Strongyloides stercoralis

In brief

What it is

Strongyloides stercoralis is a threadworm: a very small parasitic roundworm, or nematode, named for its thread-like shape. The form that matters medically is the parthenogenetic female, a worm about 2 millimeters long that lives buried in the lining of the small intestine and lays eggs without a mate ¹. Parthenogenesis means reproduction from unfertilized eggs, so a single female can keep an infection going. The stage a laboratory actually sees is not the adult but the larva passed in stool, a creature a few hundred micrometers long, a micrometer being a thousandth of a millimeter ¹.

It belongs to the soil-transmitted helminths, the group of worms picked up from ground fouled by human feces, alongside hookworm and the roundworm Ascaris ¹. But it does not behave like them. Most soil-transmitted worms are swallowed as eggs or burrow in once and are then counted by the eggs they shed; Strongyloides has a life cycle with two features that set it apart, described in the next section, and these make it both hard to measure and, in the wrong patient, deadly ^1,2.

The worm is primarily a human parasite, but it is not ours alone. A meta-analysis pooled Strongyloides in 6% of dogs (95% confidence interval 4 to 8%) and in 7% of dog owners, and a 2024 review pooled 13.3% in cats (95% confidence interval 8.3 to 18.3%) ^3,4. Whether these animals are a true reservoir that reinfects people, or simply share the same contaminated ground, is unresolved, in part because most surveys do not sequence the worms to species ^3,4. A confidence interval is the range within which the true value probably lies given the size of the studies.

How you get it: two cycles in one worm

A person is infected when filariform larvae, the slender infective stage, in warm damp soil penetrate bare skin directly ^1,18. The larvae enter the bloodstream, are carried to the lungs, break into the air spaces, climb the windpipe, are coughed up and swallowed, and arrive in the small intestine, where they mature into egg-laying females ¹⁸. This much resembles hookworm. What follows does not.

The first unusual feature is a complete free-living cycle. Larvae passed in the feces need not find a new host at all: in the soil they can grow into free-living adult males and females that mate and breed, a whole generation living and reproducing outside any animal before their offspring, as infective larvae, wait in the ground for the next person ¹. This is rare among the worms that infect people and helps the parasite saturate a community with poor sanitation ¹.

The second feature, and the dangerous one, is autoinfection. Some larvae do not wait to be excreted. While still inside the gut, rhabditiform larvae (the non-infective feeding stage) transform into infective filariform larvae and bore back through the wall of the intestine or through the skin around the anus, re-entering the same host and starting the migration over again ^1,2. Because of this internal loop, strongyloidiasis is commonly a chronic, lifelong infection rather than one that clears, a point the reviews make plainly ^1,2. The clearest illustration is clinical: a traveler developed the characteristic skin track of the worm more than 20 years after the last possible exposure, because the infection had quietly renewed itself the entire time ²². A 2022 report describes the parasite as unique in being able to remain undetected for decades ¹⁷.

In a healthy person, autoinfection is held to a low simmer by the immune system, which leans on type-2 immunity and eosinophils, the white blood cells that respond to worms ². The balance tips when that control is removed, and the two commonest ways it is removed, corticosteroid drugs and infection with the retrovirus HTLV-1, are the subjects of the two sections that follow ^2,6. Risk rises with any cause of weakened cell-mediated immunity: a 2023 narrative review lists HTLV-1, low antibody levels (hypogammaglobulinemia), steroid use, alcoholism and malnutrition as the recognized risk factors ¹⁶, a grouping a 2024 review echoes for alcohol ²⁴.

How many people carry it, and why the old number was wrong

For decades the textbooks put the number of people infected at 30 to 100 million, a figure still repeated in major reviews as recently as 2016 and 2019 ^2,6. It was always an estimate passed from paper to paper, and it was almost certainly far too low, because the worm is so easily missed that wherever investigators look harder they find more.

The current modeled estimate is much larger. In 2020, Buonfrate and colleagues took prevalence data from endemic countries between 1990 and 2016, corrected each study for the sensitivity and specificity of the test it used (how many true infections a test catches, and how reliably it clears the uninfected), and fitted a spatiotemporal statistical model, a method that borrows strength across neighboring places and years ⁵. They estimated the global prevalence in 2017 at 8.1% (95% confidence interval 4.2 to 12.4%), or 613.9 million people infected (95% confidence interval 313.1 to 910.1 million), with South-East Asia, Africa and the Western Pacific holding 76.1% of infections ⁵. That is roughly six to twenty times the old ceiling. A separate 2022 ecological niche model, which maps where the climate and soil suit the worm rather than counting infections, estimated 2.6 billion people living in suitable areas, the population at risk ⁷. These are two different quantities, and both are models, not counts.

The uncertainty is not a footnote; it is the finding. The 2020 interval runs from 313 million to 910 million, a threefold spread, and the modern trial and guideline literature simply rounds to up to 600 million or 300 to 600 million ^15,23. The reason the range is so wide is the same reason the old figure was wrong: surveillance is thin and the usual test is poor, so most infections are never recorded ¹. The 2024 Nature Reviews Disease Primers review states outright that global prevalence remains largely unknown because of limited surveillance ¹.

The United States is a case in point. Seroprevalence is reported at about 4%, concentrated in immigrants, but the worm is also acquired domestically: a 2022 case was acquired locally (autochthonously) in rural southwest Virginia ^16,17. The honest summary is that strongyloidiasis is more common than the historical number implied, that the best current estimate is a model centered near 600 million for 2017, and that no one has counted the world ^1,5.

What it does to you: from nothing to fatal

Most infections cause nothing, or little. Reviews describe the majority as subclinical, meaning silent, or marked only by vague and intermittent gut, chest and skin complaints ^1,6. The most specific sign is larva currens, Latin for running larva: a raised, itchy, serpiginous (snaking) track that moves across the skin by centimeters an hour as a larva migrates, most often around the trunk and buttocks ^18,22. Chronic infection can also bring abdominal pain, diarrhea, cough and a raised eosinophil count, but none of these is specific and the infection can run for years with no eosinophilia at all ^1,22.

The danger is what happens when the immune brake comes off. Autoinfection, normally held in check, accelerates: larval numbers multiply, and larvae migrate in huge numbers out of the gut. Hyperinfection means an overwhelming increase in worm burden along the normal migratory route; disseminated strongyloidiasis means larvae reaching organs outside that route, such as the brain, liver and skin ². As larvae pierce the gut wall they carry intestinal bacteria with them, so the clinical picture is often Gram-negative sepsis or meningitis arriving on top of the worm ².

The numbers from the severe end are stark. A 2013 systematic review assembled 244 published cases of hyperinfection and disseminated disease from 1991 to 2011 ⁸. Corticosteroids were the precipitating trigger in 67%, usually given for an unrelated condition such as a lymphoma or a rheumatic disease, and sometimes, tragically, given to treat the very symptoms the unrecognized worm was causing ⁸. Diagnosis was made by microscopy in 100% of the cases but serology had been done in only 6.5%, and the death rate was 68.5% in disseminated disease and 60% in hyperinfection ⁸. A 2023 narrative review cites disseminated-disease mortality of 87.1%, and the 2024 World Health Organization (WHO) guideline review puts the hyperinfection or disseminated case fatality above 60% ^16,23. These figures come from reported severe cases, so they describe how lethal the severe form is, not the chance that an ordinary infection becomes severe.

