LYMPHATIC FILARIAL

NEMATODES

SHAKA BOOM BOOM SHAKA


• Solomon Fallah Foa SANDY
• Solomon Patrick Brima
• Moses Tamba Momoh
• Dauda Sesay
• Alusine Sesay
• Sylvernus Momoh Kamara
• Emeric Nicholson
• Idrissa Conteh
PRESENTERS
• Abubakarr Jalloh
• Abubakarr M. Kamara
• Osman I. Kamara
• Idrissa Korie Turay
• Karifala Balla Sesay
• Amadu Sall
• Ahmed Sankoh
 Introduction
FILARIAL NEMATODE
GENERAL PROPERTIES
• Habitat: Filarial worms reside in the lymphatic system, skin, subcutaneous tissue and
rarely body cavity
• Adult worm: Th e adult worms are slender, round measuring 2–10 cm in length
(except the female Onchocerca 35–50 cm).
• Some adult filarial worms can survive for many years in humans causing a number of
chronic obstructive and inflammatory conditions including elephantiasis and
hydrocele
• Microfilariae: The female worm produces large number of L1 larvae called as
microfilariae which are highly motile thread like larvae.
• They are usually non pathogenic but sometimes, hypersensitivity reactions can occur
against the microfilarial antigen resulting in tropical pulmonary eosinophilia (TPE).
 LYMPHATIC FILARIAL
NEMATODES
• Lymphatic filariasis is caused by
➢Wuchereria bancrofti
➢Brugia malayi
➢Brugia timori.
 Wuchereria bancrofti
History
• Indian physician Sushruta was the first to describe
elephantiasis.
• Microfilaria of W. bancrofti was first discovered by Demarquay
(1863) in hydrocele fluid from a patient in Cuba Wucherer
(1868) had detected the microfilaria in urine and Lewis (1872)
in blood Bancroft was the first to describe the female worm in
1877, followed by the discovery of adult male by Bourne
(1888) Manson (1899) had described the periodicity of the
microfilaria and the role of insect vector.
 Wuchereria bancrofti
Epidemiology
W. bancrofti, is the most widely distributed
filarial parasite of humans
• Approximately two billion people residing in
80 countries are at risk; while an estimate of
nearly 110 million people are infected
• It is found throughout the tropics and
subtropics with highest prevalence in Asia
(India-5%, China) and Sub-Saharan Africa (8%)
and other places like Pacific Islands, areas of
South America, and the Caribbean Basin
• In general, W. bancrofti is nocturnally
periodic, except in Pacific Islands; where it is
sub-periodic.
 Wuchereria bancrofti
Morphology
Adult worm
• Adult worms are located in the lymphatic vessels and lymphnodes.
• They are long, slender, creamy white thread like filariform shaped with
tapering ends
• Adult males (4 cm × 0.1 mm) are smaller than females (6–10 cm × 0.2–0.3
mm)
• Male worms can be differentiated from female worms by their small size,
corkscrew like tail and presence of two spicules (helps in copulation) at
posterior end
• Both adult male and female remain coiled together
• Females are viviparous
 Wuchereria bancrofti
Morphology
Larva
• Like other nematodes, there
are four larval stages. The first
stage larva is called as
microfilaria.
• The third stage larva is called as
filariform larva
 Wuchereria bancrofti
Morphology
Microfilaria
• Microfilariae are the diagnostic forms, found in the blood vessels.
• It measures 240–300 μm × 7.5–10 μm covered by a long hyaline sheath
(360 μm) within which it moves
• The head end is blunt while the tail end is Pointed In unstained film.
• Microfilariae are transparent and colorless.
• But when stained with Giemsa or other Romanowsky stains they look pink
with a column of violet nuclei which are present throughout the body
except near the head and the tail end.
• Nuclei are also absent in few places which represent various primordial
organs.
 Wuchereria bancrofti
Life Cycle
Host: W. bancrofti completes its life cycle in two hosts.
1. Definitive host: Man
2. Intermediate host: Mosquito named Culex
quinquefasciatus is the principle vector worldwide.
Rarely Anopheles (rural Africa) or Aedes (Pacific Island)
can serve as a vector.
• Infective form: Third stage filariform larvae are the
infective form found in the proboscis of the
mosquito.
• Mode of transmission: L3 filariform larvae get
deposited in skin by the insect bite.
• Residents living in the endemic areas are exposed to
about 50–300 L3 larvae every year.
 Wuchereria bancrofti
Human cycle

