Strongyloidiasis is an intestinal infection caused by 2 species of the parasitic nematode Strongyloides. The most common and clinically important pathogenic species in humans is S stercoralis (see the following image). S fuelleborni is found sporadically in Africa and Papua New Guinea. Distinctive characteristics of this parasite are its ability to persist and replicate within a host for decades while producing minimal or no symptoms (individuals with an intact immune system) and its potential to cause life-threatening infection (hyperinfection syndrome, disseminated strongyloidiasis) in an immunocompromised host (60-85% mortality rate).[1, 2, 3]

View Image

Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

The symptoms related to strongyloidiasis may reflect the nematode's systemic passage, its local cutaneous involvement, or both. During chronic uncomplicated infections, the larvae may migrate to the skin, where they can cause cutaneous strongyloidiasis, known as larva currens because of the quick migratory rate of the larva. Infection is clinically characterized by watery diarrhea, abdominal cramping, and urticarial rash. In malnourished children, strongyloidiasis remains an important cause of chronic diarrhea, cachexia, and failure to thrive.

This condition can also be a health consequence of captivity. During the World War II, allied military personnel held by the Japanese experienced deprivation, malnutrition, and exposure to tropical diseases.[4] Certain tropical diseases have persisted in these survivors, notably infections with S stercoralis, with studies 30 years or more after release documenting overall infection rates of 15%. Chronic strongyloidiasis may produce a linear urticarial larva currens rash, with such individuals at risk of fatal hyperinfection if immunity is suppressed.

Patient Education

Travelers to endemic areas should wear footwear when walking on the beach and other areas with soil. Community education in endemic areas should include sewage management, avoidance of soil contaminated with feces or use of feces for fertilizer, wearing of protective clothing when handling sewage or contaminated soil, and wearing of shoes while outdoors.


The life cycle of Strongyloides stercoralis is complex and unique among the intestinal nematodes. This worm has 2 types of life cycles—a free-living life cycle (rhabditiform larvae) and a parasitic life cycle (filariform infective larvae)—with 3 developmental stages: adult, rhabditiform larva, and filariform larva.

The first type of life cycle allows development of nonparasitic adults, both males and females, in the soil, which can indefinitely maintain infestation of the soil. This free-living phase is occasionally termed the heterogonic life cycle.

The second type of life cycle allows noninfective new larvae to molt in the human host into infective filariform larvae. Infective larvae can penetrate the intestine and set up a new cycle, commonly termed the hyperinfective or autoinfective cycle. In this setting, unlike in other intestinal nematodes of humans, the larvae can increase in numbers without reinfection from outside. This life-cycle variation is responsible for the decades-long persistence of infection in untreated hosts.

The adult female worm is a minute, slender, almost transparent worm that measures approximately 2.2-2.5 mm long and has a diameter of 50 µm. The adult female worm lives in tunnels between the enterocytes in the small bowel of humans.

A parasitic male exists, but it is found only in experimentally infected dogs and has no role in human infections. Parasitic males are shorter and broader than females and are easily eliminated from the intestine. Only adult females are found in infected humans.

Humans are the principal host of S stercoralis. Dogs, cats, and other mammals can also harbor the worm and may serve as reservoir hosts.

Stage 1

Human infection is acquired by penetration of the skin or mucous membranes by infective filariform larvae, either from autoinfection or from contact with infected soil or other material contaminated with human feces (fecal-oral route) (see the image below). This is facilitated by a potent histolytic protease that is secreted by the organism. At the portal of entry, the larvae cause petechial hemorrhages, which are accompanied by intense pruritus, congestion, and edema.

View Image

First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

The larvae migrate into the pulmonary circulation via the lymphatic system and venules. Larvae migrate up the pulmonary tree, where they are swallowed, and reach the GI system. In the intestine, S stercoralis can produce an inflammatory reaction and induce a malabsorption syndrome when it attaches to the mucosal folds.

Stage 2

Migration of infective larvae traditionally has been believed to occur via the lymphatic vessels and venules. These larvae reach the pulmonary circulation, where, once in the pulmonary capillaries, the larvae produce hemorrhages, which form the avenue of penetration into the alveolar space. An inflammatory response associated with eosinophilic infiltration follows, and the sequence of events that occurs in the lungs results in pneumonitis. The larvae migrate up the pulmonary tree, where they are swallowed (see the following image) and finally enter the intestine.

View Image

Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Stage 3

When they reach the small bowel, they molt twice and mature into adult females (2 mm × 0.05 mm in diameter). (All parasitic adult worms are female.) The parasitic females produce eggs via parthenogenesis. Each adult female may live up to 5 years and continue the reproductive cycle. Their eggs hatch into noninfective rhabditiform larvae within the intestine, which may then be passed through the stool into the environment, where they mature into adult males and females (see the image below). Compared with hookworms, adult Strongyloides organisms lie embedded in the intestinal folds. The traditional migratory pathway is now perceived to exist in conjunction with an equally significant direct migration from the skin to the duodenum.

Strongyloides is the only helminth to secrete larvae (and not eggs) in feces. Typically, larvae appear in feces approximately 1 month (about 28 days) after skin penetration, but the incubation period is unknown. As long as the patient is infected, which can be for several decades, the infection is communicable. The excreted rhabditiform larvae may again live freely in soil or be transformed into filariform larvae awaiting another human host. Alternatively, they may cause autoinfection.

View Image

Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.


Autoinfection involves premature transformation of noninfective larvae (rhabditiform, 0.25 mm × 0.015 mm) into infective larvae (filariform, 0.5 mm × 0.015 mm), which can penetrate the intestinal mucosa (internal autoinfection) or the skin of the perineal area (external autoinfection), thus establishing a developmental (parasitic) cycle within the host. Infection can be maintained by repeated migratory cycles for the remainder of the host’s life.

Millions of filariform larvae reach the skin by means of the circulation or direct invasion from body cavities; they can migrate through all levels of the dermis and involve the subcutaneous tissue. The infective filariform larvae reenter the circulation by 1 of 3 methods: (1) The larvae penetrate the mucosa of the colon and cause indirect endoautoinfection; (2) the larvae penetrate the mucosa of the upper small intestine and cause direct endoautoinfection; or (3) the larvae penetrate the perianal skin and cause exoautoinfection. The last method has been associated with the development of larva currens.

After entering the circulation, the larvae are carried to the lungs, where the cycle repeats itself. This mechanism accounts for the chronicity and frequent recurrence of the disease in patients who no longer live in areas in which the disease is endemic.

Autoinfection is kept in check by a normal host immune response. However, in patients with impaired cell-mediated immunity, autoinfection may give rise to the 2 most severe forms of strongyloidiasis: hyperinfection syndrome (stage 4) and disseminated strongyloidiasis (stage 5).

Stage 4

The pathophysiology that results from the hyperinfection cycle, which leads to dissemination in a compromised host, is not well understood. Patients receiving high-dose corticosteroids[5] or patients with human T-cell lymphotrophic virus type I (HTLV-I) are at particularly increased risk.

Hyperinfection syndrome represents an acceleration of the normal life cycle of S stercoralis, leading to excessive worm burden without the spread of larvae outside the usual migration pattern (eg, gastrointestinal tract, lungs) (see the following image). The larvae do not exit the host in feces and instead molt into the infective filariform larva within the intestinal lumen. These larvae are then capable of penetrating the bowel wall and traveling throughout the body.

View Image

Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Stage 5

Disseminated strongyloidiasis involves widespread dissemination of larvae to extraintestinal organs (eg, central nervous system [CNS], heart, urinary tract, endocrine organs), which are outside the realm of the parasite's ordinary life cycle (see the image below). All organs and tissues may be invaded, along with the small intestine. In these severe forms, translocation of enteric bacteria may occur, leading to polymicrobial bacteremia and occasionally meningitis with enteric pathogens. The enteric pathogens may be carried on the filariform larvae or may enter the circulation through intestinal ulcers. The CNS, liver, and lungs are the most common destinations of the autoinfectious larvae.

View Image

Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.


