| disease | Amoebic Dysentery |
Entamoeba histolytica (dysentery amoeba) (Entamoeba histolytica Schaudinn, 1930), primarily resides in the colon, causing amoebic dysentery or amoebic colitis. The dysentery amoeba is also the most significant pathogenic species among the Rhizopoda, and under certain conditions, it can spread to the liver, lungs, brain, urogenital system, and other areas, forming ulcers and abscesses.
bubble_chart Epidemiology
This disease is prevalent worldwide, especially in tropical and subtropical regions, but amoebic infections and outbreaks also occur in colder areas, even within the Arctic Circle. The infection rate is closely related to local environmental sanitation, economic conditions, and dietary habits. It is estimated that about 10% of the world's population is infected, with some areas having infection rates as high as 50%. In China, the distribution is generally higher in rural areas than in cities. In recent years, due to improvements in sanitation and living standards, acute amoebic dysentery and abscess cases have become relatively rare, except in certain regions. Most cases are chronic, lingering, or typical cases, as well as carriers, scattered in distribution.
(1) Source of pestilence: Chronic sexually transmitted disease patients, convalescent patients, and healthy carriers are the sources of pestilence for this disease. Cysts have strong resistance and can survive for more than 12 days in damp and low-temperature environments, and 9 to 30 days in water. However, cysts have weaker resistance to dryness, high temperatures, and chemical agents. For example, they die quickly at 50°C, survive only a few minutes in dry environments, and cannot survive for long in 0.2% hydrochloric acid, 10-20% saline, or condiments like soy sauce and vinegar. 50% alcohol can quickly kill them.
(2) Transmission routes: Entamoeba histolytica can be transmitted in the following ways: ① Cyst contamination of water sources can cause outbreaks in the area; ② Using feces as fertilizer, unwashed and uncooked vegetables are also important transmission factors; ③ Cyst contamination of fingers, food, or utensils; ④ Flies and cockroaches can come into contact with feces, carry cysts on their bodies, and vomit feces, contaminating food and becoming important vectors of transmission.(3) Epidemiological characteristics: Entamoeba histolytica is widely distributed. In temperate regions, the disease can occasionally become epidemic, while in tropical and subtropical regions, the epidemic situation is particularly severe. Since the liberation of China, the infection rate of amoebiasis has significantly decreased. For example, from 1973 to 1978, Beijing Capital Hospital examined 38,075 cases, with a positive rate of 0.52%; Fujian Medical University examined 216 children in Hui'an in 1976, with a positive rate of 4.63%; Jiamusi Medical College in Northeast China reported in 1980 that among 487 suburban middle school students examined, the positive rate was only 0.4%; in 1979, a general survey of 557 farmers in Leqing, Zhejiang, showed a positive rate of 3.2%. The incidence of the disease varies with time, being more common in autumn and less so in summer. The incidence rate is higher in males than in females, and higher in adults than in children, which may be related to the ingestion of cyst-containing food or age-related immunity.
The morphological changes of Entamoeba histolytica can be divided into the trophozoite stage, precyst stage, and cyst stage. The trophozoite stage is further divided into two types: large and small. The large trophozoite is large and mainly lives in the intestinal wall tissue; the small trophozoite is small, lives in the intestinal lumen, and leads a commensal life, capable of forming cysts. Therefore, the former is also known as the tissue-type large trophozoite (referred to as the large trophozoite), and the latter is known as the commensal encysting-type small trophozoite (referred to as the small trophozoite).
1. Trophozoite:
⑴ Large trophozoite: Chinese Taxillus Herb in the tissue is the pathogenic form of Entamoeba histolytica. The active large trophozoite varies greatly in size, with a diameter of 12-60μm, commonly 15-30μm. The body is divided into endoplasm and ectoplasm, with the ectoplasm being transparent, accounting for about one-third of the whole body, and the endoplasm being denser and granular. During movement, the ectoplasm extends, often forming a single pseudopod, moving directionally in an amoebic motion. Initially, the ectoplasm extends a tongue-like or finger-like pseudopod, followed by the endoplasm flowing into the pseudopod, causing the entire body to move in the direction of the pseudopod extension. Red blood cells engulfed by it are often seen in the endoplasm. After staining with iron Sappan Wood, a round nucleus can be seen, vesicular in shape, 4-9μm in size, averaging 5.3μm, with a layer of evenly sized and neatly arranged chromatin particles on the inner edge of the nuclear membrane, and a small round nucleolus in the center, which may be slightly eccentric, and sometimes a reticular nuclear fiber can be seen between the nucleolus and the nuclear membrane.
