Strongyloidiasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Strongyloidiasis is an infection caused by a roundworm (nematode), Strongyloides stercoralis. Transmission occurs predominantly in tropical and subtropical areas but can also be found in countries with temperate environments including the southeastern U.S. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. S stercoralis in humans usually produces an asymptomatic chronic infection of the gastrointestinal tract that can remain undetected for several decades. Usually there are no unique clinical symptoms to suggest infection, although abdominal bloating and eosinophilia are common in many infected patients. In some patients a disseminated or hyperinfection syndrome can develop with the dissemination of larvae to extra-intestinal organs, and that can result in mortality rates exceeding 90%. Risk factors and predisposing conditions include immunosuppressive therapies with corticosteroids and other medications, HTLV-1 infection, organ transplantation, immune reconstitution syndrome, hematologic malignancies (lymphoma), tuberculosis, and malnutrition. Diagnosis is generally made by the detection of larvae in the stool. Ivermectin, thiabendazole, and albendazole are the most effective medicines for treating the infection. Excellent recovery after treatment should be expected in immunocompetent patients.

Strongyloides was first discovered in 1876 by the French physician Louis Alexis Normand while working in the naval hospital in Toulon; he identified the adult worms and sent them to Arthur Réné Jean Baptiste Bavay, chief health inspector, who observed that the worms were the adult forms of the larvae found in stool. In 1883, the German parasitologist Rudolf Leuckart made initial observations on the life cycle of parasite. Belgian physician Paul Van Durme described the mode of infection through the skin. The German parasitologist Friedrich Fülleborn described autoinfection and the mechanism by which strongyloidiasis involves the intestine. Strongyloidiasis was investigated further during the 1940s, as persons who had acquired the infection abroad and then received immunosuppression developed hyper-infestation syndrome.

Strongyloidiasis may be classified as acute or chronic based on the duration of symptoms and as hyper infection syndrome or disseminated strongyloidiasis based on the organ system involvement.

Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin and enter a venous or lymphatic vessel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host’s intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, and maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis.

Strongyloidiasis is a human parasitic disease caused by the nematode (roundworm) Strongyloides stercoralis or sometimes S. fülleborni.

Strongyloidiasis can mimic other worm infections like Ascaris lumbricoides, Trichuris trichiura, hookworm infections (Necator americanus and Ancylostoma duodenale), Enterobius vermicularis (pinworm) and gastrointestinal pathologies such as peptic ulcer disease, intussusception in children, and bile duct stone.

The global prevalence of Strongyloides is unknown, but recent studies estimate that there are between 30–100 million infected persons worldwide, mainly in tropical and subtropical countries. Strongyloidiasis is more common in the pediatric age group (ages 2-10 years).

Common risk factors in the development of strongyloidiasis include immunosuppressive therapies with corticosteroids and other medications, HTLV-1 infection, organ transplantation, immune reconstitution syndrome, hematologic malignancies (especially lymphoma), tuberculosis, and malnutrition

Most fatal infections caused by S.stercoralis can be prevented by early detection and treatment of asymptomatic chronic infections. Screening is highly recommended to detect latent S.stercoralis infection before the start of chemotherapy or immunosuppression/steroid therapy in patients at risk. Repeated stool examination for ova and parasites or agar culture of stool may be the most appropriate approach.

If strongyloidiasis is left untreated, the infection can disseminate and transform into hyper-infection syndrome which has a mortality rate of 90%. Complications that can develop as a result of strongyloidiasis are disseminated strongyloidiasis (especially in patients with HIV or other immunocompromised conditions ), eosinophilic pneumonia, malnutrition, and malabsorption. With appropriate treatment, people should make a full recovery. Treatment needs to be repeated often. Infections that are severe or widespread often have a poor outcome, especially in people with a suppressed immune system.