Strongyloidiasis is caused by the nematode (roundworm) Strongyloides stercoralis. The genus Strongyloides is classified in the order Rhabditida, and most members are soil-dwelling microbiverous nematodes. Most of the 52 species of Strongyloides do not infect humans. S stercoralis is the most common human pathogen. Other species include S myopotami and S procyonis. These species have animal hosts and are thus responsible for zoonotic infections.[6]

Infections are initiated when exposed skin contacts contaminated soil. Autoinfection commonly occurs allowing infection to persist decades. The longest documented asymptomatic infection was more than 65 years. Hyperinfection is typically triggered by drug-induced or disease-associated defects in cellular immunity, which allows a massive increase in parasite burden and dissemination to nearly all organ systems.

Risk factors for severe strongyloidiasis include the following:

No evidence exists of direct person-to-person transmission in a household. Strongyloides larvae have been detected in the milk of mothers with chronic infection, suggesting vertical transmission. Evidence in dogs also shows transmission in breast milk.[17] No studies indicating transmammary transmission in humans exist. Cadaveric donors of renal transplants have been implicated as sources of fatal hyperinfection syndromes in transplant recipients.[18]

Zoonotic infections by Strongyloides species are similarly contracted by contact with sand or soil that contains infected animal droppings, including feces from raccoons and nutria. Infections are reported among veterinarians and laboratory workers who work in temperate climates and are exposed to larvae from horses. Zoonotic forms of Strongyloides infection can also produce creeping skin eruptions identical to those of S stercoralis infection.


United States statistics

The true prevalence of S stercoralis is likely underestimated, because infection is often subclinical. Strongyloidiasis is uncommon in the United States, although endemic foci exist in rural areas of the southeastern states and the Appalachia region (especially in eastern Tennessee, Kentucky, and West Virginia) and Puerto Rico,[19] with prevalence rates close to 4%. Populations in whom strongyloidiasis is more prevalent include patients in long-term institutionalized care (mental health facilities, prisons), immigrants or refugees from tropical and subtropical countries (eg, Southeast Asia, Africa, Middle East),[20] and persons who were stationed in Southeast Asia during World War II[21] and the Vietnam War.

In one study, Southeast Asian immigrants living in Washington, DC, were found to have a 38% incidence of infection.[22] Similarly, a Canadian epidemiology study of Southeast Asian immigrants to Canada demonstrated infection in 11.8% in the Vietnamese population and a 76.6% seroprevalence in Cambodian immigrants.[23] Sudanese Lost Boys and Girls and Somali Bantu refugees demonstrated 46% and 23% respective seropositive rate.[24] Five percent of Vietnam veterans reporting mild symptoms demonstrated S stercoralis infection.

Infections acquired in the United States, while not usually associated with larva currens, are not clinically silent; the infected individuals usually have a chronic relapsing illness of mild to moderate severity. Among veterans of the US military forces who served in Southeast Asia, the prevalence of larva currens in those with confirmed strongyloidiasis is high, with studies showing a range of 30% to 90%.[25, 26]

International statistics

Globally, prevalence rates of strongyloidiasis are as high as 40% in certain areas where suitably moist soil and improper disposal of human waste coexist, especially West Africa, the Caribbean, and Southeast Asia, as well as Colombia, tropical sections of Brazil, and temperate sections of Spain.[27, 28] The disease is estimated to affect 100-200 million people worldwide in 70 countries.

The international prevalence of larva currens among patients with strongyloidiasis varies, with rates in the range of 30-90% in Southeast Asia. High rates of larva currens are also reported in Latin America. A stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found strongyloidiasis due to S stercoralis in the stool of 69 (8.7%) of 792 participants.[29]

Racial and age differences in incidence

No racial predilection is apparent for Strongyloides infection; however, Southeast Asia appears to have the highest endemic percentage, and it is highly prevalent in some tropical Aboriginal communities in Australia.[30] Larva currens is most frequently seen in white patients with an infection acquired in Southeast Asia.

Although Strongyloides infection is represented in all ages, infection may most frequently initially occur in childhood, as children are most likely to play outdoors in contaminated soil with bare feet.[31] Advanced age is also a risk factor for severe strongyloidiasis, because it may be associated with an immunosuppressed state.


Acute and chronic strongyloidiasis carry a good prognosis in immunocompetent hosts. However, untreated infection can persist for the remainder of the patient's life because of autoinfection. Most immunocompetent individuals who develop strongyloidiasis have asymptomatic chronic infections that result in negligible morbidity. A patient's prolonged absence from an endemic area is no guarantee of freedom from infection.

Severe strongyloidiasis (hyperinfection syndrome and disseminated strongyloidiasis) carries a high mortality rate (up to 80%) because the diagnosis is often delayed. This relates to its nonspecific presentation and the host's immunocompromised status. Death from Strongyloides infection is typically iatrogenic and frequently occurs after an asymptomatic infected person is treated with immunosuppression.[32] Gram-negative sepsis is a common consequence of hyperinfection and carries a 50% mortality rate.[33] Disseminated strongyloidiasis may be relatively common in high-risk populations and may be frequently misdiagnosed as isolated gram-negative sepsis or acute respiratory distress syndrome.

(See Complications under Clinical.)

History and Physical Examination

The clinical manifestations of Strongyloides infections vary, depending on the acuity of infection and the underlying host response.[34] The vast majority of patients with strongyloidiasis have uncomplicated disease. As many as 50% of patients remain asymptomatic and can survive decades undiagnosed.

Symptomatic infections typically manifest in gastrointestinal, pulmonary, and dermatologic systems. Patients who become symptomatic do so shortly after exposure, or they develop late symptoms. Severe symptoms may develop and death may ensue, especially in individuals who are immunocompromised.

Acute infection is generally characterized by gastrointestinal (GI) and pulmonary symptoms, whereas chronic infection is characterized by skin involvement.

Severe strongyloidiasis (hyperinfection, disseminated disease) may be insidious; occasionally, symptoms may have an abrupt onset. Fever is almost always present in disseminated disease.[35] Invasion of larvae into tissue is potentially massive. As a result, patients present with an exaggeration of the symptoms of established infection found in patients who are immunocompetent. In addition, as larvae penetrate the intestinal wall, they may allow enteric flora to escape, causing bacteremia, sepsis, meningitis, and endocarditis. Thus, a diagnosis of severe strongyloidiasis should be suspected with unusual GI or pulmonary symptoms or an unexplained Gram-negative bacilli sepsis.

Gastrointestinal manifestations

Gastrointestinal symptoms are vague, including epigastric abdominal cramping, indigestion, anorexia, weight loss, nausea, vomiting, chronic diarrhea, constipation, pruritus ani, bloating and, rarely, small bowel obstruction. Strongyloides is an important cause of failure to thrive and cachexia in immunocompetent children.

In classic cases, diarrhea is profuse, watery, and mucoid. Periods of alternation between diarrhea and constipation may occur. Malabsorption of fat and vitamin B-12 has been reported in chronic infections and has been successfully treated by deworming.

Prolonged malabsorption of both fat and protein can lead to a celiac-like syndrome, characterized by steatorrhea, hypoalbuminemia, and peripheral edema, such as a syndrome of infantile infection caused by S fulleborni described in western Papua New Guinea. These children have diarrhea that becomes protracted in the first months of life, respiratory distress, failure to thrive, protein-losing enteropathy, and a kwashiorkor-like appearance (with ascites and pleural effusions) due to hypoalbuminemia ("swollen baby" sickness).

In severe hyperinfection syndrome or disseminated disease, abdominal symptoms are similar to those of chronic infection, but they are more severe. Gut flora invade host tissues either through penetration of infective larvae from bowel lumen or through damaged intestinal epithelium. Escherichia coli and Klebsiella species are the most common organisms involved. Bloody stools and/or blood diarrhea may occur along with severe abdominal pains. Massive GI tract bleeding has also been reported.[36]

Pulmonary manifestations

Symptomatic pulmonary strongyloidiasis that results from migrating larvae is observed in 10% of patients. Initial infection may trigger wheezing[37] and mild cough.

Migration of the larvae through the lungs produces a pneumonitis that resembles Loeffler syndrome. Symptoms include a productive cough, at times with blood-streaked sputum, dyspnea, and fever. Strongyloidiasis can also produce a clinical syndrome that mimics either asthma or pneumonia.