• Larvae penetrate the skin, enter into lymphatic vessels and

migrate to the local lymph nodes where they molt twice to
develop into adult worms in few months
• Adult worms reside in the afferent lymphatics or cortical sinuses
of the lymph nodes where they mate and start laying the
(microfilariae).
• Male worms die after mating where as the female worms live for
5–10 years. A gravid female can discharge 50,000
microfilariae/day
• Prepatent period: Range from 80 days to 150 days.
 Wuchereria bancrofti
Mosquito cycle
• When the mosquito bites an infected man, the
microfilariae are ingested. Culex bites in night where
as Aedes bites in daytime
• Microfilariae come out of the sheath within 1–2
hours of ingestion and penetrate the stomach wall
and migrate to thoracic muscle in 6–12 hours where
they become sausage shaped (short and thick)
• L1 larvae molt twice to develop L2 (long and thick
form) followed by L3 (long and thin form). The highly
active L3 larvae migrate to the labella (distal part of
proboscis) of the mosquito and serve as the infective
stage to man
• Under optimum conditions, the mosquito cycle takes
around 10–14 days.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Infection caused by W. bancrofti is termed as
wuchereriasis or bancroftian filariasis.
• The disease can present as
– Classical filariasis
– Occult filariasis.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis
• It occurs due to blockage of lymph vessels and lymph
nodes by the adult worms. The blockage could be due to
mechanical factors or allergic inflammatory reaction to
worm antigens and secretions.
• The affected lymph nodes and vessels are infiltrated
with macrophages, eosinophils, lymphocytes and
plasma cells.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis
• The vessel walls get thickened and the lumen narrowed
or occluded, leading to lymph stasis and dilatation of
lymph vessels.
• The worms inside lymph nodes and vessels may cause
granuloma formation
• Inflammatory changes damage the valves in lymph
vessels, further aggravating lymph stasis.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis
• Increased permeability of lymph vessel walls lead to leakage of
protein-rich lymph into the tissues.
• This produces the typical hard pitting or brawny edema of
filariasis.
• Fibroblasts invade the edematous tissues, laying down fibrous
tissue, producing the nonpitting gross edema of elephantiasis.
• Recurrent secondary bacterial infections cause further damage.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis Clinical manifestations:
• The most common presentations of lymphatic filariasis
are
• Asymptomatic (Subclinical)
• Microfilaremia,
• Acute Adenolymphangitis (AOL)
• Chronic Lymphatic Disease.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis Clinical manifestations:
• Acute Adenolymphangitis (AOL)
– High fever
– Lymphatic inflammation (lymphangitis and
lymphadenitis)
– Transient local edema.
• Chronic Lymphatic Disease.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Classical filariasis Clinical manifestations:
• Chronic Lymphatic Disease includes
– Hydrocele
– Lymphorrhagia
– Elephantiasis
 Wuchereria bancrofti
Pathogenesis and Pathology
• Occult fllariasis
• It occurs as a result of hypersensitivity reaction to
microfilarial antigens, not directly due to lymphatic
involvement.
• Microfilariae are not found in blood, as they are
destroyed by the allergic inflammation in the tissues.
 Wuchereria bancrofti
Pathogenesis and Pathology
• Occult fllariasis Clinical manifestations:
– Massive eosinophilia (30-80%)
– Hepatosplenomegaly
– Pulmonary symptoms like dry nocturnal cough, dyspnea and
asthmatic wheezing.
– Occult filariasis has also been reported to cause arthritis,
glomerulonephritis, thrombophlebitis, tenosynovitis, etc.
– Classical features of lymphatic filariasis are absent.
• Meyers Kouwenaar syndrome is a synonym for occult filariasis.
 Wuchereria bancrofti
Laboratory Diagnosis
• The diagnosis of filariasis depends on the clinical
features, history of exposure in endemic areas and on
laboratory findings.
• The laboratory tests that can be used for diagnosis
 Wuchereria bancrofti
Treatment
• Diethylcarbamazine is the drug of choice. It is given
orally in a dose of 6 mg/ kg body weight daily for a
period of 12 days amounting to a total of 72 mg of DEC
per kg of body weight.
• It has both macro and microfilaricidal properties.
• Following treatment with DEC severe allergic reaction
(Mazzotti reaction) may occur due to death of
microfilariae. It kills both microfilaria and adult worm.
