INTRODUCTION — Anaerobes have been encountered in infections at virtually all anatomic sites, although the frequency of recovery is highly variable. This topic will focus on common infections that involve anaerobic flora endogenous to the host.
Histotoxic clostridial infections are reviewed separately by individual pathogen and/or syndrome (eg, tetanus, botulism, Clostridioides [formerly Clostridium] difficile infection, gas gangrene, neutropenic enterocolitis due to Clostridium septicum). The history of anaerobes, the composition of normal flora in humans, and the pathophysiology, clinical clues, and recovery of these organisms are also discussed separately. (See "Anaerobic bacteria: History and role in normal human flora" and "Pathophysiology, clinical clues, and recovery of organisms in anaerobic infections".)
CLINICAL CLUES TO ANAEROBIC INFECTION — Clinical clues to anaerobic infection include:
●Putrid drainage (considered diagnostic of anaerobic infection)
●Polymicrobial flora on Gram stain of exudates
●Infection involving normal flora of adjacent mucosal surfaces, such as the upper respiratory tract, the gastrointestinal tract, and the female genital tract
●Infection characterized by abscess formation
ANTIMICROBIAL SELECTION — Most anaerobic infections are treated empirically, since the process of recovery and in vitro testing is long, tedious, and often limited in availability and, perhaps most importantly, the bacteriologic patterns are predictable based on published reports and knowledge of the flora at adjacent mucocutaneous sites (table 1) [1-45]. Antimicrobial susceptibility testing is rarely performed in clinical laboratories for the following reasons:
●Cultures usually yield a polymicrobial flora or may be falsely negative due to inadequate sampling, transport, or anaerobic culture techniques.
●The infecting flora is usually polymicrobial, requiring the tedious task of separating multiple different bacteria for identification and susceptibility testing.
●Poor quality control of in vitro antibiotic sensitivity testing limits use of these tests.
●The practical application of these observations is that complete culture results with susceptibility tests are often labor intensive, time consuming, expensive, and incomplete. Results other than Gram stain are not available in a clinically relevant time frame. Thus, antibiotic decisions for anaerobic pathogens are often best made based upon predicted susceptibility patterns according to the Gram stain and the anatomical site of infection. In contrast, appropriate therapy for the aerobic component of mixed infection is determined based upon culture and susceptibility testing results that typically can be completed more quickly.
Based on these practical issues, the 2012 edition of Clinical and Laboratory Standards Institute (CLSI, formerly the National Committee for Clinical Laboratory Standards [NCCLS]) Working Group on Anaerobic Susceptibility Testing has restricted recommending this testing to the following settings [46]:
●To monitor local and regional resistance patterns
●To test new antimicrobial agents
●To select antibiotics that are critical for individual patient management because of:
•Critical illness
•Known resistance of an organism or species
•Persistent infection despite appropriate antibiotics
•Difficulty with empiric decision based on precedent
•To confirm antimicrobial activity when long courses of antibiotics are required
Most clinical laboratories will not perform susceptibility tests unless they are specifically requested. In addition, many hospitals do not offer this service, those that do often use techniques that are not considered reliable, and the results are usually available only after therapeutic decisions have been made.
General in vitro susceptibility patterns of various antibiotics against anaerobes are summarized in the table (table 2). The preferred drugs, which remain active against most clinically important anaerobes, are metronidazole, a carbapenem, or a beta-lactam-beta-lactamase inhibitor. Recommendations for the management of intra-abdominal infections are presented below.
The management of anaerobic infections involving other sites is discussed separately. (See "Complications, diagnosis, and treatment of odontogenic infections" and "Deep neck space infections in adults" and "Ludwig angina" and "Aspiration pneumonia in adults" and "Lung abscess in adults" and "Management and complications of tubo-ovarian abscess" and "Postpartum endometritis".)
ANTIMICROBIAL RESISTANCE — Despite the lack of emphasis on in vitro testing as described above, a clear correlation has been noted between antimicrobial in vitro activity and patient survival after treatment for anaerobic bacteremia [47,48] (see 'Antimicrobial selection' above). This was illustrated in a prospective observational study of 128 patients with Bacteroides bacteremia [47]. The mortality rate among patients who received inactive therapy by in vitro testing was higher than in patients who received active therapy (45 versus 16 percent). Clinical failure and microbiologic persistence were also higher for patients who received inactive therapy (82 and 42 percent, respectively) than for patients who received active therapy (22 and 12 percent, respectively).