The trigger is usually a drug. The COVID-19 pandemic made the point in real time: because dexamethasone became standard for severe COVID-19, hyperinfection appeared in people given steroids, sometimes fatal, as in a Cuban-born man with rheumatoid arthritis, and sometimes survived after treatment, as in a Bangladeshi man given steroids and baricitinib ^25,26. The common thread is that a short or long course of immune-suppressing treatment, started without anyone checking for the worm, is what tips a silent lifelong infection into a lethal one ^8,25.

The HTLV-1 link: why this worm belongs in a cancer season

Human T-cell lymphotropic virus type 1 (HTLV-1) is a retrovirus that infects T cells, a kind of white blood cell, for life. It is the proven cause of adult T-cell leukemia/lymphoma (ATLL), a cancer of those cells, and the International Agency for Research on Cancer (IARC) lists HTLV-1 among the 12 Group 1, meaning proven, infectious causes of human cancer in its 2026 global burden analysis ⁹. ATLL develops in roughly 3 to 5% of people infected with the virus, usually decades after infection ²⁷. The virus and the worm share the same tropical geography, so people often carry both ¹⁹.

The reason the two are linked runs through the immune system. A 2020 review sets out the mechanism: HTLV-1 shifts the immune response away from type-2 immunity, the arm that controls worms, toward type-1, and in co-infected people the virus reaches a higher proviral load, the amount of viral DNA carried in the blood cells ¹⁹. Weaker worm control means heavier strongyloidiasis and more treatment failures, which is why HTLV-1, alongside steroids, is one of the two classic triggers of hyperinfection ^6,28. A 2022 review confirms that Strongyloides is found more often, and is harder to clear, in people with HTLV-1 ²⁸.

The claim that matters for a cancer season runs the other way: that the worm may help cause the leukemia, not merely ride along with the virus. The evidence for this is real but limited, and it is important to say exactly how strong each piece is. A 2011 review states that ATLL arises significantly earlier and more often in people co-infected with Strongyloides, and offers this as an argument for the worm acting as a leukemogenic co-factor, meaning a second factor that helps the virus drive the cancer ¹⁰. A 2013 study of co-infected patients found an immune profile (lower tumor necrosis factor-alpha and higher soluble interleukin-2 receptor) that shifted toward normal after the worm was treated, and noted that the one patient who went on to develop ATLL was co-infected; the authors concluded the worm may be a cofactor ²⁰. A 2003 study of a girl with infective dermatitis and strongyloidiasis found HTLV-1 replicating in a pattern of persistent oligoclonal expansion (growth of a few dominant clones of infected cells) resembling leukemia, long before any leukemia ²⁷.

What these do and do not show should be stated plainly. They are co-infection series, small immunological studies and mechanistic arguments. They establish a consistent association and a plausible pathway, in which chronic worm infection drives repeated division of the infected T cells the virus has colonized, giving mutations more chances to accumulate ^10,20. They do not amount to a cohort study demonstrating that treating strongyloidiasis lowers the risk of ATLL, and no such trial has been reported here. On IARC's scale the proven carcinogen in this story is HTLV-1; the worm's role is an association with mechanistic support, not an established cause ^9,10. The practical takeaway is less contested: in anyone with chronic strongyloidiasis, especially without eosinophilia or with repeated treatment failure, HTLV-1 should be sought, and vice versa ¹⁰.

Why it is missed

Strongyloides is called the most neglected of the common parasites largely because the test most laboratories reach for cannot find it ¹⁶. In chronic infection the worm sheds few larvae, and sheds them intermittently, so a single stool examined under the microscope catches only a fraction of infections. In a 750-sample study against serology, a single microscopy read had a sensitivity of 6%, meaning it detected 6 of every 100 true infections; agar plate culture of the same raw stool managed 3% and an older culture method 0% ¹³. Sensitivity is the share of real infections a test detects.

Serology, which detects antibodies to the worm in blood, is far more sensitive and is the recommended screening test in places where the infection is uncommon. In one study its sensitivity against a composite reference was about 95%, compared with 57% for real-time polymerase chain reaction (PCR, a method that copies and detects the worm's DNA) and 45% for agar plate culture ¹². The weakness of serology is the mirror image of its use: it can read falsely negative in exactly the immunosuppressed patients most at risk, because they make fewer antibodies, and falsely positive in people infected with other worms ¹³. Recombinant-antigen versions, built from defined worm proteins, improve specificity and can even track cure, with antibody levels falling a median 93.9% a year after treatment in one small study ²⁹. A 2025 Bayesian analysis of 498 immunosuppressed patients in north India put serology sensitivity at only 74.5% (95% credible interval, the Bayesian counterpart of the confidence interval, 62.7 to 84.5%), well below the roughly 95% seen in people with intact immunity, while serology and stool PCR used together performed best, at 87.5% sensitivity ³⁰; point-of-care rapid tests using defined worm antigens are beginning to move serologic screening to the bedside ³¹.

Culture and molecular methods help most when the stool is cultured first. Agar plate culture, in which larvae crawl across a plate and drag bacterial trails behind them, is a WHO reference method but is slow and labor-intensive ^12,23. A 2026 study found that agar plate culture and PCR run on the cultured stool each detected about 85% of infections, while PCR on fresh, uncultured stool detected only 42% ³². Real-time PCR comes into its own in the immunosuppressed, where it diagnosed donor-derived infection in two transplant recipients whom other tests would likely have missed ³³.

The cruelest trap is the blood count. A raised eosinophil count is the classic laboratory hint of a tissue worm and often prompts testing, but it fails in both directions here. Chronic strongyloidiasis frequently runs without high-grade eosinophilia, as in the 20-year larva currens case, and, worse, the corticosteroids that unleash hyperinfection also suppress eosinophils, erasing the very clue that might have led to the diagnosis before the steroids were given ^6,10,22. For that reason a 2011 review urges that strongyloidiasis not be ruled out by a normal eosinophil count ¹⁰.

