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What is Intestinal Amebiasis?
Amebiasis (also spelled amoebiasis) is an intestinal infection caused by the microscopic protozoan parasite Entamoeba histolytica, a single-celled organism belonging to the class of amoebae. It is a disease of global importance and, despite being largely preventable through basic sanitation and hygiene measures, remains one of the most significant parasitic causes of morbidity and mortality worldwide.
The World Health Organization has estimated that Entamoeba histolytica infects approximately 50 million people globally each year, causing symptomatic disease in 10–20 million of them. It is responsible for an estimated 40,000 to 100,000 deaths annually, primarily in developing countries with inadequate sanitation infrastructure, making it one of the leading parasitic killers in the world, second only to malaria in terms of deaths attributable to protozoan infections.
Entamoeba histolytica is capable of living within the large intestine (colon) of its human host without causing any detectable harm or symptoms, a state known as asymptomatic carriage or luminal colonization. However, in a significant proportion of infected individuals, the parasite invades the intestinal wall, triggering a spectrum of gastrointestinal disease ranging from mild discomfort to life-threatening complications:
- Colitis (inflammatory disease of the colon)
- Acute dysentery (severe bloody diarrhea with mucus)
- Chronic or recurrent diarrhea
In a minority of cases, the parasite breaches the intestinal barrier and disseminates through the bloodstream to cause extraintestinal disease, most commonly:
- Amebic liver abscess (the most common form of extraintestinal amebiasis)
- Pulmonary amebiasis (typically from direct extension of a liver abscess)
- Cerebral amebiasis (rare but potentially fatal)
- Skin involvement (perianal or cutaneous amebiasis)
In countries with well-developed sanitation systems, such as most of Western Europe and North America, indigenous cases are rare.
Causes
Geographic Distribution
Amebiasis is a globally distributed disease, but its burden falls disproportionately on populations living in regions characterized by tropical or subtropical climates, high population density, inadequate sanitation infrastructure, and limited access to clean drinking water. The highest-burden regions include:
- Sub-Saharan Africa
- Mexico and Central America
- Parts of South America, particularly Brazil, Colombia, and Peru
- South and Southeast Asia, with India, Bangladesh, and parts of Indonesia particularly affected
- Parts of the Middle East
Within these regions, rural communities and periurban slums, where open defecation is common and sewage treatment is absent, bear the greatest burden.
The disease’s geographic concentration is not a reflection of the parasite’s inherent tropical requirement, but rather of the sanitary conditions that allow it to propagate. The parasite’s cysts (the environmentally resistant form) can survive in contaminated soil and water, and their spread is directly linked to practices such as the use of untreated human feces as agricultural fertilizer (night soil farming), the contamination of water sources with raw sewage, and the absence of hygienic food preparation.
The Pathogen: Entamoeba histolytica
Entamoeba histolytica exists in two distinct morphological forms during its lifecycle:
1. Trophozoite (active, invasive form): The trophozoite is the actively motile, feeding, and reproducing form of the parasite. It measures 10–60 micrometers in diameter and propels itself using pseudopodia (cytoplasmic extensions). Trophozoites inhabit the lumen of the large intestine, where they feed on bacteria, food particles, and cellular debris. In invasive amebiasis, trophozoites penetrate the intestinal mucosa using a combination of mechanical force via their pseudopodia and enzymatic destruction. They secrete proteases, phospholipases, and a pore-forming protein called amoebapore that directly lyses host cells. This explains the species name histolytica, meaning “tissue-dissolving”.
Trophozoites are fragile and rapidly destroyed outside the host body: they are killed by gastric acid if ingested, cannot survive desiccation, and are not infective by the oral route. Transmission of amebiasis therefore does not occur via trophozoites.
2. Cysts (resistant, infective form): When conditions in the colon become unfavorable (dehydration, nutrient depletion, pH changes during transit toward the rectum), trophozoites transform into cysts, a dormant, environmentally resistant form enclosed within a thick protective wall. Cysts measure 10–20 micrometers in diameter and contain 1–4 nuclei.
Cysts are the infective form responsible for person-to-person and environmental transmission. They can:
- Survive several months in contaminated soil, water, and on food surfaces at ambient temperature
- Withstand exposure to the chlorine concentrations used in standard water treatment (standard chlorination does not reliably kill E. histolytica cysts)
- Be rendered non-infective by heating (cooking food thoroughly) and by freezing (storage below -5°C)
When cysts are ingested by a new host, they pass through the stomach (protected from gastric acid by their cyst wall), excyst in the small intestine, and develop into trophozoites in the large intestine, completing the cycle.
