some laboratory evidence shows that spermicidal creams can
kill HIV, there is no conclusive evidence if it can prevent transmission.
The risk of HIV transmission from a pregnant woman to her baby is
significantly reduced if she takes AZT during pregnancy, labour and delivery and
her baby takes it for the first six weeks of life.Nevirapine is also found to be useful.
Having a sexually transmitted disease (STD) can increase a person’s
chances of getting HIV through sexual contact. Hence it is necessary to treat STD as
soon as possible.
All donated blood must be screened for HIV as well as for Hepatitis B
and Syphilis.

TREATMENT

Three classes of drugs are available for treatment of AIDS.

1. Nucleoside analogue Reverse Transcriptase Inhibitors (NRTIs). These were

first antiretroviral drugs that were developed for inhibiting the replication of HIV in
the early stage by inhibiting an enzyme called Reverse Transcriptase. The drugs
include Zidovudine (Retrovir, AZT), Lamivudine (Epivir,
3TC), Didanosine (Videx, ddI), Zalcitabine (Hivid, ddC), Stavudine (Zerit, d4T)
and Abacavir (Ziagen).

The major reported side effect of Zidovudine is bone marrow suppression,

which causes a decrease in the number of red and white blood cells. The drugs ddI,
ddC and d4T can damage peripheral nerves, leading to tingling and burning
sensation in hands and feet. Treatment with ddI can also cause pancreatitis,
and ddC may cause mouth ulcers. Approximately 5 percent of people treated
with Abacavir experience hypersensitivity with rash along with fever, fatigue,
nausea, vomiting, diarrhea and abdominal pain. Symptoms usually appear within the
first 6 weeks of treatment and generally disappear when the drug is discontinued.

2. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs). These drugs bind

directly to the enzyme, Reverse Transcriptase. There are three NNRTIs currently
approved for clinical use: Nevirapine (Viramune),Delavirdine (Rescriptor)
and Efavirenz (Sustiva). A major side effect of all NNRTIS is appearance of rash.
In addition, people taking Efavirenz may also have side effects such as abnormal
dreams, sleeplessness, dizziness and difficulty concentrating.

3. Protease Inhibitors (PIs). They interrupt HIV replication at a later stage in its
life cycle by interfering with an enzyme known as HIV protease. This causes HIV
particles in the body to become structurally disorganized and noninfectious. Among
these drugs
are Saquinavir (Fortovase), Ritonavir (Norvir), Indinavir (Crixivan),Nelfinavir (
Viracept), Amprenavir (Agenerase) and Lopinavir (Kaletra).

The triple cocktail treatment, also known as Highly Active

Antiretroviral Therapy (HAART), is the closest thing that medical science has to
an effective therapy, which has the ability to disrupt HIV at different stages of
replication. Reverse transcriptase inhibitors, which usually make up two drugs in the
HAART regimen, restrain an enzyme crucial in the early stage of HIV replication.
Protease inhibitors hold back another enzyme that functions near the end of the HIV
replication process.

As of now, there is no vaccine to prevent HIV infection.

ANIMAL DISEASES
VIRAL DISEASES
SWAMP FEVER
Equine Infectious Anaemia (EIA), also known as swamp fever is a horse disease
caused by a retrovirus and transmitted by bloodsucking insects. The EIA virus is mechanically
transmitted from one horse to another by the bloodsucking horse flies, deer
flies (Tabanus), stable flies (Stomoxys spp.), mosquitoes and possibly midges. Symptoms
include recurrent fever, weight loss, an enlarged spleen, anemia, and swelling of the lower
chest, abdominal wall, penile sheath, scrotum, and legs. Horse tires easily due to a recurrent
fever and anemia, may relapse to acute form even several years after the original attack.
The EIA virus is a slow acting virus of the lenti-retrovirus group. Retroviruses cause
leukemia in cats, mice and cattle, arthritis, pneumonia and neurological diseases in small
ruminants and acquired immune deficiency syndrome (AIDS) in humans. These viruses
localize and multiply in macrophages of many organs, especially in the s pleen, liver, kidney,
and lymph nodes, where they take over the cell and sit and wait to become activated. Upon
activation, the cell reproduces more viruses, which bursts free from the cell to infect other
cells. This causes recurring cycles, in which the horse seems normal and then ill.
There is no known treatment that can eliminate the virus from the body. To date there
are no satisfactory vaccines for EIA. The Coggins’ test is an agar gel diffusion (AGID) test,
which is a practical diagnostic test for identifying horses infected with EIA. This test is used to
detect the EIA antibody.

EQUINE ENCEPHALOMYELITIS
Equine encephalomyelitis is an inflammation of the brain and spinal cord that affects
horses but is also deadly for humans. The virus was isolated, characterized, and vaccines
were produced in the 1930s. The viruses responsible for causing these diseases are
members of a family of viruses called the alphavirus. The mosquito transmits the virus from
small infected animals such as birds and rodents to horses.
The warm, humid weather of the summer is good for mosquito breeding and this is when
outbreaks are more common. Transmission of EEE is not horse to human, but bird or rodent
to human via the mosquito.

Approximately two days after equine infection with encephalomyelitis, there is an

infection and low-grade fever. The first apparent signs are at four to five days. At that time, the
animal generally has a fever and rapid heart rate, is showing signs of anorexia, depression,
and variable other neurological signs. As the illness progresses the brain stem and spinal cord
are affected. Muscle weakness becomes apparent and there are behavioural changes and
dementia. Notable symptoms include aggression, head pressing, wall leaning, compulsive
circling, and blindness. Other signs might include uncontrolled twitching of the eyeball, and
facial muscle paralysis. As the disease progresses, a semi-comatose and convulsive state
occurs. Death usually follows two or three days later. If the animal survives, residual nervous
system problems result.
Encephalomyelitis vaccines are available for horses from several different companies. They
are packaged as single or combination vaccines.

AFRICAN HORSE SICKNESS

African horse sickness (AHS) is a highly infectious non-contagious, vector born viral
disease affecting all species of Equidae. It is classified as an Orbivirus of family Reoviridae, of
which there are 9 serotypes. All serotypes are distributed throughout Africa, although there is
a variation in their temporal distribution. It is endemic to the African continent, and is
characterised by respiratory and circulatory damage, accompanied by fever and loss of
appetite. The disease manifests in three ways, namely the lung form, the heart form and the
mixed form.

The lung (dunkop) form is characterised in the following manner:

 Very high fever (up to 41 degrees).

 Difficulty in breathing, with mouth open and head hanging down.
 Frothy discharge may pour from the nose.
 Sudden onset of death.
 Very high death rate (90%).

The heart (dikkop) form is characterised in the following manner:

 Fever, followed by swelling of the head and eyes.

 In severe cases, the entire head swells.
 Loss of ability to swallow and possible colic symptoms may occur.
 Terminal signs include bleeding in the membranes of the mouth and eyes.
 Slower onset of death, occurring 4 to 8 days after the fever has started.
 Lower death rate (50%).

This disease is spread by insect vectors such as midges but can also be transmitted
by species of mosquitoes including Culex, Anopheles and Aedes, and species of ticks such
as Hyalomma and Rhipicephalus.

There is currently no treatment for AHS. Control of outbreak in an endemic region

involves quarantine, vector control and vaccination.

JAPANESE B-ENCEPHALITIS
This is a fatal disease of pigs, horses, sheep, birds and man. The infection is caused
by a flavivirus, a single stranded RNA virus. It is transmitted by the bite of the Culex
tritaeniorhynchus mosquito. The virus multiplies at the site of the bite and in regional lymph
nodes before viraemia develops that can lead to inflammatory changes in the heart, lungs,
liver, and reticulo-endothelial system. The endemic area for Japanese encephalitis spreads
across Asia from Pakistan to the coast of Siberia and includes Japan.
The incubation period is 6 to 16 days. There is fever, headache, nausea, diarrhea, vomiting,
and myalgia, which may last for several days. This may be followed by a spectrum of
neurological disease ranging from mild confusion, to agitation, to overt coma. It is more
common in children, while headache and meningism are more common in adults. Tremor or
other involuntary movements are common.

Japanese Encephalitis-VAX was a formalin-inactivated vaccine derived from mouse

brain against Japanese B Encephalitis, produced since 1992 by BIKEN (Japan). The new
vaccine available in the UK is the Japanese Encephalitis Green Cross vaccine (GC vaccine).

SWINE POX
Swinepox is a worldwide disease of pigs caused by a virus of the family Poxviridae
and the genusSuipoxvirus, which can survive outside the pig for long periods of time and is
resistant to environmental changes. Symptoms include small circular red areas 10-20mm in
diameter that commence with a vesicle containing straw-coloured fluid in the centre. After two
to three days the vesicle ruptures and a scab is formed which gradually turns black.
The disease is most frequently seen in young pigs but all ages may be affected. After
an incubation period of 1 week, small red areas may be seen most frequently on the face,
ears, inside the legs, and abdomen. These develop into papules and, within a few days,
pustules develop that change into small vesicles. The centres of the pustules become dry and
scabbed and are surrounded by a raised, inflamed zone. Later, dark scabs form, giving
affected piglets a spotted appearance. These eventually drop or are rubbed off without leaving
a scar. The early stage of the disease may be accompanied by mild fever and dullness. Virus
is abundant in the lesions and can be transferred from pig to pig by the biting
louse (Haematopinus suis). The disease also may be transmitted, possibly between farms, by
other insects acting as mechanical carriers. Recovered pigs become immune. There is no
specific treatment. Eradication of lice is important.

FOWL POX
Fowl pox is a worldwide disease of poultry caused by viruses of the family Poxviridae
and the genusAvipoxvirus. There are two forms of the disease. The first is cutaneous
form (dry pox) that is spread by biting insects, especially mosquitoes that causes lesions on
the comb, wattles, and beak. The second form isdiphtheritic form (wet pox), which is spread
by inhalation of the virus and causes a diphtheritic membrane to form in the mouth, pharynx,
larynx, and sometimes the trachea. Symptoms include weight loss, reduced egg production,
lesions, small whitish or yellowish areas, nodules or scabs, raised white or opaque nodules
which may join to form yellow, cheesy, necrotic lesion. The virus, abundantly present in the
lesions is transmitted by contact to pen mates through abrasions of the skins. Mosquitoes and
other biting insects can have a mechanical role in the transmissions. Modified live fowl pox
virus vaccines are available commercially.

COW POX
Cow pox is a disease of the skin that is caused by a virus known as the Cow pox virus.
The pox is related to the vaccinia virus, and got its name from dairy maids touching the
udders of infected cows. The cow pox virus is within the family Poxviridae and the
genus Orthopoxvirus. The ailment manifests itself in the form of red blisters and is transmitted
by touch from infected animals to humans. When it is gone, the person is immune to small
pox. Cow pox virus has been found only in Europe and in adjacent parts of the former Soviet
Union. Despite its name, the reservoir hosts of cow pox virus are rodents, from which it can
occasionally spread to cats, cows, humans, and zoo animals, including large cats and
elephants. Transmission to humans has traditionally occurred via contact with the infected
teats of milking cows. However, currently, infection is seen more commonly among domestic
cats, from which it can be transmitted to humans.

The pathology of the skin lesions caused by cow pox virus is similar to that of small
pox. However, there is greater epithelial thickening and less rapid cell necrosis. There is also
more involvement of the mesodermal tissues. The most significant pathological feature of cow
pox is the presence of two types of cytoplasmic inclusion bodies: irregular B-type inclusion
bodies, and numerous large, homogenous, acidophilic, A-type inclusion bodies.

Human cow pox usually responds to treatment with antivaccina immunoglobulin.

However, this should be restricted to the most severe cases. Usually, the lesions regress
spontaneously. Identification and isolation of animals infected with cow pox can help decrease
the incidence of human infections.

FOOT & MOUTH DISEASE

Foot-and-mouth disease (FMD) or hoof-and-mouth disease is a highly contagious and
sometimes fatal viral disease of domestic animals such as cattle, water buffalo, sheep, goats
and pigs, as well as antelope, bison and deer. It is caused by foot-and-mouth disease virus.
Seven main types of Foot and Mouth Virus are believed to exist that belong to
the genus Aphthovirus of the family Picornaviridae. Picornaviruses are tiny viruses (27-30 nm
across) that are not enveloped with an icosahedral capsid and contain a single strand of
positive sense RNA.

The disease is characterised by high fever that declines rapidly after two or three
days; blisters inside the mouth that lead to excessive secretion of stringy or foamy saliva and
to drooling; and blisters on the feet that may rupture and cause lameness. Adult animals may
suffer weight loss from which they do not recover for several months as well as swelling in the
testicles of mature males, and in cows, milk production can decline significantly.Symptoms of
the Foot and Mouth in Cattle include, Slobbering and smacking lips, Shivering, Tender and
sore feet, Reduced milk yield, Sores and blisters on feet and Raised temperature.
 BACTERIAL DISEASES
ANTHRAX Anthrax is an infectious disease caused by a bacterium called Bacillus anthracis,
which can change into spores that can last for a long time in the environment before
germinating. It is carried by wild and domestic animals in Asia, Africa and parts of Europe.

There are two main types of anthrax. The cutaneous anthrax starts as a skin bump
that ulcerates, which is not generally a serious illness. The second type
is inhalational anthrax, is normally less common and symptoms begin as a flu-like illness
which progresses to pneumonia, respiratory failure and septicaemia, which can lead to shock
and death. There is a third type, intestinal anthrax, but this is a very rare form of food
poisoning and results in fever and severe gut disease.

Cutaneous anthrax tends to occur through direct contact with the skin or tissues of
infected animals. The early stages of the lesion are noticed about 3 days from exposure,
although the incubation period can be up to 60 days. Inhaled anthrax usually shows up about
2-3 days after exposure and can be fatal within the next 2-3 days. The spores can be inhaled
directly into the lungs. Spores with food cause the intestinal form of the disease.

Normally 95 percent of anthrax cases are cutaneous and are caused by direct contact
with abrasions on the skin. There have been no known cases of person-to-person spread of
anthrax pneumonia and it is not thought to be a significant health risk.

Treatment can be done with Ciprofloxacin and doxycyline are also used as prophylaxis
for people who have been exposed. Early treatment is needed if inhaled anthrax is suspected.
There is an immunisation against anthrax but it takes five doses of vaccine over the course of
a year to get immunity. This makes immunisation too slow to deal with accidental or deliberate
exposure. It is normally offered to those who handle infected animals, and laboratory staff who
work with the bacteria. Swabs and smears can be taken from infected exposed people and
blood can be analysed for the presence of the bacteria.

LEPTOSPIROSIS
It is a bacterial disease that affects humans and animals. It is caused by bacteria of
the genus Leptospira. Symptoms of leptospirosis include high fever, severe headache, chills,
muscle aches, and vomiting, and may include jaundice (yellow skin and eyes), red eyes,
abdominal pain, diarrhea, or a rash. If the disease is not treated, the animal could develop
kidney damage, meningitis, liver failure, and respiratory distress. In rare cases death occurs.
Treatment is done with antibiotics.

ANAPLASMOSIS
Anaplasmosis is a type of tick fever that is caused by invasion of red blood cells by the
rickettsial blood parasite Anaplasma ovis. In cattle, the disease is caused by A.
marginale or A. centrale. Transmission is through insect vectors, especially horse flies, ticks
and flies. Ticks are the natural vectors and a range of tick species has been shown to be
capable of transmitting infection, e.g. Boophilus, Dermacentor, Rhipicephalus, Ixodes,
Hyalomma, Argas and Ornithodoros. There is also some evidence that it can be transmitted
to the fetus in the womb. Cattle over 2 years of age become very ill and approximately 50%
die unless treated. Usually, once the cattle become infected, and if they survive, stay infected
for life. They are "immune carriers"—they do not get sick, but act as a reservoir for other
susceptible animals.

The important symptoms are fever, anemia and jaundice or yellowing of the mucous
membranes. In cattle, the severity of the disease is directly related to age, with adults showing
the greatest difficulty. Additionally, a drop in milk production, weight loss, depression,
dehydration, constipation and lack of appetite may be observed. Some animals which recover
remain weak and emaciated through life.

Most of the sick animals die within a few days of the fever starting, if they are not
treated. The use oftetracyclines or imidocarb diproprionate is effective, however, the drug
mush be administered early in the disease. Tick control by acaracide dipping is widely used in
endemic areas. Anaplasmosis vaccines are readily available and are highly effective. The
most commonly used vaccine is a live Anaplasma centrale vaccine used either singly or in
combination with Babesia bovis vaccine.

