Atlas of Medical Helminthology and Protozoology - Text

Fourth edition
Helminthology
and Protozoology
IW
%v
P.L. Chiodini
A.H. Moody
D.W. Manser
Atlas of
Medical
Helminthology
and Protozoology
Commissioning Editor: Timothy Horne
Project Development Manager: Jim Killgore
Designer: Sarah Russell
Project Manager: Nancy Arnott
Fourth Edition
Atlas of
Medical
Helminthology
and Protozoology
Peter L, Chiodini bsc PhD frcp FRCPath
Tropical Diseases,
Consultant Parasitologist, Department of Clinical Parasitology, The Hospital for
Honorary Professor, The London School of Hygiene and Tropical Medicine, London, UK
Anthony H. Moody MPhh MiBioi c.Bioi fibms

Laboratory Manager, Department of Clinical Parasitology, The Hospital for
Tropical Diseases, London, UK
David W. Manser bsc ms c fibms
Biomedical Scientist, Department of Clinical Parasitology, The Hospital for Tropical Diseases, London, UK
Illustrated by Robert Britton
Churchill
Livingstone
EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS STDNEY TORONTO 2001
CHURCHILL LIVINGSTONE
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First published 2001

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Preface
Since this atlas was first published, major advances in laboratory workers and clinicians. Common to all these
immunology and molecular biology have transformed our disciplines is a need to understand the life cycles and
understanding of the parasitic diseases which affect morphology of the organisms they confront. It is hoped that
humans. The programme to eradicate Guinea worm is well this edition of the atlas will provide an appropriate
advanced and real progress is being made towards a introduction. The strong emphasis on diagnosis has been
malaria vaccine. However, none of the parasites described retained and since diagnostic parasitology still relies
in the first edition have yet been consigned to history heavily on morphology, we have strengthened this area
Indeed, Cyclospora and the microsporidia are newly with the introduction of colour illustrations and
recognised as important human pathogens even since the photom icrogr a p h s
third edition, and in some geographical areas the malaria
situation is worse, with the spread of multi-drug resistant We hope this book will help to kindle enthusiasm for the
Plasmodium falciparum malaria. There is a great deal left to effort to control these parasites and the diseases they cause.
be done.
London R L* C
team 2001 A. H. M,
Effective action against parasitic disease requires a
approach, including epidemiologists, biologists, diagnostic
D.W. M.
Acknowledgement
This atlas first originated from the Royal Army Medical Major-General, GO Cowan undertook revision for the third
College, London. The late Major-General HC Jeffrey and the edition and an abridged version of his introduction is
late RM Leach wrote the first two editions. Colonel, later included in this latest edition.
viii Atlas of Helminthology and Protozoology

Contents
Introduction 1
gjjMMHHnmnHnAnRMMHHHnnnnni
Helminthology 3 Protozoology 39
Nematode (round) worms 5

An outline classification of the parasitic protozoa
of humans 40
Enterobius vermicularis (thread or pin worm) 5
Trichuris trichiura (whip worm) 6

Intestinal protozoa 41
Ascaris lumbricoides (round worm) 7
Coccidia 41
Hookworms 8
/sospora belli 41
Strongyloides stercoraiis 9
Cryptosporidium parvum 42
Trichinella spiralis 10
Cyclospora cayetanensis 43
Wuchereria bancrofti (fi lari a sis) 12
Sa rcocys t is horn in is 44
Brugia malayi 13
Loa loa (eye worm) 14
Microsporidia general characteristics 45
Amoebae 47
On chocerca vo l vu l us (blinding worm ) 1 5
Entamoeba histolytica (causing amoebiasis) 48
Other filarial worms 16
Other intestinal amoebae 54
Dracunculus medinensis (Guinea worm) 17
Intestinal flagellates 56
Phasmid nematodes 18
Giardia intest inalis (G. Iambi ia) 56
Toxocara cams (dog round worm) 18
Chilomastix mesnili 56
Toxocara cati (cat round worm) 18
Trichomonas specie s 57
Gnathostorm spinigerum 19
Intestinal eiliates 58
Cutaneous larva migrans (creeping eruption) 19
Balantidium coli 58
Cestode (tape) worms 20

Tissue protozoa 59
Taenia solium (pork tape worm) 20
Toxoplasma gondii 59
Taenia saginata (beef tape worm) 21
Dwarf tape worms 22

Malaria parasites 61
Hymenolcpis nana 22
Hymenolepis diminuta worm) 22(rat tape Life cycle 62
Diphyllobothrium latum (fish tape worm) 23 Morphology 63
Larval forms of cestode infection in humans 24 Pathology and Clinical features 68
Echinococcus granulosus (dog tape worm) 25 Laboratory diagnosis 69
Echinococcus multilocularis 26
Body-fluid and tissue flagellates 70
Trematode (flat) worms 27 Leishmaniasis 71
Schistosoma species (blood flukes) 27 Visceral leishmaniasis (kala azar) 72
Schistosomiasis 29 Cutaneous leishmaniasis 73

Mucocutaneous leishmaniasis (espundia) 73
Clonorchis sinensis, syn. Opisthorchis sinensis (Oriental liver
fluke) 30 Diagnosis of leishmaniasis 73
Opisthorchis felineus, Opisthorchis viverrini (cat liver Trypanosomiasis 74

African type: sleeping sickness 74
fluke) 31
Fasciola hepatica (sheep liver fluke) 32 South American type: Chagas' disease 76
33 Laboratory diagnosis of trypanosomiasis 78

Fasciolopsis buski
Heterophyes heierophyes 34
34
Recapitulation 79
Metagon im us yokogawai
Paragonimus westermani (lung fluke) 35 Luminal intestinal protozoa 79
Common helminth ovo 36 Index 81
Atlas of Helminthology and Protozoology ix

Introduction
The protozoan and the helminth, as regards tropical pathology, The definitive host is that in which sexual reproduction
are in the ascendant. occurs (e.g. mosquitoes for malaria) or in which the mature
Sir Patrick Manson (1899) form of the parasite occurs (e.g. humans for African
trypanosomiasis). An intermediate host is another animal

Parasites to the Ancient Greeks were those who sat at essential to the completion of the life cycle (e.g. snails for
another's table and paid for their meal with flattery. In schistosomiasis).
biology, a parasite is an animal or plant living in or on
another {the host) and drawing nourishment from it. This Parasites cause disease in humans by:
definition could include viruses, bacteria and fungi as well
mechanical effects, e.g. hydatid cyst
as protozoa and helminths, but historically the first group
invasion and destruction of host cells, as in malaria
has been studied in microbiology the second in
allergic or inflammatory immune reaction by the host to
parasitology. In tropical diseases, Manson 's dictum remains
the parasite, e.g. toxocariasis and trypanosomiasis
valid today.
competition for specific nutrients, e.g. Diphyllobo thrium
latum for vitamin B p
Protozoa are small, unicellular organisms, which contain a
or there may be no obvious disease, as in Taenia saginata
nucleus and functional organelles. They reproduce quickly
in humans.
and a sexually in the host, but may have a sexual phase of
their life cycle in another host or vector.
Diagnosis in parasitic diseases depends on:
Helminths (worms), which are metazoa, are larger, a history of exposure and the clinical pattern of illness in
multicellular organisms, normally visable to the naked eye the patient
in their adult form. They reproduce sexually, usually within identification of the parasite itself in excreta (stool,
the host, and have pre-adult stages (ova, larvae) which live urine), blood, or specific tissues
externally or in other hosts. m indirect evidence of the parasite by testing the patient's
blood for antibodies
Transmission of parasites requires: detection of parasite antigens in clinical specimens
detection of parasite DNA or RNA in clinical specimens.
a source or reservoir which may be human or animal
a route of infection, e.g. ingestion, penetration or an
insect vector.
Atlas of Helminthology and Protozoology 1

Helminthology
Worms of medical importance
r
8MW MHHHHHnHHHI
Nematodes Cestodes Trematodes

worms)
(tape (flukes)
(round worms)
* Unsegmented - Segmented * Unsegmented
* Possess scolex, neck and proglottids Leaf-like or cylindrical

* Possess mouth, oesophagus and anus
-Important in further diagnosis * Generally hermaphroditic
Hermaphroditic
in general, sexes separate Reproduction (digenetic)
Reproduction
* Reproduction -Oviparous -Oviparous
-Sometimes multiplication within larval forms -Multiplication within larval forms
-Oviparous
-Larvipamus * Infection generally by encysted larvae * Infection mainly by larval stages entering
intestinal tract, sometimes through skin
* Infection by
-Ingestion of eggs, or
-Penetration of larvae through surfaces, or
-Arthropod vector, or
-Ingestion of encysted larvae
4 Helminthology
Nematode (round) worms
Enterobius vermicularis (thread or pin worm)
Life cycle
Maturation
in humans
15-26 days
Contaminated
hands, food, drink,
clothing, dust.
Autoinfection
by scratching
Very frequent
Caecum and
lower ileum
Gravid female /
crawls through
anus to oviposit
on perianal skin
Mature in hours
(viable for months)
Distribution
350 million infected worldwide, often group or institutional

infection.
o
o
Pathology and Clinical features 00 P
Most infections are asymptomatic. Perianal itching may be Clear adhesive tape slide 55 x 25 pm
troublesome. In females, migrating worms may cause pruritis
vulvae or vaginitis. Rarely, urinary tract infection or
appendicitis can occur. Migration into the peritoneal cavity

has been recorded.
Laboratory diagnosis
Mild eosinophilia.
Ova can be recovered from the perianal area using clear
adhesive tape or a cotton swab moistened with saline. Early
morning collection before washing gives best recovery. In
females, ova may occasionally be recovered from urine.

Trichuris trichiura (whip worm)
Life cycle
Maturation
in humans
3 months
Contaminated
soil, food, etc.
Mainly caecum
r~i V t'I tj tf i
i
m -H
n HE
Maturation in soil 3-5 weeks
Pathology and Clinical features Ovum
Light infections may be asymptomatic. Heavy infections can

result in the trichuris dysentery syndrome, rectal prolapse,
rectal bleeding, anaemia, growth stunting and growth
retardation in children.
Eosinophilia may occur.

Ova may be recovered in faeces by concentration methods.
Distribution
L3 billion infected worldwide.
6 Helminthology
Ascaris lumbricoides (round worm)
Life cycle
Hards carry infective ova from

soil contaminated with human
excreta, vegetables, dust, etc.
Normal form Decorticated

60-45 gm
Adult life span

10-12 months
Embry onated Unfertilized
Larvae penetrate the mucosa, enter the lymphatics and

venules, migrate to the right heart and lungs, break out
into the alveoli, moult twice, ascend the respiratory tree
and descend the oesophagus to mature In the intestine.
Maturation in humans 2 months.
Mature in 1-2 weeks. Viable months -years Eosinophilia
Pathology and Clinical features
Larvae can cause pneumonitis with eosinophilia. Adult worms

can cause obstruction of the small intestine, bile ducts and
trachea; also appendicitis, pancreatitis and peritonitis. Children
may vomit up a bolus of adult worms, or cough up immature
worms.
Ova may be recovered from faeces by concentration methods.

Rarely larvae can be found in sputum, and must be
distinguished from those of Strongyloides. Eosinophilia is
present in the larval invasion stage,

No specific serology is currently available.
200-350 x 4-6 mm.

Distribution Smooth cuticle, unstriated, n on-segmented
1.47 billion infected worldwide.

Hookworms
Ancylostoma duodenale Necator americanus
New world
Old world
Buccal capsule
Buccal capsule
Cutting plates
2 pairs of teeth
Eosinophilia
bifid tips, spicules
tips tridigitate Anaemia
fused and barbed
Enter circulation, and via

heart, lungs, respiratory
tree and oesophagus

70 x 38 ^im
migrate to the intestine.
60 x 40 \xrr\
Maturation in humans
35 days
Allergy
Ground itch
"Worm
Ovum Ovum
Rhabditiform larva Filariform larva
Pathology and Clinical features Laboratory diagnosis
Ground itch may follow skin penetration by filariform larvae. Eosinophilia.
Pneumonitis can result from larval migration through the Ova may be recovered from faeces by concentration methods.
lungs. Adult worms in the jejunum ingest blood. Occult Rhabditiform larvae may be seen in old faecal specimens and
gastrointestinal bleeding occurs. Iron deficiency anaemia and must be distinguished from Strongyloides by the appearance
its sequelae in heavy infections. of the buccal cavity.
Distribution
900 million infected worldwide.
8 Helminthology
Strongyloides stercoralis
Rhabditiform larva
250 x 20 (im
Strongyloides filariform larva
Filariform larva
600 x 20 \im
9 enters mucosa, lays

eggs which hatch to
rhabdrtiform larvae.
Larvae mature in duodenum These then make their
(or bronchus) way to bowel lumen
Rhabditiform larvae Rhabditiform larvae metamorphose

passed in faeces in bowel to filariform larvae
Eosinophilia
Larvae enter circulation and

via heart, lungs, respiratory
New host Same host Same host
skin bowel wall
tree and oesophagus reach
intestine. Maturation m
humans 17 days
Survive weeks
in soil
Direct cycle Autoinfection
Under unfavourable
environmental
conditions
metamorphose to
infective filariform
larvae
Skin penetration by larvae may cause local irritation.
Free living Migrating larvae can cause pneumonitis, and ectopic larvae
can sometimes be found in the brain and other viscera. A
characteristic serpiginous urticarial rash (larva currens) is
seen on the trunk and buttocks.

