Amoebic Dysentery

AMOEBIC DYSENTERY This is also called amoebiasis, loeschiasis or tropical dysentery, the latter because of its early endemicity and greater incidence in the tropical areas.

The causal organism E. histolytica (Loesch 1871) affects man alone in nature, though the dog, cat, guinea-pig and rat have been infected experimentally. The E. histolytica in its life-cycle in man passes through three stages—a large vegetative stage when living within the tissues, giving rise to ulceration and passage of blood and mucus; a pre-cystic stage found in convalescents and carriers, when the amoebae are much smaller and live on the mucous membrane within the bowel, from which they may pass into the membrane and assume the larger vegetative form ; and a cystic stage. The amoebae increase in numbers by division of the parent into two. In the pre-cystic stage they contract into smaller, rounded or ovoid forms, develop a firm outer wall and become transformed into cysts with one to four characteristic nuclei and chromatoid rods which possibly act as food stores. It is by swallowing these cysts that man is infected. They do not resist drying, but retain their vitality for two weeks if kept moist in the faeces or in water. They can therefore be transmitted by direct contamination with faeces, through handling soiled linen, by flies carrying them to food, by soil or by drinking contami nated water ; and prophylaxis must be directed accordingly. The cysts pass through the stomach unchanged; in the small intestines they germinate, and amoebulae are set free. These grow, divide and penetrate into the submucous layer of the large bowel where they continue to proliferate and destroy the tissue, thus leading to haemorrhage and outpouring of mucus. Locally, a flask-shaped ulcer is formed, with roughened undermined edges at the orifice, and such ulcers are frequently joined by submucous tunnels.

Symptoms.

Clinically the disease is characterized by its chronicity and tendency to recrudescence. The onset is insidious, the sufferer first noticing debility and lassitude with an increase of stools, soft and mixed with blood and mucus. These may clear up after a few days and be the only signs noticed, or may recur months later. Most often the initial stage is followed by an acute exacerbation of symptoms, dependent in their degree upon the extent of the ulceration in the large bowel, the most markedly affected sites being the entire colon, the caecum, flexures and appendix, sigmoid and rectum. Stools become still more frequent, even up to 4o or 5o in 24 hours, and the ulceration gives rise to abdominal pain and, if at the rectum, to severe tenesmus. In un complicated cases there is but slight rise of temperature or other symptoms of toxaemia as the entamoeba produces no toxin. Diagnosis is quickly made by microscopical examination of the stools.

Occasionally infection with other bowel organisms supervenes, and gangrene may follow, or the amoebae may perforate the large bowel, giving rise to peritonitis, or, penetrating a blood-vessel and being conveyed by the blood stream they may cause an abscess in the liver, or, most exceptionally, in the brain or lung. Healing is brought about by the development of fibrous tissue at the sites of the ulcers.

Treatment.

The specific treatment is ipecacuanha, or its alkaloid, emetine. Combined hypodermic injections of emetine hydrochloride with oral administration of ipecacuanha (Bra zilian), or of bismuth subnitrate in large doses, to attack the amoebae from within and without have given striking results. The toxic action of emetine on the heart must be watched. Added to the specific treatment in acute cases there is the general and symptomatic, which may include an early free flushing of the bowel by a dose of castor oil with tinct. opii. added; later fol lowed by magnesium (or sodium) sulphate in hourly or two-hourly half or drachm doses for 12 or 24 hours. Morphia may be neces sary to relieve the abdominal pain and straining. The diet must be light and easily assimilated, and raw food should be withheld.

The symptoms subside in one to three weeks, the patient re gains his general health after suitable convalescence and no further trouble may follow. However, not infrequently the scar tissue formed in healing leads to thickening of the bowel wall, partial loss of peristalsis or constriction producing chronic con stipation; or again the entamoeba may persist in the lumen of the bowel, ready to enter its wall and renew symptoms when conditions so favour.

Therapy Notes.

Treatment to eliminate the entamoeba in its pre-cystic form from within the lumen of the bowel of the carrier is not yet on an equally satisfactory basis. Emetine hydro chloride injections have no effect upon it. An important measure to avoid recrudescence is to maintain the general health and avoid indiscretions in diet. Intravenous injections and colonic lavage with neosalvarsan have been much used to supplement oral treat ment by the French. Amoebic hepatitis and small abscess of the liver respond well to injections of emetine hydrochloride, but a large abscess needs surgical intervention. A carrier should, if possible, live in the temperate zone.