Strongyloides infection can present in various forms. The majority of people infected with Strongyloides are asymptomatic. The symptomatic spectrum of strongyloidiasis ranges from subclinical in acute and chronic infection to severe and fatal in hyper infection syndrome. On acquiring the infection, there may be respiratory symptoms (Löffler’s syndrome). The infection may progress to chronic stage with mainly digestive symptoms. On reinfection there may be respiratory, skin, and digestive symptoms. Finally, hyper infection syndrome sets in and cause symptoms in many organ systems, including the central nervous system.

The physical examination findings in strongyloidiasis vary and are usually dependent on the worm burden and the involved organ.

The diagnosis of strongyloidiasis is made by presence of clinical signs and symptoms, eosinophilia, and positive serological findings. Definitive diagnosis of strongyloidiasis is generally made by the detection of larvae in the stool. Sputum examination may rarely be used to identify organisms in cases of hyperinfection. Agar tracking (detection of larval tracks on agar culture plates) has been shown to be more sensitive than the conventional stool examination. However, agar tracking is usually unavailable on a routine basis in clinical microbiology laboratories. Immunodiagnostic tests for strongyloidiasis are indicated when the infection is suspected and the organism cannot be demonstrated by repeated examinations of stool. Enzyme immunoassay (EIA) is currently recommended because of its greater sensitivity (90%). Antibody test results cannot be used to differentiate between the past and current infection. In disseminated cases of strongyloidiasis, larvae can be detected in sputum by simple wet-mount in fluid from a bronchoalveolar lavage (BAL).

X rays can be helpful in the diagnosis of strongyloidiasis. Radiographic findings are variable, depending upon the stage and extent of infection which includes pulmonary infiltrates, when present, may be alveolar or interstitial, diffuse or focal, uni- or bilateral. Lung consolidation, occasional cavitation, and even abscess formation can also be found. Plain abdominal radiographs and contrast studies can reveal worm masses in bowel loops. Chest radiographs are explained by pulmonary migration of the parasites and by different types of bacterial super-infection, particularly gram-negative bacilli.

There are no specific CT findings associated with strongyloidiasis. However, in cases of abdominal obstruction due to worm burden, CT can demonstrate collapsed loops of the bowel distally and radial distribution of several dilated, fluid-filled bowel loops.

There are no specific MRI findings associated with strongyloidiasis.

There are no specific ultrasound findings associated with strongyloidiasis.

There are no other specific imaging findings associated with strongyloidiasis infection.

Upper and lower GI endoscopy, skin biopsy, and BAL fluid examination are some other diagnostic tests that are employed in diagnosing strongyloidiasis when there is a negative stool exam.

Ivermectin, thiabendazole, and albendazole are the most effective medicines for treating strongyloidiasis infection. Ivermectin is the drug of choice, and albendazole is considered the least effective. Thiabendazole is not generally used in the U.S. due to adverse events, but it is still used in other countries. All patients with strongyloidiasis (even asymptomatic patients) require treatment. Complete obstruction with inadequate decompression, lack of response within an interval of 24-48 hrs, volvulus, intussusception, or perforation should be managed surgically.

Strongyloidiasis is usually managed with medical therapy. However, surgery may be indicated when medical management fails or complications arise.

The prevention of strongyloidiasis is best achieved through improvements in personal hygiene and environmental sanitation.

Secondary preventive measures of strongyloidiasis are similar to primary preventive measures.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Strongyloides was first discovered in 1876 by the French physician Louis Alexis Normand while working in the naval hospital in Toulon; he identified the adult worms and sent them to Arthur Réné Jean Baptiste Bavay, chief health inspector, who observed that the worms were the adult forms of the larvae found in stool. In 1883, the German parasitologist Rudolf Leuckart made initial observations on the life cycle of parasite. Belgian physician Paul Van Durme described the mode of infection through the skin. The German parasitologist, Friedrich Fülleborn described autoinfection and the mechanism by which strongyloidiasis involves the intestine. Strongyloidiasis was investigated further during the 1940s, as persons who had acquired the infection abroad and then received immunosuppression developed hyper-infestation syndrome.^[1]