⑵ Small trophozoite: The small trophozoite lives in the intestinal lumen, feeding on intestinal bacteria and contents, does not engulf red blood cells, and is smaller in size in physiological saline smears, with a diameter of 12-30μm, its size not easily distinguishable from the large trophozoite, with indistinct boundaries between endoplasm and ectoplasm, and food vacuoles containing bacteria. After staining with iron Sappan Wood, the nuclear structure is the same as that of the large trophozoite.
3. Cyst: Spherical, with a diameter of 5-20μm, a cyst wall about 0.5cm thick, transparent, strongly refractive, and not stained by eosin. Under low magnification, it appears as a round transparent body, with internal structures not clearly visible. Under high magnification, chromatoid bodies and reflective round nuclei can be faintly seen. When stained with iodine, the entire cyst appears light brown, relatively clear, with 1-4 nuclei, occasionally 8. In single or binucleate cysts, brown-stained glycogen vacuoles and transparent rod-like chromatoid bodies (possibly polyribosomes) can be seen. When forming mature infectious quadrinucleate cysts, the chromatoid bodies and glycogen vacuoles gradually disappear. After staining with iron Sappan Wood, the glycogen vacuoles dissolve into vacuoles during the staining process, and the chromatoid bodies become clearer, rod-shaped with blunt ends.
(II) Observation under an electron microscope:
1. Trophozoite
⑴ Cell surface structure: Through scanning electron microscopy, Mccaul et al. (1977) first discovered that the surface of the trophozoite has microfilopodia 2-3μm long. Lushbaugh et al. (1979) reported that the surface of living trophozoites is wavy, with fine wrinkles, irregularly protruding trabeculae, and distinct lobopodia as well as longer filopodia, the number of which varies. Transmission electron microscopy shows that these filopodia range in length from a few μm to over 30μm, with a diameter of up to 0.1μm, and their surface has a unit membrane structure, formed by the extension of the plasma membrane. The microfilopodia and filopodia described by the above two authors seem to be the same.
Transmission electron microscopy reveals that the plasma membrane of the trophozoite is a typical unit membrane, consisting of two thin electron-dense layers (each 35-40Å thick) with a transparent and wider middle layer (45-50Å), totaling 120Å in thickness (Ludvik, 1970). The plasma membrane of amoebae obtained from intestinal tissue is covered with a fuzzy coat approximately 300Å thick, whereas cultured amoebae lack this feature. This may be a secretion of the parasite or an antigen-antibody complex, which remains to be confirmed.
⑵Cytoplasm: Through transmission electron microscopy, it was observed that the cytoplasm of the trophozoite of Entamoeba histolytica contains many vesicular structures, including vacuoles, food vacuoles, and numerous glycogen particles of varying sizes. The food vacuoles vary in size (0.5～12μm), and their membrane structure is the same as the plasma membrane, suggesting that they are formed by the plasma membrane during phagocytosis; the vacuoles contain a type of food, which may be related to the specific digestive enzymes present in each food vacuole. There are also microtubules and smaller vacuole-like lysosomes [diameter (5～20)×10-9m]; the endoplasmic reticulum formed by the membrane is sparse, appearing as small tubules or vesicles, with no ribosomes attached to its surface. Additionally, ribosomes aggregated into a helical configuration can be seen.
⑶Nucleus: Irregularly round, the nuclear membrane is a typical unit membrane, 12×10-9m thick, with many nuclear pores, most of which have a diameter of 5×10-9m, the nucleoplasm is granular, with an electron density higher than the cytoplasm, and the inner edge of the nuclear membrane has chromatin particles clustered into abdominal masses, which are rich in ribonucleic acid (RNA), as determined by 3H-uridine labeling to be the site of RNA synthesis and abdominal mass (Albach et al., 1977), and also determined to have deoxyribonucleic acid (DNA) by the consumption of 3H-thymidine. It is speculated that they may be the morphological basis of certain types of messenger ribonucleic acid (mRNA), with definitive conclusions awaiting the purification and generation and transformation analysis of these particles. The nucleolus is central but irregular, composed of many very small dense electron particles.
