Intestinal helminths, strongyloidiasis and schistosomiasis

• Soil-transmitted helminths (roundworm, hookworm and whipworm) and schistosomiasis are cheaply treated, often in a day or two with a single oral drug, yet between them they affect well over a billion people, almost all in poor communities with poor sanitation. ^[3]
• Strongyloidiasis is different: the worm can live for decades and multiply inside one person, so a single corticosteroid course in an apparently well patient can trigger a rapidly fatal hyperinfection syndrome.
• These three intestinal roundworms do not multiply in the human host and re-infect through contaminated soil or water; hookworm larvae in particular can burrow through bare skin.
• Schistosomiasis is a blood-fluke infection picked up from freshwater; the danger comes from the body's reaction to eggs that lodge in the liver, gut or bladder, and praziquantel is the drug of choice for every species. ^[8]
• Drug treatment is short and safe; the real management is choosing whom to treat, when to repeat doses, how to prevent re-infection with clean water, sanitation and footwear, how to care for special groups, and how to protect immunosuppressed patients from Strongyloides.

By the end of this page you should be able to:

1. Describe the life cycle and transmission of roundworm, hookworm, whipworm, Strongyloides stercoralis and the main Schistosoma species, and explain why treatment is cheap while control is hard.
2. Recognise the clinical pictures of ascariasis, hookworm disease, trichuriasis, strongyloidiasis (including hyperinfection), and intestinal and urogenital schistosomiasis.
3. Order sensible investigations and interpret an eosinophil count, stool and urine microscopy, serology and imaging.
4. Prescribe albendazole, ivermectin, mebendazole, pyrantel and praziquantel with correct dose, route, duration and cautions.
5. Recognise hyperinfection syndrome and disseminated strongyloidiasis, explain why corticosteroids trigger it, and manage it as an emergency.
6. State the public health and preventive measures, including screening before immunosuppression and mass drug administration.

Clinically these split into three groups. First, the large roundworms that do not multiply in people and re-infect only from the environment: Ascaris, Trichuris and hookworm. Second, Strongyloides stercoralis, whose autoinfection lets one patient harbour it for life, with fatal consequences during immunosuppression. Third, the schistosomes, whose adults live in the vasculature and whose disease comes from the host response to their eggs. ^[3]

The intestinal and (briefly) urogenital forms of schistosomiasis are covered here; hepatic portal fibrosis shares the same drug target, so management is identical. ^[9]

Soil-transmitted helminths. WHO estimates that about 1.5 billion people, roughly 24% of the world's population, carry at least one STH, making these among the commonest infections on earth. ^[3] More than 260 million pre-school children, 654 million school-age children, 108 million adolescent girls and 138.8 million pregnant or lactating women live in areas of intense transmission and need treatment and prevention. ^[3] Over 600 million people are estimated to be infected with Strongyloides stercoralis, which shares the poor-sanitation map but is seldom detected by routine programmes. ^[3] Transmission is highest in sub-Saharan Africa, China, South America and Asia. There is no direct person-to-person spread, and eggs in faeces need about 3 weeks in soil to become infective. ^[3]

Schistosomiasis. An estimated 253.7 million people required preventive treatment in 2024, of whom more than 100.5 million received it, and transmission has been reported from 79 countries. ^[10] Deaths are estimated at 14,353 per year globally, likely an underestimate. ^[10] At least 93.9% of those needing treatment live in Africa, mostly in poor rural agricultural and fishing communities. ^[10] The forms and their maps: Schistosoma mansoni in Africa, the Middle East, the Caribbean, Brazil, Venezuela and Suriname; S. japonicum in China, Indonesia and the Philippines; S. mekongi in Cambodia and Lao PDR; S. haematobium in Africa and the Middle East. ^[10]

Strongyloides. Global prevalence is largely unknown because surveillance is limited; clues are birth, residence or travel in the tropics with poor sanitation, and the infection can persist for decades. ^[6]

Transmission determines who is at risk, how to diagnose and how to prevent. ^[1]

• Ascaris lumbricoides. Infection follows ingestion of mature eggs from vegetables, water or hands contaminated with soil. ^[3] Worms do not multiply in people, so intensity depends on re-exposure.
• Trichuris trichiura. Eggs from faecally contaminated soil or food are swallowed; heavy infection means many worms.
• Hookworm. Eggs hatch in soil and release larvae that penetrate bare skin (especially the feet); Ancylostoma duodenale can also be swallowed. ^[3]
• Strongyloides stercoralis. Filariform larvae in soil penetrate skin or mucous membranes, and the key feature is autoinfection, where larvae re-invade the same person and sustain infection for decades. ^[5]
• Schistosomiasis. Larval forms released by freshwater snails penetrate the skin during water contact; eggs in stool or urine re-contaminate water to complete the cycle. ^[10]

