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Strongyloidiasis is caused by the nematode (roundworm) Strongyloides stercoralis. S. stercoralis is a soil-dwelling nematode capable of producing infection in humans and other mammals. Other Strongyloides species include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.[1]

  • S. stercoralis is a parasite common in wet tropical areas and usually only seen in the UK in travellers who have returned from such areas.
  • Infection is most often acquired by walking barefoot on contaminated soil.
  • Strongyloidiasis can be either acute or chronic in nature. The chronic form of the infection is well documented in individuals who have been prisoners of war in the Far East.
  • Infection can be asymptomatic for many years. It is therefore very important to eradicate the parasite prior to starting immunosuppressive treatment or chemotherapy, as failure to do so may result in a hyperinfection syndrome due to dissemination of the larvae to several organs, which is associated with a high mortality rate.[2]
  • S. stercoralis is thought to have infected 100 million people worldwide.
  • Prevalence rates of strongyloidiasis are as high as 50% in certain areas where moist soil and improper disposal of human waste co-exist, especially in West Africa, the Caribbean, Southeast Asia, tropical regions of Brazil, Cambodia, and temperate regions of Spain.

The life cycle of Strongyloides spp. is more complex than that of most nematodes, involving both parasitic and free-living stages.

  • Free-living cycle:
    • The rhabditiform larvae passed in the stool can either moult twice and become infective filariform larvae, or moult four times and become free-living adult males and females, which then mate and produce eggs from which rhabditiform larvae hatch.
    • The filariform larvae either penetrate the human host skin to initiate the parasitic cycle or develop into free-living worms living in the soil independently of a human or mammalian host.
  • Parasitic cycle:
    • Filariform larvae in contaminated soil penetrate the human skin and travel via the bloodstream to the lungs, from where they migrate through the bronchial tree to the pharynx, and are then swallowed and reach the small intestine.
    • In the small intestine the filariform larvae moult twice and become adult female worms. The females live threaded in the epithelium of the small intestine and produce eggs, which yield rhabditiform larvae, which can either be passed in the stool or can cause autoinfection.
  • In autoinfection, the larvae become infective filariform larvae, which can penetrate either the intestinal mucosa or the skin of the perianal area. In either case, the filariform larvae travel via the blood stream to the lungs, through the bronchial tree, the pharynx and then the small intestine where they mature into adults, or they may disseminate widely in the body.
  • Autoinfection may explain the persistence of infections for many years in people who have not been in an endemic area and hyperinfections in immunodepressed individuals.
  • Strongyloidiasis has a variable effect on the host. Individuals may be asymptomatic for many years or may develop a series of acute or chronic nonspecific symptoms.
  • In other cases, specific symptoms make the diagnosis more obvious - eg, the migratory rash. Symptoms that may occur include:
    • Skin involvement:
      • Larva currens (a linear lesion which may advance at a rate of 10 cm/hour) often occurs on the buttocks, groin and trunk.
      • Urticarial rashes on the buttocks and waist areas.
    • Gastrointestinal involvement:
      • Abdominal discomfort and bloating.
      • Profuse watery diarrhoea, sometimes alternating with constipation.
      • Malabsorption.
      • Weight loss.
    • Pulmonary involvement (including Löffler's disease) can occur during pulmonary migration of the filariform larvae:
      • Cough.
      • Bronchospasm.
      • Haemoptysis.
      • Shortness of breath.
    • Disseminated strongyloidiasis (occurs in immunosuppressed patients) can present with abdominal pain, distension, shock, pulmonary and neurological complications, and septicaemia. Disseminated strongyloidiasis is potentially fatal.
  • In a massive hyperinfection, the larvae cause lung haemorrhage when passing from the capillaries to the alveoli.
  • The vast numbers of larvae also penetrate other organs which are not normally involved in the usual life cycle - eg, urinary tract, central nervous system and liver.
  • Bacterial infection also occurs due to leakage from the damaged bowel. The bacteria are carried on the surface of the larvae to produce meningitis, pneumonia and septicaemia, which are frequently the immediate cause of death in patients with hyperinfection syndrome.
  • Hyperinfection syndrome may occur due to immunosuppression of the host and particularly by treatment of the host with steroids.[5]
  • It is therefore particularly important to exclude and treat the infection in any person who has spent time in the tropics or subtropics, prior to initiating treatment with immunosuppressive agents or steroids.
  • Definite diagnosis may be difficult unless larvae are seen in the stool. Often a high index of suspicion is needed.
  • FBC may show an eosinophilia. Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.
  • Microscopic identification:
    • Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid. Examination of serial samples may be necessary.
    • Larvae may be detected in sputum from patients with disseminated strongyloidiasis.
  • Antibody detection:
    • Antibody detection tests for strongyloidiasis are indicated when the infection is suspected and the organism cannot be demonstrated by microscopic identification.
    • Enzyme immunoassay is currently recommended because of its greater sensitivity (90%).
    • Immunocompromised people with disseminated strongyloidiasis usually have detectable IgG antibodies despite their immunodepression.
    • Cross-reactions in patients with filariasis and some other nematode infections may occur.
    • Antibody test results cannot be used to differentiate between past and current infection.
    • Serology monitoring may be useful in the follow-up of immunocompetent treated patients: antibody levels decrease markedly within six months after successful chemotherapy.
  • CXR: may show pulmonary infiltrates, consolidation or cavitations.

