ANAEROBIC INFECTIONS : CLINICAL ASPECTS
Bacteroides, Fusobacterium, and peptostreptococci, alone or together with other faculta-tive or obligate anaerobes, are responsible for the overwhelming majority of localized abscesses within the cranium, thorax, peritoneum, liver, and female genital tract. As indi-cated earlier, the species involved relate to the pathogens present in the normal flora of the adjacent mucosal surface. Those derived from the oral flora also include dental infec-tions and infections of human bites.
In addition, anaerobes play causal roles in chronic sinusitis, chronic otitis media, aspi-ration pneumonia, bronchiectasis, cholecystitis, septic arthritis, osteomyelitis, decubitus ulcers, and soft tissue infections of patients with diabetes mellitus. Dissection of infection along fascial planes (necrotizing fasciitis) and thrombophlebitis are common complica-tions. Foul-smelling pus and crepitation (gas in tissues) are signs associated with, but by no means exclusive to, anaerobic infections. As with other bacterial infections, they may spread beyond the local site and enter the bloodstream. The mortality rate of anaerobic bacteremias arising from nongenital sources is equivalent to the rates with bacteremias due to staphylococci or Enterobacteriaceae.
The key to detection of anaerobes is a high quality specimen, preferably pus or fluid taken directly from the infected site. The specimen needs to be taken quickly to the mi-crobiology laboratory and protected from oxygen exposure while on the way. Special anaerobic transport tubes may be used or any air from the syringe in which the specimen was collected may be expressed. Actually, a generous collection of pus serves as an ade-quate transport medium unless transport is delayed for hours.
A direct Gram-stained smear of clinical material demonstrating Gram-negative and/or Gram-positive bacteria of various morphologies is highly suggestive, often even diagnos-tic of anaerobic infection. Because of the typically slow and complicated nature of anaer-obic culture, the Gram stain often provides the most useful information for clinical decision-making. Isolation of the bacteria requires the use of an anaerobic incubation at-mosphere and special media protected from oxygen exposure. Although elaborate systems are available for this purpose, the simple anaerobic jar is sufficient for isolation of the clinically significant anaerobes. The use of media that contain reducing agents (cysteine, thioglycollate) and growth factors needed by some species further facilitates isolation of anaerobes. The polymicrobial nature of most anaerobic infections requires the use of selective media to protect the slow growing anaerobes from being overgrown by hardier bacteria, particularly members of the Enterobacteriaceae. Antibiotics, particularly aminoglycosides to which all anaerobes are resistant, are frequently used. Once the bacte-ria are isolated, identification procedures including morphology, biochemical characteri-zation, and metabolic end-product detection by gas chromatography may begin.
As with most abscesses, drainage of the purulent material is the primary treatment, in as-sociation with appropriate chemotherapy. Antimicrobics alone may be ineffective because of failure to penetrate the site of infection. The selection of antimicrobics used is empiric to a degree; such infections typically involve mixed species, and cultural diagnosis is de-layed by the slow growth and the time required to distinguish multiple species. In addi-tion, antimicrobial susceptibility testing methods are slow and less standardized than they are for the rapidly growing bacteria. The usual approach involves selection of antimicro-bics based on the expected susceptibility of the anaerobes known to produce infection at the site in question. For example, anaerobic organisms derived from the oral flora are of-ten susceptible to penicillin, but infections below the diaphragm caused by fecal anaer-obes such as B. fragilis are usually resistant to β-lactams. These latter infections are most likely to respond to clindamycin, metronidazole, or a cephalosporin such as cefoxitin, which is not inactivated by the β-lactamases produced by anaerobes.
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