An Important Distinction: E. histolytica vs. E. dispar
A critically important diagnostic consideration is that Entamoeba histolytica is morphologically indistinguishable from Entamoeba dispar, a closely related, non-pathogenic species that is ten times more prevalent in human populations and colonizes the gut without ever causing disease. Under standard light microscopy, the cysts and trophozoites of these two species appear identical. This distinction has profound clinical implications, because diagnosing E. dispar as E. histolytica would lead to unnecessary antiparasitic treatment, while failing to distinguish them could result in under-treatment of true amebiasis.
Additional non-pathogenic Entamoeba species that must be distinguished from E. histolytica include Entamoeba coli, Entamoeba hartmanni, and Entamoeba moshkovskii.
Risk Factors
While amebiasis can potentially affect individuals of any age, sex, race, or ethnicity, certain conditions substantially increase susceptibility to infection and to developing severe disease:
Immunocompromising conditions: Any condition that impairs the immune system, particularly cellular immunity, increases both the risk of acquiring symptomatic amebiasis and the likelihood of developing severe or extraintestinal disease:
- HIV/AIDS: one of the most significant individual risk factors; HIV-infected individuals are at dramatically higher risk of severe and disseminated amebiasis
- Malignancy (cancer): particularly hematological cancers (leukemia, lymphoma) and solid tumors treated with chemotherapy
- Malnutrition: impairs both innate and adaptive immune responses; protein-calorie malnutrition is extremely common in endemic regions and substantially increases disease severity
- Immunosuppressive medications: corticosteroids, methotrexate, biologic agents, and medications used in organ transplant recipients
- Alcoholism: Chronic heavy alcohol use impairs hepatic immune function and is specifically associated with a higher risk of amebic liver abscess, the most common form of extraintestinal amebiasis
- Extremes of age: infants and very young children (whose immune systems are still developing) and the elderly (with age-related immune decline) are at higher risk of severe disease
- Pregnancy: particularly in the third trimester, associated with more severe disease and higher rates of hepatic and pulmonary dissemination
Travel history: A recent history of travel to an endemic region is the most important epidemiological risk factor for amebiasis in high-income countries. Even short-duration travel (days to weeks) to endemic areas carries a risk of fecal-oral infection through contaminated food or water. Longer-term travelers, expatriates, aid workers, and military personnel deployed in endemic areas face higher cumulative exposure.
Living conditions and practices:
- Residence in crowded settings with shared sanitation facilities (refugee camps, prisons, institutions for people with intellectual disabilities)
- Men who have sex with men (MSM), particularly those with multiple partners, face elevated risk of direct fecal-oral sexual transmission
Transmission
Understanding the transmission routes of Entamoeba histolytica is essential for both individual prevention and public health control.
The key principle: the parasite is transmitted exclusively via the fecal-oral route, that is, by ingestion of matter contaminated with human feces containing viable E. histolytica cysts.
Active trophozoites and recently passed feces: the trophozoite form is present only in the living host and in freshly passed feces. Within hours of excretion, trophozoites outside the body are destroyed by desiccation, temperature changes, and gastric acid if ingested. They are therefore not infective by the oral route and play no role in transmission.
Cysts: by contrast, cysts are hardy, environmentally stable, and can remain infective for months in cool, moist environments. Cysts can withstand standard chlorination of drinking water (necessitating additional filtration or boiling for safe water in endemic areas).
Specific transmission pathways:
Direct person-to-person transmission:
- Fecal-oral contact via hands: the classic route, inadequate hand hygiene after defecation or after handling contaminated material (for example, diapers/nappies), followed by touching food or the mouth
- Sexual transmission: particularly direct anal-oral contact (rimming) and fecal contamination during anal intercourse, a recognized transmission route in MSM communities
- Childcare settings: changing diapers in nurseries or daycare centers, if hand hygiene is not meticulously maintained
Indirect transmission via contaminated food and water:
- Contaminated water: drinking or using water from wells, streams, or untreated municipal supplies contaminated with sewage; water used to wash salads and vegetables; ice made from contaminated water
- Contaminated food: raw fruits and vegetables (particularly leafy greens and root vegetables) grown with raw sewage as fertilizer or irrigated with contaminated water; shellfish harvested from polluted water
- Food handling: food prepared by an infected individual with inadequate hand hygiene
The role of animals:
- Other mammals, including household pets such as dogs and cats, and non-human primates, can occasionally harbor E. histolytica transiently. However, these animals do not typically excrete cysts in their feces in quantities sufficient to contribute meaningfully to human transmission, and they are not considered a significant reservoir host. The human host is the primary and most important reservoir of E. histolytica.
