Intestinal Amoeba Overview

Intestinal Amoeba

• Intestinal amoeba are single-celled protozoa that change shape constantly.
• Locomotion is achieved through an organ called a pseudopodium.
• Classified by habitat: intestinal amoeba (large intestine of humans/animals) and free-living amoeba (small free-living and opportunistic pathogens).
• Pathogenic intestinal amoeba include Entamoeba histolytica.
• Non-pathogenic intestinal amoeba include E. dispar, E. moshkovskii, E. coli, E. polecki, E. hartmanni, E. gingivalis, Endolimax nana, Iodamoeba butschlii.
• Entamoeba histolytica is prevalent in the tropics and subtropics.
• The majority of Entamoeba histolytica cases are asymptomatic.
• It is a common diarrheal pathogen in long-term travelers (>6 months).
• The highest burden of the disease occurs in the tropics of China, Central and South America, and the Indian subcontinents, affecting 10% of the world's population.
• Families of infected people, male homosexuals, those in mental institutions, prisons, and children institutions have a higher prevalence of infection.
• All ages are susceptible, but the rate is lower in infants & children. Females and males have similar likelihood of infection but invasive amebiasis is more common in males.

Classification of Amoeba

• Amoeba are a type of single-celled protozoa.
• They have the ability to constantly change their shape.
• The presence of a pseudopodium (an organ of locomotion) results in their ability to change shape.

Etiological Agent

• Infection is caused by Entamoeba histolytica.
• E. histolytica resides in the human colon, specifically within the mucous and submucous layers of the large intestine.
• Morphology presents in three forms: trophozoite, precyst, and cyst.
• Trophozoite: the vegetative form found in tissues; irregular shape, 12-60 µm in size; moves unidirectionally using pseudopodia.
• Cytoplasm contains ectoplasm and endoplasm with nuclei, food vacuoles, and phagocytosed red blood cells within the endoplasm.
• Trophozoite is the only form that resides within tissues
• Cysts (10-20 µm, round, thick-walled): highly resistant to harsh digestive environments; survive in external environments. Contains 1-4 nuclei, chromatoid bars (RNA aggregates), and a glycogen mass.
• Cysts are the infectious form.

Life Cycle

• The life cycle occurs within a single host (humans).
• Mature quadrinucleated cysts are the infectious form and are ingested with contaminated food or water.
• In the intestines, cysts transform into trophozoites.
• Trophozoites reside in the lumen of the small intestine, specifically the lower small bowel, and within mucosal crypts in the colon.
• Trophozoites feed on nutrients and bacteria.
• Trophozoites encyst within the colon's lumen, transforming back into cysts, and are discharged in feces.

Pathogenesis

• Infection by E. histolytica is initially asymptomatic in 90% of cases.
• Under particular conditions (host and parasite factors), E. histolytica becomes invasive.
• E. histolytica can cause tissue lysis.
• Factors that increase susceptibility increase invasive potential: poor nutrition, stress, altered colon flora, and low host resistance.
• Trophozoites invading colonic mucosa lead to characteristic ulcerative lesions and profuse bloody diarrhea (amoebic dysentery).
• Males and females are affected equally in terms of infection.

Complications of Intestinal Amebiasis

• Initial lesions of amebic invasion begin as small foci of necrosis within the large bowel mucosa.
• These foci progress into ulcers with a distinctive flask shape (wide base, narrow neck).
• Ulcers can be superficial (heal without scarring) or deep(heal with scarring).
• Ulcers typically locate in the ileocecal region, sigmoidorectal region, or can affect the entire large intestine.
• Confluence of ulcers leads to sloughing of mucosa, leading to secondary bacterial infection.
• Invasive disease can extend to complications such as: fulminant colitis, amoebic appendicitis, intestinal perforation, and amoebic peritonitis and other extraintestinal sites.

Pathogenesis of Extraintestinal Amebiasis

• About 5-10% of patients with intestinal amoebiasis develop extraintestinal amoebiasis 1-3 months after intestinal infection.
• Liver is the most common site of extraintestinal infection, followed by lungs, brain, genitourinary tract, and spleen.
• Characterized by the development of abscesses typically in the upper right lobe of the liver. Abscesses can be multiple.
• Extra-intestinal disease can cause: rupture into lungs or pericardium, skin lesions, right pleura infection, subphrenic abscesses, and peritoneal infection (spreading through blood).

Diagnosis of Intestinal Amebiasis

• Laboratory diagnosis for intestinal disease includes stool microscopy (detecting cysts or trophozoites), stool culture, stool antigen detection (copro-antigen), serology (antibody detection), molecular diagnosis (PCR), and sigmoidoscopy (mucosal scrapings).

Diagnosis of Extraintestinal Amebiasis

• Laboratory tests for extraintestinal amebiasis often include microscopy (detecting trophozoites in pus), molecular diagnosis (PCR of pus), serology, ultrasonography (to visualize the abscess site and extent).

Treatments

• Metronidazole or tinidazole are the drugs of choice for intestinal and hepatic amoebiasis.
• Fluid and electrolyte replacement, symptomatic treatment also recommended for treatment.
• Specific dosage and duration vary depending on the type of amebiasis and/or drug.

Prevention and Control

• Health education, especially for food handlers, children, and maids.
• Good personal hygiene habits (handwashing).
• Good sewage disposal practices.
• Do not use feces as fertilizer.
• Detect and treat cases.
• Boiling of water; thorough cleaning of fruits and vegetables.
• Avoid sexual practices that allow fecal-oral contact.

Prognosis

• The prognosis for amebiasis depends on the location of the infection and the patient's general health prior to infection.
• If infection is limited to the intestines and the patient is healthy, prognosis is generally good.
• Patients with ameboma, peritonitis, and liver infection can have higher mortality rates; fulminant colitis has the highest risk of mortality (>50%).