Risk is environmental and socioeconomic: poor sanitation, poverty, rural residence, agriculture or fishing, unsafe water and bare feet in endemic areas. ^[10] Migration and travel matter: tropical infection presents in temperate cities years after exposure. ^[5] For Strongyloides the key risks are pharmacological immunosuppression (especially corticosteroids), HTLV-1 infection, haematological malignancy, organ transplantation and residence or travel in endemic areas, as in CDC screening guidance. ^[4]

STH infections impair nutrition in several ways: worms feed on host tissues including blood (hookworms most), causing chronic intestinal blood loss and iron deficiency anaemia; they increase malabsorption and some cause loss of appetite; roundworm may compete for vitamin A. ^[3] Roundworm larvae migrate through the lung before settling in the gut; whipworm lives in the caecum and damages colonic mucosa; hookworm attaches to the small-bowel wall and bleeds. ^[1][3] Intensity of infection determines severity, and millions of low-intensity infections cause only modest illness. ^[1]

This is the mechanism that makes Strongyloides dangerous. Rhabditiform larvae in the gut develop into infective filariform larvae that can penetrate the intestinal wall or the skin around the anus and re-infect the same host. ^[5] A healthy immune response holds the numbers down. When immunity is impaired (most notoriously by high-dose corticosteroids for asthma or chronic obstructive pulmonary disease exacerbations), autoinfection accelerates: thousands of larvae disseminate, carrying gut bacteria with them. ^[5] Hyperinfection is confined to gut and lung; disseminated disease reaches many other organs. ^{[5] [6]}

The adult lives harmlessly in the veins; damage is done by eggs trapped in tissue. ^[10] The granulomatous and fibrotic response to these eggs produces disease, with target organs determined by where eggs deposit: S. mansoni and S. japonicum in bowel and liver, S. haematobium in urinary and genital tracts. ^[9][10]

Most light infections are silent. ^[1][3] Heavy infection gives pulmonary migration symptoms (cough, wheeze, transient eosinophilic infiltrates, often called Löeffler syndrome) during larval passage, followed by abdominal pain, bloating, nausea and anorexia once adults mature in the small intestine. ^[1] Serious complications are intestinal obstruction from a tangled mass of worms (commonest in heavily infected children), biliary or pancreatic obstruction when an adult migrates up a duct, and cholangitis. ^[1] Adults may be vomited or passed per rectum.

Attachment to the small intestine causes chronic blood loss, so the dominant problem is iron-deficiency anaemia proportional to worm burden, presenting as fatigue, dyspnoea on exertion, pallor and, in severe cases, heart failure. ^[1][3] Larvae cause a pruritic erythematous "ground itch" at the entry site (usually the feet), ^[1] with malabsorption, abdominal pain and, in children, impaired growth. ^[3]

Light infection is usually asymptomatic; heavier infection causes abdominal pain, diarrhoea and, when the mucosa is inflamed, dysentery with blood and mucus. ^[3] With very heavy infection Trichuris dysentery syndrome develops: chronic mucoid bloody diarrhoea, growth faltering and anaemia in children, occasionally rectal prolapse. ^[1] Whipworm can also cause appendicitis-like pain. ^[1]

Acute infection begins with a pruritic erythematous rash at larval entry, followed by tracheal irritation, dry cough and transient wheeze as larvae pass through the lungs, then diarrhoea, constipation, abdominal pain and anorexia when they reach the gut. ^[5]

Chronic infection is often completely silent; symptomatic patients complain of epigastric pain, postprandial fullness, heartburn and brief intermittent diarrhoea or constipation, with occult or massive gastric and colonic haemorrhage and a colitis-like picture documented. ^[5] Cutaneous findings include chronic urticaria and larva currens, a serpiginous or urticarial rash that advances up to 10 cm per hour, usually along the buttocks, perineum and thighs. ^[5] Up to 75% of those with chronic strongyloidiasis have mild peripheral eosinophilia or raised IgE. ^[5]