• Single stool microscopy (ova and parasites)A technologist looks for moving larvae in stool; in chronic infection the larval output is low and intermittent, so one sample misses most infections ^2,13.The default first test almost everywhere, and the method by which 100% of a large series of severe cases were finally diagnosed ⁸Against serology, a single microscopy read detected only 6% of infections in one 750-sample study ¹³.Most light, chronic infections; it is the reason the worm is called the most neglected parasite ¹⁶.
• Serology (antibody ELISA, or enzyme-linked immunosorbent assay)Detects antibodies to the worm; the most sensitive screening test in low-burden settings, and recombinant-antigen versions can track cure ^12,29.Screening migrants and patients before immunosuppression ^12,34Sensitivity about 95% against a composite reference in one study ¹².Can read falsely negative exactly when it matters most, in the immunosuppressed, and falsely positive with other worm infections ¹³.
• Agar plate cultureStool is spread on an agar plate; migrating larvae drag bacteria into visible tracks over days ¹².A World Health Organization (WHO)-endorsed reference method and a confirmatory test ^12,23Sensitivity 45% against a composite reference, rising to about 85% when polymerase chain reaction (PCR, which copies and detects the worm's DNA) is run on the cultured stool ^12,32.Slow, labor-intensive, and still misses light infections; raw stool performs far worse than cultured stool ³².
• Stool real-time PCRDetects worm DNA in stool and can catch infection in the immunosuppressed when microscopy and serology fail ³³.Confirmation, donor-derived transmission work, and research ^13,33Sensitivity about 38% against serology (ELISA) on a single raw sample ¹³ and about 57% against a composite reference ¹²; higher on cultured stool.Light infections on a single raw specimen; not yet standardized across laboratories ¹.
• Peripheral eosinophil countA raised eosinophil count is a classic clue to a tissue-invading worm, but it is a signpost, not a diagnosis ¹⁰.As a prompt to test for the worm, especially in migrants ³⁴Unreliable: chronic infection can run without high-grade eosinophilia, and steroids erase the count ^10,22.The patient about to become most dangerous, because the drug that unmasks the worm also removes its warning sign ^6,10.

The screening that does not happen

Because the worm is lifelong and lethal mainly when immunity is suppressed, the logical defense is to find and clear it in two groups: migrants from endemic areas, and anyone about to be immunosuppressed. Both are screened far less than they should be.

For migrants, a systematic review for the European Centre for Disease Prevention and Control concluded that antibody serology is the most effective screening test in low-endemicity settings and that short-course ivermectin is highly effective and cost-effective; economic modeling even suggested that presumptive treatment, meaning treating every arriving migrant with a single dose of ivermectin without testing first, is likely cost-effective, though the review cautioned that the feasibility of that strategy has not been demonstrated in clinical studies ³⁴. The certainty of evidence for screening techniques was rated low ³⁴.

For patients facing immunosuppression, the gap is documented in the dead. In the 2013 review of 244 severe cases, only 3 of 29 transplant patients had any mention of pre-transplant serological screening, and serology had been performed in just 6.5% of all severe cases ⁸. The remedy is not unknown: transplant guidelines recommend screening candidates and donors from endemic areas and treating before immunosuppression, and in 2024 the US organ-allocation network moved toward universal donor screening after cases of donor-derived infection ^35,36. The worm can pass from an infected organ donor to recipients, where it was caught by stool PCR in two patients who received organs from one donor ³³. Where screening is impossible before urgent steroids, several authors argue for presumptive ivermectin in anyone with the relevant exposure history ^25,37.

The through-line is that the tools exist and the policy is catching up, but the default remains to give the immune-suppressing drug first and think of the worm only when a patient is already in the intensive care unit with sepsis and larvae in the sputum ^8,25.

What is done about it

Ivermectin is the drug of choice, given as a single oral dose of 200 micrograms per kilogram of body weight ^1,23. Its advantage over the alternative is settled by trials. A Cochrane review of 7 randomized trials and 1,147 participants found ivermectin cured more people than albendazole (risk ratio 1.79, 95% confidence interval 1.55 to 2.08) and matched the older drug thiabendazole for cure while causing fewer side effects ¹⁴. An early trial in 301 Zanzibari children found single-dose ivermectin cured 83% against 45% for three days of albendazole, and a trial in 42 Thai patients found 76.2% against 38.1% for a week of albendazole ^38,39. Albendazole is therefore the weaker alternative, used when ivermectin cannot be, not an equal.

One tidy assumption was overturned. Because autoinfection keeps the parasite cycling, it seemed obvious that repeated doses, timed to catch newly matured larvae, should cure more people than one dose. The Strong Treat trial tested exactly this in 309 patients in Europe and found no benefit: a single dose of ivermectin cleared 86% at 12 months (102 of 118) against 85% for four doses (96 of 113), with more side effects in the four-dose group, and the trial was stopped early for futility ⁴⁰. For ordinary, non-disseminated infection, one dose is now preferred ⁴⁰. This did not test severe or disseminated disease, where optimal dosing is still undefined ^8,40.

Moxidectin is the emerging alternative, and it comes out of veterinary medicine. It is a macrocyclic lactone, the same drug class as ivermectin, long used in animals and now approved for human onchocerciasis (river blindness), and it is being repurposed against intestinal worms ⁴¹. The decisive trial, in 726 adults in Laos and Cambodia, compared a single 8-milligram dose of moxidectin with single-dose ivermectin: cure rates were 93.6% and 95.7%, a difference of 2.1 percentage points that fell within the pre-set non-inferiority margin, with similar, mild side effects ¹⁵. A systematic review of the two available trials (821 adults) reached the same conclusion, with the important caveat that neither trial enrolled immunocompromised, very young or very old patients, so moxidectin cannot yet be recommended for them ⁴². Pharmacometric modeling suggests moxidectin's single 8-milligram dose plateaus near 87% cure in heavier infections and proposes a two-dose regimen three weeks apart to catch the autoinfection cycle; moxidectin's attractions are a fixed dose and lower cost ^15,43.

A second drug from the veterinary cabinet is close behind moxidectin. Emodepside, a dewormer repurposed from animal medicine and now in human development for river blindness (onchocerciasis) and soil-transmitted worms, works by a mechanism distinct from ivermectin and moxidectin, which is part of why it is being pursued as a hedge against resistance to the two macrocyclic lactones ^31,44. A 2025 phase 2a (early-stage) dose-ranging trial in 202 adults in Laos gave a single oral dose and found a predicted cure rate rising from 78.3% (95% confidence interval 59.4 to 89.9%) at 5 milligrams to a plateau of 89.1% (81.6 to 93.7%) at 15 milligrams, against an observed 88.0% (68.8 to 97.5%) for single-dose ivermectin in the same trial; the main side effect was short-lived drowsiness and no serious events occurred ⁴⁴. As with the moxidectin trials, this was an early study, and its authors frame emodepside as a promising new candidate rather than an approved treatment ⁴⁴.

Treating the severe form is harder and less evidence-based. Ivermectin remains the mainstay, but the dose and duration in hyperinfection and dissemination are not defined by trials, and patients are often too ill to swallow ⁸. When the oral route fails, clinicians have reached again into the veterinary cabinet: a kidney-transplant recipient with disseminated disease was cured with subcutaneous veterinary ivermectin, though drug levels accumulating above 40 nanograms per milliliter after the course were linked to encephalopathy, a brain disturbance ⁴⁵. For prevention before immunosuppression, a review reasons from treatment data that ivermectin, 200 micrograms per kilogram daily for two days and repeated in two weeks, is a reasonable prophylaxis, while acknowledging no trial has tested it as such ³⁷.