Established infection may have no signs or symptoms, or
Indirect cycle Direct cycle present with larva currens alone. Diarrhoea, abdominal pain,
bloating and sometimes malabsorption can be found.
The Strongyloides hyperinfection syndrome results from
massive autoinfection with filariform larvae in the presence
Laboratory diagnosis of severe immunosuppression or cachexia. Risk factors
include steroid and/ or cytotoxic therapy, HTLV1 infections,
Eosinophilia may be present, but its absence does not exclude
HIV infections, malignancy severe malnutrition and other
diagnosis* It is essential to examine fresh specimens.
severe systemic disorders. Clinical features include diarrhoea,
Rhabditiform larvae can be seen in faeces by direct microscopy
gastrointestinal haemorrhage or perforation, pneumonitis,
or by concentration methods. Filariform larvae may also be
Gram-negative bacterial meningitis or septicaemia with high
seen in faeces, sputum and other body fluids, particularly
mortality.
in immunocompromised hosts. Faecal culture using charcoal
is an important diagnostic method. Duodenal aspiration and
Distribution
the string test' are also recommended isolation methods.
Serology by ELISA is useful in chronic infection. 70 million infected worldwide*

Trichinella spiralis
Life cycle
A given host can be definitive or intermediate, but two hosts,
Others:
both carnivores, are required to complete the cycle $
horses Swill,
dogs
foxes
cats Viviparous
wild pigs
bears
badgers Rat
seals A,
3-4 x 0.6 mm
/ i Larva
Actual size 90-100 x 6 limn
Humans are
infected by
eating raw or
Infected flesh is digested by gastric juices; the larvae are set free and develop into
undercooked
adults duodenum. The gravid ? burrows into mucosa and releases larvae which
in
infected pork,
enter circulation and are disseminated throughout the body
pork products or
honsemeat
Eosinophil ia and high serum CPK in the acute phase, At the

encystment stage, use muscle biopsy, muscle crush preparation
and serology (IFAT or ELISA).
Distribution Encysted larva

in muscle
10 Helminthology
Invasion
Intestinal inflammation leading to diarrhoea.
Inflammatory response leading to periorbital oedema,

haemorrhages under nails, muscle pains and myocarditis.
Dissemination
Migration may occur through any tissue but larval encystment
is only in striated muscle. A granulomatous response develops
elsewhere.
i
Localization
Especially muscles of respiration and tongue. Long term;
eventual fibrosis and degeneration, resulting in calcification.
Organization Laboratory diagnosis
At and larvae may be found

the diarrhoeal stage, adults
occasionally in faeces* Eosinophilia is high. At the encystment
stage, use muscle biopsy, muscle crush preparation and

serology (IFAT or ELISA).

Wuchereria bancrofti (filariasis)
Adults
Development in mosquito
Maturation time The larvae penetrate stomach,
2-3 weeks migrate to thoracic muscles,
May survive develop, then migrate to head,
several months mature and now infective
Nocturnal Head bluntly rounded

periodicity 9 80-100 x 0.25 mm
6 40 x 0.1 mm
Localization Microfilaria
Culex
230-320x 10
Mansonia
jim
Aedes
Anopheles
Microfilariae Tail pointed,

enter lymph channels free from nuclei
and mature Microfilariae appear in the
blood 1 year after infection
Sheathed
Distribution
17
Eosinophilia.
Microfilariae are found in peripheral blood collected between
Adult worms in the lymphatic channels cause proliferation 10pm and 2am, or at midday for W. bancrofti var. pacifica. Thick
of the lining of the endothelium. Surrounding infiltration of blood films are examined stained or unstained, concentration
eosinophils, macrophages, lymphocytes and giant cells causes by Knotts method will increase sensitivity. Filtration of dtrated
filarial granulation tissue leading to obstruction, secondary blood through a 5 micron pore size polycarbonate membrane
infection, fibrosis and calcification. The results of this are acute is the method of choice.
lymphangitis, filarial abscess, lymphadenopathy, elephantiasis, Microfilariae can also be found in chylous exudate, chylous
hydrocoele and chyluria. Tropical pulmonary eosinophilia urine and in hydrocoele fluid.
(TPE) occurs in individuals who are hyper-responsive to filarial Serology. ELISA is of use. Patients with TPE have high
antigens, giving rise to nocturnal cough, wheeze and low- filarial antibody levels. A specific W. bancrofti antigen
grade fever. immunochromatographic test is now commercially available.
12 Helminthology
Brugia malayi
Life cycle
Nocturnal periodicity
Mosquitoes
Life cycle as for

W. bancrofti (
p. 12)
Marcson/a
Anopheles
Aedes
As for Wuchereria bancrofti except for the specific antigen test.

Sheathed
Microfilaria
Two discrete
nuclei in tip
of tail
The adults resemble
W, bancrofti but are smaller
Distribution
These are similar to those of Wuchereria, but Brugia more

commonly affects the upper limbs. Hydrocoele, other genital
lesions and chyluria are rare.

Loa loa (eye worm)
Life cycle
Adults
6 30-36x0.6 mm
9 70 x 0.5 mm
Chrysops
Diurnal periodicity
Adult filanae migrate
under conjunctiva
Microfilariae invade
WCuticular bosses
{
subcutaneous tissue
and become adults
Life span
Maturation time Microfilariae lose sheath, penetrate stomach wall,
year 1-15 years
1 tissue,mature and migrate through body to mouthpaits.
Insect row infective. Maturation time 1012 days
Allergy
Gravid 9 discharges
microfilariae into
blood vessels
L Chronic
may
pruritus,
develop, skin
dead worms may
thicken,
papules
may
form abscesses
Calabar swelling
lasting hours to days
Reaction to
migrating adult
Microfilariae found
in peripheral blood
Eosinophilia
Microfilaria
250-300 x 6-8,5 |im
Distribution
33 million infected, mostly in the great river basins of Africa,

e.g> Congo, Niger.
Transient subcutaneous (Calabar) swellings due to

hypersensitivity to adult excretory products.
The adult worm may appear under the conjunctiva and can
be removed surgically Symptoms include fatigue, chronic
pruritus, rarely encephalopathy or nephropathy
Eosinophilia.
Microfilariae are found in blood by day (between noon and
14:00 hours). Nuclepore membrane filtration or centrifugation
after lysis of the blood (Knott's method) can be used.
Serology ELISA detects antibodies to filarial antigens but
is non-specific.
14 Helminthology
Onchocerca volvulus (blinding worm)
Life cycle
Simulium
Principally dammsum
(Buffalo fly)
No periodicity
Maturation time
6 days or more
Subcutaneous nodule
Adult 6 & 2 filariae
Cellular reaction,
then fibrosis
Dermatitis
Microfilaria
Unsheathed tail is tapered and free of nuclei

150-368 x 5-9 pm
Adults
J 19-42 cm. x 130-210 urn
34-50 cm. x 270-400 Jim
Pathology and Clinical features Distribution
Fibrous nodules develop round the adult worms, especially 17 million infected worldwide-
over the iliac crests. There may be some lymphatic obstruction;
elephantiasis lias been noted in Africa. The microfilariae cause
itching, excoriation, urticaria, depigmentation, lichenification,

sowda' and lymphadenopathy. When invading the eye, they
can cause inflammatory lesions in any part of the eye such as
sclerosing keratitis, choroid ore tiniti s and optic atrophy.
Blindness may ensue.
Where microfilariae cannot be demonstrated, a Mazzotti
test(DEC provocation test) can be useful.
Eosinophilia.
Adult worms can be detected in excised nodules,
microfilariae in the anterior chamber of the eye (slit lamp),
skin snips and raTely in blood and urine.
Specific serodiagnosis by ELISA and PCR for parasite DNA
on skin samples is in use.

Other filarial worms
These worms are much less pathogenic. Microfilariae of other

species are unsheathed,may be found in the blood and tissues
and differentiation from Wuchereria and Brugia is necessary.
Filtration requires 3 micron pore size membrane, because
of the smaller size of these microfilariae*
No periodicity.
Mansonella perstans
Nuclei continue to tip
Found in Tropical Africa and the coasts of Central and South
America. The vector is the midge Culicoide s. Microfilariae can
be found in the blood*
Mansonella streptocerca
Found in Africa. The vector is the midge Culicoides. Microfilariae
can be found in the skin. Blunt tail, tapered and curved into a crook
1 80-240 x 3 pm
Mansonella ozzardi
Found in South America and the Caribbean. The vector is the
midge Culicoides,
Microfilariae can be found in the blood and skin.
175-240 x 4.5 Jim
16 Helminthology
Dracunculus medinensis (Guinea worm)
Life cycle
9 Adult
Infected
drinking water
Larvae migrate to
loose connective tissue
Life span
and become adults
in humans
12 months
Gravid $ migrates
to superficial tissue
Calcified Guinea worm in

Larvae
X-ray of leg
Guinea worm 500-750 x 15-25 \im
in cydops after
two moults, larvae
metamorphose to
H
infective larvae
in 21 days
Cyclops
0.2 mm long
The gravid female causes and a burning

itching, urticaria 70 000 infected worldwide.
sensation, A blister appears which bursts to become an ulcer
(usually leg) with discharge of embryos and some fibrosis.
The adult female may be seen protruding from the ulcer. There
is often secondary bacterial infection, and sometimes arthritis
of the knee and ankle. Worms may fail to emerge, die and
calcify
Eosinophilia.
Larvae may be found in fluid from the ulcer. Areas where dracunculiasis is endemic (based on reported
cases in 1997). (Map reprinted from Weekly Epidemiological
Record 1997; 72(6};33-35; prepared by WHO/UNICEF
HealthMap Programme & CTD/DRA, Geneva: WHO.)

Phasmid Nematodes
Toxocara canis (dog round worm)
Morphology
Toxocara ; body is bent ventraily Toxascaris: body is bent dorsally.
Life cycle and occurrence Laboratory diagnosis
Ocular larva migrans (OLM) and visceral larva migrans (VLM) Eosinophil! a.
usually occur as distinct entities without overlap. VLM occurs Serology, Antibody detection by ELISA on serum. A vitreous
in younger children and gives rise to fever, pneumonitis and sample may be required in OLM. Examination of
hepatomegaly. Myocarditis, convulsions, psychiatric changes environmental soil samples for ova by concentration techniques
or encephalopathy may occur. OLM presents as unilateral may be an aid to control.
visual loss, often with squint* Retinal detachment,
Lung-respiratory
endophthalmitis or papillitis may occur.
In an incompatible host, the larvae

hatch in intestine, gain circulation
and are carried to viscera where
they cause granuJomata
Toxocara cati (cat round worm)

Life cycle
Human incompatible
host Visceral larva
migrans (as above)
Cycle like Ascaris or 65-70 p.rr

Toxocara canis cats,
.
in
not humans
18 Helminthology
Gnathostoma spinigerum
Morphology
Stout, reddish-coloured worms
Bulbous head
Ring of hooklets
Ovum in definitive host
Pair of fleshy lips Non-embryoriated

round mouth
Plug at one end
Leaf-like spines Superficially
anterior half pitted
67-70 x 38-40 pm
Life cycle and occurrence

stage larvae
1st 2nd 3rd
Hatches to
larvae armed Ingested by
New host
with spines cyclops
Occasionally humans are infected by 3rd stage larvae but

they cannot reach maturity. The larvae migrate to skin,
subcutaneous tissue, muscle and brain
./
Cutaneous
larva migrans
\
Visceral larva
migrans
1
G ran ulo mate
Abscesses
j n superficial
tissues
(or gnathostomiasis)
Laboratory diagnosis Distribution
ELISA for antibody detection* Histology or mophology of South East Asia, mainly Thailand,
worm if excised.
Cutaneous Larva Migrans (creeping eruption)

Caused by non-human hookworm larvae.
Normal cycle
Arrcyfostoma braziiiense
Pierce
Ancytosioma caninum skin
Uncinaria stenocsphaia
Blood Intestine
Filariform larvae New host
If they successfully invade humans, the intensely itchy infection lasts for months. Produce serpiginous
tunnel
Especially feet and

legs, buttocks Move 1-2 cm per day
Fail to penetrate the skin fully
and burrow in lower epidermis

MRHEBHKfBa
mm mmmrnmm*. MHrinPHIPIIMMPP
Cestode (tape) worms
Taenia solium (pork tape worm)

Life cycle
Usual Definitive host

Intermediate host liberated embryo, via (and reservoir)
bloodstream to tissue, especially muscle
Human
cysticercosis
Cysticercus is tibe rated, scolex e vagin ates, Infection with adult
attaches itself to mucosa of small intestine.
Develops to adult. Maturation time 3 months.
Life span up to 25 years
Development of cysticercus Section of human brain showing

(Cysticercus cellulosae 5 x 810 mm} viable larva of T soiium
r

Scolex Proglottid
Infection by larvae (cysticercosis). Cysticerci, generally
multiple, may occur in any site but are more frequent in the
brain and muscle. They excite reaction in the area, especially
when they die, winch manifests as inflammation, fibrosis and
later some calcification. This leads to focal CNS syndromes,
especially epilepsy
Infection with adults. Often there can be no pathology,
but there might be mild irritation of intestinal mucosa.
Eosinophilia.
Larval infections. There are several methods, including
histological examination of biopsy material, serology (TFAT,
ELISA, EITB) and radiology (CT or MRI scan of the brain.
X-ray of the thigh muscles).
Distribution
Pure infection with the adult. Gravid segments, ova and
scolex can be found in faeces. The uterine branches of the 5 million people infected worldwide. Taenia solium is endemic
mature segments can be demonstrated by injection of Indian in pig-rearing areas of the world where hygiene and animal
ink through the uterine pore. husbandry are poor.
20 Helminthology
Taenia saginata (beef tape worm)
Life cycle
Definitive host
and reservoir
Intermediate host,
liberated embryo
Motile segments rupture

and release eggs
Scot ex Ovum
30-40 pm
Scolex evaginates in small

intestine and attaches itself
to mucosa of jejunum
Gravid segment
5-10 m
1000-2000 segments
Strobile Uterus with 15-30 lateral branches

1 620 x 57 mm
Usually there is no pathology as Cysticercus bovis is unknown

Maturation time 8-10 weeks,
in humans. Occasionally there is vague alimentary upset.
Life span up to 25 years
Laboratory diagnosis Distribution
Gravid segments, ova and scolex can be found in faeces. Taenia saginata is found in beef-eating areas, especially in the
Uterine branches of the mature segments may be seen in a tropics.
crush preparation between two glass slides, or by Indian ink

preparation, as in T. solium. Ova are also found on the perianal
skin (on clear adhesive tape slides).