Symptoms
Incubation Period and Natural History
After ingestion of infective cysts, the incubation period before symptoms develop ranges from 7 to 28 days, though it may occasionally be shorter (a few days) or extend to several months in some individuals. The duration of symptomatic illness, in the majority of treated cases, is approximately two weeks.
Asymptomatic Carriage
The most important clinical fact about Entamoeba histolytica infection is that the majority of infected individuals, approximately 80–90%, remain entirely asymptomatic despite harboring the parasite in their intestine. In these individuals, the parasite exists as a luminal commensal without invading the intestinal wall, causing no discernible symptoms and producing no detectable pathology. However, they are potentially infectious to others through cyst excretion in their feces, making asymptomatic carriers an important, though often unidentified, source of ongoing transmission.
Symptomatic disease develops in only approximately 10–20% of infected individuals, and the factors that determine why some people develop invasive disease while others remain asymptomatic carriers are not fully understood. They likely include the virulence characteristics of the specific E. histolytica strain, the host’s immune status and genetic factors, and the composition of the intestinal microbiome.
Intestinal (Luminal) Amebiasis
The mildest symptomatic form, sometimes called non-dysenteric colitis or amebic colitis, presents with:
- Abdominal pain: typically crampy, intermittent, and most pronounced in the lower abdomen (particularly the right iliac fossa and cecal region), though it can be diffuse.
- Diarrhea: loose, watery stools, typically 3–8 times per day. Stools may contain mucus and occasionally small amounts of blood.
- Excessive flatulence (meteorism).
- Fatigue and general malaise.
- Unintentional weight loss in more prolonged cases.
- Tenesmus: a painful, distressing feeling of incomplete bowel evacuation. It is a persistent urge to defecate even when the rectum is empty or nearly empty. This symptom reflects rectal and sigmoid colon inflammation and is a characteristic feature of amebic colitis.
Symptoms typically wax and wane over weeks and can become chronic if untreated, alternating with periods of relative improvement before recurring.
Amebic Dysentery
Amebic dysentery represents the more severe form of invasive intestinal amebiasis, in which Entamoeba histolytica trophozoites invade deeply into the colonic mucosa and submucosa, causing extensive ulceration and hemorrhage. Its clinical features include:
- Severe abdominal pain and tenderness: diffuse or localized abdominal pain, often accompanied by marked tenderness to palpation, particularly in the right lower quadrant
- Grossly bloody stools: the hallmark of dysentery, with frank blood visible in the stool rather than merely occult blood
- Mucoid, liquid, bloody stools: stools are typically liquid, containing large amounts of mucus and streaked or mixed with blood
- Very frequent defecation: characteristically, patients with amebic dysentery may pass stool 10–20 or more times per day, a debilitating frequency that rapidly leads to dehydration and electrolyte imbalance
- Fever: typically moderate (38–39°C), reflecting systemic inflammation; high fever may indicate secondary bacterial superinfection or extraintestinal dissemination
- Nausea and vomiting: common accompaniments, contributing to dehydration
- Signs of dehydration: tachycardia, hypotension, reduced skin turgor, dry mucous membranes; these can be potentially life-threatening in severe cases, particularly in young children and the elderly
It is important to clinically distinguish amebic dysentery from bacillary dysentery (caused by Shigella species) and from Campylobacter enterocolitis, as the treatment differs. Both can present with bloody diarrhea, fever, and tenesmus, and microbiological confirmation is therefore essential.
Extraintestinal Amebiasis
In a small but clinically significant proportion of cases, E. histolytica trophozoites penetrate the intestinal wall, enter the portal circulation, and disseminate hematogenously to distant organs.
Amebic liver abscess (ALA), the most important form of extraintestinal amebiasis:
- Develops in approximately 1–3% of cases of intestinal amebiasis.
- Men are affected far more commonly than women (male-to-female ratio approximately 7–10:1), for reasons not fully understood.
- The right lobe of the liver is affected in approximately 80% of cases (reflecting the preferential flow of portal blood from the right colon to the right hepatic lobe).