TULAREMIA
It is caused by the bacterium Francisella tularensis found in animals, especially
rodents, rabbits, and hares. Symptoms of tularemia could include: sudden fever, chills,
headaches, diarrhoea, muscle aches, joint pain, dry cough and progressive weakness.
People can also catch pneumonia and develop chest pain, bloody sputum and can have
trouble breathing and even sometimes stop breathing. Other symptoms include ulcers on the
skin or mouth, swollen and painful lymph glands, swollen and painful eyes, and a sore throat.

Disease can spread by being bitten by an infected tick, deerfly or other insect, eating
or drinking contaminated food or water, breathing in the bacteria, F. tularensis. Tularemia is
not known to be spread from person to person. The disease can be fatal if it is not treated with
the right antibiotics. The drug of choice for treating tularemia is streptomycin or gentamicin,
although other antibiotics also are also effective.

Several precautions can protect individuals from tularemia.

 Avoid drinking, bathing, swimming or working in untreated water where infection may be
common among wild animals.
  Use impervious gloves when skinning or handling animals, especially rabbits.
 Cook the meat of wild rabbits and rodents thoroughly.
 Avoid being bitten by deer flies and ticks.

RELAPSING FEVER

Louse-borne relapsing fever

Borrelia recurrentis is the only agent of louse-borne disease. Pediculus humanus, is
the specific vector. Louse-borne relapsing fever is more severe than the tick-borne variety.
It occurs in poor living conditions, famine and war conditions. Mortality rate is 1% with
treatment but 30-70% without treatment. Diagnosis includes severe jaundice, severe change
in mental status, severe bleeding, and prolonged QT interval on ECG.

Lice that feed on infected humans acquire the Borrelia organisms that then multiply in
the gut of the louse. When an infected louse feeds on an uninfected human, the organism
gains access when the victim crushes the louse or scratches the area where the louse is
feeding. B. recurrentis infects the person via mucous membranes and then invades the
bloodstream. Cattle lice can spread the disease in animals.

Tick-borne Relapsing Fever

Other relapsing infections are acquired from other Borrelia species, such
as Borrelia hermsii or Borrelia parkeri, which can be spread from rodents, and serve as a
reservoir for the infection, via a tick vector. Borrelia hermsii and Borrelia recurrentis cause
very similar diseases although the disease associated with Borrelia hermsii has more relapses
and is responsible for more fatalities, while the disease caused by B. recurrentis has longer
febrile and afebrile intervals and a longer incubation period.
Tick-borne relapsing fever is found primarily in Africa, Spain, Saudi Arabia, Asia, and certain
areas in the Western U.S. and Canada. It is Borrelia duttoni transmitted by the soft-bodied
African tick Ornithodoros moubatathat is responsible for the relapsing fever found in Central,
East and southern Africa.

BOVINE TUBERCULOSIS
There are three types of TB – human, avian, and bovine. Human TB is rarely
transmitted to non-humans, avian TB is typically restricted to birds, and bovine TB – or cattle
TB – is the most infectious, capable of infecting most mammals. Bovine TB is caused by the
bacterium Mycobacterium bovis, which is part of the Mycobacterium tuberculosis complex.
Bovine TB is spread through the exchange of respiratory secretions between infected and
uninfected animals. Bacteria released into the air through coughing and sneezing can spread
the disease to uninfected animals. Non-cerviid animals are most likely to contract TB from
feeding on infected tissues from deer carcasses.
 Bovine TB is a chronic disease and it can take years to develop. M. Bovis grows very
slowly and only replicates every 12-20 hours. The lymph nodes in the animal's head usually
show infection first and as the disease progresses. Lesions will begin to develop on the
surface of the lungs and chest cavity. Non-cerviid animals do not develop the disease as
extensively and lesions are usually not found in lungs or other tissues.
Infected lymph nodes will contain one or more necrotic nodules, which may vary in size and
be filled with yellow-green or tan pus. Coughing, nasal discharge, and difficulty in breathing
can result in cases where the lungs become severely affected. In some instances, superficial
lymph nodes in the neck will develop large abscesses that may rupture and drain through the
skin.

Diagnosis is done by removal of suspicious looking lymph nodes for further testing. M.
Bovis is unique among the bacteria because they have a lot of waxy material in their cell
walls. Because of the waxy material (known as mycolic acid), the usual stains for looking at
bacteria with a microscope do not work.

Since there are no effective vaccines for the disease, a combination of wildlife disease
surveys and deer management strategies are being used to eliminate the disease in wild deer.
Humans can be skin-tested to determine if they have been exposed to TB.

PROTOZOAN DISEASES

PIROPLASMOSIS
Equine piroplasmosis is caused by the protozoan parasites Theileria
equi (formerly Babesia equi) andBabesia caballi, which is approximately twice the size of T.
equi. EP affects horses, donkeys, mules, and zebras and sometimes dogs. The wild zebra
population is an important reservoir for the disease in Africa. Adult and nymphal ticks are
capable of transmitting the disease. While obtaining a blood meal from an infected horse, the
tick ingests infected equine red blood cells. As the erythrocytes are digested in the tick's
digestive tract, parasite trophozoites are released and undergo sexual reproduction, resulting
in the production of zygotes. Zygotes develop into sporozoites, which undergo division and
spread via the tick's haemolymph to its salivary glands. The
causative agents are then transmitted when the infected tick
bites a susceptible horse.

Genera of ticks that transmit EP agents include Dermacentor,

Hyalomma, Rhipicephalus, and Boophilus. Approximately 15
species of ticks are capable of transmitting EP agents.

Once infected, a horse can take 7 to 22 days to show

signs of illness. Clinical signs of acute EP are nonspecific, and
mimic many other diseases and conditions. Signs observed are the result of red blood cell
destruction, complement activation, and release of inflammatory mediators (including
bradykinin, histamine, and 5-hydroxytryptamine). The severity of clinical signs reflects the
number of cells destroyed and the degree of activation of the complement and inflammatory
cascades.

Treatment via medication is instituted in affected horses. Diminazene diaceturate,

phenamidine isethionate, and amicarbalide diisethionate are effective in eliminating clinical
signs of B. caballi infection. Buparvaquone and other antitheilericidal drugs demonstrate some
efficacy against T. equi, and may eliminate the parasite when combined with
imidocarb. Theileria equi is more refractory to treatment than B. caballi, and higher dosages of
imidocarb are required.

Because EP agents are transmitted by ticks, tick control is a vital preventive measure.
Infected horses must be quarantined and isolated to reduce exposure to ticks. Pets and
wildlife, including rodents must be prevented from entering the isolation area, as they may
carry ticks capable of transmitting EP agents. No vaccine is available.

THEILERIASIS
Theileriasis, also called east coast fever, is a tick born disease of cattle, sheep and
goats caused by protozoan blood parasites, Theileria annulata, Theileria parva and Theileria
ovis of the Genus Theileria, Family Theileriidae and Order Piroplasmida.
Animals are infected through the bite of vector ticks.

Ticks possess large numbers of infective parasite Sporozoites, which develop in the
salivary glands during the first two to four days of engorgement of nymph or adult ticks. The
first visible stages are found in lymphocytes and the infected lymph nodes shows an increase
in mitotic figures. Within next several days parasites are increasingly apparent in the local
nodes and elsewhere in the lymphoid and reticulo-endothelial tissue.

Clinical signs include loss of appetite, dullness, depression, high temperature,

salivation, lacrimation, difficulties in breathing, anaemia, haemoglobinuria, jaundice,
convulsion and death. Other symptoms include, enlargement of lymph glands, pale mucous
membrane and nodules in the skin, enlargement of liver, spleen, kidney and gall bladder and
presence of necrotic ulcers in the abomasums of stomach.

Diagnosis involves microscopic examination of blood with Giemsa’s stain, presence of

punched necrotic ulcers in abomasum of dead animal and serological test

Treatment is done by administering Oxytetracycline, Berenil, Antihistamins and

Multivitamins.
TRYPANOSOMIASIS
Animal trypanosomiases include the following: Chagas; Nagana or Animal African
trypanosomiasis, also called 'Souma' or 'Soumaya' in Sudan; Surra; Mal de caderas of
central South America; Murrina de caderasof Panama; Dourine; Cachexial
fevers; Gambian horse sickness of central Africa; Baleri of Sudan;
Kaodzera or Rhodesian trypanosomiasis; Tahaga of camels
in Algeria; Galziekte or bilious fever of cattle or gall sickness
of South Africa and Peste-boba of Venezuela.

African animal trypanosomiasis (AAT) is a disease

complex caused by tsetse-fly-transmitted Trypanosoma
congolense, T. vivax, or T. brucei in cattle but can cause
serious losses in pigs, camels, goats, and sheep. Infection of
cattle results in acute or chronic disease characterized by
intermittent fever, anemia, occasional diarrhea, and rapid loss of condition and often
terminates in death. In southern Africa the disease is widely known as nagana, which is
derived from a Zulu term meaning "to be in low or depressed spirits"— a very apt description
of the disease.

Ruminants are widely known to be active reservoirs of the trypanosomes. Wild

Equidae, lions, leopards, and wild pigs are all susceptible and can also serve as carriers of
trypanosomes. Of the three African animal trypanosomes, only T. vivax occurs in the
western Hemisphere in at least 10 countries in the Caribbean and South and Central America.

In Africa, the primary vector for T. congolense, T. vivax, and T. brucei is the tsetse fly.
These trypanosomes replicate in the tsetse fly and are transmitted through saliva when the fly
feeds on animals. The three main species of tsetse flies for transmission of trypanosomes
are Glossina morsitans, which favors the open woodland of the savanna; G. palpalis, which
prefers the shaded habitat immediately adjacent to rivers and lakes; and G. fusca, which
favors the high, dense forest areas. Trypanosomiasis is also mechanically transmitted by
other biting flies of the genera Tabanus, Haematopota, Liperosia,
Stomoxys and Chrysops flies.

Initial replication of trypanosomes is at the site of inoculation in the skin, where

swelling and a sore is caused. Trypanosomes then spread to the lymph nodes and blood and
continue to replicate. T. congolenselocalizes in the endothelial cells of small blood vessels
and capillaries. T. brucei and T. vivax localize in tissue. Antibody does not clear the infection,
for the trypanosome has genes that can code for many different surface-coat glycoproteins
and change its surface glycoprotein to evade the antibody.
 The cardinal clinical sign observed in AAT is anemia. Within a week of infection, there
is usually a pronounced decrease in hemoglobin, red blood cell, and white blood cell levels,
and within 2 months these may drop to below 50 percent of their pre-infection values. Also
invariably present are intermittent fever, oedema and loss of condition.
In the early phases of infection, especially with T. vivax and T. congolense, the parasite can
readily be observed by microscopic examination of a wet-mount of blood slides. Thick blood
films and stained with Giemsa are also a good technique.

Fly eradication and drug prophylaxis are effective trypanosomiasis control

methods. Some of the older drugs such as the quinapyramine
derivatives Antrycide and Antrycide Prosalt are still used and give effective protection
against T. brucei infection in horses, camels, and cattle. The drug pyrithidium bromide is
useful in the prophylaxis of T. vivax and T. congolense infections in cattle, sheep, and goats
and can give protection for up to 6 months. The most widely used of the newer drugs
is isometamidium chloride. Homidium bromide has also been found to be an effective drug
in Kenya, and the newly introduced arsenical Cymelarsan is effective in treatment of T.
brucei infection. A very widely used drug is diminazine aceturate, which is effective against
all three African animal trypanosomes. The isometamidium drugs are also excellent
chemotherapeutic agents as are the quaternary ammonium compounds Antrycide,
Ethidium and Prothidium.

No vaccine is currently available for African animal trypanosomiasis.

COCCIDIOSIS
Coccidiosis is the name given to a group of closely related diseases caused by a
protozoan parasite called Eimeria, which develops inside cells lining the intestine. As the
parasites reproduce they cause bleeding and massive swelling of the gut. This leads to a
huge loss of liquid and the bird is unable to absorb the nutrients from its food. Out of 11
species of Coccidia, the most common species are Eimeria tenella, E. acervulina and E.
maxima, which cause chronic intestinal coccidiosis.

Eimeria tenella develops in the cells of the cecca which are the two blind sacs near the end of
the intestine. It is one of the most pathogenic coccidia to infect chickens.

E. necatrix develops in the small intestine and later in the caecum, within deeper tissues of
the small intestine and is a major pathogen of poultry.

E. accervulina and E. maxima develop in epithelial cells, primarily in the upper part of the
small intestine.
 The Sporozoite stage is the infective stage that contains special proteins and enzymes
that allow it to penetrate the cell wall. Once inside the cell the sporozite begins its
development through various stages. More parasites are produced during these stages, they
in turn move on and in to healthy cells to begun the cycle again. The result is weakened cell
walls that allow moisture to leak and damaged blood vessels. This loss of blood and fluid is
often fatal to the bird. Coccidiosis is passed to another bird during the oocyst stage, which is
an egg-like structure that is excreted by the bird and can remain inactive for many weeks and
still infect another bird. The infection starts when an oocyst is ingested. Once ingested,
symptoms may appear as early as 4-6 days later.

Symptoms of the disease include listlessness, lethargy, weight loss and blood in the
droppings or elsewhere in the body, diarrhoea, and dehydration are all common signs of
Coccidiosis. The birds may also appear to have dirty or wet vents and may eventually die.
A controlled dose of coccidial vaccine is administered once to day-old chicks, initiating
the development of natural immunity against Eimeria. Vaccination eliminates the need for
withdrawal times, which are required when anticoccidials are used, as well as concerns about
possible drug residues in poultry meat. Vaccination is also used to restore sensitivity to
anticoccidials by replacing resistant, in-house strains of Eimeria with drug-
sensitiveEimeria strains.

LEISHMANIASIS
Leishmaniasis is primarily a zoonotic disease in which wild and domestic animals such
as the fox, jackal, rodents and wolves serve as reservoir hosts. Other animals in the
surrounding areas can become infected and these are referred to as secondary or incidental
hosts. The only proven vector of the Leishmania is the blood-sucking female sand fly of the
genus Phlebotomus in the old world and Lutzomyia in the new world. Visceral leishmaniasis is
caused by the parasites Leishmania donovani, Leishmania
infantum and Leishmania archibaldi in the old world and
by Leishmania chagasi in the new world.

The sand fly vector becomes infected when feeding on the

blood of an infected individual or an animal reservoir host. The
parasites live in the macrophages as round, non-motile amastigote
fiorm (3-7 micrometers). The macrophages are ingested by the fly
during the blood-meal and the amastigotes are released into the
stomach of insect. Almost immediately the amastigotes transform in
to a motile, elongated (10-20 micrometers), flagellate promastigote form. The promastigotes
then migrate to the alimentary tract of the fly, where they multiply by binary fission. Four to five
days after feeding, the promastigotes move forward to the proboscis of the insect. When the
sand fly next feeds on a mammalian host, it's proboscis pierces the skin and saliva containing
anti-coagulant is injected into the wound to prevent the blood from clotting, the promastigotes
are transferred to the host along with the saliva. Once in the host the promastigotes are taken
up by the macrophages where they rapidly revert to the amastigote form. The leishmanias are
able to resist the microbiocidal action of the acid hydrolases released from the lysozymes and
so survive and multiply inside the macrophages, eventually leading to the death of the
macrophages. The released amastigotes are taken up by the additional macrophages and so
the cycle continues. Ultimately all the organs containing macrophages and phagocytes are
infected, especially the spleen, liver and bone marrow.
Common symptoms include high undulating fever often with 2-3 peaks in 24 hours and
drenching sweats which can easily be misdiagnosed as malaria; Chills, rigors, weight loss,
fatigue, poor appetite, cough, burning feet, insomnia, abdominal pain, joint pain, anorexia,
epistaxis and diarrhoea. Clinical sings include splenomegaly, hepatomegaly and
lymphadenopathy.

The two pentavalent antimonial compounds, sodium stibogluconate and meglumine

antimoniatehave been used as first-line chemotherapeutic agents against all forms of
leishmaniasis including visceral leishmaniasis. If treatment with pentavalent antimonials is
unsuccessful a preparation of an aromatic diamidine, pentamidine isethionate
(Pentamidine) or pentamidine dimethane sulphonate (Lomidine) is used.Amphotericin
B, which is a macrolide, is another drug of second choice used in the treatment of
leishmaniasis.There are three preparations of lipid associated Amphotericin B currently under
trial for treatment of leishmaniasis: AmBisome (Vestar, USA), Amphocil (Liposome
technology Inc, USA) and Amphotericin B lipid complex (Bristol Meyers Squibb, USA).

