Brachyspira pilosicoli

[2][3] It appears as a characteristic "false brush border" due to its end-on attachment to enterocytes of the colon where it interferes with intestinal absorption.

[4] B. pilosicoli is unique from other Brachyspira species because it colonizes a variety of domestic animals including pigs, chickens, dogs, wild birds, rodents, and humans.

[2] Although spirochetes have been described dating back to 1877,[8] it would be another hundred years before Brachyspira pilosicoli would be first described in 1980 and recognized as a causative agent of diarrhea and dysentery in pigs.

This name reflected the microscopic description of how the spirochete organisms coat the enterocytes creating an appearance similar to a healthy brush border, despite the ongoing colitis and mucoid diarrhea.

This, however, was disputed by Dr. Claude O. Burdick who suggested that the "false brush border" was simply normal intestinal microvilli sectioned tangentially, giving a spirochete-like morphology.

[5][23] A distinguishing feature of B. pilosicoli is that it belongs to a group of gram-negative bacteria that contain lipooligosaccharide in their outer membrane instead of lipopolysaccharide.

[23] It was previously thought that B. pilosicoli could be differentiated from other Brachyspira species because it is hippurate hydrolysis positive; however, hippurate-negative strains have also been documented.

[4][23] B. pilosicoli attaches in an end-on manner to the mucosal epithelium of the large intestine and interferes with water absorption in the GI tract.

[7] This disruption to the colonic enterocytes and associated microvilli causes the symptoms of diarrhea and slow growth that are characteristic of intestinal spirochetosis.

[7] 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 with microvilli disruption in some compared to invasion and destruction of enterocytes in others.

[26] In general, the virulence factors within the genus Brachyspira are thought to be involved primarily in chemotaxis and motility, adherence and invasion, and hemolysis.

[7] The decreased feed intake and body weight gain associated with the disease cause significant economic impacts for producers.

[30] Chicks hatched from hens colonized with Brachyspira pilosicoli have reduced growth rates and experience wet feces.

[2] Transmission occurs most commonly from contact with wildlife or other domestic animals carrying the bacteria, as well as from contaminated people or equipment.

[4] Specifically, the spirochete is passed in feces and may survive for prolonged periods in natural water systems such as lakes and ponds, from which it can be isolated.

[35] Specifically, if hygiene in a village is poor due to lack of modern sanitation and reliance on nearby streams as a sole source of water, the fecal-oral transmission of B. pilosicoli is favored.

[26] Largely as a consequence of the considerable genetic similarities between strains of B. pilosicoli infecting humans, swine, and poultry, the potential to adapt to various hosts exists.

[40] These cases are likely examples of human infections of pathogenic B. pilosicoli from enteric commensal populations as a consequence of increased microorganism virulence or diminished host defenses.

Intestinal spirochetosis. Spirochetes disrupt absorption in the intestine by attaching to the surface of colonic enterocytes.
Opportunities for interspecies transmission of B. pilosicoli are more likely to occur in households where animals and humans live in close proximity.