Strongyloides stercoralis (Parasitic Roundworm)- A Threadworm

Strongyloides stercoralis is a parasitic roundworm that belongs to the phylum Nematoda and the order Rhabditida. It is commonly known as threadworm because of its slender and thread-like appearance. It is one of the smallest nematodes that infect humans, measuring about 2.5 mm in length and 0.05 mm in width.

Strongyloides stercoralis causes a disease called strongyloidiasis, which is characterized by chronic intestinal infection that can persist for decades without symptoms. However, in some cases, especially in immunocompromised individuals, the infection can become severe and life-threatening, leading to hyperinfection syndrome or disseminated strongyloidiasis.

Strongyloides stercoralis has a complex life cycle that involves both free-living and parasitic stages. The free-living stage occurs in the soil, where the worm can reproduce sexually or asexually. The parasitic stage occurs in the human host, where only female worms are found embedded in the mucosa of the small intestine. The female worms produce eggs by parthenogenesis, which hatch into rhabditiform larvae that are either excreted in the feces or undergo autoinfection.

The main mode of transmission of Strongyloides stercoralis is through skin penetration by the infective filariform larvae that are present in the contaminated soil or water. The larvae can also be transmitted by organ transplantation, transplacental or transmammary routes, or zoonotic infection from dogs or nonhuman primates.

Strongyloides stercoralis is a global health problem that affects more than 600 million people worldwide, mainly in tropical and subtropical regions, but also in temperate areas. It is associated with poverty, poor sanitation, and agricultural activity. It is also endemic in some parts of the United States and Europe, especially among immigrants, refugees, travelers, and military veterans who have lived in endemic regions.

Strongyloidiasis is a neglected tropical disease that requires more attention and research to improve its diagnosis, treatment, and prevention. It is often underdiagnosed because of its low sensitivity of stool microscopy and its nonspecific clinical manifestations. It is also often undertreated because of its potential for relapse and reinfection due to autoinfection. It is also often overlooked because of its low awareness among health professionals and the general public.

Therefore, it is important to increase the knowledge and understanding of Strongyloides stercoralis as a threadworm that can cause serious health consequences if left untreated.

Strongyloides stercoralis is a parasitic roundworm that causes strongyloidiasis, a chronic and potentially fatal infection of the human gastrointestinal tract and lungs. It is also known as dwarf threadworm or military worm, because of its small size and its association with soldiers in tropical regions.

The first description of S. stercoralis was made by a French physician named Auguste Normand in 1876, who observed the larvae in the diarrheic feces of French soldiers stationed in CochinChina (now Vietnam). He named the parasite Anguillula stercoralis, meaning "little eel of feces".

However, Normand did not recognize the parasitic nature of the larvae, and thought they were free-living nematodes that had accidentally ingested by the soldiers. He also did not notice the adult worms in the intestinal mucosa, which are very difficult to detect by conventional methods.

The true life cycle and pathogenicity of S. stercoralis were revealed later in the early 1900s by several researchers, including Arthur Looss, Thomas Bancroft, Charles Stiles, and Arthur Hassall. Looss discovered the skin penetration by the infective filariform larvae, Bancroft described the autoinfection and hyperinfection phenomena, Stiles and Hassall proposed the current name of the parasite, and Hassall also demonstrated the presence of adult female worms in the intestinal mucosa.

Since then, S. stercoralis has been recognized as a cosmopolitan parasite that can infect humans and other mammals, especially in tropical and subtropical regions where soil contamination with feces is common. It has also been associated with various clinical manifestations, ranging from asymptomatic carriage to severe disseminated disease, especially in immunocompromised individuals.

• Strongyloides stercoralis is a parasitic roundworm that infects humans and other animals. It is sometimes called a threadworm because of its slender shape and twisted uterus.
• S. stercoralis has a cosmopolitan distribution in tropical and subtropical regions, but may also occur in temperate areas during summer months . It is common in Brazil, Colombia, and in the Far East—Myanmar, Thailand, Vietnam, Malaysia, and the Philippines. It is also endemic in the southeastern United States and southern Europe, although most cases in the US occur in immigrants, refugees, travelers, and military veterans who have lived in endemic regions.
• The infection of S. stercoralis is associated with fecal contamination of soil or water . Hence, its prevalence is higher in areas with poor sanitation and areas associated with agricultural activity. It is found more frequently in socio-economically disadvantaged persons and in institutionalized populations.
• Strongyloides infection is not limited to human hosts. Dogs and nonhuman primates are susceptible to infection and this may play an important role in transmission. Other animal-associated Strongyloides spp., such as S. myopotami (nutria), S. procyonis (raccoons), and possibly others, may produce mild short-lived cutaneous infections in human hosts (larva currens, “nutria itch”), but do not cause true strongyloidiasis.
• Other species of Strongyloides that are naturally parasitic in humans, but with restricted distributions, are S. fuelleborni in central Africa and S. kellyi in Papua New Guinea.

