Nematodes

• Nematodes are unsegmented worms.

• Nematodes have separate sexes.
• Nematodes have four larval molts.
• The severity of disease depends upon the
worm load, since nematodes cannot
multiply in their host, except
Strongyloides stercoralis.
• Löeffler's syndrome: transient pulmonary
infiltrates with peripheral
eosinophilia.     
 Historical aspect
• Anisakiasis was first recognized in the
Netherlands (Van Thiel et al., 1960).
• The patient was diagnosed as acute
localized enteritis of terminal ileum.
• Surgical operation revealed that a
small nematode was penetrating the
mucus membrane.
• The larva was identifed as 3rd-stage
larva of Anisakis simplex.
 Geographic Distribution

• Worldwide, with higher incidence in

areas where raw fish is eaten, e.g.,
Japan, Pacific coast of South
America, the Netherlands.
• Anisakis simplex: herring worm
• Pseudoterranova decipiens: cod or seal
worm
 Epidemiology

• In adult males: raw marine food

• Northern Europe: raw or “green”
herring marinated with vinegar and salt
or smoked.
• Japan: sashimi from squid, cod, salmon
or mackerel.
 Anisakis
• Adult stages of Anisakis simplex or
Pseudoterranova decipiens reside in the
stomach of marine mammals, where
they are embedded in the mucosa, in
clusters. 
Stomach, Pink Whale Liver, Alaska Pollack
 Anisakis
• Unembryonated eggs produced by adult
females are passed in the feces of
marine mammals. 
• The eggs become embryonated in water,
and first-stage larvae are formed in the
eggs. 
• The larvae molt, becoming second-stage
larvae, and after the larvae hatch from
the eggs, they become free-swimming . 
 Anisakis
• Larvae released from the eggs are
ingested by crustaceans. 
• The ingested larvae develop into third-
stage larvae that are infective to fish
and squid. 
• The larvae migrate from the intestine
to the tissues in the peritoneal cavity
and where they grow up to 3 cm in
length. 
 Anisakis
• Upon the host's death, larvae migrate
to the muscle tissues, and through
predation, the larvae are transferred
from fish to fish. 
• Fish and squid maintain third-stage
larvae that are infective to humans
and marine mammals. 
 Anisakis
• When fish or squid containing third-stage
larvae are ingested by marine mammals,
the larvae molt twice and develop into
adult worms. 
• The adult females produce eggs that are
shed by marine mammals. 
Third stage larvae of anisakids are commonly found in the flesh and the body cavity of a large
number of fishes as well as in cephalopods that serve as paratenic hosts.
Anisakis in Mackerel
Anisakis
 Anisakis
• Humans become infected by eating raw or
undercooked infected marine fish.
• After ingestion, the anisakid larvae
penetrate the gastric and intestinal
mucosa causing the symptoms of
anisakiasis.
 Fate of Larvae
• One-third of the Anisakis larvae eaten
with marine organisms are evacuated
through the anus, one-third die in the
walls of the stomach and intestine, and
one-third die forming granuloma or after
penetrating the abdominal cavity.
• To enter the abdominal cavity, the wall
of the digestive tract must be
penetrated.
 Anisakis: Clinical Features
• Within hours after ingestion of infected
larvae, violent abdominal pain, nausea,
and vomiting may occur. 
• Occasionally larvae are coughed up. 
• If the larvae pass into the bowel, a
severe eosinophilic granulomatous
response may occur 1 to 2 weeks
following infection, causing symptoms
that mimic Crohn's disease.
 Anisakis: Lab Diagnosis

• Gastroscopic examination: the 2 cm

larvae can be removed when directly
visualized.
 Endoscopic Features
(a) Existence of Anisakis larvae
(b) Edematous hypertrophic gastric folds
(c) Increased gastric secretion and gastric
peristalsis
(d) Mucosal lesions through which Anisakis
larvae penetrated: 46%- edema, 25%-
redness, 19%- coagulation, 6%-
hemorrhage, and 4%- ulceration
(e) Erosive gastritis
 Anisakis: Lab Diagnosis
• Histopathologic examination of tissue
removed at biopsy or during surgery
(finding on laparotomy a
granulomatous lesion with a worm.)
• Differential diagnosis: acute
appendicitis, Crohn's disease, gastric
ulcer, or gastrointestinal cancer.
 Anisakis in Tissue, x-section.
Worm within eosinophilic granuloma
 Anisakis: Treatment

