Pathogenesis of Anaerobic Infections
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p310-311
2025-09-16
304
Infections caused by anaerobes commonly are caused by combinations of bacteria that function in synergistic pathogenicity. Although studies of the pathogenesis of anaerobic infections have often focused on a single species, it is important to recognize that the anaerobic infections most often are caused by several species of anaerobes acting together to cause infection.
B. fragilis is a very important pathogen among the anaerobes that are part of the normal microbiota. The pathogenesis of anaerobic infection has been most extensively studied with B. fragilis using a rat model of intra-abdominal infection, which in many ways mimics human disease. A characteristic sequence occurs after colon contents (including B. fragilis and a facultative anaerobe such as E. coli) are placed via needle, gelatin capsule, or other means into the abdomens of rats. A high percentage of the study animals die of sepsis caused by the facultative anaerobe. However, if the animals are first treated with gentamicin, a drug effective against the facultative anaerobe but not Bacteroides species, few of the animals die, and after a few days, the surviving animals develop intra-abdominal abscesses from the Bacteroides infection. Treatment of the animals with both gentamicin and clindamycin, a drug effective against Bacteroides species, prevents both the initial sepsis and the later development of abdominal abscesses.
The capsular polysaccharides of Bacteroides are important virulence factors. A unique feature of infections with B. fragilis is the ability of the organism to induce abscess formation as the sole infecting organism. When injected into rats’ abdomens, purified capsular polysaccharides from B. fragilis cause abscess formation, but those from other bacteria (eg, Streptococcus pneumoniae and E. coli) do not. The mechanism by which the B. fragilis capsule induces abscess formation is not well understood.
Bacteroides species have lipopolysaccharides (endotoxins) but lack the lipopolysaccharide structures with endotoxic activity (including β-hydroxymyristic acid). The lipopolysaccharides of B. fragilis are much less toxic than those of other Gram-negative bacteria. Thus, infection caused by Bacteroides does not directly produce the clinical signs of sepsis (eg, fever and shock) so important in infections caused by other Gram-negative bacteria. When these clinical signs appear in Bacteroides infection, they are a result of the inflammatory immune response to the infection.
B. fragilis elaborates a number of enzymes important in disease. In addition to proteases and neuraminidases, production of two cytolysins acts together to cause hemolysis of erythrocytes. An enterotoxin capable of causing diarrhea and whose gene is contained on a pathogenicity island is found in the majority of isolates that are recovered from blood cultures.
B. fragilis produces an SOD and can survive in the presence of oxygen for days. When a facultative anaerobe such as E. coli is present at the site of infection, it can consume all available oxygen and thereby produce an environment in which Bacteroides species and other anaerobes can grow.
F. necrophorum likewise possesses important virulence factors that enable it to cause Lemierre’s syndrome and other seriously invasive infections. One of these factors is a leukotoxin likely responsible for the necrosis seen with these infections. Other factors include a hemagglutinin, a hemolysin, and lipopolysaccharide (endotoxin). In addition, F. necrophorum is capable of causing platelet aggregation. The exact pathogenic interplay, if any, among these factors in the pathogenesis of human infections remains to be elucidated.
Many anaerobic bacteria produce heparinase, collage nase, and other enzymes that damage or destroy tissue. It is likely that enzymes play a part in the pathogenesis of mixed anaerobic infections, although laboratory experiments have not been able to define specific roles.
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