Strongyloides stercoralis is a nematode (roundworm) that can live in two different forms: as a free-living worm in the soil, or as an intestinal parasite in humans and other animals. The habitat of S. stercoralis depends on its life cycle stage and mode of transmission.

Free-living form

The free-living form of S. stercoralis consists of adult male and female worms that mate and produce eggs in the soil. The eggs hatch into rhabditiform larvae, which are the first stage of the larval development. The rhabditiform larvae can either molt twice and become infective filariform larvae, which are the third stage of the larval development and can penetrate human skin, or they can molt four times and become free-living adult worms, which can continue the soil cycle .

The free-living form of S. stercoralis is found in moist, warm, and shaded soil that is contaminated with human or animal feces . The optimal temperature for the development of the larvae is between 25°C and 30°C. The larvae can survive for several weeks in the soil, depending on the environmental conditions.

Parasitic form

The parasitic form of S. stercoralis consists of adult female worms that live embedded in the mucosa of the small intestine (duodenum and jejunum) of humans and other animals . The adult female worms produce eggs by parthenogenesis (asexual reproduction), which hatch into rhabditiform larvae within the mucosa or the intestinal lumen. The rhabditiform larvae can either be passed in the stool and enter the soil cycle, or they can transform into filariform larvae and cause autoinfection, which is the reinfection of the same host by penetrating the intestinal wall or the perianal skin .

The parasitic form of S. stercoralis is found mainly in tropical and subtropical regions, where poor sanitation and hygiene practices facilitate the transmission of the infection . However, cases have also been reported in temperate areas, especially during summer months or among travelers, immigrants, refugees, and military veterans who have lived in endemic regions . S. stercoralis infection is also common in rural and remote communities, institutional settings, and among socially marginalized groups. In addition, some animals, such as dogs and nonhuman primates, can serve as reservoir hosts for S. stercoralis and may play a role in its transmission to humans .

Strongyloides stercoralis is a nematode (roundworm) that can exist in both parasitic and free-living forms. In the parasitic form, only the female worms are found in the human host, while the male worms are free-living in the soil. The female worms are thin, semi-transparent, and colorless, and measure about 2.5 mm long and 0.05 mm wide. The male worms are shorter and broader, measuring about 0.6-1 mm long and 40-50 µm wide.

The female worms have a mouth with three small lips at the anterior end, and a pointed tail at the posterior end. They have a cylindrical esophagus that occupies the anterior one-third of the body, and an intestine that occupies the posterior two-thirds. The anus is located mid-ventrally near the tail. The reproductive system consists of paired uteri, vagina, and vulva. The vulva is situated at the junction of the middle and posterior thirds of the body. The uteri contain thin-walled transparent eggs that are oval in shape and measure 50-60 µm by 30-35 µm. The female worms are ovoviviparous, meaning they produce eggs that hatch within their bodies.

The male worms have a mouth with two lips at the anterior end, and two spicules at the posterior end. The spicules are used to penetrate the female during copulation. They have a similar esophagus and intestine as the female worms, but they also have a genital primordium, which is a rudimentary reproductive organ. The male worms do not parasitize humans, but they can mate with free-living female worms in the soil.

The morphology of Strongyloides stercoralis can be summarized in the following table:

The life cycle of Strongyloides stercoralis is complex, alternating between free-living and parasitic cycles and involving autoinfection . The following diagram illustrates the main stages of the life cycle:

Free-living cycle

In the free-living cycle, rhabditiform larvae are passed in the stool of an infected definitive host, such as a human or a dog. These larvae develop into either infective filariform larvae (direct development) or free-living adult males and females that mate and produce eggs, from which rhabditiform larvae hatch and eventually become infective filariform (L3) larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle . This second generation of filariform larvae cannot mature into free-living adults and must find a new host to continue the life cycle.