Antibiotic resistance among anaerobic bacteria is increasing [49-53] and could lead to worse patient outcomes. Resistance rates vary widely among different geographic regions and institutions, and some antibiotic regimens that were well accepted in the 1970s and 1980s are no longer considered adequate for empiric use (table 2). The most significant changes have been with major reductions in the in vitro activity of clindamycin, cefoxitin, cefotetan, and moxifloxacin against Bacteroides fragilis and related strains (often referred to as B. fragilis group, including Parabacteroides distasonis, B. ovatus, B. thetaiotaomicron, B. uniformis, B. vulgatus, B. caccae, and B. eggerthii). These are the major anaerobic pathogens causing intra-abdominal sepsis and bacteremia [49,54].
A national survey in the United States of resistance patterns of over 5000 B. fragilis group isolates from 1997 to 2004 [45] and other studies have revealed the following findings [55,56]:
●The frequency of clindamycin resistance in B. fragilis increased from 3 percent in 1987 to 26 percent from 1997 to 2004 [45,57]. Some centers have reported clindamycin resistance rates of B. fragilis to be as high as 44 percent, with even higher rates observed among some members of the B. fragilis group [49,55].
●Resistance to moxifloxacin in the national survey increased to 38 percent for B. fragilis, and, for cefoxitin, the resistance rate was 10 percent [45].
●Resistance rates for other antibiotics were [45]:
•Ampicillin-sulbactam – 3 percent
•Piperacillin-tazobactam – 0.5 percent
•Tigecycline – 4 percent
●Carbapenems (ertapenem, doripenem, meropenem, and imipenem) are generally equally active against anaerobes with <1 percent of B. fragilis strains showing resistance in some studies [45,58,59]. Other studies have reported higher rates [55,60,61]. As an example, in one large study, up to 5 percent of isolates were resistant to carbapenems [55].
●A surveillance study of clinical isolates of B. fragilis from Canada from 2010 and 2011 showed that 98 to 99 percent of isolates were susceptible to metronidazole, imipenem, and piperacillin-tazobactam [52]. Lower rates of susceptibility were seen for tigecycline (81 percent), cefoxitin (66 percent), moxifloxacin (56 percent), and clindamycin (52 percent).
●There has also been a substantial reduction in the susceptibility of the B. fragilis group to clindamycin and moxifloxacin in other studies. Among 1957 clinical isolates in the United States collected between 2006 and 2009, up to 60 percent of strains were resistant to clindamycin and up to 88 percent were resistant to moxifloxacin [55].
●The same group reported that only one of several hundred strains of B. fragilis was resistant to metronidazole [55]. Depending on the species, 0 to 23 percent of B. fragilis group isolates were resistant to cefoxitin. Approximately 5 percent of isolates were resistant to tigecycline.
●Other reports of metronidazole-resistant B. fragilis in the United States have been rare [62-64].
●Two cases of multidrug-resistant (MDR) B. fragilis have been reported in the United States; the isolates from these cases were resistant to metronidazole, carbapenems, piperacillin-tazobactam, and clindamycin, among other agents [63,64].
A surveillance study from a hospital in Taiwan has reported increasing rates of anaerobe resistance to various antibiotics [61]. Of more than 2500 B. fragilis isolates, nearly 30 percent were nonsusceptible (intermediate or resistant) to ampicillin-sulbactam between 2000 and 2004, but 48 percent were nonsusceptible in 2007. There was also a significant increase in resistance to ampicillin-sulbactam among other Bacteroides spp, Prevotella spp, and Fusobacterium spp. An increase in clindamycin resistance was also observed among isolates of B. fragilis, Fusobacterium spp, and anaerobic gram-positive cocci other than Peptostreptococcus anaerobius. However, it is unclear if these resistance patterns represent an atypical experience that is geographically restricted, nonstandardized culture techniques, or an important emerging trend.
The high rate of resistance of the B. fragilis group to clindamycin and moxifloxacin has been an increasing trend in the United States and Europe, but beta-lactam-beta-lactamase inhibitor combinations remain active against most isolates. Carbapenem resistance is now being reported, but it remains rare in most of the world.
