Amoebiasis, giardiasis and cryptosporidiosis

• The intestinal protozoa in this topic - Entamoeba histolytica, Giardia duodenalis, Cryptosporidium species and Cyclospora cayetanensis - are all caught by the faecal-oral route. They can look alike clinically, so the diagnosis is made in the stool.
• Amoebiasis is the one that turns invasive: most people carry E. histolytica without symptoms, about 90%, but a minority develops bloody diarrhoea or an amoebic liver abscess, sometimes years after travel. ^[1][3][2]
• Giardiasis is the commonest parasitic gut infection in the United States and gives malabsorptive, greasy stools; it usually runs 2 to 6 weeks and is treated with a nitroimidazole. ^[5][9]
• Cryptosporidiosis and cyclosporiasis are usually self-limited in healthy people, but in a person with advanced HIV disease they become life-threatening, chronic and difficult to clear. ^[6][7][9]
• Treatment follows the organism, not just the symptom: metronidazole or tinidazole for amoebiasis and giardiasis, nitazoxanide for cryptosporidiosis in immunocompetent patients, trimethoprim-sulfamethoxazole for cyclosporiasis. ^[2][4][6][8]

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

1. Explain why E. histolytica disease is the exception among the intestinal protozoa, and describe how it reaches the liver.
2. Recognise the presentation of amoebic colitis and amoebic liver abscess, interpret stool and serological tests, and know when and how to treat or drain.
3. Distinguish giardiasis, cryptosporidiosis and cyclosporiasis on the basis of incubation, stool character and patient factors, especially HIV infection.
4. Prescribe the correct drug, dose, route and duration for each condition, and adapt it for children, pregnant patients and immunocompromised hosts.
5. Outline the HIV cross-check: why antiretroviral therapy matters more than any antiparasitic for cryptosporidiosis, cyclosporiasis and isosporiasis.
6. Cross-check your patient with the MedGrasp topic "Gastroenterology: infectious diarrhoea and foodborne illness" for rehydration and for when antibiotics are and are not justified.
7. Adapt diagnosis and treatment to a low-resource setting where microscopy or PCR may not be available.

It is useful to keep them separate.

• Amoebiasis stands apart because it is invasive. E. histolytica trophozoites can cross the colonic mucosa, enter the portal circulation and form extraintestinal abscesses, most often in the liver. ^[3]
• Giardiasis is a luminal infection of the small bowel. It does not invade, but it damages the brush border and causes malabsorption. ^[5]
• Cryptosporidiosis and cyclosporiasis are coccidian infections of the small bowel that in healthy people are usually mild and self-limited, but become chronic and dangerous in immunocompromise. ^[6][7][9]

Isospora belli behaves like cryptosporidiosis and cyclosporiasis in advanced HIV disease and is treated with the same drug. It is mentioned here so that it is not missed. ^[9]

Amoebiasis is the heaviest burden. About 50 million people are estimated to be infected each year with E. histolytica, and although roughly 90% remain asymptomatic, those who become ill most often have bloody diarrhoea or an amoebic liver abscess. The disease is estimated to cause 55,000 deaths and 2.2 million disability-adjusted life-years lost annually, mainly in low-income countries. ^[3]

Tropical and subtropical parts of Central and South America, Asia and Africa are most affected; particular countries include Bangladesh, India, Brazil, Colombia, Mexico and China. In some areas, such as parts of Mexico, Turkey, China, Saudi Arabia, Yemen, Egypt and South Africa, amoebiasis accounts for up to 20 to 40% of reported infectious diarrhoea. ^[3]

In high-income countries most cases are imported. In the United Kingdom, E. histolytica is a notifiable laboratory finding with about 100 infections reported per year, probably an underestimate; the GeoSentinel network found it to be the third most commonly isolated infection among returning travellers with gastrointestinal illness, responsible for between 0.3 and 10% of visitor diarrhoea. Only about 8% of infected people in one Australian study had no prior travel history, so acquisition without travel does occur. ^[3]

