SUMMARY BackgroundLymphogranuloma venereum (LGV) is a recognized cause of proctitis. Symptoms, endoscopy and histology findings are similar in IBD and LGV proctitis.

From the earliest reports of what has since become the pandemic of human immunodefi ciency virus (HIV) infection, a close association between HIV infection and a previously un common mycobacterial disease-that due to infection with Mycobacterium avium complex (MAC)-was evident. 1 Then and since, clinically significant disease due to MAC is restricted to HIV-positive people in industrialized countries. Later it was realized that M. tuberculosis is associated with HIV infection to the extent that, in sub-Saharan Africa, tuberculosis is clinically the most important opportunistic disease in HIV-positive people.2 A significant proportion of the population there is latently infected with M. tuberculosis, and it is thought that HIV infection, by its progressive destruction of cell mediated immunity, permits the reactivation of tuberculous lesions. What about M. /eprae and HTV? Tn Africa, which today has the greatest number of HTV-infected people of all the continents, leprosy is still relatively common. Further, India has the greatest number of known cases of leprosy in the world, and appears to be on the rising curve of an HTV epidemic potentially as significant as that in Africa.3 So, an interaction between the two infections could be important. In fact, despite expectations,4-7 little interaction has been observed. The potential interactions and complications are many. HTV infection could: I increase the probability of infection with M. /eprae; 2 increase the probability of clinical leprosy developing in a dually infected person; 3 alter the clinical pattern of leprosy; 4 alter the response to anti leprosy chemotherapy.

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The specialty of tropical medicine originated from the needs of the colonial era and is removed from many of the health care requirements of tropical countries today. Tropical medicine concentrates on parasitic diseases of warm climates, although other infections and diseases related to poverty rather than climate dominate medicine in developing countries challenged by population pressure, civil strife, and migration. In the new century, tropical medicine would best be absorbed into the specialty of infectious diseases, which should incorporate parasitic diseases, travel medicine, and sexually transmitted diseases. Pressing questions for health care and research in developing countries concern the provision of appropriate services for problems such as HIV/AIDS, tuberculosis, sexually transmitted diseases, and injuries. The question of how to provide appropriate clinical care in resource poor settings for the major causes of morbidity and premature mortality has been neglected by donors, academic institutions, and traditional tropical medicine.

The prevalence of infection with human immunodeficiency virus type 1 (HIV 1) is lower in west Africa than in other parts of Africa. Human immunodeficiency virus type 2 (HIV 2) has been isolated from west African patients and may be transmitted by heterosexual contact. The prevalence of antibodies to HIV 1 and HIV 2 was studied by enzyme linked immunosorbent assay (ELISA) among various groups of subjects in The Gambia, west Africa—namely, prostitutes, blood donors, patients with suspected infection with HIV, patients attending clinics for sexually transmitted diseases, and patients with tuberculosis. Four cases of the acquired immune deficiency syndrome (AIDS) due to infection with HIV 1 were detected, of which three had been acquired abroad. No other subject was found to be positive for antibodies to HIV 1. The prevalence of antibodies to HIV 2 among the patients attending clinics for sexually transmitted diseases was found to have increased from 0/117 in 1984 to 10/185 (5%) in the last six months of 1986. One out of 278 blood donors was positive for antibodies to HIV 2 as were 10 out of 80 patients with suspected AIDS. HIV 2 seems to be transmitted sexually, and, although it has been present for only a short time, it seems to be endemic in The Gambia and is pathogenic.

Chronic splenomegaly in 131 Kenyan patients was investigated at Kenyatta National Hospital, Nairobi. Patients were allocated to diagnostic groups on the basis of clinical, haematological, parasitological, histological, radiological and endoscopic data. The major diagnostic groups were hyper-reactive malarial splenomegaly, our preferred name for tropical splenomegaly syndrome, (31%), hepatosplenic schistosomiasis (18%), visceral leishmaniasis (5%) and "indeterminate splenomegaly", where no diagnosis could be reached (12%). Another 20% of patients were suffering from various non-schistosomal forms of portal hypertension. A number of specific and rarer causes accounted for the rest of the cases. The tribal and geographical distribution of patients with chronic splenomegaly was compared with the pattern of general medical admissions. Splenomegaly was more frequent than expected in Kamba and Luo patients. Hyper-reactive malarial splenomegaly and hepatosplenic schistosomiasis were common in both groups, whereas visceral leishmaniasis was almost restricted to the Kamba and indeterminate splenomegaly was especially prevalent in the Luo. Malarial antibody and immunoglobulin levels differed significantly between the various diagnostic categories of patients and controls. Malarial serology can be diagnostically useful for chronic splenomegaly, provided results are interpreted in their geographical context.

In a study of forty asymptomatic volunteers from northern Nigeria; 35 (87.5%) had histological gastritis and 32 (80%) were infected by Helicobacter pylori. All but one of the patients infected by Helicobacter Pylori had histological gastritis. This high prevalence of H. Pylori infection in young, asymptomatic subjects, occurs in an area with a low prevalence of duodenal ulcer. The possible reasons for this are discussed.

Eighty-five patients with chronic splenomegaly and proven oesophageal varices were studied at Kenyatta National Hospital, Nairobi. The major defined groups were hepatosplenic schistosomiasis (24%), cirrhosis (20%) and portal vein occlusion (11%). Hyper-reactive malarial splenomegaly (tropical splenomegaly syndrome) was considered as the cause of oesophageal varices in only one patient. In 26% of cases liver biopsy was non-diagnostic and the extrahepatic portal vein was demonstrated radiologically to be patent. Such patients were thought to be suffering from idiopathic portal hypertension, not previously described elsewhere in Africa. Hepatitis B surface antigen was detected in 12% of controls and in 58% of patients with cirrhosis (p less than 0.001). Some serological marker of previous hepatitis B virus infection was present in 92% of patients with cirrhosis and in 79% of controls. Kamba patients from Machakos and Kitui Districts were significantly more prevalent than expected among these 85 cases of portal hypertension.