2. Cyst: Proctor et al. (1973) collected cysts of Entamoeba histolytica from feces and observed them with transmission electron microscopy, finding that the cyst wall has two layers, the outer layer being a low electron density villous coat, 40nm thick, and the inner layer being a high electron density fibrous structural layer, 80nm thick. The entire cyst wall is 120nm thick. Inside the inner layer of the cyst wall is the plasma membrane surrounding the cytoplasm, 10nm thick, with osmophilic bodies (osmophilic) distributed at intervals on its inner edge, 30～80nm in size. The cytoplasm contains many organelles, similar to those seen in trophozoites. Glycogen particles are abundant, scattered throughout the cytoplasm, some clustered into abdominal masses. The chromatoid bodies are composed of electron-dense particles. There are also many vacuoles of varying sizes, some containing food residues. The size of the nucleus averages 1.7×1.6μm, with the nuclear membrane and nuclear subcutaneous nodes being the same as in trophozoites.
bubble_chart Pathological Changes
The pathogenesis of amoebiasis is a complex process involving the interaction between the parasite and the host, influenced by multiple factors. The invasive power of Entamoeba histolytica is primarily manifested in its lytic destruction of host tissues. It has been previously demonstrated that amoebae possess various proteolytic enzyme activities, but these have not been successfully isolated. In the 1970s, initial stage [first stage], experiments showed that the destructive effect of living trophozoites on host cells is characterized by contact lysis. Cytochemical analysis of acid phosphatase in dysentery amoebae indicated that the active substances are located in the plasma membrane and food vacuole membrane, leading to the proposition of the "membrane-bound enzyme" theory. Additionally, enzymes capable of hydrolyzing gelatin, casein, fibrin, and hemoglobin were extracted from living dysentery amoebae. Experiments and electron microscopy observations revealed that trophozoites can not only phagocytose red blood cells but also kill white blood cells. Lushbaugh et al. (1979) also isolated an enterotoxin from the soluble extract of amoebae, which has cytotoxic properties and plays a significant role in the pathogenesis of amoebic dysentery.
The issue of amoebic strains, recent studies have shown that the virulence of amoebae is hereditary, but the intensity of virulence varies among strains. Strains from tropical regions with high incidence rates of amoebic dysentery, due to long-term adaptation to tissue environments, possess stronger virulence; whereas strains from cold and temperate regions have weaker virulence and more carriers. However, the virulence of strains is not fixed and can be enhanced through animal passage or weakened after long-term in vitro culture, but can be increased again by transmission from one meridian to the next through animal inoculation. The emergence of virulence is also interrelated with bacteria present in the intestinal lumen. Some self-experiments have shown that ingesting only washed, non-virulent dysentery amoebic cysts results in a carrier state, and subsequent ingestion of intestinal cells from patients leads to dysentery. This synergistic effect promoting pathogenesis is likely because bacteria provide the physicochemical conditions necessary for amoebic proliferation and activity, such as creating suitable redox potentials and hydrogen ion concentrations, while also potentially weakening the host's systemic or local resistance, or even directly damaging the intestinal mucosa, providing opportunities for amoebae to invade tissues.
The immune status of the host also plays a crucial role in whether amoebae can invade tissues. Dysentery amoebae must breach the host's defense barriers to invade and proliferate in tissues. Clinical and experimental data indicate that factors such as malnutrition, infection, intestinal dysfunction, and mucosal injury, which lower the host's systemic or local immune function, all facilitate amoebic invasion of tissues. In populations or experimental animals with low nutritional standards, the incidence and pathological indices of amoebiasis are significantly higher than in those with balanced diets, and are less susceptible to drug control; patients with cold-damage disease, schistosomiasis, subcutaneous nodules, or other intestinal or systemic infections are more prone to amoebiasis and find it harder to cure once infected.
The large trophozoites of Entamoeba histolytica invade the intestinal wall causing amoebiasis, commonly affecting the cecum, followed by the rectum, sigmoid colon, and appendix, with the transverse and descending colon being less commonly involved, and sometimes affecting the entire large intestine or part of the ileum.
