Chapter 273 Amebiasis Edsel Maurice T. Salvana, Robert A. Salata Entamoeba histolytica infects up to 10% of the world’s population; endemic foci are particularly common in the tropics, especially in areas with low socioeconomic and sanitary standards. In most infected individuals, E. histolytica parasitizes the lumen of the gastrointestinal tract and causes few symptoms or sequelae. The 2 most common forms of disease caused by E. histolytica are amebic colitis with parasitic invasion of the intestinal mucosa and amebic liver abscess with dissemination of the parasite to the liver. Etiology Two morphologically identical but genetically distinct species of Entamoeba commonly infect humans. Entamoeba dispar, the more prevalent species, does not cause symptomatic disease. E. histolytica, the pathogenic species, causes a spectrum of disease and can become invasive. Patients previously described as asymptomatic carriers of E. histolytica based on microscopy findings were likely harboring E. dispar. Five other species of nonpathogenic Entamoeba can colonize the human gastrointestinal tract: E. coli, E. hartmanni, E. gingivalis, E. moshkovskii, and E. polecki. Infection is acquired through the ingestion of parasite cysts, which measure 10-18 mm in diameter and contain 4 nuclei. Cysts are resistant to harsh environmental conditions including the concentrations of chlorine commonly used in water purification but can be killed by heating to 55°C. After ingestion, cysts are resistant to gastric acidity and digestive enzymes and germinate in the small intestine to form trophozoites. These large, actively motile organisms colonize the lumen of the large intestine and may invade the mucosal lining. Infection is not transmitted by trophozoites, as these rapidly degenerate outside the body and are unable to survive the low pH of the stomach if swallowed. Epidemiology Prevalence of infection with E. histolytica varies greatly depending on region and socioeconomic status. Most prevalence studies have not distinguished between E. histolytica and E. dispar, and thus the true prevalence of E. histolytica infection is not known. It is estimated that infection with E. histolytica leads to 50 million cases of symptomatic disease and 40,000-110,000 deaths annually. Amebiasis is the 3rd leading parasitic cause of death worldwide. Prospective studies have shown that 4-10% of individuals infected with E. histolytica develop amebic colitis and that <1% of infected individuals develop disseminated disease, including amebic liver abscess. These numbers vary by region; for example, in South Africa and Vietnam, liver abscesses form a disproportionately large number of the cases of invasive disease due to E. histolytica. Amebic liver abscesses are rare in children and occur equally in male and female children; in adults, amebic liver abscesses occur predominantly in men. Amebiasis is endemic to Africa, Latin America, India, and Southeast Asia. In the USA, amebiasis is seen most frequently in immigrants from and in travelers to developing countries. Residents of mental health institutions and men who have sex with men are also at increased risk for invasive amebiasis. Food or drink contaminated with Entamoeba cysts and direct fecal-oral contact are the most common means of infection. Untreated water and night soil (human feces used as fertilizer) are important sources of infection. Food handlers shedding amebic cysts play a role in spreading infection. Direct contact with infected feces also results in person-to-person transmission. Pathogenesis Trophozoites are responsible for tissue invasion and destruction. These attach to colonic epithelial cells by a galactose and N-acetyl-D-galactosamine (Gal/GalNac)-specific lectin. This lectin is also thought to be responsible for resistance to complement-mediated lysis. Once attached to the colonic mucosa, amebae release proteinases that allow for penetration through the epithelial layer. Host cells are destroyed by cytolysis and apoptosis. Cytolysis is mediated by trophozoite release of amoebapores (pore-forming proteins), phospholipases, and hemolysins. Amoebapores may also be partially responsible for the induction of apoptosis that occurs in mice with amebic liver disease and colitis. Early invasive amebiasis produces significant inflammation, due in part to parasite-mediated activation of nuclear factor-κB (NF-κB). Once E. histolytica trophozoites invade the intestinal mucosa, the organisms multiply and spread laterally underneath the intestinal epithelium to produce the characteristic flask-shaped ulcers. Amebae produce similar lytic lesions if they reach the liver. These lesions are commonly called abscesses, although they contain no granulocytes. Well-established ulcers and amebic liver abscesses demonstrate little local inflammatory response. Immunity to infection is associated with a mucosal secretory IgA response against the Gal/GalNac lectin. Neutrophils appear to be important in initial host defense, but E. histolytica–induced epithelial cell damage releases neutrophil chemoattractants, and E. histolytica is able to kill neutrophils, which then release mediators that further damage epithelial cells. The disparity between the extent of tissue destruction by amebae and the absence of a local host inflammatory response in the presence of systemic humoral (antibody) and cell-mediated responses may reflect both parasite-mediated apoptosis and the ability of the trophozoite to kill not only epithelial cells but neutrophils, monocytes, and macrophages. The sequencing of the E. histolytica genome has led to further insights into the pathogenesis of E. histolytica disease. The genome is functionally tetraploid, and there is evidence of lateral gene transfer from bacteria. It has been demonstrated that the amoebapore-A (Ap-A) gene along with other important genes can be epigenetically silenced using plasmids with specifically engineered sequences or short hairpin RNAs. Transcriptional profiling using proteomics and microarrays have likewise identified several candidate virulence factors. Several classes of proteases that may be associated pathogenesis have been identified, including a novel E. histolytica rhomboid protease 1 (EhROM1), which may be involved in immune evasion. Clinical Manifestations Clinical presentations range from asymptomatic cyst passage to amebic colitis, amebic dysentery, ameboma, and extraintestinal disease. E. histolytica Only gold members can continue reading. 