• In 1876, Louis Alexis Normand, a French physician, discovered Strongyloides for the first time.
• Later in the same year, Professor Arthur Réné Jean Baptiste Bavay at the French Conseil Supérieur de Santé gave a detailed description of Strongyloides.
• In 1883, Karl Georg Friedrich Rudolf Leuckart, a German parasitologist, discovered the alternation of generations involving parasitic and free-living phases.
• The discovery that infection occurred through the skin was made by Belgian physician Paul Van Durme whose studies were based on the work of Arthur Looss.
• The German parasitologist Friedrich Fülleborn described autoinfection and the way by which strongyloidiasis involves the intestine.
• In 1940, detailed studies on disseminated infections of Strongyloides in immunosuppressed patients were described.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Strongyloidiasis may be classified as acute or chronic based on the duration of symptoms and as hyper infection syndrome or disseminated strongyloidiasis based on the organ system involvement.

Strongyloidiasis may be classified as acute or chronic based on the duration of symptoms and as hyper infection syndrome or disseminated strongyloidiasis based on the organ system involvement.^[1]

• Acute strongyloidiasis: If the duration of symptoms is less than 4-6 weeks.

• Chronic strongyloidiasis:  If the symptoms persist for more than 6 weeks.

• Hyperinfection syndrome: The strongyloidiasis infection is limited to the GI tract and the lungs
• Disseminated strongyloidiasis: Multiple organ systems are involved.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin of the host, enter a venous or lymphatic channel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host’s intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis.

Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin of the host, enter a venous or lymphatic channel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host’s intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis. ^[1][2][3][4]

• Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities

• The incubation period of strongyloidiasis is unknown but it takes 28 days for larvae to appear in urine after the initial exposure.

• The principal definitive hosts of S.stercoralis are humans, but infection in dogs can also occur. The Strongyloides life cycle includes the following stages:

Free-living cycle:

• The rhabditiform larvae passed in the stool can either become infective filariform larvae (direct development) or free living adult males and females.
• These adult forms mate and produce eggs from which rhabditiform larvae hatch, which eventually become infective filariform larvae.
• The filariform larvae penetrate the human host skin to initiate the parasitic cycle.

Parasitic cycle:

• Filariform larvae in contaminated soil penetrate the human skin and by various, often random, routes migrate into the small intestine.
• The larvae migrates via the bloodstream to the lungs, where they are eventually coughed up and swallowed.
• There is also evidence that larvae can migrate directly to the intestine via connective tissues.
• In the small intestine, they molt twice and become adult female worms.
• The female worms live in the epithelium of the small intestine and produce eggs through parthenogenesis, which yield rhabditiform larvae.
• The rhabditiform larvae can either be passed in the stool or cause autoinfection.
• In autoinfection, the rhabditiform larvae can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection).
• In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunosuppressed individuals.

• The initial host immune response to Strongyloides infection is production of immunoglobulin E and eosinophilia in blood and tissues, which presumably prevents dissemination and hyper-infection in the immunocompetent host.^[5][6]
• Adult female worms in otherwise healthy and asymptomatic individuals may persist in the gastrointestinal tract for years.
• If infected persons become immunocompromised, the reduction in cellular and humoral immunity may lead to an abrupt and dramatic increase in parasite load with systemic dissemination.

Prevalence of strongyloidiasis is higher in patients with conditions such as:

• Systemic rheumatic diseases
• Chronic renal failure
• Diabetes mellitus
• Malnutrition
• Alcoholism

• Strongyloides stercoralis is a nematode.
• Female worms can grow 2.5 mm-long, male worms can grow to only about 0.9 mm (0.04 in) in length.^[7]
• Both sexes worms possess a tiny buccal capsule and cylindrical esophagus without a posterior bulb.
• In the free-living stage, the esophagi of both sexes are rhabditiform.
• Males can be distinguished from females by two structures the spicules and gubernaculum.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Strongyloides stercoralis is the scientific name of a human parasitic roundworm causing the disease of strongyloidiasis.

