Strongyloidiasis

Section Contents

Key Points
Background & Epidemiology
Transmission & Life cycle
Pathogenesis & Clinical Presentation
Diagnosis
Treatment
Prevention
Assessment: Did It Get It? (DIG IT)
Other Media Resources (Optional)
References

Key Points

Strongyloidiasis is a parasitic infection caused by the nematode Strongyloides stercoralis.
Infection occurs when infective larvae, present in fecally contaminated soil, penetrate the intact skin.
The life cycle is very complex and consists of two separates phases: a free-living phase and a parasitic phase.
S. stercoralis can complete its entire life cycle inside the human host (autoinfection), allowing it to persist for decades.
Strongyloides infection has an acute and a chronic phase. Further, in those taking corticosteroids, co-infected with HTLV-1 and/or other immunosuppressive conditions, a hyperinfection syndrome can occur.
Ivermectin is the drug of choice for treatment.

Background & Epidemiology

Strongyloidiasis is a parasitic infection caused by the soil-transmitted helminth Strongyloides stercoralis. Because of its uniqueness, we gave it a separate lesson! Other species (S. fuelleborni, S. fuellerborni kellyi) will not be discussed in this module. S. stercoralis has a worldwide distribution, but it is primarily seen through tropical and subtropical areas.

Although the exact prevalence is unclear, an estimated 30-100 million people are infected worldwide. Infection by S. stercoralis occurs by skin penetration of infectious larvae present in soil, which occurs frequently while walking barefoot in endemic areas.

Transmission & Life cycle

It involves two separate phases, a free-living (in the environment) and a parasitic phase (in the human). Click below to learn more on each:

Free-living phase

Parasitic phase

Occurs when filariform larvae (L3) penetrate the host’s intact skin. Upon entry, it finds its way to the venous and lymphatic circulation, it's carried into the pulmonary capillaries, and ruptures into the alveolar space, where it molts from L3 to L4, leaving behind its larval cuticle. It then actively crawls up the respiratory tree into the pharynx, where it is swallowed. Larva undergoes a final molt in the small intestine and the adult female finds its definitive habitat in the crypts of the small intestine. Egg production begins and these are released into the lumen. Once in the lumen, two things may happen:

Eggs usually hatch within the host, releasing rhabditiform larva (L1) in the stool. L1 larva can either mature back to infective filariform larva (L3) in the proper soil (enters free-living phase, indirect cycle) OR directly infects a new host (direct cycle). Please know that only in individuals with very severe diarrhea, you may find eggs in stool - although it is rare;
OR
Autoinfection: occurs when L1 larva molts into infective L3 larva within the intestinal lumen, which may re-penetrate the intestinal mucosa or the perianal region, allowing for a new cycle to start. Low levels of autoinfection are known to be common, allowing the parasite to persist for decades!

Figure 1. Strongyloides larva

Note: In immunocompromised patients (especially those on corticosteroids or co-infected with HTLV-1) a hyperinfection syndrome can occur where there is an accelerated autoinfection cycle, and a BIG burden of worms (sometimes >200,000) undergo the gut-pulmonary cycle. More about hyperinfection is coming up!

Figure 2. Life cycle of Strongyloides stercoralis

Pathogenesis & Clinical Presentation

During the parasitic phase, Strongyloides can have different presentations at each phase of the life cycle:

Acute infection

It is reflective of the initial larval passage through the skin, lungs and GI tract, which lasts 1-2 weeks. There is something you MUST remember: most infections are asymptomatic! Eosinophilia is present in the acute phase (except in immunosuppressed individuals or those co-infected with pathogens that can falsely mask an eosinophilic response because of an elevation of neutrophils or lymphocytes).

When symptoms are present, they include:

Cutaneous: i. Ground itch: mild pruritic papular rash at the site of larval penetration (heteroinfection); ii. Larva currens: serpiginous, pruritic, linear tracks, classically of rapid progression, reflective of larval migration through the skin (autoinfection). Larvae can move over 10 cm every 3-4 hours over a period of 1-2 days, before re-entering the circulation.
Pulmonary: i. Löeffler's syndrome: is a transient hypersensitivity response to larval pulmonary migration, that presents with cough, fever, and eosinophilia. It mimics asthma-like symptoms.
Gastrointestinal: "dyspepsia-like symptoms", inc. epigastric discomfort, bloating, and diarrhea.