- Classic presentation: right upper quadrant pain (often pleuritic in character, worse with breathing), fever, and hepatomegaly (enlarged, tender liver).
- Importantly, concurrent active intestinal symptoms are present in fewer than 50% of patients with amebic liver abscess. Many have had no recent diarrhea or bowel complaints, which makes the diagnosis more challenging.
- Complications include spontaneous rupture of the abscess into the pleural space (causing amebic empyema), peritoneum (causing peritonitis), or pericardium (causing cardiac tamponade).
Pulmonary amebiasis:
- Most commonly results from direct extension of a right lobe liver abscess through the diaphragm into the right pleural space or lung
- Presents with right-sided chest pain, cough, and breathlessness
- May produce a characteristic “anchovy sauce” colored sputum if the abscess communicates with a bronchus
Cerebral amebiasis:
- Extremely rare but almost universally fatal if not recognized and treated promptly
- Results from hematogenous spread from the intestine or liver
- Presents with rapidly progressive neurological deterioration
Diagnosis
The laboratory diagnosis of amebiasis is considerably more challenging than might be expected, and this difficulty has important clinical consequences. Both delayed diagnoses and misdiagnoses are common.
Stool Examination (Microscopy)
Traditionally, the definitive diagnostic test for intestinal amebiasis has been the microscopic examination of stool samples for the presence of Entamoeba histolytica cysts or trophozoites. However, this approach has significant limitations:
- High false-negative rate: a single stool examination has a sensitivity of only 25–33%. To achieve acceptable sensitivity (approaching 85–90%), at least three separate stool specimens collected on different days must be examined. Ideally, these should include both formed stool (for cysts) and fresh diarrheal stool (for trophozoites).
- Expertise required: reliable microscopic identification of E. histolytica cysts and trophozoites requires considerable laboratory expertise and experience
- Morphological indistinguishability from non-pathogenic species: the most critical limitation, E. histolytica is morphologically identical to Entamoeba dispar (a non-pathogenic commensal that is 10 times more common) under standard light microscopy. A positive stool microscopy for “E. histolytica/dispar” in an asymptomatic individual is therefore most likely to represent E. dispar colonization rather than true E. histolytica infection. This distinction is clinically essential, as E. dispar does not require treatment.
- Other non-pathogenic Entamoeba species can also be confused with E. histolytica
Antigen detection tests (enzyme-linked immunosorbent assay, ELISA): Antigen detection tests using stool samples have significantly improved the accuracy of diagnosis. Monoclonal antibody-based ELISA tests that specifically detect E. histolytica antigens (but not E. dispar antigens) are available and are substantially more sensitive (>90%) and specific (>95%) than microscopy alone. These tests are recommended by the WHO as the preferred first-line diagnostic approach where available.
Polymerase chain reaction (PCR): PCR-based molecular detection of E. histolytica DNA in stool samples offers the highest available sensitivity and specificity, and can definitively distinguish E. histolytica from all other Entamoeba species. PCR is increasingly available in reference laboratories and is the diagnostic gold standard in high-resource settings.
Serological Testing (Blood Tests)
Serum anti-Entamoeba histolytica antibody testing (ELISA, indirect hemagglutination assay, immunofluorescence):
- Serological tests detect host IgG antibodies directed against E. histolytica antigens
- They are positive in approximately 90–95% of patients with amebic liver abscess and in approximately 70–80% of patients with invasive intestinal amebiasis
- They are recommended when extraintestinal amebiasis (particularly amebic liver abscess) is suspected
- Important limitation: antibodies can persist for months to years after resolution of infection, meaning a positive serology may reflect past rather than current infection. In endemic areas, where prior exposure is common, seropositivity rates in the general population can be high, reducing the diagnostic specificity of a positive serology for acute disease.
Imaging Studies
In patients with suspected amebic liver abscess, imaging is essential for both diagnosis and management:
- Abdominal ultrasound: the first-line imaging modality, highly sensitive (over 90%) for detecting liver abscesses. The classic sonographic appearance is a well-defined, hypoechoic, or heterogeneous rounded lesion, most commonly in the right lobe. Ultrasound can also guide diagnostic aspiration when needed.
- CT scan (computed tomography): provides more detailed anatomical characterization, helps identify complications (rupture into adjacent structures), and is particularly useful in atypical cases or when the ultrasound findings are inconclusive.
- MRI: occasionally used for further characterization.