In severe (disseminated) disease, pneumonitis may cause hemoptysis and difficulty in breathing. In addition, cough, hemoptysis, dyspnea, wheezing, pleuric pain, tachypnea can occur, and acute respiratory distress syndrome (ARDS) may require mechanical ventilation.

Dermatologic manifestations

Skin penetration by infective larvae can elicit ground itch, a cutaneous eruption of pruritic papulovesicular lesions. Typically, skin penetration is on the feet but may be at any site that contacted infected soil (eg, around the anus [within 12 cm] or anywhere on the trunk and thighs).

Larva currens (racing larvae), the pathognomonic rash of Strongyloides infection, is an intensely pruritic linear or serpiginous urticarial rash that may consist of 1 or more such bands and creeps 5-15 cm/h up the body. The rash, likely an allergic response to the migrating filariform larvae, often manifests as a pruritic wheal or linear urticaria. This dermatologic manifestation may last hours to days but in autoinfection cycles can recur over weeks, months, and years. In an individual who has already been sensitized, a second, creeping, urticarial rash may appear, which is caused by an allergic reaction to the larvae penetrating the skin. Excoriation and impetigo are common.

Rarely, in disseminated strongyloidiasis, a rapidly progressive, diffuse, petechial purpuric eruption may be present secondary to vessel injury during larval migration.[38] Characteristic purpuric periumbilical skin lesions should raise the suspicion for its diagnosis; it often portends a fatal outcome in cancer patients.[39] There have also been case reports of multiple atypical dermatologic presentations in hyperinfection cases.[40]

Neurologic and other manifestations (severe strongyloidiasis)

An altered mental status, focal seizures, meningitis, brain abscess or nuchal rigidity may indicate central nervous (CNS) involvement. Symptoms of meningitis may include headache, nausea, vomiting, and, in extreme cases, coma.

Granulomatous hepatitis and parasitic invasion of the heart, kidney, peritoneum, lymph nodes, pancreas, prostate, ovaries, thyroid, or parathyroid may be present in disseminated disease.

A case report demonstrated infertility as a presentation for disseminated strongyloidiasis with larvae found in ejaculate and conception occurring after treatment. Another patient experienced years of recurrent abdominal pain and fever with recurrent eosinophilic oophoritis who had positive Strongyloides serology and clinical response to treatment.[41]


Strongyloidiasis can lead to gastrointestinal (GI), pulmonary, dermatologic, neurologic, and other complications, as well as death.

GI complications include the following:

GI hemorrhage: Life-threatening GI bleeding has been described in a patient with hyperinfection syndrome; the bleeding was found to be from microaneurysms ("berry aneurysms") in the superior and inferior mesenteric arteries

Pulmonary complications include the following:

Dermatologic complications include larva currens, purpura of the trunk and proximal extremities, and chronic urticaria.

Neurologic complications include meningitis due to enteric bacteria and brain abscess.

Vascular complications include hyperinfection syndrome presenting as bacteremia (occasionally recurrent) due to enteric microorganisms (eg, Escherichia coli, Klebsiella pneumoniae, Enterococcus species including vancomycin-resistant E faecium, Streptococcus bovis).

Renal complications can rarely include nephrotic syndrome[44] (eg, minimal-change nephrotic syndrome[45] ). Resolution of the proteinuria occurs after administration of antihelmintic therapy with ivermectin. Incidence of nephrotic syndrome in children in the developing world is increased in those with underlying strongyloidiasis.[46] In addition, the syndrome of inappropriate antidiuretic hormone (SIADH) has been observed in patients with severe Strongyloides infection.[47]

Rarely, a musculoskeletal complication such as reactive arthritis may occur.

Approach Considerations

Identify patients at risk for strongyloidosis, and perform appropriate diagnostic tests before they begin immunosuppressive therapy. Search for S stercoralis larvae before initiating immunosuppression in anyone who has traveled to an endemic area, even if it was decades earlier.[7]

In patients with an appropriate geographic history, rule out strongyloidiasis by means of thorough evaluation, including several stool examinations for ova and parasites, special larvae detection techniques, and/or serology in all transplant candidates or others who are likely to receive a prolonged course of steroids or other immunosuppressive medications. Complete eradication of the parasite before the initiation of immunosuppressive therapy is essential in patients with uncomplicated infections to ensure that hyperinfection syndrome does not develop. In general, falling eosinophilia and Strongyloides antibody titers are indications of successful treatment.

Hematologic Studies

The white blood cell (WBC) count is usually within the reference range in acute and chronic strongyloidiasis; it is often elevated in severe strongyloidiasis. Peripheral leukocytosis may occur in the early stages of the infection.

Peripheral eosinophilia (>600/mL) probably represents an immune response to larvae migrating through host tissues. This finding is common during acute infection (10-40% to as high as 75-80%), intermittent during chronic infection (often the only abnormal laboratory test result), and frequently absent in severe strongyloidiasis and in the immunocompromised host. A normal eosinophil count with an untreated known Strongyloides infection may be a poor prognostic sign.

Severe infection may be associated with anemia, thrombocytopenia, and a prolonged prothrombin time (PT) because of decreased levels of clotting factors.

Obtain blood cultures in all patients in whom Strongyloides infection is suspected, because enteric pathogens often cause coinfection, most commonly Escherichia coli and Klebsiella species.

Microscopy and Culture of Stool for Ova and Parasites

Strongyloides larvae are secreted in feces and excretion may be intermittent, releasing as few as 50 eggs per day.[52] This can complicate identification. Larvae are seen in stool approximately 1 month after skin penetration. Unlike the eggs of other parasitic nematodes, the eggs of S stercoralis are not usually found in the feces; instead, they embryonate within the intestine and develop into larvae, which are deposited in the soil. Ova are almost never observed during a strongyloidiasis infection unless severe diarrhea occurs; results from this examination are typically negative during acute infection.

Children with S fuelleborni infection shed eggs rather than larvae in the feces, and the infection is easily diagnosed using microscopic techniques.


Microscopically identify Strongyloides stercoralis larvae (definitive diagnostic test). The larvae resemble those of hookworms, but they can be distinguished by their short buccal cavity.

Examine stool directly in wet mounts (very low yield) (see the image below) or after ethyl acetate-formalin concentration occurs.

View Image

Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

Several fresh stool specimens may need to be examined before a positive result is found. Single stool examination yields a low sensitivity (approximately 30%) in chronic strongyloidiasis, because larval output is low and intermittent. Thus, perform at least 3 stool examinations on consecutive days, because this may increase the sensitivity to 70-80%. More than 90% sensitivity for stool samples is seen if 7 or greater samples are examined.


Several specialized stool culture techniques have been advanced that exploit the ability of S stercoralis to enter a free-living cycle of development. In all of these methods, fecal material is cultured in a vessel for approximately 1 week, during which filariform larvae crawl out of the stool suspension.[28]

Enhance larvae recovery by using special methods such as the Baermann funnel method (larvae migrate from stool samples to warmed water and are detected in the centrifuged fluid), the Harada-Mori filter paper method (stool is spread onto a filter paper strip and cultured in a test tube containing a little water; filariform larvae appear in the water after 7-10 d), and the agar plate method, when needed. The modified agar plate method appears to be the most sensitive and efficient method.

Charcoal fecal culture (26°C) for 1 week, using the Baermann concentration method, is best for detecting hatched larvae. However, the availability of this cumbersome test in clinical practice is highly variable. False-positive test results can occur in patients with hookworm infection.


Serodiagnosis can be helpful but is not readily available, and false-negative results may occur. Several immunodiagnostic assays have been developed, including skin testing with larval extracts, indirect immunofluorescence using killed larvae, filarial complement fixation testing, indirect agglutination testing, radioallergosorbent testing for specific immunoglobulin E (IgE) (total serum IgE level is usually elevated), gelatin particle indirect agglutination (GPIA), Western blot analysis, enzyme-linked immunosorbent assay (ELISA) for IgG antibodies and immunoprecipitation technique combined with a recombinant antigen.[53]

Often, establishing a diagnosis and confirming a cure of strongyloidiasis is difficult. Strongyloides -specific antibody levels may be used for serologic follow-up for strongyloidiasis.[54] They may indicate reversion to negative serostatus after successful ivermectin therapy, which is frequent.


A stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found the ELISA test had a negative predictive value of 98% and is an excellent screening test for strongyloidiasis.[29] With the greatest accuracy for diagnosis of strongyloidiasis,[55] ELISA testing has been shown to detect the disease in approximately 85-90% of patients (82-95% sensitivity[56] ). However, its sensitivity may be lower in severely immunocompromised patients or in those with HTLV-1 infection, and ELISA cannot be used to differentiate between past and present infection, making the test less helpful in endemic areas. In addition, the anti-strongyloides antibody can persist for years even after successful treatment. In patients with eosinophilia, Strongyloides serology may be helpful.[57]

If ELISA results are positive, continue efforts to establish a parasitologic (microscopic) diagnosis because of cross-reactivity with other nematode infections (8-16%). This test is also useful for monitoring a patient's response to therapy (antibody titers decrease markedly within 6-12 mo of successful therapy).

ELISA can be performed at the National Institutes of Health (Laboratory for Parasitic Diseases) and the Centers for Disease Control and Prevention (CDC). The reliability of some serologies run by commercial laboratories is variable.

Other assays

A study of an anti-Strongyloides IgG enzyme immunoassay (EIA) showed it to be rapid and easy to perform, and it may be a good option when a parasitologic stool examination is negative, as well as in immunosuppressed patients.[58]

S stercoralis–specific recombinant antigens such as 31-kDa recombinant antigen (NIE) and S stercoralis immunoreactive antigen (SsIR) can help overcome the limitations of antibody-based assays.[59] A luciferase immunoprecipitation systems assay has been described, which may eventually prove to be more accurate than existing ELISA testing.[60, 61]

Polymerase chain reaction (PCR) on stool specimens has also been described but is currently under investigation.[61, 62, 63] A 2018 systematic review found that nucleic acid amplification tests have a sensitivity of 71% and a specificity of 93%.[64]

In a study that evaluated gelatin particle agglutination test (GPAT) and ELISA results in endemic regions of Thailand, the GPAT was judged to be more practical for screening for strongyloidiasis than the conventional ELISA.[65]

Radiologic Studies


Obtain a chest radiograph to reveal possible patchy alveolar infiltrates in acute strongyloidiasis. In severe strongyloidiasis, findings are diverse; the chest radiograph may depict diffuse interstitial infiltrates, segmental or diffuse alveolar infiltrates, or pleural effusions. In severe cases, bronchopneumonia (either segmental or lobar opacities) may be seen. In these patients, clinical progression to acute respiratory distress syndrome may occur. Occasionally, pulmonary effusions may occur. Lung cavitation and abscesses have been described in association with secondary bacterial infection.

A plain abdominal radiograph may reveal loops of a dilated small bowel, or ileus, in severe strongyloidiasis; other findings may include duodenal edema, with loss of the mucosal pattern; ulcerations; strictures; rigidity, and tubular narrowing. The strictures and ulcerations may mimic inflammatory bowel disease.

Barium swallow and barium enema findings may be normal, may exhibit bowel dilatation, or may indicate stenosis with ulceration.

CT scanning

Obtain a computed tomography (CT) scan of the abdomen and pelvis to reveal any nonspecific thickening of the bowel wall.

Pulmonary CT scans may reveal fine miliary nodules or diffuse reticular interstitial opacities. Pulmonary infiltrates in disseminated strongyloidiasis. These infiltrates consist of foci of hemorrhage, pneumonitis, and edema.

Endoscopy and Histologic Features

Findings from upper and lower gastrointestinal endoscopy may range from normal-appearing mucosa to severe duodenitis and colitis. The most common abnormal duodenal endoscopic finding is edematous mucosa, white villi, and erythematous mucosa. In some cases, the larvae are identified with duodenal biopsy.[66]

Duodenal biopsy histopathologic examination identified larvae in 71.4% of immunosuppressed patients.[66] Thus, in addition to stool analysis, endoscopic observation and biopsies are very important.[67]

Strongyloides stercoralis larvae are typically found in the proximal part of the small intestine, embedded in the mucosal lamina propria, where they produce mild to moderate degrees of edema, cellular infiltration, partial villous atrophy, and, occasionally (in severe strongyloidiasis), ulcerations. In long-standing infections, fibrosis may develop.

Entero-Test (String Test) and Duodenal Aspiration

This test offers than simple stool examination.

Conduct an Entero-Test (string test) or a duodenal aspiration to examine duodenal fluid for Strongyloides species larvae. These tests produce a higher likelihood of larval recovery than a stool examination. However, results may be negative if larvae are located too far down in the lower intestine. The reported sensitivity ranges from 40% to 90%.

The Entero-Test capsule consists of a textured string within a gelatin capsule. One end of the string is taped to the cheek and the capsule is swallowed; after several hours or overnight, the terminal portion of the string ideally unravels into the duodenum. If it does, the end of the string should be bile stained, and mucous secretions can be wiped onto a slide using gloved hands. Examination of the slide should reveal larvae.

Sputum and CSF Examination, Bronchial Washing, and BAL

In hyperinfective and disseminated Strongyloides infection, larvae can be recovered from extraintestinal sites, including sputum, bronchoalveolar fluid, and in some cases, cerebrospinal fluid (CSF), urine, semen, ascites, gastroesophageal biopsy, and skin biopsy. In these cases, sputum examinations, bronchial washings, and bronchoalveolar lavages (BALs) frequently reveal filariform and/or rhabditiform larvae.

When observing the agar plate of sputum cultures, the microorganisms that are part of the normal respiratory flora may be found outside the area of streaking as groups of colonies arranged in a characteristic pattern. This laboratory phenomenon is a result of migrating larvae on the agar plates, and, in an appropriate clinical setting, is considered diagnostic of S stercoralis infection.

Perform a lumbar puncture if central nervous system (CNS) involvement is suspected. Perform CSF analysis (elevated protein levels, decreased glucose levels, pleocytosis with neutrophilic predominance) to evaluate for acute bacterial meningitis. A Gram stain may exhibit gram-negative rods or, rarely, gram-positive cocci in chains (Enterobacteriaceae, Streptococcus species). A wet mount preparation may reveal S stercoralis larvae.

Skin Biopsy

In acute or chronic infection, skin biopsy is usually neither necessary nor sufficient, because parasites are rarely visualized. When they are, speciation is difficult.

In severe infection, skin biopsy may be useful, because filariform larvae are often observed. Larvae can be observed in all levels of the dermis and occasionally in the subcutis. Obtain specimens from the purpuric eruptions, because these areas contain the largest amount of larvae.

Other findings include edema, extravasated red blood cells (RBCs), and some lymphocytes in the superficial dermis. The larvae range in size from 9 to 15 µm and contain a triradiate digestive tract.

Approach Considerations

All persons found to harbor Strongyloides organisms should be treated, even if they are asymptomatic, because of the risk of hyperinfection. However, for infected pregnant patients, clinicians may prefer to defer treatment for strongyloidiasis until after the first trimester. All of the anthelmintic medications discussed in this article are US Food and Drug Administration (FDA) category C agents.

Strongyloides species are the hardest worms to eradicate. Treatment of early infection is with symptomatic support, because specific therapy is more effective once intestinal infection is established. Posttherapy stool examinations at 6 and 12 months posttreatment are recommended to verify Strongyloides eradication and to exclude other parasitic infections.[68] A posttreatment/pretreatment ratio of 0.6 or less suggests successful treatment. Patients with hyperinfection should undergo multiple followup stool examinations starting at two weeks posttreatment.[69]

Empiric corticosteroid administration used to treat wheezing is problematic, because it may cause life-threatening hyperinfection. Thus, Strongyloides hyperinfection syndrome, usually precipitated by immune suppression, should be considered in patients who have resided in endemic regions.[70] Attempts at the detection and eradication of this infection are recommended to prevent this potentially fatal complication.