The conclusion from these observations is that B. fragilis is the major anaerobic pathogen in blood cultures and at infected sites with intra-abdominal and pelvic infections. Antibiotic selection is generally made empirically based on susceptibility test results from sentinel laboratories. These reports indicate that the most predictably active drugs are metronidazole, carbapenems, and beta-lactam-beta-lactamase inhibitor combinations. These agents are generally active against other anaerobic bacteria as well. Clindamycin and fluoroquinolones no longer have reliable activity against B. fragilis. Note that there have been substantial changes in the susceptibility of B. fragilis in recent years and some geographic idiosyncrasies as well, so these dynamic changes need to be followed. Most intra-abdominal infections are caused by not only anaerobic but also aerobic and/or microaerophilic bacteria; the latter pathogens are usually easily cultured, and treatment decisions for them can be based on conventional methods.
Infections above the diaphragm usually reflect the orodental flora, which does not include the B. fragilis group. Major anaerobic pathogens in orodental and pulmonary infections are Fusobacterium, Prevotella, and peptostreptococci. Many of these strains produce beta-lactamase, making all beta-lactams (penicillins and cephalosporins) poor options. The favored oral agents for empiric use are metronidazole, clindamycin, and amoxicillin-clavulanate [65]. It is important to note that most of these infections have a mixed flora that includes microaerophilic and aerobic streptococci, which are not susceptible to metronidazole.
ANTIMICROBIALS BY CLASS
●Penicillins – Penicillin G, ampicillin, and amoxicillin are equally active versus anaerobes and are often preferred except for infections involving the B. fragilis group, other gram-negative anaerobes producing beta-lactamase, and some Clostridia (C. ramosum, C innocuum) and Prevotella spp. Methicillin, nafcillin, and oxacillin are generally inferior to penicillin G. Carbenicillin, piperacillin, and ticarcillin are generally active against anaerobes but are considered suboptimal for infections involving B. fragilis. The beta-lactam-beta-lactamase inhibitors show good activity against anaerobes including the B. fragilis group [66]. B. distasonis is an exception.
●Carbapenems – Imipenem, ertapenem, doripenem, and meropenem have good activity against anaerobes including the B. fragilis group [67]. Use of doripenem has been associated with increased mortality in patients with ventilator-associated pneumonia. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Other agents'.)
●Chloramphenicol – Chloramphenicol has good activity against anaerobes, but use in the United States is rare because of hematologic toxicity.
●Macrolides – Macrolides have good in vitro activity against many anaerobes other than B. fragilis and other gram-negative anaerobes, but the published clinical experience is limited.
●Clindamycin – Clindamycin was once a preferred antimicrobial agent for anaerobic infections including B. fragilis bacteremia [68], but resistance has emerged with B. fragilis, Prevotella, some peptostreptococci, and some Clostridia [56]. (See 'Antimicrobial resistance' above.)
●Fluoroquinolones – Moxifloxacin was previously the preferred agent in the fluoroquinolone class for infections involving anaerobes including the B. fragilis group. However, as noted above, resistance rates as high as 57 percent for B. fragilis have been reported more recently [56].
SITES OF INFECTION
Central nervous system infections — Pyogenic intracranial infections that commonly involve anaerobic bacteria include cerebral and epidural abscess and subdural empyema [1]. Since meningitis rarely involves these bacteria, growth of an anaerobe in cerebrospinal fluid (CSF) cultures suggests a parameningeal collection, shunt infection, or contamination. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Infections of cerebrospinal fluid shunts and other devices" and "Intracranial epidural abscess".)
The most extensively studied of these infections is cerebral abscess, which is usually a polymicrobial infection with some variation in bacteriologic patterns, depending upon the primary source of the abscess. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Treatment and prognosis of bacterial brain abscess".)
Infections of the upper airways — Anaerobic bacteria are involved in a variety of infections of the oral cavity and adjacent structures. Organisms isolated in oral infection reflect the contiguous normal oral flora. The dominant isolates are the Bacteroides oralis group, the pigmented Prevotella (formerly B. melaninogenicus group), Porphyromonas asaccharolytica, Fusobacterium spp, Peptostreptococcus spp, microaerophilic streptococci, and aerobic streptococci.