HELMINTHIC DISEASES

TAPE WORMS
The small intestinal tapeworms of major importance in sheep
are Moniezia expansa, Thysaniezia giardi,and Avitellina centripunctata. Other cestodes, such
as Stilesia globipunctata and Thysanosoma actinoides occur less frequently, or only in
specific regions. Stilesia hepatica parasitizes the bile ducts of sheep and other ruminants.
There are three common species that affect dogs and cats: Dipylidium caninum which can
infect dogs, cats and people uses the flea larvae as intermediate hosts; Taenia
pisiformis which infects dogs uses the rabbit; Taenia taeniaeformis which infects cats uses the
rat or mouse. The other most common tapeworms that infect dogs and cats are: Dipylidium
caninum, Taenia species, Echinococcus granulosus and E. multiocularis, Diphyllobothrium
latum and Spirometra mansonoides.

Echinococcus granulosus, also called the Hydatid worm or Hyper Tape-worm, is a

cyclophyllid cestode that parasitizes the small intestine of caniids as an adult, but which has
important intermediate hosts such as livestock and humans, where it causes hydatid
disease. In caniids, E. granulosus causes a typical tapeworm infection, and produces eggs
that are passed with the dog's faeces. Intermediate hosts include herbivores such as sheep,
deer, moose, kangaroos, and wallabies, and any other organism (including humans) that
ingests dog faeces. By an accidental ingestion in humans, oncospheres hatch in the
duodenum, penetrate the intestine and are carried via the bloodstream to various organs.
Hydatid cysts form in organs like liver (60-70 %), lungs and brain. The metacestode cysts
develop over years in most cases and have to be surgically removed after diagnosis.

Taeniasis results from either T. saginata or T. solium and relates to the adult worm in
the gut. Light infection may be asymptomatic and heavier infection leads to epigastric pain,
diarrhoea and vomiting.Cysticercosis is caused by T. solium by larval cysts that infiltrate the
lung, liver, eye or brain. This results in inflammation leading to clinical features such as,
blindness, neurology.

Treatment is by administering the drug Niclosamide or praziquantel (single dose).

There has been suggestion to use a purgative before and after to improve expulsion of the
tapeworm.

Taenia saginata, also known as Taeniarhynchus saginata or the Beef tape worm is a
parasite of both cattle and humans that occurs where cattle are raised by infected humans
maintaining poor hygiene and where meat is eaten without proper cooking. The disease is
relatively common in Africa, some parts of Eastern Europe, the Philippines, Mexico, and Latin
America.
Hymenolepis nana causes hymenolepiasis in mammals like rodents and humans and
is carried by beetles. H. nana has 3 modes of infection: (1) an indirect 2-host cycle involving
rodents as primary definitive hosts and grain beetles, fleas, or other insects that feed on
contaminated rodent droppings as intermediate hosts; (2) an oral-anal cycle in which eggs are
passed from one human to another or recycle externally in a single host; and (3) internal
autoinfection, whereby eggs hatch within the gut.

NEMATODES
There are two types of Roundworm in dogs and cats, Toxocara canis and Toxascaris
leonine, which affect the intestines and causes a pot-bellied
appearance. Hookworms (Ancylostoma caninium) occur in the intestines and can also be
transmitted to humans. Hookworm is a small, thin worm that hooks on to the intestinal wall
and sucks the blood from its victim, which causes anaemia and perhaps
death. Whipworms (Trichuris vulpis)are long, thin worms that live in the dog's colon and are
not visible by the naked eye. They attach themselves to the intestinal walls, causing intestinal
bleeding, anaemia, weight loss, flatulence, diarrhoea with blood or mucus in the stool and lack
of energy.
DOG HEARTWORM
Heartworm (Dirofilaria immitis) is spread by mosquitoes, which become infected from
biting dogs that carry the disease. These dog worms destroy the muscle and tissue of the
heart, which can cause congestive heart failure and result in death. At this advanced stage,
your dog would experience pot-belly, coughing, lack of energy and dull coat. Acute heartworm
disease in cats can result in shock, vomiting, diarrhoea, fainting, and sudden death. Chronic
infection can cause loss of appetite, weight loss, lethargy, exercise intolerance, coughing, and
difficulty breathing.

Heartworms go through several life stages before they become adults infecting the
heart of the host animal. The microfilariae circulate in the bloodstream of dog for as long as
two years, waiting for the next stage in their life cycle in the gut of a blood sucking mosquito.
When ingested by a mosquito, the microfilariae undergo a series of moults to the infective
third larval stage and then migrate to the salivary glands of the mosquito, where they wait to
infect another host through mosquito bite.

The current drug is melarsomine dihydrochloride (Immiticide), which has a greater

efficacy and fewer side effects than previously used
drug, thiacetarsamide sodium (Caparsolate), which makes it a safer alternative for dogs.

HORSE STOMACH WORM

Stomach Worms (Draschia megastoma & Habronema muscae) larvae are ingested by
fly maggots in manure. The worms develop inside the maggots. Mature flies then deposit the
larvae on the lips, nostrils, wounds and other naturally moist areas of the horse, from where
they are swallowed as the horse licks the infested area, or they stay in a wound and create
oozing, expanding the sores. Larvae deposited in the eyes can cause conjunctivitis. Larvae
that are eaten can cause gastritis and tumour-like growths which may rupture.

POULTRY EYE WORM

Oxyspirura mansoni is a widely distributed spiruroid nematode parasite found under
the nictitating membrane in the eye of turkeys, chickens, peafowl, quail, and grouse; larvae
develop to the infective stage in cockroaches. Eggs pass down tear ducts, are swallowed and
pass out in faeces, hatch after ingestion by cockroach. Larvae become infec tive for final host
in 50 days. After ingestion by the final host larvae pass from crop up oesophagus and through
tear ducts to eye. Eggs appear in faeces of final host in 32 days.

LIVER FLUKES
There are two liver flukes that commonly infect cattle: Fasciola hepatica and Fasciola
magna, the formeris the most common liver fluke of cattle. It is greyish-brown, leaf-shaped,
flatworms with two suckers at the front end. Thriving in the liver of infected cattle, flukes
disrupt the normal liver functions such as synthesizing glucose, secreting bile, and
synthesizing and storing vitamin A. Eggs from the animal may be deposited in water where
they hatch into miracidium. If snails are present, the conversion
from miracidium to cercaria to metacercariamay occur inside the body of snail. The
cysts are formed on vegetation, from where they are ingested by cattle or sheep. The
intestinal wall is penetrated, followed by the migration of the parasite to liver where significant
damage is caused.

The damage to the liver by flukes can be extensive and diarrhoea, weight loss, and
jaundice can be observed. Each fluke can cause the loss of 0.5 ml of blood per day from the
liver. A moderate infestation in cattle of 100-200 flukes can lead to blood loss of up to half a
litre each week that can cause severe anaemia.
Arthropod vectors of diseases
Many species of insects transmit diseases among humans and in animals,
while some species are blood suckers that cause pain, irritation and allergies.
Some of the arthropod borne diseases reach epidemic proportions, in which
situation vector control becomes as important as the disease itself. Detail studies
of biology, seasonal history and transmission capacities of these vectors are very
important for devising effective control strategies. The following vectors are
described.

 Bed bugs
 Mosquitoes
 Sucking Lice
 House fly
 Sand fly
 Fleas
 Tsetse fly
 Tabanus
 Stomoxys
 Ticks & Mites
 
 BED BUGS
 (Cimex lectularis; Cimex hemipterus)
Cimex lectularis is found in temperate countries while Cimex hemipterus (=C. rotundatus) occurs in
tropical countries. Bed bugs are not known to transmit any disease, although they are suspected to be
vectors of kala-azar and relapsing fever.
 Body is reddish-brown, dorsoventrally flattened. Proboscis is segmented and is used for piercing
the host skin and sucking blood. Maxillary palps are absent. Antenna is 4-segmented. Pronotum is shield
like having lobes on either side of the head. Tarsis is 3-segmented. Wings are absent but rudimentary
pads are present. There are stink glands all over the body which emit a characteristic foul odor. In male
posterior end of abdomen is produced into a lobe and is hairy with a spine -like aedeagus. In female
abdomen is broadly rounded posteriorly having small hairs. Fourth abdominal segment in female
possesses an organ of Berlese on the ventral side to the right side of the middle. This is a pouch -like
structure in which sperms are stored after copulation. Sperms from here bore through the walls and
tissues and fertilize eggs in the ovaries.
 Eggs are whitish, 1.0 mm long, flask-shaped, having reticulated surface and an operculum on the
anterior side. They are laid among the bedding, in cracks and crevices of the walls and floor or any other
hidden situations. Many females lay their eggs in groups at one place. Fecundity is 75-200 eggs/female.
Incubation period is generally 6-10 days but in hot season may be reduced. Nymphs similar to the adults
and suck blood. First instar nymphs are semitransparent and later instars are s traw yellow. There are 5
nymphal instars which take about 30 days to become adults. Adults are nocturnal and both sexes suck
blood. They can resist starvation up to six months. The starving individuals look light coloured and
extremely thin. They can regain dark brown colour and original form after sucking blood.

 Control of bedbugs
 Cement plastering of cracks on the floor and walls and periodic white washing of the house and
maintenance of cleanliness helps to eradicate bugs.
 Exposing bedding and infested articles in the sun periodically and boiling clothes in water kills
them
  MOSQUITOES(C ulex, Aedes and Anopheles)(Diptera: Culicidae)There are over 3000 species of
mosquitoes in the world which are distributed from the tropics to the altitude of 4300 meters. They are
also found 1160 meters below the sea level in the gold mines in south India. They are virtually
distributed everywhere except in Iceland and poles.

 Disease transmission

Mosquito Desease Causative organisms Distribution
species transmitted
Culex pipiens Filariasis Wuchereria bancrofti Eastern India
fatigans
Yellow fever Flavivirus Africa, S. America
Aedes egypti Dengue fever Dengue virus All over India
Chickengunya India

Malaria Plasmodium species All over India, Asia,

Anopheles Africa
stephensi Filariasis Wuchereria bancrofti Tamil Nadu in India
W. malayi
Mansonioides
annulifera

 Identification characters
 Males of all species have rudimentary maxillae and mandibles so that they cannot suck blood but
can suck fluids and nectar from flowers. They also possess very bushy whorl plumose antennae and tip
of abdomen with characteristic male genitalia. On the other hand females have short hairs on the
antennae and needle-like maxillae and mandibles for piercing the skin of host for sucking blood. Other
characteristics are given below according to the species.

 LIFE CYCLE
 Eggs are laid on the surface of water and have some device to keep them afloat for oxygenation.
Blood meal is essential for the development of ovaries and maturation of ova and hence female sucks
blood. Incubation period in all species is about 2 days. Larva has head, thorax and a long abdomen.
Thorax is the bulkiest part of the body. There are paired eyes, antennae and feeding brush that drives a
current of water along with food particles towards the mouth. Abdomen is 10-segmented, 8-9 segments
are fused to form a complex spiracular apparatus or respiratory apparatus. Anal gills are located on the
tenth segment. Respiratory siphon is located on the 9th segment and internally divided by a septum into
two chambers. Thorax and abdomen have long hairs on the lateral sides. There are 4 larval instars and
larval period ranges between 6 and 8 days. Pupa is comma shaped, having cephalothorax and abdomen.
Cephalothorax has a pair of respiratory tubes called respiratory trumpets and a pair of eyes. Abdomen is
8 segmented and has caudal paddles and hairs at the tip. Pup a does not feed but moves about actively.
 Pupal period is two days. During adult emergence, the cephalothorax of pupa breaks on the outer surface
and imago comes out, sits on the pupal case for sometime to dry up its wings and then flies away. Total
life cycle takes 10-12 days.

 Culex pipiens fatigans. It is dull whitish mosquito having unspotted wings and makes humming sound
when flying. There are overlapping scales and six transverse whitish bands on the abdomen. Scutellum
in dorsal view looks trilobed and each lobe has a bunch of long hairs. Thorax has no markings on the
dorsal side. Maxillary palps of female are short, 3-5 segmented, while in male they are long and equal to
or longer than proboscis. While resting it sits parallel to the ground. There are about 240 species
in India out of which 4-5 are vectors of diseases. It breeds in cesspools, drains, disused wells and
stagnated water. Polluted water is preferred for breeding.
 Eggs are long cigar-shaped, whitish in colour and deposited on the surface of water in a raft of
50-100 eggs, which help the eggs to float. Egg incubation period is 2 days . Larva is aquatic, with head,
thorax and 10-segmented abdomen and bunches of long hairs on the thorax and abdomen. Respiratory
siphon on the 9th abdominal segment is long and narrow and is thrust out of water for air breathing,
while the body hangs at an angle of about 45 degrees. Head bears a pair of eyes, antennae, maxillary
palps and feeding brush. There are long bunches of hairs and anal gills on the tip of abdomen but the
gills are inadequate respiratory organs. Larva is also called wriggler. There are 4 larval instars with a
total larval period of 6-8 days. Pupa is coma-shaped, with long and narrow respiratory trumpets on the
cephalothorax. Abdomen is curved with caudal paddles on the last segment for swimming. It does not
feed but swims actively. Pupa is also called tumbler. Pupal period is two days and pupa comes to the
surface before adult emergence.

 Aedes egypti: This is called zebra mosquito as it has black and white bands on the abdomen and legs. It
belongs to the same subfamily as Culex and hence has structural similarities with it. Thorax is black with
a pair of sickle like white markings on the dorsal side. Scutellum is trilobed wit h three bunches of long
hairs on the posterior margin. Maxillary palps of female are small but those of male equal to proboscis or
longer. The species breeds in tree holes, broken containers, flower pot, puddles, coolers and other small
water collections. Eggs are laid singly on water surface. They are blackish with small pits on the surface
which help them to float on water. They hatch in two days. Eggs can also be laid in moist soil where they
can remain dormant for months. Larva is also black in colour and has a short and barrel shaped spiracle.
It is a bottom feeder and has structural similarities with Culex larvae. Pupa is deep coma shaped, black
with white markings and having three abdominal segments attached to cephalothorax. Respiratory
trumpet is funnel-shaped, narrow at base and gradually broadening at the apex. Pupal period is only two
days.

 Anopheles spp.: There are 44 species out of which six species are known vectors of malaria in India.
 Adults are dull whitish in colour having wings with blackish spots and dark veins. They make no noise
while flying. There may be scattered scales on the abdomen. Thorax without any markings on the dorsal
side and scutellum not lobed and has uniformly distributed hairs on its posterior margin. Maxillary palps
in both sexes are equal to proboscis but in male they are clubbed at the tip. Adult in resting position
 makes an angle of 45 degrees against the surface. Eggs are laid singly on the surface of water. They
possess a pair of floats which prevent them from drowning. Larva rests parallel to the water surface and
has palmate hairs on the sides of abdomen for that. Respiratory siphons are absent and there are a pair of
respiratory openings instead. Larval period is about a week. Pupa is deep coma shaped in which 5
abdominal segments are attached to cephalothorax. Abdomen is 8 segmented. Respiratory trumpet wine -
glass shaped, with a stalk and parallel-sided body. Adults emerge in 2-3 days.

 MOSQUITO CONTROL
 Mosquito control efforts have not been successful because of the ability of mosquitoes to develop
resistance against insecticides very quickly and their capacity to inhabit a variety of environmental
conditions. The following measures are generally adopted to reduce mosquito populations.

 Personal preventi ve measures
 Use of mosquito nets is an effective method to prevent adults from biting and transmitting
malaria. Application of mosquito repellent chemicals, such as citronella oil, dimethylphthalate, odomos
cream or pyrethrum cream also prevent mosquitoes from sucking blood. Mosquito repelling fumigants,
e.g. tortoise mosquito coil contains pyrethrum in it and Goodknight mats or Allout liquids contain
synthetic pyrethroids such as deltamethrin, decamethrin and allethrin. They effectively repel and confuse
mosquitoes.

 Anti-larval measures
 Removal of breeding places effectively reduces mosquito population. Broken pots, old tyres, tins
and other containers should be removed from the surroundings as they serve as breeding places
for Aedes. Coolers and overhead water tanks should be periodically cleaned or treated with potassium
permagnate to kill the larvae. Small water bodies, ditches and ponds that cannot be filled should be
sprayed with light diesel or petroleum oil that makes a thin film on the water surface and clogs
respiratory siphons of larvae. Use of Paris green (copper aceto -arsenite) also kills larval and pupal
stages. Biological control of larvae and pupae in ponds has been achieved by releasing larvivorous
fishes, such as the native Gambusia andNothobranchius guntheri introduced by CIBC from Africa.
These fishes actively feed on the larvae and can aestivate in mud when ponds dry up in the summer
months. Naiads of dragonflies and damselflies are also effective predators of mosquito larvae and pupae.

