| disease | Entamoeba Histolytica Infection |
| alias | Amoeba Dysentery, Dysentery |
The pathogenic protozoa of invasive amoebiasis, primarily found in the colon, causes amoebic dysentery and various types of amoebiasis. It is globally distributed, most commonly seen in tropical and subtropical regions.
bubble_chart Epidemiology
Amoebiasis is globally distributed, with high-prevalence areas located in Mexico, eastern South America, Southeast Asia, West Africa, and other tropical and subtropical regions between 10° north and 10° south latitude. The average infection rate exceeds 20%, reaching 57–87% in some areas like Egypt. Reports indicate that in recent years, the infection rate in China has ranged between 0.7% and 2.17%, predominantly in regions with poor economic conditions, sanitation, and living environments, with higher rates in rural areas than in cities. Human infections primarily occur through oral transmission between individuals, with the main transmission route being water sources contaminated by feces containing cysts. Contamination of community water sources often leads to outbreaks and unusually high infection rates in the area. Other transmission pathways include contamination of hands, food, or utensils. Poor hygiene habits make cyst carriers dangerous sources of transmission, while insects such as flies and cockroaches also play a role in spreading cysts. Due to the lack of effective acquired immunity, individuals who have had amoebiasis remain susceptible. Susceptibility is not correlated with gender or age, and the higher incidence observed among males in epidemiological statistics is often related to lifestyle habits and occupational factors.
Whether small trophozoites can invade tissues and cause pathological changes is determined by multiple factors, mainly including:
1. Changes in the host's physiological functions, such as malnutrition, infection, intestinal dysfunction, intestinal membrane injury, etc., leading to a decrease in host resistance;2. Under the synergistic action of suitable bacterial species (bacteria can provide favorable physicochemical conditions for the growth and reproduction of amoebae), promoting the proliferation of amoebae. Additionally, they can directly damage the host's intestinal membrane, facilitating the invasion of amoebae and enhancing their pathogenicity, among other effects.
bubble_chart Pathological Changes
The majority of parasite colonies proliferated from post-cyst trophozoites cause primary lesions in the ileocecal region or, in a few cases, the sigmoid colon. Except in severe cases, primary lesions are confined to the mucosal layer, appearing as slightly raised congestive foci with central pinpoint ulcerations upon colonoscopy. In acute cases, proliferating trophozoites can breach the muscularis mucosae, spreading and multiplying in the loose submucosal layer, leading to liquefactive necrotic foci and forming flask-shaped ulcers with narrow openings and broad bases. The size of these ulcers ranges from a few millimeters to over ten millimeters. If accompanied by bacterial infection, microscopic examination reveals abundant neutrophil infiltration around the necrotic foci. In severe cases, ulcers may penetrate deep into the muscular layer or coalesce with adjacent ulcers, causing extensive mucosal sloughing. Thus, amoebic ulcers often exhibit significant perforation of the muscular layer. In mild or subacute cases, intestinal wall damage can vary from tiny mucosal ulcers to granulomatous ulcers. Chronic cases may develop amoebomas due to mucosal hyperplasia. Amoebic trophozoites in the intestinal submucosa or muscular layer can invade veins, becoming lodged in hepatic sinusoids and causing secondary amoebiasis. Initially, multiple small necrotic foci with peripheral leukocyte infiltration constitute the hepatitis stage. Depending on the host's condition, one or occasionally multiple foci may coalesce and develop into liver abscesses. The abscess center consists of a necrotic area with chocolate-colored contents, while trophozoites cluster at the periphery, at the junction between the inflammatory lesion and normal tissue (abscess wall). Large liver abscesses can grow to the size of an infant's head. Additionally, dysentery amoebae may spread hematogenously or directly through the diaphragm into the thoracic cavity, leading to pulmonary abscesses. Rarely, they may invade the mediastinum, pericardium, brain, spleen, or other sites, causing localized abscesses. Amoebic ulcers may also develop at sites of liver abscess perforation through the abdominal wall, surgical incisions, or perianal skin. Involvement of genital organs can result in amoebic vaginitis or prostatitis.
The clinical manifestations of amoebiasis are highly variable, often presenting with a prolonged and fluctuating course. According to the WHO's clinical classification, it can be divided into asymptomatic carrier infections and symptomatic invasive infections. The former accounts for over 90% of cases, mostly involving non-invasive species of the complex. The latter is further categorized into intestinal amoebiasis (including amoebic dysentery, enteritis, amoeboma, amoebic appendicitis, etc.) and extraintestinal amoebiasis (including amoebic liver, lung, brain abscesses, and cutaneous amoebiasis, etc.). Classic amoebic dysentery, characterized by acute abdominal dysentery with colicky pain, tenesmus, and bloody mucoid stools, is now less common. Most cases present as subacute or chronic persistent enteritis, accompanied by symptoms such as abdominal distension, weight loss, and anemia. Extraintestinal amoebiasis is most frequently seen as amoebic liver abscess, resulting from hematogenous spread, often affecting the right lobe of the liver. It typically has a slow onset, with remittent fever, hepatomegaly, liver pain, progressive weight loss, anemia, and nutritional edema. A history of intestinal amoebiasis is common. Amoebic lung abscess is rare and can be either hepatogenic or enterogenic in origin. The former usually results from direct rupture of an amoebic liver abscess, while the latter spreads via the bloodstream, with lesions not confined to the right lower lobe. In very rare cases, liver abscesses may rupture into the pericardium or abdominal wall. Intestinal amoebae can also spread to the perianal region, vagina, urethra, etc., causing abscesses or inflammation in these areas. Common complications include enteritis, amoeboma, and amoebic appendicitis.