Travel usually precedes disease by weeks to months; symptoms develop after, not during, travel and can appear months or even more than 20 years after the last visit to an endemic area. Men are affected more often than women, up to 72 to 76% of adult cases of amoebic liver abscess, possibly in part because of alcohol-related liver injury increasing susceptibility. Postmenopausal women also have an increased risk of amoebic liver abscess. ^[3]

Giardiasis is the most common parasitic gut infection in the United States, with more than 1 million people becoming ill every year. It occurs in every region of the United States and worldwide. Children are more likely to become ill than adults, and infection spreads easily in childcare settings and from untreated or recreational water. ^[5]

Cryptosporidiosis is the leading cause of waterborne disease in the United States. Symptoms begin 2 to 10 days after infection, most often around 7 days, and last 1 to 2 weeks. Many healthy people are asymptomatic. ^[7]

Cyclosporiasis is endemic in tropical and subtropical countries and appears seasonal, though the seasonality varies by setting and is not well understood. In the United States it causes outbreaks linked to imported fresh produce. ^[8]

All four parasites are transmitted faecal-orally, by soiled hands, contaminated food or water, or surfaces and objects. Giardia is notable for its low infective dose: swallowing just a few organisms can cause illness. Cyclospora oocysts must mature outside the host for at least 1 to 2 weeks in favourable conditions before they become infective, so direct person-to-person transmission is unlikely. ^[5][8]

Risk factors and exposures:

• Amoebiasis: travel to or residence in a tropical endemic region; male sex; men who have sex with men; postmenopausal women; immunosuppressive medication, especially corticosteroids; alcohol-related liver disease; poor sanitation. ^[3][1]
• Giardiasis: close contact in childcare settings; limited access to safe drinking water; swallowing untreated water from lakes, rivers, springs or shallow wells or swallowing water from pools and splash pads; weakened immune system; contact with faeces during sex; contaminated environments. ^[5]
• Cryptosporidiosis: contaminated water, swimming pools and water play areas, animal contact, childcare and institutional settings, immunocompromise. ^[6][7]
• Cyclosporiasis: travel to endemic areas, consumption of contaminated fresh produce, tropical and subtropical residence. ^[8]

Corticosteroids and other immunosuppressants make amoebiasis dangerous. Amoebic colitis can mimic inflammatory bowel disease symptomatically and endoscopically, and steroid use has been associated with rapid progression, colonic perforation, amoeboma formation, rectovaginal fistula, extraintestinal spread, emergency surgery in more than half of cases and death in a quarter. ^[3]

E. histolytica has a two-stage life cycle: an infective cyst and an invasive trophozoite. Cysts survive in the environment for days to weeks. After ingestion, excystation in the small intestine releases trophozoites that migrate to the colon. There the parasite's Gal/GalNAc lectin allows attachment to the epithelium, and tissue injury follows from amoebapores, cysteine proteases and an interleukin-1 and interleukin-8 mediated inflammatory response, producing the characteristic flask-shaped submucosal ulcer. Trophozoites reaching the portal circulation can seed the liver, producing an abscess containing brown necrotic "anchovy paste" material. ^[3]

Most ingested cysts release non-pathogenic organisms, and about 90% of carriers remain asymptomatic. Why only a minority develop invasive disease is not fully known; host genetic susceptibility and the microbiome are suspected. ^[2][3]

Giardiasis localises to the proximal small bowel. Trophozoites attach to the epithelium without invading it, but disrupt the brush border, leading to malabsorption and the greasy, floating, foul-smelling stools typical of the disease. ^[5][9]

Cryptosporidium and Cyclospora parasitise the epithelial cells of the small intestine. Cryptosporidium has a chlorine-resistant oocyst, which is why it is the leading waterborne protozoal pathogen, and its oocysts can be shed for weeks after symptoms resolve. Cyclospora infects through mature oocysts that must sporulate in the environment. ^[6][7][8]

About 10 to 20% of people infected with E. histolytica become ill. ^[1] When symptomatic, the picture is:

• Amoebic colitis (about 10% of carriers within a year). ^[3] A several-week history of gradually worsening cramping abdominal pain, weight loss and watery, mucoid or bloody diarrhoea. Fever occurs in less than 40% and is often low grade. ^[3]
• Amoebic liver abscess, the most common extraintestinal manifestation, affecting about 1% of infected people. ^[3]