Hyperinfection and disseminated strongyloidiasis are the life-threatening forms: abdominal pain, nausea, vomiting, diarrhoea, ileus, bowel oedema and intestinal obstruction; mucosal ulceration with massive haemorrhage and peritonitis; cough, wheeze, dyspnoea, pneumonitis and respiratory failure; aseptic or gram-negative meningitis (larvae in cerebrospinal fluid); and systemically protein-losing enteropathy with hypoalbuminaemia, ascites, oedema and syndrome of inappropriate secretion of antidiuretic hormone (SIADH). ^[4][5] Peripheral eosinophilia is frequently absent. ^[5] Gram-negative sepsis recurs because migrating larvae carry gut flora through mucosal walls. ^[5] Case-fatality approaches 90%. ^[4][5]

Acute schistosomiasis (Katayama syndrome) follows 14 to 84 days after exposure and resembles serum sickness: fever, headache, myalgia, rash and respiratory symptoms, usually with marked eosinophilia and hepatosplenomegaly. ^[8][9]

Chronic intestinal schistosomiasis (S. mansoni, S. japonicum, S. mekongi, S. intercalatum) produces abdominal pain, diarrhoea, constipation and blood in the stool from eggs in the bowel wall, progressing to bowel-wall ulceration, hyperplasia and polyposis; heavy infection causes hepatic fibrosis, portal hypertension, splenomegaly and ascites dominating the late picture. ^[9][10]

Urogenital schistosomiasis (S. haematobium) begins as terminal haematuria and dysuria, becomes chronic frequency and obstruction, and over years damages bladder (fibrosis, calcification) and kidneys and raises bladder-cancer risk. ^[10] It also causes female genital schistosomiasis (cervix, fallopian tubes, vagina) with discharge, bleeding, pain and infertility, and male genital disease with haematospermia and prostatic or seminal vesicle changes. ^[10]

Other sites. Ectopic egg deposition in the spinal cord (S. mansoni or S. haematobium) or brain (S. japonicum) is rare but produces granulomas acting as space-occupying lesions with transverse myelitis or seizures. ^[9] Katayama syndrome can be unusually severe in travellers, sometimes with paralysis. ^[10]

The parasites in this page overlap in presentation: abdominal pain, altered bowel habit, weight loss and anaemia can mean infection with any STH, several schistosome species, giardiasis, amoebiasis, inflammatory bowel disease, coeliac disease or colon cancer. Use distribution, exposure and eosinophils to narrow.

No single test is perfect; eosinophilia is often the clue rather than the proof. ^[4][5]

Full blood count. Peripheral eosinophilia is common in chronic strongyloidiasis (up to 75% of patients) and in acute schistosomiasis, but it is frequently absent in hyperinfection. ^[5] Anaemia dominates in hookworm. Raised IgE supports strongyloidiasis. ^[5]

Stool examination. For the STHs and intestinal schistosomiasis, microscopy for eggs is the first-line test; the Kato-Katz technique is standard. ^[10] Strongyloides rhabditiform larvae are the target rather than eggs, and a single stool exam is insensitive: serial examinations (up to seven) may be needed for high sensitivity. ^[5] Specialised methods include Baermann concentration, Horadi-Mori filter-paper culture and nutrient agar plate culture. ^[5]

Urine. For urogenital schistosomiasis, filtration of a midday urine through nylon, paper or polycarbonate for eggs is standard; reagent strips for microscopic haematuria screen children well. ^[10]

Serology. Antibody tests for Strongyloides are sensitive but cross-react with filarial parasites, schistosomes and Ascaris, so specificity suffers; antibodies may persist for months after cure, though a significant proportion become negative within 6 months of successful treatment. ^[5] Recombinant-antigen assays are more specific. For schistosomiasis, serology and antigen (circulating cathodic antigen, CCA) support diagnosis in light infections and non-endemic settings. ^[10] Serology is often used to screen before immunosuppression in endemic or travel-exposed patients. ^[4]

Respiratory sampling. In hyperinfection, larvae are often seen in bronchoalveolar lavage fluid. ^[5] Duodenal aspirate is more sensitive than stool for strongyloidiasis. ^[5]

Imaging. In schistosomiasis, abdominal ultrasonography assesses periportal fibrosis and portal hypertension, and CT or MRI can show disease extent. ^[10] For suspected intestinal obstruction with ascariasis, plain abdominal radiograph shows dilated loops and sometimes a mass of worms. Cardiac and lung findings are non-specific in strongyloidiasis.