(1) Acute phase: Intestinal mucosal cells are damaged, leading to erosion and superficial ulcers. If the condition progresses, the lesions deepen, involving the submucosal layer, forming typical flask-shaped ulcers with a small mouth and a large base. The base of the ulcer is the mucosal layer, and the cavity is filled with brownish-yellow necrotic material containing dissolved cell fragments, mucus, and trophozoites. When the contents are discharged, it results in clinically dysentery-like stools. The mucosa between the ulcers is mostly intact, differing from the lesions of bacterial dysentery. Amoebas continue to progress into the submucosal layer, and due to the loose tissue, the protozoa spread along the longitudinal axis of the intestine, causing extensive tissue dissolution and forming many interconnected honeycomb-like areas. There is significant inflammatory reaction around the lesions, generally limited to infiltration of lymphocytes and a few plasma cells. If there is secondary bacterial infection, there may be a large infiltration of neutrophils. The lesion sites are prone to capillary thrombosis, petechial hemorrhage, and necrosis. Due to the destruction of small blood vessels, the discharge contains more red blood cells. In severe cases, the lesions can penetrate deep into or even through the serosal layer, but because the progression of the lesions is gradual, the serosal layer tends to adhere to adjacent tissues, so acute intestinal perforation is rare. Since amoebic ulcers are generally deep and prone to eroding blood vessels, they can cause significant intestinal bleeding. During the healing process of the lesions, the tissue reaction subsides, lymphocytes disappear, and are replaced by connective tissue.
(2) Chronic phase: The characteristics of this phase are hyperplasia of the intestinal mucosal epithelium, granulation tissue appearing at the base of the ulcer, and fibrous tissue proliferation around the ulcer. Tissue destruction and healing often coexist, leading to thickening of the intestinal wall and narrowing of the intestinal lumen. Connective tissue occasionally proliferates in a tumor-like manner, forming amoebomas, which are commonly found in the anus, the junction of the anus and rectum, the transverse colon, and the cecum. Amoebomas can sometimes be extremely large and hard, making it difficult to distinguish them from large intestine cancer.
Amoebic trophozoites can enter the portal venous bloodstream, forming abscesses in the liver, and can also flow into tissues and organs such as the lungs, brain, and spleen in the form of emboli, forming abscesses.
bubble_chart Clinical Manifestations
The incubation period of amoebic dysentery varies, ranging from 1-2 weeks to several months or more. Although patients may have been infected with Entamoeba histolytica cysts for a long time, they only coexist in a commensal relationship. Clinical symptoms begin to appear when the host's resistance weakens and intestinal infections occur. Based on different clinical manifestations, it can be divided into the following types:
(1) Asymptomatic carriers: Although patients are infected with Entamoeba histolytica, the amoebae only exist in a commensal relationship. More than 90% of people do not develop symptoms and become cyst carriers. Under appropriate conditions, they can invade tissues, cause lesions, and lead to symptoms. Therefore, from the perspective of controlling the source of pestilence and preventing disease, sufficient attention should be paid to cyst carriers, and they must be treated.
(2) Acute atypical amoebic dysentery: The onset is relatively slow, with no obvious systemic symptoms. There may be abdominal discomfort, only loose stools, sometimes diarrhea several times a day, but lacking typical dysentery-like stools, resembling general enteritis. Trophozoites can be found in stool examinations.
(3) Acute typical amoebic dysentery: The onset is often slow, starting with abdominal pain and diarrhea. The frequency of stools gradually increases, reaching 10-15 times a day. There is varying degrees of abdominal pain and tenesmus during defecation, the latter indicating that the lesion has spread to the rectum. The stool contains blood and mucus, mostly dark red or purplish-red, pasty, with a foul smell. In severe cases, it may be bloody stools or white mucus covered with a small amount of bright red blood. Systemic symptoms are generally mild, with possible early fever and elevated white blood cell count. Trophozoites can be found in the stool.
(4) Acute fulminant amoebic dysentery: The onset is sudden, with poor overall nutritional status, severe illness appearance, significant toxic symptoms, high fever, shivering, delirium, obvious abdominal pain and tenesmus. The stool is purulent and bloody, with a foul smell, and may also be watery or rice-water-like, occurring more than 20 times a day, accompanied by vomiting, collapse, and varying degrees of dehydration and electrolyte imbalance. Blood tests show increased neutrophils. It is prone to complications such as intestinal bleeding or perforation, and if not treated properly, death from toxemia can occur within 1-2 weeks.
(5) Chronic persistent amoebic dysentery: Usually a continuation of acute infection, with alternating diarrhea and constipation, lasting for months or even years without cure. During intermittent periods, the patient may appear healthy. Recurrences are often triggered by improper diet, overeating, alcohol consumption, cold exposure, fatigue, etc., with diarrhea 3-5 times a day, yellow pasty stools, and trophozoites or cysts can be found. Patients often experience periumbilical or lower abdominal dull pain, varying degrees of anemia, weight loss, malnutrition, etc.
