Strongyloidiasis

Strongyloidiasis is an intestinal nematode infection caused by Strongyloides stercoralis. It differs from other soil transmitted helminths in its capacity for autoinfection.

In autoinfection, larvae mature and re-invade the host directly within the intestine or perianal skin, without an external soil phase. The infection can therefore persist and self perpetuate within a single host for decades without further external exposure.

This characteristic underlies the main clinical risk: hyperinfection syndrome and disseminated disease. This severe, frequently fatal complication is triggered by immunosuppression (most classically corticosteroid therapy) in a patient with previously asymptomatic, longstanding and often unrecognised chronic infection.

Pathophysiology and the autoinfection cycle

• Infective filariform larvae penetrate the skin from contaminated soil. This is the initial, conventional exposure route, mirroring hookworm transmission.
• Larvae migrate to the lungs and are swallowed. They mature into adult female worms in the small intestine, which reproduce parthenogenetically (without a male worm).
• The eggs hatch within the intestine and release rhabditiform larvae. Most are passed in stool to continue the conventional external life cycle.
• A proportion mature directly into infective filariform larvae within the intestine. They penetrate the intestinal mucosa or perianal skin and re-invade the same host. This autoinfection cycle allows chronic, low level infection to persist indefinitely without further external exposure.
• Hyperinfection syndrome occurs when host immune control of the autoinfection cycle is lost. The classic cause is corticosteroid therapy, even at relatively modest doses and including short courses given for unrelated indications in a patient with unrecognised chronic infection.
• Larval proliferation accelerates massively, with overwhelming larval migration through the lungs and gut wall. Migrating larvae carry enteric bacteria into the bloodstream and central nervous system, so secondary Gram negative bacteraemia and meningitis frequently accompany it. Mortality is substantial.

• Chronic, low level intestinal infection is frequently asymptomatic or causes only mild, non specific gastrointestinal symptoms (intermittent abdominal pain, bloating, altered bowel habit). It often goes unrecognised for years to decades after the original, sometimes remote, exposure.
• Larva currens is a distinctive serpiginous urticarial rash, typically on the buttocks, groin or trunk. It advances several centimetres per hour, a rate far exceeding that of cutaneous larva migrans caused by other organisms.
• Larva currens reflects autoinfective larval migration through the skin. Where present, it is a relatively specific and useful clue to chronic strongyloidiasis.
• Hyperinfection syndrome and disseminated disease cause severe abdominal pain, distension, diarrhoea (which may be bloody), and respiratory symptoms (cough, wheeze, haemoptysis, progressing to respiratory failure). These reflect massive larval migration through the gut and lungs.
• Features of secondary Gram negative sepsis accompany them, and meningitis occurs where larvae have carried bacteria into the central nervous system. This is a medical emergency with substantial mortality even with treatment.
• Eosinophilia is present in a substantial proportion of chronic, uncomplicated infection. It is characteristically absent or reduced in hyperinfection syndrome, reflecting the immunosuppressed state that allowed the complication. This can mislead clinicians who rely on eosinophilia as a general marker of parasitic infection.
• Seek a history of past residence in or travel to an endemic tropical or subtropical region, however remote, in any patient being considered for significant immunosuppression, particularly corticosteroids.
• Chronic, asymptomatic infection acquired decades earlier can trigger fatal hyperinfection if it is unrecognised and untreated before immunosuppression starts.

• Stool microscopy looks for larvae rather than eggs, because eggs typically hatch within the intestine before passage.
• A single sample has limited sensitivity, because larval output in chronic infection is characteristically low and irregular. Multiple samples, or concentration techniques such as the Baermann technique or agar plate culture, improve yield considerably where available.
• Serological testing is substantially more sensitive than stool microscopy for chronic infection. It is the preferred screening approach in patients with relevant epidemiological exposure who are being considered for immunosuppressive therapy.
• Serology cannot reliably distinguish active from past, cleared infection. Sensitivity may also be reduced in significant immunosuppression because the antibody response is attenuated.
• Hyperinfection syndrome and disseminated disease are diagnosed by identifying larvae in sputum, bronchoalveolar lavage fluid or stool. In the most severe cases, larvae may be found in essentially any body fluid or tissue sample because of the extent of dissemination.
• Blood cultures are also important, given the frequent association with secondary Gram negative bacteraemia.
• Unrecognised chronic infection can be catastrophic once immunosuppression starts. Consider screening (serology, with or without stool examination) in any patient with relevant epidemiological exposure who is being considered for significant immunosuppressive therapy, particularly corticosteroids, chemotherapy or biologic agents.
• Screening allows pre-emptive treatment before immunosuppression is commenced.

• Uncomplicated, chronic intestinal infection is treated with ivermectin 200 micrograms per kg orally once daily for two days. It is the treatment of choice because it is more effective than albendazole for this organism.
• Some protocols add a repeat course after two weeks, particularly for heavier or more longstanding infection, to improve the likelihood of eradicating the autoinfective cycle.
• Albendazole 400 mg twice daily for seven days is an alternative where ivermectin is unavailable or contraindicated. Its efficacy against this organism is generally inferior to ivermectin.
• Hyperinfection syndrome and disseminated disease are a medical emergency. They need prolonged, sometimes repeated, courses of ivermectin, with daily dosing continued until larvae are no longer detectable in relevant specimens.
• Subcutaneous ivermectin may be needed in patients with significant ileus that limits reliable oral or enteral absorption. It is obtained through compassionate use or specialist pharmacy arrangements, because most jurisdictions have no licensed parenteral formulation.
• Add broad spectrum antibiotics covering the enteric organisms responsible for the frequently associated secondary bacteraemia. Where feasible, reduce or stop any contributing immunosuppressive therapy.
• Give empirical ivermectin before or alongside immunosuppressive treatment in any patient who needs urgent immunosuppression that cannot reasonably be delayed and who has confirmed strongyloidiasis, or a relevant epidemiological exposure history with testing pending or unavailable.
• The reasons are the severe, frequently fatal consequences of unrecognised hyperinfection and the comparatively low risk and cost of empirical antiparasitic treatment.
• Prevention in endemic regions means avoiding walking barefoot on potentially contaminated soil, which blocks the initial, conventional transmission route.
• For established infection, the priority is awareness of the diagnosis and proactive screening of any patient with relevant remote exposure who is being considered for immunosuppressive therapy of any kind. Fatal hyperinfection syndrome is entirely preventable with timely recognition and pre-emptive treatment.