Dwarf tape worms
Hymenolepis nana
Life cycle
Autoinfection
*
in children
Segment
Broader
No intermediate
than long
host required
45 x 35 nm
Polar filaments
Ova passed in
faeces 30 days Pathology and Clinical features

after infection
Often there are none, but with heavy infection there may be
abdominal pain and diarrhoea. Anaemia and nervous
symptoms, including dizziness and irritability can occur in
Liberated embryo children.
penetrates villus and
becomes cysticercoid in
4 days, Cysticercoid
re-enters lumen, attaches
mucosa and
itself to
develops into adult worm Eosinophilia may be present. Ova found in faeces.
in 1012 days.
Distribution
36 million people are infected worldwide.
Hymenolepis diminuta (rat tape worm)

4 suckers
Life cycle
No hooks
300-600 x 4 mm
Intermediate host Host
Accidental ingestion
by human of 800-1000
infected insect segments
Segment
Resembles 1:-..^
H. nana
Ovum
Cysticercoid 70 x 50 pm
liberated, attaches
itself to mucosa No polar filaments
and develops to (hexacanth embryo)

adult worm
Generally there is no effect on the host
Embryo hatched
in gut, penetrates Laboratory diagnosis
intestinal
wall, develops
into cysticercoid
Ova in faeces.
in body cavity
Distribution
Worldwide, but rare in humans.
22 Helminthology
Diphyllobothrium latum (fish tape worm)
Life cycle
Human infected by
eating raw or
undercooked fish
Maturation
time 3 weeks
Life span
several Plerocencoid liberated in
Reservoir: /ears intestine, scolex evaginates

and attaches itself to mucosa
of small Intestine
-cats
-many wild
mammals
2nd intermediate host:
Plerocercoid in fish
(Carp, Trout)
(Sparganum) /
70 x 45 jim operculated
Procercoid liberated, penetrates
Hatches in 9-12 days
intestinal wall, develops into
hatches Plerocercoid (sparganum) in muscle
or viscera
Coracidium
1st intermediate host:
Procercoid in cyclops
ingested ******
Ciliated Sparganosis
Free swimming (see p. 26)
Coracidlum penetrates intestinal

and develops into procercoid
wall
in body cavity
2-7 x 10-12 mm
2x 1 mm
2 suctorial grooves or bothria
Scolex Strobila Segment
Generally there is none, but occasionally there can be 16 million infected worldwide in eastern seaboard of Canada
megaloblastic anaemia (through absorption of vitamin B12 and America, Brazil, Baltic States, parts of West Africa, North
by the worm). Siberia and South East Asia.
Eggs and gravid segments can appear in faeces. Megaloblastic

anaemia {low serum B12X
Cestode {tape) worms 23

Larval forms of cestode infection in humans
Sparganosis
Life cycle of such tapeworms
Sparganosis is caused by the extra-intestinal presence in the

human body of larvae of non-human tapeworms of the genus
Spirometra.
Morphology of spargana White, ribbon-like, motile structures

1-3 x 0.2-0. 7 cm
Pathology and Clinical features Types of spargana

Infestation with living larvae causes a painful oedema tons Most Spargana do not proliferate in human tissues. Sparganum
reaction. Dead larvae cause intense local inflammatory pwliferum is a very rare parasite in which sparganum
reactions. There are numerous eosinophils and there can be proliferates by lateral budding.
abscess formation. There can be ocular sparganosis in the soft
tissues near the eye, resulting in severe damage. Invasion of Laboratory diagnosis
the CNS may occur.
c.-\ Diagnosis of the disease is by examination of biopsy material
or excised larvae.
iW
1
' j
iV er
Distribution
o/
Oh The Far East mainly but occasionally elsewhere.
24 Helminthology
v
Echinococcus granulosus (dog tape worm)

Life cycle
Echinococcus granulosus causes hydatid disease.
Cyst in offal, esp. liver Adult

30-36 hooks in two rows
4 suckers
Immature
Intermediate host:
Definitive host:
Sheep, cattle etc. and
other herbivores a
Dog and other
canines Mature
Proglottids
Hydatid cyst
Surrounding host
tissue reaction
forming false
capsule
Laminated
membrane From
parasite Contamination by
Germinal
food and fingers
membrane
Human
intermediate
host
Cyst fluid
Hydatid sand Salts

Remains of germinal Enzymes
epithelium
Brood capsules
Protoscolices
Secondary
seeding from
ruptured cyst
Invaginated Evaginated on
entry into host
Liberated embryo
in cyst
penetrates mucosa,
carried by blood
stream to various sites
8%
abdominal
Brood capsules of Echinococcus granulosus /
n
Intraosseous cyst
Spreads along
medulla by budding
outside cyst.
Intraosseous cyst Semisolid; no fibrosis.

Echinococcus multilocularis
Life cycle
Host:
Foxes, wolves, etc.
Intermediate host:
Rodents
Ovum
^ Ova
by
ingested
eating fruit
contaminated with
fox droppings
Cycle as for
Germinal epithelium breaks through cuticular
layers, metastasizes to other sites
granulosus
Multllocular cyst (usually sterile)
Pathology and Clinical features of hydatid

disease
Echinococcus granulosus
Unilocular cysts. There is usually surrounding inflammatory
Eos in penetration of dead protoscolices
reaction and fibrosis. After years, the cyst may die, shrink and
calcify. There is general allergic reaction with eosinophilia,
bronchospasm, etc. Pressure effects can cause local tissue Laboratory diagnosis of hydatid disease
damage and obstruction of natural channels. Rupture or
Use serological tests on serum (e.g. ELISA, complement fixation,
leakage of the cyst can accentuate the allergic reaction. There
counter current immu noelectrophoresis
for Arc 5 or
can be anaphylactic shock and sometimes secondary
immunoblot). Microscopy of cyst fluid from operative
implantation, for example in the peritoneal region. There can
specimens can be used to assess viability of profoscolices.
also be secondary infection with formation of abscess.
Histological examination of a removed specimen is another
Osseus possibility
cysts. is no fibrosis although there
Usually there is
some cellular infiltration. Destruction of the bone can

sometimes lead to spontaneous fracture. Distribution
1 million infected worldwide. multilocularis is rare in humans,

Echinococcus multilocularis
but occurs in Northern Europe, Asia, North America and
Alveolar cysts. There are local pressure effects and allergy. Arctic regions. E, granulosus widespread
is in sheep-rearing
Germinal epithelium can act like a neoplasm with local areas of the world. Eradication is well advanced in Australia
infiltration or distant metastases. and New Zealand.
26 Helminthology
i .-i mini i i i mm mu mm i
Trematode (flat) worms

Schistosoma species (blood flukes)
Life cycle for all species
Vary in size according

to species and sex
Range 6.4-20 x 0,25-1 mm
Few \ Miracidium Cercaria
minutes
Development within snail host

4-8 weeks
Primary sporocysts 1
Secondary sporocysts 2
Developing cercariae 3
Life cycle in humans
Immature schistosomes
Carried in circulation
throughout body, generally
only survive and mature in
portal veins
Mature adults
Migrate to pelvic
or mesenteric venous
plexuses, 9 lays eggs
in small venules
Ova
Cercariae
1 . Pass through tissue
to lumen of viscera Lose tails, penetrate skin
and are voided of host in 3-5 minutes
2. Some gain general and enter circulation
via lymphatics
and may
circulation
land up anywhere
Trematode (flat) worms 27

Schistosoma species (blood flukes) (Continued)
Morphology Distribution
S. haematobium S. haematobium: 78 million
Ovary posterior half
4-5 testes
Tegument slightly
tuberculated
Terminal spine
Ovum 20-30 ova in uterus 112-170 x 40-70 pm
Host: Bulinus
S. nmnsoni S< mansoni: 57 million
Ovary anterior half
Lateral spine
Ovum Q _
1 - 4 ova in uteru s 140180 x 4570 (^.m
Host: Biomphalaria
S. japonicum S. japonicum: 69 million
Ovary central W ^
i V !
3 6-8 testes fcjSr

^ \ .
r t?
W
7ff
Tegument smooth f
< &
Lateralknob '
J *
Ovum 50-100 ova in uterus 70-1 05 x 50-80 pm

H
J ro
l_/
JL
Host: Oncomeknia
28 Helminthology
Schistosomiasis
Pathology
Penetration of the skin by cercariae (1) General

Skin penetration may not be apparent. Human and some non-
human Schistosoma species cause cercarial dermatitis
(swimmer's itch). This manifests with papules, macules, vesicles
and intense itching.
Migration and maturation of immature worms (2)
There are general toxic and allergic symptoms including

urticaria with eosinophilia, fever, abdominal pain and tender
hepatospienomegaly This is known as Katayama or snail
fever
Damage by eggs in tissue (3)

Resulting damage depends on the severity of the parasite
load. An inflammatory granuloma forms with epithelial, giant,
plasma and eosinophil cells and fibroblasts (Hoeppli reaction).
There is subsequent fibrosis and calcification. Such damage

may be local and/or ectopic.
Urinary schistosomiasis (4) Particular

Caused by S. haematobium. Initial toxic and allergic symptoms 4 6
are not marked, but the bladder and ureter are typically
involved with hyperaemia, terminal haematuria, dysuria and
frequency of micturition, papules, papillomata and ulceration.
Hypertrophy of the bladder can lead to later contraction. There
may be cystitis and calculus formation, with calcification and
squamous cell carcinoma. Fistulae may develop. There can
also be hydroureter and hydronephrosis. Ectopic lesions are
less severe than in other species. Genital schistosomiasis may
lead to lumpy semen, haematospermia or wart-like lesions
on the vulva.
Intestinal schistosomiasis (5)

Caused by S. mansoni There are marked initial toxic and
allergic symptoms. The large intestine and rectum are typically
involved with polyposis, papules, abscesses, ulcers,

papillomata, fistulae and ova in faeces. The bladder is
sometimes involved, with pathology as for urinary

schistosomiasis as above. There can be ectopic lesions; the
liver is frequently involved (receiving eggs via the portal vein
with inflammatory reaction and fibrosis leading to periportal
('pipe-stem') fibrosis with portal hypertension, oesophageal
varices, splenomegaly and ascites; there can also be lesions in
the brain, spinal cord and lungs.
Oriental schistosomiasis (6)
Caused by S. japonicum. Initial toxic and allergic symptoms

are marked and can lead to myocarditis and death. Intestinal
lesions are similar to those with S. mansoni infection, and the
small intestine is often involved. The Ever is infected as in Eosinophilia may be present.
S, mansoni. Hepatic involvement occurs as for S. mansoni. The Ova found in terminal urine by Nuclepore filtration or after
brain may also become involved. centrifugation. Ova may also be found in semen. Ova may
also be found in faeces directly or using formalin-ether
concentration, rectal scrapings or biopsies.
Serology. ELISA tests (using soluble egg antigen) are useful
6-12 weeks post-exposure. In many chronic cases, the diagnosis
will be made by serology alone.

Clonorchis sinensis, syn. Opisthorchis sinensis (Oriental liver fluke)
Life cycle
Ingestion of
Metacercaria in raw or
under cooked fish
Actual size
Duodenum
_Encysied
metscercariae
I ntra hepatic
bile duct
.immature
adult
Animal reservoirs:
Ova dogs, cats, etc.
Ovum
29 x 16
with operculum
2nd intermediate
1st intermediate
host A
ingested host
Cyprinoid
Carp
liberates Cercaria
3-4 weeks
Metacercaria
v in muscle
free swimming stage offish
24-48 hours \
Jntramolluscan phase
Important snail hosts:
Butinus
Parafossatvius
Alocinma
Sponocysts producing Rediae producing

rediae 1st generation cercariae 2nd generation

Adult flukes inhabit the distal bile ducts with epithelial 28 million infected worldwide.
proliferation, surrounding inflammatory reaction and
ascending cholangitis. Sometimes there is secondary bacterial
infection with jaundice and septicaemia. There can also be
eosinophilia. All this can lead to thick, dilated fibrous ducts
with adenomata of epithelium, bile duct stenosis and
cholangiocarcinoma. Many cases are asymptomatic. Acute
infection may lead to tender hepatomegaly. Chronic infection
can result in anorexia, low-grade fever, epigastric pain and
tender hepatomegaly
Ova are found in faeces and in bile (via duodenal aspiration
r
or 'string test ).
30 Helminthology
Clonorchis sinensis (continued)
Morphology
Ovum
Oral sucker
Qperculate
Ovary la bed Caeca 29x16 pm
embryonated
0 Ventral sucker
T
T Uterus coiled
Vitellaria in middle third

Testes
branched
10-20x3-4 mm
Opisthorchis felineus, Opisthorchis viverrini (cat liver fluke)
Morphology
Adult Oral sucker Ovum
Opercuiate
Ovary lobed Ventral sucker 30 x 11 pm
embryonated
0
T Uterus coiled
T
Cercaria
Testes lobed Vitellaria transverse
obliquely placed in middle third
Pigmented
eye spots
Excretory bladder,
Lancet shaped
long and sac-like
7-12 x 2-3 mm
Life cycle
Humans often
infected by
eating raw fish
Cercaria released
Direct into fli/Z/nus 1st after 2 -3 months
intermediate host

There are proliferative changes in the bile ducts* If the infection
is massive or repeated then there may be chronic cholangitis. Metacercariae

excyst in
Clinical features are similar to those of clonorchiasis.
duodenum
Migrate through
common bile duct
Laboratory diagnosis to the smaller
intra hepatic ducts
Ova can be found in faeces* Mature in
3-4
Distribution
O. felineus, is found mainly in Eastern Europe and Russia.