 Anti-adul t measures
 Trapping of adults by hanging black cloths to serve as hiding places during day time and then
killing the adults by spraying insecticide should be done daily. UV electrocuting traps should be us ed to
attract and kill adults. Destruction of tall grasses and bushes serve as resting places for mosquitoes in day
time and hence should be removed from the surrounding areas. Use of malathion and endosulfan
aerosols in the colonies periodically has been effective in reducing their populations. Aerial sprays of
pyrethrum, carbaryl, carbofuran, arprocarb mixed with mineral oil are still effective in killing adults.
Synthetic pyrethroids are quite effective and new chemicals used against mosquitoes but are
prohibitively expensive.
  Spray of DDT 5%, BHC 6% or malathion and endosulfan dust 5% in houses and cots and beds
kills them. Dusting helps to eradicate them more effectively.
 Predators of bed bugs
 Small red house ant, Monomorium pharaonis.
 Rduvius personatus, the assassin bug.
 The pseudoscorpion, Chelifer cancroids.

Human Louse
(Pediculus humanus)
DISEASES TRANSMITTED BY LICE

1. Epidemic typhus: This disease is caused by a PPLO, Ricketsia

prowazeki, which multiplies in the gut of lice. Spores are released through
faeces within 5 days of infection and can remain viable for 4 months in the
dry conditions. They get into the human system through contact with
blood, through wounds, conjunctive or by inhalation into lungs. The
disease spreads in epidemic form and is capable of causing 100% fatality.
Reservoir hosts are sheep and goats.
2. Trench fever: This is caused by Ricketsia quintana. The disease was
common among soldiers during the world war II, when soldiers had to
spend several days trapped in trenches and lice transmitted the disease in
epidemic form. The mode of transmission is similar to the epidemic
typhus.
3. Relapsing fever: This disease is transmitted by a spirochaet, Borrelia
recurrentis which breeds in the haemolymph of the louse and escapes
when the louse is crushed or dies due to the parasite. It gets into the human
blood through wounds or scratches. This disease spread in great epidemic
form during the World War I and II.
4. Local urticaria and itching: This is also called the Vagabond disease.
Itching, rashes and discoloration of the skin takes place due to the allergic
reaction to the bites and blood sucking by lice.

Pediculus humanus
This is a 2-3 mm long insect with dorsoventrally flattened body. Head is
small with reduced eyes and small, 5-segmented, filiform antenna. Mouthparts are
highly modified, with a chitinous, spine-like stabber for puncturing the host skin.
There is no proboscis or maxillary palps or other structures of usual mouth parts.
Legs form a clinging apparatus by having a single curved claw that opposes a tibial
thumb. Tarsus is single segmented. Tip of abdomen of female is bifid while that of
male rounded and armed with a chitinous pointed aedeagus, which is the male
copulatory organ. Blood is sucked by the pumping action of pharynx. Both adults
and young of both sexes feed on blood. Their mouthparts are in the form of fine
stylets which, except when feeding, are
withdrawn within the head. When food is required the skin of the host is pierced by
means of the stabber which is thrust out and then gradually pushed farther and
farther into the flesh. At the same time a salivary secretion which prevents
coagulation of the host’s blood is injected into the wound and enables the insect to
suck it up without clots forming in the delicate mouth-parts. The adults can take up
to one milligram of blood at a time. It is probable, however, as adults cannot live
long without feeding, that they prefer to take smaller quantities at frequent intervals.
At temperatures at which they remain capable of active movement they survive
starvation, after a meal, for about three days at 30°C and five days at 24°C. At lower
temperatures they survive for about a week after feeding, but it must be remembered
that at these lower temperatures they are not capable of active movement. When a
louse takes a very large meal, blood may sometimes be seen flowing from its anus.
At other times overeating results in a rupture of the gut and allows the blood to
mingle with the body fluids; this causes the death of the louse within a
comparatively short time. Adults are capable of fairly rapid active movement. They
have been recorded as moving at a rate of 9 inches per minute; but they never move
in straight lines.
Fecundity of female is 150-300 eggs/female. The eggs (called nit) are oval in
shape. 0.8 mm long, with an operculum on one end and are glued to the host hair by
a gelatinous sleeve. Incubation period is 6-7 days. Nymphs that hatch from the eggs
are similar to the adults in structure as well as in habits. They grow by sucking blood
of the host and mould twice to become adults. Nymphal period is 9 days that
includes 3 instars. Total life cycle is completed within 15-16 days. Adults survive
for 4-6 weeks. There are two forms of the human louse—head louse and the body
louse, which differ in the following details:

Head louse (Pediculus humanus Body louse (Pediculus humanus

capitis) corporis)

1. Found on head, among hairs. 1. Found on body and in

2. Longevity is 4 weeks. clothing.
3. There is no seasonal 2. Longevity is about 6 weeks.
variation. 3. There is greater density of
4. The louse is found more on lice in winter months.
children. 4. Occurs uniformly on all age
5. Spreads through head contact. groups.
6. Black in colour. 5. Spreads through clothing, bed
etc.
 6. Dull whitish in colour.

The Crab louse (Phthirus pubis)

This species is restricted to the pubic region of human beings. Thoracic
region is very broad and abdomen narrower than the thorax, 5-segmented and bears
small paired appendages. They are sluggish lice and are not known to transmit any
diseases. Fecundity is 50 eggs/female. The eggs hatch in 7-8 days and nymphs take
27-33 days to develop into adults. Otherwise they are similar to the human louse.
Body is much broader in proportion to its length and the legs have the appearance
of being attached to the edge of the somewhat flattened body rather than to the
underside. Its movements are slow and deliberate and are made with a somewhat
crablike motion. As its common name implies, it is usually found infesting hairs of
the pubic and perianal regions of both sexes. Like
Pediculus human us it is world-wide in its distribution, but much rarer, so that
infestations of Phthirus pubis are less frequently seen.

CONTROL OF LICE
Cleanliness and hygiene eradicates lice. In case of severity of infestation,
clean shaving of head brings relief. Application of kerosene mixed with olive oil in
equal ratio on the head kills lice. Lindane ointment, malathion (Lycil) and Mediker
shampoo (also contains malathion) or any insecticide mixed with oil kills all lice on
head. The application has to be repeated every week to kill nymphs emerging from
eggs. Body lice can be controlled by steaming or boiling of clothes and bedding or
rinsing clothes in weak insecticide solution.
THE HOUSE FLY
(Musca domestica and Musca vicina)

House fly is larger insect, 6-7 mm long, greyish with blackish markings and
with a wing span of 13-15 mm and having two wings, posterior wings modified in a
pair of halteres or balancers. Wings when folded over the abdomen at rest diverge
posteriorly. Mouth parts are sponging type or haustellate, which are adapted to feed
on liquid diet only. When they have to feed on solids such as sugar crystals, they
first vomit the contents of stomach over it and dissolve food in it before swallowing.
Eyes are very large, covering major part of the head and antennae small aristate.
They are very agile and expert fliers, capable of landing upside down on the roof.
They can fly up to 80 feet high. Adult longevity is generally 2-3 months but may be
reduced to 2-3 week in hot weather.
 Houseflies breed in cow dung heaps, filth, compost and other decaying
matter that has a lot of moisture content. Fecundity is 700-950 eggs/female. Eggs are
laid in about 6 batches spread in 3-4 days and placed beneath the surface of the
medium. Adults can survive for 1-3 months. Eggs are creamy white, elongated, 1
mm long and 0.25 mm wide. Incubation period ranges between 12 and 24 hours but
in summer eggs can hatch within 6 hours.
Larva is called maggot, is creamish in colour, narrow anteriorly and broad
posteriorly and truncated. There is no distinct head anteriorly but a distinct black
spine or oral hook that helps in feeding and moving about in filth. Anterior part of
thorax contains a hard chitinous cephalopharyngeal skeleton. On the posterior end of
the abdomen there are a pair of spiracles located in a pair of D-shaped depression.
Full grown larva is 1.25 mm long. There are 4 larval instars and the larval period is
5-10 days depending on the temperature. Larva feeds on decaying organic matter
and avoids light and high temperature. For pupation the larva has to migrate to drier
place or compact soil.
Pupa is barrel shaped, dark brown and shorter than the larva. Posterior end
has two spiracles for breathing. Pupa is a dormant stage but can move vertically up
to one foot to reach near the surface before adult emergence. Pupal period is 3-5
days but can be less in hot weather. The entire life cycle may be completed in 8-16
days.

Diseases transmitted by housefly

Disease Causative organism

1. Cholera Vibrio cholerae
2. Typhoid Salmonella typhi
3. Paratyphoid Salmonella paratyphi
4. Amoebic dysentery Entamoeba histolytica
5. Bacillary dysentery Shigella dysenteryi
6. Poliomyelitis Polio virus
7. Trachoma eye disease Virus
8. Eggs of many species of Cestodes and nematodes
Parasitic worms

MODE OF TRANSMISSION
Housefly transmits diseases in two ways:
1. External carriage: When housefly sits on filth and dung etc., pathogenic
organisms get attached onto the lower side of oral disc, hairs of tibia and tarsi
and on abdomen. When the same fly sits on food items meant for human
 consumption, the pathogens are release into it and get into the human system
through contamination.
2. Internal carriage: In this mode pathogens are swallowed and retained in the
gut. Housefly has a habit of regurgitating stomach contents on the food material
before swallowing it. It also defecates frequently in the form of fly specks. As
the alimentary canal of house fly contains pathogens, in both ways it releases
pathogens in the articles of human consumption. Even utensils containing fly
specks can transmit pathogens if not washed properly.

CONTROL OF HOUSE FLIES

Removal of breeding places: Cow dung and other manures should be
removed and buried in special pits and covered with soil. In dairies proper drainage
system should be installed so that hygiene and dryness could be maintained.
Household refuse should be kept in covered bins and not dumped in the
surroundings. Maintenance of cleanliness is an effective method to bring down
house fly population.
Treatment of breeding places: Where it is not possible to remove garbage
heaps and cowdung immediately, it should be covered with a layer of insecticide
dust such as 5% DDT or BHC dust to prevent flies to feed and lay eggs. Pyrethrum
and neem oil can also be used in rural areas.
General precautions: Windows and doors should be made fly proof by
covering them with wire mesh. Food material should be stored inside covered
almirahs, fridges or covered containers. Eating utensils should not come in contact
with flies or should be washed again before use. Particular care should be taken
where large scale cooking is done as in marriages and parties.
Control of adults: Adults can be killed by spraying insecticide such as
Baygon, malathion, lindane, endosulfan, carbaryl or synthetic pyrethroids. Sugar
baits containing the above mentioned insecticides are quite effective in killing
adults. UV emitting electrocuting traps are quite effective in attracting and killing
adults and can be commonly seen in shops and restaurants.
Biological control: Fowls scratch the soil and manure with their legs and
feed on the maggots of houseflies. A pupal parasite, Spalangia, has been found to be
very effective in destroying pupae of houseflies.
SANDFLIES
(Diptera: Psychodidae)
There are about 33 species of sand flies in India, some of which are known to
transmit diseases. They are smaller than mosquitoes. Wings are rhomboidal in shape,
narrow at both ends; hairy and held vertically up over the abdomen. Wing venation
is characteristic of sand flies having 8 longitudinal veins. They move by hopping
action. Antenna is 16 jointed and whorl plumose and there is no difference in the
antennae of males and females. Female mouth parts are of piercing and sucking type
 while male mouth parts are poorly developed and adapted for sucking nectar and
fruit juices. Legs are long and slender adapted for hopping movement. Ninth and
tenth abdominal segments are modified as genitalia. Male genitalia have prominent
superior and inferior claspers and median lamellae and aedeagus. Adults can bite
through the mosquito netting as they are small in size and can easily squeeze
through the holes of mesh.

LIFE CYCLE
Eggs are laid in moist soil with organic matter and aeration. Breeding places
include backyard of houses, cattle sheds, crack and crevices in houses with
accumulated moisture and organic matter. Eggs are whitish, torpedo shaped, with
striations on the surface, gradually turning darker as the embryo develops.
Incubation period is 6-9 days.

Larva is apodous, hairy maggot, without eyes and with a pair of sharp
mandibles. Apex of abdomen has a tube like stigmata or respiratory spiracle on the
ventral side. Tip of abdomen has a pair of long and a pair of short caudal bristles,
which are kept erect while walking. Body is covered with rows of spines. Full grown
larva is 5 mm long. There are 5 larval instars and the larva can go up to one foot in
soil during development. Total larval period is 21-28 days.
Pupa has cephalothorax and abdomen that is curved upwards. It is a dormant
stage that does not feed but is mobile and comes to the surface before emergence of
the adult. Pupal period is about 10 days. Complete life cycle takes 37-47 days.

Diseases transmitted by sand flies.

Disease name Causative organism Sandfly species Distribution

Kala-azar Leishmania donovani Phlebotomus NE India,
argentipes TN
Oriental Sore Leishmania tropica
P. sergenti; P. C&N
Sandfly fever Virus papatasii India

Espundia Leishmania Phlebotomus Whole

(naso- braziliensis papatasii India
Pharyngeal
leish-maniasis P. intermedius S. America

Carrion’s Bartonella
disease bacilliformis
P. varrucarum S. America
CONTROL
Dusting or spraying of houses with BHC, malathion, endosulfan, carbaryl
etc. kills the adults and other stages. Cleanliness in houses and surroundings and
plastering of cracks and crevices also reduces adult population. Cleanliness in
breeding places and treatment of these places with insecticides is an effective control
measure. Larvae are difficult to control since they burrow deep into the soil but
burying the garbage dumps and treatment with insecticides helps in controlling
them.
FLEAS
(Siphonaptera)
(Pulicidae, Ceratophyllidae, Sarcopsyllidae)
Fleas are small wingless insects, 2-3 mm long, with highly sclerotised, laterally
compressed bodies and reddish-brown colour. Antennae short, stout, pectinate or
clubbed and concealed in a groove. Mouth parts are modified for piercing and
sucking. Legs adapted for clinging with curved claws. Hind leg longer, modified for
jumping. Body bears backwardly directed spines that help them to move through the
hairs of the hosts. Maleabdomen is directed upwards at the apex and flat. Apical part
of abdomen possesses a coiled cirrus organ which is the copulatory organ of the
male. Female abdomen is directed straight backwards and carries a small pouch-like
structure called spermatheca which stores sperms after copulating with the male.

LIFE CYCLE: Fleas breed in dark and secluded places with high moisture
contents, such as dusty floors, under carpets, rat burrows, granaries, chicken houses
and godowns. Female lays 300-400 eggs in lifetime and the incubation period is 2-3
days (maximum 12 days). Larvae yellowish-brown, caterpillar-like, 13-segmented,
hairy and move about actively, feeding on decaying organic matter and on faeces of
the adult fleas. Larva is about 4 mm long and does not have eyes, antennae and legs
but has long bristles on the body, which also help it in locomotion. There are 3
instars and larval period ranges between 7 and 10 days. Pupation takes place in a
very tough, dull whitish cocoon that is concealed in dust particles. Pupal period is 7
days. Pupa may hibernate for up to one year. Total life cycle is completed in about
20 days under favourable conditions. After emergence adults hop on to the passing
rats or other hosts and start sucking blood. They suck more blood than necessary and
a lot of undigested blood passes along with faeces that form food for the larvae. An
adult can jump up to 8 inches high and 13 inches in length. Longevity of the adult is
about 2 years and it can resist starvation up to 6 months.

SPECIES OF FLEAS
 There are about 200 species of fleas in India but few common species are
given below.
1. Human flea (Pulex irritans). This is a cosmopolitan species, more common in
hilly areas. Man is the preferred host but can feed on other animals also. It is a
combless flea and not a vector of plague. Its mesopleuron is without a ridge
like crest or carina.
2. Rat flea (Xenopsylla cheopis). This is a combless flea found on rats and is the
vector of dreaded plague. It looks like human flea but mesopleuron has a crest
or carina just above the middle coxa. It breeds in rat dwellings and frequently
bites human beings.
3. Dog and Cat flea (Ctenocephalides canis and C. felis). These are combed fleas
found on dogs and cats. They possess both the genal and pronotal combs and
spines all over the body.
4. Combed Rat flea (Nosopsylla or Ceratophyllus sp.). This species is similar to
the other rat fleas but bears a pronotal comb. Genal comb is absent. The
European species N. fasciatus is a vector of plague but the Indian species, N.
nilgiriensis is not a vector of plague.
5. Broken-headed mouse flea (Leptopsylla segnis). This species is found on
mouses. Both genal and pronotal combs are present. Eyes are absent and the
antennal grooves of both sides join on the dorsal side, giving an appearance of
head divided into two parts or broken headed appearance.
6. Rat flea (Stivalius ahale). This species is found in the foot hill of south India. It
resembles Nosopsylla but is larger with a rounded head having a lot of bristles
and reduced eyes. It has only pronotal comb and is a vector of plague in south
India.
DISEASE TRANSMISSION
Fleas transmit plague that is caused by the safety pin bacillus called Yersinia
pestis or Pasturella pestis.The disease is caused in man as well as in rats and
produces three types of symptoms in man.
1. Bubonic plague. The bacillus infects lymphatic system, causing swelling and
pain in the lymph glands but no fever occurs. Rats also suffer from similar
symptoms.
2. Septicemic plague. Infection spreads to the blood vascular system causing fever.
There is headache and pain in the back. Sudden chilliness, blood-shot eyes, rapid
pulse, thick speech and high fever are other symptoms. In the case of prolonged
illness spleen enlarges and becomes brick-red in colour and liver is also enlarged.
Comma and death can occur due to heart failure in about a week.
3. Pneumonic plague. In this case bacillus multiplies in the lungs and pleural
cavity, causing pneumonia-like symptoms. Yellowish fluid fills the lungs and
pleural cavity, causing excessive coughing and heavy breathing. Infection can spread
directly from man to man through droplets release during coughing. This is the most
dangerous type of plague as it spreads very fast by droplet infection, particularly in
high population density areas and brings about quick deaths.

