The main causes are amoebic dysentery and, to a lesser extent, mild bacillary dysentery. Examination under the microscope of fresh (still warm) faeces is important in order to identify motile trophozoites. The normal bacterial intestinal flora is maintained in amoebic dysentery. In case of severe amoebic colitis there may be some fever. Amoebic dysentery is treated with medication against the trophozoites (tinidazole = Fasigyn®, metronidazole = Flagyl®) followed by medication against any remaining intestinal cysts (diloxanide furoate= Furamide®). Other, less common causes of bloody diarrhoea without fever are acute schistosomiasis (eosinophilia, worm eggs), massive trichuriasis (microscopy), ulcerative colitis (rare in the topics) and Balantidium coli (microscopy).
Ileocaecal intussusception can present with acute bloody diarrhoea followed by intestinal obstruction. The intussuscipiens forms the outer layer, the intussusceptum is the inner part. Occasionally there is intermittent haematochezia. A mass can sometimes be felt in the abdomen. The condition usually affects children between 3 and 18 months old. Rapid surgical intervention is required. Unlike children, 70-90% of adults with intussusception have an underlying condition. Malign tumours such as an adenocarcinoma of the colon or the small intestine (metastatic melanoma, lymphoma, sarcoma) have been reported. Carcinoid tumours, polyps, lipomas, neurofibromas, hyperplastic lymph follicles or Meckel’s diverticulum may also be responsible. A firmly lodged foreign object (food, faecalith) or endometriosis in the intestine can be responsible for mechanical traction.
Food poisoning with Clostridium perfringens can cause necrotising enteritis. After the Second World War this became known as “darmbrand". In the dialect of Papua New Guinea the disorder is known as “pigbel”. The anaerobic Gram-positive bacterium is frequently present in the flora of the colon, so there must be other factors present to cause the onset of the disease. The bacterium, better known as the causative agent of gas gangrene, can produce various toxins. The bacterial strains which produce toxins can be classified into types A, B, C, D and E. All types produce alpha-toxin, which is a lecithinase (phospholipase C). Clostridium perfringens type C, responsible for pigbel, produces alpha- and beta-toxins. The alpha-toxin is coded by a chromosomal gene (cpa), the beta-toxin is coded by a gene on a plasmid. These can be detected by PCR. Beta-toxins can be vaccinated against, considerably reducing the risk of disease. The toxins in the intestine is usually destroyed by proteases. In case of undernourishment there is an important deficiency in proteases such as trypsin, and as a result the toxins can remain active. If there are trypsin inhibitors present as well, such as are found in sweet potatoes, the remaining small amount of trypsin is neutralised. Adult Ascaris worms produce trypsin inhibitors. If the intestine has reduced motility, the toxin remains in contact with the wall for a prolonged period of time and cause transmural necrosis. It is often necessary to carry out a partial resection of the small intestine. Pigbel has been recognised in Papua New Guinea since 1961. The disorder is seen mainly in undernourished and parasite-infested children after eating a rich meal with sweet potatoes and infected pigmeat (pig intestines are also eaten). Meals such as this are sometimes prepared on the occasion of a great feast at which the host expresses his social standing by slaughtering and serving a large number of pigs. The illness can therefore occur in epidemics. Besides supportive therapy, treatment is based on antibiotics (chloramphenicol, benzylpenicillin or other, broad-spectrum antibiotics), type C antiserum and mebendazole. Sometimes surgery has be be performed. Vaccination against type C toxin is useful.