O. viverrini occurs in Thailand.

Fasciola hepatica (sheep liver fluke)
Encysted
metacercaria
Usual host sheep
Ovum
Hatches^ Cercaria
915 days
Miracidium
Intermediate host:
Human eats
invades
watercress with
encysted
metacer caria e
Intramolluscan cycle
Sporocysts -* Rediae
- Cercaria e
Accidental
host
Ovum Important snail hosts:
Lymnaea
Conical projection
Succinea
Shoulders
Actual
size of Metacercariae excyst in
adult duodenum, pass through
intestinal wall, peritoneal
cavity, liver capsule, fiver
substance, to reach biliary
passages to mature

immature worms through the liver can cause
Transit of
mechanical and toxic irritation with toxaemia, necrosis and
second ary Development in the bile ducts causes cystic
fibrosis, Duodenum
enlargement, endothelial hyperplasia and adenomata, and
secondary inflammatory infiltration causing fibrosis and Ova
Laid in biliary passages, pass to
cholangitis. There can be secondary bacterial infection causing intestine and voided in faeces
abscesses. Eosinophilia is marked. Worms can appear

ectopically in lungs, brain, eyes, etc. with similar reactions. If
raw sheep or goat's liver, infected by the adult fluke, is eaten Laboratory diagnosis
there can be local irritation and pharyngeal infection (Halzoun),
Ova are found in faeces. Serology (IFAT) is available.
Acute infection may present with fever, tender
hepatomegaly, epigastric pain, anorexia and vomiting. Jaundice
Distribution
may occur. In chronic infection, there may be no symptoms
or epigastric/right upper quadrant pain, hepatomegaly and The fluke is found in all sheep-rearing countries. About 1
vomiting. million people are infected worldwide.
32 Helminthology
Fasciolopsis buski
Life cycle
There is localized inflammation at the site of attachment with 15 million infected worldwide.
haemorrhages and occasional abscesses. There is also
eosinophilia. Lightly infected individuals may be

asymptomatic. Diarrhoea, abdominal pain, anorexia, nausea
and vomiting may occur.
Ova, and sometimes adults, are found in faeces*

Heterophyes heterophyes
Morphology
Adult
Ovum
Oral sucker
Scales, especially anterior 28-30 x 15-17 jam Operculate

Embryonated
Ovary
Caecae
0 Ventral sucker
TT Genital sucker armed
with spines
Uterus, coiled Armed with spines

Vitellaria in posterior third Pigmented eyespots
Very small 1-1.7 x 0.3-0. 4 mm
Life cycle
Definitive hosts: Raw or inadequately

cooked fish ingested
Metacercariae
excyst
Adult attached
Ovum direct to
to wail of small Cercaria Meta cercaria

intestine on or in mullet
Pathology and Clinical features Sporocyst - Rediae

-> Cercaria
There is a mild inflammatory reaction. Infected individuals
may be asymptomatic or have abdominal pain, diarrhoea,
anorexia and nausea. Ectopic ova have been found in the heart Distribution and laboratory diagnosis
and brain. Found and the Far
in the Nile Delta East. Ova in faeces.
Metagonimus yokogawai
Morphology
Ovum
Adult
Oral sucker
27 x 16 pirn Operculate
Pharynx (like Heterophyes) Embryonated
Ovary round
Caecae
0
TT
Ventral sucker Cercaria
(like Heterophyes)
Uterus colled
Testes Conspicuous seminal

round receptacle
Very small (one of smallest human flukes) Tail keefed

1 .5 x 0-6 mm
Life cycle
Uncooked fish
Definitive hosts

Adult in Ovum direct to
small
intestine
Metacercaria on
or in mullet
Sporocyst Rediae
Cercaria
Causes mild inflammatory reaction in the intestine.
Occasionally ectopic ova can cause granulomata in other Distribution
organs of the body especially the liver and brain. Prevalent in the Far East
34 Helminthology
Paragonimus westermani (lung fluke)
Life cycle
Life span 5~6 years
Also other mammals,

e.g. civet cat
Excyst in small intestine, Congested

pass through intestinal collapsed
wall, penetrate diaphragm lung with
and pleural cavity come to inflammatory
rest in lung infiltrate
Raw crab
or crayfish
meat
Ova voided in sputum
or swallowed and
voided in faeces
Metacercaria
250-500 jam
Adult Ovum
Miracidium
which is
ingested by:
80120 x 50-60 |im
7-12x4-6 mm
3-5 mm thickness
Main snail hosts: Intra-molluscan phase

Melanie (Semisulcospira) spp. Sporocyst^Rediae ->Cercariae Laboratory diagnosis
Ova are found in sputum after KOH digestion or faeces after
formalin-ether concentration. Serological tests, when available,
are CF or ELISA (using extract of adult flukes as antigen) or
gel diffusion. Chest X-ray or CT can also be used.

Distribution
The initial invasion has little pathological effect on the host,
On localization in the lungs, there is tissue reaction leading 5 million infected worldwide.
to formation of a fibrous tissue capsule (of a slate blue colour)
containing worms (generally in pairs), ova and inflammatory
infiltrate. The capsule is connected with the respiratory
passages. Secondary complications of these lung cysts include
bronchiectasis, abscess formation and haemoptysis.
Localization in other sites can cause cysts in any part of the
body (for example the brain, causing epilepsy). Eosinophilia
is a general manifestation. Chronic infection may be
asymptomatic. Cough, brown gelatinous sputum, chest
discomfort, shortness of breath and pleuritic chest pain may
occur.

mMm
Common helminth ova
Enterobius vermicutans Hookworm

Trichuris trichiura
Fresh Developed
Hymenoiapis diminuta Diphylfobothrium latum

Hymenolepis nana
Taenia spp.
Schistosoma haematobium Schistosoma mansoni Schistosoma japonicum
Paragonimus westermani
Ctonorchis sinensis
Fasciola hepatica and Fasciolopsis busks
Red blood cell
200
36 Helminthology
)
(a) Ascaris ovum (e) Toxocara cams ova
(b) Trichuris ovum () Hookworm ( Ancylostoma ovum
(c) Hymenole pis nana ovum
(d) Schistosoma mansoni ovum (h) Fasciola hepatica ovum
Common helminth ova 37

Protozoology
WM
i
An outline classification of the parasitic protozoa of humans
Empire Kingdom Phylum Class Order Genus
Eukaryota Archezoa Haeckel 1694 Metamonada Trepomonadea Diplomonadida Giardia
Enteromonadida Enteromonas
Retortamonadea Retortamoradida Chilomastix
Retortamonas
Microspora Micros porea Micrasponda Encephalitozoon
Enterocytozoon
Nosema
Septata
Trachipieistophora
Protozoa Goldfuss 1618 Peroolozoa Heteroiobosea Schizopyrenida Naegteria
Parabasaia Trichomonadaa Trichomonadida Dientamoeba

Trichomonas
Euglenozoa Kinetoplastidea Trypan osomatida Leishmania
Trypanosoma
Ciliophora Litostomatea Vestibulifeiida Balantidium
Apicomplexa (Sporozoa) Coccidea Eimeiiida Cryptosporidium
Cyclospora
isospora
Sarcocystis
Toxoplasma
Haematozoea Haemosporida Plasmodium

Piroplasmida Babesia
Rhizopoda Lobosea Acanthopodida Acanthamoeba

Baiamuthia
Entamoebidea Euamoebida Endolimax
Entamoeba
lodamoeba
Af\ Prnin7nnlnnw
Intestinal protozoa
Coccidia
Classification
Phylum Apicomplexa
Class Coccidea
Sexual-asexual cycle in same host
>
Parasitize intestinal ephithelium
Order Eimeriida
f
Growth period in host cell
1 1 1 1
Genus Isospora Sarcocystis Toxoplasma Cryptosporidium Cyclospora
Isospora belli (causing coccidiosis in humans)
Life cycle
Motile microgairiete released from

o, mature microgametocyte
Contaminated
fertilizes
food and drink
Mature macrogametocyte
Small intestine
and caecum
Zygote secretes
cyst wall
x
Sporogony
Sexual cycle
Sporozoites in host cell or
gut lumen
\ liberated
Nucleus divides
into2 sporoblasts
Penetrate cells of villi
Sporozoite
Further cells Each secretes cyst wail

\ invaded to become sporocyst
Transform into - Schizogony

trophozoites/# Asexual cyci*
in mucosal
cells
Merozoite Nucleus and cytoplasm divide
v
toform 4 sporozoites in each
sporocyst
* Cell
ruptures
Immature or mature
/sospora belli oocyst oocyst found in faeces
Schizont

Small bowel mucosal atrophy. Watery diarrhoea or Oocysts are seen in formalin- ether concentration of faeces or
steatorrhoea, weight loss and sometimes cholecystitis occur modified Ziehl-Neelsen or auramine-stained faecal smears.
in AIDS. Intraepithelial parasites may be seen in small bowel biopsies.
Coccidia (continued)
Cryptosporidium parvum
Type I Meront
Sporozoite
Ingested
(inhaled?)
Merozoite
Autoinfection
ThicK-walled oocyst Thin-walied oocyst

(sporulated) (sporulated) Type II Meront
Oocysts (ZN) Oocysts (au ranine)
Microgamont
Merozoite
Macrogamont

In the immunocompetent, there is short-term enteropathy Oocysts (4-5 \im in diameter) are found in faeces, using
with self-limiting diarrhoea. In the immunocompromised, for modified Ziehl-Neelsen stain, auramine or specific FITC
example a patient with AIDS or a child with severe combined labelled monoclonal antibody staining. They can also be found
immunodeficiency, there is chronic diarrhoea with in faecal concentrates, duodenal aspirates and duodenal
malabsorption and weight loss. Extra intestinal infection of biopsies. The oocysts are very small (5 pirn in diameter) and
the respiratory tract, biliary tract and pancreas may occur, round. Parasites may also be seen in small bowel biopsies,
Sucrose floatation is an alternative to formalin -ether
concentration.
Distribution
Cryptosporidia have a cosmopolitan distribution. Human and

farm animal strains exist; both can cause human disease.
Human infection is usually waterborne.
42 Protozoology
Cyclospora cayetanensis
Life cycle
Cyclospora
Oocysts are 8-1G Jim in diameter with a central morula of retractile spheres when unsporulated. These mature into a final
division of 2 sporocysts.

Acute onset of diarrhoea, followed by steatorrhoea. Colicky Oocysts are seen in faeces unsporulated when first passed.
abdominal pain and malaise. Partial villous atrophy may be Diagnosis is either by formalin -ether concentration, modified
seen. Ziehl-Neelsen stain or by auto fluorescence.
Distribution
Widespread, probably worldwide.
Unsporulated Speculated
Coccidia (continued)
Sarcocystis hominis
Probable life cycle
Definitive host:
Human
Oocyst
Occasionally humans can act as intermediate hosts for Sarcocystis of other animals*
Morphology
Cyst in human muscle Enlarged portion of

Miescher's tube x 100 Miescher's tube showing
Rainey's corpuscles (each
12-16 x 4-9 gm}; from
a human case

The intestinal stages produce diarrhoea and abdominal pain* Oocysts or free sporocysts are found in faeces. Histological
The clinical significance of muscle cysts is unknown* examination of biopsy specimens may show the sexual stages
in the intestinal epithelium.
Histology is the only way to diagnose the presence of
sarcocysts, although these are almost invariably incidental
findings.
44 Protozoology
Microsp oridia - general characteristics
All are obligate intracellular parasites- The vast majority of When spores are ingested by a new host, the cells are
species are in invertebrates, especially insects, lower vertebrates penetrated by means of an apparatus known as the polar tube.
and fish. Only a few have been reported from warm-blooded When this is fully extended, the sporoplasm passes through
vertebrates. the tube, to be inoculated into the cytoplasm of the host cell.
They are considered to be primitive organisms. Their Following infection, there follows a phase of multiplication
evolutionary history has been predicted from their prokaryote- by binary or multiple fission (merogony). The transition to
like ribosomal characteristics the absence of a separate 5.8S the spore-producing stage (sporogony) is heralded by the
rRNAand the nucleotide sequence of the small subunit (16S) secretion of an electron dense surface coat this will form
rRNA. They have no mitochondria. The infective stages are the future exospore layer of the spore wall. The primary
highly-resistant spores. These are very uniform in size for a sporogonic cells are sporonts, which divide into sporoblasts,
given species. which mature into spores, which are released when the host
cell ruptures.
Common species of microsporidia reported from humans. Most are AIDS associated.
Infections of the gastrointestinal tract and urinary system can be detected by the presence of spores in faeces or urine. Spores
from these sites can be visualized by staining them with the modified trichrome stain.
The spores of microsporidia are very small- 1 x 0.5 pm (See below)
Enterocytozoon bieneusi spores
Microsporidia (continued)
Exospore
Anchoring disc
Endospore
Cytoplasmic membrane
Polar tube
Nucleus
Posterior vacuole
Microsporidian spore
Life cycle
Alternative staining methods for microsporidial spores in
fnfective stage
Spore stool samples are modified trichrome stain and uvitex 2B or
calcofluor fluorescence.
Merogony I
Production of
sporoblasts
Production
of spores
I
Infective spores released into the gut lumen
46 Protozoology
Amoebae
Entamoeba
* Generally one nucleus in trophozoite
* Small karyosome at or near centre
- Nuclear membrane lined with
chromatin granules
* Forms cysts
Endoiimax
Generally one nucleus in trophozoite
- Large irregular karyosome attached
to nuclear membrane
No peripheral chromatin
Forms cysts
iodamoeba
* Generally one nucleus in trophozoite
* Large karyosome surrounded by
achromatic granules
- No peripheral chromatin
* Forms cysts
Dientamoeba
* Minute
* Generally binucleate
* Centrai particulate karyosome
* No peripheral chromatin
* No cystic stage
Species
Entamoeba histolytica! dispar Endoiimax nana iodamoeba butschiii Dientamoeba fragilis

Entamoeba colt
Entamoeba hartmanni
Entamoeba polecki
Entamoeba histolytica (causing amoebiasis)
Cysts from the
environment
Extra intestinal lesions
Invasion
Invasion
Encystation
when dehydrated
in bowel lumen
Invasion
of large intestine & Passed in
diarrhoea 1 Discharges
undigested food
Discharge'
1
in necrotic Excy station Precyst

debris in small intestine Passed in Condenses to
semi -formed' spherical mass
stool
Cyst
Secretes tough
cyst wall
Metacyst
Dissemination liberated from Food inclusions
cyst wall -glycogen
Chromidial bars
Cytoplasm divides
Ulceration, forming Two consecutive mitoses
occasionally metacystic pnoduce4
1
nuclei
amoeboma trophozoites
formation Invasion
Glyoogen and chromidial bars
-less conspicuous
-may disappear
Passed in semi-formed
or formed stool
Invasion
lnvasion j
Invasion
Important note
E. d/spar has a similar
life cycle but is regarded
To the environment as nominvasive and not
in faeces responsible for clinical
disease
Trophozoite
Outside the host