The diagnosis of amoebiasis, in addition to being based on the patient's complaints, medical history, and clinical manifestations as diagnostic criteria, importantly relies on etiological diagnosis. The detection of amoebic pathogens in feces is the only reliable diagnostic criterion. Typically, the detection of large trophozoites is considered indicative of active infection, while the detection of small trophozoites or cysts is only considered as an infection.
(1) Clinical manifestations: When making a diagnosis, intestinal amoebiasis should not be overlooked, as amoebiasis lacks specific clinical manifestations. The disease has a slow onset, mild toxic symptoms, is prone to recurrence, and the intestinal symptoms or dysentery-like diarrhea vary in severity. Therefore, for cases of intestinal disorders or dysentery-like diarrhea where the cause of the disease is not yet clear, or where treatment with sulfonamides or antibiotics has been ineffective, amoebiasis should be suspected.
(2) Etiological examination:
1. Fecal examination:
(1) Examination of live trophozoites: The direct saline smear method is commonly used to examine active trophozoites. For acute dysentery patients with pus and blood in the stool or amoebic colitis patients with loose stools, the container should be clean, the stool sample fresh, and the delivery to the laboratory as quick as possible. In cold seasons, attention should also be paid to keeping the sample warm during transport and examination. During examination, take a clean slide, add a drop of saline, then use a bamboo stick to pick up a small amount of stool and smear it in the saline, cover with a coverslip, and then examine under a microscope. Typical amoebic dysentery stool is soy sauce-red and mucoid, with a special fishy odor. Microscopic examination may reveal mucus containing more aggregated red blood cells and fewer white blood cells, and sometimes Charcot-Leyden crystals and active trophozoites can be seen. These characteristics can distinguish it from bacterial dysentery stool.
(2) Cyst examination method: Clinically, the iodine smear method is commonly used, which is simple and easy to perform. Take a clean slide, add a drop of iodine solution, then use a bamboo stick to pick up a small amount of stool and smear it thinly in the iodine solution, cover with a coverslip, and then examine under a microscope to identify the characteristics and number of cell nuclei.
2. Amoeba culture: There are several improved artificial culture media, commonly used ones include Locke's solution, egg, serum culture medium, nutrient agar serum saline culture medium, agar peptone biphasic culture medium, etc. However, the technical operation is complex, requires certain equipment, and the positive rate of amoeba artificial culture is not high in most subacute or chronic sexually transmitted disease cases, so it is not suitable as a routine examination for amoeba diagnosis.
3. Tissue examination: Direct observation of mucosal ulcers through sigmoidoscopy or fiber colonoscopy, and performing tissue biopsy or smear of scrapings, has the highest detection rate. It is reported that cases with lesions in the sigmoid colon and rectum account for about two-thirds of symptomatic patients. Therefore, all suspected patients who are able should undergo colonoscopy, smear of scrapings, or biopsy. The sampling of trophozoites must be at the edge of the ulcer, and slight bleeding at the site after clamping is appropriate. For the examination of pus cavity puncture fluid, in addition to paying attention to sexual characteristics, samples should be taken from the wall of the pus cavity, where trophozoites are more easily found.
(3) Immunodiagnosis: In recent years, various serological diagnostic methods have been reported both domestically and internationally. Among these, indirect hemagglutination (IHA), indirect fluorescent antibody (IFAT), and enzyme-linked immunosorbent assay (ELISA) have been extensively studied, but their sensitivity varies among different types of cases. IHA has a relatively high sensitivity, with a positive rate of 98% for intestinal amebiasis and 95% for extraintestinal amebiasis, while the positive rate for asymptomatic carriers is only 10-40%. The sensitivity of IFA is slightly lower than that of IHA. ELISA is highly sensitive and specific, showing promising potential for development. The complement fixation test is also significant for diagnosing extraintestinal amebiasis, with a positive rate exceeding 80%. Other tests, such as the gelatin diffusion precipitin test and intradermal test, also have auxiliary diagnostic value. In recent years, there have been reports of successful detection of amebic-specific antigens in feces and pus using sensitive immunological techniques. In particular, the application of monoclonal antibodies against amebic trophozoites has provided a reliable, sensitive, and interference-resistant tracing tool for detecting pathogenic substances in host excretions using immunological techniques.