Surgical intervention may be required in the rare instance of acute abdominal symptoms (peritonitis) due to bowel obstruction or infarction in the context of severe strongyloidiasis.

Intensive care and transfer

Immunocompromised hosts may require hospitalization and intensive care in disseminated infection. Consider contact isolation in these patients, because sputum, stool, vomitus, and other bodily excreta may contain infective (filariform) larvae.

Patients with hyperinfection syndrome often have complications of sepsis, shock, and acute respiratory distress syndrome (ARDS). Any patient suspected of disseminated disease should receive care in a facility properly equipped for intensive management.

Anthelmintic Therapy

Strongyloides infection should be suspected in a patient with nonspecific gastrointestinal, respiratory, or recurrent dermatologic symptoms of unclear etiology with risk factors for Strongyloides infection. Conduct definitive treatment with anthelmintic drugs, although these medications target adult worms and are not very effective against larvae in the initial infection.

Strongyloides infections should be treated even in the absence of symptoms as hyperinfection syndrome carries a high mortality rate. Disseminated strongyloidiasis requires treatment for at least 7 days or until the parasite can no longer be identified in clinical specimens. Concomitant infections should be treated aggressively, and any immunosuppressants, including exogenous corticosteroids, should be quickly tapered.[71] Corticosteroid therapy must be avoided, because hyperinfection and death may occur.

Anthelmintic treatment may have to be repeated or the duration prolonged in patients with hyperinfection syndrome. Relapses may occur despite proper therapy.

Anthelmintic agents

For acute and chronic strongyloidiasis, the CDC recommends ivermectin 200 μg/kg orally for 1-2 days as first-line therapy. Relative contraindications include concomitant Loa loa infection, weight less than 15 kg, pregnancy, and breastfeeding. Alternatively, albendazole 400 mg orally twice a day for one week can be given. Relative contraindications include hypersensitivity to benzimidazole compounds and first trimester of pregnancy.[72] A 2016 review of 7 trials found that ivermectin was more efficacious than albendazole and better tolerated than thiabendazole. Cure rates for ivermectin, albendazole, and thiabendazole were 74%-84%, 48%, and 69%, respectively. The main issue with thiabendazole was GI side effects.[73]

Patients with hyperinfection and disseminated disease should be treated with ivermectin 200 μg/kg per day orally until stool and/or sputum examination findings are negative for 2 weeks. Rectal administration is recommended for patients with malabsorption or who are unable to tolerate oral therapy. Every effort should be made to reduce or stop immunosuppressants in these patients.[72]

Patients in whom treatment fails to elicit a response should undergo screening for HTLV-1 infection.[74]

Antibiotic Therapy and Supportive Care

Provide antibiotic therapy directed toward enteric pathogens if bacteremia or meningitis is present or suggested; treat such bacterial complications for 2-4 weeks with antibiotics according to the results of in vitro testing against the bacterial isolate(s).

Provide supportive treatment as indicated (eg, intravenous fluids if volume depletion, blood transfusion if gastrointestinal or alveolar hemorrhage, mechanical ventilation if respiratory failure). Symptomatic treatment should be initiated. Pruritic dermatologic manifestations should be treated with antihistamines. Inhaled beta-agonists may improve wheezing; steroids should be avoided as they will worsen the infection. The use of leukotriene synthesis inhibitors for wheezing may also worsen infection, because leukotrienes are shown to play a potential role in the immunity against Strongyloides infection.

Medication Summary

The goals of pharmacotherapy in strongyloidiasis are to eradicate the infection, reduce morbidity, and prevent complications.

Several anthelmintic drugs are available for established infection. Thiabendazole was a therapeutic option for strongyloidiasis but has been discontinued. Albendazole and mebendazole have been used in patients with Strongyloides stercoralis infection, but results have varied. Ivermectin has been shown to be more effective than albendazole.

Patients with hyperinfection and disseminated disease should be treated with ivermectin. For those too sick to tolerate or absorb oral (PO) ivermectin, rectal (PR) or subcutaneous (SC) dosing may be effective.[75] In these patients, ivermectin should be administered daily until symptoms have resolved and larvae have not been detected for at least 2 weeks.

More information regarding the medications listed in this section may be obtained from The Centers for Disease Control and Prevention (CDC) as follows (contact information updated in November 2015):

CDC Drug Service

1600 Clifton Road, MS/D09

Atlanta, GA 30333

Telephone: (404) 639-3670

Fax: (404) 639-3717



Ivermectin (Stromectol, Mectizan)

Clinical Context:  Ivermectin is the drug of choice (DOC) for acute and chronic strongyloidiasis in intestinal stages, hyperinfection syndrome, and disseminated strongyloidiasis. This drug has not been studied extensively in children, and it has been used as an adjuvant in patients with hyperinfection not responding to thiabendazole.

Ivermectin is a semisynthetic derivative of the macrolide mold product avermectin that binds selectively to glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, thereby increasing the permeability of the cell membrane with hyperpolarization and causing paralysis and cell death.

Its half-life is 16 hour, and it is metabolized in the liver. The cure rate is 97% with 2-day course. Case reports have been made of successful SC injection of ivermectin in patients unable to achieve adequate serum drug levels after PO administration.

Albendazole (Albenza)

Clinical Context:  Albendazole is an alternative to ivermectin for the treatment of acute and chronic strongyloidiasis. This agent has high-affinity binding to free beta-tubulin in parasite cells—thereby inhibiting tubulin polymerization, which results in loss of cytoplasmic microtubules—and decreases ATP production in the worm, causing energy depletion (by inhibiting glucose uptake), immobilization, then death. To avoid an inflammatory response in central nervous system (CNS), administer albendazole with anticonvulsants and high-dose glucocorticoids.


Clinical Context:  Mebendazole has variable efficacy against strongyloidiasis. This agent inhibits microtubule formation and causes worm glucose depletion and is available in chewable form for pediatric use.

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses. The effectiveness of anthelmintic agents against larvae is poor; they are more effective once established infection occurs.

What is strongyloidiasis?What education is indicated for people at risk for strongyloidiasis?What is the pathophysiology of strongyloidiasis?What is the pathophysiology of stage 1 of the Strongyloides stercoralis life cycle in strongyloidiasis?What is the pathophysiology of stage 2 of the Strongyloides stercoralis life cycle in strongyloidiasis?What is the pathophysiology of stage 3 of the Strongyloides stercoralis life cycle in strongyloidiasis?What is autoinfection in stage 3 of the life cycle of Strongyloides stercoralis in strongyloidiasis?What is the pathophysiology of stage 4 of the Strongyloides stercoralis life cycle in strongyloidiasis?What is the pathophysiology of stage 5 of the Strongyloides stercoralis life cycle in strongyloidiasis?What causes strongyloidiasis?What are the risk factors for severe strongyloidiasis?Can strongyloidiasis be transmitted from one person to another?How are zoonotic infections by Strongyloides species (strongyloidiasis) transmitted?How common is strongyloidiasis in the US?What is the international prevalence of strongyloidiasis?What are the racial and age differences in the incidence of strongyloidiasis?What is the prognosis of strongyloidiasis?What are the clinical manifestations of strongyloidiasis?What are the GI symptoms of strongyloidiasis?What are the pulmonary signs and symptoms of strongyloidiasis?What are the dermatologic manifestations of strongyloidiasis?What are the neurologic and other manifestations of strongyloidiasis?What are the GI complications of strongyloidiasis?What are the pulmonary complications of strongyloidiasis?What are the dermatologic, neurologic, vascular, renal, and musculoskeletal complications in strongyloidiasis?What are the diagnostic considerations in strongyloidiasis?What are the differential diagnoses for Strongyloidiasis?What are the approach considerations in the workup of strongyloidiasis?What are the hematologic findings in strongyloidiasis?What are stool exam findings in strongyloidiasis?What are the microscopy findings in the workup of strongyloidiasis?What stool culture techniques are available for the workup of strongyloidiasis?Which immunodiagnostic assays are used in the workup of strongyloidiasis?What is the role of ELISA testing in the workup of strongyloidiasis?What are the assay findings in strongyloidiasis?What are the radiographic findings in strongyloidiasis?What are the CT findings in strongyloidiasis?What are the endoscopic and histologic features of strongyloidiasis?What is the role of a string test (Entero-Test) or duodenal aspiration test in the workup of strongyloidiasis?What is the role of fluid analysis in the workup of strongyloidiasis?What is the role of a skin biopsy in the workup of strongyloidiasis?What are the approach considerations in the treatment of strongyloidiasis?When is intensive care or transfer indicated in the treatment of strongyloidiasis?What is the role of anthelmintic agents in the treatment of strongyloidiasis?Which anthelmintic agents are indicated in the treatment of strongyloidiasis?What is the role of antibiotic therapy and supportive care in the treatment of strongyloidiasis?What is the goal of medication in the treatment of strongyloidiasis?What are the resources for information on medications used for the treatment of strongyloidiasis?Which medications in the drug class Anthelmintics are used in the treatment of Strongyloidiasis?


Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.


Claudia D Jarrin Tejada, MD, Assistant Professor, Division of Infectious Diseases, Wayne State University Physician Group, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Additional Contributors

Hari Polenakovik, MD, FACP, FIDSA, Professor of Medicine, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.

Sylvia Polenakovik, MD, Internist, Department of Internal Medicine, Sycamore Hospital; Internist, Miami Valley Hospitalist Group, MVH; Clinical Instructor, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.


Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Ramesh A Bharadwaj, MD, Fellow in Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Emily Anne Carpenter Rose, MD, Fellow in Pediatric Emergency Medicine, Loma Linda University School of Medicine

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology

Disclosure: Lippincott Williams Wilkins Royalty Textbook editor; DLA Piper Consulting fee Consulting

Wesley W Emmons, MD, FACP Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE

Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

Ashir Kumar, MD, MBBS, FAAP, Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Disclosure: Nothing to disclose.

Mark Louden, MD, FACEP Assistant Medical Director, Emergency Department, Duke Raleigh Hospital

Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Antonio Muñiz, MD Professor of Emergency Medicine and Pediatrics, University of Texas Medical School at Houston; Medical Director of the Pediatric Emergency Department, Children's Memorial Hermann Hospital

Antonio Muñiz, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Medical Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Allison J Richard, MD Assistant Professor of Emergency Medicine, Keck School of Medicine, University of Southern California; Associate Director, Division of International Medicine; Attending Physician, Los Angeles County-University of Southern California Hospital Emergency Department

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mordechai M Tarlow, MD Clinical Associate, Department of Dermatology, University of Pennsylvania School of Medicine

Mordechai M Tarlow, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for MOHS Surgery, American Society of Cosmetic Dermatology and Aesthetic Surgery, and Sigma Xi

Disclosure: Nothing to disclose.

Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist

Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Eric L Weiss, MD DTM&H, Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Professor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.


