Strongyloides stercoralis - Host Immunity, Clinical Manifestation

Last Modified: July 19, 2026 by Reshma Maharjan

Host immunity against Strongyloides stercoralis

Since an intact immune system is absolute for the control of Strongyloides stercoralis infection, autoinfection is mostly seen in patients with suppressed cell-mediated immunity (CMI). Hyperinfection syndrome, frequent auto-infection which leads to increased worm load in the intestinal lumen, occurs in immunocompromised people.

Serum antibodies including serum IgG, IgA, IgM and eosinophils are believed to provide host immune protection against the Strongyloides stercoralis infection. The antibody and eosinophil levels are decreased in severe infections.

Clinical Manifestations of Strongyloides stercoralis

Clinical manifestations of strongyloidiasis, caused by Strongyloides stercoralis, vary according to the host immune system.

In an immunocompetent host, the parasite may persist in the host for years without producing any or minimal symptoms.

In an immunocompromised host, the parasite can cause life-threatening infections such as hyperinfection syndrome and disseminated strongyloidiasis.

Cutaneous phase

  • cutaneous phase involves invasion of the skin by Strongyloides stercoralis filariform larvae

  • within 24 hours at the site of entry the feet, manifestations such as petechial haemorrhage, congestion, and oedema occur

  • associated with intense itching

  • in previously sensitized patients, larva currens occur which is caused by external auto-infection and is a local allergic reaction to the akin penetrating larvae

  • in larva currens clinical syndromes such as linear pruritic, erythematous, and serpiginous lesions appear around the site of invasion and the route of larval migration

  • these parasitic lesions start around the perianal area and then extend to the buttocks, upper thighs, and lower abdomen

  • the spread of these lesions is at the rate of 5 mm to 10 mm per hour

Pulmonary phase

  • pulmonary phase occurs when the Strongyloides stercoralis larvae migrate through the lungs

  • common clinical syndromes include dyspnoea, wheezing, low-grade fever, cough production with blood-streaked sputum

  • other syndromes are Loeffler-like syndromes with pneumonitis, high-grade eosinophilia, and bronchopneumonia, pneumonia, or asthma

  • in serious cases, disseminated strongyloidiasis occurs

  • eggs and rhabditiform larvae can be demonstrated in the sputum

Intestinal phase

  • intestinal phase involves invasion of the intestine by adult Strongyloides stercoralis

  • in acute cases, clinical syndromes which are common include profuse water and mucoid diarrhoea, abdominal discomfort, indigestion, nausea, vomiting

  • in chronic cases, clinical syndromes include diffuse abdominal pain, vomiting, nausea, diarrhoea with occasional blood, and hyperactive or hypoactive bowel movement

  • in children, severe cases of malabsorption of fat and protein may result in steatorrhoea, hypoalbuminaemia, chronic diarrhoea, oedema of the lower and upper limbs, and cachexia

Hyperinfection syndrome

  • hyperinfection syndrome is a clinical form of strongyloidiasis caused by the infective Strongyloides stercoralis filariform larvae

  • can be defined as frequent auto-infection which leads to increased worm load in the intestinal lumen

  • does not include the dissemination to extra-intestinal sites

  • common in patients taking immunosuppressive drugs such as corticosteroids, tacrolimus, radiation, chemotherapy

  • also common in organ transplant patients, and in patients with lymphomas, leukaemia, autoimmune disease (lupus), AIDS, HTLV-1

Disseminated strongyloidiasis

  • disseminated strongyloidiasis is a clinical form caused by the infective Strongyloides stercoralis filariform larvae

  • the larvae are widely disseminated outside the intestinal tract and on organs such as the heart, central nervous system (CNS), urinary organs, and endocrine organs

  • clinical syndromes include diffuse pulmonary infiltrates, gram-negative septicemia, oedema, severe diarrhoea, paralytic ileus

  • CNS invasion leads to meningitis or brain abscess

  • prognosis is poor and mortality is high

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