The typical symptom pattern of amoebic colitis, drawn from review data, is loose or bloody diarrhoea in over 90% of patients, abdominal pain in over 60%, fever in under 40% and weight loss in under 25%. ^[3] Only about 38% of patients with an amoebic liver abscess report concurrent diarrhoea. ^[3]

An amoebic liver abscess usually presents 8 to 20 weeks, median about 12 weeks, after travel to an endemic region. Fever and a dull aching right upper quadrant pain are typical; the pain may radiate to the epigastrium, chest or shoulder. Cough or right-sided pleural pain suggests diaphragmatic abutment. Jaundice is uncommon and should prompt consideration of another cause. Physical examination shows hepatic tenderness and hepatomegaly in about 50% of cases. ^[3]

The extraintestinal spread of amoebiasis is rare but serious: lung and pleural involvement in 2 to 3% of extraintestinal cases, pericardial disease (usually from a left-lobe abscess rupturing into the pericardium), brain abscess and cutaneous ulceration have all been described. These are medical emergencies. ^[3]

A 48-year-old patient returning from work in South America with 3 months of fever and right upper quadrant pain, a solitary right-lobe liver cavity on ultrasound and positive amoebic serology is the classic vignette.

Giardia classically causes watery diarrhoea with non-specific symptoms: bloating, flatulence, nausea, anorexia and sometimes steatorrhoea. Stools are often described as foul, greasy and floating because of fat malabsorption. ^[9][5]

Symptoms usually begin 1 to 2 weeks after infection; occasionally symptoms persist for months or years. Diarrhoea is usually mild, with 2 to 5 loose stools per day. Children are more likely than adults to be symptomatic; in endemic areas repeated infection with failure to thrive is a major problem. ^[5][9]

In immunocompetent people cryptosporidiosis is usually a self-limited illness: 1 to 2 weeks of watery diarrhoea, sometimes with low-grade fever, abdominal cramps, nausea and vomiting, and often no symptoms at all. Unlike giardiasis, it is typically not associated with chronic malabsorption in healthy hosts. ^[6][7]

In a person with advanced HIV disease (CD4 count under 200 cells per microlitre) the same organism causes severe, intermittent or chronic diarrhoea that may persist until immunity is restored. Significant wasting and dehydration are common; malabsorption can be profound. ^[9]

Cyclosporiasis causes watery diarrhoea with frequent bowel movements, abdominal cramping and bloating, increased flatus, nausea and prolonged fatigue. Vomiting, body aches, headache and low-grade fever are less common. The incubation period averages about 1 week, ranging from as early as 2 days to 2 weeks or more. If untreated, illness may last from a few days to a month or longer and can follow a remitting-relapsing course. ^[8]

Complications are uncommon but include malabsorption and weight loss, cholecystitis and reactive arthritis. ^[8]

The differential depends on whether the patient has acute or persistent diarrhoea, blood in the stool and risk factors such as travel, sexual exposure and HIV infection. Ova and parasite examination will not be requested routinely unless the clinical picture is right.

Other important differentials include bacterial dysentery (Shigella, Campylobacter, non-typhoidal Salmonella, Shiga-toxin-producing E. coli and Yersinia), Clostridioides difficile infection, inflammatory bowel disease, microscopic colitis, irritable bowel syndrome, coeliac disease, tropical sprue, and other parasites such as Blastocystis or microsporidia. In a person with advanced HIV the differential also includes cytomegalovirus colitis and Mycobacterium avium complex. The MedGrasp topic "Gastroenterology: infectious diarrhoea and foodborne illness" gives the full bacterial and viral picture and the rules for rehydration and antibiotic use. ^[9]

Definitive diagnosis depends on identifying the parasite in stool. Because all four organisms are shed intermittently, two or three stool samples collected 2 to 3 days apart are usually needed. ^[9]