  1. Arsic-Arsenijevic V, Dzamic A, Dzamic Z, Milobratovic D, Tomic D. Fatal Strongyloides stercoralis infection in a young woman with lupus glomerulonephritis. J Nephrol. 2005 Nov-Dec. 18(6):787-90. [View Abstract]
  2. Weller PF, Leder KL. Strongyloidiasis. Available at Accessed: January 29, 2008.
  3. Asdamongkol N, Pornsuriyasak P, Sungkanuparph S. Risk factors for strongyloidiasis hyperinfection and clinical outcomes. Southeast Asian J Trop Med Public Health. 2006 Sep. 37(5):875-84. [View Abstract]
  4. Robson D, Welch E, Beeching NJ, Gill GV. Consequences of captivity: health effects of far East imprisonment in World War II. QJM. 2009 Feb. 102(2):87-96. [View Abstract]
  5. Fardet L, Généreau T, Poirot JL, Guidet B, Kettaneh A, Cabane J. Severe strongyloidiasis in corticosteroid-treated patients: case series and literature review. J Infect. 2007 Jan. 54(1):18-27. [View Abstract]
  6. Gonçalves AL, Machado GA, Gonçalves-Pires MR, Ferreira-Júnior A, Silva DA, Costa-Cruz JM. Evaluation of strongyloidiasis in kennel dogs and keepers by parasitological and serological assays. Vet Parasitol. 2007 Jun 20. 147(1-2):132-9. [View Abstract]
  7. Guyomard JL, Chevrier S, Bertholom JL, Guigen C, Charlin JF. [Finding of Strongyloides stercoralis infection, 25 years after leaving the endemic area, upon corticotherapy for ocular trauma]. J Fr Ophtalmol. 2007 Feb. 30(2):e4. [View Abstract]
  8. Porto AF, Neva FA, Bittencourt H, Lisboa W, Thompson R, Alcântara L, et al. HTLV-1 decreases Th2 type of immune response in patients with strongyloidiasis. Parasite Immunol. 2001 Sep. 23(9):503-7. [View Abstract]
  9. Satoh M, Toma H, Sato Y, Takara M, Shiroma Y, Kiyuna S, et al. Reduced efficacy of treatment of strongyloidiasis in HTLV-I carriers related to enhanced expression of IFN-gamma and TGF-beta1. Clin Exp Immunol. 2002 Feb. 127(2):354-9. [View Abstract]
  10. Porto MA, Alcântara LM, Leal M, Castro N, Carvalho EM. Atypical clinical presentation of strongyloidiasis in a patient co-infected with human T cell lymphotrophic virus type I. Am J Trop Med Hyg. 2005 Feb. 72(2):124-5. [View Abstract]
  11. Carvalho EM, Da Fonseca Porto A. Epidemiological and clinical interaction between HTLV-1 and Strongyloides stercoralis. Parasite Immunol. 2004 Nov-Dec. 26(11-12):487-97. [View Abstract]
  12. Thompson BF, Fry LC, Wells CD, Olmos M, Lee DH, Lazenby AJ, et al. The spectrum of GI strongyloidiasis: an endoscopic-pathologic study. Gastrointest Endosc. 2004 Jun. 59(7):906-10. [View Abstract]
  13. DeVault GA Jr, King JW, Rohr MS, Landreneau MD, Brown ST 3rd, McDonald JC. Opportunistic infections with Strongyloides stercoralis in renal transplantation. Rev Infect Dis. 1990 Jul-Aug. 12(4):653-71. [View Abstract]
  14. Schaeffer MW, Buell JF, Gupta M, Conway GD, Akhter SA, Wagoner LE. Strongyloides hyperinfection syndrome after heart transplantation: case report and review of the literature. J Heart Lung Transplant. 2004 Jul. 23(7):905-11. [View Abstract]
  15. Stone WJ, Schaffner W. Strongyloides infections in transplant recipients. Semin Respir Infect. 1990 Mar. 5(1):58-64. [View Abstract]
  16. Roxby AC, Gottlieb GS, Limaye AP. Strongyloidiasis in transplant patients. Clin Infect Dis. 2009 Nov 1. 49(9):1411-23. [View Abstract]
  17. Shoop WL, Michael BF, Eary CH, Haines HW. Transmammary transmission of Strongyloides stercoralis in dogs. J Parasitol. 2002 Jun. 88(3):536-9. [View Abstract]
  18. Said T, Nampoory MR, Nair MP, Halim MA, Shetty SA, Kumar AV, et al. Hyperinfection strongyloidiasis: an anticipated outbreak in kidney transplant recipients in Kuwait. Transplant Proc. 2007 May. 39(4):1014-5. [View Abstract]
  19. Croker C, Reporter R, Redelings M, Mascola L. Strongyloidiasis-related deaths in the United States, 1991-2006. Am J Trop Med Hyg. 2010 Aug. 83(2):422-6. [View Abstract]
  20. Dawson-Hahn EE, Greenberg SL, Domachowske JB, Olson BG. Eosinophilia and the seroprevalence of schistosomiasis and strongyloidiasis in newly arrived pediatric refugees: an examination of Centers for Disease Control and Prevention screening guidelines. J Pediatr. 2010 Jun. 156(6):1016-8, 1018.e1. [View Abstract]
  21. Gill GV, Welch E, Bailey JW, Bell DR, Beeching NJ. Chronic Strongyloides stercoralis infection in former British Far East prisoners of war. QJM. 2004 Dec. 97(12):789-95. [View Abstract]
  22. Nuesch R, Zimmerli L, Stockli R, Gyr N, Christoph Hatz FR. Imported strongyloidosis: a longitudinal analysis of 31 cases. J Travel Med. 2005 Mar-Apr. 12(2):80-4. [View Abstract]
  23. Lim S, Katz K, Krajden S, Fuksa M, Keystone JS, Kain KC. Complicated and fatal Strongyloides infection in Canadians: risk factors, diagnosis and management. CMAJ. 2004 Aug 31. 171(5):479-84. [View Abstract]
  24. Keystone JS. Can one afford not to screen for parasites in high-risk immigrant populations?. Clin Infect Dis. 2007 Nov 15. 45(10):1316-8. [View Abstract]
  25. Pelletier LL Jr. Chronic strongyloidiasis in World War II Far East ex-prisoners of war. Am J Trop Med Hyg. 1984 Jan. 33(1):55-61. [View Abstract]
  26. Pelletier LL Jr, Gabre-Kidan T. Chronic strongyloidiasis in Vietnam veterans. Am J Med. 1985 Jan. 78(1):139-40. [View Abstract]
  27. Genta RM. Global prevalence of strongyloidiasis: critical review with epidemiologic insights into the prevention of disseminated disease. Rev Infect Dis. 1989 Sep-Oct. 11(5):755-67. [View Abstract]
  28. Glinz D, Silué KD, Knopp S, Lohourignon LK, Yao KP, Steinmann P, et al. Comparing diagnostic accuracy of Kato-Katz, Koga agar plate, ether-concentration, and FLOTAC for Schistosoma mansoni and soil-transmitted helminths. PLoS Negl Trop Dis. 2010 Jul 20. 4(7):e754. [View Abstract]
  29. Yori PP, Kosek M, Gilman RH, Cordova J, Bern C, Chavez CB, et al. Seroepidemiology of strongyloidiasis in the Peruvian Amazon. Am J Trop Med Hyg. 2006 Jan. 74(1):97-102. [View Abstract]
  30. Johnston FH, Morris PS, Speare R, McCarthy J, Currie B, Ewald D, et al. Strongyloidiasis: a review of the evidence for Australian practitioners. Aust J Rural Health. 2005 Aug. 13(4):247-54. [View Abstract]
  31. Moon TD, Oberhelman RA. Antiparasitic therapy in children. Pediatr Clin North Am. 2005 Jun. 52(3):917-48, viii. [View Abstract]
  32. Reddy IS, Swarnalata G. Fatal disseminated strongyloidiasis in patients on immunosuppressive therapy: report of two cases. Indian J Dermatol Venereol Leprol. 2005 Jan-Feb. 71(1):38-40. [View Abstract]
  33. Newberry AM, Williams DN, Stauffer WM, Boulware DR, Hendel-Paterson BR, Walker PF. Strongyloides hyperinfection presenting as acute respiratory failure and gram-negative sepsis. Chest. 2005 Nov. 128(5):3681-4. [View Abstract]
  34. Toledo R, Muñoz-Antoli C, Esteban JG. Strongyloidiasis with emphasis on human infections and its different clinical forms. Adv Parasitol. 2015 Apr. 88:165-241. [View Abstract]
  35. Lam CS, Tong MK, Chan KM, Siu YP. Disseminated strongyloidiasis: a retrospective study of clinical course and outcome. Eur J Clin Microbiol Infect Dis. 2006 Jan. 25(1):14-8. [View Abstract]
  36. Csermely L, Jaafar H, Kristensen J, Castella A, Gorka W, Chebli AA, et al. Strongyloides hyper-infection causing life-threatening gastrointestinal bleeding. World J Gastroenterol. 2006 Oct 21. 12(39):6401-4. [View Abstract]
  37. Boulware DR, Stauffer WM, Hendel-Paterson BR, Rocha JL, Seet RC, Summer AP, et al. Maltreatment of Strongyloides infection: case series and worldwide physicians-in-training survey. Am J Med. 2007 Jun. 120(6):545.e1-8. [View Abstract]
  38. Ly MN, Bethel SL, Usmani AS, Lambert DR. Cutaneous Strongyloides stercoralis infection: an unusual presentation. J Am Acad Dermatol. 2003 Aug. 49(2 Suppl Case Reports):S157-60. [View Abstract]
  39. Salluh JI, Bozza FA, Pinto TS, Toscano L, Weller PF, Soares M. Cutaneous periumbilical purpura in disseminated strongyloidiasis in cancer patients: a pathognomonic feature of potentially lethal disease?. Braz J Infect Dis. 2005 Oct. 9(5):419-24. [View Abstract]
  40. Pacanowski J, Santos MD, Roux A, LE Maignan C, Guillot J, Lavarde V, et al. Subcutaneous ivermectin as a safe salvage therapy in Strongyloides stercoralis hyperinfection syndrome: a case report. Am J Trop Med Hyg. 2005 Jul. 73(1):122-4. [View Abstract]
  41. Butterfield JH, Kephart GM, Frankson JL. Eosinophilic oophoritis: association with positive Strongyloides stercoralis serology and clinical response to ivermectin. J Pediatr Adolesc Gynecol. 2006 Oct. 19(5):329-32. [View Abstract]
  42. Harish K, Sunilkumar R, Varghese T, Feroze M. Strongyloidiasis presenting as duodenal obstruction. Trop Gastroenterol. 2005 Oct-Dec. 26(4):201-2. [View Abstract]
