TROPICAL DESEASE 10

FILARIA

2.5 TREATMENT
Di-Ethyle Carbamizine (Hetrazan) rapidly eliminates microfilaria
from the blood.
It also kills and injures adults worms, impairing
reproduction.
The dosage is 2mg/kg body weight 3 times a day and
needs to be continued for 3-4 weeks.

Elephantiasis requires surgical management with Charles operation
fig.8.5

CHARLES OPERATION FOR ELEPHANTIASIS
A tourniquet is applied to the affected leg above the knee.
The thickened tissue is incised and is reflected upto the deep
faschia.
The skin from the excised tissue is taken of either with
the scalpel or a Humby knife.
This skin can now be grafted onto the deep fascia exposed and stitched in place.

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RESOURCE http://www.surgical-tutor.org.uk/default-home.htm?specialities/general.htm~right

TROPICAL DESEASE 8

2.1 EPIDEMIOLOGY
- More than 250 million persons throughout the world are
presently infected, and
both the prevalence, and distribution of the disease seems to be increasing in many parts of
Africa, and
Asia.
- The disease primarily affects Africa, Pacific Islands, South-East
Asia from Korea to India fig.9.4
- The West Indies, Central America and South America are also sites
of the disorder.
- B.Malayi infection is limited in distribution to India, Burma,
Thailand, Vietnam, Japan, Malaysia, Indonesia, Borneo, New Guinea,
and Philippines.

2.2 PATHOLOGY
Pathological changes are caused by the adult worm in the
Lymphatics, and the effects are of two types
* Inflammatory, and
* obstructive

2.2.1 INFLAMMATORY
Inflammatory response is thought to be an immediate type of
Hyper-sensitivity reaction to the larvae,
-This is evidenced by infiltration by lymphocytes, plasma cells and eosinophiles.
There is hyperplasia of the endothelium of the lymphatics.
Later there is a granulomatous reaction to the dead and dying adult
Worms, this may end in a reversible lymphatic obstruction.

2.2.2 Repetition of this process produces permanent obstruction.
2.2.3 With the addition of secondary streptococcal
infections, there is further lymphatic obstruction and tissue
becomes edamatous, thickened and fibrotic.
Intensely dilated lymphatic may rupture.


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RESOURCE http://www.surgical-tutor.org.uk/default-home.htm?specialities/general.htm~right

TROPICAL DESEASE 7

2. FILIARISIS (W.Bancrofti and B. Malayl)

The mosquito vector of the bancrofti filaria are the species
culex,
aedes and
anopheles.
Mansoni and Anopheles serve as vector for B.Malayi's disease.
Infected mosquito transmits larvae every time it feeds on the
human host.
The adult male worm of the Bancrofti variety measures about 29 mm
and female 61 mm
B. Malayi adults are about half as long.
* These worms invade lymphatics in subcutaneous, and deep
tissues producing obstruction,
acute inflammation and
Chronic scarring.
* The gravid females release microfilaria in large number
into the lymphatics
* They eventually reach peripheral blood where further
development in the life cycle depends on their ingestion by
the appropriate mosquito vector.
The life cycle is presented above

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TROPICAL DESEASES 6

Liver Abcess


1.5.3 COMPLICATIONS
* If treatment is not timely and adequate rupture into chest
with bronchopleural fistula or empyema are common
complications.
* Rupture into the peritoneal cavity, pericardium and viscera
may occur, with haemobilia and pericardial tamponade.
* Secondary bacterial infection is ominous and metastic brain
abscess can occur.

1.5.4 TREATMENT (Liver disease)
Drugs that are both tissue and luminal amoebicides should be
used.
The best drug is metronidozole.
Indications for per-cutaneous aspiration are:
* Failure to respond to medial management within 5 days
* Large left lobe abscesses
* Impending rupture
* Severe toxamia
The only other indication for open surgical drainage is proven
BACTERIAL superinfection.

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TROPICAL DISEASE 5

1.5 EXTRA-INTESTINAL AMEBIASIS

Amebic liver abscess is the most common extraintestinal
manifestation of amebiasis.
Males are more commonly affected and the greatest incidence
is in the third, fourth and fifth decades
LIVER
Invasion of the wall of the colon results in involvement of
mesenteric venules and the amebae enter into the protal
circulation.
Portal circulation favours lodging of amebae in the right lobe.
Most trophozoites are eradicated but when circumstances are
favourable tiny colonies arise and coalesce to form an abscess.
- Within the abscess trophozoitis accumulate at the periphery,
while the central portion contains variable amounts of blood,
necrotic hepatic cellular debris, and leucocytes.
- The lesion most often starts, in the portal triad, and extends
peripherally towards the capsule of the liver.
In the early stages, an area of necrotic tissue, which may contain leucocytes, connective tissue cells and occasional ameba, is surrounded by a zone of hyperemia.
- Later, a more well defined capsule develops in which ameba can
be found.
- Secondary,bacterial infection is reported in less than 5% of
cases. Microscopically THREE zones are recognised.
* A necrotic center
* A middle zone with distruction of parenchyma but with some
persistence of stroma
* A relatively normal liver tissue in which ameba can be
demonstrated
Treatment is with amebacidal drugs and surgery for drainage.

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