The Filariae Worms

These are long, thread-like nematodes that inhabit portions of the lymphatic
system, subcutaneous and deep connective tissue. They comprise some of
the most important diseases of man. Some filariae worms of medical
importance are grouped as follows, according to habitat of adult worms:
1) Lymphatic filariae (Lf) – grouped in 3 genera:
a) Wuchereria bancrofti (man only)
b) Brugia malayi (mainly man but also other mammals)
c) Brugia timori (man)
2) Subcuteneous (and connective tissue) Filariae
Onchocerca volvulus
Loa loa
Dracunculus medinensis
3) Serous cavity (or connective tissue) filariaae
Mansonella perstans
Mansonella ozzardi
Lymphatic filariasis (Lf)
Caused by 3 main species;
Wuchereria bancrofti, Brugia maleyi and Brugia timori

Lymphatic filariasis is the cause of much morbidity in man

and share with Schistosomiasis the dubious distinction
among helminth infections of increasing in incidence each
year. Mainly transmitted by mosquitoes. The female adults
are viviparous and the early stage larvae, known as
microfilariae, are found in the blood.
 Wuchereria bancrofti
W. bancfrofti (or Bancroftian filariasis) is widely distributed
in the tropical and subtropical countries. In Africa it tends to
occur approximately between 20°N and 20 ºS and in
Madagascar and along the African coast of the
Mediterranean. Scattered cases have been reported in Turkey.
In Asia, the disease maybe found along the Arabian seacoast,
India, Pakistan, Burma, Thailand, in the Philippines,
Bangladesh, Korea, Sri Lanka etc. It occurs extensively in
the Pacific Islands (e.g. Fiji, Tahiti, Samoa and New Guinea).
It used to be seen on the northern and eastern coasts of
Australia, but it is very rare now if at all. It is also common
in some Caribbean Islands – Haiti, Puerto Rico, and Trinidad;
In South America it is found in Panama, Guyana, Surinam,
Brazil etc.
Lymphatic filariasis occurs in periodic
and sub-periodic forms. The periodic
form, with marked nocturnal periodicity,
is characteristic of humid tropics of the
world and is transmitted by night biting
mosquitoes. The other form is diurnally
periodic, restricted to Polynesia, and
transmitted by mainly day biting Aedes.
 Location in the host
The adults live in the lymphatics, either of
the lower limbs, the groin or of the upper
limbs. The adults lie coiled together in the
lymphatic glands and vessels.
Sheathed microfilariae are found in the
blood
 Morphology

The adults are long, thread-like worms, (hence the

word ‘filaria’), measuring about one to two inches in
males and 2 to 4 inches for females. The head end is
slightly swollen and has 2 rows of ten papillae. The
cuticle is smooth with very fine transverse striations
and the posterior end of the females is finely
tuberculated. The female has two posterior ovaries and
is viviparous. The eggs in the uterus are enclosed in a
chorionic membrane which becomes a sheath to the
living embryos (microfilariae).
The sheathed microfilaria are emitted by the
female and travel via the lymphatics into the
blood stream whence they are ingested by
mosquitoes. They can live in the blood
circulation for 3 to 6 months. The sheath is
actually the egg shell, which is very thin and
delicate and surrounds the mf embryo as it
circulates in the blood; it is not lost until it is
digested away in the stomach of the mosquito.
The microfilariae contain a large number of
nuclei.
The World Geographical Distribution of Filariasis