At the population level, ivermectin given in mass drug administration for other diseases clears Strongyloides as a bonus: in Papua New Guinea, adding ivermectin to treatment for lymphatic filariasis (a mosquito-borne worm disease that causes the limb swelling of elephantiasis) produced seroreversion, a fall from positive to negative antibody status, in 49% of villagers at 12 months against 23% without it ⁴⁶. In 2024, WHO issued its first guideline on strongyloidiasis, conditionally recommending mass single-dose ivermectin where prevalence reaches 5% ²³. For the pharmacology, history and controversies of the drug itself, see the ivermectin reference page.

The record, and what it reversed

Strongyloides entered medicine in 1876, when the French naval physician Louis Normand, working at the naval hospital in Toulon, found the larvae in the stools of soldiers invalided home from Cochinchina (present-day Vietnam) with the chronic wasting illness then called Cochin-China diarrhea; his colleague Arthur Bavay described the worm and gave it its first scientific name the same year ⁴⁷. Over the following half-century parasitologists worked out the two features that define it, the free-living generation that breeds in soil and the autoinfective cycle by which it reinfects its own host, so the biology this page rests on was in place well before the modern clinical record began ⁴⁷. What that record then shows is a steady series of corrections, each driven by someone measuring what had only been assumed ^5,40.

The biggest correction is the burden. The 30-to-100-million figure survived in the reviews into the late 2010s before the 2020 model placed the true number near 600 million, with a lower bound still above 300 million ^2,5,6. The second correction is therapeutic: the intuitive idea that repeated dosing must beat a single dose, so natural given autoinfection, was tested and failed in 2019 ⁴⁰. The third is the arrival of a veterinary drug, moxidectin, as a genuine alternative in a 2023 trial, and of a first WHO guideline in 2024 ^15,23. The record also shows policy slowly aligning with biology, as organ-allocation screening moved toward catching the worm before immunosuppression rather than after ³⁶.

How it connects to parasites and cancer

Measured against the parasites that are proven to cause cancer, Strongyloides is not among them. The three worm infections classified by IARC as Group 1 carcinogens are all flukes, the blood fluke Schistosoma haematobium and the liver flukes Opisthorchis viverrini and Clonorchis sinensis, and the 2026 IARC burden analysis counts the parasite-attributable cancers under those three alone ⁹. A 2016 systematic review of parasites beyond that trio screened 1,266 studies and selected 19; it listed Strongyloides among parasites that have been found in cancers or tumors, but concluded that the role of such parasites in cancer remains unclear and that a cause-effect relationship has not been established ¹¹.

So the worm's connection to cancer is indirect, and it runs almost entirely through HTLV-1. The virus is the proven carcinogen; the worm tracks it, worsens with it, and is argued, on the strength of co-infection series and immune-mechanism studies, to help the virus bring on leukemia earlier ^9,10,20. That is a real but unproven link, and the honest label is association with mechanistic support, not cause ¹⁰.

There is a second, narrower way the worm touches the subject: it imitates cancer. In 1987 a colon carpeted with 50 to 100 pseudopolyps (polyp-like lumps that are not true polyps) looked like a neoplasm (a true tumor) until a biopsy found the worm, and in 2022 an 81-year-old man with colonic pseudopolyposis and negative stool tests was diagnosed only by biopsy ^17,21. These are pseudotumors, growths that mimic a tumor but are not one, and they matter for the same reason the hyperinfection cases do: a worm that can be mistaken for a cancer, or that quietly sets the stage for a virus-driven one, is a worm that gets missed ^11,21. For this season the point is not that Strongyloides causes cancer, which is unproven, but that it sits exactly where a parasite could be overlooked in a cancer story, inside an immunosuppressed patient and alongside an oncogenic virus ^9,10.

What is still unknown

How many people carry it. The best figure is a model, 613.9 million for 2017, with an interval from 313 to 910 million, and the honest statement in the current review literature is that global prevalence remains largely unknown because surveillance is thin and the usual test is poor ^1,5. There is no reliable current count for most countries, the United States included, where seroprevalence is estimated at about 4% from scattered studies ¹⁶.

Whether the worm truly helps cause adult T-cell leukemia. The association, the earlier onset in co-infection and the immune mechanism are documented, but no cohort has shown that clearing the worm lowers the leukemia risk, so causation remains unproven ^9,10,20. Whether dogs and cats are a genuine human reservoir is likewise open, because most surveys do not sequence the worms to species ^3,4.

How best to treat the patients who die. The trials that define ivermectin and moxidectin dosing were done in people who were not immunocompromised, yet it is the immunocompromised who develop fatal disease, and the dose and duration for hyperinfection and dissemination are undefined ^15,40,42. Whether presumptive treatment of all migrants, or universal screening before immunosuppression, is feasible and cost-effective in practice has not been demonstrated in clinical studies ³⁴.

How to find it reliably. Every current test fails somewhere: microscopy misses light infections, serology fails in the immunosuppressed and cross-reacts with other worms, and molecular tests are not standardized across laboratories and work best only after the stool is cultured ^12,13,32. Until a sensitive, standard test exists, the worm will keep being counted too low and diagnosed too late ¹.

Where it connects

Sources

47 sources, numbered as they are cited. Every one was checked against PubMed or its publisher before it was cited here; the note under each says what it shows and what it does not.

1. 1
   Gordon CA, Utzinger J, Muhi S, Becker SL, Keiser J, Khieu V, Gray DJ. Strongyloidiasis.Nat Rev Dis Primers · 2024 · 10(1):6doi:10.1038/s41572-023-00490-x · PMID 38272922

   A current, authoritative review. It states the parthenogenetic female lives in the small intestine, the single-generation free-living cycle in soil, skin penetration by filariform larvae, autoinfection, and that global prevalence is largely unknown because of limited surveillance; ivermectin is the treatment of choice. A review, not new primary data.

2. 2
   Nutman TB. Human infection with Strongyloides stercoralis and other related Strongyloides species.Parasitology · 2016 · 144(3):263-273doi:10.1017/S0031182016000834 · PMID 27181117

   Review by an NIH parasitologist. Uses the older 30-100 million figure, attributes chronicity to autoinfection, names corticosteroids and HTLV-1 as the main triggers of hyperinfection, and says stool microscopy is the definitive but insensitive test. Restates figures rather than measuring them.

3. 3
   Gorgani-Firouzjaee T, Kalantari N, Chehrazi M, Ghaffari S, Shahdin S. Global prevalence of Strongyloides stercoralis in dogs: A systematic review and meta-analysis.J Helminthol · 2022 · 96:e11doi:10.1017/S0022149X21000808 · PMID 35184771

   Pooled prevalence in dogs 6% (95% CI 4-8%), and 7% in dog owners. The authors suspect the figure is an underestimate from insensitive tests; the role of dogs as a human reservoir is not settled here.