The aspirated contents of an amebic liver abscess typically have a characteristic “anchovy sauce” or “chocolate sauce” appearance. This reddish-brown, thick fluid represents liquefied necrotic liver tissue. Paradoxically, viable trophozoites are only found in aspirate from the abscess wall, not in the central fluid.
Colonoscopy
Colonoscopy with biopsy of ulcerated areas is occasionally useful in patients with atypical presentations or in whom stool-based testing is negative despite high clinical suspicion of invasive amebic colitis. The characteristic colonoscopic appearance consists of discrete, flask-shaped ulcers with undermined edges and normal intervening mucosa. However, these findings require histopathological and microbiological confirmation to distinguish them from inflammatory bowel disease and other causes of colitis.
Treatment
Drug Therapy
Several effective antiparasitic drugs (amebicides) are available for the treatment of amebiasis. The choice and combination of agents depend on whether the patient has:
- Asymptomatic intestinal colonization (luminal infection without invasive disease)
- Symptomatic invasive intestinal amebiasis (amebic colitis or dysentery)
- Extraintestinal amebiasis (amebic liver abscess or other organ involvement)
Luminal amebicides are drugs that reach effective concentrations in the intestinal lumen, allowing them to eliminate colonizing cysts:
- Diloxanide furoate (500 mg three times daily for 10 days): the most commonly used luminal agent; effective against intraluminal cysts with minimal systemic absorption
- Paromomycin (25–35 mg/kg/day in three divided doses for 7 days): an aminoglycoside antibiotic poorly absorbed from the gut, making it effective against luminal parasites with minimal systemic side effects; also used in pregnancy
- Iodoquinol: an alternative luminal agent
Tissue amebicides are drugs that reach effective concentrations in the intestinal wall and in distant tissues. They eliminate invasive trophozoites:
- Metronidazole (750 mg three times daily for 5–10 days): the most widely used and clinically validated tissue amebicide; achieves high tissue concentrations and effectively kills invasive trophozoites. Side effects include nausea, metallic taste, and alcohol intolerance (disulfiram-like reaction). Should be avoided in the first trimester of pregnancy.
- Tinidazole (2 g once daily for 5 days): a second-generation nitroimidazole with similar efficacy to metronidazole. It requires a shorter treatment duration, offers better tolerability, and involves less frequent dosing. These advantages make it increasingly preferred where available.
- Ornidazole and secnidazole: additional nitroimidazole alternatives used in various countries.
Treatment regimens by clinical scenario:
| Clinical Situation | Recommended Treatment |
|---|---|
| Asymptomatic cyst carrier (if confirmed as E. histolytica by antigen or PCR testing) | Luminal amebicide alone (diloxanide furoate or paromomycin for 10 days) |
| Symptomatic intestinal amebiasis / amebic colitis | Tissue amebicide (metronidazole or tinidazole) followed by a luminal amebicide (to eliminate residual intraluminal cysts and prevent relapse) |
| Amebic liver abscess | Tissue amebicide (metronidazole or tinidazole, typically for 7–10 days) followed by a luminal amebicide; aspiration or drainage for large abscesses (>10 cm) or failure to respond to drug therapy |
The critical principle, often overlooked in practice, is that tissue amebicides (metronidazole, tinidazole) alone are insufficient. This is because they have poor activity against luminal cysts. Failure to follow tissue amebicide treatment with a luminal agent leaves residual cysts in the colon, which can re-invade tissue and cause relapse, and which continue to be shed in feces, perpetuating transmission.
Supportive Therapy
Patients with severe amebic dysentery or amebic liver abscess may require supportive measures alongside antiparasitic drug treatment:
- Rehydration therapy: oral rehydration solution (ORS) for mild to moderate dehydration; intravenous fluids for severe dehydration or patients unable to tolerate oral intake
- Electrolyte replacement: potassium, sodium, and bicarbonate supplementation as guided by laboratory values
- Nutritional support: particularly in children with persistent diarrhea and malnutrition
- Analgesics: for pain management in amebic liver abscess
Therapeutic aspiration or drainage of amebic liver abscess is recommended in specific situations:
- Abscess diameter >10 cm (higher risk of spontaneous rupture)
- Failure to respond clinically within 3–5 days of drug therapy
- Abscesses in the left hepatic lobe (higher risk of rupture into the pericardium)
- Imminent or actual rupture
- Inability to distinguish from pyogenic (bacterial) liver abscess
Prevention
Prevention While Traveling to Endemic Regions
For travelers from low-endemicity countries, such as most of Europe and North America, visiting endemic regions, the risk of acquiring amebiasis is real. However, this risk can be substantially reduced by carefully following food and water hygiene practices. These practices include the “boil it, cook it, peel it, or forget it” principle.
