Strongyloides stercoralis Infection in Alcoholic Patients

Biomed Res Int. 2016:2016:4872473. doi: 10.1155/2016/4872473. Epub 2016 Dec 26.

Abstract

The course of Strongyloides stercoralis infection is usually asymptomatic with a low discharge of rhabditoid larva in feces. However, the deleterious effects of alcohol consumption seem to enhance the susceptibility to infection, as shown by a fivefold higher strongyloidiasis frequency in alcoholics than in nonalcoholics. Moreover, the association between S. stercoralis infection and alcoholism presents a risk for hyperinfection and severe strongyloidiasis. There are several possible mechanisms for the disruption of the host-parasite equilibrium in ethanol-addicted patients with chronic strongyloidiasis. One explanation is that chronic ethanol intake stimulates the hypothalamic-pituitary-adrenal (HPA) axis to produce excessive levels of endogenous cortisol, which in turn can lead to a deficiency in type 2 T helper cells (Th2) protective response, and also to mimic the parasite hormone ecdysone, which promotes the transformation of rhabditiform larvae to filariform larvae, leading to autoinfection. Therefore, when untreated, alcoholic patients are continuously infected by this autoinfection mechanism. Thus, the early diagnosis of strongyloidiasis and treatment can prevent serious forms of hyperinfection in ethanol abusers.

Publication types

  • Review

MeSH terms

  • Alcoholism* / immunology
  • Alcoholism* / metabolism
  • Alcoholism* / parasitology
  • Alcoholism* / pathology
  • Animals
  • Humans
  • Hypothalamo-Hypophyseal System* / immunology
  • Hypothalamo-Hypophyseal System* / metabolism
  • Hypothalamo-Hypophyseal System* / pathology
  • Pituitary-Adrenal System* / immunology
  • Pituitary-Adrenal System* / metabolism
  • Pituitary-Adrenal System* / pathology
  • Risk Factors
  • Strongyloides stercoralis* / immunology
  • Strongyloides stercoralis* / metabolism
  • Strongyloidiasis* / immunology
  • Strongyloidiasis* / metabolism
  • Strongyloidiasis* / pathology
  • Th2 Cells* / immunology
  • Th2 Cells* / metabolism
  • Th2 Cells* / pathology