• The treatment of choice is endoscopic

removal of larva or surgical intervention
for obstruction and perforation. 
 Angiostrongylus
• Normally a parasite of rats.
• The worm cycles between snails and rats.
• Spends time in both brain and lung of rats.
• Humans contract the infection by eating
infected snails accidentally.
• The worms reach the human brain where
meningitis develops.
 Angiostrongylus
• The nematode Angiostrongylus
cantonensis is the most common cause
of human eosinophilic meningitis. 
• Angiostrongylus (Parastrongylus)
costaricensis causes abdominal or
intestinal angiostrongyliasis (ileocecal
inflammation).
 Geographic Distribution

• Most cases seen in Southeast Asia and

the Pacific Basin.
• Some in Africa and the Caribbean. 
• Abdominal angiostrongyliasis has been
reported from Costa Rica, and occurs
most commonly in young children.
 Adult Angiostrongylus
cantonensis
recovered from rat
lungs.
B. Adult female worm
with characteristic
barber-pole
appearance (anterior
end of worm is to
the top).
C. B. Tail of adult
male, showing
copulatory bursa and
long spicules
(arrows).
Scale bar = 1 mm. Scale bar = 85 µm.
Morphologic features of a male nematode recovered from the central nervous
system of a gibbon (Hylobates lar). The characteristics used for specific
identification of Parastrongylus cantonensis were the presence of a bursa (b),
a gubernaculum (g), and the size of spicules (s).
Life Cycle
Angiostrongylus
Intermediate Hosts of
Angiostrongylus
 Adult Worms

• Adult worms of A. cantonensis live in

the pulmonary arteries of rats.  
• The females lay eggs that hatch,
yielding first-stage larvae, in the
terminal branches of the pulmonary
arteries.  
Angiostrongylus in rat lung
 1 -Stage Larva
st

• The first-stage larvae migrate to the

pharynx, are swallowed, and passed in
the feces of rats. 
• They penetrate, or are ingested by, an
intermediate host (snail or slug). 
• After two molts, third-stage larvae are
produced, which are infective to
mammalian hosts. 
 3rd-Stage Larva

• When the mollusk is ingested by the

definitive host, the third-stage larvae
migrate to the brain where they
develop into young adults. 
• The young adults return to the venous
system and then the pulmonary
arteries where they become sexually
mature. 
 Paratenic Hosts
• Paratenic hosts are intermediate hosts
that are not essential to completion of
parasite’s life cycle.
• Various animals act as paratenic
(transport) hosts: after ingesting the
infected snails, they carry the third-
stage larvae which can resume their
development when the paratenic host
is ingested by a definitive host. 
 Human Infection

• Humans can acquire the infection by:

a) eating raw or undercooked snails or
slugs infected with the parasite
b) eating raw produce that contains a
small snail or slug, or part of one. 
 Human Infection

• The disease can also be acquired by

ingestion of contaminated or infected
paratenic animals (crabs, freshwater
shrimps). 
• In humans, juvenile worms migrate to
the brain, or rarely in the lungs, where
the worms ultimately die. 
 Human Infection

• Acute meningoencephalitis. Onset of

severe headache, nuchal rigidity, and
low-grade fever; high ICP.
• Paresthesias and cranial nerve
involvement; diplopia and strabismus.
• CSF 500 cells/cu mm or more, up to
90% eosinophils.
Section of brain Section of brain
A B
Angiostrongylus, Cervical Spine
 Diagnosis

• History of travel to or residence in

endemic area
• Eating habits and foods eaten
• Leukocytosis and eosinophilia
• Differential diagnosis: cerebral
cysticercosis, trichinosis, visceral larva
migrans, schistosomiasis, gnathostomiasis
 Treatment

• No recommended antihelminthics since

dead parasite can exacerbate tissue
reaction
• Use of anti-inflammatory agents need to
be evaluated
• Surgical intervention when necessary
 Prevention

• Boil snails and prawns for 2 minutes

• Refrigerate food at –15 oC for 24 hrs
• Careful washing and cooking of vegetables
• Safe drinking water
 Parastrongylus costaricensis

• The life cycle of Angiostrongylus

(Parastrongylus) costaricensis is similar
to that of A. cantonensis, except that
the adult worms reside in the
arterioles of the ileocecal area of the
definitive host. 
 Parastrongylus costaricensis

• In humans, A. costaricensis often

reaches sexual maturity and release
eggs into the intestinal tissues.
• The eggs and larvae degenerate and
cause intense local inflammatory
reactions and do not appear to be shed
in the stool.
Aesculapius
 Dracunculus