Amoebiasis

• Light microscopy of fresh stool is cheap and widely available, with sensitivity under 60% and specificity 95%. Cysts may be seen in formed stool; trophozoites only in a fresh, loose "hot" stool examined within about 20 minutes. Microscopy cannot reliably separate E. histolytica from non-pathogenic E. dispar and E. moshkovskii. ^[3][9]
• Antigen detection (ELISA) reaches about 88% sensitivity and over 80% specificity and can be performed on stool or on liver abscess aspirate. ^[3]
• PCR is the gold standard for intestinal amoebiasis, with 92 to 100% sensitivity and 89 to 100% specificity, and is recommended where available. ^[3]
• Serology is useful for amoebic liver abscess, with over 90% sensitivity and specificity, but is less sensitive for intestinal disease (about 60%) and stays positive for years, so it is not suitable in endemic areas. ^[3]
• Liver abscess aspirate microscopy is unhelpful: trophozoites are seen in less than 20% of cases. ^[2][3]
• PCR on liver aspirate or stool, and amoebic serology, are the most useful confirmatory tests. ^[2][3]

Giardiasis

Diagnosis is clinical when the exposure and symptom picture is right, and confirmed by detecting cysts or trophozoites (or cyst antigen) in stool. The MedGrasp principle that testing is unnecessary in straightforward acute watery diarrhoea still applies, but stools for Giardia should be requested when diarrhoea is prolonged, malabsorptive or occurs in a traveller or child in childcare. Antigen and molecular assays are more sensitive than microscopy. ^[5][4][9]

Cryptosporidiosis

Routine stool ova and parasite examination may miss Cryptosporidium. Acid-fast or immunofluorescent staining, antigen detection or PCR should be requested deliberately. In the United States, cryptosporidiosis is often diagnosed on antigen-based panels, but sensitivity varies. Coinfection with other enteric pathogens is common in children. ^[6][7]

Cyclosporiasis

Testing for Cyclospora is not routine in most laboratories, even when stool is sent for parasites. A request must state the suspicion explicitly. Modified acid-fast staining, autofluorescence and PCR all improve detection. ^[8]

Amoebic liver abscess endpoints

For an amoebic liver abscess, imaging is essential. Ultrasound and CT show a solitary right-lobe cavity in most cases, with "anchovy paste" or chocolate-brown aspirate when drainage is performed. Because imaging and serology overlap with pyogenic abscess and malignancy, the history of travel and the clinical response to metronidazole help. The MedGrasp topic "Gastroenterology: liver abscess and parasitic liver disease" covers the imaging and drainage details. ^[2][3]

The first step is always the same: assess hydration. Reduced-osmolarity oral rehydration solution is first-line for mild to moderate dehydration, and intravenous isotonic fluid (lactated Ringer's or normal saline) is needed for severe dehydration or shock. Continue feeding during rehydration. ^[9]

Intestinal disease. The presence of cysts alone should not lead to treatment. When amoebic colitis is confirmed, the tissue agent is metronidazole (500 mg by mouth three times daily for 5 days in adults; 15 mg per kilogram three times daily for children) or tinidazole (2 g once daily for 3 days in adults; 50 mg per kilogram once daily, maximum 2 g, for children), followed by a luminal agent (such as paromomycin) where available to clear cysts. ^[2]

MSF guidance gives exactly these doses; CDC summarises the same principle as one antibiotic if the patient is asymptomatic and a second antibiotic afterwards if symptomatic. ^[1][2] Guidelines and formularies differ on the precise adult dose and on whether a luminal agent follows; follow the local guideline. ^[2]

Amoebic liver abscess. Use the same tissue agent, longer: tinidazole as for colitis but for 5 days, or metronidazole as for colitis but for 5 to 10 days. ^[2] Most abscesses are cured by drugs alone, even large ones. Clinical response usually occurs within 72 to 96 hours. ^[2][3]

Drainage is unnecessary for uncomplicated amoebic abscess and should not be done. Reserve it for failure to respond after 3 to 4 days, left-lobe abscess with risk of pericardial rupture, size over 10 cm, imminent rupture, or diagnostic uncertainty. ^[2][3]

First-line treatment is a nitroimidazole. MSF gives:

• Tinidazole: 2 g by mouth as a single dose in adults; 50 mg per kilogram (maximum 2 g) in children. ^[9]
• Metronidazole: 2 g by mouth daily for 3 days in adults; 30 mg per kilogram daily for children. ^[9]

Alternative agents include nitazoxanide, albendazole, mebendazole, paromomycin, quinacrine and furazolidone. Paromomycin is useful when a nitroimidazole is contraindicated, for example in early pregnancy, because it is poorly absorbed. Nitazoxanide is licensed and available in age-based suspensions. ^[4][9]

Practical points for giardiasis:

• Rehydrate first; dehydration can be particularly dangerous in pregnant patients and infants. ^[4]
• Test of cure is not routine; if symptoms persist, send three stool samples over several days.
• If Giardia is still present, consider reinfection before changing therapy.
• Confirm that the full dose was taken for the full duration.
• If infection is confirmed and reinfection and under-dosing have been excluded, combination therapy using drugs from different classes is effective.
• Wait at least 2 weeks after the last dose before re-examining stool.
• Persistent positivity after combination therapy suggests an underlying immunodeficiency. ^[4]

In immunocompetent patients nitazoxanide is the only FDA-approved drug. ^[6]

• Adults: 500 mg by mouth twice daily for 3 days.
• Children 1 to 3 years: 100 mg twice daily for 3 days.
• Children 4 to 11 years: 200 mg twice daily for 3 days. ^[6]

Reported efficacy is a clinical cure (resolution of diarrhoea) in 72 to 88% and a parasitological cure in 60 to 75% of immunocompetent patients. Retesting stool at least 1 week after the last dose is only needed if symptoms do not resolve; longer courses or repeated 3-day courses are sometimes used. ^[6]

In healthy people cryptosporidiosis is usually not treated at all: it resolves spontaneously in 1 to 2 weeks. ^[6][7][9]

HIV cross-check. Nitazoxanide has not been shown to be superior to placebo in HIV-infected or otherwise immunocompromised patients, and it is not approved for them. For cryptosporidiosis, cyclosporiasis and isosporiasis in advanced HIV, the most effective intervention is treating the underlying HIV infection with antiretroviral therapy; patients remain at high risk of dehydration and death until immunity returns. ^[6][9]

Nutrition, hydration and infection control matter as much as any drug. Patients with cryptosporidiosis should avoid swimming for 2 weeks after symptoms resolve, because oocysts can be shed for weeks. ^[6]

Trimethoprim-sulfamethoxazole is the treatment of choice. ^[8]

• Adults: TMP 160 mg plus SMX 800 mg (one double-strength tablet) by mouth twice daily for 7 to 10 days. ^[8]
• MSF uses the same adult dose but for 7 days. ^[9]
• Children from 2 months to 18 years: 8 to 10 mg TMP and 40 to 50 mg SMX per kilogram per day in two divided doses for 7 to 10 days. ^[8]
• Immunocompromised patients need longer courses. ^[8][9]

If TMP-SMX is not feasible because of allergy or intolerance:

• Observation with symptomatic treatment is acceptable, because most healthy patients recover spontaneously in 1 to 3 weeks. ^[8][9]
• Nitazoxanide and ciprofloxacin have uncertain efficacy and should only be considered. ^[8]
• Desensitisation to TMP-SMX should be reserved for selected patients who require treatment and have been evaluated by an allergist. ^[8]

Many drugs do not work for cyclosporiasis and should not be used: albendazole, azithromycin, diloxanide, doxycycline, metronidazole, nalidixic acid, quinacrine, tetracycline, tinidazole, and trimethoprim alone. Ciprofloxacin may have only modest activity. ^[8]

Special precautions: TMP-SMX interferes with folate metabolism and should only be used in pregnancy if the benefit justifies the risk; it should be avoided when nursing premature, jaundiced, ill or stressed infants and those with glucose-6-phosphate dehydrogenase deficiency; safety in children under 2 months has not been systematically evaluated. ^[8]

