Human infection with Strongyloides stercoralis and other related Strongyloides species

Abstract

The majority of the 30-100 million people infected with Strongyloides stercoralis, a soil transmitted intestinal nematode, have subclinical (or asymptomatic) infections. These infections are commonly chronic and longstanding because of the autoinfective process associated with its unique life cycle. A change in immune status can increase parasite numbers, leading to hyperinfection syndrome, dissemination, and death if unrecognized. Corticosteroid use and HTLV-1 infection are most commonly associated with the hyperinfection syndrome. Strongyloides adult parasites reside in the small intestine and induce immune responses both local and systemic that remain poorly characterized. Definitive diagnosis of S. stercoralis infection is based on stool examinations for larvae, but newer diagnostics - including new immunoassays and molecular tests - will assume primacy in the next few years. Although good treatment options exist for infection and control of this infection might be possible, S. stercoralis remains largely neglected.

Keywords: Strongyloides stercoralis; Strongyloidiasis; anthelmintic therapy; autoinfection; corticosteroids; hyperinfection.

Figures

Fig. 1

Immune responses in Strongyloides stercoralis infection as a function of time after infection initiation. The infective L3 larval parasites initiate infection at skin sites and activate a variety of different cell types such as innate lymphoid cells (ILCs), macrophages (MAC), dendritic cells (DCs), natural killer cells (NK), eosinophils (Eos) and basophils/mast cells (Baso/MC). At this relatively early phase of infection (or by the time the adult worms are established in the small intestine) the parasite induces the differentiation of a small number of effector Th1/Th17 and a relatively larger number of Th2 cells which together with IgE antibody, may lead to attrition of some of the parasites. At the time of patency (when larval production occurs) there is an expansion of Th2/Th9 CD4+ cells, a further contraction of Th1/Th17 cells and the induction of alternatively activated macrophages (AAM). With the evolution of chronic longstanding infection, there is an associated expansion of IL-10- and/or TGFβ-producing regulatory T cells (Tregs) and a small contraction of Th2/Th9 cells.