Chronic infection

Low-level cycles of autoinfection can occur, which perpetuates the infection for decades. Eosinophilia is present. We can't emphasize it enough: most cases are asymptomatic! However, when symptoms do occur, they include:

Gastrointestinal: epigastric pain and/or diarrhea.
Respiratory: (less common) simulates "asthma-like" symptoms.
Cutaneous: recurrent urticaria, or larva currens phenomenon. The latter classically is seen in the trunk (internal autoinfection) and in the buttocks, perianal region (external autoinfection) - the site where the L3 larvae re-penetrate the intact skin in the autoinfection cycle.

Hyperinfection & disseminated strongyloidiasis

Hyperinfection Syndrome:
This occurs when a large number of Strongyloides L3 larvae undergo an intensified gut–lung migration cycle. During this process, the larvae can transport intestinal bacteria—such as Escherichia coli, Klebsiella pneumoniae, Enterococcus spp., and Streptococcus spp.—into the bloodstream and alveoli. Clinically, hyperinfection may present with bacteremia/sepsis, pneumonitis/pneumonia, or ulcerative enteritis and upper gastrointestinal bleeding due to the heavy parasitic load in each body site.

Disseminated Strongyloidiasis:
Dissemination happens when larvae migrate erratically beyond their normal gut–lung life cycle. This can result in bacterial infections in nearly any organ system, including bacterial meningitis, peritonitis, or infections elsewhere depending on the underlying illness. Larvae may be detected in cerebrospinal fluid (CSF), and other normally sterile sites - such as the peritoneal fluid. A distinctive clinical sign is a purpuric rash around the periumbilical area and thighs, referred to as “thumbprint purpura.” Unlike uncomplicated infections, disseminated disease is often associated with eosinopenia (a lack of eosinophils) due to elevated levels of endogenous catecholamines.

NOTE: Severe disease occurs in immunocompromised patients, especially those using corticosteroids, co-infected with HTLV-1, and/or other immunosuppressive conditions (e.g., HIV/AIDS, malnutrition, transplantation, cancer-related therapies).

What is Löeffler's syndrome?

Answer

Löeffler's syndrome is a transient hypersensitivity reaction to the larval cuticle during the L3 to L4 molting process. Once the cuticle disappears, the respiratory symptoms go away and appear in other body sites where the larva is present.

Diagnosis

As with all diseases, diagnosis starts with a clinical suspicion in the right epidemiological context (ask yourself: What is the presentation? Who is the host?). Clinical and epidemiological diagnosis is supported with various diagnostic modalities. In the case of Strongyloides, diagnosis is challenging because there is no gold standard test, but available diagnostics include:

Acute infection:
1. Stool microscopy (direct smear): sensitivity is low, and requires serial testing. Might be more helpful among individuals with high parasitic burden (e.g., AIDS). Concentration techniques (i.e., Baermann concentration) are preferred, but are not widely available.
  1. Different from other helminthiasis, stool examination will show
    rhabditiform larvae (L1)! NOT eggs. L3 larvae are rarely seen because
    they re-penetrate the mucosa before being released with stool.
2. Agar plate culture: after placing a stool sample in an agar plate, larvae can
  carry enteric bacteria through the plate, showing centrifugal tracks. Modifications using cellophane paper are available, click here to read more!
3. PCR: highly sensitive and specific, but not widely available.
4. Serology: can be initially negative. Does not differentiate between previous or past infection. Useful in non-endemic areas.
  
