Periportal fibrosis, liver and spleen sizes among S. mansoni mono or co-infected individuals with human immunodeficiency virus-1 in fishing villages along Lake Victoria shores, North-Western, Tanzania

Humphrey D Mazigo, David W Dunne, Domenica Morona, Therese E Lutufyo, Safari M Kinung’hi, Geofrey Kaatano, Fred Nuwaha

The pathogenesis of S. mansoni infection involves chronic inflammatory responses to parasite eggs which can be associated with a characteristic periportal fibrosis (PPF) and the progression to severe hepatosplenic disease. The effects of HIV-1 co-infection and the influence of CD4(+) cell numbers on these clinical manifestations of chronic S. mansoni are not known. To understand the effects of HIV-1 co-infection on these morbidities, we examined S. mansoni ultrasound-detectable morbidities in relation to HIV-1 infection and CD4(+) cell counts, and other factors in fishing communities where the two infections are present. Ultrasonographical examination was conducted during a cross-sectional study of 1,671 (aged 21-55 years) individuals in North-Western Tanzania. Blood samples were obtained for HIV-1 screening and CD4(+) cell quantification. A single stool sample was examined for S. mansoni eggs using the Kato-Katz technique. A questionnaire was used to collect socio-demographic-economic information. The prevalence of PPF (grade C-F) was 13.79% and 15.01% for the HIV-1 infected and non-infected individuals (P = 0.72). Male gender (P< 0.001), age group 21-30 years (P< 0.028) and, residential time of 11-20 (P< 0.01) and ≥21 years (P< 0.01) were associated with PPF in S. mansoni infected individuals. The height-adjusted measurements of the left liver lobe were significantly larger in HIV-1/S. mansoni co-infected compared to S. mansoni only-infected individuals (t = -2.0702, P< 0.039). Predictors of the height-adjusted measurements of the left liver lobe and spleen were age, male gender, malaria infection, fishing occupation, village of residence and heavy intensity of S. mansoni infection. After accounting for these factors, neither HIV-1 infection nor CD4(+) cell counts predicted PPF, hepatosplenomegaly, measurements of the liver or spleen. Height-adjusted ultrasound measurements of the left liver lobe did not correlate with the CD4(+) cells counts in co-infected individuals (r = -0.16, P = 0.084). S. mansoni-related PPF, liver and spleen enlargement are prevalent in the study population. The intensity of S. mansoni infection was associated with the enlargement of liver, spleen and hepatosplenomegaly. The PPF grades observed were similar in both HIV-1/S. mansoni co-infected and in those only infected with S. mansoni. There was no evidence that HIV-1 infection or CD4(+) cells counts were associated with these S. mansoni morbidities.