Strongyloidosis B78.1

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 10.04.2021

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larva currens; Strongyloidiasis

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Leuckart, 1883; van Durme 1901; Looss, 1905; Fülleborn, 1914

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Parasitic nematode infection by Strongyloides spp.

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Strongyloides stercoralis, Strongyloides fuelleborni (mainly in Africa and Papula New Guinea), Strongyloides f. kellyi and others: The partogenetic female adults are 2.0-2.5mm long and 30-50um thick (see figure). They are predominantly localized in the mucosa of the duodenum and upper jejunum and lay fully embryonated eggs in the mucosa and crypts of the intestinal wall.

The small (0.7mm x 14um) males are found only occasionally or are absent altogether.

The 0.3-0.5mm long first larvae hatch while still in passage through the intestinal tract. They are called "rhabditiform" because of their esophagus equipped with a terminal bulb. During the further development 2 ways are possible:

  1. Direct development: The initial larvae develop within a few days into 500-700um large, vividly motile filiariform infectious larvae that can penetrate human skin.
  2. Indirect development: However, under suitable conditions, these initial larvae may mature into free-living, non-parasitic adults about 1.0mm in size. These lay eggs, which in turn may hatch into rhabditiform larvae. The survival of the free-living infective larvae depends on external conditions. If they dry out, they die quickly. As with hookworms, infection again occurs by penetration through the skin. Subsequent migration is through the right heart, lungs, bronchial system and passage into the esophagus. 2-3 weeks after infection, the adults reach the small intestine and begin egg production.
  • Internal autoinfection: In this case, the rhabditiform larvae develop into filariform infectious larvae while still in the intestinal tract. Autoinfection appears to occur primarily in the colon. It is favored by constipation and decreased peristalsis. The filiform larvae penetrate the mucosa and then travel through the heart, lungs, and esophagus to reach the small intestine, where they mature into adults. This form of autoinfection appears to occur primarily in infected individuals continuously at low levels and is responsible for the long persistence of infection.
  • External autoinfection: The filiariform larvae excreted in the stool re-enter the skin via contamination with stool particles. They then undergo a migration phase with pulmonary passage and maturation into adult dwarf nematodes.
  • Hyperinfection syndrome: In the case of immunosuppression (e.g. HIV infection), a massive autoinfection can occur with dissemination of the larvae to all organs.

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Worldwide, more than 70 million people are infected; in endemic areas, up to 60% of the population is affected. Furthermore, primates(S.fuellborni) are apparently affected, from which the infection can also spread to humans ( Janwan P et al. 2020).

Mostly distributed in subtropical or tropical regions, especially Southeast Asia, Africa and South America. Rare in Europe (especially in mines).

Highly frequent occurrence in patients with HIV infection.

Internal and external auto-infection leads to a chronic persistent infection. In the case of immune incompetence (see below HIV), a threatening hyperinfection syndrome can develop.

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The infectious filarial larvae penetrate the skin (usually during barefoot walking) and enter the gastrointestinal tract via the bloodstream, lungs and trachea. Female dwarf threadworms lay eggs in the mucosa of the duodenum and jejunum from which non-infectious larvae hatch (3 weeks after infection in faeces detectable). In the rectum, further development into infectious larvae. These in turn penetrate the skin in the buttock area (autoinfection).

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Occurrence is possible at any age. In endemic areas infestation mostly during childhood.

Clinical features
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The incubation period for strongyloidiasis is:

  • 12-18 hours for skin reaction
  • 7 days for pulmonary reaction
  • 14 days for intestinal symptoms.

Linerar, serpiginous, itchy erythema and plaques(larva currens), which correspond to cutaneous larva migrans, frequently form at the entry sites of the filiariform infection larvae, especially in people who have already been sensitized by previous infections. These regress within a few days. In infections by free-living larvae, these typical linear structures occur preferentially on the foot and ankle. In external autoinoculation, they are found on the buttocks and perianally.

During pulmonary passage, pneumonitis with dry cough and other symptoms of Löffler 's syndrome may occur about 1 week after infection if the infestation is extensive.

Uncomplicated intestinal infection is associated with variable symptoms: most common are persistent or recurrent abdominal pain, often in the epigastrium with variable diarrhea, occasionally with mucopurulent or bloody admixtures. Furthermore, nausea or vomiting.

The dermatological picture is that of a fast-moving (racing larva) larva currens. It is not uncommon for urticaria to accompany the disease.

Extensive infections may be accompanied by alternating fever, weakness and weight loss.

In hyperinfection syndrome , dissemination of larvae to all organs occurs (disseminated strongyloidiasis). Larvae may be present in large numbers: lungs, liver, intestinal wall, less frequently in the CNS. Specifically:

  • Gastrointestinal: Sprue-like symptomatology, colitis, steatorrhea, hypalbuminemia, generalized edema. Complicative: necrotizing jejunitis.
  • Lung: severe pneumonia with fever, cough dysplneo, hemoptysis, obstructive-restrictive ventilatory disorder.
  • CNS (rare): headache, mental syndromes, meningismus, convulsions, paralysis
  • Laboratory: massive signs of inflammation; often no eosinophilia!

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Diagnosis is made by detecting the larvae in the stool. Detection of mobile larvae in freshly deposited stool (usually the examination of several stool samples is necessary).

Strongyloides larvae cannot be found with the necessary sensitivity in SAF-fixed stools!

Good results are obtained by culture of the larvae, which are made visible by migration in semi-solid culture media. For this purpose, native stool with the appropriate notation is required.

Eggs and larvae may be detectable in duodenal secretions.

Always blood eosinophilia, high IgE, in case of lung involvement: neutrophilia

Detection of specific antibodies ( ELISA).

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Cave! The use of systemic glucocorticoids can cause a transition to disseminated strongyloidosis!

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Mebendazole (e.g. Vermox) 2 times/day 300 mg p.o. on 3 consecutive days; repeated after 2-4 weeks.

Alternatively: Tiabendazol (Mintezol) 2 times/day 2-3 tbl. p.o. (= 25 mg/kg bw) for 2-3 days, max. daily dose of 3 g. Stool controls monthly for at least 3 months.

In severe cases: Ivermectin (e.g. Mectizan) 170-200 μg/kg bw as ED, if necessary repeat every 2 weeks if larvae are detected in the stool.

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Symptomless course in immunocompetent patients often over years. With therapy almost always healing. In immunocompromised patients up to 80% of cases lethal.

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Wear sturdy shoes in endemic areas.

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To prevent infections in laboratory or hospital personnel, precautions must be taken against contact with larval stool or sputum.

Notifiable occupational skin disease!

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Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 10.04.2021