Noninvasive intestinal amebiasis: Entamoeba histolytica colonization without invasion.

PURPOSE OF REVIEW: Entamoeba histolytica infection remains a major cause of morbidity and mortality worldwide. Although research with the organism began in the late nineteenth century, our understanding of the natural history of the infection remains incomplete and is heavily based on expert opinion. Most persons infected with E. histolytica are carriers with the organism colonizing the large intestine. Host defense mechanisms that prevent invasive diseases are poorly understood. A timely review could lead to renewed interest. RECENT FINDINGS: We herein review 2012 and 2013 publications related to the epidemiology, diagnosis, management and potential mechanisms that enable noninvasive E. histolytica colonization without invasion. SUMMARY: There are several publications that advance our knowledge in the first three categories listed above, but studies of mechanisms for noninvasive E. histolytica colonization are glaringly few.

Luminal host-defense mechanisms against invasive amebiasis.

Most humans infected with the virulent protozoan parasite Entamoeba histolytica do not develop invasive disease. Available evidence indicates that beneficial bacteria and the mucus gel layer in the colon lumen protect the host mucosa. Glycosidases produced by some normal colonic bacteria and luminal proteases degrade the key adherence lectin on E. histolytica trophozoites and decrease their adherence to epithelial cells. The mucus gel layer prevents those trophozoites that escape the hydrolases from reaching the epithelial cells. Trophozoite mucosal invasion is triggered only when both protective mechanisms are lost, as might occur during an unrelated pathogenic enteric bacterial infection. A newly developed gnotobiotic model of intestinal amebiasis should enable testing of this hypothesis and provide clues to help design practical studies in humans.

Visceral angioedema: an under-recognized complication of angiotensin-converting enzyme inhibitors.

Cough and upper airway angioedema are well-recognized adverse reactions of angiotensin-converting enzyme inhibitor (ACEI) therapy. Visceral angioedema is an infrequent and often unrecognized complication of ACEI therapy. We describe a patient in whom the diagnosis was delayed for > 2 years. A 60-year-old woman with hypertension on treatment with enalapril presented with complaints of abdominal pain and diarrhea for 2 days. Physical examination was significant for diffuse abdominal tenderness and hypotension. Laboratory data were normal except for leukocytosis and elevated creatinine. Computed tomography (CT) of the abdomen showed diffuse small bowel wall thickening. ACEI-induced visceral angioedema was considered, enalapril was discontinued and supportive care was provided. Patient's symptoms and CT appearance improved 48 and 72 hours, respectively, after stopping enalapril. She remained symptom-free 1 year after discharge.