Parasitic cycle

In the parasitic cycle, filariform larvae in contaminated soil penetrate human skin when skin contacts soil, and migrate to the small intestine. It has been thought that the L3 larvae migrate via the bloodstream and lymphatics to the lungs, where they are eventually coughed up and swallowed. However, L3 larvae appear capable of migrating to the intestine via alternate routes (e.g. through abdominal viscera or connective tissue). In the small intestine, the larvae molt twice and become adult female worms. The females live embedded in the submucosa of the small intestine and produce eggs via parthenogenesis (parasitic males do not exist), which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection .

Autoinfection

Autoinfection is a unique feature of Strongyloides stercoralis that allows the infection to persist for years or even decades in the host without exposure to external sources of infection . Autoinfection occurs when rhabditiform larvae in the gut become infective filariform larvae that can penetrate either the intestinal mucosa or the skin of the perianal area, resulting in reinfection of the host. Once the filariform larvae reinfect the host, they are carried to the lungs, pharynx and small intestine as described above, or disseminate throughout the body. Autoinfection may be quite common and may contribute to the development of hyperinfection syndrome, a severe form of strongyloidiasis that occurs in debilitated, malnourished, or immunosuppressed individuals .

One of the most remarkable features of Strongyloides stercoralis infection is the possibility of autoinfection and hyperinfection, which can lead to severe and potentially fatal complications.

Autoinfection

Autoinfection is the process by which rhabditiform larvae, instead of being excreted in the stool, transform into infective filariform larvae and re-enter the host through the intestinal mucosa or the perianal skin. This allows the parasite to maintain its life cycle within the same host for years or even decades, without requiring an external environmental phase.

Autoinfection can occur in two ways:

• Internal autoinfection: The rhabditiform larvae develop into filariform larvae within the intestinal lumen and penetrate the intestinal wall, reaching the bloodstream and lymphatics. From there, they migrate to the lungs, trachea, and pharynx, where they are swallowed and return to the small intestine, completing the cycle .
• External autoinfection: The rhabditiform larvae are excreted in the stool and develop into filariform larvae in the perianal region or other moist areas of the skin. They then penetrate the skin and follow the same migratory route as in internal autoinfection .

Autoinfection can result in a chronic asymptomatic or mild infection that persists for a long time, even after leaving an endemic area. However, it can also predispose to hyperinfection syndrome under certain conditions.

Hyperinfection

Hyperinfection syndrome is a life-threatening complication of strongyloidiasis that occurs when there is an accelerated multiplication and dissemination of filariform larvae throughout the body, involving multiple organs and systems . Hyperinfection syndrome is characterized by high parasite burden, severe eosinophilia, and polymicrobial sepsis.

Hyperinfection syndrome is most frequently associated with subclinical infection in patients receiving high-dose corticosteroids or other immunosuppressive drugs. Subsequent impaired host immunity leads to accelerated autoinfection and an overwhelming number of migrating larvae . Other risk factors include human T-cell lymphotropic virus type 1 (HTLV-1) infection, malnutrition, alcoholism, chronic renal failure, diabetes mellitus, hematologic malignancies, organ transplantation, and HIV infection .

The clinical manifestations of hyperinfection syndrome vary depending on the organs involved and may include diarrhea, abdominal pain, intestinal bleeding or perforation, pulmonary symptoms (cough, wheezing, hemoptysis), respiratory failure, skin lesions (urticaria, larva currens), meningitis, encephalitis, septicemia, endocarditis, myocarditis, nephritis, and liver abscesses . The diagnosis is based on the detection of filariform larvae in stool, sputum, urine, cerebrospinal fluid, blood, or tissue samples. The treatment consists of ivermectin or albendazole combined with supportive care and antibiotics for secondary bacterial infections . The prognosis is poor, with mortality rates ranging from 15% to 87%.

Hyperinfection syndrome is a medical emergency that requires early recognition and prompt treatment. Prevention strategies include screening and treating asymptomatic carriers of S. stercoralis , especially before initiating immunosuppressive therapy or traveling to endemic areas .

Strongyloides stercoralis is a soil-transmitted helminth that can cause chronic and sometimes fatal infection in humans. The pathogenesis and clinical features of this parasite depend on the stage of the life cycle, the host immune status, and the degree of parasite burden.

Pathogenesis

The pathogenesis of S. stercoralis involves two main aspects: tissue invasion by the infective filariform larvae (L3) and mucosal infection by the adult female worms.

