Intestinal strongyloidiasis and hyperinfection syndrome

Abstract

In spite of recent advances with experiments on animal models, strongyloidiasis, an infection caused by the nematode parasite Strongyloides stercoralis, has still been an elusive disease. Though endemic in some developing countries, strongyloidiasis still poses a threat to the developed world. Due to the peculiar but characteristic features of autoinfection, hyperinfection syndrome involving only pulmonary and gastrointestinal systems, and disseminated infection with involvement of other organs, strongyloidiasis needs special attention by the physician, especially one serving patients in areas endemic for strongyloidiasis. Strongyloidiasis can occur without any symptoms, or as a potentially fatal hyperinfection or disseminated infection. Th2 cell-mediated immunity, humoral immunity and mucosal immunity have been shown to have protective effects against this parasitic infection especially in animal models. Any factors that suppress these mechanisms (such as intercurrent immune suppression or glucocorticoid therapy) could potentially trigger hyperinfection or disseminated infection which could be fatal. Even with the recent advances in laboratory tests, strongyloidiasis is still difficult to diagnose. But once diagnosed, the disease can be treated effectively with antihelminthic drugs like Ivermectin. This review article summarizes a case of strongyloidiasis and various aspects of strongyloidiasis, with emphasis on epidemiology, life cycle of Strongyloides stercoralis, clinical manifestations of the disease, corticosteroids and strongyloidiasis, diagnostic aspects of the disease, various host defense pathways against strongyloidiasis, and available treatment options.

Figure 1

Life cycle of Strongyloides stercoralis. Complete life cycle of Strongyloides stercoralis with both parasitic and free living cycles along with the cycle leading to autoinfection and hyperinfection syndrome. The cycle involving the mechanism of autoinfection is shown on the right side of the figure with the cycle elucidating the concept of hyperinfection and disseminated infection on the left side of the figure (adapted from: Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control & Prevention; Permission via phone taken from Ms. Melanie at (770) 488–4063).

Figure 2

Corticosteroids and strongyloid hyperinfection syndrome. The pathophysiological pathway showing the mechanism of corticosteroids leading to strongyloid hyperinfection syndrome and disseminated infection. Corticosteroids along with cortisol act on specific receptors called glucocorticoid receptors (GCRs) available on CD4+ Th₂ cell membrane causing apoptosis and thus T cell dysfunction. Corticosteroids also increase ecdysteroid like substances in the body which act as molting signals for eggs and rhabditiform larvae, leading to increased number of filariform larvae [41,57].