Mode of infection
When a flea sucks blood from a plague-infected rat, it gets bacillus into the
crop along with the blood meal. The bacilli get attached to the spines of
proventriculus and form mucilaginous colonies there, multiplying very fast, blocking
the passage of blood into the intestine. Such fleas are called blocked fleas that
always remain hungry as the blood does not pass into the intestine. Hence they keep
biting and sucking blood repeatedly but regurgitating it in the same wound as the
stomach is already full of blood and bacilli. In doing so, they keep transmitting
bacilli from their stomach to the new hosts. Blocked fleas can survive up to 40 days
and transmit disease continuously.

Murine typhus
This is another disease transmitted by Xenopsylla cheopis. It is a mild
typhoid fever caused by the PPLO, Rickettsia mooseri. The causative organism
multiplies in the gut of flea and is excreted through faeces. Man gets infected either
by contamination of wounds by the flea faeces or by inhalation of dust containing
faeces.

Tape worm
Some fleas act as intermediate hosts for the tape worms like, Dipylidium
caninum and Hymenolepis diminuta.

Control of fleas
Control of rats is an effective method of controlling fleas. Trapping, baiting
and fumigation can eradicate rats. Cyanogas fumigation kills not only rats but also
all stages of fleas in the rat burrows. Fumigation should be done every 2-3 months.
Construction of rat proof godown having metalled doors and meshed windows is
also an effective method to keep the rats away from human dwellings.
Dusting the houses, floors, godowns and other places frequented by rats
should be done frequently using residual insecticides such as BHC, endosulfan,
dieldrin, aldrin etc. This will kill all stages of fleas as they breed in dust and
abandoned corners.
Patients suffering from plague can be treated with streptomycin injections or
oral doses of antibiotics such as tetracycline, sulphadiazene, chloramphenicol,
doxycycline, azithromycin etc. given two or three times in a day.
 TSETSE FLY Tsetse fly belongs to genus Glossina of family Glossinidae and is
pronounced tse-tse or teet-see or set-see. They are large biting flies found in Africa that suck blood of
vertebrates and transmit several protozoan diseases.

Tsetse flies are similar to other large flies but can be distinguished as they fold their wings completely
when at rest so that one wing rests directly on top of the other. Adults are yellowish to brownish, with a
piercing proboscis and a hatchet-shaped cell in the center of each wing. The arista of the third antennal
segment has branched setae. Larvae breathe through a pair of posterior spiracles and in the third instar
via a pair of lateral lobes, which contain three air chambers and open through numerous spiracles.

Female tsetse flies are viviparous, which involves the retention of a single egg that develops to the third
larval stage before being deposited. The egg within the uterus hatches in 3–4 days, giving rise to the
first instar larva that obtains nourishment from secretions of a pair of uterine glands from the mother.
The larvae are deposited in soil where they burrow and feed and pupate for 4–5 weeks. The young adult
emerges from the pupa and both sexes suck blood. Males are not fully fertile until several days after
emergence, and females are able to mate two to three days after emergence. The first larval offspring is
deposited about 9–12 days after the female emerges. Tsetse flies females live up to 14 weeks while
males live for around 6 weeks.
Tsetse flies have about thirty four species and sub-species that are placed in a single genus, Glossina.
Some species transmit trypanosome species that cause trypanosomiasis or sleeping sickness in humans
caused by Trypanosoma brucei gambiense and T. brucei rhodesiense. In animals, they
transmit nagana, in cattle, horses, pigs and antelopes which is caused by Trypanosoma brucei brucei,
T. congolense and T. simiae and surra in horses and pigs caused by Trypanosoma suis.

Tsetse transmit trypanosomes in two ways:

Mechanical transmission involves direct transmission of trypanosomes taken from an infected host
into an uninfected host. The fly feeds on an infected host and acquires trypanosomes in the blood meal
and then, if within a short period it feeds on an uninfected host and regurgitates infected blood and
saliva into the tissue of uninfected animal, it has transmitted the protozoans.

Biological transmission requires a period of incubation of the trypanosomes within the tsetse stomach
where the protozoans reproduce through several generations to become infective stage. Tsetse infected
by trypanosomes are thought to remain infected for the remainder of their lives.

TABANUS

(The Horsefly)
Tabanus quinquevittatus
T. striatus

T. atratus

T. rubidus

Horseflies are moderately sized, heavy bodied insects, 6-20 mm long with
cloudy wings and large banded eyes. Females have strong, blade-like, piercing and
sucking mouthparts for sucking blood of animals but males do not feed on blood but
feed on vegetable material or nectar. Thorax is pubescent, yellowish. Larvae have
girdle like transverse bands on the body and are found in moist soil, mud, rotting
vegetation or in aquatic situations. Pupae are elongated and cylindrical and are found
in dry places, generally 1-2 inches below the surface. Pupal period may be as long as
three weeks.

They transmit horse disease called, SURRA that is caused by the

protozoan, Trypanosoma evansi and T. theileri.They also transmit Anthrax among
cattle. The flies are active in warm and sunny days and fly very fast.

Stomoxys calcitrans

(The Stable fly)

The stable flies look like over-sized houseflies, which are 6.5 mm long, greyish-brown with dark
markings and short checkered abdomen. Both sexes suck blood of mammals. Mouth parts are piercing
and sucking type and prominent. When at rest wings are kept at an angle. Average life span is about
20 days with a maximum of about 2 months.

They breed in decaying grass, horse dung or manure where the eggs are laid which hatch in 1-
5 days. Female fecundity is about 800 eggs per female. Larvae resemble housefly larvae and feed and
grow in horse dung. Pupae are formed in dry places.

Stable flies transmit the following pathogens that cause a variety of diseases like SURRA
disease of horses.

Trypanosoma evansi

T. gambiense

T. rhodesiensi s
T. brucei

Leishmania tropica

L. maxicana

Bacillus anthracis

Brucella abortis

Habronema microstoma

TICKS & MITES

TICKS
Boophilus annulatus

Ixodes ricinus

Hyalomma detritum

Haemaphysali s bispinosa

Amblyomma variegatum

Ticks are vectors of cattle fever, tick fever and several other pathogens that cause
enlargement of spleen and discoloration of urine. Ticks are generally whitish to bluish-gray in colour
with oval body wrapped in a tough and wrinkled skin. They prefer to suck blood from soft parts of the
host body, like ear pinna or base of the tail. Being Arachnids, they have 4 pairs of legs, a pair of
chelicerae modified for piercing and sucking and a pair of pedipalps. Female detaches from the host
and lays eggs in soil, where the eggs hatch into a 6-legged larval stage called seed-tick. The seed tick
grows in soil and finding an opportunity attaches on to the host and changing into a 4-legged nymph
which eventually molts to become adult. Life cycle takes about 60 days.

Diseases transmitted

Bovine piroplasmosis (caused by the protozoan, Babesia species. Horse tick fever is caused by 2
species of Babesia.Theileriasis is a disease of goat and sheep caused by the protozoan, Theileria
parva. Anaplasmosis is a protozoan disease caused by Anaplasma marginale. The Indian tick
typhus is caused by Rick ettsia conori in cattle in UP and Assam. Lyme disease is also transmitted by
ticks. KFD (Kyasanur Forest Desease) is a viral disease transmitted by ticks.
Control: Ticks can be controlled by hand-picking or by spraying lindane, carbaryl, malathion or
arsenic trioxide.

MITES
Sarcoptes scabei – Mange mite

Psoroptes equiovis; P. ovis; P. equi

Mites infect man, horse, goat, sheep, cattle, dog etc. They are very tiny, about 0.1 mm, oval in
shape and pale to greyish in colour. Adult possess 8 stubby legs while larvae are 6-legged. Eyes are
absent. Mouth parts are piercing and sucking type. Some species burrow in skin and make galleries or
wounds which causes intense itching. Later, fluid-filled pimples are formed which are covered with
scabs. These contain abundant mites and are the chief sources of infection by contact. Host may lose
hairs due to infection.

Control: Mites can be controlled by the application of Benzyl benzoate, Benzocaine-ethyl p-

aminobenzoate, Srobiton mono-ocleate, Lindane and sulphur ointment or by giving bath with lime-
sulphur, nicotine and lindane.

SNAKES OF INDIA
(Dr. Girish Chandra)

Out of about 2,000 species of snakes found in the world, about 272 occur in India,
which range from the 10 cm long worm snake to more than 6 meter long pythons and king
cobras. They constitute approximately 10 percent of the total snake species found in the world
and 80% of them are non-poisonous. The venomous snakes include only about 58 species
and there are only 4 species of snakes that are dangerous to man, namely, Cobra, Krait,
Russell’s viper and Saw-scaled viper.

NON-POISONOUS SNAKES

Common Worm Snake (Typhlops braminus Rhamphotyphlops braminus)

or
This snake resembles a worm, growing to a maximum length of 12 cm. It is small and
worm–like with smooth shiny scales and a blunt head and tail. They are reddish brown or
black and superficially look like earthworms. Worm snakes live underground in ant and termite
nests. They are also found under logs, moist leaves and humus in wet forest, dry jungle and
city gardens.
Indian Rock Python (Python molurus)
Indian Rock Python is found in the estuarine mangrove forest, the arid scrub jungles
and the cool dense rain forests. These large, thick bodied snakes have smooth scales and a
bright pattern of blotches. Like other pythons are non-venomous. They prey mainly on mice
and birds, although jackals, civets, and even wild boar and deer are occasionally eaten.
Snake can be 20 feet long and weigh up to 100 kilos. Usually sluggish, they have a peculiar
method of locomotion in a straight line, pushing forward with its ribs. Two races, the Indian
rock python and the reticulated python are common throughout India. Eggs vary in number
and are laid from March-June. The eggs hatch about 58 days after being laid. The oldest
python recorded in captivity was 22 year old.

Common Sand Boa (Eryx conicus)

It is a thick and round snake, 1 to 2 feet long. Its tail is very short, sharply tapering,
and conical. The head is covered by small scales. It is grey with yellowish-brown blotches on
the back forming a sort of irregular chain. Some specimens are of a dark-brown or blackish
colour, with irregular grey stripes across the back. The young are more brilliantly coloured.
The snake has a projecting snout, with the mouth
placed under it. The snout is adapted for burrowing
into the ground. Its belly-plates are narrow. The
eyes are very small, the pupil being vertically
elliptical and the iris speckled yellow. It burrows and
lives in holes, which are not very deep. It is an
extremely sluggish snake and is commonly seen in
a snake-charmer’s basket. It lives on small
mammals like mice and squirrels.

Red Sand Boa (Eryx johnii)

It is a species of snake found in Afghanistan, Pakistan, Iran, and India.
It can be identified by the presence of a mental groove, a pronounced angular ridge on the
muzzle, a blunt tail and costal scales numbering over 53. Food is mainly mammals such as
rats, mice and other small rodents which are killed by constriction. Ovoviviparous with up
to 14 young born at a time

Common Wolf snake (Lycodon aulicus)

It is a terrestrial slender bodied snake, brown in colour with yellow cross-bars which
are obvious near the head and diminishes near the tail. Found in Pakistan, Sri Lanka, India,
Nepal, Myanmar, Thailand, Malaysia, Indonesia, Philippines, Seychelles and China. A small
slender snake found throughout India. In the hills, it occurs at an elevation of about 2000 mts.

Barred Wolf Snake (Lycodon striatus)

 It is a terrestrial slender bodied snake, generally brown in colour with many cross-bars.
Found in Sri Lanka, NW India, Pakistan, USSR, S Turkmenistan, W Tajikistan, Uzbekistan,
Iran, Afghanistan and Pakistan.

Banded Kukri (Oligodon arnensis)

This is a small snake with prominent cross bands on its body. Found all over India and
up to an elevation of 200 mts. in the eastern Himalaya.

Striped Keelback (Amaphiesma stolata)

A small to medium-sized snake, this is closely related to and resembles the water
snakes and is found all over India and up to an elevation of 2,000 mts. in the hills.

Green Keelback (Macropisthodon plumbicolor)

A medium-sized keel-scaled snake found in the forested regions of India up to an
elevation of 1,500 mts.

Checkered Keelback Watersnake (Xenochropis (=Natrix)

piscator)
A medium-sized keeled snake found all over India up
to an elevation of about 3,000 mts. Brownish coloured with
chess board arrangement of spots, grows to a length of one
metre. It has two tear-marks just below the eyes. Shows
extreme aggression and readily bites anything but the bite is
completely harmless. It feeds mainly on small fishes and water frogs. Average length is more
than 4 ft. Found near fresh water lakes and paddy fields in Afghanistan, Pakistan, Sri Lanka,
India, Burma, Thailand, Laos, Vietnam, West Malaysia, China, Taiwan and Indonesia.

Olive Keel-back (Atretium schistosum)

It is a species of snake found in Sri Lanka, India and Nepal. It can be distinguished by
a single inter-nasal, 19 costals at mid body and 8 to 9 supra–labials.
It Lives in water or among the surrounding vegetation. Largely diurnal and feeds mainly on
frog, fish and crabs. A small to medium-sized snake found in central and peninsular India up
to an elevation about 1,000 mts.

Trinket Snake (Elaphe helena)

It is a terrestrial snake. It feeds on frogs, toads, etc. A medium-sized, slender snake
found all over India up to an elevation of about 4,000 mts. in the Himalayas.

Rat Snake (Ptyas mucosus)

 It is a terrestrial snake. The Rat snake can grow up
to 11 feet in length. Colours varied due to different climatic
conditions and change in habitats. The Rat snake has
black tear marks just below the labial. They have
numerous cross bars near the tail. It is voracious feeder of
rats and mice and frogs. Their size and colour are similar
to the cobras. Rat snakes are found wherever rats and
frogs/toads are prevalent. So, of course, they are often found in rice fields and in human
habitation. The colour varies from jet black in the hills to yellowish or brown. The female lays
about 8 to 16 eggs and the young start their diet on frogs.

Fasciolated Rat snake or Banded Racer (Argyrogena (=Coluber) fasciolatus)

This harmless, olive-brown snake is beautifully ornamented with black and white cross
bars that gradually disappear along the mid body. This can be plucky and aggressive if
irritated. It feeds on small mammals and amphibians. It is found throughout India, although it
is fairly common southwest India. Little is known about breeding habits. Oviparous, It is found
in India, Sri Lanka, Pakistan, Nepal and Bangladesh. Average size is over 1 metre. Anal 2,
supra–labials 8, 3rd divided, 4th and 5th touching eye, 5th and 6th highest touching temporal.

Bronze-back Tree Snake (Dendrelaphis tristis; D. pictus)

It is a species of tree-snakes found in Sri Lanka, India, Pakistan and Nepal. It is a long
slender snake with a bronze coloured line running down its back. It has a pointed head. It
feeds mainly on tree geckos, frogs and small birds. It gracefully moves through thick
vegetation. It broadens it neck to show white and bluish interscale coloration when disturbed.
This harmless snake prefers the tree tops to life on the ground. It is perfectly camouflaged
among the leaves because of its uniform ruddy brown skin. It springs on its prey and feeds
largely on lizards and tree frogs and occasionally on birds. This oviparous snake lays its eggs
between September-February. The 6-7 eggs in a clutch hatch 4-6 weeks after egg-laying and
the gestation period is 4-6 months.

Flying snake or Golden tree snake (Chryopelea Ornata)

This beautiful and harmless black snake has narrow pale
greenish-yellow cross bars. It prefers trees but also frequently
spotted in the grass and on low bushes. It feeds largely on geckos
and other lizards. The 6-12 eggs are laid in May, while hatchlings
have been recorded in June. They prefer to live on large trees and
appear to glide for some distance.