  43. Komenaka IK, Wu GC, Lazar EL, Cohen JA. Strongyloides appendicitis: unusual etiology in two siblings with chronic abdominal pain. J Pediatr Surg. 2003 Sep. 38(9):E8-10. [View Abstract]
  44. Morimoto J, Kaneoka H, Sasatomi Y, Sato YN, Murata T, Ogahara S, et al. Disseminated strongyloidiasis in nephrotic syndrome. Clin Nephrol. 2002 May. 57(5):398-401. [View Abstract]
  45. Hsieh YP, Wen YK, Chen ML. Minimal change nephrotic syndrome in association with strongyloidiasis. Clin Nephrol. 2006 Dec. 66(6):459-63. [View Abstract]
  46. Copelovitch L, Sam Ol O, Taraquinio S, Chanpheaktra N. Childhood nephrotic syndrome in Cambodia: an association with gastrointestinal parasites. J Pediatr. 2010 Jan. 156(1):76-81. [View Abstract]
  47. Hayashi E, Ohta N, Yamamoto H. Syndrome of inappropriate secretion of antidiuretic hormone associated with strongyloidiasis. Southeast Asian J Trop Med Public Health. 2007 Mar. 38(2):239-46. [View Abstract]
  48. Pirisi M, Salvador E, Bisoffi Z, Gobbo M, Smirne C, Gigli C, et al. Unsuspected strongyloidiasis in hospitalised elderly patients with and without eosinophilia. Clin Microbiol Infect. 2006 Aug. 12(8):787-92. [View Abstract]
  49. Nuesch R, Zimmerli L, Stockli R, Gyr N, Christoph Hatz FR. Imported strongyloidosis: a longitudinal analysis of 31 cases. J Travel Med. 2005 Mar-Apr. 12(2):80-4. [View Abstract]
  50. Masseau A, Hervier B, Leclair F, Grossi O, Mosnier JF, Hamidou M. [Strongyloides stercoralis infection simulating polyarteritis nodosa]. Rev Med Interne. 2005 Aug. 26(8):661-3. [View Abstract]
  51. Qu Z, Kundu UR, Abadeer RA, Wanger A. Strongyloides colitis is a lethal mimic of ulcerative colitis: the key morphologic differential diagnosis. Hum Pathol. 2009 Apr. 40(4):572-7. [View Abstract]
  52. Anamnart W, Pattanawongsa A, Intapan PM, Maleewong W. Factors affecting recovery of Strongyloides stercoralis larvae: an approach to a newly modified formalin-ether concentration technique for diagnosis of strongyloidiasis. J Clin Microbiol. 2010 Jan. 48(1):97-100. [View Abstract]
  53. Buonfrate D, Formenti F, Perandin F, Bisoffi Z. Novel approaches to the diagnosis of Strongyloides stercoralis infection. Clin Microbiol Infect. 2015 Jun. 21 (6):543-52. [View Abstract]
  54. Page WA, Dempsey K, McCarthy JS. Utility of serological follow-up of chronic strongyloidiasis after anthelminthic chemotherapy. Trans R Soc Trop Med Hyg. 2006 Nov. 100(11):1056-62. [View Abstract]
  55. Gam AA, Neva FA, Krotoski WA. Comparative sensitivity and specificity of ELISA and IHA for serodiagnosis of strongyloidiasis with larval antigens. Am J Trop Med Hyg. 1987 Jul. 37(1):157-61. [View Abstract]
  56. Rodrigues RM, de Oliveira MC, Sopelete MC, Silva DA, Campos DM, Taketomi EA, et al. IgG1, IgG4, and IgE antibody responses in human strongyloidiasis by ELISA using Strongyloides ratti saline extract as heterologous antigen. Parasitol Res. 2007 Oct. 101(5):1209-14. [View Abstract]
  57. Salvador F, Sulleiro E, Sánchez-Montalvá A, Saugar JM, Rodríguez E, Pahissa A, et al. Usefulness of Strongyloides stercoralis serology in the management of patients with eosinophilia. Am J Trop Med Hyg. 2014 May. 90(5):830-4. [View Abstract]
  58. Bon B, Houze S, Talabani H, Magne D, Belkadi G, Develoux M, et al. Evaluation of a rapid enzyme-linked immunosorbent assay for diagnosis of strongyloidiasis. J Clin Microbiol. 2010 May. 48(5):1716-9. [View Abstract]
  59. Krolewiecki AJ, Ramanathan R, Fink V, McAuliffe I, Cajal SP, Won K, et al. Improved diagnosis of Strongyloides stercoralis using recombinant antigen-based serologies in a community-wide study in northern Argentina. Clin Vaccine Immunol. 2010 Oct. 17 (10):1624-30. [View Abstract]
  60. Ramanathan R, Burbelo PD, Groot S, Iadarola MJ, Neva FA, Nutman TB. A luciferase immunoprecipitation systems assay enhances the sensitivity and specificity of diagnosis of Strongyloides stercoralis infection. J Infect Dis. 2008 Aug 1. 198(3):444-51. [View Abstract]
  61. Montes M, Sawhney C, Barros N. Strongyloides stercoralis: there but not seen. Curr Opin Infect Dis. 2010 Oct. 23(5):500-4. [View Abstract]
  62. Taniuchi M, Verweij JJ, Noor Z, Sobuz SU, Lieshout L, Petri WA Jr, et al. High throughput multiplex PCR and probe-based detection with Luminex beads for seven intestinal parasites. Am J Trop Med Hyg. 2011 Feb. 84(2):332-7. [View Abstract]
  63. Basuni M, Muhi J, Othman N, Verweij JJ, Ahmad M, Miswan N, et al. A pentaplex real-time polymerase chain reaction assay for detection of four species of soil-transmitted helminths. Am J Trop Med Hyg. 2011 Feb. 84(2):338-43. [View Abstract]
  64. Buonfrate D, Requena-Mendez A, Angheben A, Cinquini M, Cruciani M, Fittipaldo A, et al. Accuracy of molecular biology techniques for the diagnosis of Strongyloides stercoralis infection-A systematic review and meta-analysis. PLoS Negl Trop Dis. 2018 Feb. 12 (2):e0006229. [View Abstract]
  65. Sithithaworn J, Sithithaworn P, Janrungsopa T, Suvatanadecha K, Ando K, Haswell-Elkins MR. Comparative assessment of the gelatin particle agglutination test and an enzyme-linked immunosorbent assay for diagnosis of strongyloidiasis. J Clin Microbiol. 2005 Jul. 43(7):3278-82. [View Abstract]
  66. Kishimoto K, Hokama A, Hirata T, Ihama Y, Nakamoto M, Kinjo N, et al. Endoscopic and histopathological study on the duodenum of Strongyloides stercoralis hyperinfection. World J Gastroenterol. 2008 Mar 21. 14(11):1768-73. [View Abstract]
  67. Mittal S, Sagi SV, Hawari R. Strongyloidiasis: endoscopic diagnosis. Clin Gastroenterol Hepatol. 2009 Feb. 7(2):e8. [View Abstract]
  68. Biggs BA, Caruana S, Mihrshahi S, Jolley D, Leydon J, Chea L, et al. Management of chronic strongyloidiasis in immigrants and refugees: is serologic testing useful?. Am J Trop Med Hyg. 2009 May. 80 (5):788-91. [View Abstract]
  69. Krolewiecki A, Nutman TB. Strongyloidiasis: A Neglected Tropical Disease. Infect Dis Clin North Am. 2019 Mar. 33 (1):135-151. [View Abstract]
  70. Robson D, Beeching NJ, Gill GV. Strongyloides hyperinfection syndrome in British veterans. Ann Trop Med Parasitol. 2009 Mar. 103(2):145-8. [View Abstract]
  71. Fardet L, Généreau T, Cabane J, Kettaneh A. Severe strongyloidiasis in corticosteroid-treated patients. Clin Microbiol Infect. 2006 Oct. 12(10):945-7. [View Abstract]
  72. CDC. Parasites - Strongyloides: Resources for Health Professionals. Centers for Disease Control and Prevention. Available at December 31, 2018; Accessed: June 19, 2019.
  73. Henriquez-Camacho C, Gotuzzo E, Echevarria J, White AC Jr, Terashima A, Samalvides F, et al. Ivermectin versus albendazole or thiabendazole for Strongyloides stercoralis infection. Cochrane Database Syst Rev. 2016 Jan 18. CD007745. [View Abstract]
  74. Gotuzzo E, Arango C, de Queiroz-Campos A, Istúriz RE. Human T-cell lymphotropic virus-I in Latin America. Infect Dis Clin North Am. 2000 Mar. 14 (1):211-39, x-xi. [View Abstract]
  75. Fusco DN, Downs JA, Satlin MJ, Pahuja M, Ramos L, Barie PS, et al. Non-oral treatment with ivermectin for disseminated strongyloidiasis. Am J Trop Med Hyg. 2010 Oct. 83(4):879-83. [View Abstract]
  76. Datry A, Hilmarsdottir I, Mayorga-Sagastume R, Lyagoubi M, Gaxotte P, Biligui S, et al. Treatment of Strongyloides stercoralis infection with ivermectin compared with albendazole: results of an open study of 60 cases. Trans R Soc Trop Med Hyg. 1994 May-Jun. 88(3):344-5. [View Abstract]
  77. Marti H, Haji HJ, Savioli L, Chwaya HM, Mgeni AF, Ameir JS, et al. 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 Nov. 55(5):477-81. [View Abstract]
  78. Suputtamongkol Y, Premasathian N, Bhumimuang K, Waywa D, Nilganuwong S, Karuphong E. Efficacy and safety of single and double doses of ivermectin versus 7-day high dose albendazole for chronic strongyloidiasis. PLoS Negl Trop Dis. 2011. 5(5):e1044. [View Abstract]
  79. Steinmann P, Zhou XN, Du ZW, Jiang JY, Xiao SH, Wu ZX, et al. Tribendimidine and albendazole for treating soil-transmitted helminths, Strongyloides stercoralis and Taenia spp.: open-label randomized trial. PLoS Negl Trop Dis. 2008. 2(10):e322. [View Abstract]
  80. Santiago M, Leitão B. Prevention of strongyloides hyperinfection syndrome: a rheumatological point of view. Eur J Intern Med. 2009 Dec. 20(8):744-8. [View Abstract]
  81. Cohen J, Powderly WG. Infectious Diseases. 2nd ed. New York, NY: CV Mosby; 2004:503-15,. 1186-7.
  82. Long SS, Pickering LK, Prober CG. Principles and Practice of Pediatric Infectious Diseases. 2nd ed. New York, NY: Churchill Livingstone; 2003. 1337-9.

Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).