FILARIAL

WORM

Long, slender worms

with tapering ends
Adult forms are found
in tissues
Three types of
infections (based on
site)
Table 20.15 Clinical from of filariasis and its causative
agent

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  Caused by Wuchereria and Brugia
 Wuchereria bancrofti: 90% of the cases
 Brugia malayi causes the rest
LYMPHATIC  Brugia timori rarely causes lymphatic filariasis
 In India more than 90% of cases are reported from
FILARIASIS nine states—Bihar, Uttar Pradesh, the coastal areas of
Gujrat and Maharashtra and coastal parts of Tamil
Nadu, Andhra Pradesh, Orissa and West Bengal.

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 MORPHOLOGY
• Adult
Morphologically, adult worms of
Wuchereria and Brugia are
indistinguishable
The male and female adult worms are long,
transparent and filiform
Both ends taper with a slightly swollen
head
Male and females usually remain tightly
coiled together in the lymph nodes
Fig. 20.33 Adults of W. bancrofti (Source: CDC, DPDx)

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 • Larvae
Microfilariae of various species are different;
differentiated by their morphological features
Sheathed microfilariae: Larvae retain a part of the
chorionic envelope of the egg as a hyaline sheath
MORPHOL Seen in both Wuchereria and Brugia
OGY The larvae have somatic cells known as nuclei which
are distributed from the head to the tail end
In Wuchereria bancrofti, the tail tip is free of nuclei
in Brugia malayi, the tail has two nuclei—one at
extreme end and a second one just above the tip

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Table 20.16 Characteristics of filarial worms
causing lymphatic filariasis
 LIFE CYCLE
Human beings: Definitive
hosts
Mosquitoes (Culex,
Anopheles and Aedes) are
intermediate hosts
Culex mosquito: Vector in
urban and semi-urban areas
Anopheles plays: In rural
areas.
Aedes: Mainly in the
Pacific Islands

Fig. 20.34 Schematic diagram of the life

cycle of W. bancrofti/B. malayi
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 Mosquitoes ingest microfilariae when
Mosquitoes ingest microfilariae when they bite an
they bite
infected host
an infected host
Ex-sheathing
Ex-sheathing of the of thestage
larval larval stage occurs
occurs
LIFE
LIFECYCLE
CYCLE Microfilariae
Microfilariae undergo
undergo three moultings
three moultings to
to mature into
mature
actively into
motile 3rdactively motile 3rd stage
stage larvae
larvae
Infective form: 3rd stage larvae
Infective form: 3rd stage larvae

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 Fig. 20.35 The
life cycle of
filarial worms

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 Lymphatic obstruction and inflammatory
damage to lymphatics
Valvular damage in the lymphatic vessels and
resulting in lymphedema due to antigen and toxic
metabolites released by worms causing infiltration
PATHOGENE of plasma cells, eosinophils and macrophages
After the death of worm: Severe lymphatic
SIS obstruction due to increased granulomatous
reaction causes blockage and fibrosis of lymph
vessels
Altered CMI and humoral immunity
Increase in eosinophil count and IgE levels

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CLINICAL FEATURES
Incubation period is 8–16 months
Asymptomatic lymphatic filariasis: Patients are asymptomatic
in endemic areas
Acute infection: High fever, lymphatic inflammation and
transient local edema
Regional lymph nodes are enlarged and lymphatic channels
appear thick and indurated
Scrotal tenderness and pain may be present

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CLINICAL FEATURES
Chronic infection: Damage over 10–15 years
Progressively leads to lymphangitis, lymphedema and other
complications
Severe lymphatic obstruction
Fibrosis, chronic lymphedema and elephantiasis(commonly
affects the lower limbs, genital organs and breasts)
Symptoms: Lymph scrotum, lymphuria

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CLINICAL FEATURES
• Occult filariasis (tropical pulmonary eosinophilia)
Caused by a hypersensitivity reaction to microfilarial antigens
Symptoms: Dry cough, wheezing, fever and loss of appetite
Chest X-ray: Diffuse interstitial infiltrates with increased bronchoalveolar
markings
Eosinophils counts raised up to 5,000 per mm3 of blood, and IgE levels are
elevated

