Filariasis - Surgical menifaststaions and

Filariasis
Dr.Rahul Kadam
Asist Proff
General Surgery

WHAT IS Filariasis
•Filariasis (or philariasis) is a parasitic disease
caused by an infection with roundworms of
the Filarioidea type. These are spread by
blood-feeding black flies and mosquitoes.
This disease belongs to the group of
diseases called helminthiasis.
•Eight known filarial nematodes use
humans as their definitive hosts.

Parasites
• White, slender roundworms
• Three types: Wuchereria
bancrofti,
Brugia malayi,
Brugia timori
• Live for 5-7 years, produce
millions of offspring
•Block the lymphatic system
• Network of channels and
lymph nodes that help
maintain fluid levels in
the body
• Blockage leads to edema
(collection of fluid in
tissues)

Mosquitos are Vectors and
spread the Infection
•Amosquito is the intermediate host
and carrier. The most common
vectors/carriers are:
•in Africa: Anopheles species
•in the Americas:
Culex
quinquefasciatus
•in the Pacific and in Asia: Mansonia
and Aedes species.

Wucheraria bancrofti
• Primary causative agent of lymphatic
filariasis
• Overt bancroftian filariasis : 115 million
cases worldwide (45.5 million India, 40
million sub-Saharan Africa)
• Widespread throughout the subtropics and
tropics (for e.g. Central Africa, India,
Thailand, Malaysia, Phillipines, Pacific
Islands, Haiti, coastal Brazil)

Geographical Distribution Of Wuchereria
bancrofti

Wuchereria bancrofti
Pathogenesis
Mode of infection – inoculative method – Mosquito bite.
Transmitting agent – female mosquitoes ( Culex, Aedes,
Anopheles )
• In India – Culex pipens fatigans ( C. p. quinquefasciatus)
Infective form – 3rd stage larvae.
Portal of entry – skin.
Site of localisation – lymphatic system.
Biological incubation period – 8 to 12 months.

In endemic areas, infection is mostly asymptomatic .
• Tolerate microfilaria, immune response being inhibited.
Infective larvae enter thru bite → lymphatics → moult,
releasing their body proteins, secretions & other products.
• In some, they cause irritation – directly or hypersensitivity.
Typical manifestations produced by the adult worms.
Living microfilaria circulating in blood – not known to
produce any pathogenic effect, except in Occult filariasis.

Histopathological changes
1. Males & females of W.bancrofti lodged in lymph
node.
2. Lymphoedema / Lumph varices.
3. Obliterative endolymphangitis
4. Occlusion of lymph vessel
Strangulating the parasite – degeneration
5. A parasitic onion developing around
degenerated
parasite.
6. Hyaline scar

Causes of Lymphatic obstruction
1. Mechanical blocking.
2. Obliterative endolymphangitis.
Endothelial proliferation & inflammatory
thickening of walls.
3.Excessive fibrosis of lymphatic
vessels.
4.Fibrosis of afferent lymph nodes.
5. Allergic inflammatory reactions.

Causes of Lymphangitis
1. Mechanical irritation
2. Liberation of metabolites of growing larvae &
secretion of some toxic fluid by fertilised
females
3. Absorption of toxic products liberated from
dead worms undergoing disintegration.
4. 2° bacterial infection

Inflammatory changes damage the valves ,
aggravating
lymph stasis.
Increased permeability of vessel walls → leakage
of protein rich lymph into the tissues.
Brawny edema / hard pitting edema.
Fibroblasts invade → laying down fibrous
tissue → non pitting gross edema of
elephantiasis.

Occult Filariasis
Occult filariasis Classical filariasis
Lesion by microfilarias Developing worms & Adults
Lesion not only in lymph
nodes, but lungs, liver,
spleen
Lymph nodes, lymphatic
system
Eosinophilic granuloma a/c inflammation followed by
epitheloid granuloma
Microfilaria present in
affected tissues, but not in
blood
Microfilaria present in blood
Complement fixation
test highly sensitive
Not so sensitive

Clinical manifestations
Asymptomatic
Filariasis
Symptomatic
Filariasis
Inflammatory Phase Obstructive Phase

Clinical Features
•Chronic manifestations: Hydrocoele (most common ),
elephantiasis, Chyluria
•Acute manifestations: Acute inflammatory episodes
'DLA'(dermatolymphangioadenitis) , 'filarial fever' ,
tropical pulmonary eosinophilia, acute inflammatory
reaction
•Asymptomatic Presentations
•Other Syndromes: arthritis (typically monoarticular),
endomyocardial fibrosis, tenosynovitis,
thrombophlebitis, glomerulonephritis, lateral popliteal
nerve palsy, and others.