This topic and the MedGrasp topic "Gastroenterology: infectious diarrhoea and foodborne illness" agree on the key points: most acute diarrhoea is self-limited; rehydration comes first; antibiotics are reserved for dysentery, enteric fever, severe cholera and symptomatic Shigella; antimotility agents should be avoided with fever or bloody diarrhoea. Intestinal protozoa are a major cause of persistent, often travel-related diarrhoea there. Microscopic diagnosis and treatment of protozoa belong here; the gastroenterology topic's organism table usefully cross-checks incubation periods and clinic picture. ^[9][10]

• Amoebic colitis: progression to fulminant colitis in 0.5%; three-quarters of those develop toxic megacolon or perforation, with mortality around 40%. Immunosuppressed, alcoholic, diabetic and pregnant patients are at greatest risk. ^[3]
• Amoebic liver abscess: rupture into the peritoneum, pleura, pericardium or lung; brain abscess; and, rarely, death (mortality in uncomplicated disease is around 1 to 3%). ^[3][2]
• Giardiasis: malabsorption and failure to thrive in children; refractory or recurrent infection; post-infectious irritable bowel syndrome is reported after giardiasis. ^[4][5][9]
• Cryptosporidiosis: severe dehydration, wasting and electrolyte disturbance in immunocompromised hosts. Chlorine resistance means outbreaks in swimming pools and water play areas are common. ^[6][7]
• Cyclosporiasis: prolonged relapsing illness, malabsorption and weight loss; reactive arthritis and cholecystitis are uncommon complications. ^[8]

Corticosteroids for suspected inflammatory bowel disease must wait until amoebiasis has been excluded, because the colitis can mimic IBD and steroids accelerate disaster. ^[3]

In immunocompetent hosts these infections are curable and rarely fatal. Amoebic liver abscess mortality in uncomplicated disease is around 1 to 3%, worse with encephalopathy, hyperbilirubinaemia, hypoalbuminaemia or large abscess size. ^[3]

Untreated cryptosporidiosis in advanced HIV can be fatal or permanently disabling because of malabsorption and dehydration, and cryptosporidiosis and cyclosporiasis in these patients are opportunistic infections rather than self-limited ones. ^[9]

Prevention rests on safe water, food hygiene and sanitation:

• Wash hands with soap and water before preparing food and eating and after using the toilet or changing nappies.
• Avoid swallowing water while swimming; Cryptosporidium is chlorine resistant, so pool hygiene matters. Patients with cryptosporidiosis should avoid swimming for 2 weeks after symptoms resolve. ^[6][7]
• Boil lake, river or spring water for at least 1 minute before drinking or cooking (3 minutes above 6,500 feet / 2,000 m) to kill Giardia. ^[5]
• Peel fruit and vegetables in endemic areas; avoid unpasteurised dairy, fountain drinks with ice and street-vendor food. ^[1]
• Use condoms and dental dams and avoid sexual contact while symptomatic; several of these parasites spread during sex. ^[1][5]
• There is no licensed vaccine for these protozoal infections; none should be expected.
• Mass antibiotic chemoprophylaxis is not recommended and contributes to antimicrobial resistance. ^[10]

Screening points:

• Screen for intestinal amoebiasis before starting immunosuppression for possible inflammatory bowel disease; a single stool PCR is the most reliable test. ^[3]
• In immunocompromised patients, consider cryptosporidiosis, cyclosporiasis and isosporiasis early and test specifically rather than waiting for routine stool examination. ^[8][9]
• A travel history is essential for any patient with persistent diarrhoea; disease can present months or years after exposure. ^[3]

Pregnancy. Dehydration is the immediate danger for mother and fetus, so rehydration is the priority. TMP-SMX and nitroimidazoles in pregnancy must be weighed against fetal risk and local protocol; paromomycin is sometimes favoured because it is poorly absorbed. Albendazole and other alternatives should follow the local formulary and specialist advice. ^[4][8]

Children. Children carry the highest risk of severe dehydration and failure to thrive from these infections. Use the paediatric doses above, continue feeding and rehydrating. Antimotility agents are avoided in bloody or febrile diarrhoea. ^[9][4]