4. 4
   Zhao H, Bradbury RS. Feline strongyloidiasis: An insight into its global prevalence and transmission cycle.One Health · 2024 · 19:100842doi:10.1016/j.onehlt.2024.100842 · PMID 39026543

   Pooled Strongyloides prevalence in cats 13.3% (95% CI 8.3-18.3%). The review states it remains inconclusive whether cats are a reservoir for human infection, and that most data do not resolve the worms to species.

5. 5
   Buonfrate D, Bisanzio D, Giorli G, Odermatt P, Fürst T, Greenaway C, French M, Reithinger R, Gobbi F, Montresor A, Bisoffi Z. The Global Prevalence of Strongyloides stercoralis Infection.Pathogens · 2020 · 9(6):468doi:10.3390/pathogens9060468 · PMID 32545787

   The current modeled global estimate: prevalence 8.1% (95% CI 4.2-12.4%) in 2017, or 613.9 million (95% CI 313.1-910.1) people, built by spatiotemporal modeling of prevalence data from 1990 to 2016 corrected for test performance. A model of reported data, not a worldwide count; the wide interval is the uncertainty.

6. 6
   Krolewiecki A, Nutman TB. Strongyloidiasis: A Neglected Tropical Disease.Infect Dis Clin North Am · 2019 · 33(1):135-151doi:10.1016/j.idc.2018.10.006 · PMID 30712758

   Review. Opens with 30 to 100 million people infected, most subclinical; corticosteroid use and HTLV-1 are most commonly associated with hyperinfection. This is the old burden figure that the 2020 modeled estimate overturns.

7. 7
   Fleitas PE, Kehl SD, Lopez W, Travacio M, Nieves E, Gil JF, Cimino RO, Krolewiecki AJ. Mapping the global distribution of Strongyloides stercoralis and hookworms by ecological niche modeling.Parasit Vectors · 2022 · 15(1):197doi:10.1186/s13071-022-05284-w · PMID 35676740

   Ecological niche modeling estimates 2.6 billion people living where conditions suit the worm. This is population at risk by climate and soil, not people infected; it is a far larger and different number from the 613.9 million prevalence estimate.

8. 8
   Buonfrate D, Requena-Mendez A, Angheben A, Muñoz J, Gobbi F, Van Den Ende J, Bisoffi Z. Severe strongyloidiasis: a systematic review of case reports.BMC Infect Dis · 2013 · 13:78doi:10.1186/1471-2334-13-78 · PMID 23394259

   Systematic review of 244 published cases of hyperinfection and disseminated disease, 1991-2011. Steroids were the trigger in 67%; diagnosis was by microscopy in 100% and serology in only 6.5%; fatality was 68.5% in disseminated and 60% in hyperinfection; only 3 of 29 transplant cases mention pre-transplant serology. A review of case reports, so it describes the severe end, not the risk of becoming severe.

9. 9
   Rumgay H, Georges D, Huang Y, Hirabayashi M, Shah R, de Martel C, Park JY, Soerjomataram I, Clifford GM. Global burden of cancer attributable to infections in 2024: a worldwide incidence analysis.Lancet Oncol · 2026 · 27(10):1237-1248doi:10.1016/S1470-2045(26)00307-4 · PMID 42805198

   IARC burden analysis: 2.3 million new cancers (12% of all cancer) attributable to 12 Group 1 infectious agents in 2024. HTLV-1 is one of the 12; the three Group 1 parasites are all flukes. Strongyloides is not on the list. A modeled burden estimate built on GLOBOCAN with no uncertainty intervals, not a cohort study.

10. 10
    Pays JF. [Combined infection with HTLV-1 and Strongyloides stercoralis].Bull Soc Pathol Exot · 2011 · 104(3):188-99doi:10.1007/s13149-011-0175-z · PMID 21800110

    French-language review (English abstract read). Argues HTLV-1 raises larval numbers and anthelmintic failure, shifts Th1/Th2 toward Th1, and lowers IgE and eosinophils; states that adult T-cell leukemia arises significantly earlier and more often in co-infection, which it offers as an argument for the parasite as a leukemogenic co-factor. Also warns that chronic strongyloidiasis can occur without eosinophilia. This is a reasoned argument, not a cohort result.

11. 11
    Machicado C, Marcos LA. Carcinogenesis associated with parasites other than Schistosoma, Opisthorchis and Clonorchis: A systematic review.Int J Cancer · 2016 · 138(12):2915-21doi:10.1002/ijc.30028 · PMID 26840624

    Systematic review: of 1,266 studies, 19 were evaluated; Strongyloides is named among parasites found in cancers or tumors, but the authors state the role of parasites beyond the three flukes remains unclear and a cause-effect relationship is not established.

12. 12
    Buonfrate D, Perandin F, Formenti F, Bisoffi Z. A retrospective study comparing agar plate culture, indirect immunofluorescence and real-time PCR for the diagnosis of Strongyloides stercoralis infection.Parasitology · 2017 · 144(6):812-816doi:10.1017/S0031182016002559 · PMID 28073382

    On 223 samples, against a composite reference, serology was most sensitive at 95%, real-time PCR 57% and agar plate culture 45%. Retrospective, non-endemic setting; it concludes serology is the best screening test and culture and PCR are confirmatory.

13. 13
    Swan C, Phan T, McKew G. Clinical Performance of Real-Time Polymerase Chain Reaction for Strongyloides stercoralis Compared with Serology in a Nonendemic Setting.Am J Trop Med Hyg · 2022 · 107(2):355-358doi:10.4269/ajtmh.21-1289 · PMID 35895584

    On 750 stool samples in a low-burden population, with ELISA as the reference, sensitivities were 38% for real-time PCR, 6% for microscopy, 3% for agar plate culture and 0% for Harada-Mori culture, with 100% specificity. Shows how badly single stool tests undercount chronic infection; serology itself can be falsely negative with immunosuppression.

14. 14
    Henriquez-Camacho C, Gotuzzo E, Echevarria J, White AC, Terashima A, Samalvides F, Pérez-Molina JA, Plana MN. Ivermectin versus albendazole or thiabendazole for Strongyloides stercoralis infection.Cochrane Database Syst Rev · 2016 · 2016(1):CD007745doi:10.1002/14651858.CD007745.pub3 · PMID 26778150

    Cochrane review of 7 trials and 1,147 participants: ivermectin cured more than albendazole (risk ratio 1.79, 95% CI 1.55-2.08, moderate-quality evidence) and matched thiabendazole for cure with fewer adverse events; a second ivermectin dose gave no benefit in a small subgroup. Pooled trial data, not a single trial.

15. 15
    Sprecher VP, Hofmann D, Savathdy V, Xayavong P, Norkhankhame C, Huy R, Khieu V, Sayasone S, Hattendorf J, Keiser J. Efficacy and safety of moxidectin compared with ivermectin against Strongyloides stercoralis infection in adults in Laos and Cambodia: a randomised, double-blind, non-inferiority, phase 2b/3 trial.Lancet Infect Dis · 2024 · 24(2):196-205doi:10.1016/S1473-3099(23)00507-8 · PMID 37949090

    The primary head-to-head trial: 726 adults in Laos and Cambodia, single-dose moxidectin 8 mg vs ivermectin 200 micrograms/kg; cure 93.6% (95% CI 90.5-96.0) vs 95.7% (93.0-97.6), difference -2.1 points, within the -10 point non-inferiority margin. No immunocompromised patients, no children; cure read at 14-21 days, not 12 months. Swiss National Science Foundation funded.

