Classification and external resources

Larva of Strongyloides stercoralis, the roundworm that causes strongyloidiasis
ICD-10 B78
ICD-9 127.2
DiseasesDB 12559
MedlinePlus 000630
eMedicine article/999614-overview
MeSH D013322

Strongyloidiasis is a human parasitic disease caused by the nematode (roundworm) Strongyloides stercoralis, or sometimes S. fülleborni. It can cause a number of symptoms in people, principally skin symptoms, abdominal pain, diarrhea and weight loss. In some people, particularly those who require corticosteroids or other immunosuppressive medication, Strongyloides can cause a hyperinfection syndrome that can lead to death if untreated. The diagnosis is made by blood and stool tests. The drug ivermectin is widely used in the treatment of strongyloidiasis.

It is thought to affect 30–100 million people worldwide, mainly in tropical and subtropical countries. Worldwide efforts are aimed at eradicating the infection in high-risk groups. Strongyloidiasis was first described in France in 1876.


Signs and symptoms

Strongyloides infection occurs in five forms. On acquiring the infection, there may be respiratory symptoms (Löffler's syndrome). The infection may then become chronic with mainly digestive symptoms. On reinfection (when larvae migrate through the body), there may be respiratory, skin and digestive symptoms. Finally, the hyperinfection syndrome causes symptoms in many organ systems, including the central nervous system.[1][2]

Uncomplicated disease

Frequently asymptomatic. Gastrointestinal system symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Löffler's syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Blood eosinophilia is generally present.

Strongyloidiasis can become chronic and then become completely asymptomatic.

Disseminated disease

Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become immunosuppressed. It presents with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. The worms enter the bloodstream from the bowel wall, simultaneously allowing entry of bowel bacteria such as Escherichia coli. This may cause symptoms such as sepsis (bloodstream infecion),[citation needed] and the bacteria may spread to other organs where they may cause localized infection such as meningitis.[3]

Dissemination can occur many decades after the initial infection[4] and has been associated with high dose corticosteroids, organ transplant, HIV,[5][6] lepromatous leprosy, tertiary syphilis, aplastic anemia, malnutrition, advanced tuberculosis and radiation poisoning.[7] It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are often unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is very small, so screening is usually not cost-effective, except in endemic areas.

Laboratory diagnosis

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, and not always sufficient, because direct stool examination is relatively insensitive.

The stool can be examined in wet mounts:

  • directly
  • after concentration (formalin-ethyl acetate)
  • after recovery of the larvae by the Baermann funnel technique
  • after culture by the Harada-Mori filter paper technique
  • after culture in agar plates

Culture techniques are the most sensitive, but are not routinely available in the West. In the UK, culture is available at either of the Schools of Tropical Medicine in Liverpool or London. Direct examination must be done on stool that is freshly collected and not allowed to cool down, because hookworm eggs hatch on cooling and the larvae are very difficult to distinguish from strongyloides.

Finding strongyloides in the stool is negative in up to 70% of tests. It is important to undergo frequent stool sampling as well as duodenal biopsy if a bad infection is suspected. The duodenal fluid can be examined using techniques such as the Enterotest string or duodenal aspiration. Larvae may be detected in sputum from patients with disseminated strongyloidiasis.


The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin. Ivermectin does not kill the strongyloides larvae only the adult worms therefore repeat dosaging may be necessary to properly eradicate the infection. There is an auto-infective cycle of roughly two weeks in which Ivermectin should be re-administered however additional dosaging may still be necessary as it will not kill strongyloides in the blood or larvae deep within the bowels or diverticuli. Other drugs that are effective are albendazole and thiabendazole (25 mg/kg twice daily for 5 days—400 mg maximum (generally)).[6] All patients who are at risk of disseminated strongyloidiasis should be treated. It is not clear what the optimal duration of treatment for patients with disseminated infectious should be.[5]

Treatment of strongyloides can be difficult and has been known to live in individuals for upwards of 1–2 years after treatment. Continued treatment may be necessary if symptoms persist. Treatment should be continued until symptoms resolve themselves.


The disease was first recognized in 1876 by the French physician Louis Alexis Normand, working in the naval hospital in Toulon; he identified the adult worms, and sent them to Arthur Réné Jean Baptiste Bavay, chief inspector for health, who observed that these were the adult forms of the larvae found in the stool. In 1883 the German parasitologist Rudolf Leuckart made initial observations on the life cycle of the parasite, and Belgian physician Paul Van Durme (building on observations by the German parasitologist Arthur Looss) described the mode of infection through the skin. The German parasitologist Friedrich Fülleborn described autoinfection and the way by which strongyloidiasis involves the intestine. Interest in the condition increased in the 1940s when it was discovered that those who had acquired the infection abroad and then received immunosuppression developed hyperinfestation syndrome.[8]


  1. ^ Montes M, Sawhney C, Barros N (Oct 2010). "Strongyloides stercoralis: there but not seen". Curr Opin Infect Dis 23 (5): 500–4. doi:10.1097/QCO.0b013e32833df718. PMC 2948977. PMID 20733481. 
  2. ^ Marcos LA, Terashima A, Dupont HL, Gotuzzo E (Apr 2008). "Strongyloides hyperinfection syndrome: an emerging global infectious disease". Trans R Soc Trop Med Hyg 102 (4): 314–8. doi:10.1016/j.trstmh.2008.01.020. PMID 18321548. 
  3. ^ Graeff-Teixeira C, da Silva AC, Yoshimura K (Apr 2009). "Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance". Clinical Microbiology Reviews 22 (2): 322–48. doi:10.1128/CMR.00044-08. PMC 2668237. PMID 19366917. 
  4. ^ Gill GV, Beeching NJ, Khoo S, et al. (2004). "A British Second World War veteran with disseminated strongyloidiasis". Trans R Soc Trop Med Hyg 98 (6): 382–6. doi:10.1016/j.trstmh.2003.11.002. PMID 15099996. 
  5. ^ a b Kramer MR, Gregg PA, Goldstein M, Llamas R, Krieger BP. (1990). "Disseminated strongyloidiasis in AIDS and non-AIDS immunocompromised hosts: diagnosis by sputum and bronchoalveolar lavage". South Med J 83 (10): 1226–9. doi:10.1097/00007611-199010000-00024. PMID 2218668. 
  6. ^ a b Gompels MM, Todd J, Peters BS, Main J, Pinching AJ. (1991). "Disseminated strongyloidiasis in AIDS: uncommon but important". AIDS 5 (3): 329–32. doi:10.1097/00002030-199103000-00015. PMID 2059374. 
  7. ^ Purtilo DT, Meyers WM, Connor DH (1974). "Fatal strongyloidiasis in immunosuppressed patients". Am J Med 56 (4): 488–93. doi:10.1016/0002-9343(74)90481-1. PMID 4818417. 
  8. ^ Cox FE (October 2002). "History of Human Parasitology". Clin. Microbiol. Rev. 15 (4): 595–612. doi:10.1128/CMR.15.4.595-612.2002. PMC 126866. PMID 12364371. 

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