• From Gr. drakontion, little dragon

• During ancient times, illness inferred by
the universally recognized symbol of
medicine, the Greek asklepios (Roman
aesculapius), which consists of a one-
headed snake wrapped around a stick.
Dracunculiasis: Removal of worm
 Dracunculus
• Class: SECERNENTEA
• Subclass: SPIRURIA
• Order: SPIRURIDA
• Superfamily: DRACUNCULOIDEA
• Family: DRACUNCULIDAE
• Scientific name - Dracunculus
medinensis
• Common name - Guinea worm, medina
worm, serpent worm
 Dracunculiasis
• In the early 1990s, 3-5 million cases of
dracunculiasis occurred worldwide
each year.
• By 1996, only 152,805 cases were
reported, mostly from Sudan.
• Eighteen endemic countries: India,
Pakistan, Nigeria, Cameroon,
Ghana, and Sudan.
Africa India
 Mortality/Morbidity
• Death due to dracunculiasis is low and
not caused by the primary infection
but by the secondary infection of the
worm's exit site which leads to sepsis.
• Morbidity is a major concern: cellulitis
or abscess requires prompt attention,
and pain from the exit sites often can
incapacitate patients for weeks.
 Dracunculiasis
• Humans become infected by drinking
unfiltered water containing copepods
(small crustaceans) which are infected
with larvae of D. medinensis.
• Following ingestion, the copepods die
and release the larvae, which
penetrate the host stomach and
intestinal wall and enter the abdominal
cavity and retroperitoneal space. 
juveniles

Dracunculus medinensis
 Dracunculiasis
• After maturation into adults and
copulation, the male worms die and
the females (length: 70 to 120 cm)
migrate in the subcutaneous tissues
towards the skin surface.
• One year after infection, the female
worm induces a blister on the skin of
the distal lower extremity, which
ruptures. 
 1 2
3

4
 Dracunculiasis
• When this lesion comes into contact
with water, a contact that the patient
seeks to relieve the local discomfort,
the female worm emerges and releases
larvae. 
• The larvae are ingested by a copepod
and after two weeks (and two molts)
develop into infective larvae
• Ingestion of the copepods closes the
cycle.
 Intermediate host

genus Cyclops

copepod
in joint
 Filariasis: Causal Agents

• 8 main species infect humans:

1) Lymphatic: Wuchereria bancrofti,
Brugia malayi, Brugia timori
2) Cutaneous: Loa loa, Onchocerca
volvulus, Mansonella streptocerca
3) Body cavity: Mansonella perstans, M.
ozzardi
 Epidemiology
• 120 million people in 83 countries of
the world are infected with lymphatic
filarial parasites.
• 1 billion are at risk of acquiring the
infection.
• Ninety percent of these infections are
caused by Wuchereria bancrofti, and
most of the remainder by Brugia
malayi.
 Distribution

Lymphatic Filariasis is found in the tropics and subtropics of India, China, Indonesia, Southeast Asia, Africa,
South America, and the Pacific.
Elephantiasis
Elephantiasis
 Life Cycle of Filaria

• The filarial life cycle, like that of all

nematodes, consists of 5
developmental or larval stages in a
vertebral host and an arthropod
intermediate host and vector.
• Adult female worms produce thousands
of first-stage larvae or microfilariae that
are ingested by a feeding insect vector.
 Life Cycle of Filaria

• During a blood meal, an infected

mosquito introduces third-stage filarial
larvae onto the skin of the human
host.  They develop into adults that
commonly reside in the lymphatics . 
• The female worms measure 80 to 100
mm in length and 0.24 to 0.30 mm in
diameter, while the males measure
about 40 mm by 0.1 mm. 
 Life Cycle of Filaria

• Adults produce microfilariae measuring

244 to 296 μm by 7.5 to 10 μm, which
are sheathed and have nocturnal
periodicity, except the South Pacific
microfilariae, which have the absence
of marked periodicity. 
 Life Cycle of Filaria
• The microfilariae migrate into lymph
and blood channels moving actively
through lymph and blood. 
• A mosquito ingests the microfilariae
during a blood meal. 
• After ingestion, the microfilariae lose
their sheaths and reach the thoracic
muscles through the wall of the
proventriculus and cardiac portion of
the mosquito's midgut.
 Life Cycle of Filaria