Histology. Duodenal biopsy may show parasites in gastric crypts or duodenal glands with eosinophilic infiltration. ^[5] Eggs in rectal or bladder biopsy can confirm schistosomiasis.

Aetiological diagnosis rests on demonstrating the parasite (eggs or larvae), supported by serology where appropriate. For population control, WHO uses broad programmes without individual diagnosis, treating at-risk groups in endemic areas. ^[3] Individual clinical diagnosis, by contrast, requires matching exposure, symptoms and a positive test.

Severity is driven by intensity of infection. For the STHs, heavy infections cause obstruction, dysentery or anaemia, while light infections are often harmless. ^[1][3] For schistosomiasis, WHO recommends treating children at least 2 years old and pregnant women in mass campaigns, with preschool-aged children diagnosed and treated individually using paediatric praziquantel. ^[10] Paediatric dispersible praziquantel (arpraziquantel) has shown high efficacy and a favourable safety profile in children 3 months to 6 years. ^[8]

The single most important point is that all of these infections are curable with cheap oral drugs, so the clinical task is deciding whom, when and how often to treat, and how to prevent re-infection. ^[2][3][8]

Guideline editions used here: the CDC clinical care pages for soil-transmitted helminths (updated 3 June 2024), Strongyloides (16 February 2024, clinical overview 11 February 2026) and schistosomiasis (4 March 2024); WHO fact sheets on soil-transmitted helminth infections (18 January 2023) and schistosomiasis (23 February 2026); the Jourdan 2018 Lancet seminar; the Gordon 2024 Nature Reviews Disease Primers article; and the Lo 2025 review of the WHO strongyloidiasis guideline. ^{[1][4][6][7][9][10]}

The CDC 2024 guidance provides these adult and paediatric doses (the same for adults and children unless noted): ^[2]

Albendazole, ivermectin and mebendazole are pregnancy category C. WHO allows albendazole or mebendazole in the second and third trimesters during mass campaigns, and ivermectin is excluded from mass campaigns in pregnancy. ^[2] Albendazole and ivermectin have limited safety data in children under 6 years or under 15 kg: WHO guidance for mass campaigns allows albendazole from 1 year of age and ivermectin from a height of 90 cm. ^[2] FDA has not approved albendazole for ascariasis or hookworm, nor albendazole or ivermectin for whipworm, but all are widely used off-label and donated for mass deworming. ^{[2] [3][4] [8]}

Chronic infection can be eradicated: the CDC first-line is ivermectin 200 micrograms per kg orally for 1 to 2 days, with albendazole 400 mg orally twice daily for 7 days as the alternative. ^[4] Cochrane evidence and the CDC text agree ivermectin is more effective than albendazole, and albendazole should be used only when ivermectin is unavailable (for example because of possible Loa loa co-infection). ^[4][6] Follow-up stool examination 2 to 4 weeks after treatment confirms clearance, with retreatment if larvae persist. ^[4] Strongyloides is not sensitive to albendazole or mebendazole in mass-campaign doses, so does not benefit reliably from STH programmes. ^[3][7]

This is an emergency. ^[4][5]

• Stop or reduce immunosuppression if possible, especially high-dose corticosteroids. ^[4][5]
• Give ivermectin 200 micrograms per kg per day orally until stool and sputum (and BAL if sampled) are negative for at least 2 weeks. ^[4]
• If ileus or malabsorption prevents oral dosing, published case reports show efficacy with rectal administration; where neither route is possible, an Investigational New Drug exemption for veterinary subcutaneous ivermectin has been granted by FDA in isolated cases. ^[4]
• Treat bacterial superinfection aggressively (gram-negative meningitis, bacteraemia, peritonitis) with broad-spectrum antibiotics plus supportive care; larvae carry gut flora. ^[5]
• Screen contacts and siblings only where local protocol calls for it; the immediate patient is the priority. ^[5]

Both the acute and the chronic forms of strongyloidiasis can be silent, and a patient starting corticosteroids (especially for an asthma or chronic obstructive pulmonary disease flare) may develop hyperinfection weeks later. ^[4][5] Empiric corticosteroids for wheezing in a patient from an endemic area are particularly dangerous. ^[5] Prevention is better and cheaper than treating hyperinfection, where mortality approaches 90%. ^[4][5]