• Tissue invasion: The L3 larvae penetrate the skin, usually through the feet or legs, and release hydrolytic enzymes that facilitate their entry into the blood or lymphatic vessels. They then migrate to the lungs, where they break through the alveolar walls and ascend the bronchial tree to the pharynx. They are then swallowed and reach the small intestine, where they molt twice and become adult female worms. The tissue invasion by the L3 larvae can cause local inflammation, hemorrhage, edema, and allergic reactions at the site of entry and along their migratory route. The pulmonary manifestations include cough, wheezing, dyspnea, hemoptysis, eosinophilic pneumonia, and Loeffler syndrome (transient pulmonary infiltrates with eosinophilia). The larval migration can also cause systemic symptoms such as fever, malaise, anorexia, weight loss, and urticaria.
• Mucosal infection: The adult female worms reside in the mucosa or submucosa of the duodenum and jejunum, where they produce eggs by parthenogenesis. The eggs hatch into rhabditiform larvae (L1), which are either excreted in the stool or undergo autoinfection. Autoinfection is a unique feature of S. stercoralis that allows the parasite to persist for decades in the host by transforming into infective L3 larvae within the intestine or perianal skin and re-entering the circulation or tissues. The mucosal infection by the adult worms can cause damage to the intestinal epithelium, resulting in inflammation, ulceration, bleeding, malabsorption, protein-losing enteropathy, and bacterial translocation. The intestinal manifestations include abdominal pain, diarrhea, nausea, vomiting, bloating, constipation, and peritonitis.

The pathogenesis of S. stercoralis can be influenced by several factors, such as:

• The degree of parasite burden: A higher number of worms can cause more tissue damage and inflammation, leading to more severe symptoms and complications.
• The host immune status: A normal immune response can limit the parasite multiplication and dissemination, resulting in asymptomatic or mild infection. However, immunosuppression due to corticosteroids, chemotherapy, HIV infection, organ transplantation, malignancy, or other conditions can impair the host defense mechanisms and facilitate autoinfection and hyperinfection. Hyperinfection is a potentially fatal complication of S. stercoralis that involves a massive increase in parasite load and dissemination to extraintestinal organs such as the liver, spleen, kidney, brain, heart, and skin. Hyperinfection can cause septic shock, meningitis, encephalitis, myocarditis, nephritis, endophthalmitis, and disseminated intravascular coagulation.
• The presence of co-infections: S. stercoralis can interact with other pathogens such as bacteria (e.g., Escherichia coli), viruses (e.g., human T-cell lymphotropic virus type 1), fungi (e.g., Candida albicans), or protozoa (e.g., Giardia lamblia), which can alter its life cycle or pathogenicity. For example, HTLV-1 infection can enhance autoinfection and hyperinfection by increasing the production of interleukin-5 (IL-5), a cytokine that stimulates eosinophil activation and IgE synthesis.

Clinical features

The clinical features of S. stercoralis infection vary depending on the stage of infection, the host immune status, and the degree of parasite burden. They can be classified into three main categories: acute infection (larval penetration and migration), chronic infection (intestinal parasitism), and hyperinfection syndrome (disseminated infection).

Acute infection

Acute infection occurs within days to weeks after exposure to contaminated soil or water. It is characterized by:

• Cutaneous manifestations: These include pruritus, erythema, papules, vesicles, pustules, or nodules at the site of larval penetration. In sensitized hosts, a characteristic serpiginous rash called larva currens (racing larvae) can develop, which moves rapidly along the skin (up to 10 cm/hour) and is usually seen on the buttocks, perineum, and thighs.
• Pulmonary manifestations: These include cough, wheezing, dyspnea, hemoptysis, eosinophilic pneumonia, and Loeffler syndrome. The pulmonary symptoms usually resolve spontaneously within a few weeks.
• Systemic manifestations: These include fever, malaise, anorexia, weight loss, and urticaria. They are more common in heavy infections or in immunocompromised hosts.