Immunocompromised hosts, including HIV. As above: cryptosporidiosis, cyclosporiasis and isosporiasis are opportunistic infections in advanced HIV. Start or optimise antiretroviral therapy, rehydrate, and use longer courses where an antiparasitic is indicated; the gut symptoms will not reliably clear until immune reconstitution occurs. Test specifically rather than relying on routine stool examination. ^[6][8][9]

Men who have sex with men. E. histolytica carriage and disease are more common; transmission can follow sexual contact. Clinical outcomes appear similar irrespective of CD4 count in one review, but any immunocompromise worsens disease in practice. ^[3]

Older adults. Amoebiasis-related deaths are most prevalent in men over 75, and dehydration from any diarrhoeal illness is more dangerous; low thresholds for admission and rehydration. ^[3]

• Ultrasound is often the only imaging; for amoebic liver abscess, a trained clinician can recognise many lesions with basic views. ^[2]
• Clinical clues carry weight where tests are unavailable: fever, right upper quadrant pain and hepatomegaly in a patient from an endemic region should raise suspicion for amoebic abscess even without recent travel. ^[2][3]
• An amoebic liver abscess can be cured with oral metronidazole alone, without drainage, even when large. ^[2][3]
• Where stool testing is not possible, parasitic diarrhoeas cannot be distinguished clinically, nor can they be distinguished from non-parasitic diarrhoea. Empirical treatment with a nitroimidazole and co-trimoxazole, together or in succession, may be tried in prolonged diarrhoea or steatorrhoea; in patients with HIV follow the HIV chapter's empirical guidance. ^[9]
• ORS, food and water hygiene and safe isolation of stool are the backbone of control, from amoebiasis to cholera. ^[10][9]
• Boiling water for at least 1 minute protects against Giardia; because Cryptosporidium is chlorine resistant, boiling or filtration is preferred. ^[5][6]
• Several of these drugs and reagents may be unavailable; paromomycin, tinidazole and nitazoxanide are particularly often missing, and metronidazole plus co-trimoxazole may be all that is on the shelf. Keep doses to those in the guidelines and do not overdose a child because a larger tablet is to hand.

• E. histolytica is the only species of Entamoeba that causes disease; most carriers are asymptomatic, and invasive disease (colitis, liver abscess) follows in a minority. ^[3]
• About 50 million infections and 55,000 deaths occur each year worldwide; about 90% of carriers are asymptomatic and 10% of cyst carriers develop invasive amoebiasis within a year. ^[3]
• Amoebic colitis shows diarrhoea in over 90%, abdominal pain in over 60%, fever in under 40% and weight loss in under 25%; liver abscess affects about 1% and presents 8 to 20 weeks after travel. ^[3]
• E. dispar is about 10 times more common worldwide and is non-pathogenic; symptom-free carriers may have it rather than E. histolytica. ^[1]
• Giardiasis is the commonest parasitic gut infection in the United States (over 1 million cases a year), with incubation of 1 to 2 weeks and duration of 2 to 6 weeks, and is treated with tinidazole or metronidazole. ^[5][9]
• Cryptosporidiosis is the leading waterborne disease in the United States, incubates 2 to 10 days and is usually self-limited; nitazoxanide cures 72 to 88% clinically in immunocompetent people. ^[6][7]
• Cyclosporiasis incubates about 1 week, can last up to a month and relapses; TMP-SMX is the treatment of choice, and many common drugs are ineffective against it. ^[8]
• In advanced HIV, cryptosporidiosis, cyclosporiasis and isosporiasis are opportunistic infections; antiretroviral therapy is more important than any antiparasitic. ^[9]
• Corticosteroids for suspected inflammatory bowel disease must wait until amoebiasis has been excluded by stool PCR. ^[3]
• Prevention is water, food and hand hygiene; boil water for 1 minute for Giardia, and boil or filter for Cryptosporidium because it resists chlorine. ^[5][6]

Gastroenterology: infectious diarrhoea and foodborne illness (rehydration, investigation, when antibiotics help). Gastroenterology: liver abscess and parasitic liver disease (amoebic liver abscess imaging and drainage). HIV infection (opportunistic intestinal infections, antiretroviral therapy). Approach to diarrhoea; dehydration and oral rehydration solution. Malabsorption and chronic diarrhoea.