Royal Snake (Spalerosophis diadema)

A medium to large-sized snake found in the drier tracts of Rajasthan, Punjab,
Haryana, Uttar Pradesh, Jammu hills and Himachal Pradesh up to an elevation of 2,000 mts.
Green Wine Snake or Green whip snake (Ahaetulla (=Dryophis) nasuta)
A medium to large-sized snake found all over India, except in the northwest and parts
of the Gangesplain. They may occur at elevation of about 2,500 mts. preferring low bushes
and trees. Parrot green in colour with faint yellow and blue lines. It moves very fast from
branch to branch on trees and bushes.

Common Cat Snake (Boiga trigonata)

A small to medium-sized snake found all over India up to an elevation of 3000 mts. in
the Himalayas. They are nocturnal in habit and prefer to spend the daylight hours in a cool
place.

Dog-Faced Watersnake (Cerebrus rhynchops)

A medium-sized snake found in the coastal tracts. They live in muddy and rocky areas
in estuaries, mangrove swamps, salt pans and deserted areas. It is grey with black marking on
the back, and two stripes running behind each eye. It is a rough, dull snake, one of the six
species of “rear fanged” swamp snakes in India.On land this snake is one of the “side
winders”. In rapid movement, it does a kind of sideways leap. All brackish water snakes give
birth to about 10 to 30 young at a time.

Indian Egg eater (Elachistodon westermanni)

It is a rare species of egg-eating snake found in Bangladesh, India, and Nepal. Also
called the Westermann’s snake, it belongs to the monotypic genus Elachistodon. Recent
discoveries of the species from Maharashtra and Gujarat suggest that the species may be
more widespread. The snake has special adaptations with vertebral hypapophysis, a
projection of the backbone into the oesophagus that helps in cracking eggs. After an egg has
been swallowed whole, these projections hold it and then puncture and crack the shell. The
contents are then be swallowed and the collapsed shell is regurgitated. Egg-eating snakes are
mainly arboreal, enabling them to access eggs in birds’ nests. Generally less than 1 m in
length, it is a slender grey-brown snake with two V-shaped markings on the top of its head
and a regular pattern of dark markings along its back.

POISONOUS SNAKES OF INDIA

There are three types of venomous snakes: Opisthoglyph are the rear-fanged
snakes, the fangs with a ‘groove’ that venom flows down. The
Boomslang (Dispholidus typus) and the Twig snake (Thelotornis kirtlandi)are
examples. Proteroglyphs are the fixed front fang snakes that have non-movable front fangs.
Examples of this type of snake are the
cobras (Naja), kraits (Bungarus), mambas (Dendroaspis), and
coral (Micrurus) snakes.Solenoglyph have movable front fangs which fold back into the
mouth until they are needed. Examples include rattlesnakes (Crotalus), eyelash
vipers (Bothriechis), and copperheads (Agkistrodon).

King Cobra (Ophiophagus hannah)

The third largest snake in India, the king cobra is also one of the most courageous,
poisonous and aggressive snakes. Their hood is relatively less inflatable than that of the
Indian Cobra. The body is blackish brown with lighter bands running throughout its entire
length. King cobra has a voracious appetite and their staple diet is snakes but they also eat
lizards and rats. Mating has been observed in March, with copulation lasting for about an
hour. The eggs are laid 5-6 weeks after mating. A maximum of 51 eggs have been recorded.
King cobras can reach 18 feet (5.5 meters) in length, making them the longest of all
venomous snakes. When confronted, they can raise up to one-third of their bodies straight off
the ground and still move forward to attack. They will also flare out their iconic hoods and emit
a bone-chilling hiss that sounds almost like a growling dog. Their venom is not the most
potent among venomous snakes, but the amount of neurotoxin they can deliver in a single bite
is up to 7 ml that is enough to kill 20 people or an elephant.

Indian Cobra (Naja naja)

One of the most poisonous snakes found in India, the cobra has the
most distinctive features as its hood. There are three races mainly the Indian
Spectacled Cobra (Naja naja naja), the mono-ocellate cobra (Naja naja
kaouthia) and the black cobra. Cobra feed principally on rats, frogs and
toads, but can also take in lizards and snakes and also earthworm, ants,
cockroaches and eggs. Mating occurs in January and 12-22 eggs are laid in
April-May, which hatch within 45 to 69 days.

Bamboo pit viper (Trimersurus gramineus)

All vipers give birth to live young which hatch from eggs inside the mother’s uterus.
They can be distinguished from all other groups of snakes by the presence of the loreal pit
(heat sensitive pit enabling the snake to locate and capture its prey). This beautiful but
poisonous snake has a glossy green back and yellowish white bottom. It is usually sluggish
during the day but when provoked it anchors itself firmly by its prehensile tail with an open
mouth. It prefers hilly forests and bamboo forests.

Russell’s viper (Daboia =Vipera russelli)

This is a medium to large-sized snake with a characteristic bright pattern on its body.
Found all over India, both in the plains and hills up to an elevation of about 3,000 mts. This
snake grows to a maximum length of166 cm. The average length is about 120 cm on the
mainland, although island populations do not attain this size. The head is flattened, triangular
and distinct from the neck. The snout is blunt, rounded and raised. The nostrils are large, in
the middle of a large, single nasal scale. The lower edge of the nasal touches the naso–
rostral. The supra–nasal has a strong crescent shape and separates the nasal from the naso–
rostral on the anterior. The rostral is as broad as it is high. The body is stout, the cross-section
of which is rounded to cylindrical. The dorsal scales are strongly keeled; only the lower row is
smooth. It feeds primarily on rodents, especially murid species. However, they will eat just
about anything, including rats, mice shrews, squirrels, domestic cats, land crabs, scorpions
and other arthropods. Adults are reported to be persistently slow and sluggish unless pushed
beyond a certain limit, after which they becomes fierce and aggressive. Juveniles, on the
other hand, are generally more active and will bite with minimal provocation.

Saw-scaled Viper (Echis carinatus)

A small-sized snake found all over India, usually in the plains. They may occur in
areas as high as 2,000 mts. in the north–western
Himalayas. Size ranges between 38 and 80 cm in
length, but usually no more than 60 cm. Head distinct
from neck, snout very short and rounded. The nostril
between three shields and head covered with small
keeled scales, among which an enlarged supra ocular
is sometimes present. They move about mainly by
side winding: a method at which they are considerably proficient and alarmingly quick. It feeds
on rodents, lizards, frogs, and a variety of arthropods, such as scorpions, centipedes and
large insects. The population in India is ovoviviparous. In northern India, mating takes place in
the winter with live young being born from April through August.

Himalayan pit viper (Gloydius himalayanus)

It is a venomous pit viper species found along the southern slopes of the Himalayas in
Pakistan, India and Nepal. Medium-sized snake, with distinct elongated head covered with
large symmetrical scales; a distinct pit between eye and nostril. Dorsum light brown, gray to
dark brown. A median series of dark brown blotches, alternating with lateral row of spots. A
broad dark band from eye to the angle of mouth. Supralabials light with dark mottling. Ventrum
light gray with dark clouding and fine spotting. This snake frequents rocky wooded hill sides,
where it lives in caverns and crevices among rocks, hibernates in winter from October to April.
Basks in bright sunny winter days, habitually sluggish. Feeds mainly on skinks and other
mountain lizards.

Common Krait (Bungarus caeruleus)

Found almost all over India, they are nocturnal in habit. Commonly found in northeast
India, Bihar, Orissa, Madhya Pradesh, Andhra Pradesh and Uttar Pradesh up to an elevation
of 1500 mts. It is easily identified by its triangular body cross-section and the marked vertebral
ridge consisting of enlarged hexagonal vertebral shields along the middle of the dorsal side.
The head is not distinct from neck. The eye is black. It has arrow-head like yellow markings on
its black head and has yellow lips, lore, chin and throat.

Banded Krait or (Bungarus fasciatus)

They are medium to large-sized snake with prominent
yellow and black bands on the body. The banded krait has been
recorded to grow up to a length of 2 metres in M.P., Bihar, Orissa,
U.P. and Assam. Sometimes there is a black spot on the head. It
feeds on other snakes.

Sleder Coral Snake (Callophis melanurus)

A small slender snake found in most parts of the country except parts of central and
northeast India, Bihar, Orissa, Madhya pradesh, Andhra Pradesh and Uttar Pradesh up to an
Elevation of 1500 mts. A small and slender snake that has uniform pale brown body
colouration. This snake can be identified by its non-evident neck, blunt snout, widely spaced
nostrils which nearly are as wide apart as the eyes and small Supra-ocular compared to the
Frontal. Its head is mottled and dotted with black from which its specie name has been
derived. The tip of its tail may also have a similar colouration and it could serve to act as a
decoy. Some specimens have a brown colouration. Little is known about its behaviour. It
appears to be inactive and sluggish by day.

Hook-nosed Sea Snake or Beaked sea snake (Enhydrina schistosa)

This is a medium-sized snake having a flattened body and tail. Found along the coast
and coastal islands. They are seasonally found in the deep sea though they prefer coastal
areas. These snakes are generally found in the coast and coastal islands of India. They are
amongst the most common of the 20 kinds of sea snakes found in that region. They are active
both during the day and at night. They are able to dive up to 100 m and stay underwater for a
maximum of five hours before resurfacing. Sea snakes are equipped with glands to eliminate
excess salt. They are venomous, but not aggressive and are thus handled by the fishermen
without fear, though they are thrown back into the sea upon sight. The venom of this snake is
rated four to eight times as toxic as cobra venom. About 1.5 milligrams of its venom is
estimated to be lethal. The principal food is fish.

Dwarf Sea snake (Hydrophis caerulescens)

Scales on thickest part of the body are quadrangular or hexagonal in shape. There
are 14-18 maxillary teeth behind front fangs. Ventrals 253-334 and distinct throughout, though
not twice as large as the adjacent body scales. Colour bluish grey above, whitish below, with
40-60 broad bands. This snake ooccurs in Indian Ocean, Coasts of China, South China Sea
and Australia.
Model organisms for research ORGANISMS COMMONLY USED IN SCIENTIFIC
RESEARCH Some organisms by virtue of being easy to handle and breed and to maintain large colonies in the
laboratory, have become popular experimental animals. Some of them have been in use for such a long time

that information available on their biology, anatomy, physiology, genetics etc. is overwhelming. That makes

them suitable organisms for further scientific investigations. Details on some of these animals are given below.

 Escherichia coli
 Saccharomyces cerevisiae
 Neurospora crassa
 Arabidopsis thaliana
 Caenorhabditis elegans
 Drosophila melanogaster
 Mus musculus


Escherichia coli
 (Dr. Girish Chandra)



 BIOLOGY

 E. coli is facultative anaerobic Gram-negative non-sporing rod-like bacterium
that ferments lactose. It is catalase positive, oxidase negative and indole positive
bacillus. They can grow at a temperature ranging from 7 to 46°C and can grow at a
minimum water activity of 0.95. They are fairly acid tolerant and can grow at pH values
ranging from 4.4 to 10.

 Escherichia coli (Migula 1895) is a bacterium that is commonly found in the
lower intestine of warm-blooded animals. Most strains are harmless, but some, such as
serotype O157:H7, can cause serious food poisoning in humans. The harmless strains
are part of the normal flora of the gut and can benefit their hosts by producing
vitamin K2 and B12 or by preventing the establishment of pathogenic bacteria within
the intestine.E. coli has the ability to survive for brief periods outside the body which
makes them an ideal organism for fecal contamination.

 Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and
neonatal meningitis. In rarer cases, virulent strains are also responsible for hæmolytic-
uremic syndrome (HUS), peritonitis, mastitis, septicemia and Gram-negative
pneumonia.
 There is a particularly strain called E. coli O157:H7 that causes food poisoning.

 The complete sequence of the genome of a harmless laboratory strain of E.
coli (K-12) was reported in 5 September 1997 issue of Science, whose genome consists
of a single molecule of DNA containing 4,639,221 base pairs. These encode 4288
proteins and 89 RNAs. Many of the genes were already known but the function of 38%
of the genes (ORFs) remains to be discovered.

 More than 700 serotypes of E. coli have been identified. The different E.
coli serotypes are distinguished by their “O” and “H” antigens on their bodies and
flagella, respectively. The E. coli serotypes that are responsible for the numerous
reports of contaminated foods and beverages are those that produce Shiga toxin (Stx),
so called because the toxin is virtually identical to that produced by another bacterium
known asShigella dysenteria type 1.


 SPECIAL FEATURES

 The bacteria can be grown easily and its genetics is comparatively simple and
easily- manipulated, making it one of the best-studied prokaryotic model organisms, and
an important species used in biotechnology.

 Bacteria make useful tools for genetic research because of their relatively small
genome size compared to eukaryotes. E. coli cells only have about 4,400 genes whereas
humans contain approximately 30,000 genes. Also, bacteria, including E. coli, live their
entire lifetime in a haploid state, with no second allele to mask the effects of mutations.

 Bacteria typically grow much faster than more complex organisms. E.
coli grows rapidly at a rate of one generation per twenty minutes under typical growth
conditions. This allows for preparation of large cultures overnight and genetic
experimental results can be obtained in hours instead of days, months or years.

 Most gene cloning techniques were developed using this bacterium. E. coli is
readily transformed with plasmids and other vectors, and preparation of competent cells
is not complicated. Transformations with other microorganisms are often less
successful.


 CONTRIBUTIONS TO RESEARCH STUDIES

 Because of its long history of laboratory culture and ease of manipulation, E.
coli also plays an important role in modern biological engineering and industrial
microbiology. The work of Stanley Norman Cohen and Herbert Boyer in E. coli,
using plasmids and restriction enzymes to create recombinant DNA, became a
foundation of biotechnology.

 One of the first useful applications of recombinant DNA technology was the
manipulation of E. coli to produce human insulin. Modified E. coli have been used in
vaccine development, bioremediation, and production of immobilized enzymes. E.
coli cannot, however, be used to produce some of the more large, complex proteins
which contain multiple disulfide bonds and, in particular, unpaired thiols, or proteins
that also require post-translational modification for activity.

 E. coli is frequently used as a model organism in microbiology studies.
Cultivated strains (E. coli K12) are well-adapted to the laboratory environment and,
unlike wild strains, have lost their ability to live in intestine. Many lab strains lose their
ability to form biofilms.

 In 1946, Joshua Lederberg and Edward Tatum first described the
phenomenon known as bacterial conjugation using E. coli as a model bacterium, and
it remains the primary model to study conjugation. E. coliwas an integral part of the
first experiments to understand phage genetics, and early researchers, such asSeymour
Benzer, used E. coli and phage T4 to understand the topography of gene structure.
Prior to Benzer's research, it was not known whether the gene was a linear structure, or
if it had a branching pattern.
 SACCHAROMYCES CEREVISIAE

 (Dr. Girish Chandra)



 The word "Saccharomyces " derives from Greek term that means "sugar
mold". "cerevisiae" comes from Latin word meaning "of beer". Saccharomyces
cerevisiae is commonly known as "bakers yeast" or "brewers yeast". The yeast ferments
sugars present in the flour or added to the dough, giving off carbon dioxide and alcohol
(ethanol) to gain energy from the breakdown of carbohydrates. The CO is trapped as
2

tiny bubbles in the dough, which rises. Most modern brewers use highly cultured
isolates, e.g. Saccharomyces carlsbergensis, named after the Carlsberg Brewery in
Copenhagen.

 Saccharomyces belongs to kingdom Fungi because it has a cell wall made of
chitin, it has no peptidoglycan in its cell walls, and its lipids are esters. It also uses
DNA template for protein synthesis and it has larger ribosomes. It is considered yeast
because it is a unicellular organism so it can not form a fruiting body like other fungi
do.

 BIOLOGY

 Saccharomyces cerevisiae has both asexual and sexual reproduction. There are
two forms in which yeast cells can survive and grow, haploid and diploid. The haploid
cells undergo a simple lifecycle of mitosis and growth. The diploid cells similarly
undergo a simple lifecycle of mitosis and growth, but under conditions of stress can
undergo sporulation, producing a variety of haploid spores, which can go on to
conjugate to produce diploid stages again. These diploid cells can go through mitosis,
which they call budding or they can undergo meiosis and from an ascus which will split
into four ascospores. These haploids can then germinate and become haploid yeast
again (Madigan, 457).