Strongyloides stercoralis is a nematode, 2.5 mm-long, that is a parasite of humans. The adult parasitic stage lives in tunnels in the mucosa of the small intestine. The genus Strongyloides contains 53 species and S. stercoralis is the type species. S. stercoralis has been reported in other primates and occasionally in dogs. However, it seems that the species in dogs is typically not S. stercoralis, but another species S. canis. Non-human primates are more commonly infected with S. fuelleborni and S. cebus although S. stercoralis has been reported in captive primates. Other species of Strongyloides naturally parasitic in humans, but with restricted distributions, are S. fuelleborni in central Africa and S. kellyi in Papua New Guinea.

For S. stercoralis first stage larvae (L1) pass out in the feces and develop in feces on the ground to infective larvae (IL). This development can occur via two routes: directly from L1 to IL via three moults or indirectly. The indirect route results first in the development of free-living adult females and males which mate, females lay eggs which hatch and then develop to IL. The direct route gives IL faster (3 days) versus the indirect route (7-10 days), However, the indirect route results in an increase in the number of IL produced. Speed of development of IL is traded off for increased numbers. The free-living males and females of S. stercoralis die after one generation; they do not persist in the soil.

The infectious larvae penetrate the skin when there is contact with the soil. Some of them enter the superficial veins and ride the blood vessels to the lungs, where they enter the alveoli. They are then coughed up and swallowed into the gut, where they parasitise the intestinal mucosa (duodenum and jejunum). However, research in dogs has shown that most of the larvae that penetrate the skin migrate randomly through the body until they reach the small intestine. Only females will reach reproductive adulthood in the intestine. Female strongyloides reproduce through parthenogenesis. The eggs hatch in the intestine and young larvae are then excreted in the feces. It takes about two weeks to reach egg development from the initial skin penetration. By this process, S. stercoralis can cause both respiratory and gastrointestinal symptoms. Adult worms can live up to a year in dogs.

An unusual feature of S. stercoralis is autoinfection. Only one other species in the Strongyloides genus, S. felis, has the trait of autoinfection. Autoinfection is the development of L1 into small infective larvae in the gut of the host. These autoinfective larvae penetrate the wall of the lower ileum or colon or the skin of the perianal region, enter the circulation again, up to the lungs, and back down to the small intestine thus repeating the cycle. Autoinfection makes strongyloidiasis due to S. stercoralis an infection with several unusual features.

Persistence of infection is the first of these important features. Because of autoinfection, humans have been known to still be infected up to 65 years after they were first exposed to the parasite (e.g. Vietnam veterans). Once a host is infected with S. stercoralis, infection is life-long unless effective treatment eliminates all adult parasites and migrating autoinfective larvae.

Strongyloidiasis in immunocompetant individuals is usually an indolent disease. However, in immunocompromised individuals strongyloidiasis can cause a hyperinfective syndrome (also called disseminated strongyloidiasis). This hyperinfective syndrome has a mortality rate of close to 90%.

Immunosuppressive drugs, such as those used for tissue transplantation, (especially corticosteroids) can increase the rate of autoinfection to the point where there is an overwhelming number of larvae migrating through the lungs, and in many cases this can prove fatal. Additionally, diseases such as HTLV-1 (Human T-cell Lymphotropic Virus 1), which enhance the Th1 arm of the immune system and lessen the Th2 arm, increase the disease state. Another consequence of autoinfection is that the autoinfective larvae can carry gut bacteria back into the body. About 50% of people with hyperinfection present with bacterial disease due to enteric bacteria. Finally, a unique effect of autoinfective larvae is larva currens due to the larvae migrating rapidly through the skin. Larva currens appears as a red line that appears, moves rapidly (>5 cm/day) and then quickly disappears. It is pathogonomic for autoinfective larvae and can be used as a diagnostic criterion for strongyloidiasis due to S. stercoralis.

