AMOEBIASIS / MedUrgent

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AMOEBIASIS


According to the WHO definition, it is a condition in which the protozoan parasite Entemoeba histolytica is harbored by some patients regardless of their symptoms. Geographically, it is a world-wide disease, although it is more prevalent in the tropics and sub-tropics. It is primarily a parasite of the large bowel where it mostly affects the cecum and ascending colon and in severe infections, it extends into the ilium and appendix.

Poor sanitation and overcrowding account for the occurrence of epidemics of amoebic dysentery. More severe infection is seen in pregnant women, younger children, immunocompromised patients, and those on corticosteroid medications. Cysts transmit the disease and are resistant to drying, cold and routine chlorination of water. Trohozoites are not infective as they are destroyed by the acid in the stomach.

AETIOLOGY

It is caused by Entemoeba histolytica, a protozoan which may persist in a cystic form in chronic carriers but may become virulent and cause acute dysentery. Transmission is via the fecal-oral route following ingestion of contaminated water, raw fruits or vegetables, although insects and flies have been implicated in transmission of the parasite.

There are certain conditions that may make this organism invasive. These include:

Virulence and the amount of the organisms, host's resistance, genetic makeup and nutritional status i.e. decreased protein intake are important contributing factors. Damage to the intestinal mucosa by any process e.g. bacillary dysentery, malaria, schistosomiasis and worm infestations may activate the organism leading to acute or chronic amoebic dysentery.

PATHOGENESIS

The pathogenicity of the organism is related to its ability to attach to the colonic mucus layer and disrupt local immune mechanisms. The cyst after ingestion releases 4 trophozoite within the large intestine and under favorable conditions invasion takes place. It starts with lysis and necrosis of the mucosa by means of proteolytic enzymes released by the trophozoite. These invade the intestinal wall and submucosa forming a very characteristic patchy lesion, the amoebic ulcer. This is a flask-shaped ulcer due to lysis circumferentially.

The mucosa in between the ulcers is normal and there is little cellular reaction. The area may be covered by exudates due to edema, hyperemia and sloughs. The cecum, transverse colon and sigmoid colon are usually involved. Peristalsis is increased. Healing occurs with little scar formation, but occasionally fibrosis and strictures may be detected.

An amoeboma which is a granuloma may develop. Occasionally, blood vessel found at the base of the ulcers may be injured leading to bleeding. Should the ulcers become deeper, this may lead to perforation and acute abdomen.

Though extensive intestinal involvement appears to favor dissemination, it can occur with few intestinal lesions. Dissemination to the liver most frequent leads to amoebic abscess or abscesses. The abscess may rupture into the peritoneal cavity leading to peritonitis or through the diaphragm into the lung or pleura causing lung abscess or pleural effusion. Extension into the skin in the perianal region may occur rarely leading to painful ulcer.

WHO Classification

1- asymptomatic or carrier state: this occur even if the intestine is invade.

2- Symptomatic: This is further divided into:

  a) The intestinal group, which is composed of amoebic dysentery, post amoebic dysenteric colitis, amoeboma and amoebic appendicitis

  b) Extra-intestinal dissemination which results in non-suppurative hepatitis and amoebic liver abscess.

  c) The skin or cutaneous group, which occurs if the skin is invaded.

  d) Other organs to be affected e.g. brain, meninges, lung and spleen.

   

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