ABSTRACT
On the basis of their relationship to oxygen, microorganisms may be classified as strict aerobes which require molecular oxygen as a terminal electron acceptor, microaerophiles which require reduced oxygen tension and which grow in the presence of 5% CO2, facultative anaerobes which require oxygen under aerobic conditions but can also use organic compounds in a series of oxidation-reduction reactions to grow anaerobically, and anaerobes which cannot grow in the presence of molecular oxygen. There is, however, an oxygen gradient within which anaerobic bacteria fall, based upon their capability to neutralize toxic oxygen molecules. Microaerotolerant species produce superoxide dismutase and are able to scavange superoxide anions (O2) which prevent the secondary generation of OH radicals, and singlet oxygen (1O2), all of which are highly toxic to the bacterial cell. Additionally, many anaerobes involved in human infections, e.g. Bacteroides species and Propionibacterium, produce catalase-and peroxidase-inactivating hydrogen peroxide (H2O2), aborting the generation of O2 radicals. Most human anaerobic infections are caused by microaerotolerant anaerobes of the genera Clostridium, Peptostreptococcus, Fusobacterium, and Bacteroides. Strict anaerobes are either devoid of superoxide dismutase or produce small quantities. Anaerobic bacteria are widely distributed in nature in oxygen-free niches and colonize many sites on the human body including skin (Proprionibacteriun). In the colon, the predominant bacterial flora is anaerobic, exceeding 1011 organisms /gram of colon content and outnumbering facultative species by 1000 : 1. Anaerobes are closely associated with
mucosal surfaces in the oral cavity (gingival crevices, tonsilar crypts) and genitourinary tract. In their ecological niche, anaerobic bacteria are generally harmless. When introduced, however, into devitalized tissue with a low redox potential, devastating life-threatening infections may ensue. Usually, infections are polymicrobic and contain aerobic species which diminish oxygen concentrations, thereby facilitating growth of anaerobic species. Anaerobic bacteria have been incriminated in a wide range of human infections, including aspiration pneumonia, pelvic infections, brain abscesses, especially after dental manipulation, intrauterine infection, abdominal infections, subcutaneous infections, bacteremia, and, rarely, endocarditis. Of special note are clostridial gas gangrene, botulism and tetanus. In the oral cavity, two potentially devastating infections can occur, Ludwig’s angina and Lemierre’s syndrome. Ludwig’s angina is a severe, rapidily progressive cellulitis of the floor of the mouth, involving the submandibular and sublingual spaces arising from the second and third submandibular molars. Unimpeded, there is local lymphadenitis, bacteremia, and involvement of the cervical fascia with focal cellulitis. Lemierre’s syndrome is an uncommon, but potentially lifethreatening entity, that consists of oropharyngeal infection with bacteremia, usually caused by Fusobacterium mortiferum. Infection rapidly progresses to jugular vein septic thrombopheblitis, with embolization to the lungs and other tissues. Anaerobic bacteria produce many tissue-destructive exoenzymes, some species-specific. Acute necrotizing gingivitis, or trench mouth, is an ulcerative process affecting the marginal gingivae, with a propensity to spread to the tonsils or pharynx
Figure 249 Clostridium perfringens India ink preparation of culture smear counterstained with crystal violet, showing distinct capsules. A similar preparation may be used to confirm C. perfringens directly in tissue exudates
Figure 252 Clostridium perfringens Colonies on 5% sheep blood agar after 48-h growth, showing double zone of β-hemolysis
Figure 250 Clostridium perfringens Massive myonecrosis of thigh with crepitation extending to the ankle. Tissue destruction is due to local production of toxins, including α-toxin and lecithinase. Gas in tissue occludes blood supply, adding to gangrenous presentation. Patients also have systemic toxemia
Figure 253 Clostridium perfringens Hemorrhagic, painful, oozing bullous lesions on back and shoulder of neutropenic leukemia patient who developed non-traumatic spontaneous cellulitis and myonecrosis. Note the linear creases in skin and rupture of bullous lesions due to pressure of gas formation in tissue. Note also the bluish discoloration of the skin
Figure 251 Clostridium perfringens Numerous stout bacilli with rounded to square ends in smear of necrotic tissue excised from leg of patient with myonecrosis. Note absence of inflammatory response and presence of clear, circular areas denoting gas bubbles in proteinaceous matrix
Figure 248 Clostridium perfringens Gram stain of culture, showing typical stout bacilli with rounded ends
Figure 254 Clostridium perfringens Buttocks of patient with spontaneous gangrenous myonecrosis, with bluish discoloration of skin and edema of the surrounding tissue. This entity may also be caused by Clostridium septicum
(Vincent’s angina). Spread to involve the facial tissue (cancrum oris, noma) is a major complication. Gramstained smears of these lesions will show a predominance of Gram-negative cigar-shaped fusobacterial organisms and spirochetes (Borrelia vincenti).