• There the microfilariae develop into

first-stage larvae and subsequently into
third-stage infective larvae.
• The third-stage infective larvae
migrate through the hemocoel to the
mosquito's proboscis and can infect
another human when the mosquito
takes a blood meal.
 Life Cycle of Filaria

• Some microfilariae have a unique

circadian periodicity in the peripheral
circulation over a 24-hour period.
• The arthropod vectors, mosquitoes and
flies, also have a circadian rhythm in
which they obtain blood meals.
• The highest concentration of
microfilariae usually occurs when the
local vector is feeding most actively.
 Filariasis

• For W. bancrofti, humans are the

exclusive host
• Certain strains of B. malayi can also
infect some feline and monkey species,
but the life-cycles in humans and in
these other animals generally remain
epidemiologically distinct so little
overlap exists.
 Incubation Period

• There is an asymptomatic incubation

period of at least 6 months and up to 6
years.
• As this may lead to difficulty in
diagnosis, some have suggested routine
post-travel serologic screening for
those individuals with >1 year exposure
in an endemic area.
 Risk to the Traveller
• Risk is low with an increased risk in the
long term traveller, missionaries, field
scientists, and volunteers, as disease
usually requires repeated exposure to
the particular infected vector over
months to years.
• As the adult worm cannot multiply in the
human host, disease manifestations will
depend on the frequency of bites as well
as the worm burden.
 Asymptomatic Presentations
• Of all the patients with lymphatic
filariasis at least half appear clinically
asymptomatic, though they have
microfilariae circulating in their blood
and essentially all have hidden damage
to their lymphatic (as evidenced by
lymphoscintigraphy) and/or renal
systems (microscopic hematuria and/or
proteinuria).
 Asymptomatic Presentations

• The state of asymptomatic

microfilaraemia is associated with a
highly down-regulated immune system,
but it is as yet unclear how, when or
even whether these individuals will
progress to develop one of the more
overt clinical manifestations of filarial
disease.
 Asymptomatic Presentations
• A second asymptomatic 'presentation'
exists in individuals previously termed
‘endemic normals’
• No microfilaraemia but parasite
antigen present in blood (which will
disappear after appropriate
treatment).
 Expatriate Syndrome
• Individuals who have grown up outside
of the endemic regions and then
moved to these regions and acquired a
filarial infection manifest prominent
signs and symptoms of inflammatory
(including allergic) reactions to the
mature or maturing parasites.
 Expatriate Syndrome
• In bancroftian filariasis (when military
personnel or other migrants to
endemic areas have acquired these
infections), they have usually been
lymphangitis, lymphadenitis, genital
pain (from inflammation of the
associated lymphatics), along with
hives, rashes and other 'allergic-like'
manifestations, including blood
eosinophilia.
 Expatriate Syndrome
• The reason for these different clinical
presentations lies almost certainly in
the different immunoregulatory
responses to filarial antigens between
those with long (including prenatal)
exposure to these antigens and those
meeting them for the first time.
Microfilaria of Wuchereria bancrofti, thick blood smears stained
with hematoxylin. The microfilaria is sheathed, its body is gently
curved, and the tail is tapered to a point. The nuclear column (the
cells that constitute the body of the microfilaria) is loosely packed,
the nuclei can be visualized individually and do not extend to the
tip of the tail. The sheath is slightly stained with hematoxylin.
 Vectors

• The major vectors for W. bancrofti are

culicine mosquitoes in most urban and
semi-urban areas, anophelines in the
more rural areas of Africa and
elsewhere, and Aedes species in many
of the endemic Pacific islands.
 Culex vectors

• Culex quinquefasciatus breeds in

polluted water bodies such as
cesspits, drains, septic tanks, unused
wells, storm water canals.
Vector of Bancroftian Filariasis
•Culex quinquefasciatus is the principal vector of bancroftian filariasis in India.
 Anopheles Vectors

• The genus Anopheles is important in the

transmission of periodic W.bancrofti in
Africa, Southern Asia and the island of New
Guinea.
• A significant vector of periodic B.malayi in
Southern Asia. New transmission and
distribution records include A. gambiae
from the island of Grande Comore, and A.
flavirostris from Sabah.
Aedes

Anopheles
 Aedes vectors:

• Aedes species such as A.polynesiensis,

A.samoanus are mainly
distributed in Samoa and French
Polynesia and A.poecilius in
Phillippines
 Brugian Vectors