S. stercoralis has a very low prevalence in societies where faecal contamination of soil is rare. Hence, it is a very rare infection in developed market economies and is less prevalent in urban areas in developing countries than in rural areas. Strongyloidiasis was first described in the nineteenth century in French soldiers returning home from expeditions in IndoChina. Today, the countries of the old IndoChina (Vietnam, Cambodia and Laos) still have endemic strongyloidiasis, typical prevalence being 10% or less. Regions of Japan used to have endemic strongyloidiasis, but control programs have probably reduced prevalence markedly. Strongyloidiasis appears to have a high prevalence in some areas of Brazil and Central America. Strongyloidiasis is endemic in Africa, but the prevalence is typically low (1% or less). Pockets of strongyloidiasis have been reported from rural Italy, but current status is unknown. In the Pacific islands strongyloidiasis is rare although there have been reports of cases from Fiji. In tropical Australia, some rural and remote Australian Aboriginal communities have very high prevalence of strongyloidiasis . In some African countries (e.g., Zaire) S. fuelleborni was more common than S. stercoralis in parasite surveys from the 1970s, but current status is unknown. In Papua New Guinea, S. stercoralis is endemic, but prevalence is low. However, in some areas another species, S. kellyi, is a very common parasite of children in the PNG highlands and Western Province.

Knowledge of the geographic distribution of strongyloidiasis is of significance to travelers who may acquire the parasite during their stay in endemic areas.

Ivermectin is the drug of first choice for treatment . Thiabendazole was used previously, but owing to its high prevalence of side effects and lower efficay, it has been superseded by ivermectin and as second line, albendazole. However, these drugs have little effect on the majority of these autoinfective larvae during their migration through the body. Hence, repeated treatments with ivermectin have to be administered to kill adults which develop from the autoinfective larvae.

• Overview of taxonomy of Strongyloides genus.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2], Furqan M M. M.B.B.S[3]

Strongyloidiasis can mimic other worm infections like Ascaris lumbricoides, Trichuris trichiura, hookworm infections (Necator americanus and Ancylostoma duodenale), Enterobius vermicularis (pinworm) and gastrointestinal pathologies such as peptic ulcer disease, intussusception in children, and bile duct stone.^[1][2][3]

The table below summarizes the findings that differentiate strongyloidiasis from other nematode infections:

• Strongyloidiasis, when it involves the gastrointestinal tract, presents with abdominal pain and must be differentiated from other GI disorders like peptic ulcer disease, intussusception, and bile duct stone.
• The table below summarizes the findings that differentiate strongyloidiasis from peptic ulcer disease, intussusception, and bile duct stone:

The table below summarizes the findings that differentiate intestinal strongyloidiasis from other conditions that may cause abdominal pain and diarrhea^[5][6][7]

The table below summarizes the findings that differentiate pulmonary strongyloidiasis from other conditions that may cause cough, wheezing, dyspnea and hemoptysis^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The global prevalence of Strongyloides is unknown, but experts estimate that there are between 30–100 million infected persons worldwide, mainly in tropical and subtropical countries. Strongyloidiasis infection is more common in the pediatric age group (ages 2-10 years).

• The global prevalence of Strongyloides is unknown, but recent studies estimate that there are between 30–100 million infected persons worldwide.

• The incidence of strongyloidiasis is approximately 600-1,000 per 100,000 individuals in the United States.
• The incidence of strongyloidiasis is approximately 460-1,000 per 100,000 individuals in immigrant populations.

• Strongyloides is known to exist on all continents except for Antarctica, but it is most common in the tropics, subtropics, and in warm temperate regions.

• Strongyloidiasis occurs in all age groups but it is more common in the pediatric age group (ages 2-10 years).

• Males are more commonly affected by strongyloidiasis than females.
• The male to female ratio is approximately 2-3 to 1.^[1]

• There is no racial predilection to strongyloidiasis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Common risk factors in the development of strongyloidiasis include immunosuppressive therapies with corticosteroids and other medications, HTLV-1 infection, organ transplantation, immune reconstitution syndrome, hematologic malignancies (especially lymphoma), tuberculosis, and malnutrition.

