Opportunistic protozoan diarrhoea.

In the developed world, a significant increase in the incidence of protozoan diarrhoea was observed following the AIDS epidemic. The profound immunodeficiency associated with advanced HIV disease produced increased susceptibility to opportunistic protozoan infections. The resultant profuse diarrhoea, malabsorption and weight loss contributed to the high morbidity and mortality rates associated with the epidemic. The success of highly active antiretroviral therapy (HAART) in suppressing viral replication has led to a reduced incidence of AIDS-related opportunistic infections and this has contributed to decreased morbidity and mortality. In this review, we examine current management practices for HIV-related opportunistic protozoan diarrhoea

Elevated mucosal addressin cell adhesion molecule-1 expression in acquired immunodeficiency syndrome is maintained during antiretroviral therapy by intestinal pathogens and coincides with increased duodenal CD4 T cell densities.

Reduced intestinal CD4 T cell numbers and gastrointestinal disease are common features of acquired immunodeficiency syndrome (AIDS). Duodenal lymphocyte densities and mucosal addressin cell adhesion molecule (MAdCAM)-1 expression were analyzed in patients with AIDS after highly active antiretroviral therapy (HAART). Compared with human immunodeficiency virus (HIV)-seronegative individuals, HAART-naive patients with AIDS displayed reduced duodenal CD4 T cell densities. After HAART, AIDS patients with opportunistic intestinal pathogens displayed greater increases in duodenal lamina propria (LP) CD4 T cell densities than patients without such infections. Duodenal MAdCAM-1 expression was elevated in all HAART-naive patients with AIDS but remained elevated only in the intestinal pathogen group after HAART. The data suggest that, in HIV-1 infection, lymphocyte migration to the intestine may be promoted by increased MAdCAM-1 expression. After HAART, opportunistic intestinal pathogens maintain elevated MAdCAM-1 expression, which results in prominent increases in LP CD4 T cell densities in the absence of HIV-mediated CD4 T cell destruction.