16. 16
    Yeh MY, Aggarwal S, Carrig M, Azeem A, Nguyen A, Devries S, Destache C, Nguyen T, Velagapudi M. Strongyloides stercoralis Infection in Humans: A Narrative Review of the Most Neglected Parasitic Disease.Cureus · 2023 · 15(10):e46908doi:10.7759/cureus.46908 · PMID 37954715

    Narrative review. Gives US seroprevalence as 4%, mostly in immigrants, and reported mortality of disseminated disease as 87.1%; lists HTLV-1, hypogammaglobulinemia, steroids, alcoholism and malnutrition as risk factors. A narrative review, so the figures are drawn from the sources it cites.

17. 17
    Yousaf O, Carreon A, Mohsin I. A Rare Cause of Pedunculated Polyps Caused by Strongyloides.Eur J Case Rep Intern Med · 2022 · 9(3):003008doi:10.12890/2021_003008 · PMID 35402330

    An 81-year-old man in rural southwest Virginia with colonic pseudopolyposis mimicking colitis and negative stool studies, diagnosed by biopsy. States the worm is unique among parasites in that it can remain undetected for decades. One case, and a reminder of autochthonous US infection.

18. 18
    Ly MN, Bethel SL, Usmani AS, Lambert DR. Cutaneous Strongyloides stercoralis infection: an unusual presentation.J Am Acad Dermatol · 2003 · 49(2 Suppl):S157-60doi:10.1067/mjd.2003.338 · PMID 12894109

    A case report whose discussion lays out the migratory route (skin or mucosa, venous system, lungs, trachea, swallowed, small intestine) and the skin signs: larva currens in chronic disease, petechiae and purpura in dissemination. One patient; the route description is textbook, not measured here.

19. 19
    Dykie A, Wijesinghe T, Rabson AB, Madugula K, Farinas C, Wilson S, Abraham D, Jain P. Human T-cell Leukemia Virus Type 1 and Strongyloides stercoralis: Partners in Pathogenesis.Pathogens · 2020 · 9(11):904doi:10.3390/pathogens9110904 · PMID 33137906

    Review of the co-infection. HTLV-1 endemic areas overlap with high Strongyloides prevalence; co-infection is associated with higher HTLV-1 proviral load and a shift of the immune response from Th2 toward Th1 that weakens control of the worm. The authors say the clinical implications remain elusive and more work is needed.

20. 20
    Salles F, Bacellar A, Amorim M, Orge G, Sundberg M, Lima M, Santos S, Porto A, Carvalho E. Treatment of strongyloidiasis in HTLV-1 and Strongyloides stercoralis coinfected patients is associated with increased TNF-alpha and decreased soluble IL2 receptor levels.Trans R Soc Trop Med Hyg · 2013 · 107(8):526-9doi:10.1093/trstmh/trt052 · PMID 23843560

    Small human study: co-infected patients had lower TNF-alpha and IFN-gamma and higher soluble IL-2 receptor, and anthelmintic treatment reversed both; the one patient who developed adult T-cell leukemia was co-infected. The authors conclude the worm may be a cofactor in that leukemia. Few patients, a single leukemia event; hypothesis-generating.

21. 21
    Carp NZ, Nejman JH, Kelly JJ. Strongyloidiasis. An unusual cause of colonic pseudopolyposis and gastrointestinal bleeding.Surg Endosc · 1987 · 1(3):175-7doi:10.1007/BF00590927 · PMID 3509735

    A man with rectal bleeding whose right colon was carpeted with 50-100 pseudopolyps of 3-4 mm; biopsy found the worm in the bowel wall. One case; the lesion mimicked a tumor and was diagnosed only on biopsy.

22. 22
    Bailey KE, Danylo A, Boggild AK. Chronic Larva Currens Following Tourist Travel to the Gambia and Southeast Asia Over 20 Years Ago.J Cutan Med Surg · 2015 · 19(4):412-5doi:10.1177/1203475415575247 · PMID 25775620

    A case of larva currens (the fast-moving serpiginous skin track) more than 20 years after exposure, illustrating lifelong infection unless treated and the absence of high-grade eosinophilia. One case.

23. 23
    Lo NC, Addiss DG, Buonfrate D, et al. Review of the WHO guideline on preventive chemotherapy for public health control of strongyloidiasis.Lancet Infect Dis · 2024 · 25(3):e146-e152doi:10.1016/S1473-3099(24)00595-4 · PMID 39481419

    Summarizes the first WHO guideline on strongyloidiasis (2024): where prevalence is 5% or higher by Baermann or agar plate culture, WHO conditionally recommends mass drug administration with single-dose ivermectin 200 micrograms/kg for everyone aged 5 years and older. Puts burden at 300-600 million and hyperinfection or disseminated case fatality above 60%. A conditional recommendation, written partly by the guideline authors.

24. 24
    Pillai RK, Pillai RK, Illankovan VR, Kumarasamy V, Reddy S, Gowtham K, Dhanasekaran M, Subramaniyan V. Understanding Strongyloides stercoralis infection and its relationship to chronic alcohol abuse.Toxicol Rep · 2024 · 13:101754doi:10.1016/j.toxrep.2024.101754 · PMID 39434865

    Review arguing that chronic alcohol use impairs T-cell and B-cell immunity and so favors the infection and hyperinfection; cites a global figure over 600 million. A mechanistic review, not an epidemiological measurement of the alcohol association.

25. 25
    Hamze H, Tai T, Harris D. Strongyloides hyperinfection syndrome precipitated by immunosuppressive therapy for rheumatoid arthritis and COVID-19 pneumonia.Trop Dis Travel Med Vaccines · 2023 · 9(1):15doi:10.1186/s40794-023-00201-0 · PMID 37794447

    A Cuban-born patient who died of hyperinfection after dexamethasone for severe COVID-19 on a background of prolonged immunosuppression. One fatal case; it recommends empiric treatment for at-risk patients given steroids.

26. 26
    Sharma R, Islam M, Alam MK, Das S, Islam R, Ghose A. Strongyloides Hyperinfection Syndrome Following Immunosuppressant Therapy for COVID-19: A Case Report With Literature Review.Clin Case Rep · 2024 · 12(12):e9689doi:10.1002/ccr3.9689 · PMID 39649493

    A Bangladeshi man who developed hyperinfection after about a month of corticosteroids plus baricitinib for COVID-19 pneumonia and survived after albendazole and ivermectin. One case; shows that steroid-sparing immunosuppressants can also unmask the infection.

