Filarial worms are thread-like nematodes that infect approximately 250 million people worldwide through mosquito transmission. They inhabit different areas of the body and can cause diseases like elephantiasis. The female worms release microfilariae that circulate in the blood and are ingested by mosquitoes, where they develop into infective larvae that can infect other humans, completing the life cycle. Common filarial worms include Wuchereria bancrofti, which resides in the lymphatic system and causes elephantiasis, Brugia malayi which is similar but transmitted by different mosquitoes, Onchocerca volvulus which causes river blindness and resides in subcutaneous nodules, and Loa lo

2. Filarial worms
Filarial worms are thread-like nematodes of which
there are at least 8 species for which humans, especially
in tropical regions, are the definitive host.
Approximately 250 million people worldwide are
infected with these worms which are spread by
mosquitoes.
Different species inhabit different locations in the
body. Some live in the lymphatic system, others
subcutaneously and others in the abdominal cavity.
Introduction

3.  The female worms are viviparous and give birth to
larvae known as microfi lariae.
The microfi lariae released by the female worm, can
be detected in the peripheral blood or cutaneous tissues,
depending on the species.
The microfilariae are picked up by mosquitoes where
they develop, become infective and can infect another
person.
Introduction

4. Periodicity: Depending on when the largest
number of microfi lariae occur in blood, fi larial
worms can exhibit nocturnal, diurnal periodicity or
no periodicity at all.
The basis of periodicity is unknown but it may be an
adaptation to the biting habits of the vector

5. Nocturnal periodicity: When the largest
number of microfi lariae occur in blood at night, e.g.
Wuchereria bancrofti
Diurnal periodicity: When the largest number
of microfi lariae occur in blood during day, e.g. Loa
loa
Nonperiodic: When the microfilariae
circulate at constant levels during the day and
night, e.g. Onchocerca volvulus
Subperiodic or nocturnally subperiodic:
When the microfi lariae can be detected in the blood
throughout the day but are detected in higher
numbers during the late afternoon or at night.
Note: The microfi lariae are found in capillaries and
blood vessels of lungs during the period when they are
not present in the peripheral blood.

6. Once the microfi lariae are classifi ed on the basis of
sheath as ‘sheathed’ or ‘unsheathed’, their further diff
erentiation can be done on the characteristic
arrangement of nuclei

7. Differentiating features of various microfi lariae on the basis of presence of
nuclei in tail end

10. Wuchereria bancrofti
Habitat:
The adult worms reside in the lymphatic system of
man. The microfi lariae are found in blood .
Disease
• Wuchereria bancrofti causes filariasis
• Elephantiasis is a striking feature of this disease
Important Properties
• Humans are infected when the female mosquito
(especially Anopheles and Culex species) deposits
infective larvae on the skin while biting
• The larvae penetrate the skin, enter a lymph node,
and, after 1 year, mature to adults that produce
microfilariae.

11. • These circulate in the blood, chiefly at night, and are
ingested by biting mosquitoes
• Within the mosquito, the microfilariae produce
infective larvae that are transferred with the next bite
• Humans are the only definitive hosts.

12. Life Cycle
W. bancrofti passes its life cycle in 2 hosts (Fig. 21.5).
Definitive host: Man. No animal host or reservoir is
known for W. bancrofti.
Intermediate host: Female mosquito, of different
species acts as vectors in different geographic areas.
The major vector in India and most other parts of Asia
is Culex quinque fasciatus (C. fatigans).
Infective form: Actively motile third-stage filariform
larva is infective to man.
Mode of transmission: Humans get infection by bite of
mosquito carrying filariform larva.

13. Life Cycle

14. Pathogenesis & Clinical Findings
1-Adult worms in the lymph nodes cause inflammation
that eventually obstructs the lymphatic vessels, causing
edema. Massive edema of the legs is called elephantiasis.
Note that microfilariae do not cause symptoms

15. 2-Early infections are asymptomatic. Later, fever,
lymphangitis, and cellulitis develop. Gradually, the
obstruction leads to edema and fibrosis of the legs and
genitalia, especially the scrotum
3- Elephantiasis occurs mainly in patients who have
been repeatedly infected over a long period
4- Tropical pulmonary eosinophilia is characterized by
coughing and wheezing, especially at night
5- These symptoms are caused by microfilariae in the
lung that elicit an immediate hypersensitivity reaction
characterized by a high immunoglobulin E (IgE)
concentration and eosinophilia

17. Thick blood smears taken from the patient at night
reveal the microfilariae

18. Control of Vector Mosquito:
control would be elimination of breeding places
by providing adequate sanitation and
underground waste water disposal system.
 €Chemical control: Using antilarval chemicals.
 Detection and Treatment of Carriers.
Treatment: Drug of choice is DEC and ivermectin.
Supportive and surgical management in some cases.
Treatment & Control

20. Brugia Malayi
Introduction Brugia malayi is a nematode causing
lymphatic filariasis in South East Asia. There are two
strains of B. malayi;
1. The nocturnal periodic strain which is widely
distributed in Asia, the microfilariae being in their
highest concentrations between the hours of
10pm and 2am.
2. The sub-periodic strain which is found in Malaysia,
Indonesia and the Philippines where humans
exhibit a microfilaremia all the time with the
highest numbers being detected between noon
and 8pm.