• For the Brugian parasites Mansonia

species serve as the major vector, but
in some areas anopheline mosquitoes
are responsible for transmitting the
infection. Brugian parasites are
confined to areas of east and south
Asia, especially India, Malaysia,
Indonesia, the Philippines, and China.
 Brugian Vectors

• Vectors of brugian filariasis: M. annulifera,

M. uniformis and M. indiana.
• These vectors require the presence of
hydrophytes (water weeds) for completing
their life cycle. The larvae of these
mosquitoes get attached to the roots of
water plants like Pistia, Eichornia and
Salvinia to draw oxygen.
 Brugian Filariasis

• During a blood meal, an infected

mosquito introduces third-stage filarial
larvae onto the skin of the human host,
where they penetrate into the bite
wound . 
• They develop into adults that
commonly reside in the lymphatics. 
 Brugian Filariasis
• The adult worms resemble those of W.
bancrofti but are smaller. 
• Female worms measure 43 to 55 mm in
length by 130 to 170 μm in width, and
males measure 13 to 23 mm in length
by 70 to 80 μm in width. 
• Adults produce microfilariae measuring
177 to 230 μm in length and 5 to 7 μm
in width, which are sheathed and have
nocturnal periodicity. 
 Brugian Filariasis
• The microfilariae migrate into lymph
and enter the blood stream reaching
the peripheral blood. 
• A mosquito ingests the microfilariae
during a blood meal. 
• After ingestion, the microfilariae lose
their sheaths and work their way
through the wall of the proventriculus
and cardiac portion of the midgut to
reach the thoracic muscles.
 Brugian Filariasis

• There the microfilariae develop into

first-stage larvae and subsequently into
third-stage larvae. 
• The third-stage larvae migrate through
the hemocoel to the mosquito's
proboscis and another human can be
infected when the mosquito takes a
blood meal.
 Knott Centrifugation Technique

Hematoxylin

B. malayi:
subterminal and
terminal nuclei
Brugia malayi
 Tropical Eosinophilia
• Weingarten’s syndrome
• Subacute or chronic form of B. malayi
or W. bancrofti filariasis occurring in
the tropics (India) with episodic
nocturnal wheezing and coughing,
marked blood eosinophilia, and
interstitial thickening and diffuse
nodular mottling in the lung fields.
• Microfilariae are confined to the lungs.
 Laboratory Diagnosis
• For such assessments one must take into
account the parasites' possible nocturnal
periodicity in selecting the optimal blood
drawing time (10 p.m.-2 a.m. for most
brugian filariasis and bancroftian
infections).
 Laboratory Diagnosis
For examining blood, hydrocoele fluid,
articular effusions and urine:
2) spread 20 microliters evenly over a
clean slide and let dry
3) stain with Giemsa or a similar stain
4) Wet smear: dilute 20-40 microliters of
anti-coagulated blood with water or 2%
saponin, which will lyse the RBC but
allow the microfilariae to remain motile
and thus more readily identifiable.
 Laboratory Diagnosis
• Knott's concentration technique: 1 ml of
anti-coagulated blood mixed with 10 ml
of 2% formalin is centrifuged; examine
the sediment either unstained or fixed
and stained.
• the microfilariae are non-motal and
generally straight, and they can be easily
missed if the viscous sediment is not
searched diligently.
 Laboratory Diagnosis
• Membrane filtration: the most sensitive
technique for quantitating microfilariae
in blood, urine or other body fluids.
• Polycarbonate (Nuclepore®) filters with
a 3 µm pore size. Anti-coagulated blood
or other fluid is passed through a
Swinnex holder containing the filter,
followed by a 35 ml of pre-filtered water
that lyses the RBC. A volume of air then
follows the water, and the filter is
removed, placed on a slide and stained.
 Laboratory Diagnosis
• Immunoassay for antigen detection of
circulating filarial antigens: rapid-
format immunochromatographic test
for detection of W. bancrofti antigens.
• Useful diagnostic approach because
microfilaremia can be low and
variable. 
 Laboratory Diagnosis

• Molecular diagnosis using polymerase

chain reaction for W. bancrofti and B.
malayi.
• Identification of adult worms is
possible from tissue samples collected
during nodulectomies (onchocerciasis),
or during subcutaneous biopsies or
worm removal from the eye (loiasis).
 Laboratory Diagnosis

• Antibody detection is of limited value:  