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 LABORATORY
DIAGNOSIS
Samples: Peripheral blood—best
collected at night or after administering
a dose of diethylcarbamazine (DEC) 2
mg/kg body weight; collected after 30–
60 minutes of giving the medicine—
DEC provocation test
Microscopy: Direct wet mount of
EDTA blood shows motile microfilariae
Other samples: Urine or hydrocele
Fig. 20.36 Algorithm of approach to fluid
the laboratory diagnosis of filariasis

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LABORATORY DIAGNOSIS
Thick and thin films made
Stained with Giemsa/Leishman or polychrome methylene blue
QBC: Acridine orange is used to stain after centrifugation of blood
in capillary; examined under a fluorescent microscope
Detection of circulating antigen: ELISA and
immunochromatographic (ICT) lateral flow assay
Detect the filarial antigen of Wuchereria (Og4C3 ELISA)
Not yet available for Brugia
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LABORATORY DIAGNOSIS
Biopsy of lymph nodes: The adult worm can be demonstrated in
biopsy (rarely used)
Molecular methods: PCR
Indirect evidence:
Detection of antibody
Skin hypersensitivity reaction
Blood tests—eosinophilia and elevated IgE

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• TREATMENT
Diethylcarbamazine (DEC) 6 mg/kg body weight for 12 days
Albendazole 400 mg twice daily for 21 days
Both DEC and albendazole kill the adult as well as larval form of the parasite
PREVENTION
Mass drug administration (MDA)—DEC and albendazole along with vector
control in endemic areas
Under the National Vector-Borne Control Programme

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 Table 20.17 Blood flukes pathogenic to humans

 Blood flukes reside in the venous plexus of the

SCHISTOSOMES OR intestine and bladder of humans

BLOOD FLUKES  Cause schistosomiasis

 Five species

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Fig. 20.37 Schistosoma (a) egg of S. mansoni, (b) egg of S. haematobium, (c) egg of S. japonicum and (d) cercaria
larva (Source: CDC, PHIL, Image IDs 4841, 4842, 4843 and 8556)

 Adults are cylindrical with a thick syncytial tegument

MORPHOLOGY 

Sexes are separate
Male and female worms coexist in the venous plexus

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 • Egg
Operculated with a projection or spine.
The size and position of the spine vary
across species
Larva
MORPHOLOG
Y Three larval forms: miracidium,
sporocyst and cercaria
The infective form is the cercaria larva,
which is oval and elongated with a
bifurcated tail
Larva lives for about 24–72 hours
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LIFE CYCLE
• Fig. 20.38 Life cycle
of schistosomes

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 CLINICAL FEATURES

Acute schistosomiasis
Cercarial dermatitis: The cercaria penetrates the skin, causing maculopapular, itchy
rash
Seen in all Schistosoma infections and is known as the swimmer’s itch

Katayama syndrome
In S. mansoni and S. japonicum infections

4–8 weeks after the infection

Nocturnal fever, headache, cough, myalgia and abdominal tenderness

Lymphadenopathy and hepatosplenomegaly may

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 LABORATORY TREATMENT
DIAGNOSIS
DC shows eosinophilia Drug of choice is praziquantel with or
Chest X-ray shows diffuse without steroids.
pulmonary infiltrates
Serum contains antibodies to
Schistosoma
Schistosome egg in feces

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CHRONIC SCHISTOSOMIASIS
Depend on the site involved
Chiefly due to tissue reaction and reaction to mucosal injury
Allergic reaction to eggs
Granuloma due to eggs
Complications: nephrosclerosis, liver abscess, pulmonary
hypertension or encephalitis

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 By chronic infection with
HEPATOSPLENIC Schistosoma parasites residing
SCHISTOSOMIAS in the mesenteric plexus
IS

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 LABORATORY DIAGNOSIS
Samples: Urine, stool, biopsy specimen, and blood

Microscopy: Eggs of S. haematobium can be detected in urine or bladder biopsy

Eggs of Schistosoma infecting the intestines can be detected in stool samples and
intestinal biopsy
All eggs except those of Schistosoma haematobium are acid-fast

Serology:
Antigen detection: ELISA-based assay
Antibody detection: ELISA and enzyme-linked immunetransfer blot assay
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TREATMENT AND CONTROL
Praziquantel is the drug of choice

Proper disposal of human feces and eradication of intermediate hosts

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