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Brachyspira pilosicoli draft
B. pilosicoli attaches in an end-on manner to the mucosal epithelium of the large intestine and interferes with water absorption in this portion of the GI tract. This end-on attachment of spirochetes to the colonic enterocytes creates the appearance of a "false brush border" and is a common feature in spirochetosis in all animal species. Experimental infections in pigs have also shown invasion of and degeneration of epithelial cells in addition to surface colonization of enterocytes. Inflammation of the mucosa due to spirochete attachment may lead to a thickened mucosa, focal lesions with an exudate of mucus and white blood cells, and dilated colonic crypts. This disruption to the colonic enterocytes and associated microvilli causes the symptoms of diarrhea and slow growth that are characteristic of intestinal spirochetosis. However, there may be variability in the characteristics of colonization and severity of infection in different individuals and between species, such as purely end-on attachment and microvilli disruption versus invasion and destruction of enterocytes in different species and severity of infection. For instance, diet may affect degree of colonization and disease, and disease can vary from subclinical disease to severe. Originally thought to be non-invasive in humans, attaching to just the luminal surface of the intestinal mucosa, more recent studies have found that there can be cell destruction associated with intestinal spirochetosis in humans. Cases of more severe diarrhea are associated with heavier spirochete burden, increased cell destruction, and blunted microvilli.

Although virulence factors in Brachyspira pilosicoli have not been extensively characterized, various surface proteins have been identified that are known to be linked to virulence in other bacterial species and which may allow colonization of the intestinal mucosa by B. pilosicoli. These include proteins involved in chemotaxis and motility, hemolysins involved in damage to enterocytes and subsequent inflammation, ankyrin-like proteins that can enter host cells and allow interaction of bacteria with host cells. No secreted proteins were found that could contribute to virulence like are seen in some other Brachyspira species. In general, the virulence factors within genus Brachyspira are involved primarily in chemotaxis and motility (B. pilosicoli exhibits chemotaxis towards mucin and has flagella which allows penetration of mucus and interaction with the enterocytes), adherence and invasion (B. pilosicoli attaches end-on without disrupting enterocyte membrane to create "false brush border" but can also invade crypts and epithelium), hemolysis (B. pilosicoli may be weakly beta-hemolytic which can contribute to cytotoxicity to host cells and lesions; hemolysins also aid in obtaining nutrients such as cholesterol and phospholipids from host cells). Lipooligosaccharides in the cell wall may be associated with mucosal inflammation. Brachyspira species do not have genes that encode any adhesins or toxins.