1) Substantial antigenic cross reactivity
exists between filaria and other
helminths
2) a positive serologic test does not
distinguish between past and current
infection.
 X-Ray Diagnosis
• Conventional X-rays are rarely helpful.
• Ultrasound exam of the lymphatics
(especially scrotal lymphatics in men,
and the breast and retro-peritoneal
lymphatics in women) can reveal rapidly
moving ("dancing") adult worms.
• Lymphoscintigraphy can identify
functional and gross anatomical
abnormalities of the lymphatics.
 Treatment
1. Effective eradication of microfilaria:
Diethylcarbamazine (eliminates adult
worms slowly)
2. Ivermectin single dose of 200-400
mg/kBW: not macrofilaricidal
3. Corticosteroids for symptomatic relief
4. Surgery
5. Supportive: pressure bandaging
 Prevention of Filariasis
• The principal strategies for
interrupting transmission of infection:
1) to identify endemic areas
2) implement community-wide
programmes to treat the entire at-risk
population. This breaks the cycle of
transmission between mosquitoes and
humans.
 Prevention of Filariasis
• Community-wide prophylaxis: once-
yearly single doses of two drugs,
albendazole plus either ivermectin or
diethylcarbamazine, for four to six years.
• Individual prophylaxis: prophylactic
regimen of DEC (6 mg/kg per day x 2
days each month) could be effective in
preventing the acquisition of infection.
 Onchocerca volvulus
• Convoluted filaria; river blindness
• Man is the only host
• Habitat: subcutaneous tissues
• Geographic distribution: Africa, Central
and South America
• Morphology: female- 40mm x 300 micra
male- 30 mm x 150 micra
 Clinical Diseases
1. Skin lesions: urticaria, papules,
edema, lichenified skin, peau d’
orange
2. Eye lesions: conjunctivitis (lacrimaion
and photophobia); keratitis; iritis,
iridocyclitis, secondary glaucoma;
blindness
3. Inguinal lymphadenopathy: scrotal
enlargement
 Diagnostic Tests
• Examination of skin snips will identify
microfilariae of Onchocerca volvulus. 
• Get skin snips via corneal-scleral
punch, or more simply with a scalpel
and needle. 
• The sample is incubated for 30-120
minutes in saline or culture medium;
examine for microfilariae that have
migrated from the tissue to the liquid
phase of the specimen.
 Onchocerca volvulus
no sheath present; the tail is tapered
and is sharply angled at the end.

Loa loa

sheathed, with a relatively dense nuclear

M. perstans column; its tail tapers and is frequently
coiled, and nuclei extend to end of tail.
 Loiasis
• Loa loa
• Habitat: subcutaneous tissues
• Calabar swelling: a transient
subcutaneous swelling marking the
migratory course through the tissues of
the adult filarial eye worm of the
genus Loa
• No reservoir hosts
 Pathogenesis
• Hypersensitivity to secretions of adult
worms
• Tissue swellings are hot and
erythematous, occurring in the
extremities and periorbital tissues
• Rarely, adult parasite in CSF
associated with meningoencephalitis
Loa loa
 Loa Loa Filariasis
• The vector for Loa loa filariasis are day-
biting flies from two species of the genus
Chrysops, C. silacea and C. dimidiata. 
• During a blood meal, an infected fly
introduces third-stage filarial larvae onto
the skin of the human host, where they
penetrate into the bite wound.  The
larvae develop into adults that commonly
reside in subcutaneous tissue. 
 Loa Loa Filariasis

• Female worms measure 40 to 70 mm in

length and 0.5 mm in diameter, while
males measure 30 to 34 mm in length
and 0.35 to 0.43 mm in diameter. 
• Adults produce microfilariae measuring
250 to 300 μm by 6 to 8 μm, which are
sheathed and have diurnal periodicity. 
 Loa Loa Filariasis

• During the day they stay in peripheral

blood, but are found in the lungs
during the noncirculation phase. 
• The fly ingests microfilariae during a
blood meal. 
• Microfilariae have been recovered from
spinal fluids, urine, and sputum. 
 Loa Loa Filariasis

• After ingestion, the microfilariae lose

their sheaths and migrate from the fly's
midgut through the hemocoel to the
thoracic muscles of the arthropod.
• There the microfilariae develop into 1st-
stage then 3rd-stage infective larvae. 
• The third-stage infective larvae migrate
to the fly's proboscis and can infect
another human when the fly takes a
blood meal.
 Expatriate Syndrome
• In loiasis, these manifestations have
included primarily Calabar swellings,
hives, rashes and occasionally asthma.
 Loa loa: Treatment
1. Diethylcarbamazine
2. Corticosteroids
3. Surgery