27. 27
    Gabet AS, Kazanji M, Couppie P, Clity E, Pouliquen JF, Sainte-Marie D, Aznar C, Wattel E. Adult T-cell leukaemia/lymphoma-like human T-cell leukaemia virus-1 replication in infective dermatitis.Br J Haematol · 2003 · 123(3):406-12doi:10.1046/j.1365-2141.2003.04565.x · PMID 14616998

    A girl with infective dermatitis and strongyloidiasis carried extremely high HTLV-1 proviral loads with persistent oligoclonal expansion of infected T cells resembling the pattern seen in adult T-cell leukemia, which occurs in 3-5% of HTLV-1 carriers. One patient; shows a leukemia-like replication pattern, not leukemia, and does not isolate the worm from the dermatitis.

28. 28
    Rosadas C, Taylor GP. HTLV-1 and Co-infections.Front Med (Lausanne) · 2022 · 9:812016doi:10.3389/fmed.2022.812016 · PMID 35187000

    Review of HTLV-1 co-infections. Reports a higher frequency of Strongyloides in people living with HTLV-1 and higher treatment failure, but notes it is unclear whether this reflects greater susceptibility or shared exposure. A review; calls for large prospective studies.

29. 29
    Prato M, Tamarozzi F, Tais S, Rizzi E, Mazzi C, Buonfrate D. Evaluation of the SsIR/NIE recombinant antigen ELISA for the follow up of patients infected by Strongyloides stercoralis: a diagnostic study.Parasitology · 2024 · 151(3):295-299doi:10.1017/S0031182024000027 · PMID 38185819

    A recombinant-antigen ELISA tracked cure: in 38 paired sera about 95% showed a fall in optical density after treatment, median 93.9%. Small, and the positivity threshold was not predefined, so it is promising for follow-up rather than ready for routine use.

30. 30
    Mewara A, Sharma N, Dhir V, Dhooria S, Pandiarajan V, Prakash G, Rana SS, Singh S, Agarwal R. Prevalence and Diagnostic Performance of Molecular and Serological Tests for Strongyloides stercoralis Infection in Immunosuppressed Patients from North India.Am J Trop Med Hyg · 2025 · 114(2):269-274doi:10.4269/ajtmh.25-0566 · PMID 41662748

    In 498 immunosuppressed patients in north India (16.9% infected by a composite reference), Bayesian latent class analysis put ELISA serology sensitivity at 74.5% (95% credible interval 62.7-84.5), well below the ~95% in immunocompetent people, while ELISA plus real-time PCR together reached 87.5% sensitivity. Quantifies the failure of serology in the immunosuppressed and supports combined testing.

31. 31
    Clark EH, Nutman TB. Recent advances in Strongyloides screening, diagnostics, therapeutics, and management.Curr Opin Infect Dis · 2026 · 39(5):422-428doi:10.1097/QCO.0000000000001217 · PMID 42592788

    Review of current screening, diagnostics and treatment. Notes molecular assays supplanting microscopy where feasible, a shift to IgG/IgG4 point-of-care rapid tests using recombinant NIE/SsIR antigens, the 2024 WHO conditional recommendation for ivermectin mass drug administration, moxidectin non-inferiority (93-94% cure), and emodepside as a mechanistically distinct option with 80-90% predicted cure in early trials. A narrative review; it still quotes the old 30-100 million burden figure.

32. 32
    Tamarozzi F, Degani M, Scarso S, Negrelli S, Tais S, Rizzi E, Carrara A, La Marca G, Treggiari D, Ursini T, Buonfrate D. An Agar-Free, Glass Bead-Based Method for the Culture of Strongyloides stercoralis: An Exploratory Diagnostic Sensitivity Study.Diagnostics (Basel) · 2026 · 16(5):711doi:10.3390/diagnostics16050711 · PMID 41827987

    Of 110 serology-positive samples, 26 were positive by at least one method; agar plate culture and PCR after culture were most sensitive at 84.62%, PCR on fresh stool only 42.31%. Confirms that culturing the stool first beats testing it raw, and that the worm is targeted for WHO control.

33. 33
    Gómez-Junyent J, Paredes-Zapata D, de las Parras ER, González-Costello J, Ruiz-Arranz A, Cañizares R, Saugar JM, Muñoz J. Real-Time Polymerase Chain Reaction in Stool Detects Transmission of Strongyloides stercoralis from an Infected Donor to Solid Organ Transplant Recipients.Am J Trop Med Hyg · 2016 · 94(4):897-9doi:10.4269/ajtmh.15-0610 · PMID 26880781

    Two transplant recipients acquired the worm from one infected donor and were diagnosed by stool real-time PCR. Shows donor-derived transmission and that molecular testing can catch it where microscopy and serology fail in immunosuppressed patients. Two cases.

34. 34
    Agbata EN, Morton RL, Bisoffi Z, Bottieau E, Greenaway C, Biggs BA, Montero N, Tran A, Rowbotham N, Arevalo-Rodriguez I, Myran DT, Noori T, Alonso-Coello P, Pottie K, Requena-Méndez A. Effectiveness of Screening and Treatment Approaches for Schistosomiasis and Strongyloidiasis in Newly-Arrived Migrants from Endemic Countries in the EU/EEA: A Systematic Review.Int J Environ Res Public Health · 2018 · 16(1):11doi:10.3390/ijerph16010011 · PMID 30577567

    A GRADE-assessed review for the European Centre for Disease Prevention and Control: antibody serology is the most effective screening test in low-endemicity migrants, short-course ivermectin is highly effective, and presumptive single-dose ivermectin for all migrants is likely cost-effective but its feasibility has not been shown in clinical studies. Certainty for screening techniques was low.

35. 35
    Camargo LFA, Kamar N, Gotuzzo E, Wright AJ. Schistosomiasis and Strongyloidiasis Recommendations for Solid-Organ Transplant Recipients and Donors.Transplantation · 2018 · 102(2S Suppl 2):S27-S34doi:10.1097/TP.0000000000002016 · PMID 29381575

    Consensus recommendations to screen transplant candidates and donors from endemic areas and to treat before immunosuppression. Expert guidance, not a trial.

36. 36
    Hogan JI, Mehta SA. Strongyloides stercoralis infection in solid organ transplant recipients.Curr Opin Infect Dis · 2024 · 37(5):367-375doi:10.1097/QCO.0000000000001046 · PMID 39082077

    Review of donor-derived infection and of the Organ Procurement and Transplantation Network's recent move toward universal donor screening, with guidance on treating hyperinfection and on repeat treatment during later immunosuppression. A review of evolving policy.

37. 37
    Santiago M, Leitão B. Prevention of strongyloides hyperinfection syndrome: a rheumatological point of view.Eur J Intern Med · 2009 · 20(8):744-8doi:10.1016/j.ejim.2009.09.001 · PMID 19892301

    Review of prophylaxis before immunosuppression. Found no trial restricted to rheumatic patients and reasons from treatment studies that ivermectin has the best safety, cost and efficacy; suggests 200 micrograms/kg/day for 2 days repeated within 2 weeks. The regimen is inferred from treatment data, not tested as prophylaxis.