Wuchereriasis
Does not kill, but cause great suffering, disfiguration &
disability.
Metabolites of growing larvae in highly reactive individuals
→ allergic manifestations -
• malaise, headache, nausea, vomiting , low grade fever,
urticaria, pruritis, fugitive swellings, lymphoedema.
Fugitive swellings – raised, painless, tender, diffuse, red
areas on skin
Symptoms may appear much earlier.
Fails to demonstrate microfilaria in blood.

Lymphadenitis
Inguinal lymph nodes most often
affected.
Swollen nodes may be painful and
tender.

Lymphangitis
Red streaks underneath the skin.
Lymphatics of testis & spermatic
cord are frequently involved
→ Epidymo-orchitis and Funiculitis

Filarial fever
High fever of sudden onset, often with rigor, lasting for 2 or 3
days.
Temperature comes down by crisis with profuse sweating.
Associated with localizing sign of inflammation of lymphatic
vessel.
Examination of blood → transient leukocytosis, increased
neutrophils, presence of microfilaria.

Lymphangiovarix
Dilatation of lymph vessels ; varicosity.
Results from collateral circulation & lymph stasis.
Commonly occur in inguinal, scrotal, testicular & abdominal

Lymphorrhagia
Rupture of lymph varices → release of lymph / chyle.
Depends on the sites involved.
Lymph scrotum, lymphocoele, chyluria, chylous diarrhoea,
chylous ascites, chyothorax.
Chyluria :-
Due to rupture of varicose chyle vessels thru mucous
membrane of urinary tract.
Milk white in colour.
Contains fat particles, albumin, fibrinogen.
Microscopical examination – microfilaria, few RBCs

Hydrocoele
Due to obstruction of lymph vessels
of spermatic cord & also by
exudation from the inflamed testes
and epididymis.
Fluid – clear & straw coloured ,
sometimes – cloudy, milky or
haemorrhagic.

Lymphoedema
Starts as swelling around the
ankle, spreading to the back
of the foot & leg.
Also effect arms, breast,
scrotum, vulva…
Hard & Non Pitting

Elephantiasis
Affected part becomes enormously enlarged, producing
tumour like solidity.
Most commonly in leg, but may also involve arm, breast,
scrotum, penis & vulva.
 Causes –
1. Fibrotic constriction of all afferent lymphatics.
2. Recurrent attacks of lymphangitis over years.
3. Hypertrophy & Hyperplasia – result of excess protein in
exudate.

Pathological Anatomy -
• Surface of skin – rough, fissured & even papillomatous.
• On section – skin cuts like an unripe pear, is
thickened, dense & fibrous.
• Subcutaneous tissues – edematous ( blubbery )
appearance – dilated & thickened lymphatics & veins
seen.
Histology – granulation tissue.
Blood Microfilaria – generally absent

Occult Filariasis
(Meyers – Kouwenaar Syndrome)
 Clinical conditions not due to lymphatic involvement, but
due to hypersensitivity reactions to filarial antigens.
 Massive eosinophilia, > 3000cells/mm3.
 Generalised lymph node enlargement, Hepato-splenomegaly,
pulmonary symptoms & absence of microfilaria in blood.
 Microfilaria does not reach peripheral blood, because they are
destroyed in tissues.
 Host reaction – Eosinophil granuloma

Filarial complement fixing antibody present in high titre.
Serological tests with filarial antigens are strongly positive.
Non specific antibody production → biological false
positive
reaction in serological tests for syphilis.
Prompt response to DEC confirms the diagnosis.
Also reported to cause arthritis, glomerulonephritis,
thrombophlebitis, tenosynovitis & dermatoses.

Tropical Pulmonary Eosinophilia
( Eosinophilic Lung / Weingarten’s Syndrome )
A manifestation of Occult filariasis.
Low fever, loss of weight, paroxysmal cough with
scanty
sputum, dyspnoea, asthmatic wheezing &
splenomegaly.
Blood eosinophil count – above 3000/mm3. IgG levels ↑.
Chest Xray – increased bronchovascular markings,
diffuse
mottled shadows resembling Miliary TB.

Direct Evidence Indirect Evidence
Microfilaria Adult Allergic tests Immunological
tests
A sheathed
microfilaria
having pointed
tail tip free of
nuclei
1. In peripheral
blood.
2. In chylous
urine
3. In exudate
of
lymph
varix.
4. In hydrocoele
fluid.
1. In biopsied
lymph node.
2. Calcified
worm
by X ray.
1. Blood
examination –
Eosinophilia.
2. Intradermal
test.
( wheal over
2cm after 30
min )
1. Demonstration of
antibody to filarial
antigens
2. Demonstration of
filarial antigens in
blood.
Lab Diagnosis

Microfilariae not found in peripheral blood in
following cases :-
1. During early allergic manifestations
2. In occult filariasis
3. Case of Elephantiasis – due to lymphatic
obstruction
4. After an attack of lymphangitis, due to death of
adult worm.
Nocturnal periodic – Night blood samples,
collected between 10pm to 4am

Unstained Film
Examination under low power microscope –
• actively motile microfilariae lashing the blood cells
around.
May be conveniently made next morning –
• as microfilariae retain their viability & motility for a day or
two at room temp.
By using a simple counting chamber, microfilaria in
the wet
mount can be counted.