 Wuchereria bancrofti
Treatment
• Antihistamines or corticosteroids may require to control
the allergic phenomenon.
• The administration of DEC can be carried out in three
ways:
– Mass therapy
– Selective treatment
– Diethylcarbamazine medicated salts
 Wuchereria bancrofti
Treatment
• Antihistamines or corticosteroids may require to control
the allergic phenomenon.
• The administration of DEC can be carried out in three
ways:
– Mass therapy
– Selective treatment
– Diethylcarbamazine medicated salts
 Wuchereria bancrofti
Treatment
• Ivermectin: In doses of 200 μg/kg can kill the
microfilariae but has no effect on adults. It is not used in
India. It is used in regions of Africa.
• Tetracyclines or doxycycline for 4-8 weeks also have an
effect in the treatment of filariasis by inhibiting
endosymbiotic bacteria (Wolbachia species) that are
essential for the fertility of the worm.
 Wuchereria bancrofti
Treatment
• Ivermectin: In doses of 200 μg/kg can kill the
microfilariae but has no effect on adults. It is not used in
India. It is used in regions of Africa.
• Tetracyclines or doxycycline for 4-8 weeks also have an
effect in the treatment of filariasis by inhibiting
endosymbiotic bacteria (Wolbachia species) that are
essential for the fertility of the worm.
 Wuchereria bancrofti
Supportive treatment
• Chronic condition may not be curable by antifilarial drugs and
require other measures like elevation of the affected limb, use of
elastic bandage and local foot care reduce some of the symptoms
of elephantiasis.
• Surgery is required for hydrocele.
• Medical management of chyluria includes bed rest, high protein
diet with exclusion of fat, drug therapy with DEC and use of
abdominal binders.
• Surgical management of refractory case includes endoscopic
sclerotherapy using silver nitrate.
 Wuchereria bancrofti
Prophylaxis
• The two major measures in prevention and control of
filariasis are:
– Eradication of the vector mosquito.
– Detection and treatment of carriers.
Brugia Malayi
 Brugia Malayi
History and Distribution
• the genus Brugia was named after Brug, who in 1927 described a new
type of microfilaria in the blood of natives in Sumatra.
• The adult worm of 8. malayi was described by Rao and Maplestone in
India (1940).
• Besides B malayi, the genus includes B. timori, which parasitizes
humans in Timor, Indonesia and a number of animal species, such as B.
pahangi and B. patei infecting dogs and cats.
• The geographical distribution of B. malayi is much more restricted than
that of W. bancrofti.
• It occurs in India and Far-East, Indonesia, Philippines, Malaysia,
Thailand, Vietnam, China, South Korea and Japan.
 Brugia Malayi
Morphology
Adult worms:
• The adult worms of B. malayi are generally similar to those of W.
bancrofti, though smaller in size.
Microfilariae:
• The microfilariae of B. malayi, although sheathed are different in a
number of respects from Microfilaria bancrofti.
• Mf malayi is smaller in size, shows kinks and secondary curves, its
cephalic space is longer, carries double stylets at the anterior end, the
nuclear column appears blurred in Giemsa-stained films and the tail tip
carries two distinct nuclei, one terminal and the other subterminal
 Brugia Malayi
Life Circle
• The life cycle of 8. malayi is similar to that or W.
bancrofli; however, the intermediate host of Brugia are
vectors of genera Mansonia, Anopheles and Aedes. In
India, main vectors are Mansonia annulifera and M.
uniformis.
• Pathogenicity, clinical features, laboratory diagnosis and
treatment are similar to W. bancrofti.
 Brugia Malayi
Prevention
• The breeding of Mansonia mosquito is associated with
certain plants such as Pistia.
• In absence of these plants, mosquito cannot breed. Thus
in countries like Sri Lanka and India where M. annulifera
is the chief vector of B. malayi, the transmission of the
parasite can be effectively reduced by removal of these
plants in addition to the methods described in W.
bancrofti.
Brugia Malayi
 Brugia Timori
• Is limited to Timor and some other islands of Eastern Indonesia.
• The vector of B. timori is Anopheles barbirostris, which breeds in rice
fields and is a night feeder.
• Definitive host: Man. No animal reservoir is known.
• The microfilaria is larger than Mf malayi. The sheath of Mf timori fails to
take Giemsa stain with 5-8 nuclei present in the tail.
• lesions produced by B. timori are milder than those of bancroftian or
malayan filariasis.
• A characteristic lesion is the development of draining abscesses caused
by worms in lymph nodes and vessels along the saphenous vein, leading
to scarring.