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Chapter 273 Amebiasis Edsel Maurice T. Salvana, Robert A. Salata Entamoeba histolytica infects up to 10% of the world’s population; endemic foci are particularly common in the tropics, especially in areas with low socioeconomic and sanitary standards. In most infected individuals, E. histolytica parasitizes the lumen of the gastrointestinal tract and causes few symptoms or sequelae. The 2 most common forms of disease caused by E. histolytica are amebic colitis with parasitic invasion of the intestinal mucosa and amebic liver abscess with dissemination of the parasite to the liver. Etiology Two morphologically identical but genetically distinct species of Entamoeba commonly infect humans. Entamoeba dispar, the more prevalent species, does not cause symptomatic disease. E. histolytica, the pathogenic species, causes a spectrum of disease and can become invasive. Patients previously described as asymptomatic carriers of E. histolytica based on microscopy findings were likely harboring E. dispar. Five other species of nonpathogenic Entamoeba can colonize the human gastrointestinal tract: E. coli, E. hartmanni, E. gingivalis, E. moshkovskii, and E. polecki. Infection is acquired through the ingestion of parasite cysts, which measure 10-18 mm in diameter and contain 4 nuclei. Cysts are resistant to harsh environmental conditions including the concentrations of chlorine commonly used in water purification but can be killed by heating to 55°C. After ingestion, cysts are resistant to gastric acidity and digestive enzymes and germinate in the small intestine to form trophozoites. These large, actively motile organisms colonize the lumen of the large intestine and may invade the mucosal lining. Infection is not transmitted by trophozoites, as these rapidly degenerate outside the body and are unable to survive the low pH of the stomach if swallowed. Epidemiology Prevalence of infection with E. histolytica varies greatly depending on region and socioeconomic status. Most prevalence studies have not distinguished between E. histolytica and E. dispar, and thus the true prevalence of E. histolytica infection is not known. It is estimated that infection with E. histolytica leads to 50 million cases of symptomatic disease and 40,000-110,000 deaths annually. Amebiasis is the 3rd leading parasitic cause of death worldwide. Prospective studies have shown that 4-10% of individuals infected with E. histolytica develop amebic colitis and that <1% of infected individuals develop disseminated disease, including amebic liver abscess. These numbers vary by region; for example, in South Africa and Vietnam, liver abscesses form a disproportionately large number of the cases of invasive disease due to E. histolytica. Amebic liver abscesses are rare in children and occur equally in male and female children; in adults, amebic liver abscesses occur predominantly in men. Amebiasis is endemic to Africa, Latin America, India, and Southeast Asia. In the USA, amebiasis is seen most frequently in immigrants from and in travelers to developing countries. Residents of mental health institutions and men who have sex with men are also at increased risk for invasive amebiasis. Food or drink contaminated with Entamoeba cysts and direct fecal-oral contact are the most common means of infection. Untreated water and night soil (human feces used as fertilizer) are important sources of infection. Food handlers shedding amebic cysts play a role in spreading infection. Direct contact with infected feces also results in person-to-person transmission. Pathogenesis Trophozoites are responsible for tissue invasion and destruction. These attach to colonic epithelial cells by a galactose and N-acetyl-D-galactosamine (Gal/GalNac)-specific lectin. This lectin is also thought to be responsible for resistance to complement-mediated lysis. Once attached to the colonic mucosa, amebae release proteinases that allow for penetration through the epithelial layer. Host cells are destroyed by cytolysis and apoptosis. Cytolysis is mediated by trophozoite release of amoebapores (pore-forming proteins), phospholipases, and hemolysins. Amoebapores may also be partially responsible for the induction of apoptosis that occurs in mice with amebic liver disease and colitis. Early invasive amebiasis produces significant inflammation, due in part to parasite-mediated activation of nuclear factor-κB (NF-κB). Once E. histolytica trophozoites invade the intestinal mucosa, the organisms multiply and spread laterally underneath the intestinal epithelium to produce the characteristic flask-shaped ulcers. Amebae produce similar lytic lesions if they reach the liver. These lesions are commonly called abscesses, although they contain no granulocytes. Well-established ulcers and amebic liver abscesses demonstrate little local inflammatory response. Immunity to infection is associated with a mucosal secretory IgA response against the Gal/GalNac lectin. Neutrophils appear to be important in initial host defense, but E. histolytica–induced epithelial cell damage releases neutrophil chemoattractants, and E. histolytica is able to kill neutrophils, which then release mediators that further damage epithelial cells. The disparity between the extent of tissue destruction by amebae and the absence of a local host inflammatory response in the presence of systemic humoral (antibody) and cell-mediated responses may reflect both parasite-mediated apoptosis and the ability of the trophozoite to kill not only epithelial cells but neutrophils, monocytes, and macrophages. The sequencing of the E. histolytica genome has led to further insights into the pathogenesis of E. histolytica disease. The genome is functionally tetraploid, and there is evidence of lateral gene transfer from bacteria. It has been demonstrated that the amoebapore-A (Ap-A) gene along with other important genes can be epigenetically silenced using plasmids with specifically engineered sequences or short hairpin RNAs. Transcriptional profiling using proteomics and microarrays have likewise identified several candidate virulence factors. Several classes of proteases that may be associated pathogenesis have been identified, including a novel E. histolytica rhomboid protease 1 (EhROM1), which may be involved in immune evasion. Clinical Manifestations Clinical presentations range from asymptomatic cyst passage to amebic colitis, amebic dysentery, ameboma, and extraintestinal disease. E. histolytica Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Rumination, Pica, and Elimination (Enuresis, Encopresis) Disorders Adolescent Pregnancy Neisseria gonorrhoeae (Gonococcus) Blastomycosis (Blastomyces dermatitidis) Stay updated, free articles. Join our Telegram channel Join Tags: Nelson Textbook of Pediatrics Expert Consult Jun 18, 2016 | Posted by admin in PEDIATRICS | Comments Off on Amebiasis Full access? Get Clinical Tree
