BackgroundThe HIV epidemic in sub-Saharan Africa has had a major impact on infectious disease, and there is currently great interest in the impact of HIV on intestinal barrier function. A three year longitudinal cohort study in a shanty compound in Lusaka, Zambia, carried out before anti-retroviral therapy was widely available, was used to assess the impact of HIV on susceptibility to intestinal infectious disease. We measured the incidence and seasonality of intestinal infection and diarrhoea, aggregation of disease in susceptible individuals, clustering by co-habitation and genetic relatedness, and the disease-to-infection ratio.MethodsAdults living in a small section of Misisi, Lusaka, were interviewed every two weeks to ascertain the incidence of diarrhoea. Monthly stool samples were analysed for selected pathogens. HIV status and CD4 count were determined annually.ResultsHIV seroprevalence was 31% and the prevalence of immunosuppression (CD4 count 200 cells/μL or less) was 10%. Diarrhoea incidence was 1.1 episodes per year and the Incidence Rate Ratio for HIV infection was 2.4 (95%CI 1.7–3.3; p < 0.001). The disease-to-infection ratio was increased at all stages of HIV infection. Aggregation of diarrhoea in susceptible individuals was observed irrespective of immunosuppression, but there was little evidence of clustering by co-habitation or genetic relatedness. There was no evidence of aggregation of asymptomatic infections.ConclusionHIV has an impact on intestinal infection at all stages, with an increased disease-to-infection ratio. The aggregation of disease in susceptible individuals irrespective of CD4 count suggests that this phenomenon is not a function of cell mediated immunity.

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Ten outbreaks of Salmonella gallinarum-pullorum infections on poultry farms in Zambia were investigated. Three cases were seen in day-old broiler chickens and were diagnosed by culture as S. gallinarum-pullorum and characterized as pullorum disease because the mortality was only in the first few weeks. Another case was diagnosed by culture from broiler parent stock. Day-old chicks from two of the three cases were supplied by a hatchery. Five cases in 5-to-18-month-old layer chickens were diagnosed by culture as S. gallinarum-pullorum and characterized as fowl typhoid because of the clinical disease appearing after 5 months of age and the typical lesions of fowl typhoid. The last case was in 5-month-old village-bred fowls and was diagnosed by culture and clinical manifestation as fowl typhoid. Outbreaks of S. gallinarum-pullorum are still manifest in Zambia. Clinically, both pullorum disease and fowl typhoid were observed, and it was indicated that hatchery infection plays an important role in the transmission of S. gallinarum-pullorum.

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