38. 38
    Marti H, Haji HJ, Savioli L, Chwaya HM, Mgeni AF, Ameir JS, Hatz C. A comparative trial of a single-dose ivermectin versus three days of albendazole for treatment of Strongyloides stercoralis and other soil-transmitted helminth infections in children.Am J Trop Med Hyg · 1996 · 55(5):477-81doi:10.4269/ajtmh.1996.55.477 · PMID 8940976

    Randomized trial in 301 Zanzibari children: single-dose ivermectin 200 micrograms/kg cured 83% vs 45% for three days of albendazole. An early, direct comparison in children.

39. 39
    Suputtamongkol Y, Kungpanichkul N, Silpasakorn S, Beeching NJ. Efficacy and safety of a single-dose veterinary preparation of ivermectin versus 7-day high-dose albendazole for chronic strongyloidiasis.Int J Antimicrob Agents · 2007 · 31(1):46-9doi:10.1016/j.ijantimicag.2007.08.014 · PMID 18023151

    In 42 Thai patients, single-dose ivermectin cured 76.2% vs 38.1% for 7 days of albendazole (intention-to-treat). The ivermectin used was a veterinary parenteral preparation given by mouth; one patient developed acute pustulosis. Small, open-label.

40. 40
    Buonfrate D, Salas-Coronas J, Muñoz J, Maruri BT, Rodari P, Castelli F, Zammarchi L, Bianchi L, Gobbi F, Cabezas-Fernández T, Requena-Mendez A, Godbole G, Silva R, Romero M, Chiodini PL, Bisoffi Z. Multiple-dose versus single-dose ivermectin for Strongyloides stercoralis infection (Strong Treat 1 to 4): a multicentre, open-label, phase 3, randomised controlled superiority trial.Lancet Infect Dis · 2019 · 19(11):1181-1190doi:10.1016/S1473-3099(19)30289-0 · PMID 31558376

    In 309 patients in Europe, four doses of ivermectin were no better than one (86% vs 85% cleared at 12 months) and were tolerated less well; the trial was stopped for futility, overturning the assumption that more doses help non-disseminated infection. It did not test severe or disseminated disease.

41. 41
    Fabara SP, Patel G, Jain N, Bishev D, Tama B, Caputi A, Zarrate D, Al-Tawfiq JA, Tirupathi R. Can Moxidectin Be an Anthelmintic Alternative for Trichuris trichiura and Strongyloides stercoralis: A Systematic Review.Cureus · 2022 · 14(7):e27074doi:10.7759/cureus.27074 · PMID 36000107

    Review noting that moxidectin is a long-established veterinary drug, now FDA-approved for human onchocerciasis, under study for other worms. Context for the moxidectin work; not a trial itself.

42. 42
    Henriquez-Camacho C, Pérez-Molina JA, Buonfrate D, Rodari P, Gotuzzo E, Luengo B, Plana MN. Ivermectin vs moxidectin for treating Strongyloides stercoralis infection: a systematic review.Parasitology · 2024 · 151(13):1466-1472doi:10.1017/S0031182024001215 · PMID 39819639

    Systematic review of the two ivermectin-vs-moxidectin trials (821 adults, Cambodia and Laos): moxidectin was non-inferior and as safe, moderate-quality evidence. Neither trial included immunocompromised, very young or very old patients, so moxidectin cannot yet be recommended for them.

43. 43
    Hofmann D, Smit C, Sayasone S, Pfister M, Keiser J. Optimizing moxidectin dosing for Strongyloides stercoralis infections: Insights from pharmacometric modeling.Clin Transl Sci · 2021 · 15(3):700-708doi:10.1111/cts.13189 · PMID 34889057

    Pharmacometric modeling suggests a single 8 mg dose of moxidectin plateaus cure near 87% in heavier infections, and proposes a two-dose regimen 3 weeks apart to catch the autoinfection cycle. Simulation, not a trial, and it frames autoinfection as the reason a single dose may not cure.

44. 44
    Taylor L, Many S, Jeanguenat H, Hattendorf J, Sayasone S, Keiser J. Efficacy and safety of ascending doses of emodepside in comparison with ivermectin in adults infected with Strongyloides stercoralis in Laos: a phase 2a, dose-ranging, randomised, parallel-group, placebo-controlled, single-blind clinical trial.Lancet Infect Dis · 2025 · 25(11):1254-1264doi:10.1016/S1473-3099(25)00255-5 · PMID 40580974

    Phase 2a dose-ranging trial in 202 adults in Laos: a single oral dose of emodepside, an anthelmintic repurposed from veterinary medicine, gave a predicted cure rate rising from 78.3% (95% CI 59.4-89.9) at 5 mg to a plateau of 89.1% (81.6-93.7) at 15 mg, against an observed 88.0% (68.8-97.5; 22 of 25) for single-dose ivermectin; the main adverse event was transient somnolence and no serious events occurred. An early-phase trial in a general adult population; funded by the European Research Council and the Uniscientia Foundation. Positions emodepside as a promising candidate, not an approved treatment.

45. 45
    Donadello K, Cristallini S, Taccone FS, Lorent S, Vincent JL, de Backer D, Jacobs F. Strongyloides disseminated infection successfully treated with parenteral ivermectin: case report with drug concentration measurements and review of the literature.Int J Antimicrob Agents · 2013 · 42(6):580-3doi:10.1016/j.ijantimicag.2013.07.015 · PMID 24269075

    A kidney-transplant recipient with disseminated disease who could not take oral drugs was cured with subcutaneous veterinary ivermectin; serum levels of 15.6-19.7 ng/mL worked, but accumulation above 40 ng/mL after stopping was linked to encephalopathy. One case; parenteral ivermectin is unlicensed for people.

46. 46
    Tobon Ramos JA, Maure T, Carias L, Lew D, Goss C, Samuel A, Tavul L, Fischer PU, Weil GJ, Laman M, Robinson LJ, Pomat W, King CL. Impact of mass drug administration with ivermectin, diethylcarbamazine, and albendazole for lymphatic filariasis on hookworm and Strongyloides stercoralis infections in Papua New Guinea.PLoS Negl Trop Dis · 2025 · 19(3):e0012851doi:10.1371/journal.pntd.0012851 · PMID 40063867

    Within a cluster-randomized trial, adding ivermectin to mass drug administration drove Strongyloides seroreversion in 49% of villagers at 12 months vs 23% without it. Shows the collateral benefit of ivermectin-containing programs; serology, not larvae, was the endpoint.

47. 47
    Grove DI. Human strongyloidiasis.Adv Parasitol · 1996 · 38:251-309doi:10.1016/s0065-308x(08)60036-6 · PMID 8701797

    Authoritative historical and clinical review, the standard source for the parasite's discovery: Louis Normand found the larvae in 1876 in French troops returning from Cochinchina with Cochin-China diarrhea, and Arthur Bavay named the worm the same year, with the free-living cycle and autoinfection established over the following decades. The PubMed record carries no abstract; the discovery date and names are corroborated by independent historical reviews.