(4) Diagnostic treatment: If clinical suspicion is high and the diagnosis cannot be confirmed through the above examinations, a full dose of emetine injection or oral administration of drugs such as anlidine and metronidazole can be given. If the effect is significant, a preliminary diagnosis can also be made.
bubble_chart Treatment Measures
(1) General Treatment: During the acute phase, bed rest is mandatory, and intravenous fluids may be administered as necessary. Depending on the condition, a liquid or semi-liquid diet is provided. Chronic patients should enhance their nutrition to strengthen their constitution.
(2) Pathogen Treatment:
1. Metronidazole (Flagyl): It has a strong killing effect on amoebic trophozoites and is relatively safe, making it the first-choice drug for both intestinal and extraintestinal amoebiasis. The dose is 400-800 mg orally, three times a day for 5-10 days; for children, 50 mg per kilogram of body weight per day, divided into three doses, for 7 days. Side effects such as nausea, abdominal pain, dizziness, and flusteredness may occur occasionally but do not require special treatment. It is contraindicated in the first three months of pregnancy and in nursing mothers. The efficacy rate is 100%.
2. Tinidazole: A derivative of nitroimidazole compounds. The dose is 2 g per day; for children, 50 mg per kilogram of body weight per day, taken once in the morning for 3-5 days. Occasional side effects include loss of appetite, abdominal discomfort, constipation, diarrhea, nausea, and cutaneous pruritus. Its efficacy is similar to or better than metronidazole.
3. Emetine: Highly effective against tissue trophozoites but ineffective against luminal amoebae. It is very effective in controlling acute symptoms but has a low cure rate and should be used in combination with halogenated quinolines. The dose is 1 mg per kilogram per day, not exceeding 60 mg per day for adults, usually 30 mg per dose, twice a day, administered by deep subcutaneous or intramuscular injection for 6 days.
It has significant dermatitis medicamentosa potential. Patients should rest in bed during treatment, and blood pressure and pulse should be measured before each injection, with attention to heart rhythm and blood pressure drops. Toxic reactions include vomiting, diarrhea, abdominal colicky pain, weakness, myalgia, tachycardia, hypotension, precordial pain, and ECG abnormalities, with occasional arrhythmias. It is contraindicated in young children, pregnant women, and those with cardiovascular or kidney diseases. If retreatment is needed, it should be at least 6 weeks apart.
4. Halogenated Quinolines: Mainly act on luminal rather than tissue amoebic trophozoites. Effective for mild cases and cyst passers, often used in combination with emetine or metronidazole for severe or chronic cases.
Iodoform, 0.5 g, three times a day orally for 10 days, or 1% iodoform solution 100-150 ml for retention enema. Main side effects are diarrhea, with occasional nausea, vomiting, and abdominal discomfort. Contraindicated in those allergic to iodine and with thyroid disease.
5. Others: Diloxanide furoate, 0.5 g orally, three times a day for 10 days; Paromomycin, 15-20 mg per kilogram of body weight per day, divided doses orally for 5-7 days; Phanquinone, 0.1 g orally, three times a day for 10 days. All three drugs act on luminal amoebae.
6. Chinese Herbal Medicine: Java brucea fruit, 15-20 seeds, encapsulated and taken orally, three times a day for 7 days; Garlic, 6 g per day, eaten raw in divided doses for 10 days; Chinese pulsatilla root, 15-20 g made into a decoction, taken in three doses for 10 days.
Except for metronidazole, a combination of two or more drugs is often necessary to achieve better results.
(3) Treatment of Complications: Under active and effective treatment with metronidazole and emetine, all intestinal complications can be alleviated. Patients with fulminant forms and mixed bacterial infections should receive additional antibiotics. Massive intestinal bleeding may require blood transfusion. Surgical treatment is necessary for intestinal perforation, peritonitis, etc., and should be performed under metronidazole and antibiotic treatment.
The prognosis for intestinal amoebiasis is good if treated promptly. However, the prognosis is poorer for complications such as intestinal bleeding, perforation, diffuse peritonitis, and metastatic abscesses in the liver, lungs, or brain. Post-treatment stool examinations for parasites should continue for about six months to detect possible relapses early.
Treat patients and cyst carriers by ensuring drinking water is boiled, avoiding raw vegetables, and preventing food contamination. Control fly breeding and eliminate flies. Screen and treat food industry workers who are cyst excretors or chronic patients, and maintain personal hygiene such as washing hands before meals and after using the toilet.