Chronic infection

Chronic infection occurs when the parasite establishes a long-term residence in the intestinal mucosa or submucosa. It is characterized by:

• Intestinal manifestations: These include abdominal pain, diarrhea, nausea, vomiting, bloating, constipation, and peritonitis. The diarrhea can be intermittent or persistent, and may contain blood or mucus. The abdominal pain can mimic peptic ulcer disease or appendicitis. The intestinal symptoms can be aggravated by food intake or stress. In severe cases, malabsorption, protein-losing enteropathy, and bacterial translocation can occur, leading to nutritional deficiencies, hypoalbuminemia, edema, and sepsis.
• Cutaneous manifestations: These include pruritus and urticaria, especially around the perianal area and buttocks. Larva currens can also recur in chronic infection.
• Pulmonary manifestations: These include chronic cough, wheezing, asthma-like symptoms, and bronchiectasis. Larvae can be detected in the sputum of some patients.
• Hematological manifestations: These include eosinophilia (>500/cumL of blood), which is a constant finding in chronic infection. However, eosinophilia may be absent in hyperinfection syndrome or in immunosuppressed hosts. Total serum immunoglobulin E (IgE) level is also elevated in more than half of the patients.

Hyperinfection syndrome

Hyperinfection syndrome occurs when the parasite undergoes a massive increase in multiplication and dissemination due to autoinfection. It is characterized by:

• Severe intestinal manifestations: These include profuse diarrhea (which may be watery or bloody), abdominal pain, distension, ileus, obstruction, perforation, peritonitis, and septic shock. The stool may contain large numbers of larvae.
• Severe pulmonary manifestations: These include respiratory distress, hemoptysis, pulmonary hemorrhage, pneumonia, empyema, and respiratory failure. The sputum may contain large numbers of larvae.
• Disseminated infection: This involves the spread of larvae to extraintestinal organs such as the liver, spleen, kidney, brain, heart, and skin. This can cause organ dysfunction and failure, as well as secondary bacterial or fungal infections. The clinical manifestations depend on the organ involved and may include meningitis, encephalitis, seizures, coma, myocarditis, arrhythmias, nephritis, renal failure, endophthalmitis, blindness, skin ulcers, abscesses, and disseminated intravascular coagulation.

Hyperinfection syndrome is a life-threatening complication that requires prompt diagnosis and treatment. It has a high mortality rate (>50%) even with appropriate therapy.

pathogenesis... - Online Biology Notes

Strongyloides stercoralis infection can be diagnosed by various methods, depending on the availability of resources, the stage and severity of the infection, and the clinical presentation of the patient. The main methods are:

• Microscopy: This is the most widely used and accessible method for diagnosis, but it has low sensitivity and specificity. It involves examining fresh or concentrated stool samples under a microscope for the presence of rhabditiform larvae, which are the diagnostic stage of S. stercoralis. The rhabditiform larvae have a short buccal cavity, a notched tail, and an esophagus that occupies about half of the body length. They can be distinguished from hookworm larvae, which have a longer buccal cavity, a pointed tail, and an esophagus that occupies only one-third of the body length. However, microscopy may miss many cases of infection, especially in chronic or low-intensity infections, because of the irregular and low output of larvae in the stool. Therefore, multiple stool samples (at least three) should be collected and examined to increase the diagnostic yield. Alternatively, duodenal aspirates or biopsies can be obtained by enterotest or endoscopy and examined for larvae, which may increase the sensitivity of microscopy .

• Stool culture: This is a more sensitive method than microscopy, but it requires more time and expertise. It involves culturing stool samples on various media, such as agar plates, charcoal cultures, filter paper tubes, or Baermann funnels, and allowing the rhabditiform larvae to develop into free-living adult worms or infective filariform larvae. The culture can be examined after 2-7 days for the presence of S. stercoralis worms or larvae . The agar plate method has been reported to have a sensitivity of 96% in detecting S. stercoralis.

• Serology: This is a highly sensitive and specific method for diagnosis, but it may not be available in resource-limited settings. It involves detecting antibodies against S. stercoralis antigens in serum samples using various techniques, such as enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination (IHA), or immunofluorescence assay (IFA). Serology can detect both acute and chronic infections, as well as asymptomatic carriers. However, serology cannot distinguish between active and past infections, and it may cross-react with other helminth infections . ELISA has been reported to have a sensitivity of 95% and a specificity of 93% for S. stercoralis diagnosis.

• Molecular diagnosis: This is a novel and promising method for diagnosis, but it is still under development and validation. It involves detecting S. stercoralis DNA in stool samples using polymerase chain reaction (PCR) or other molecular techniques. Molecular diagnosis has the potential to be more sensitive, specific, and rapid than other methods, and it may also allow for quantification of parasite load and differentiation of species or strains . A real-time PCR assay has been developed and tested for S. stercoralis detection in fecal samples, achieving 100% specificity and high sensitivity.

