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The history of B. hominis is unique. Few infectious agents have provoked the many misconceptions that plague this enigmatic parasitic ameba. Conflicting descriptions of its nature and pathogenesis have continued throughout the 20th century. As seen by the greatly expanded number of reports in recent years, B. hominis is now a major subject of study, particularly for evidence of disease causation. Physicians are treating patients with intestinal disease caused by B. hominis. Many mild cases resolve in about 3 days without treatment, but others are acute and chronic disease is common. As with E. histolytica, the carrier state is often seen without symptoms. Treatment is usually with metronidazole, but emetine (for refractory infections), trimethoprim-sulfamethoxazole, and pentamidine are also effective. In fecal samples, this complex protozoan appears in a variety of cell forms which makes microscopic diagnosis difficult. As yet, no specific fluorescent-antibody test is available for diagnosis. A culture method to demonstrate the more easily recognized CB form is available, but probably not feasible for most diagnostic laboratories. The common cell forms are the CB form, the granular (mitochondria) form, and the ameba form. The unexpected size range of these forms in clinical material, from yeast size (ca. 7 microns) to giant cells of 20 to 40 microns, makes diagnosis difficult Pseudopodia may be demonstrated by the ameba form in heated microscope stage culture chambers. The anaerobic B. hominis has no cyst form. Its mitochondria are uniquely anaerobic and have no cytochrome protein or oxidative mitochondrial enzymes. Because of its many cell forms and anaerobic mitochondria, B. hominis is an organism of great interest for morphologic and biochemical study. Reproduction is asexual, usually by binary fission. Shizogony occurs in cultured cells. The CB appears to be an organelle whose specific purpose is for reproduction by shizogony. From 2 to 30 progeny are derived from schizogony. The ameba form reproduces by plasmotomy; it has no CB. The pathology of B. hominis infections has been studied in gnotobiotic guinea pigs in which inflammation of the intestinal mucosa and invasion of the superficial layers were seen. Only limited studies of human pathology are available. Those who have studied mucosal histopathology report inflammation and cellular changes that resolve after treatment. More study in this area is strongly indicated (32, 44, 57, 62, 67, 75). Ultrastructural details of B. hominis major forms, except for the schizont, are complete. The organism has no cell wall. The concentric CB takes up as much as 95% of the cell. The major organelles, which include multiple nuclei, Golgi apparatus, mitochondria, endoplasmic reticulum, fat, and other inclusions, are confined in two or four opposed pods in a thin band of peripheral cytoplasm between the spherical entire plasma membrane and the CB membrane. The pods buldge the CB membrane inward. There is evidence of a bacteroid endosymbiont. Education about B. hominis is needed. Entry of recent findings into new textbooks is imperative for its understanding among medical practitioners. Laboratory workers need to be aware of it for many reasons. The College of American Pathologists includes B. hominis in its proficiency testing samples and requires that it be reported from clinical samples.