(1) Intestinal complications:
1. Intestinal perforation: Acute intestinal perforation mostly occurs in patients with severe amoebic intestinal disease. This is the most life-threatening complication of intestinal amoebiasis. Perforation can cause intestinal contents to enter the abdominal cavity due to intestinal wall lesions, leading to localized or diffuse peritonitis. The perforation sites are commonly found in the cecum, appendix, and ascending colon. Chronic perforation first forms intestinal adhesions, which often lead to localized abscesses or internal fistulas into nearby organs.
2. Intestinal hemorrhage: The incidence is less than 1%, and it generally occurs in patients with amoebic dysentery or granulomas, caused by ulcers invading the intestinal wall blood vessels. Massive bleeding is often due to ulcers reaching the submucosal layer, invading large blood vessels, or destruction by granulomas. Although massive bleeding is rare, once it occurs, the condition is critical and often leads to shock due to blood loss. Minor bleeding is usually caused by superficial ulcer oozing.
3. Appendicitis: Since amoebic intestinal disease often affects the cecum, the appendix is frequently involved. Autopsies of colonic amoebiasis cases reveal appendicitis in 6.2% to 40.9% of cases, while domestic reports indicate that only 0.9% involve the appendix. The symptoms are similar to bacterial appendicitis, with both acute and chronic presentations. However, if there is a history of amoebic dysentery and obvious tenderness in the lower right abdomen, this condition should be considered.
4. Amoeboma: The intestinal wall produces a large amount of granulation tissue, forming a palpable mass. It mostly occurs in the cecum but can also be found in the transverse colon, rectum, and anus, often accompanied by pain, closely resembling a tumor and difficult to distinguish from intestinal cancer. When the mass enlarges, it can cause intestinal obstruction.
5. Intestinal stenosis: In chronic patients, fibrous tissue repair of intestinal ulcers can lead to cicatricial stenosis, accompanied by abdominal colicky pain, vomiting, abdominal distension and fullness, and obstructive symptoms.
6. Perianal amoebiasis: This condition is relatively rare and is often misdiagnosed clinically. When there are skin injuries, anal fissures, anal canal inflammation, or cryptitis, amoebic trophozoites can directly invade the skin, causing perianal amoebiasis. Seasonal disease changes can occur secondary to ligation treatment for hemorrhoids and fistulas. Occasionally, amoebic trophozoites can infect perianal tissues through the bloodstream, leading to brown, foxtail millet-sized rashes that are flat and raised with unclear edges, eventually forming ulcers or abscesses that discharge pus and secretions. It is easily misdiagnosed as rectal-anal canal cancer, basal cell carcinoma, or subcutaneous skin nodules.
(2) Extraintestinal complications: Amoebic trophozoites can spread from the intestines through the bloodstream or lymphatic system to distant organs, causing various extraintestinal complications. The most common is liver abscess, followed by infections in the lungs, pleura, pericardium, brain, peritoneum, stomach, gallbladder, skin, urinary system, and female reproductive system.
Amebic intestinal disease needs to be differentiated from bacterial dysentery, schistosomiasis, intestinal tuberculosis, intestinal cancer, and chronic nonspecific ulcerative colitis.
(1) Bacterial dysentery: The onset is acute, systemic toxic symptoms are severe, antibiotic treatment is effective, and stool microscopy and bacterial culture are helpful for diagnosis.
(2) Schistosomiasis: The onset is relatively slow, the course is long, there is a history of contact with infected water, hepatosplenomegaly, increased eosinophils in the blood, schistosome eggs or hatched miracidia can be found in the stool, and eggs can be detected in intestinal mucosal biopsies.
(3) Intestinal tuberculosis: Most cases have primary subcutaneous node lesions, patients experience consumptive fever, night sweats, nutritional disorders, etc.; stools are often yellow and porridge-like, with mucus and little pus or blood, alternating diarrhea and constipation. Gastrointestinal X-ray examination aids in diagnosis.
(4) Intestinal cancer: Patients are older, often have changes in bowel habits, stools become thinner, there is progressive anemia, and weight loss. In advanced stages, abdominal masses can often be palpated, and X-ray barium enema and fiber colonoscopy aid in diagnosis.
(5) Chronic nonspecific ulcerative colitis: Clinical symptoms are difficult to distinguish from chronic amebiasis, but stool examination does not reveal amebae, and when anti-amebic treatment is ineffective, this disease should be considered.