 SPECIAL FEATURES

 Saccharomyces cerevisiae is a widely used model organism in science, and
therefore also is one of the most studied, along with E. coli. S. cerevisiae has obtained
this important position because of its established use in industry for making beer, bread
and wine and in ethanol production. It is also easy to manipulate and culture in the lab.
Additionally, yeasts are comparatively similar in structure to human cells, both being
eukaryotic. The availability of the S. cerevisiae genome sequence and the knowledge of
complete set of deletion mutants have further enhanced its utility as a model for
understanding the regulation of eukaryotic cells.

 Saccharomyces cerevisiae has been a very important genetic tool. It has been
used in genetic studies for many decades. Since it is very small and unicellular, large
 numbers of the yeast can be grown in culture in a very small space, in much the same
way that bacteria can be grown. However, yeast has the advantage of being an
eukaryotic organism, so that the results of genetic studies with yeast are more easily
applicable to human genetics.

 Saccharomyces cerevisiae reproduces abundantly and quickly, producing large
number of haploid cells, which can mate with an appropriate strain, undergoing
karyogamy and growing as a diploid organism. The diploids can undergo meiosis to
form ascospores, which are a recombinant haploid progeny unlike either parent. Mitosis
and meiosis can be more easily studied in these organisms.


 CONTRIBUTIONS TO RESEARCH

 Lee Hartwell, from the Fred Hutchison Cancer Research Center in Seattle, won
the Nobel Prize in Medicine in 2001 for his pioneering work on the mitosis genes
in S. cerevisiae. He shared the prize with R. Timothy Hunt and Paul M. Nurse of the
Imperial Cancer Research Institute in London, who worked on another species of
yeast, Schizosaccharomyces pombe. The genes they discovered and characterized in the
yeast as a model organism have led to some important discoveries in fighting cancer in
humans.

 Approaches have been developed by yeast scientists, which can be applied in
many different fields of biological and medicinal science. These include Yeast
hybrids for studying protein interactions, synthetic genetic array analysis for studying
gene interaction, and tetrad analysis. Many proteins important in human biology were
first discovered by studying their homologs in yeast, for instance, cell cycle proteins,
signaling proteins, and protein-processing enzymes. The petite mutation
in S. cerevisiae is of particular interest in genetic studies.

 Saccharomyces cerevisiae is one of the most important fungi in the history of
the world. This yeast is responsible for the production of ethanol in alcoholic drinks.
There are two ways Saccharomyces cerevisiaebreaks down glucose. One way is
through aerobic respiration in the presence of oxygen but when oxygen is not available,
the yeast will grow through anaerobic fermentation to gain two ATPs and produce two
by products, namely, carbon dioxide and ethanol. So if this yeast is grown in a
container lacking oxygen it will produce ethanol. Both of these processes use haploid
forms of the yeast for this process. In industry they isolate one strain, either a or ?, of
the haploid form to keep them from undergoing mating. In baker’s yeast there is a
strain where the production of carbon dioxide is more prevalent than ethanol.

  One important use of this yeast is that “live yeast supplementation to early
lactating dairy and goats significantly increased milk production”.

 Saccharomyces cerevisiae, which can proliferate in both haploid and diploid
stages, has been used extensively in aging research. The budding yeast divides
asymmetrically to form a mother cell and a bud. Two major approaches, study of life
span of buds and the stationary phase have been used to determine senescence and life
span in yeast.

 The demand for suitable genetically modified (GM) S. cerevisiae strains for
producing biofuel, bakery products and beverages or for the production of
biotechnological products (e.g. enzymes, pharmaceutical products) is continuously
growing. Numerous specialized S. cerevisiae wine producing strains were obtained in
recent years that possess a wide range of properties, capable of satisfying the demands
of modern winemaking industry.

 The unlocking of transcriptome, proteome and metabolome complexities will
contribute decisively to the knowledge of genetic make-up of commercial yeast strains
and will influence wine strain improvement via genetic engineering.

 Yeast extract hydrolysate from Saccharomyces cerevisiae helps to prevent
bacterial and fungal diseases in treated plants. It appears to act by enhancing the plant’s
natural defense mechanisms. The active ingredient is approved for use on all food
crops, as well as on turf and ornamental plants. Yeast extract is a common food
flavoring and has a long history of use as a plant fertilizer. No risks to human health or
to environment are known to occur by the use of yeast extract hydrolysate.
Neurospora crassa
Neurospora crassa is a type of red bread mold of the phylum Ascomycota. The genus
name, meaning "nerve spore" refers to the characteristic striations on the spores that
resemble axons.

BIOLOGY

Neurospora crassa produces two kinds of spores:

Conidia are spores produced by asexual reproduction,

by mitosis of the haploid nuclei of the active, growing fungus.

Ascospores, on the other hand, are formed following

sexual reproduction. If two different mating types are allowed to
grow together, they will fuse to form a diploid zygote. Meiosis of this zygote then gives rise to
the haploid ascospores.

Specialized hyphae,
called conidial anastomosis tubes (CATs), are produced by all
types of conidia and by conidial germ tubes
of Neurosporacrassa. The CAT is shown to be a cellular
element that is morphologically and physiologically distinct from
a germ tube and under separate genetic control. In contrast to
germ tubes, CATs are thinner, shorter, lack branches, exhibit
determinate growth, and home toward each other.

SPECIAL FEATURES

N. crassa is used as a model organism because it is easy to grow and has a haploid
life cycle that makes genetic analysis simple since recessive traits will immediately show up
in the offspring. Its entire genome of seven chromosomes has been
sequenced. Neurospora was used by Edward Tatum and George WellsBeadle in their
experiments for which they won the Nobel Prize in Physiology or Medicine in 1958

Neurospora is particularly well suited for genetic studies because:

 It can be grown quickly on simple culture medium.

 It spends most of its life cycle in the haploid condition so any recessive mutations will
show up in its phenotype.
 When the diploid zygote undergoes meiosis, the nuclei produced by Meiosis I, Followed
by Meiosis II, followed by one mitotic division are confined to a narrow tube, the ascus.
 The nuclei cannot slip past one another, if the zygote nucleus is heterozygous for a gene
and no crossing over near that locus occurs during meiosis I, the ascus will finally have
four spores at one end containing one allele and four spores at the other end containing
the other alleles.

The filamentous fungus Neurospora crassa, which has played an important role in the
development of modern genetics, has several unique genome-defense mechanisms, including
a process called repeat-induced point mutation. The draft genome sequence has revealed
several unusual features, which suggest that the evolution of N. crassa has been greatly
influenced by these defense mechanisms.

In 1941 Beadle and Edward L. Tatum decided to examine step by step the chemic al
reactions in a pathway. They used Neurospora crassa as an experimental organism. It had a
short life-cycle and was easily grown. Since it is haploid for much of its life cycle, mutations
would be immediately expressed and the meiotic products could be easily inspected.
Chromosome mapping studies on the organism facilitated their work.

Neurospora can be grown on a minimal medium and it’s nutritional requirements could be
studied by its ability to metabolize sugars and other chemicals. The scientists could add or
delete nutrients from the mixture of the medium. It is able to synthesize all amino acids and
other chemicals needed for its growth, thus mutants in synthetic pathways would easily show
up. X-rays induced mutations in Neurospora, and the mutated spores were placed on growth
media enriched with all essential amino acids. Crossing the mutated fungi with non-mutated
forms produced spores which were then grown on media supplied with only one of the 20
essential amino acids. If a spore lacked the ability to synthesize a particular amino acid, such
as Pro (proline), it would only grow if the Proline was in the growth medium. Biosynthesis of
amino acids is a complex process with many chemical reactions mediated by enzymes, which
if mutated would shut down the pathway, resulting in no growth.

Neurospora crassa has proven to be an excellent organism for studying various aspects of
biology of mitochondria by biochemical and genetic approaches. As N. crassa is an obligate
aerobe and its mitochondria are more similar to mammalian mitochondria than those of yeast.
The recent sequencing of the genome of N. crassa and a gene knockout project that is under
way make the organism even more attractive.

CONTRIBUTION TO SCIENCE
George Beadle and Edward Tatum during the late 1930s and early 1940s
established the connection Garrod suspected between genes and metabolism. They used X
rays to cause mutations in Neurospora, which affected a single gene and single enzyme in
specific metabolic pathways. Beadle and Tatum proposed the "one gene one enzyme
hypothesis" for which they won the Nobel Prize in 1958.

ARABIDOPSIS THALIANA

Arabidopsis thaliana is a small flowering plant native to Europe, Asia, and

northwestern Africa. A spring annual with a relatively short life cycle, Arabidopsis is popular
as a model organism for understanding the molecular biology of plants. Its genome is one of
the smallest plant genomes that was completely sequenced. Its
common name is mouse-ear cress.

Kingdom: Plantae
Angiosperms
Eudicots
Rosids
Order: Brassicales
Family: Brassicaceae
Genus: Arabidopsis
Species: A. thaliana

BIOLOGY
Arabidopsis is native to Europe, Asia, and northwestern Africa. It is an annual plant,
20–25 cm tall, with leaves forming a rosette at the base and few leaves also on the flowering
stem. The basal leaves are green to slightly purplish in colour, with coarsely serrated margin;
the stem leaves are smaller, unstalked, with entire margin. Leaves are covered with small
unicellular hairs called trichomes. The flowers are 3 mm in diameter.. The fruit is a siliqua 5–
20 mm long, containing 20–30 seeds.

Arabidopsis can complete its entire life cycle in 6 weeks. The central stem that
produces flowers grows after about three weeks, and the flowers naturally self-pollinate. In the
lab Arabidopsis may be grown in petridishes or pots, under fluorescent lights or in a
greenhouse.

SPECIAL FEATURES

Arabidopsis is widely used as one of the model organisms for studying plant sciences,
including genetics and plant development. As a photosynthetic organism, Arabidopsis requires
only light, air, water and a few minerals to complete its life cycle. It has a fast life cycle that
produces numerous self progeny in limited space requirements and is easily grown in a
greenhouse or indoor growth chamber.

The small size of its genome (about 157 million base pairs and five chromosomes)
makes Arabidopsisthaliana useful for genetic mapping and sequencing. Arabidopsis has one of
the smallest genomes among plants and is the first plant genome to be sequenced in 2000 by
the Arabidopsis Genome Initiative. Much work has been done to assign functions to its
27,000 genes and the 35,000 proteins they encode.

The plant's small size and rapid life cycle are useful for cultivation in a small space and
it produces several thousand seeds. It takes about six weeks from germination to mature seed.

Homeotic mutations in Arabidopsis result in the change of one organ to another — in

the case of the Agamous mutation. For example, stamens become petals and carpels are
replaced with a new flower, resulting in a recursively repeated sepal-petal-petal pattern.

Finally, plant transformation in Arabidopsis is routine, using Agrobacterium

tumefaciens to transfer DNA to the plant genome. The current protocol, termed "floral-dip",
involves simply dipping a flower into a solution containing Agrobacterium, the DNA of
interest, and a detergent. This method avoids the need for tissue culture or plant regeneration.

The availability of a broad base of knowledge about Arabidopsis and the previously
developed research toolkit invites scientists to establish new techniques, develop new
approaches, and test new concepts in Arabidopsis prior to their application in other species.

Some of its advantages as a model organism are as follows:

 It has one of the smallest genomes in the plant kingdom: 115,409,949 base pairs of DNA
distributed in 5 chromosomes (2n = 10).
 Very little of this is "junk" DNA, so most of the DNA encodes its 25,498 genes.
 Transgenic plants can be made easily using Agrobacterium tumefaciens as the vector to
introduce foreign genes.
 The plant is small — a flat rosette of leaves from which grows a flower stalk 6–12 inches
high.
 It can be easily grown in the lab in a relatively small space.
 Development is rapid. It only takes 5– 6 weeks from seed germination to the production
of a new crop of seeds.
 It is a prolific producer of seeds (up to 10,000 per plant) making genetics studies easier.
 Mutations can be easily generated by irradiating the seeds or treating them with
mutagenic chemicals.
 It is normally self-pollinated so recessive mutations quickly become homozygous and
thus expressed.
 However, Arabidopsis can easily be cross-pollinated to do genetic mapping and to
produce strains with multiple mutations.

CONTRIBUTION TO SCIENCE

The first mutant in Arabidopsis was documented in 1873 by Alexander

Braun, describing a double flower phenotype. However, it was not until 1943 that Friedrich
Laibach proposed Arabidopsis as a model organism. His student Erna Reinholz published her
thesis on Arabidopsis in 1945, describing the x-ray mutagenesis

In the 1950s and 1960s John Langridge and George Rédei played an important role in
establishingArabidopsis as a useful organism for biological laboratory experiments by writing
several scholarly reviews which were instrumental in introducing the model to the scientific
community. The breakthrough year forArabidopsis as the preferred model plant came in 1986
when T-DNA mediated transformation was first published, which coincided with the first gene
to be cloned and published.
 Observations of homeotic mutations led to the formulation of the ABC model of flower
development byE. Coen and E. Meyerowitz. According to this model floral organ identity
genes are divided into three classes:class A genes, which affect sepals and petals, class
B genes, which affect petals and stamens and class C genes, which affect stamens and carpels.
These genes code for transcription factors that combine to cause tissue specification in their
respective regions during development.

Arabidopsis was used extensively in the study of the genetic basis of phototropism,
chloroplast alignment, and stomatal aperture and other blue light- influenced processes. These
traits respond to blue light, which is perceived by the phototropin light
receptors. Arabidopsis has also been important in understanding the functions of another blue
light receptor, cryptochrome, which is especially important for light entrainment to control the
plants circadian rhythms.

In 2005, scientists at Purdue University proposed that Arabidopsis possessed an

alternative form of DNA repair, which they called "parallel path of inheritance". It was
observed in mutations of the HOTHEAD gene. Plants mutant in this gene exhibit organ fusion,
and pollen can germinate on all plant surfaces, not just the stigma.
CAENORHABDITIS ELEGANS
(Dr. Girish Chandra)

C. elegans is a vermiform and bilaterally symmetrical nematode with a cuticular

integument, four main epidermal muscle cords and a fluid- filled pseudocoelom. In the wild,
they feed on bacteria growing on decaying vegetable matter. They are generally hermaphrodite
but occasionally males also occur. In 1960's Sydney Brenner began using it for the study of
genetics of development and neurobiology.

BIOLOGY

C. elegans eggs are laid by the hermaphrodite forms. After hatching, they larvae pass
through 4 larval stages. When crowded or in the absence of food, C. elegans can enter an
alternative third larval stage called the dauer state. Dauer larvae are stress-resistant and do not
age. Hermaphrodites produce all their sperms in the L4 stage (150 sperms per gonadal arm)
and then switch over to producing oocytes. The sperms are stored in the same area of the gonad
as the oocytes until the first oocyte pushes the sperm into the spermatheca. The male can
inseminate a hermaphrodite, which prefers to use male sperms (both types of sperms are stored
in the spermatheca). When self-inseminated the wild-type worm will lay approximately 300
eggs. When inseminated by a male, the number of progeny can exceed 1,000. At 20°C, the
laboratory strain of C. elegans has an average life span of approximately 2–3 weeks and a
generation time of approximately 4 days. Hermaphrodites can mate with males or self-fertilize.

C. elegans has five pairs of autosomes and one pair of sex chromosomes. Sex in C.
elegans is based on an X0 sex-determination system. Hermaphrodite C. elegans have a
matched pair of sex chromosomes (XX); the rare males have only one sex chromosome (X0).

SPECIAL FEATURES

Strains are cheap to breed and can be frozen. When subsequently thawed they remain
viable, allowing long-term storage.

Because the complete cell lineage of the species has been determined, C. elegans has
proven especially useful for studying cellular differentiation.

From a research perspective, C. elegans has the advantage of being a multicellular

eukaryotic organism that is simple enough to be studied in great detail. The developmental fate
of every single somatic cell has been mapped out. In both sexes, a large number of additional
cells (131 in the hermaphrodite) are eliminated by programmed cell death (apoptosis).

C. elegans is one of the simplest organisms with a nervous system. In the

hermaphrodite, this comprises 302 neurons whose pattern of connectivity has been completely
mapped out.

A useful feature of C. elegans is that it is relatively easy to disrupt the function of

specific genes by RNA interference (RNAi). Gene silencing in this way can sometimes allow a
researcher to infer what the function of that gene may be. The nematode can be soaked in a
solution of double stranded RNA, the sequence of which is complementary to the sequence of
the gene that the researcher wishes to disable. Alternatively, worms can be fed on genetically
transformed bacteria which express the double stranded RNA of interest.

C. elegans has also been useful in the study of meiosis. As sperm and egg nuclei move
down the length of the gonad, they undergo a temporal progression through meiotic events
 The organism has also been identified as a model for nicotine dependence as it has
been found to experience the same symptoms humans experience when they quit smoking.

Caenorhabditis elegans is a microscopic (1 mm) nematode that normally lives in soil.

