Some parasitic infections can remain dormant and asymptomatic for years after infection, only to cause serious illness decades later.
Strongyloidiasis is caused by infection with the nematode strongyloides.
For practical purposes, most human infections are caused by Strongyloides stercoralis. While an exotic infection, it is presented to illustrate a number of points:
- some parasitic infections can remain dormant and asymptomatic for years after infection, only to cause serious illness decades later
- immune suppression can lead to overwhelming infection and death, before the diagnosis is even considered
- transplant-associated infection can be due to reactivation or come from an infected donor organ
- diagnosis requires a variety of specimens and techniques
- risk for travellers to endemic areas should be further investigated because of the long term potential risks.
Strongyloides stercoralis distribution is in most tropical environments, including northern Australia, but also in some sub-tropical and temperate environments.
Infection is acquired when the infective filariform larval stage of the worm penetrates intact skin or mucosa, usually when contact is made with soil contaminated with faeces from infected humans.
Larvae then travel via the venous circulation to the lungs, where they traverse the lungs, then up the trachea, past the epiglottis and down the oesophagus, settling to develop into the adult female worm mainly in the duodenum and upper small bowel. Here, the adult female can live for more than 60 years laying eggs in the mucosa that develop into larvae that are shed in the faeces.
These larvae are non-infectious (rhabditiform larvae) initially but they can develop into infectious (filariform) larvae before they have departed the host’s gastrointestinal tract.
These infective larvae can then penetrate the colonic mucosa and perianal skin, again via the venous system and lungs to cause reinfection (auto-infection). Shedding of filariform larvae means that direct infection of others can occur but how commonly is not known.
In most people, there are never any symptoms of infection. If they do occur, then there are three recognised syndromes: acute infection; chronic infection; hyperinfection syndrome/disseminated strongyloidiasis (see table for clinical features and diagnosis). Keeping infection in check is a balance between the worm and the host’s immune system.
Specimens to be collected, and their ability to confirm the diagnosis, depend on the type of illness. Most persons do not present until much later, but larvae are said to appear in the faeces 2–4 weeks after infection occurs.
In practice, serology is often used as the main screening test in most persons, except those with hyperinfection/disseminated infection, where larvae are generally easily and rapidly identified, provided the correct specimen is accompanied by appropriate discussion with the laboratory, as they can still be missed.
Determining who should be screened for strongyloidiasis, and what test algorithm to use, has become topical since cases started to appear in transplant patients, either with reactivation of infection, or through receipt of a transplant from a strongyloides-infected donor organ.
Interestingly, cyclosporin provides some protection compared with tacrolimus and related anti-rejection drugs. Certainly, if transplant patients are to be screened with serology it is best done before immune suppression as the latter can cause false negative results.
Diagnosis of strongyloidiasis is important as treatment with ivermectin (two daily doses of 200mcg/kg repeated two weeks later) is probably curative, except in hyperinfection and disseminated disease where repeated treatments are often required.
Treatment of asymptomatic persons in endemic areas is problematic as repeated exposure means that reinfection is likely while ever exposed. More work is required to determine the best strategy for management of infection in that setting.
Clin Infect Dis 2009; 49(9):1411-23
Tags: , Pathology