Safe drinking water practices:
- Drink only commercially bottled water from sealed, tamper-evident containers. Before drinking, verify that the bottle seal is intact
- When bottled water is unavailable, boil water vigorously for at least 1 minute before drinking (this kills E. histolytica cysts reliably)
- Never consume tap water, well water, or stream water without boiling, not even for brushing teeth
- Avoid drinks with ice cubes in restaurants and street vendors. The ice is typically made from local tap water and may contain E. coli or other contaminants. histolytica* cysts that survive standard chlorination
- Carbonated bottled drinks are generally safe, as the carbonation and acidity create an inhospitable environment for cysts
Safe food practices:
- Eat only thoroughly cooked hot foods: cooking kills E. histolytica cysts reliably. Avoid undercooked or raw meat, fish, and eggs.
- Avoid raw fruits and vegetables that cannot be peeled: leafy salads, herb garnishes, and unpeeled fruits may have been irrigated with contaminated water or washed with tap water. Only eat raw fruits if you peel them yourself immediately before eating.
- Avoid unpasteurized dairy products: milk, soft cheese, cream, and yogurt that have not been pasteurized may be contaminated. Drink only pasteurized, commercially packaged dairy products.
- Avoid street food from vendors who cannot guarantee safe preparation: street food represents a high-risk category in endemic areas, as temperature control, water sourcing, and hand hygiene are often inadequate. When street food must be eaten, prefer items that are freshly cooked and served piping hot from clean equipment.
- Avoid raw shellfish: oysters, clams, and other shellfish filter large volumes of water and can concentrate pathogens to dangerous levels if sourced from polluted waters.
There is currently no vaccine against Entamoeba histolytica, though research into potential vaccine candidates is ongoing.
Preventing Spread From Infected Individuals
Once an infected individual is identified and treated, preventing onward transmission requires strict adherence to personal hygiene and safe food handling:
-
Rigorous hand washing with soap and water:
- After every visit to the toilet
- After changing diapers or handling infant feces
- Before handling, preparing, or eating food
- After contact with soil or potentially contaminated surfaces
-
Complete the full course of antiparasitic treatment: elimination of intestinal carriage (through the luminal amebicide component of treatment) is essential to stop cyst shedding and prevent ongoing transmission to household members and the community.
-
Sanitation measures in endemic regions: at the community and public health level, the most powerful preventive interventions are:
- Access to clean, treated drinking water
- Adequate sewage treatment and disposal
- Sanitary latrines and elimination of open defecation
- Safe disposal of human waste: ending the use of untreated human feces as agricultural fertilizer
- Health education about fecal-oral transmission and hand hygiene
-
In healthcare settings: standard infection control precautions (gloves, hand hygiene, appropriate disposal of fecal material) are sufficient to prevent healthcare-associated transmission.
Sources and Bibliography
- Centers for Disease Control and Prevention (CDC): Amebiasis
- World Health Organization (WHO). (1997). Amoebiasis: Report of a WHO Expert Consultation. Weekly Epidemiological Record.
- Lozano R, et al. (2012). Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. The Lancet, 380(9859):2095–2128.
- Haque R, et al. (2003). Amebiasis. New England Journal of Medicine, 348(16):1565–1573.
- Stanley SL Jr. (2003). Amoebiasis. The Lancet, 361(9362):1025–1034.
- Petri WA Jr, et al. (2009). Entamoeba histolytica and other intestinal protozoan infections. In: Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th edition. Churchill Livingstone.
- Shirley DT, et al. (2018). A Review of the Global Burden, New Diagnostics, and Current Therapeutics for Amebiasis. Open Forum Infectious Diseases, 5(7):ofy161.
- Blessmann J, et al. (2002). Real-time PCR for detection and differentiation of Entamoeba histolytica and Entamoeba dispar in fecal samples. Journal of Clinical Microbiology, 40(12):4413–4417.
- PLoS Speaking of Medicine Blog. (2015). One Million Deaths: Parasites.
- Hamzah Z, et al. (2006). Differential diagnosis of Entamoeba histolytica and Entamoeba dispar. Asian Pacific Journal of Tropical Medicine. PMC2754014