21. The life cycle of B. malayi is similar to that of
W. brancofti;
however, the intermediate host of Brugia are
vectors of genera Mansonia, Anopheles and
Aedes. In India, main vectors are Mansonia
annulifers and M.uniformis.
Pathogenecity, clinical featues, laboratory
diagnosis, and treatment are similar to W.
brancofti.

22. Distinguishing features of Microfi laria
bancrofti and Microfi laria malayi.

24. Onchocerca volvulus
Disease
• Onchocerca volvulus causes onchocerciasis (river
blindness) Important Properties
• Humans are infected when the female blackfly,
Simulium, deposits infective larvae while biting
• The larvae enter the wound and migrate into the
subcutaneous tissue, where they differentiate into
adults, usually within dermal nodules
• The female produces microfilariae that are ingested
when another blackfly bites
• The microfilariae develop into infective larvae in the
fly to complete the cycle
• Humans are the only definitive hosts

25. life cycle is completed in 2 hosts.
Definitive host: Humans are the only defi nitive
host.
Intermediate hosts: Day-biting female black fl ies
of the genus Simulium (black flies).
The vector Simulium species breed in ‘fast-fl owing
rivers; and therefore, the disease is most common
along the course of rivers. Hence, the name ‘river
blindness’.
life cycle

26. life cycle

27. Clinical features:
Subcutaneous nodule formation (onchocercoma).
Ocular manifestations – sclerosing keratitis,
secondary glaucoma, optic atrophy,chorioretinitis.
It is the second major cause of blindness in world.
Diagnosis:
Demostration of microfi laria from skin snips and
aspirated material form subcutaneous nodules.
Demonstration of IgG4 antibody and PCR.
Treatment:
Ivermectin is the drug of choice except in areas
coendemic for O. volvulus and L. loa.

29. Loa loa Introduction Loa loa, also known as the
African eye worm, is a filarial nematode endemic in
the rain forests of West and Central Africa. It is
transmitted by Chrysops species, also known as
mango flies or horse flies and humans are the only
known reservoir. It is estimated that 2-13 million
humans are infected with the larvae. Adults migrate
in the subcutaneous tissues of man and monkeys,
with them eventually migrating across the eyeball
under the conjunctiva.
Loa loa

31. Pathogenicity and Clinical Features
The pathogenesis of loiasis depends on the migratory
habit of the adult worm.
Their wanderings through subcutaneous tissues set
up temporary foci of inflammation, which appear as
Subcutaneous swellings (calabar swellings), ocular
granuloma, edema of eyelid, andproptosis.
Complications like nephropathy,encephalopathy,
and cardiomyopathy can occur but are rare.

32. Diagnosis: Demostration of adult worm from
skin and conjunctiva. Demonstration of microfilaria
in peripheral blood during day. High eosinophil
count.
Treatment: DEC with simultaneous
administration of corticosteroid of other drugs
which may be used. Ivermectin or albendazole.

34. Morphology
•One of the largest nematodes known.
•Adult females have been recorded up to 800 mm
long
•Few males known do not exceed 40 mm.
•The mouth is small and triangular and is
surrounded by a quadrangular, sclerotized plate.
•Lips are absent.
•The esophagus has a large glandular portion
•Spicules of the male are unequal and 490 to 730
um long. The gubernaculum ranges from 115 to
130 um long.

35. Life cycle
Habitat: The adult females of D. medinensis are
usually found in the subcutaneous tissue of the legs,
arms and back in man.
D. medinensis passes its life cycle in two hosts.
Definitive host: Man
Intermediate host: Cyclops, in which embryos
undergo developmental changes. There is no animal
reservoir.
Infective form: Third-stage larva present in the
hemocele of infected cyclops.
Mode of transmission: Humans get infected by
drinking unfi ltered water containing infected cyclops.

36. Incubation period: About 1 year.
The adult worm, which is viviparous discharges
larvae,which are ingested by the fresh water
crustacean Cyclops, the intermediate host.

37. Life cycle

38. Pathogenesis
 Year – asymptomatic
Before blister symptoms
Nausea, vomiting, erythema, urticarial rash &
pruritis, blister – reddish papule with vesicular centre
souround induration
Common site – feet ankle metatarsal
 Secondary bacterial infections of opening possible.
 Retreating worm can draw bacteria under skin as
well.
 There may be later symptoms
 fibrosis of the skin, muscles, tendons and joints
(may interfere with locomotion or use of limbs)

40. LAB DIAGNOSIS:
 Detection of adult worm
-Gravid female worm appears at the surface of skin
-After death may become calcified can be detected
radiological

41. Detection of larva:
Contact with water – large amount of larva discharges
 Microscopic examination
 Serology:
• Antibody seen in serum by elisa & fluorescents
antibody test
• Skin test
• Antigen is injected intradermal to see wheal reaction

42. Treatment
• Removal of worm:
• by twisting it around
• take weeks to months
•Metronidazole, Niridazole, Membendazol
• Surgical removal of worm

43. Control:
•Filter, boil, or treat water with chlorine to kill
intermediate host.
•Finely-meshed cloth or, better still, a filter made
from a 0.15 mm nylon mesh, is all that is needed to
filter out the copepods from the drinking water.
•Avoid bathing or wading in drinking water.
•Village-based volunteers demonstrating the use of
cloth filter on a clay pot to filter drinking water.
• Construction of copings around well heads or the
installation of boreholes with hand pumps.
• Borehole is a deep and narrow well.
• Coping is a cap/cover over a well
• Key is to prevent copepod growth by controlling
sunlight. Light increases the food source of the
copepod.