Die rapidly
Patient
Not infective by Resistant
or earner
natural route Infective
Via
* Polluted water
Viability Infected food handlers
* Moist, cool conditions Flies contaminating food
up to 12 days
Night soil cultivation
* In water 9-30 days
* Direct contact
48 Protozoology
Morphology
General - nomenclature
Trophozoite (Vegetative) Precyst or unripe cyst Ripe cyst
Important note
Membrane
, dispar is morphologically
Chromatin lining membrane identical to E. histolytica but
Fibril network the trophozoites are not

haematophagous
Karyosome
Cytoplasm
Particular - Includes differentiation from Entamoeba cofi, an Intestinal commensal.
Unstained preparations
E. histolytica Trophozoite E. coll
Granular Cytoplasm Conspicuously granular
Clear finger-like Pseudopodia Blunt
JW
M
Active
Purposeful
Generally invisible
Red blood cells (RBCs)

Movement
Nucleus
Inclusions
Sluggish
Ring
Not purposeful
eccentric
retractile granules with
karyosome
Vacuoles, crystals, vegetable w *

*
cells, bacteria, no RBCs
15-60 (im 1550 |im
Precyst and unripe cyst

Granular Cytoplasm Granular
May be retractile ring Nucleus Visible as retractile ring
Rod-like retractile chromidial Inclusions May be slender retractile
bars chromidial bars
Glycogen masses Glycogen masses
Ripe cyst
Round Shape Round
Retractile Wall Conspicuous retractile
double outline
1-4 retractile nuclei with Nuclei 1 -8 retractile nuclei with
central karyosome eccentric karyosomes
10-20 pm Retractile chromidial bars Inclusions Only rudimentary slender 10-33

often present chromidial bars
Pathology
Invasion of the large intestine

Mucosa
Muscularis mucosae
Submuoosa
Muscle layers
p
^r^=fl H2af&
'
1 '
,
iff '
Subserosa The primary Invasion of mucosa via crypts
ulcer Repair may:

Ly
-overtake necrosis with healing
keep pace with necrosis causing persistent
superficial lesions
Site of entry
Initiallyminute then irregular ulcer shape, 'Flask-shaped' Lag behind -extension
typically flask-like edges overhanging floor;
necrotic lysed tissue; amoebae invading
around discharge; necrotic debris, mucus
and amoebae
Extension in Muscularis mucosae relatively resistant
mucosa Accumulation of amoebae superficial to it
Lateral extension of lytic necrosis

Invasion elsewhere
in large bowel
Formation Abscesses may coalesce under intact
of sinuses mucosa
Later mucosa may slough with widespread
ulceration
Deep Muscularis mucosae eventually pierced

extension (directly or via vessels)
Deep necrosis of sub-mucosa even muscle

5
and sub-serosa
Complications and sequelae
Perforation
Peritonitis
Haemorrhage (rare)
Haemorrhage
Surrounding inflammatory reaction and

Secondary infection
fibroblastic proliferation
Amoeboma (rare)
A mass under oedematous mucosa with
(Clinically simulates neoplasm) internal abscesses of necrotic tissue and amoebae
-surrounding granulomatous tissue zone with eosinophils,
-intussusception
-obstruction
lymphocytes and fibroblasts
-outer firm nodular fibrous tissue
Invasion of blood vessels Extraintestinal lesions-page 52
Direct extension outside bowel
r
Entamoeba histolytica (causing amoebiasis) (continued)
Extra intestinal lesions in amoebiasis
Haematogenous spread Further haematogenous spread Further haematogenous spread
t t
Invasion of Secondary invasion, Further
large intestine
Formation
especially in liver of abcesses
direct
extension
*
Direct extension
Almost normal tissue

invaded by amoebae
Later some (slight)
polymorph infiltration
Red brown fluid

Cellular debris with
Cutaneous amoebiasis Fibrin thrombus containing amoebae stromal trabeculae
Spreading trice trapped in small vessels Usually bacterlaily
- irregular margins * Amoebae digest pathways into tissue sterile
Necrotic floor * Multiple small foci of necrosis
* Amoebae laterally Essentially no surrounding reaction Zone of stroma of organ
Direct extension
Haematogenous spread
Brain
May rupture into

bronchus {anchovy
sauce sputum)
Pleura-pulmonary
abscess
(Cardiac Ectopic sites
tamponade)
abscess
>
Secondary to
1
Concomitant with _ Liver
involvement
Skin of
1
Independent of
abdominal
wall after Progression
rupture or to abscess(es)
surgery
Peritoneal cavity and

other abdominal organs
Perianal skin,
balanitis, vulvitis
52 Protozoology
Diagnosis depends primarily on demonstration of haematophagous trophozoites of E. histolytica in stool samples, aspirates
from intestinal and other organs, biopsy material (pinch biopsy at proctoscopy or sigmoidoscopy and surgical biopsy from
elsewhere) and in mucus from rectal ulcers. ELISAs are available for the detection of Entamoeba antigen and specific E. histolytica
lectin antigen in faecal samples. Serology is the method of choice for diagnosis of amoebic liver disease.
Faecal appearances in amoebic dysentery
Character
Naked eye Faecal matter Always present
Mucus Not tenacious
Not abundant
Microscopic 1. Bacteria Numerous

2. Pus cells Scanty, well preserved
3, Red blood celts Often in rouleaux
4. Large macrophages Not a feature
5. Charcot- Leyden crystals May be present but are non-specific
6. Haennatophagus trophozoites of E. histolytica Present
Cu Itu re U sually lim ited to refers nee or resea rch a boratories

I
;
I ecti n ELI SA is used for specific identification
of E. histolytica from cyst or trophozoite. Enzyme electrophoresis from cultured trophozoite

Is an alternative.
Notes
Vegetative , histolytica when seen is actively motile and moves purposefully There are finger Tike, clear pseudopodia and
ingested red cells. No nucleus can be seen. Precysts or cysts found in semi-formed or solid stool have typical nuclear characteristics
(1-4 nuclei) and glycogen and ehromidial bars can be demonstrated.
Diagnostic tests
Polymorph leucocytosis. Examination of stool samples may show cysts and trophozoites of E. histolytica. Serological tests (IFAT,
ELISA, cellulose acetate precipitin, latex agglutination) but serology is positive inno more than 75% of cases of amoebic colitis.
Examine aspirated material for E, histolytica. Histology of rectal and colon biopsy material.
Other intestinal amoebae
Life cycle
Morphology
Unstained
Vegetative forms (trophozoites)
Entamoeba colt Endoiimax nana lodamoeba Dientamoeba Entamoeba Entamoeba dispar Entamoeba
butschiii fragilis histolytica hartmanni
, f
e> *
Size 15-50 p.m 8-10 pm 8-20 jj,m 5-12 pm 15-60 pm 15-60 pm 15-60 p.m
Motility Sluggish Sluggish Fairly active Very active Very active Active Active
Ectoplasm Little Little Little Abundant Abundant Abundant Abundant
Pseudopodia Blunt, mainly Blunt, mainly Blunt, clear Leaf-like, dear Finger-like, clear Finger-like r
dear Finger-like, clear
granular granular
Endoplasm All have granular cytoplasm with food particles, bacteria, crystals, RBCs
Ingested No ingested RBCs No ingested RBCs
vegetable cells, often in vacuoles. No ingested RBCs
Nucleus Ring of Generally Generally Two, collection Generally Generally Generally

refractive dots invisible invisible of dots invisible invisible invisible
Precyst
(round up, discharge food particles, bacteria, etc.)
Glycogen Often prominent Rare Conspicuous None Diffuse,soon soon

Diffuse, Diffuse, soon
vacuole disappears disappears disappears
Chromidial Rarely seen Rare None None Large Large Large

bars bars
retractile retractile bars refractile bars
Cysts
Size
$
10-33 p.m

5-14 pun 5-18
0
pirn None 10-20 jim 10-20 |im 8-10 |im
Shape Spherical or oval Oval Irregular None Spherical Spherical Spherical
Wall Thick Thin Thin None Thin Thin Thin
Glycogen Diffuse central None Well-defined None Sometimes Sometimes Sometimes

vacuoles persists persists persists
Chromidial Not usual None None None Sometimes Sometimes Sometimes

bars present present present
Nuclei 1-8 4 (at one end) 1 only None 1-4 1-4 1-4
numbers
54 Protozoology
Stained
Entamoeba coli Endoiimax nans lodamoeba Dientamoeba Entamoeba Entamoeba dispar Entamoeba
bQtschlii fragitis histolytica hartmannii
Cytoplasm With haematoxylin, stains bluish-grey RBCs also

indusions stain black
Stain black except glycogen as clear area
Nuclear
characteristics
Membrane
&Thick Thin
Q
Thick
00
Very delicate

Delicate
Chromatin on Coarse None Sometimes None Fine granules

membrane granular
Karyosome Coarse, generally Large Large lateral Central granules Small central
eccentric irregular
Fibril network May be chromatin No chromatin No chromatin Delicate fibrils Not often seen
particles
Harmless Harmless
Pathogenicity Harmless Harmless Harmless Disputed Invasive commensal commensal
commensal commensal commensal
Non-invasive Non-in vasive
Entamoeba coli cysts lodamoeba bQtschlii cysts Entamoeba histolytica! dispar cysts
Intestinal flagellates
Diagnosis Distribution
Trophozoites or cysts are found in stool samples or duodenal These protozoa have a worldwide distribution,
aspirates. Duodenal string test and stool antigen detection
ELISA are also possible for the detection of Giardia.
Giardia intestinalis (G, lamblia)
Life cycle
Cysts from
environment
Common Trophozoite
bile duct Sucking disc
Excy station
Blepharoplasts G. tambiia trophozoites
Multiplication
Binary fission 2 nuclei
14 x 7 jim Cyst (iodine stained)
(Thin nuclear membrane
Ency station with no granules. Thick wall
Central karyosome) (unstained)
2 axonemes 2-4 Nuclei
Granular
Parabasal body
Cysts to
environment
4 pairs of flagella
cytoplasm
Remains
Blepharoplasts of locomotor
8-12 |u.m apparatus
Unstained
-colourless
-motile with jerky movement
Pathogenicity
Common inhabitant of upper part of small intestine
Enteropathy, diarrhoea, steatorrhoea
G. lamblia cyst
Chilomastix tnesnili
Life cycle
Cysts from
environment
Trophozoite 6 flagellae
-3 free anteriorly
1 in mouth
2 surrounding mouth
Blepharoplast
Single nucleus
-well-defined thin nuclear membrane
-minute central or eccentric karyosome
Cytostome
Cysts to
Spiral groove environment
Anterior projection
Thick unstained
cell wall
Cytostome and remains of

locomotor apparatus
Unstained Single nucleus

-colourless or pale green -well-developed membrane
-actively motile, jerky -central or lateral karyosome
-no nucleus seen, only
7-10 [im
retractile granules
Pathogenicity Commensal-apparently harmless
56 Protozoology
Trichomonas species
Trophozoite
4 free flags ae anteriorly
1 1
Blepharoplast
(mass or granules)
One flagellum
attached by
Single nucleus
undulating
-delicate nuclear membrane
membrane
-central karyosome
Cytostome
15 pm
Vacuole with bacteria,

rarely RBC
Axostyle
No cystic
form
is known
Unstained
-colourless
-nucleus generally invisible
-axostyle as hyaline spike
T. hominis
This is illustrated above. The trophozoite inhabits the small and large intestine. There is no proof as yet that it has any
pathogenicity*
T. vaginalis
Morphologically this is the same as T. hominis (above) but there is no free posterior flagellum beyond the undulating membrane.
There is a marked parabasal body It inhabits the urethra in the male and the vagina in the female, and is a cause of urethritis
and vaginitis*
Demonstration of T. vaginalis is made by direct microscopy or after staining with acridine orange fluorescence stain* Cultures
can be made using Feinberg-Whittington or Diamond's medium.
Intestinal ciliates
Balantidium coli
Found in South and Central America/ parts of Asia and some Pacific islands*
In its vegetative state, recognizable by the oval shape/ coarse cilia, contractile vacuoles and the horseshoe- or kidney-shaped
macronucleus* Reproduction is by binary fission.
Vegetative Cytostome
Cilia
Macronucleus
Micronucleus
in concavity
Contractile
vacuole
50-100 x 40 70 fim
Life cycle
Cysts from
environment
Encystation
Multiply
by binary
fission Cysts to
environment
*V~i^ Reservoir pig

Problems occur in the ileum, colon and rectum but there is no
extra intestinal spread. The parasite is a cause of dysentery,
although the ulcers are wider mouthed than those of amoebic
dysentery. Secondary infection is frequent. The main
complication is perforation.
Trophozoites are found in diarrhoea and, in a fresh specimen,

can be seen in active rotational movement* Cysts are found in
semi-formed and formed stools.
58 Protozoology
Tissue protozoa
Toxoplasma gondii
Toxoplasma has a very wide mammalian host range.
Morphology
Tachyzoite Central karyosome
Pointed end Habitat
\ nucleus-ovoid, crescentic,
pyriform-nearer one end
Tachyzoite s: single (free
or intracellular) or
(pseudxysts)
in masses
Blue cytoplasm In nucleated cells, especially
macrophages
Paranucleus stains Nuclear membrane
as a small red dot
Bradyzoites (similar to
tachyzoites but less active

metabolically) in tissue cysts
Life cycle
Cat is definitive host:
Unsporulated oocysts
.passed in faeces
Cysts containing
bradyzoites in tissues
Ingested cysts in of intermediate host
meat (raw or
infective
undercooked)
Tachyzoites
transmitted
through
Oocysts In feed,
placenta
water, or soil
ingested by
intermediate
host ^
Contaminated Sporuiated oocysts

food and water
Intermediate hosts
Infected fetus
Tissue protozoa 59
Toxoplasma gondii (continued)
Congenital infection Other routes of infection
Woman may have affected child though

herself shows no signs of disease
Cerebral abscess
Frequently seen in patients with
HiV infection
C
"
'
\
'Gland ular-fever-tike' syndrome
\ J r '
Chorioretinitis
Acute fever
V J
Atypical
pneumonia
Lymphadenopathy
Enlarged
Congested
f
Chorioretinitis Micro \
J Atypical pneumonia
Serous effusions Parasitized
mononuclears
in bronchi /
Micro \
Reactive hyperplasia
Conspicuous
collections of
histiocytes / i
Diagnosis is usually made serologically by demonstration of specific antibodies. Methods include Latex agglutination, ELISA
and TSAGA, The gold standard' for Toxoplasma serological diagnosis is the Sabin- Feld man dye test.
Lymph node biopsy should not be required to diagnose Toxoplasma but if performed because another diagnosis was suspected,
the findings are as stated above.
Toxoplasma tachyzoites
j
60 Protozoology
x
Malaria parasites
Classification
Class Haematozoea
Order Haemosporida
* Sexual and asexual generations in different hosts
Parasitic in fixed tissue cells and RBCs of vertebrate host
Family Plasmodiidae
Include human malaria parasites
Produce pigment in asexual cycle in RBCs of vertebrates
- Produce gametocytes in RBCs of vertebrates
Sporogony (sexual cycle) In invertebrates
Genus Plasmodium
* Schizogony (asexual cycle) in:
-RBCs
-other tissue ceils of vertebrate host
* Pigment derived from haemoglobin of infected RBC