  Figure 3. Strongyloides larvae in stool
Chronic infection:
1. Stool microscopy/PCR: frequently negative, due to the low and inconsistent shedding of larvae released in stool.
2. Agar plate: in certain endemic areas, agar plate is considered test of choice during chronic infection. Serial examination can improve sensitivity.
3. Serology (ELISA - IgG): sensitivity is high, but can cross react with other helminths. Only shows past exposure. Test of choice during chronic infection in non-endemic areas.
Hyperinfection & Disseminated syndrome:
1. Serology
2. Stool & sputum microscopy: because of high burden of migrating larvae, they may be seen in stool AND in sputum! Don't forget to send both!

Figure 4. Phases of strongyloidiasis

Treatment

The drug of choice for Strongyloides stercoralis is ivermectin!

Uncomplicated (acute or chronic) infection: in books you will find that treatment of choice is ivermectin 200 mcg/kg/day for 1-2 days. Certain experts will argue that a single dose 150-200 mcg/kg/d is usually sufficient, but dose might be repeated 14-30 days later if eosinophilia has not improved.
- In immunocompromised individuals, 1-2 doses should be repeated 14 days later.
Hyperinfection & disseminated syndrome: ivermectin is still the drug of choice, but duration is debated. You should be managing this in consultation with an expert!
- Rectal or parenteral formulation has been used off-label.
- Reduce immunosuppression as possible.

Flip the card to learn more management pearls!

Answer

NUMBER ONE - screen patients at risk with serology before starting immunosuppressive therapy or those with HTLV-1 infection.

NUMBER TWO - Ivermectin is contraindicated in patients with Loa Loa co-infection (screen based on epidemiological risk!). More on this in Filarial Nematodes.

Prevention

Avoid contaminating soil with human stool (e.g., proper disposal of human waste).
Avoid coming in contact with contaminated soil (e.g., wearing shoes in endemic areas).
Screen and treat patients at risk! (as noted in management pearls).

NOTE: high-risk occupations in endemic areas include those involved in agriculture, gardening, septic tank cleaners, among others.

Assessment: Did I Get It? (DIG IT)

DIG ITs are online modules designed to reinforce key learning points for you! Please choose the best answer, then check all of the answer choices for more learning pearls

Begin Assessment

Other Media Resources (Optional)

Podcast Recording

References

View All References

Despommier, D.D. et al. (2019) Parasitic Diseases. Seventh Edition. Parasites Without Borders, Inc. NY.
Gordon, C.A., Utzinger, J., Muhi, S. et al. Strongyloidiasis. Nat Rev Dis Primers 10, 6 (2024).
Zainol DA, Anuar NS, Abdul Halim NSS, et al. Systematic Review of Strongyloides stercoralis Infection Diagnosis in Southeast Asia: Insights from Parasitological, Molecular, and Serological Approaches. Am J Trop Med Hyg. 2024 Aug 13;111(4):724- 735.
Abad CLR, Bhaimia E, Schuetz AN, Razonable RR. A comprehensive review of Strongyloides stercoralis infection after solid organ and hematopoietic stem cell transplantation. Clin Transplant. 2022 Nov;36(11):e14795.
Taheri B, Kuo HC, Hockenbury N, et al. Strongyloides stercoralis in the US Military Health System. Open Forum Infect Dis. 2023 Mar 18;10(3):ofad127.
Buonfrate D, Fittipaldo A, Vlieghe E, Bottieau E. Clinical and laboratory features of Strongyloides stercoralis infection at diagnosis and after treatment: a systematic review and meta-analysis. Clin Microbiol Infect. 2021 Nov;27(11):1621-1628.
Barkati, S., Greenaway, C. and Libman, M.D. (2021) ‘Strongyloidiasis in immunocompromised migrants to non-endemic countries in the era of COVID-19: What is the role for presumptive ivermectin?’, J of Travel Med, 29(1).
Blumberg, L. et al. (2021) Oxford Handbook of Tropical Medicine. Oxford: Oxford University Press.
Reyes Romero, H., Navarro Rojas, P. and Reyes Barrios, H. (2013) Medicina tropical y enfermedades del viajero Vol Tomo II. Caracas: Consejo de Desarrollo Científico y Humanístico Universidad Central de Venezuela.

This lesson was last updated September 8 2025

Strongyloidiasis