FILARIASIS
 Developmental Cycle
Male and female adult worms live in the lymphatics where
they can survive for 10 to 18 years
Lymphatic filariasis is transmitted to man by various
mosquito species – Anopheles, Culex and Aedes species.
Transmission by the Anopheles mainly occurs in rural areas
which are favourable for this mosquito to breed, whereas
Culex transmit mainly in urban areas.
Adults live in lymph glands and vessels where they block
flow of lymph fluids. The females release sheathed
microfilariae (mf) which travel via the lymphatics into the
peripheral blood six months to one year after infection. In
most parts of the world the microfilariae show a marked
nocturnal periodicity; they are found in the peripheral
circulation from about 22.00 to 02.00 hours, whilst during
When microfilariae are ingested with a blood meal by a
suitable species of mosquito they undergo 3 stages of
development in the insect host. They lose their sheath within
about 15 to 30 minutes in the stomach of the insect. Some
penetrate the stomach wall and migrate to the thoracic
muscles in about 1 to 24 hours.
Here they metamorphose into sausage shaped larvae and
after further development in about 10 days they migrate to
the head where they enter the proboscis and migrate to the
tip (the labilla) of the proboscis. The larvae emerge from the
labilla when the mosquito takes a blood meal, and penetrate
man through the puncture caused by the proboscis.
The penetration is likely to be more successful in areas of
high humidity where the skin will be moist. However, the
mosquito secretes a drop of fluid before feeding, which
supports the survival of the larvae on the skin for a short
period of time. On entering they migrate to the lymph
glands where they molt twice before maturing into male
and female adult worms. The female produces microfilariae
about six months to one year after infection. The adults
may also be found in dilated lymphatic vessels anywhere in
the body causing lymphatic obstruction. They can live up to
17 years.
The development in the mosquito is necessary therefore
man to man transmission does not occur
 Clinical manifestation
Many cases are symptomless for years or throughout life and
the only evidence of infection is the presence of micfrofilariae
in the blood. In the cases showing symptoms there may be
recurring attacks of acute lymphagitis (inflammation of the
lymph ducts), with inflamed tender lymph nodes, headache,
nausea and sometimes urticaria, from about the third month
after entry of the larvae.
The most serious clinical manifestations are due to
disturbances of the lymphatic system, which may result in
lymphadenitis (inflammation of the lymph nodes),
lymphodema, lymphoceles, chyluria (lymph containing fat in
the urine) and, in males, genital lesions including hydrocoele
and lymph scrotum leading in time to the disfiguring
elephantiasis.
The nature of lesions varies in
different parts of the world, reflecting
different sites of obstruction. In
Africa, elephantiasis is less common
than in the Pacific Islands (with gross
elephantiasis of the arm, breast, legs,
scrotum or vulva, and hydrocoele in
males –with a probable reduction in
fertility) and it is usually confined to
the legs. Hydrocoele is common in
East Africa.
The adults of the nocturnal periodic strains of W.
bancrofti usually develop in the lymphatics of the
lower limbs and groin while those of the
subperiodic Pacific strain are also found in the
lymphatics of the upper limbs. It is estimated that
there are at least 250 million cases in the world,
with the resulting debilitation continuously affecting
the economies of the developing countries.
 Pathogenesis
The earliest signs occur 4 weeks after infection and involve
the lymph glands as a result of an immunological response by
the host. There is a marked cell-mediated response in the
lymph gland followed by an antibody-mediated response in
the afferent lymphatics caused by antimicrofilarial antibody.
This response is the cause of the local gland enlargement in
early filariasis. The early symptoms are reversible following
chemotherapy, but later as a result of collagen deposit and
probable streptococcal infection the lymphatics are
permanently destroyed by fibrous obliteration which causes
elephantiasis, a process which is not reversible.
The presence of numerous living worms leads to dilatation
of the afferent lymphatic vessels and leakage of lymph into
the tissues (causing lymphodoema), with increase in tissue
fluid content. The later stage of elephantiasis presents with
hyperplasia (abnormal cell increase in an organ) and fibrosis
(excessive fibrous tissue) of affected tissues, in which the
oedema becomes hard and the skin thickens and folds, often
with verrucous (warty lesion) growths. Dead worms calcify
and become surrounded by fibrosis and may form lymphatic
abscesses, obliterating the lymphatics and adding to the
pathogenesis. In addition there could be secondary infection
with streptococcus and this combined with collagen deposit,
the lymphatics are permanently destroyed.
Scrotum extending beyond the knees. Upper limbs, scrotum and lower limbs
 Other conditions:
 
Chyluria – results from rupture of obstructed and
dilated small intestinal lymphatics into the urinary
tract so the chyle (milky lymph from emulsified
fats) no longer returns to the blood. This results in
the loss of fat with loss of weight, electrolyte,
protein and other deficiencies.
Occular filariasis – adult worms may invade the
orbit giving rise to proptosis (forward projection or
displacement especially of the eyeball), keratitis or
glaucoma
 
 Differential Diagnosis
Observation of various telltale clinical manifestations listed above; e.g.
varicose groin glands, filarial glandular enlargement, Chyluria and
elephantiasis.
Laboratory examination
This can be done by finding the microfilaria in the blood;
Blood thick smear slide, stained with a Romanowsky stain, e.g. Giemsa
stain for microfilaria
Membrane filters – blood filtered through either a Millipore or
Nucleopore membrane. The filter may be examined fresh or stained as
above. This method is very sensitive.
ICT card test - Examination for the circulating filarial antigen (CFA) due
to infection with microfilariae can be done using
Immunochromatographic (ICT) card test. In this test 100µl of finger-
prick blood is obtained using heparinized capillary and the blood
specimen transferred to an ICT card, the card closed and results read
after 10 minutes to determine if individual is infected or not.
DEC given at a small dose during the day can provoke the nocturnal mf
from the lungs and into the peripheral circulation during the daytime.
 Treatment

Diethylcarbamazine (DEC) (Banocide, Hetrazan, Notezone) – destroys

microfilaria and also capable of killing the adult worms when given at a
dose of 2-6 mg/kg body weight per day for 2 to 3 weeks. When given at
6mg/kg body weight it should be divided into 3 daily doses of 2mg/kg.
Other drugs used include:
Furapyramidone – in China. Said to be active against mf and adults.
Metrifonate - given at a dose of 10-15mg/kg every 14 days for 5 to 16
doses– specifically good for mf but also kills adults in a proportion of
cases. Where Schistosoma haematobium occurs this drug will also kill
the Schistosome worms.
 
Control
-Mass chemotherapy with DEC
-Vector control including insecticide treated bednets
-Combined methods
-Personal prophylaxis
 Brugia malayi

Most aspects similar to W. bancrofti, Mf with 2 isolated nuclei at the tip of

the tail. No nuclei at the end of tail for the W. bancrofti.
It is distributed in South and South-East Asia from India in the West to
Korea in the East. The worms resemble those of W. bancrofti and the life
cycle is similar. However B. malayi exhibits both diurnal and nocturnal
periodicities and the worms inhabit the lymphatic glands and lymph
vessels usually of the lower limbs and groin. This filariasis also affects
other animals including monkeys, cats, civets and pangolins.
 
Brugia timori

The only difference from the other two is that the sheath does not stain in
Giemsa. It has a small distribution in the South-east Indonesia in Timor
and Flores Islands. It is nocturnally periodic and transmitted by
Anopheles mosquitoes.