• Others: Other methods that may aid in the diagnosis of S. stercoralis infection include imaging studies (such as chest radiography or abdominal ultrasound), which may reveal characteristic findings in pulmonary or intestinal involvement; peripheral blood eosinophilia (>500/cumL), which is a common but nonspecific finding in most cases; total serum immunoglobulin E (IgE) level, which may be elevated in more than half of the patients; and sputum examination, which may reveal filariform larvae in cases of hyperinfection syndrome or disseminated infection .

  Treatments of Strongyloides stercoralis infections

Strongyloides stercoralis is a parasitic roundworm that can cause chronic and sometimes fatal infections in humans. The treatment of strongyloidiasis depends on the severity and extent of the infection, as well as the immune status of the patient. The main goals of treatment are to eliminate the adult worms from the intestine, prevent autoinfection and hyperinfection, and manage any complications.

For Acute and chronic strongyloidiasis

• The drug of choice for uncomplicated strongyloidiasis is ivermectin, which kills the adult worms but not the larvae. It is given orally at a dose of 200 micrograms per kilogram of body weight once daily for 1-2 days . Ivermectin has a high efficacy and tolerability compared to other anthelmintics.
• An alternative drug for patients who cannot take ivermectin is albendazole, which also kills the adult worms but not the larvae. It is given orally at a dose of 400 milligrams twice daily for 7 days. Albendazole has a lower efficacy and more side effects than ivermectin.
• Patients with chronic strongyloidiasis may require repeated courses of treatment to achieve cure, as the larvae can persist in the soil and reinfect the host. Follow-up stool examinations or serological tests are recommended to monitor the response to treatment.
• Patients with chronic strongyloidiasis should also receive supportive care, such as nutritional supplementation, correction of electrolyte imbalances, and treatment of any secondary bacterial infections.

For Hyperinfection syndrome/Disseminated strongyloidiasis

• Hyperinfection syndrome and disseminated strongyloidiasis are life-threatening complications of strongyloidiasis that occur in immunocompromised patients, such as those receiving corticosteroids or chemotherapy, or those with HIV/AIDS or HTLV-1 infection. These conditions are characterized by massive multiplication and dissemination of larvae throughout the body, causing severe organ damage and sepsis.
• The treatment of hyperinfection syndrome and disseminated strongyloidiasis is similar to that of uncomplicated strongyloidiasis, but with a longer duration and higher dose of ivermectin. The recommended dose is 200 micrograms per kilogram of body weight per day orally until stool and/or sputum exams are negative for 2 weeks. Alternatively, subcutaneous injections of ivermectin can be used if oral administration is not possible.
• Patients with hyperinfection syndrome and disseminated strongyloidiasis also require intensive care, such as mechanical ventilation, fluid resuscitation, broad-spectrum antibiotics, and management of any organ failure or bleeding complications.
• Patients with hyperinfection syndrome and disseminated strongyloidiasis have a high mortality rate, ranging from 15% to 87%. Therefore, early diagnosis and prompt treatment are essential to improve the prognosis.

Prophylaxis of Strongyloides stercoralis

The prevention of strongyloidiasis involves reducing the exposure to contaminated soil or water, improving sanitation and hygiene practices, and treating infected cases. Some specific measures include:

• Wearing shoes and gloves when working or walking on soil that may be contaminated with human feces.
• Washing hands thoroughly after contact with soil or feces.
• Boiling or filtering water before drinking or cooking if the source is potentially contaminated.
• Disposing of human feces safely and preventing soil contamination by using latrines or sewage systems.
• Treating all infected cases with appropriate anthelmintics to prevent transmission and autoinfection.

• Screening and treating high-risk populations, such as travelers, immigrants, refugees, military veterans, institutionalized persons, or immunocompromised patients, who may have acquired or reactivated infection from endemic areas.

The prevention of strongyloidiasis involves reducing the exposure to contaminated soil or water, improving sanitation and hygiene practices, and treating infected cases. Some specific measures include:

• Wearing shoes and gloves when working or walking on soil that may be contaminated with human feces.
• Washing hands thoroughly after contact with soil or feces.
• Boiling or filtering water before drinking or cooking if the source is potentially contaminated.
• Disposing of human feces safely and preventing soil contamination by using latrines or sewage systems.
• Treating all infected cases with appropriate anthelmintics to prevent transmission and autoinfection.

• Screening and treating high-risk populations, such as travelers, immigrants, refugees, military veterans, institutionalized persons, or immunocompromised patients, who may have acquired or reactivated infection from endemic areas.

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