* Gametocytes develop in some RBCs. These undergo sporogony (sexual cycle) in female anopheline mosquitoes
- Sporozoites produced in mosquito, infective to vertebrate host
- All malaria parasites incl uded i n th is gen us
Class P. viva P maiariae R falciparum P ovale
Causes benig n C a uses qu a rtan Causes malignant Causes ovale

tertian malaria malaria tertian malaria malaria
Life cycle
Elongation and development of motility

by zygote-ookinete (travelling vermicule)
Fertilization of female (zygote formed)
Macrogamete
Microgamete
Penetration of stomach
wall by ookinete Exflagellalion of microgametocyte
. Maturation of macrogametxyte
by reduction division
Development of oocysts
and sporozoites
Rupture of oocyst liberating

sporozoites into body cavity
Localization of many
sporozoites in salivary glands
Infective
Mosquito
mosquito
now infective
Sporozoites
Gametocytes
Primary
pre-erythrocytic
cycle in
liver cells
Trophozoite
Development
Erythrocytic of schizont
cycle
Hypnozoite
Merozoites
Dormantfor
months, reactivates
to produce a
pre-erythrocytic cycle
In R vivax and
P. ovate only
62 Protozoology
:
Morphology
Stained by Leishman or Giemsa
Schizogony (asexual cycle)
Fre- erythrocytic cycle in liver cells

Mature Ruptured
Releases
O
Merozoites
Sporozoite
Schizonts in tiver celts
No pigment at this stage
Erythrocytic stage in RBCs

General features
The parasite * Cytoplasm blue

* Chromatin red
* Pigment (from haemoglobin) varies
incolour and time of appearance
Pink spots in cytoplasm

The red cell
unoccupied by parasite
May vary in
* Size
Normal RBC
1
Shape
Brick red clefts

in cytoplasm
RBC characteristics P. max R malarias P. falciparum P. ovaie
Size Larger than Smaller, Mature RBC Larger than

mature RBC older RBC mature RBC
Colour Pale Normal Normal Pale
Shape Round Round Round Oval

May be crenated May be fimbriated
Cytoplasmic inclusions Schuffner's dots None Maurer's clefts may be James dots
present present in late trophozoites conspicuous
Morphology (continued)
Stages in thin films
Ring forms (early trophozoites)
P vivax R maiariae P falciparum P. ovale
Size 1/3 RBC Up to 1/3 RBC 1/3 RBC 1/3 RBC

Shape Delicate ring Compact ring Very delicate ring Dense ring
Chromatin Fine dot

G
One mass often
inside ring
Fine dots
G
Frequently two
O
Dense, well-defined mass
Aecol forms* Sometimes None Frequent None
Pigment None at this stage May be present None at this stage None at this stage
Multiple Sometimes Rare Frequently with Rare

parasitized cells high paras itaemia
11
Forms situated on margin of RSC
Developing trophozoites
P vivax P. malarias p falciparum P. o vale
Size Large Small but appears large Small Small

relative to size of RBC
Shape Very Irregular amoeboid Compact, often band forms Compact, with cytoplasmic Compact
vacuoiation
Chromatin Dots or threads Prominent, often as a band Dots or threads Large irregular dumps
Pigment
texture Fine Coarse Coarse Coarse
colour Yellow brown Dark brown Black Dark yellow brown
quantity Medium Abundant Medium Medium
distribution Scattered fine particles Scattered dumps and rods Aggregated in one or two clumps Scattered coarse particles
64 Protozoology
Immature schizonts
P. vivax P. mafariae R falciparum P. ovate
(rarefy seen in peripheral blood)
Size Almost fills RBC Almost fills RBC Almost fills RBC Almost fills RBC
Shape Somewhat amoeboid Compact Compact Compact
Chromatin Numerous irregular masses Few irregular masses Irregular masses Few Irregular masses
Pigment Scattered Scattered Single clump Scattered
Mature schizonts
P. vivax P. malariae P. falciparum P. ovale
(rarely seen in peripheral blood)
Size Fills RBC Nearly fills RBC Nearly fills RBC Fills 3/4 RBC
Shape Segmented Segmented daisy head Segmented Segmented
Merozoites
range 14-24 6- 12 8-32 6-12
mean 16 e 24 8
size Medium Large Small Large
Pigment Aggregated in centre Aggregated in centre Aggregated in centre Aggregated in centre

(yellow brown) (dark brown) (black) (dark yellow brown)
Stages in thin films (continued)
Microgametocytes (male)
P. viva* P. maiariaa R falciparum R ovate
Time of 3-5 days 7-14 days 7-12 days 12-14 days

appearance
Number in Many Scanty Many Scanty

bloodstream
Size 3/4 fills RBC 1/2 to 2/3 fills RBC Larger than RBC 1/2 to 2/3 fills RBC
Shape Round or ova! compact Round compact Kidney-shaped Round compact

Bluntly round ends
Cytoplasm Pale blue Pale blue Reddish blue Pale blue
Chromatin Single chromatin mass As for R vivax Fine granules scattered As for R vivax
throughout
Pigment Abundant brown granules As for P. vivax Dark granules throughout As for R vivax
throughout
Macrogametocytes (female)
Time of 3-5 days 7*14 days 7 -*12 days 12-14 days

appearance
Number in Many Scanty Many Scanty

bloodstream
Size 3/4 fills RBC 1/2 to 2/3 fills RBC Larger than RBC 1/2 to 2/3 fills RBC
Shape Round or oval compact Round compact Crescentic-sharply rounded Round compact
or pointed ends
Cytoplasm Dark blue Dark blue Dark blue Dark blue
Chromatin Compact peripheral mass As forP, vivax Compact masses near centre As forP. vivax
Pigment Small masses round periphery As forP. vivax Black, rod-like granules As forP. vivax
round nucleus
66 Protozoology
Morphology in stained thick films
Note that the parasites are not flattened in the film and so appear smaller than in thin film. The red cells are haemolyzed in
processing so there is no guide to the size, shape or colour of the RBCs. Schuffner s dots are indefinite and there are no Maurer s
clefts.
R vivax
1. Ring forms, small fine rings often broken
2. Trophozoites, markedly irregular cytoplasm
3. Schizonts, many (average 16) small merozoites
4. Gametocytes, compact parasites with features of d and 9

as described
5. White blood cell
R malariae and P. ovale

Almost identical but James' dots may be visible in the latter
1 . Ring forms, compact rings

Trophozoites, solid regular cytoplasm
2.
m 3. Schizonts, few (average 8) large merozoites
4. Gametocvtes, very difficult to distinguish from P. vivax
e 4 2r O
5. White blood cell
1. Ring forms, very small, fine rings usually unbroken

trophozoites (with vacuolated cytoplasm) and schizonts are
rarely seen in peripheral blood
2. Gametocytes, characteristic crescentic d and S forms
3. White blood cell
Plasmodium vivax, P. ovale, P. malariae and uncomplicated P. falciparum malaria have similar features with fever, rigors,
headache,
muscle aches, malaise and anorexia. Anaemia may develop and the liver and spleen may become enlarged. Because
the clinical
appearances are non-specific, malaria may be misdiagnosed, e.g. as a viral infection, with severe consequences.
Plasmodium falciparum infection can readily progress to severe malaria, the clinical criteria of which have been defined
by a
World Health Organisation working group. One or more of the following features in the presence of asexual
parasitaemia
indicate severe falciparum malaria; cerebral malaria severe anaemia renal failure pulmonary oedema or adult respiratory
distress syndrome hypoglycaemia circulatory collapse or shock * spontaneous
bleeding from the gums, nose, gastrointestinal
tract and/ or laboratory evidence of disseminated intravascular coagulation repeated generalised convulsions (more than
two in 24 hours despite cooling) * acidaemia (arterial pH < 7.25) or acidosis (plasma bicarbonate < 15 mmol/L) macroscopic
haemoglobinuria.
Other features of severe falciparum malaria include impaired consciousness less severe than coma, prostration, hyperparasitaemia,
jaundice and hyperpyrexia.
Sequence of events leading to cerebral malaria
Role of INF
(Both of the above figures after Figs 20.17 and 20,18 Hommel M, H M, Malaria (Chapter
in Gilles 20). In Cox E G, Kreier J P Wakelin
t
D, eds, Topley and Wilson's Microbiology and
Microbial Infections, Vol 5. Parasitology. London: Arnold; 1 998)
68 Protozoology
Malaria parasites in thin blood film* Stained by Leishman or Giemsa at pH 7*2
P falciparum
Rarely
seen in
peripheral
blood
It is by Field or Giemsa, Bone marrow films may also be examined. Serology (1FAT
also possible to use thick blood films stained
or ELISA) is is deployed as a retrospective test for epidemiological use
not appropriate for the detection of acute malaria but
to establish the cause of nephrotic syndrome or hyperreactive malarial splenomegaly (HM5).
Antigen Detection
P. falciparum expresses a specific antigen HRP2 on the surface of the parasitized RBC This can be detected by using
immunochromatographic antigen capture techniques (AMRAD ICT, Becton Dickinson ParaSight F). Parasite lactate dehydrogenase
(pLDH) is biochemically and antigenieally distinct from human LDH and is produced by all Plasmodium species. Gold-labelled
monoclonal and polyclonal antibodies can be used in an immunochromatographic technique to detect pLDH in whole blood
(GptiMAL, Flow Inc., Portland OR).
P. vivax trophozoites P, malar iae: late trophozoite R ovale trophozoite
P. falciparum trophozoites P. falciparum gametocyte
Body-fluid and tissue flagellates
Classification
Phylum Euglenozoa
i
Class Kinetoplastidea
Posterior Anterior
Live in bloodstream and tissues
Vector (blood-sucking invertebrates) required
Volutin
granules Flagellum
Single flagellum
Morphological stages of the Trypanosomatidae affecting humans
Leishmania spp.
Intracellular in
Amastigote macrophages
(L-D body) in humans
Lmhmania amastigotes
In midgut, then
proboscis of
sandfly (transfer
stage to human,
also in culture)
Trypanosoma spp.
Trypanosoma brucei rhodesiense

Trypanosoma brucei gambiense
In salivary glands
and proboscis of
tsetse fly (transfer
stage to human)
Trypomastigote
Trypanosoma cruzi
In mid gut, then

faeces of bug
(transfer stage
to humans)
in blood and
tissue spaces
of humans
70 Protozoology
Leishmaniasis
Distribution
Species L donovani complex L tropica L brazMens/s complex
L infantum L major L amazonensis
L do novani L aetbiopica L mexicana
L chagasi L infantum
Disease Visceral Cutaneous Muco-cutaneous

(kaia azar) (Espundia)
Life cycle and morphology of Leishmania (similar in all three species)
Promastigote form in insect Amastigote in macrophages

{and culture) of humans
Visceral 3-4 x 2 pm
14-20 pm leishmaniasis Vacuole
occasion ally
- transmitted - Remains of
by blood axoneme
transfusion
Kinetoplast(DNA)
Life cycle in insect
Species of sandflies
* Phlebotomus {Old World)
* Lutzomyia (New World)
Blockage of
proboscis by
Forward migration
topharynx
Reproduction by
binary fission
Change into
promastigote
in blood or
tissue juices
Life cycle in humans and reservoir animals
To insect
Blocked sandfly attempts

to obtain blood meal
Injects promastigotes
In blood
Remains
localized to
skin in
cutaneous
ingested by 9n tissue juices
forms
macrophages Core of parasitized
Metamorphose cells formed
into amastigotes
Reproduction
by binary fission
Localized to skin, plus In tissue juices

Rupture of
parasitized cell
further cells to mucosae In mucocutaneous forms
|

Visceral leishmaniasis (kala azar)
Distribution
Clinico'pathological correlation
* Parasitized macrophages and endothelial cells
* Splenomegaly, pain from perisplenitis
* Spleen appears congested, dark red, soft and friable. Markedly enlarged
- The capsule is thickened and, later, infarcts and fibrosis occur
* Hepatomegaly
* Liver appears enlarged, fatty congested and later may become cirrhotic
* Parasitized proliferated Kuppfer cells with atrophy of the liver cells and later fibrosis
- Lymphade nopath y
* Reactive hyperplasia with parasitized macrophages
Mechanism of pathology
Both offensive and defensive processes give rise to increased serum globulin and reversal of a/g ratio.
72 Protozoology
Visceral leishmaniasis (kala azar)
Distribution
Clinico'pathological correlation
* Parasitized macrophages and endothelial cells
* Splenomegaly, pain from perisplenitis
* Spleen appears congested, dark red, soft and friable. Markedly enlarged
* The capsule is thickened and, later, infarcts and fibrosis occur
Liver
* Hepatomegaly
* Liver appears enlarged, fatty congested and later may become cirrhotic
* Parasitized proliferated Kuppfer cells with atrophy of the liver cells and later fibrosis
* Lymphade nopath y
Reactive hyperplasia with parasitized macrophages
Mechanism of pathology
Both offensive and defensive processes give rise to increased serum globulin and reversal of a/g ratio.
72 Protozoology
Cutaneous leishmaniasis
Caused by Leishmama tropica, L. major , L. aethiopica, L infantum ,
. L. brazil iensis complex
Blocked sandfl y injects Core of cel Is parasitized Acan thesis cel ular
I Necrosis and ulceration Seco ndary nfectbn
i Granulation Healing (2-12 months)
promastigotes by amastigotes infiltration withdepressed
formed pigmented scar
Remains localized to skin Ulcer with sharp cut edges and

surrounding induration
Mucocutaneous leishmaniasis (espundia)