Common risk factors in the development of strongyloidiasis include:^[1][2]

• Occupations that increase contact with contaminated soil such as farming and coal mining
• Human T-cell lymphotropic virus-1 (HTLV-1) infection
• Immunosuppressive therapy with corticosteroids and other medications,
• Immune reconstitution syndrome
• Hematologic malignancies (lymphoma)
• Tuberculosis
• Malnutrition
• Diabetes mellitus, chronic obstructive pulmonary disease (COPD), chronic renal failure.
• Living in endemic regions.
• Alcoholics
• Travelers, immigrants

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Most fatal infections caused by S.stercoralis can be prevented by early detection and treatment of asymptomatic chronic infections. Screening is highly recommended to detect latent S.stercoralis infection before the start of chemotherapy or immunosuppression/steroid therapy in patients at risk. Repeated stool examination for ova and parasites or agar culture of stool may be the most appropriate approach.

• Most fatal infections caused by S.stercoralis can be prevented by early detection and treatment of asymptomatic chronic infections.^[1][2][3]
• Screening is highly recommended to detect latent S.stercoralis infection before the start of chemotherapy or immunosuppression/steroid therapy in patients at risk.^[4]
• Repeated stool examination for ova and parasites or agar culture of stool may be the most appropriate approach.

• In the U.S., residents of the Southeast may be at risk for strongyloidiasis by growing up in an endemic area.
• Travelers and armed forces personnel may acquire infection during overseas trips to endemic areas (e.g., southeast Asia, Central and South America, and Africa).
• Refugees and immigrants from endemic areas
• Immunocompromised patients, especially on corticosteroid therapy, are the most vulnerable population at risk for developing disseminated disease.
• Efforts to diagnose and screen individuals who harbor S.stercoralis should be made for patients who are candidates for immunosuppressive (e.g., corticosteroid) therapy with relevant geographic history and peripheral eosinophilia.

• At least three ova and parasite examinations should be performed on separate days.

• An enzyme-linked immunosorbent assay (ELISA) for detecting serum IgG (Strongyloides antibody) against a crude extract of the filariform larvae of S.stercoralis is available and should be used as a screening test for strongyloides infection.
• However, because of cross-reactivity with other antigens, definitive diagnosis must also include identification of ova and parasites in stool specimens.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

If strongyloidiasis is left untreated, the infection can disseminate and transform into hyperinfection syndrome, which has a mortality rate of 90%. Complications that can develop as a result of strongyloidiasis are disseminated strongyloidiasis (especially in patients with HIV or who are otherwise immunocompromised), eosinophilic pneumonia, malnutrition, and malabsorption. With appropriate treatment, people should make a full recovery. Treatment needs to be repeated often. Infections that are severe or widespread often have a poor outcome, especially in patients with a suppressed immune system.

If left untreated, the subclinical strongyloidiasis can disseminate and transform into hyperinfection syndrome, which has a mortality rate of 90%.^[1]

Complications that can develop as a result of strongyloidiasis are:^[2][3]

• Disseminated strongyloidiasis(especially in patients with HIV and other immunocompromised conditions)
• Polymicrobial sepsis including polymicrobial gram-negative meningitis
• Eosinophilic pneumonia
• Malnutrition
• Malabsorption
• Intestinal perforation

• With appropriate treatment people should make a full recovery.
• Sometimes, treatment needs to be repeated due to autoinfection.
• Infections that are severe or widespread often have a poor outcome, especially in patients with a suppressed immune system.
• Strongyloidiasis could be severe and life-threatening in specific groups including:
  • Those who use oral or intravenous steroids, for example, in patients with asthma, chronic obstructive pulmonary disease (COPD) exacerbations, lupus, gout, or in persons using steroids for immunosuppression or symptomatic relief
  • Those with HTLV-1 infection
  • Those with hematologic malignancies such as leukemia or lymphoma
  • Transplant recipients
• Even with treatment, disseminated strongyloidiasis and hyperinfection syndrome have a mortality rate of 90%.

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