It has become one of the "model" organisms in biology because:

 It is eukaryotic animal with physiological systems, namely, feeding, nervous, muscle,

reproductive etc. found in higher animals.
 Large numbers of nematodes can be raised in petri dishes by feeding on E. coli which is
another model organism.
 It reproduces rapidly because of the generation time of only 4 days.
 It is transparent and hence cells in the living animal can be seen under the microscope
from the fertilized egg to the 556 cells of the newly-hatched larva and later the 959
somatic cells and a variable number of germ cells of the adult worm.
 It can be easily transformed with transgenes by injecting DNA into the animal.
 It can also be treated with antisense RNA.
 It shows signs of aging before death and thus may provide general clues as to the aging
process.
 Its cells contain 5 pairs of autosomes and, usually 2 X chromosomes which are easy to
study.
 These animals are hermaphrodite, producing both sperm and eggs so reproduction is
easy. Most of the time they fertilize themselves, so that any recessive alleles quickly
become homozygous and express in the phenotype.
 On rare occasions, nondisjunction occurs during meiosis with the loss of one X
chromosome. Animals with a single X are males and are able to fertilize the eggs of the
hermaphrodites.
 C. elegans was the first multicellular eukaryote to have its entire genome sequenced. It
contains some 19 – 20,000 protein-encoding genes incorporated in 100,258,171 base
pairs of DNA.
 In contrast to other eukaryotes, some 13 – 15% of its genes are grouped in operons
containing 2 – 8 genes each.

CONTRIBUTION TO SCIENCE

C. elegans was the first multicellular organism to have its genome completely
sequenced in 1998. TheC. elegans genome sequence is approximately 100 million base pairs
long and contains approximately 20,000 genes

In 2003, the genome sequence of the related nematode C. briggsae was also
determined, allowing researchers to study the comparative genomics of these two organisms.
 In 2002, the Nobel Prize in Physiology and Medicine was awarded
to Sydney Brenner, H. Robert Horvitz and John Sulston for their work on the genetics of
organ development and programmed cell death (PCD) in C. elegans.

The 2006 Nobel Prize in Physiology or Medicine was awarded

to Andrew Fire and Craig C. Mello, for their discovery of RNA interference in C. elegans.

In 2008 Martin Chalfie shared a Nobel Prize in Chemistry for his work on green
fluorescent protein (GFP) in C. elegans.

The complete sequence of all 100,269,912 bases was finished in 2002, making it the
first genome of a multi-cellular eukaryote in which every base is known. It is high-quality
sequence with an estimated error rate of less than 1 in 100,000. The sequence was produced
jointly by the Sanger Institute in Hinxton, England and the Genome Sequencing Center in
St. Louis. Funding for the project was provided to the Genome Sequencing Center by The
National Human Genome Research Institute (NHGRI), National Institutes of Health (NIH).
DROSOPHILA MELANOGASTER
(Dr. Girish Chandra)

Drosophila melanogaster is a dipteran insect that is commonly known as the fruit fly
and is one of the most commonly used model organisms in studies in genetics, physiology and
evolution. The Greek termDrosophila means “dew lover" and melanogaster means "dark gut".

Wild type fruit flies have brick red eyes, yellowish-brown colour and transverse black
rings across the abdomen. Females are about 2.5 millimetres long and males slightly smaller
and darker. Males are distinguished from females by the sex combs (dark bristles on the fore
tarsus) and claspers on the tip of abdomen.

BIOLOGY

The developmental period for Drosophila varies from 7 days at 28 °C to11 days at
higher temperatures. Females lay about 400 eggs into rotting fruit or other decaying vegetable
material. The eggs hatch after 12–15 and larvae complete development in about 4 days by
moulting twice. Larvae feed on micro organisms that decompose fruit and on the fruit itself.
Then the larvae pupate and adults take 4 days to emerge from pupae. The total lifespan is about
30 days at 29 °C.

SPECIAL FEATURES

Drosophila melanogaster is one of the most studied organisms in biological research,

particularly in genetics and developmental biology because of the following reasons:

 It is small in size, morphologically easy to identify and easy to culture in small containers
in laboratory.
 One can anesthetize them easily and manipulate individuals with unsophisticated
equipment.
 Drosophila are sexually dimorphic, making differentiation of sexes easy.
 It is easy to obtain virgin males and females, as virgins are physically distinctive from
mature adults.
 The care and culture requires little equipment of low cost and uses little space even for
large cultures.
 It has a short generation time of about two weeks and high fecundity, so that large
numbers could be reared in short time.
 The mature larvae possess giant chromosomes in the salivary glands called polytene
chromosomes which are used in cytological studies.
 It has only 4 pairs of chromosomes; three autosomes, and one sex chromosome.
 Males do not show meiotic recombination, facilitating genetic studies.
 Genetic transformation techniques are available since 1987.
 Its genome has been completely sequenced and was first published in 2000.
 Its embryo grows outside the body and can easily be studied at every stage of
development.
 The blastoderm of embryo is a syncytium, in which nuclei are not separated by cell
membranes, so that DNA injected into the embryo can have easy access to all the nuclei.
 The genome is relatively small for an animal, less than a tenth that of humans and mice).
 Mutations can be targeted to specific genes.

THE DROSOPHILA GENOME

Drosophila has 4 pairs of chromosomes, the X/Y sex chromosomes and the autosomes
2, 3, and 4. The size of the genome is about 165 million bases that contain about 14,000 genes
(human genome has 3,400 million bases and about 22,500 genes).
CONTRIBUTIONS TO SCIENCE

Charles W. Woodworth is credited with being the first biologist to

breed Drosophila and suggesting its use in genetic research. Thomas Hunt Morgan began his
studies in 1900 on heredity using Drosophila, and described sex-linked inheritance, which
helped to confirm that genes were found on chromosomes and linked traits led to the
construction of genetic maps that showed the locations of genetic loci on chromosomes. He
reported his first finding of a white (eyed) mutant in 1910 to the academic community. His
work on Drosophilaearned him the 1933 Nobel Prize in Medicine for identifying chromosomes
as vectors of inheritance for genes. The first genetic maps of Drosophila chromosomes were
completed by Alfred Sturtevant.

About 75% of known human disease genes have a recognizable match in the genetic
code of fruit flies (Reiter et al. (2001) and 50% of fly protein sequences have mammalian
analogues.

Drosophila is being used as a genetic model for several human diseases including the
neurodegenerative disorders such as Parkinson's, Huntington's, spinocerebellar ataxia and
Alzheimer's diseases.

The fly is also being used to study mechanisms underlying aging and oxidative stress,
immunity, diabetes, and cancer, as well as drug abuse.

The use of Drosophila is a powerful tool in teaching the Life Sciences. In fact it allows
the observation of sexual dimorphism, of mutants and of the life cycle. Moreover it permits the
realization of crosses aimed to demonstrate the sex linked characters and crosses aimed to
establish if a mutation is conferred by a dominant or a recessive gene.

MUS MUSCULUS
(Dr. Girish Chandra)

MORPHOLOGY

Mus musculus, commonly known as house mice,

originated in Asia, probably in India, and then spread
throughout Europe and Africa and to the rest of the world.
It belongs to family Muridae.
 Most laboratory mice are hybrids of different sub-species, which
include, Mus musculus domesticus and Mus musculus musculus. The long history of breeding,
together with their short life-spans and breeding cycles has made mice particularly useful for
studying mammalian genetics.

House mice are 6-9 cm long, with 6-10 cm long tail. Colour varies from light brown to
black with lighter shades on the ventral side. Weight ranges from 12 to 30 grams. Many lab
forms of mice have been developed that vary in color from white to black and with spots. Lab
mice and pet mice are often white, with ears and tail having little hair, weighing 12-40 gms and
length 15-19 cms long.

Young males and females are not easily distinguished; Males have testicles which are
usually hairless and can be retracted into the body. Females have 5 pairs of mammary glands
with nipples.

BIOLOGY

Mus musculus breeds throughout the year, although wild mice may have a reproductive
season extending from April to September. Males court females by emitting characteristic
ultrasonic calls in the 30kHz-110 kHz range. Following copulation, female mice develop a
vaginal plug that prevents further copulation. The estrous cycle is 4-6 days long. Females
generally have 5-10 litters per year if conditions are suitable. Gestation period is 19-21 days.
Litters consist of 3-12 offspring, which are born naked and blind. They are fully furred after 10
days, open their eyes at 14 days, are weaned at 3 weeks, and reach sexual maturity at 5-7
weeks. Average life span is about 2 years in captivity, but individuals have lived for as long as
6 years. In the wild, most mice do not live beyond 12-18 months.

SPECIAL FEATURES

Mice are convenient in research because their physiology is similar to that of humans
and their short life cycle makes breeding easy. They are mainly used to model human diseases,
to develop new drugs and to test the safety of proposed drugs.

Mice are the most commonly used animal research models with hundreds of
established inbred, outbred, and transgenic strains. They are common experimental animals in
the studies in biology, behaviour and psychology because they are mammals, and thus share a
high degree of homology with humans.
 It consists of a complex of several separate lineages and nearly 3000 different strains of
natural mutants, and transgenic and targeted mutant mice.

The mouse genome has been sequenced, and virtually all mouse genes have human
homologs. The mouse genome is about the same size as the human genome, and the
organization of genes is strikingly similar. Mouse genome sequencing indicates that mice and
humans share about 95 percent DNA sequencing similarity. This means that any gene in
humans is likely to have an identical or very similar counterpart in the mouse genome.

Mice can also be experimented with in ways that would be considered unethical for
humans.

Mice are small, inexpensive, easy to maintain and have high reproductive rate. Several
generations of mice can be completed in a relatively short time. They become docile if raised
from birth in captivity and given sufficient human contact.

Mice possess different coat colours that includes agouti, black and albino, which helps
in making genetic studies. Many laboratory strains are inbred to make them genetically almost
identical. The different strains are identified by a letter-digit combination, for example,
C57BL/6 and BALB/c. The first such inbred strains were produced by Clarence Cook Little in
1909, who promoted mouse as a laboratory organism.

The behavioural patterns of laboratory mice are significantly different from those of
most common house mice and wild races due to years of lab breeding. They are docile and can
be handled easily.

Besides primates, such as monkeys and chimpanzees, which are costly as well as
protected animals, the most closely related animal to humans is the mouse, Mus musculus.

GENOME
Sequencing of the mouse genome was completed in late 2002. The haploid genome is
about 3 billion bases long (3000 Mb distributed over 20 chromosomes) and therefore equal to
the size of the human genome. The current estimated gene count of mice is 23,786 while
humans are estimated to have 23,686 genes, which is strikingly similar.

CONTRIBUTION OF SCIENCE

Mice were first used for genetics research by the French biologist Lucien Cuénot in
1902.
 VERMICULTURE
Vermiculture means worm farming or culturing worms for selling them either to fishermen or to
compost manufacturers. When earthworms are used for the production of compost it is
calledvermicomposting. Earthworms burrow through the soil and feed on decaying organic matter,
excreting castings that are rich in nutrients and beneficial micro-organisms, which are about 20 times
more in worm castings than in normal soil. These beneficial organisms not only make available
nutrients to the plants but also suppress the growth of pathogens leading to healthy plants.

The most common worms used in vermiculture are, red worms (Eisenia foetida, Eisenia
andrei, andLumbricus rubellus). These worms thrive at temperatures between 20-30°C and can be
cultured indoor in boxes. Other worms like Perionyx excavatus and Eudrillius eugieneare are suitable
for warmer climates.

Vermiculture Medium

Crop residues, dry leaves, cattle dung are the basic materials for culturing earthworms, along with
saw dust, coir waste, paddy husk, slurry from biogas plant, poultry waste and vegetable wastes. Earth
worm culturing should be done under shelter to avoid direct sunlight and flooding by heavy rain.

Containers for Vermiculture

Brick lined pits, plastic tubs, wooden boxes, earthen pots or any other suitable containers can be used
for culturing earthworms. The ideal size is 1 m x 1 m x 0.3 m but dimensions can be changed to suit
the amount of waste material and convenience but the depth of pit should not be more than 45 cms.
Sometimes a heap of organic matter over plain ground in shady area can also be used for culturing.

METHOD OF CULTURING EARTHWORMS

1) Select a container or dig a pit of suitable dimensions in shady areas.

2) At the bottom of the pit or container, make a wormibed of 10 cm height using coir waste, paddy
husk, sugar cane trash, old papers etc. and spread a layer of soil over it. Wet the bed by sprinkling
sufficient water over it to obtain a relative humidity of 40-45%.

3) Mix the organic waste, cattle dung and slurry from biogas plant or any other organic material and
spread it over the bed. Keep this mixture for two weeks for half digestion, during which heating of
substrate will take place and temperature will rise to 50-55°C. Add 5-10 % of neem cake in this
material. Neem cake has beneficial effect on the growth of worms and kills harmful microorganisms.

4) Once the organic feeding material has cooled down to about 30°C, introduce worms by spreading
them over the bed at the rate of 500 worms for every 100 kg of organic material.
 5) Cover the bed with jute cloth, straw or similar material to provide shade and protection to the
worms. Water has to be sprinkled over this cover to maintain the moisture content at 45-50% and
temperature between 20-30°C. The pH of the raw material should not exceed 6.5-7.

The worms feed actively on organic matter and excrete mounds of castings near the surface. In about
60 days the compost will be ready.

6) To separate the worms from compost, take out the vermicompost and spread it in a heap in
sunlight on a plastic sheet. In about two hours all the worms will move to the bottom of the heap. The
compost can be removed from the top and used in fields, and the worms from the bottom can be
carefully collected and used for further vermicomposting.

VERMICOMPOSTING TECHNIQUE FOR FARMERS

 The vermicomposting is done by digging pits 3.0 m long, 1.0 m wide and 1.0 m deep
 At the bottom of the pits, broken pieces of earthen pots or bricks are spread to provide adequate
drainage.
 Over the layer of bricks, a bed of paddy husk or dry leaves is spread and then a layer of 2.5 cm
thick soil is spread over it.
 Cattle dung and other organic wastes are then spread over the bed in about three inches thick
layer.
 This organic material is allowed half digestion for about two weeks when temperature will
increase to about 50°C.
 Worms can be introduced after this incubation period is over and when the temperature has come
down to about 30°C. About 500 earthworms are then introduced into the pit, and a layer of
paddy straw is placed over them. Water should be sprinkled and the pit is covered with coconut
fibres or paddy straw or dry leaves to protect the worms from sunlight and predators.
 Fresh layers of organic waste can be added over this material every 3 or 4 days and covered with
a layer of soil and paddy husk.
 The earthworms will move to the upper layer after finishing food material in the lower layers.
 The pit can be charged with all kinds of organic wastes in layers of about 5 cm, covered with a
layer of soil till the material reaches the top of the pit.
 When the pit is full, it should be covered with husk and a layer of soil, and left for 30-60 days,
during which compost will be fully formed.
 To procure the compost, top layer should be exposed to sunlight to force the earthworms to move
to the deeper layers, so that compost could be removed from the top.
 The worms collected at the base can be used for inoculating new vermicomposting pits.
 The quality of vermicompost is far superior to other composts in terms of nutrients and other
plant growth promoting substances.
Vermicompost production using worms such as Eisenia foetida, Lumbricus
rubellus and Eudrilus eugeniae can be enhanced by using cattle urine for moistening organic wastes
during the preliminary composting stage before the addition of worms. This simple technique can yield
vermicompost of a higher Nitrogen content. Moreover, worms have been found to become more active
and vermicompost can be harvested at least 10 days earlier if cattle urine is used

Research on the mammalian genome is now being conducted by using mice. Much of this
research is aimed at genes and DNA sequences and documenting the phenotypic expression of genes.

A technology has been developed to enable engineering of knockout strains in mice, in

which a single known gene has been selectively deleted from the genome of every cell. For human
disease genes, knocking out the homologous gene in mice can provide an excellent model system for
studying the disease. The knockout mouse may show disease conditions similar to that of human
disease. Learning how the elimination of the gene in the mouse contributes to the growth of mouse
disease may give important clues about theinvolvement of homologous genes in humans. The disease
model mouse strains are now available
for cancer,Alzheimer’s disease, arthritis, diabetes, heart disease, cystic fibrosis, and obesity.

The autosomal variation and the genetic control of GPI have been determined by a comparison
of electrophoretic patterns of F1 and backcross progeny of three inbred strains of mice.

Construction of a small library of recombinant plasmids containing Mus musculus repetitive

DNA inserts has been completed.

A precision stereotaxic procedure for mouse brain research has been developed. A new design
in mouse stereotaxic head holder and a new device used to guarantee accurate alignment of the skull in
the stereotaxic device has been designed.