All patients with strongyloidiasis require treatment, whether or not they are symptomatic, due to the possibility of developing a hyperinfection syndrome at some stage in the future.

  • Ivermectin 200 micrograms/kg daily for two days is the most effective drug for strongyloidiasis: 
    • Eradication rates with ivermectin are as high as 97%.
    • Indications of successful treatment include falling eosinophilia and antibody titres.
  • Albendazole is the alternative: 400 mg twice daily for three days, repeated after three weeks if necessary. 
  • Symptomatic treatment includes antihistamines for pruritus.
  • Immunocompromised patients may require hospital admission and intensive care for disseminated infection.
  • Appropriate antihelminthic treatment results in a cure for the majority of patients, although re-infection is common in endemic areas.
  • Disseminated strongyloidiasis is a life-threatening condition for immunosuppressed patients, with death often occurring in a few days.[2]

Infection can be reduced by good sanitation and wearing footwear in endemic areas.

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Further reading and references

  1. Strongyloidiasis; DPDx - Centers for Disease Control and Prevention

  2. Bisoffi Z, Buonfrate D, Montresor A, et al; Strongyloides stercoralis: a plea for action. PLoS Negl Trop Dis. 2013 May 97(5):e2214. doi: 10.1371/journal.pntd.0002214. Print 2013.

  3. Puthiyakunnon S, Boddu S, Li Y, et al; Strongyloidiasis-An Insight into Its Global Prevalence and Management. PLoS Negl Trop Dis. 2014 Aug 148(8):e3018. doi: 10.1371/journal.pntd.0003018. eCollection 2014 Aug.

  4. Schar F, Trostdorf U, Giardina F, et al; Strongyloides stercoralis: Global Distribution and Risk Factors. PLoS Negl Trop Dis. 2013 Jul 117(7):e2288. doi: 10.1371/journal.pntd.0002288. Print 2013.

  5. Buonfrate D, Requena-Mendez A, Angheben A, et al; Severe strongyloidiasis: a systematic review of case reports. BMC Infect Dis. 2013 Feb 813:78. doi: 10.1186/1471-2334-13-78.

  6. Wang C, Xu J, Zhou X, et al; Strongyloidiasis: an emerging infectious disease in China. Am J Trop Med Hyg. 2013 Mar88(3):420-5. doi: 10.4269/ajtmh.12-0596.

  7. British National Formulary