Caused by some infections with l. braziliensis (Central and South America), L aethiopica (Ethiopia), L mexicana.
Parasitized celtsx.
Inflammatory
infiltration
Necrosis
Later reactive
Blocked sandfly injects Cutaneous manifestations Spread to mucosae of fibrosis
promulgates like oriental sore but mouth, nose, larynx,
often weeping ulcers pharynx, ear
Secondary effects in loose mucosal tissues
* Oedema and capillary involvement * Secondary infection * Healing with fibrosis

Interference with local blood supply -Deep erosion locally
* Necrosis - extensive destruction -Spread of infection to lungs or elsewhere
Leading to:
Extensive disfiguring lesions * General constitutional upset * Bronchopneumonia

anaemia)
(fever, pain, and septicaemia
Diagnosis of Leishmaniasis
Visceral
Amastigotes can be demonstrated by staining bone marrow, lymph node fluid, nasal scrapings (in the Sudan), liver biopsy or
splenic aspiration specimens (although this can be a dangerous procedure). Rarely, amastigotes can be demonstrated in huffy
coat preparations from peripheral blood.
Cutaneous and mucocutaneous

Demonstration of the parasite is possible in stained films from slit-skin smears taken from the indurated edge of an ulcer, biopsy
of the margin of the ulcer and from mucosal scrapings in mucocutaneous type.
Culture (NNN or a liquid medium such as Schneider's Drosophila medium or 199 medium with added fetal calf serum) is
used for all types of material for diagnosis. Animal inoculation is rarely used now.
Polymerase chain reaction (PCR) can be used to diagnose and type the species of Leishmania present in biopsy or culture
material
Specific serological tests are 1FAT, ELISA, direct agglutination test (LMT), or latex agglutination for IgG antibodies. An
immunochroma og r a phic
t test for rK39 antibody detection is also available.

Trypanosomiasis
African type: sleeping sickness

Caused by either Trypanosoma gambiense (chronic sleeping sickness, found in West Africa, the Congo, Zaire) or by T rhodesiense
(acute sleeping sickness, found in Zimbabwe, Tanzania, Zambia, Angola). Both have similar life cycle and morphology.
7! rhodesiense
I rhodesiense
Bushbuck or
antelope T gambiense
Giossina spp.
Tsetse fly
I gambiense
*
Nagana
in animals
Epimastigote in vector
No animal reservoir
Trypanosomes in blood
ingested by tsetse fly Total developmental cycle in fly 20 days
Anterior station
development
Enter salivary glands via ducts

Metamorphose to epimastigotes and multiply
Re-meta morph ose to slender metacyciic
trypomastigotes

Reproduction by binary fission as trypomastigotes
Metacyciic
trypanosomes
injected by
tsetse fly
Invade and tissue spaces of Then CMS

Multiply at site bl ood strea m various orga ns particula riy But do not enter
of injection lymph nodes initially actual cells
Primary stage Secondary stage Third stage
74 Protozoology
Pathogenesis and pathology
Primary stage Secondary stage Third stage
* Parasitaemia and toxaemia

* Invasion of tissue spaces (not cells) of various organs
f
Predominantly ^
Multiplication at site of injection Lymph nodes CNS
Surrounding inflammatory reaction
* Damage to endothelial cells of blood vessels, surrounding
(perivascular) granulomatous reactions and haemorrhages
Local inflammatory lesion Toxic degeneration and pressure atrophy of tissue cells
Chronic sleeping sickness Acute sleeping sickness

Differ only in degree
(Due to T gamtose) (Due to T rhodasiensa)
C in ico-patholog ica Clinico-pathological
I I
Primary stage
correlation correlation
/
1 /
Trypanosomal
As
Firm, tender, painful
red nodule 1-3 weeks
0 j
chancre in chronic
Secondary stage predominantly blood and lymph node involvement
Fever Fever
* Low High
* Irregular * Persistent
* Recurrent
Severe toxic symptoms
General toxic symptoms * Headache
* Backache * Vomiting
* Shivering
* Headache
* Tachycardia * Oedema face
* Irregular skin rashes
* Serous effusion
(circinate) * Bone pain
- Transient oedema face Similar lesions not so
pronounced Lymphadenopathy
Lymphadenopathy Myocarditis
- Typically post-cervical
Anaemia
Later anaemia Purpura
monocytosis
Hepatitis
Slight enlargement liver,

Congested .slightly enlarged Toxic depression Slightly enlarged Toxic depression Often death at this stage
spleen
Bone marrow Bone marrow
Third stage -CNS involvement
Progressive involvement Generalized leptomeningitis May have early onset of

of the CNS Dura thickened and adherent encephalitis with rapid
Oedema with flat convolutions and development of coma

General symptoms of
progressive encephalitis dilated ventricles
Haemorrhage with softening
Focal signs uncommon
CSF turbid, increase cells and protein,
Dementia containing trypanosomes.
r
Perivascular cuffing with round and plasma Death before CNS involvement
cells, macrophages and endothelial cells or
Neuroglial proliferation Similar changes but more acute
Pressure atrophy neurones
Note on epidemiology - Vectorsof T. gambiense are riverine species, Vectors of T. rhodesiense are game-atfacking species,
hence disease often epidemic: hence disease more often sporadic:
* G. paipaiis * G. mors/fans
*
G, tachinoides * G. paiftdipes
* G. swynnertoni

Trypanosomiasis (continued)
South American type: Chagas' disease

Caused by Trypanosoma cruzi. The parasite is harboured in humans, domestic animals such as cats and dogs, and some wild
animals, notably armadillos and opossums.
Morphology
Axoneme
Trypomastigotes fn blood
of humans and gut of insect
blepharapfast
Resemble African trypanosomes except: Indistinguishable {except for site) and transitional stage
characteristic C or S shape from Leish man - Donovan bodies in hu mans
conspicuous kinetoplast of leishmaniasis
long and short forms may occur
Triatoma spp: the cone bug
Posterior station
development
These infective forms

passed in faeces
Metamorphosis to Re-metamorphosis
Trypomastigotes in blood and multiplication as to small metacyclic
ingested by bug epimastigotes trypomastigotes
Metacyclic trypanosomes in Rubbed into bite puncture,

Carried to regional
bug faeces deposited on skin abrasion or conjunctiva lymph nodes
Enter histiocytes locally
metamorphose to amastigotes
and multiply by binary fission
Some amastigotes metamorphose to trypomastigotes

and invade blood and lymph
Some amastigotes
enter further cells
Parasitized
cells rupture
Enter cells of many organs,

^ metamorphose to amastigotes
and multiply
76 Protozoology
Pathogenesis and pathology
Fundamental pathogenesis
Local invasion of histocytes
invasion and destruction of
Inflammatory reaction
tissue cells by multi plying
Fibrosis: lymph blockage
Oedema amastigote fori
with functional disability
Chagoma invasion of blood

* Myocarditis
and lymph vessels by
* Tachycardia
trypanosoma! forms
* Heart block
* Emboii
* Aneurysms
* Generalized
Invasion of local Parasitization of lymphadenopathy
lymph nodes reticule-endothelial and
Reticuloendothelial parenchymatous cells by
hyperplasia with amastigote forms which
parasitization
multiply and destroy *
Encephalitis
cells
General or focal
CNS signs and
symptoms
w No * Dissemination
multiplication Splenomegaly
to practically any
in
tissue of body
bloodstream
1
Systemic
manifestations
Hepatomegaly
Recurring
re-invasion of the
blood by trypanosomal
forms and further
dissemination
Toxic depression
marrow
of bone
Anaemia
Destruction of
intestinal nerve plexus
Megaoesoptiagus
Micro Megacolon
/ Similar in
Amastigote forms
all
in
lesions \
tissue cells e.g.
Pseudocyst
Acute symptoms
* Fever
Myocardial fibres * Swelling of eyelids

(Romana's sign)
Little surrounding tissue

reaction
Acute form (often in children) Chronic form

- Blood and reticule-endothelial cells predominantly involved * General toxic symptoms and focal signs
* Fever Death or depending on localization
* Oedema * Predominantly cardiac and CNS manifestations
Lymphadenopathy May be asymptomatic

* Enlargement of liver and spleen
* Sometimes encephalitis

Laboratory diagnosis of trypanosomiasis
African type (sleeping sickness)
Demonstration of the parasite.

Microscopy of thin and thick blood films and buffy coat preparations.
Tiypanosomes can also be seen in smears from bone marrow and
centrifuged cerebrospinal fluid (CSF) Culture is possible
but difficult.
Microscopic detection of trypanosomes in peripheral blood may

be improved by the use of a mini-anion- exchange column
or by the use of the QBC11 (Beeton Dickinson) to
concentrate the parasite.
The CSF might show increased protein and lymphocytes.
South American type (Chagas disease)

Stained smears of peripheral blood show trypanosomal forms in C or S shape. Stained films of lymph
node fluid show
amastigotes. It is possible to show trypomastigotes by animal inoculation from blood and by culture
from lymph node fluid
Histological methods from biopsy or post-mortem material. It is also possible to demonstrate the parasite through
xenodiagnosis-
clean bred tnatomid bugs fed on the patient's blood develop trypanosomes in the gut.
Serology (e g. by ELISA or IFAT) is the method of choice for the detection of chronic T. cruzi infection.
78 Protozoology
Laboratory diagnosis of trypanosomiasis
African type (sleeping sickness)

Microscopy of thin and thick blood films and buffy coat preparations.
Trypanosomes can also be seen in smeaTS from bone marrow and centrifuged cerebrospinal fluid (CSF) Culture is possible
but difficult.
Microscopic detection of trypanosomes in peripheral blood may

be improved by the use of a mini-anion- exchange column
or by the use of the
QBC11 {Becton Dickinson) to concentrate the parasite.
The CSF might show increased protein and lymphocytes.
South American type {Chagas' disease)

Stained smears of peripheral blood show trypanosoma!
forms in C or S shape. Stained films of lymph node fluid
show
amastigotes. It is possible to show trypomastigotes by animal
inoculation from blood and by culture from lymph node
fluid
Histological methods from biopsy or post-mortem material.
It is also possible to demonstrate the
parasite through xenodiagnosis:
dean bred trmtormd bugs fed on the patient's blood develop
trypanosomes in the gut.
Serology (e.g. by ELISA or IFAT) is the method of choice for the detection of chronic T. cruzi infection.
78 Protozoology
Recapitulation
Luminal intestinal protozoa
Refer to text for the following additional stained appearances:

trichrome stain for cocddia and microsporidia spp.
* modified Ziehl-Neelsen for Cydospora, Isospom and Cryptosporidium spp.
Recapitulation 79
,
Index
Cutaneous larva migrans (creeping eruption) Enterocytozoon bieneusi, 45

A A .
.
braziliense, 19 Eosinophilia, tropical pulmonary, 12
African trypanosomiasis, 74-5, 78 A. caninum 19 , Erythrocytic stage in RBCs ( Plasmodium
Allergic reaction, hydatid disease, 26 G. spinigerum, 19 spp.), 63
Alveolar hydatid cyst, 26 LE stenocephala, 19 Espundia, 73
Amoebae, 47-56 Cutaneous leishmaniasis, 73, 74 Eye worm, 14
Amoeboma, 51 Cydospora cayetanensis, 43
Ancylostoma spp., see also Hookworm Cyst
helminths F
19
braziliense,
caninum, 19 hydatid cysts, 25, 26
Fasciola hepatica (sheep liver fluke), 32, 32
duodenale 8 westermani, 35
F.
ova, 36, 37
ova, 8 protozoa, 79
Fasciolopsis buski, 33
Ascaris lumbricotdes, 7 amoeba other than Entamoeba
ova, 33, 36
ova, 7, 36, 37 spp., 54, 55, 79
Filariasis, 12-16
Ascites, 5. mansoni, 29 B , coli, 58, 79
Bancroftian (W. bancrofti), 12
C mesnili, 56, 57 Filariform larvae, S. stercoralis, 9
Entamoeba spp,, 48, 49, 50, 55, 79
B Fish tape worm, see Diphylhhothrium latum
G. lamblia, 56, 79
Flagellates
S, hominis, 44
Balanitis, E. histolytica, 52 body-fluid and tissue, 70-8
T. gondii, 59
Balantidium coli 58 ,
intestinal, 56-7
Cysticercoid, H. nana/H. diminuta, 22
trophozoites and cysts, 58, 79 Flukes, see Trematodes
Cysticercus bovis , 21
Bancroftian fUariasis (W, bancrofti), 12
Cysticercus cellubsae, 20
Beef tape worm, 21
Blackwater fever, 68
Cystitis, schistosomiasis, 29 G
Blinding worm, 15
Blood flukes, 27-9 D Gametocytes, Plasmodium spp,, 64, 65
Giardia intestinalis (G. lamblia }, 56
Body-fluid flagellates, 70-8
Diagnosis, methods, 1 cysts and trophozoites, 58, 79
Bone, hydatid (osseous) cyst, 25, 26
Dientamoeba tragi! is, 47 Gnathostoma spinigerum, 19
Bronchiectasis, P westermani 35 \
life cycle, 54
,
Brugia malayi , 13 Granuloma(ta)

morphology, 54-5, 79 M. yokogawai, 34
Dipkylhbothrium latum, 23
Schistosoma spp., 29
ova, 23, 36
c Gravid segment, T, saginata, 21
Disease mechanisms, 1
Ground itch, 8
Calabar swelling, 14 Dog round worm, see Toxocara cams
Growth effects, trichuriasis, 6
Cancer /malignancy, schistosomiasis, 29 Dog tape worm, 25
Guinea worm, 17
Cat liver fluke, 31 Dracunculus medinensis, 17
Cat round worm, 18 Dwarf tape worms, 22
Cercariae Dysentery H
to rio/c? 32
hepatica, amoebic, faecal appearance, 53
Fasciolopsis buski 33 , balantidial, 58 Haemoptysis, P. westermani, 35
H. heterophyes, 34 T, trichiura 6 ,
Halzoun, 32
M. yokogazmi, 34 Helminths (worms), 3-37
O. felineus, 31 E classification, 4
O, felineus /O, viverrini 31 ,
definition, 1
O. sinensis (C. sinensis), 30, 31 Echinococcus granulosus 25 , Hematophagous trophozoites,

