Defensive strategies of Bacillus anthracis that promote a fatal disease

Abstract

Bacillus anthracis is a Gram-positive bacterium that causes anthrax. Bacterial spores that enter the host germinate into metabolically active bacilli that disseminate throughout the body and replicate to high numbers. Two virulence factors are essential for this unrestrained growth. The first is a weakly immunogenic poly γ-D-glutamic acid capsule that surrounds the bacilli and confers resistance to phagocytosis. The second virulence factor, anthrax toxin, disrupts multiple host functions to diminish the immune response.

JMM Profile: Bacillus anthracis

“…PA forms seven-or eight-molecule complexes on eukaryotic cell membranes, to which LF and EF bind. Following endocytosis, the PA structures form channels and deliver LF and EF into the cytosol [27,35,45,50]. LF is a zinc metalloproteinase targeting mitogen-activated protein kinase kinases; it depresses key immune functions, including phagocytosis [13,45,51].…”

“…Following endocytosis, the PA structures form channels and deliver LF and EF into the cytosol [27,35,45,50]. LF is a zinc metalloproteinase targeting mitogen-activated protein kinase kinases; it depresses key immune functions, including phagocytosis [13,45,51]. EF is an adenylyl cyclase that depresses phagocyte and B-lymphocyte function and reduces immune cell chemotaxis [45,51,52].…”

“…LF is a zinc metalloproteinase targeting mitogen-activated protein kinase kinases; it depresses key immune functions, including phagocytosis [13,45,51]. EF is an adenylyl cyclase that depresses phagocyte and B-lymphocyte function and reduces immune cell chemotaxis [45,51,52]. The toxins may synergize [51] and they also have systemic effects probably including cardiac and liver depression for LF and EF, respectively [35,49].…”

“…Bacillus anthracis capsule inhibits phagocytosis, interferes with host antimicrobial peptides and probably shields cell surface antigens from the host [13,45]. Its partial depolymerisation may be locally immunosuppressive [35,53].…”

“…Existing micro-trauma to skin and alimentary mucosa probably allows spore entry; other suggested routes include gut lymphoid tissue, toxin-damaged mucosa and intact skin [1,5,16,36,42,44,45]. Inhaled spores probably reach thoracic lymph nodes via mucosal dendritic cells and perhaps also macrophages [13,46].…”