WHO's 2024 first guideline for public health control of strongyloidiasis uses a prevalence-based recommendation and targets control of strongyloidiasis morbidity in school-age children, while the individual clinical rule remains: screen or treat before immunosuppression, using serology and stool. ^{[7] [3]}

Praziquantel is effective against all major Schistosoma species and is the drug of choice; widespread clinical resistance has not occurred. ^[8] Timing matters because praziquantel acts on adult worms and requires a mature antibody response: ^[8][9]

• S. mansoni, S. haematobium and S. intercalatum: 40 mg per kg per day orally in two divided doses for one day. ^[8]
• S. japonicum and S. mekongi: 60 mg per kg per day orally in three divided doses for one day. ^[8]

For travellers, treat only at least 6 to 8 weeks after the last exposure to potentially contaminated freshwater, so adult worms have matured. ^[8] Lightly infected patients may need repeat dosing after 2 to 4 weeks because the immune response is less robust. ^[8] Where the pre-treatment stool or urine exam was positive, a follow-up exam 1 to 2 months later helps confirm cure. ^[8]

Screening follows CDC, which lists patients on or about to begin corticosteroid therapy or other immunosuppressants, those with HTLV-1 infection, haematological malignancy, organ transplant history, persistent or unexplained eosinophilia, and travel to endemic areas. ^[4] Empiric treatment of seropositive or at-risk patients before immunosuppression is common and sensible. ^[4] Adults with persistent infection rarely become seriously ill from ordinary immunosuppression, so the intensity is screening and early treatment.

Hygiene and population control. WHO targets school-age children and at-risk groups with periodic preventive chemotherapy; high-transmission areas require annual treatment. ^[10] The six 2030 targets include elimination of morbidity in pre-school and school-age children and universal access to at least basic sanitation and hygiene in STH-endemic areas. ^[3] Between 2010 and 2019, DALYs lost to STH fell by more than 50% as coverage scaled up. ^[3]

• Ascariasis. Intestinal obstruction, biliary or pancreatic obstruction, cholangitis. ^[1]
• Hookworm. Iron-deficiency anaemia, heart failure in severe cases, impaired growth. ^[1][3]
• Trichuriasis. Trichuris dysentery syndrome, rectal prolapse, anaemia. ^[1]
• Strongyloidiasis. Malnutrition, hyperinfection, disseminated strongyloidiasis with gram-negative sepsis and meningitis, death; mortality approaches 90% in severe forms. ^[4][5]
• Schistosomiasis. Hepatic fibrosis, portal hypertension, splenomegaly, ascites, bladder fibrosis and calcification, obstructive uropathy, bladder cancer, female genital schistosomiasis with infertility. ^[9][10]
• After surgery for complications or secondary procedures is rarely needed; these are medical diseases.

Treated light infections resolve quickly and fully. ^[2][3] Heavy injury (portal fibrosis in late schistosomiasis, growth faltering) may only partly reverse, but periodic treatment in childhood lowers the risk of severe late disease, and praziquantel reverses much of the morbidity. ^[10] Strongyloides, if eradicated before immunosuppression, removes a fatal risk entirely. ^[3][4] Strongyloides hyperinfection carries mortality near 90%, so early recognition dominates outcomes. ^[4][5]

Prevention beats cure at the population level. ^[3][10]

• Mass drug administration with albendazole 400 mg (or mebendazole 500 mg) for STH and with praziquantel 40 mg per kg (or 60 mg per kg) for schistosomiasis remains the WHO strategy for endemic areas. ^[3][10]
• Sanitation: sanitary disposal of faeces and urine prevents soil contamination; eggs need about 3 weeks in soil to mature, so breaking the chain matters. ^[3]
• Water: avoid bathing or swimming in infested freshwater for schistosomiasis; safe water for washing, drinking and cooking. ^[10]
• Shoes interrupt larval skin penetration for hookworm and Strongyloides. ^[3]
• Hygiene education and hand washing; deworming integrated with school and child health programmes. ^[3]
• Snail control and veterinary public health (One Health) where species overlap. ^[10]
• Fence off or drain transmission sites where practical. ^[10]
• Screen travellers and migrants after return from endemic regions where appropriate. ^[1]

For individual patients, screening for Strongyloides before steroid or immunosuppressive therapy is the highest-yield single action. ^[4]

STHs impair growth and learning, and school-based deworming is effective and cheap. ^[3] Roundworm obstruction is a surgical emergency most often in the young. ^[1] Albendazole is used from 1 year of age and ivermectin from 90 cm height in mass campaigns because of safety data gaps below those thresholds. ^[2] Praziquantel is used in children from 2 years of age in mass campaigns, and paediatric dispersible formulations have been studied down to 3 months of age in some countries. ^[8][10]