Schistosoma spp., 27 Echinococcus multilocu laris, 26 E. histolytica., 53
skin penetration, 29 Eggs, see Ova Heterophyes heterophyes, 34
Cestodes (tapeworms), 20-6 Elephantiasis Hoeppli reaction, 29
general characteristics, 4 G. volvulus 15 ,
Hookworms, 8, see also Ancylostoma spp.
larval forms, 24 W. bancrofti, 12 ova, 37
8, 36,
Chagas' disease, 76-7, 78 Encephalitozoon spp., 45
Host, definitive vs intermediate, 1
Chilomastix mesnili , 56 Endolimax nana 47 ,
Hydatid disease, 25-6
cysts and trophozoites, 56, 79 morphology, 54-5, 79
Hydrocele
Chrysops (vector), 14 Endophthalmitis, T, can is, 18
B. malayi , 13
Chyluria Entamoeba coli, 47
W. bancrofti, 12
B. malayi 13 morphology (vs E, histolytica), 49-50,
,
Hymenolepis diminuta (rat tape worm), 22
bancrofti, 12 54-5, 79
ova, 22, 36
Ciliates, intestinal, 58 Entamoeba dispar, 48
Hymenolepis nana 22 ,
Classification morphology, 54-5, 79
ova, 22, 36, 37
helminths, 4 Entamoeba hartmanni, 47
morphology, 54-5
Hypoglycaemia in malaria, 68
protozoa, 40
body-fluid and tissue flagellates, 70 Entamoeba histolytica, 47, 48-53
malaria parasite, 61 laboratory diagnosis, 53 I
Clonorchis sinensis ( Opisthorchis life cycle, 48
sinensis), 30-1 morphology, 49-50, 54-5, 79 Intraosseous cyst, 25, 26

ova, 30, 31, 36 pathology, 51-2 lodamoeba biltschlii, 47
Coccidia, 41-4 Entamoeba polecki, 47 morphology, 54-5, 79
Cone bug (vector), 76 Enterobius vermicular is, 5 Iron deficiency anaemia, I. trichiura, 6
Conjunctiva, L, loa under, 14 ova, 5, 36 Isospora belli, 41
Atlas of Helminthology and Protozoology 81

, , , , , ,
I Plasmodium spp., 61-9 (continued) T

life cycle, 62
Jaundice morphology, 63-7 Taenia spp.
C. (OJ sinensis, 30 pathophysiology, 68 ova, 20, 21, 36
F. hepatica, 32 T. saginata 21
Plasmodium falciparum 61
P. falciparum 68 laboratory diagnosis, 69 T. solium, 20
morphology, 63-7 Tapeworms, see Cestodes
K Plasmodium malarias, 61 Thread worm, 5
laboratory diagnosis, 69 Thrombocytopenia, P. falciparum, 68
Kala azar (visceral leishmaniasis), 72, 73
morphology, 63-7 Tissue protozoa, 59-60
Katayama fever, 29 flagellates, 70-8
Plasmodium ovale, 61, 62
laboratory diagnosis, 69 TNF and malaria, 68
L Toxocara cams, 18
morphology, 63-7
Plasmodium vivax 61, 62 ova, 18, 37
Larva currens, 9 ,
laboratory diagnosis, 69 Toxocara cat is, 18

Larva migrans, see Cutaneous larva
morphology, 63-7 Toxoplasma gondii, 59-60
migrans; Visceral larva migrans
Pleistophora spp., 45 Transmission of parasites, 1
Larval forms of cestodes, 24
Pork tape worm, 20 Trematodes (flukes), 27-37
Leishmania spp., 71-3
Portal vein, S. mansoni, 29 general characteristics, 4
morphology, 70, 71
Pre-erythrocytic stage, Plasmodium spp., 63 Triatoma spp. (vector), 76
Leucopenia, P. falciparum, 68
Pregnancy, placenta in malaria, 68 Trichinella spiralis, 10-11
Liver fluke
Proglottid, 7 solium, 20 Trichomonas spp., 57
cat, 31
Protozoa, 39-79 hominis, 57, 79
oriental, 30-1
sheep, see Fasciola hepatica classification, see Classification vaginalis, 57
Loa loa, 14 definition, 1 Trichuris trichiura (whip worm), 6
ova, 37
6, 36,
M Trophozoites, 79
amoebae other than Entamoeba spp.,
R
Macrogame tocytes, Plasmodium spp., 64 morphology, 54
Malaria parasite, see Plasmodium spp, Rat tape worm, see Hymenolepis diminuta L b Utschlii, 54, 79
Mansonella spp,, 16 Red blood cells (RBCs), malaria parasite B. coli, 58, 79
Megaloblastic anaemia, D. latum, 23 erythrocytic stage, 63 C. mesnili, 56, 79

Microfilariae pathophysiology, 68 Entamoeba spp., 48, 49, 50, 79
B. malayi, 13 Renal involvement, see Kidney hematophagous, 53
L. loa, 14 Rhabditiform larvae morphology, 54
O. volvulus, 15 hookworms, 8 G. lamblia, 56, 79
W. bancrofti 12 S. stercoralis, 9 Plasmodium spp.,64, 67
,
other filarial worms, 16 Ring form, Plasmodium spp., 64, 67 Trichomonas spp., 57, 79
Microgametocytes, Plasmodium spp., 64 Round worms, see Nematodes Tropical pulmonary eosinophilia, 12
Microsporidia, 45-6 Trypanosoma spp., 74-8
Mosquito as vector laboratory diagnosis, 78
B, malayi, 13 S morphology, 70
Plasmodium spp,, 62 Trypanosoma cruzi, 76-7
Sandfly (vector), 70, 71 morphology, 70, 76
W. bancrofti 12 ,
Sarcocystis hominis, 44 Trypanosoma gambiense, 74
Mucocutaneous leishmaniasis, 73
Sdijsfesoma spp., 27-9 morphology, 70
MuMocular cyst, 26
haematobium 28, 29, 36, 37 pathology, 75
japonicum 28, 29, 36
N mansoni 28, 29, 36, 37
Trypanosoma rhodesiense, 74
morphology, 70
Necator americanus, 8 ova, see Ova pathology, 75
Nematodes (round worms), 5-19 Schizogony, Plasmodium spp., 63 Try pa nosoma tidae, morphological
general characteristics, 4 Schizonts, Plasmodium spp., 64, 67 stages, 70
Nosema spp., 45 Scolex Tsetse fly (vector), 70, 74
0. latum, 23 Tumour necrosis factor and malaria, 68
O 1. saginata, 21
T. solium, 20 U
Oesophageal varices, S. mansoni, 29 Sheep liver fluke, see Fasciola hepatica
Onchocerca volvulus, 15 Sleeping sickness, 74-5, 78 Uncinaria $ tenocephala, 19
Opisthorchis felineus, 31 Snail fever, 29 Unilocular cyst, 26
Opisthorchis sinensis, see Clonorchis sinensis Snail host Urethra, Trichomonas vaginalis , 57
Opisthorchis viverrini, 31 Fasciola hepatica, 32 Urinary tract infection
Oriental liver fluke, 30-1 Fasciolopsis buski 33 , E. vermicularis, 5
Oriental schistosomiasis, 29 H. hetemphyes, 34 S. haematobium, 29
Osseous 26
cyst, 25, M. yokogawai, 34
Ova (eggs), helminth, 36-7 O. felineus , 31 V
Schistosoma spp., 36, 37, 38 O. sinensis (C. sinensis ), 30
damage caused by, 29 P. westermani, 35 Visceral Larva migrans
Schistosoma spp., 27, 28 G, spinigerum, 19
P South American trypanosomiasis, 76-7, 78 X cams , 18

Sparganosis, 24 Visceral leishmaniasis, 72, 73
Papillitis (optic), T. cams, 18 Sparganunt proUferum , 24
Paragonimus wes termani, 35 Spirometra spp., 24 W
ova, 35, 36 Squamous cell carcinoma of bladder, 29
Periorbital oedema, 7, spiralis, 11 Strobila
Whip worm, see Trichuris trichiura
Pharynx, F. hepatica 32 D. latum, 23
Worms, see Helminths
Phasmid nematodes, 18-19 Wuchereria bancrofti, 12
T. saginata, 21
Pin worm, 5 solium, 20
T,
Placenta in malaria, 68 Strongyhides stercoralis, 9
Plasmodium spp., 61-9 Subconjunctival location, L. loa, 14
classification, 61 Subungual haemorrhage, T. spiralis, 11
laboratory diagnosis, 69 Swimmer's itch, 29
82 Index
Fourth edition
Atlas of /
Medica
Helminthology
and Protozoology
in this fourth edition provides a unique diagnostic reference source
for the microbiologist, tropical disease physician and medical scientist.
The entire contents has been revised and re-structured and illustrated
with new full colour diagrams and photomicrographs.

For each organism there is a schematic life cycle, range map,
morphological drawing and microscopic
appearance. No diagnostic
laboratory should be without
this valuable resource.
Vjk CHURCHILL
LIVINGSTONE
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SCIENCE 9 '780443 062681
Entamoeba histolytica (causing amoebiasis) (continued)
Iodine preparations
histolytica
Precyst cod
Brown, diffuse Glycogen Brown, compact
e in Finely granular yellow

green
Cytoplasm Conspicuous granularity
'
e
'.h-,
*i
# Yelfow ring with central

yellow dot (karyosome)
Nucleus Nuclear
eccentric
recognised
membrane
karyosome
with
easily
Stained by iron haematoxylin
Trophozoite
Purplish brown Cytoplasm Greyish blue

Faintly granular Coarsely granular
RBC black Inclusions Vacuoles black, as

are bacteria etc.
Nucleus:
Lined with minute Membrane Thick with plaques of
black granules black chromatin
Small black central dot Karyosome Eccentric black dot

or plaque
Trace only seen Fibril network More conspicuous; may

have chromatin plaques
Precyst
Round Shape Round
As trophozoite Cytoplasm As trophozoite

Nucleus
Black chromldial Inclusions May have slender black

bodies or bars chromldial bars
Glycogen (dissolved) Glycogen (dissolved)

replaced by vacuoles replaced by vacuoles
Cyst
Grey-blue Cytoplasm Greyish- blue, granular
As precyst, less Inclusions As precyst, less

conspicuous or absent conspicuous or absent
In 2 nuclei stage glycogen
vacuoles may be
dumb- bell -shaped
Unstained, hyaline Waff Unstained, hyaline
As trophozoite 1 4 Nuclei As trophozoite 1 -8
50 Protozoology

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Fourth edition

Anthony H. Moody MPhh MiBioi c.Bioi fibms

David W. Manser bsc ms c fibms

Illustrated by Robert Britton

Harcourt Publishers Limited 2001

The right of P. L. Chiodini, A + H. Moody and D, W, Manser to be

No part of this publication may be reproduced, stored in a retrieval

First published 2001

ISBN 0443 06268 4

British Library Cataloguing in Publication Data

Library of Congress Cataloging in Publication Data

your source for books,

www. el se vi er hea Lth.com

viii Atlas of Helminthology and Protozoology

Nematode (round) worms 5

Trichuris trichiura (whip worm) 6

Cestode (tape) worms 20

Dwarf tape worms 22

Diphyllobothrium latum (fish tape worm) 23 Morphology 63

Larval forms of cestode infection in humans 24 Pathology and Clinical features 68

Echinococcus granulosus (dog tape worm) 25 Laboratory diagnosis 69

Trematode (flat) worms 27 Leishmaniasis 71

Schistosoma species (blood flukes) 27 Visceral leishmaniasis (kala azar) 72

Schistosomiasis 29 Cutaneous leishmaniasis 73

fluke) 30 Diagnosis of leishmaniasis 73

Opisthorchis felineus, Opisthorchis viverrini (cat liver Trypanosomiasis 74

33 Laboratory diagnosis of trypanosomiasis 78

Common helminth ovo 36 Index 81

Atlas of Helminthology and Protozoology ix

trypanosomiasis). An intermediate host is another animal

Atlas of Helminthology and Protozoology 1

Nematodes Cestodes Trematodes

* Unsegmented - Segmented * Unsegmented

* Possess scolex, neck and proglottids Leaf-like or cylindrical

-Ingestion of encysted larvae

350 million infected worldwide, often group or institutional

appendicitis can occur. Migration into the peritoneal cavity

Nematode (round) worms 5

Maturation in soil 3-5 weeks

Pathology and Clinical features Ovum

Light infections may be asymptomatic. Heavy infections can

Eosinophilia may occur.

L3 billion infected worldwide.

Hards carry infective ova from

Normal form Decorticated

Adult life span

Larvae penetrate the mucosa, enter the lymphatics and

Mature in 1-2 weeks. Viable months -years Eosinophilia

Pathology and Clinical features

Larvae can cause pneumonitis with eosinophilia. Adult worms

Ova may be recovered from faeces by concentration methods.

present in the larval invasion stage,

200-350 x 4-6 mm.

1.47 billion infected worldwide.

Nematode (round) worms 7

Ancylostoma duodenale Necator americanus

Enter circulation, and via

tree and oesophagus

Rhabditiform larva Filariform larva

Pathology and Clinical features Laboratory diagnosis

Ground itch may follow skin penetration by filariform larvae. Eosinophilia.

900 million infected worldwide.

Strongyloides filariform larva