Stained Film
A Thick & Thin blood smear.
Dehaemoglobinised by applying distilled water.
Fixed with methanol.
Stained with Giemsa, Leishman, Delafield’s haematoxylin or
Polychrome methylene blue stains.
Microfilaria seen under light microscope in thick film.
Morphology studied in thin film.
Species identification made.

By using a measured quantity of blood for
preparing smears, for e.g, 20mm3 pipette and
counting the total no. of microfilariae in the smear
---- microfilaria counts can be obtained.

Features Mf. bancrofti Mf. malayi
Length 250 – 300 µm 175 – 230 µm
Appearance Graceful , sweeping
curves
Kinky, with secondary
curves
Cephalic space Length = breadth Length = 2 x breadth
Stylet at anterior
end
Single Double
Excretory pore Not prominent Prominent
Nuclear column Discrete nuclei Blurred
Tail tip Pointed; free of nuclei 2 distinct nuclei, one
at tip, other sub
terminal
Sheath Faintly stained Well stained

Concentration Techniques
Employs venous blood.
When microfilaria density is low – larger volumes of blood,
Two Methods –
1. Sedimentation method –
Sample of blood first lysed with acetic acid, saponin or
other lytic substances or by freeze thawing & then
centrifuged.
Sediment is stained & microfilariae is counted.

2. Filtration Method –
 A measured quantity of blood (1-5 ml) is collected into an
anticoagulant solution → passed through membrane filters.
 Millipore & Nucleopore Filters.
 Blood cells & proteins sticking on to the filter are washed
away by repeatedly passing saline thru it.
 Filter is removed, placed on a slide, stained & examined.
 Much more sensitive - collected even during daytime.
 Disadvantages – cost , need for venepuncture

DEC Provocation Test
Oral administration of Diethyl Carbamazine (100mg or
2mg/kg body weight) induces microfilariae to appear in
peripheral blood, even during daytime.
Blood collected 20-50 min after.
Great advantage for surveys.
But may cause febrile reactions, esp. in Brugiasis.
Cannot be used in areas endemic for Onchocercasis –
severe reactions.

Treatment
DEC (Hetrazan) – drug of choice.
• Dose – 6mg/kg orally in 3 divided doses
for 12 days.
• Adverse effects – due to host
response to dying microfilariae
oFever, headache, nausea, vomiting,
arthralgia & prostration.
oAnti-histamines/corticosteroids to
control.

Prevention & Control
Eradication of vector mosquito
Detection & treatment of Carriers
• DEC -6mg/kg daily for 12 days.
• Repeated in endemic areas , every 2 yrs or so.
DEC medicated salt
Morbidity Control –
• Improved hygiene measures
• Proper treatment of 2º infection
• Proper care of the limb

Global Eradication
Programme
Whole population at risk – annual dose of 2
drugs-
• Ivermectin & Albendazole in countries of Africa-
co endemic
(150µg/kg) (400mg)
for Onchocercasis.
• DEC (6mg/kg) with Albendazole (400mg) in
other parts of world.
• Continued for 5-6 yrs for interruption of
transmission.

Brugia malayi
In India, Kerala is the largest endemic area.
Pathogenicity –
Intermediate hosts – various species.
• Mansonia species & One species of Anopheles
( A.barbirostris).
Like W.bancrofti, causes lymphangitis & elephentiasis
( Primarily of lower limbs).
Malayan Filariasis – absence of chyluria & rarity of
scrotal swellings.

By finding characteristic Microfilariae in peripheral
blood.
• 175 – 230 µm
• Kinky, with secondary curves
• Length = 2 x breadth
• Double stylet
• Prominent excretory pore
• Blurred nuclear column
• Blunt tail tip - 2 distinct nuclei, one at tip, other sub
terminal
• Sheath - Well stained
Lab Diagnosis

Treatment –
Same as for Wuchereriasis.
Prevention –
Same as for Wuchereriasis.
Certain water plants ( Pistia, Water hyacinth, Swamp
grass) – necessary for growth of Mansonoides ---
remove those.

Brugia timori
Natural vectors – Anopheles barbirostris.
Clinical manifestations milder than other lymphatic
filariasis.
Lymphangitis, Lymphadenitis, Lymphoedema
( confined below
knee) & abscess along lymph trunk/nodes.
Draining abscess – lead to scar formation

Lab Diagnosis :
By finding characteristic Microfilariae in peripheral
blood.
• Larger than Mf. malayi ( overall length- 310µm ).
• Cephalic space : length = 3 x breadth
• 5 to 7 terminal nuclei
• Sheath not stained with Giemsa stain
Treatment & Prevention :
Same as for B. malayi

Filariasis - Surgical menifaststaions and

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