1. Pathogen Examination:
(1) Stool Examination:
1) Physiological saline smear method: Suitable for purulent bloody stools of acute dysentery patients or loose stools of amoebic enteritis, mainly used to examine active trophozoites. However, the specimen must be fresh, and the faster it is sent for examination, the better. Storage at 4°C should not exceed 4–5 hours. Typical amoebic dysentery stools are soy-sauce red and mucoid with a foul odor. Microscopic examination reveals mucus containing many clumped red blood cells and fewer white blood cells, and sometimes Charcot-Leyden crystals and active trophozoites can be seen. These characteristics can differentiate it from bacterial dysentery stools.
2) Cyst concentration method: For formed stools of chronic patients, direct smear can also be used to detect cysts. Iodine staining is often performed to highlight the nuclei for differential diagnosis. However, cyst examination can be improved using concentration methods. Common methods include zinc sulfate flotation and merthiolate-iodine-formaldehyde centrifugation (MIFC, see appendix for details).
Clinically, atypical chronic amoebiasis is often difficult to detect in stool samples. Analysis shows that for asymptomatic patients or cases with lesions confined to the cecum and ascending colon, the detection rate of routine wet smears or fixed-stain smears does not exceed 30%. Submitting samples three times with intervals of more than one day can increase the positive rate to 60–80%, and submitting five times can achieve over 90%.
(2) Artificial Culture: Various improved culture media are available (see appendix). Routine diagnostic culture from stool samples typically involves bacterial culture, but the detection rate is generally low for most subacute or chronic sexually transmitted disease cases. Therefore, culture methods are not suitable for routine examination. Axenic culture requires special media and technical expertise and is more appropriate for research.
(3) Tissue Examination: Direct observation of mucosal ulcers using a sigmoidoscope or fiber colonoscope, along with biopsy or scraping smears, yields the highest detection rate. Approximately 85% of dysentery patients can be diagnosed this way. Biopsy specimens must be taken from the ulcer edge, and abscess puncture should sample the wall, noting the characteristics of the pus.
Pathogen examination requires special attention to container cleanliness and the effects of medications and treatments. Certain antibiotics, anti-parasitic drugs, laxatives, astringents, hypertonic or hypotonic enema solutions, barium meals, and contamination with the patient’s own urine can kill trophozoites and interfere with pathogen detection.
2. Immunodiagnosis
Due to the difficulty and potential misdiagnosis of amoebic disease through pathogen examination, immunodiagnosis, though an indirect auxiliary method, holds significant practical value. Since the 1960s, with the establishment of axenic culture for amoebae and the advent of specific monoclonal antibodies, pure antigens of Entamoeba histolytica and high-quality antibody tools have become available, leading to the development of various immunodiagnostic methods worldwide. In recent years, various modifications of the enzyme-linked immunosorbent assay (ELISA) have been widely used. Generally, the detection rate of specific circulating antibodies is as high as 95–100% in liver abscess patients, 85–95% in invasive intestinal disease patients, and only 10–40% in asymptomatic carriers. Antibody titers vary with disease severity, but large abscesses often correlate with high titers. Therefore, serological diagnosis is most valuable for acute cases. In seroepidemiological surveys, trends in population antibody titers can indicate regional disease prevalence. The application of monoclonal antibodies and DNA probe hybridization techniques provides specific, sensitive, and interference-resistant tools for detecting pathogen components in host blood and excreta. Reports have described the use of monoclonal antibodies to detect parasite-derived antigens in stool and pus, as well as DNA probes to identify parasite species in stool.
The methods commonly used to diagnose intestinal amebiasis include stool examination (to detect trophozoites and cysts), artificial culture (to detect trophozoites), and intestinal biopsy (to detect trophozoites) or smear examination of scrapings (to detect trophozoites). Although immunological diagnosis is an indirect auxiliary diagnostic method, it holds significant practical value.
bubble_chart Treatment Measures
1. Identify and treat patients and carriers to control the source of pestilence, with special attention to detecting and treating cyst carriers and chronic patients engaged in food-related work. If necessary, identify the parasite species to determine treatment strategies.
2. Managing feces and protecting water sources are key steps to cutting off the transmission route of amoebic Bingchuan. Conducting fecal harmless treatment based on local conditions to eliminate cysts and strictly preventing fecal contamination of water sources are critical measures for controlling amoebiasis.
3. Pay attention to food and water hygiene, develop good personal habits, eliminate pests, maintain environmental sanitation, and prevent diseases from entering through the mouth—all of these are effective measures to protect susceptible populations.
4. Currently, metronidazole (Flagyl) is the first-line drug for acute amoebiasis (including abscesses in different locations). It is well absorbed orally and has few side effects, but its concentration in the colon is relatively low, making it less effective for treating carriers alone. To cure intestinal amoebiasis, a combination of medications such as chiniofon and vioform—quinoline drugs effective against luminal amoebas—should be used. Chloroquine is also effective for extraintestinal amoebiasis. Chinese medicinals like java brucea fruit, garlic extract, and Chinese pulsatilla root also show certain efficacy with minimal side effects.
A cure can only be confirmed after 6 to 10 consecutive stool examinations show no cysts or trophozoites following treatment.
Pay attention to food and water hygiene, develop good personal habits, eliminate pests, maintain environmental cleanliness, and prevent diseases from entering through the mouth—these are all effective measures for preventing infections.