Albendazole and mebendazole are pregnancy category C and are given only if benefit outweighs risk; WHO permits use in the second and third trimesters during mass campaigns. ^[2] Ivermectin is also category C and is excluded from mass campaigns in pregnancy. ^[2] Pyrantel pamoate is category C with WHO allowance in second and third trimesters. ^[2] Praziquantel is pregnancy category B, with WHO encouragement at any stage in mass campaigns; individual clinical judgement balances treatment against disease progression. ^[8] In a pregnant patient, balance risk to the fetus against the risks of untreated heavy infection, including worsening anaemia and obstruction. ^[2][8]

Albendazole and mebendazole are minimally excreted and compatible with breastfeeding; ivermectin enters breast milk in low concentration and should be given only when maternal disease risk outweighs infant risk; praziquantel is compatible. ^{[2][8] [4]}

HTLV-1 co-infection and corticosteroids above all predispose to hyperinfection; consider Strongyloides screening in any patient from an endemic area before chemotherapy, transplant or anti-tumour-necrosis treatment and use empiric ivermectin where serology is positive. ^[4][6]

• One tablet, no infrastructure: mass deworming with donated albendazole 400 mg and praziquantel 40 mg per kg is highly cost-effective and the doses are fixed for adults and children except age or height limits. ^[2][3]
• Kato-Katz microscopy can be performed with a cheap kit; where resources are lowest, clinical and epidemiological suspicion drives treatment.
• Bare feet and poor sanitation are the modifiable exposures; shoes and latrines cost far less than repeated treatment but are harder to deliver. ^[3]
• Where CT or MRI is unavailable, clinical signs plus eggs in stool or urine carry the diagnosis. ^[9][10]
• Without ivermectin, albendazole covers STH poorly for Strongyloides, so early access to ivermectin matters most for immunosuppressed patients and prevents deaths. ^[4][7]
• In schistosomiasis, decentralising urine filtration and praziquantel delivery to schools reaches the children who carry most of the burden. ^[10]

Ascariasis and intestinal obstruction in children; iron deficiency anaemia; eosinophilia; imported infections and returned travellers; neglected tropical diseases; water, sanitation and hygiene (WASH) programmes; lymphatic filariasis and co-administered ivermectin and albendazole.

• STHs affect about 1.5 billion people (roughly 24% of the global population) and schistosomiasis about 253.7 million; both are concentrated in communities with poor sanitation and water. ^[3][10]
• Roundworm, whipworm and hookworm do not multiply in humans; intensity depends on environmental exposure and transmission. ^[3]
• Hookworm attaches to the gut wall and causes iron-deficiency anaemia; heavy roundworm causes intestinal obstruction; heavy whipworm causes dysentery and rectal prolapse. ^[1]
• Strongyloides can persist for decades by autoinfection, and corticosteroid-induced hyperinfection kills up to 90% of patients if treatment is delayed. ^[4][5]
• The first-line tests are stool microscopy (Kato-Katz) for STH and intestinal schistosomiasis, urine filtration for S. haematobium and serology where appropriate. ^[5][10]
• Albendazole (400 mg), mebendazole (500 mg) and ivermectin (200 micrograms per kg) are the standard basis of STH treatment; praziquantel is the drug of choice for all schistosome species. ^[2][3][8]
• Strongyloidiasis should be treated with ivermectin 200 micrograms per kg for 1 to 2 days, or albendazole 400 mg twice daily for 7 days if ivermectin is unavailable, followed by stool re-check at 2 to 4 weeks. ^[4]
• Hyperinfection is an emergency managed by stopping immunosuppression and giving daily ivermectin until stool and sputum are negative for 2 weeks, plus antibiotics and supportive care. ^[4][5]
• Schistosomiasis dosing is 40 mg per kg for S. mansoni, S. haematobium and S. intercalatum, and 60 mg per kg for S. japonicum and S. mekongi, in divided doses over one day. ^[8]
• Prevention combines mass drug administration with sanitation, safe water, footwear and vector or snail control, and screening before immunosuppression. ^[3][4][10]
• Most drugs are pregnancy category C except praziquantel, which is category B, and all require weighing benefit against untreated disease in pregnancy and during breastfeeding. ^[2][8]