Dental infections — Most clinically important dental infections involve anaerobes, including pulpitis (endodontal infection), periapical or dental abscess, and perimandibular space infections. These three infections usually represent a continuum. The initial lesion is endodontal; the infection progresses to the periapical region, and it may then extend through the mandible to involve the potential spaces created by fascial insertions along the mandible. Factors responsible for this progression are poorly understood, but one hypothesis is that a "network of bacteria" comprising the gingival microbiome collectively contribute [69]. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections".)
Infections of the gingival crevice and gums, including gingivitis, periodontitis, and pyorrhea, usually involve anaerobic bacteria. Major agents of the flora also found in infected perioral infections include Fusobacterium, Prevotella, Porphyromonas, and Treponema spp. An infrequent but distinct form is necrotizing ulcerative gingivitis, sometimes known as Vincent angina or trench mouth. This is a relatively fulminant infection associated with severe pain, tissue destruction, pseudomembrane formation, and putrid discharge. The bacterial agent is not well established, although anaerobic spirochetes have been detected within tissue at the advancing edge of inflammation, and antibiotic treatment directed against anaerobes is necessary. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections" and "Overview of gingivitis and periodontitis in adults".)
A possibly related necrotizing infection of the oral mucous membranes is noma, also called cancrum oris, which is characterized by destruction of soft tissue and bone. It evolves rapidly from gingival inflammation to orofacial gangrene [70]. Noma occurs most frequently in children (peak incidence at ages 1 to 4 years) with malnutrition or systemic disease and is usually fatal in the absence of antibiotic therapy [71]. (See "Noma (cancrum oris)".)
Deep neck space infections — Deep neck space infections usually arise from dental infections involving molar teeth and, less commonly, from infections of the pharynx or tonsils. The deep neck "spaces" are potential spaces formed by insertions of fascia along the mandible, and they are named by their location (eg, submandibular space). Oral flora play an important role in these infections, but they may also be caused by Staphylococcus aureus and aerobic enteric gram-negative bacilli [72]. Life-threatening forms of deep neck space infections that are important to recognize clinically include Ludwig's angina and Lemierre syndrome:
●Ludwig's angina is an infection characterized by bilateral involvement of the sublingual and submandibular spaces that causes swelling of the base of the tongue and potential airway compromise, hence "angina." Ludwig's angina is typically a polymicrobial infection involving the flora of the oral cavity, including anaerobes. (See "Ludwig angina".)
●Lemierre syndrome (eg, jugular vein suppurative thrombophlebitis) is an infection involving the posterior compartment of the lateral pharyngeal space complicated by suppurative thrombophlebitis of the jugular vein with Fusobacterium necrophorum (not F. nucleatum) bacteremia and metastatic abscesses, primarily to the lung. Studies have also implicated F. necrophorum as a possibly important cause of pharyngitis [73-77]. (See "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein".)
Peritonsillar abscess is another type of deep neck space infection that is frequently caused by anaerobic bacteria, such as F. necrophorum and Peptostreptococcus spp. (See "Peritonsillar cellulitis and abscess".)
Deep neck space infections are discussed in greater detail separately. (See "Deep neck space infections in adults".)
Miscellaneous infections — Anaerobic bacteria have been implicated with variable frequencies in chronic sinusitis, chronic otitis media [2], and mastoiditis but play a minimal role in acute otitis media or acute sinusitis. (See "Microbiology and antibiotic management of chronic rhinosinusitis" and "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and diagnosis".)
Pleuropulmonary infections — Anaerobic bacteria are relatively common and frequently overlooked pathogens in the lower airways. The infections usually arise from aspiration of oral and dental secretions that result in aspiration pneumonitis. This is generally an indolent form of pneumonia, but the early presentation is difficult to distinguish from other forms of acute bacterial pneumonia, including pneumococcal pneumonia. (See "Aspiration pneumonia in adults".)
In fact, the clues that lead clinicians to suspect anaerobic infection are typically absent during this early or pneumonitis stage of infection. As an example, patients rarely have putrid sputum and are often diagnosed as having atypical pneumonia. Nevertheless, this should be considered in patients who are aspiration prone and have an infiltrate in a dependent pulmonary segment. The usual features of anaerobic infection are seen in the later stages of disease, when there is likely to be putrid discharge and necrosis of tissue with abscess formation or empyema as well as weight loss and anemia as indicators of chronic disease. (See "Lung abscess in adults".)
Clinical clues to this diagnosis include a predisposition to aspirate, infection in a dependent pulmonary segment, and putrid sputum [78]. The indolent course of many of these infections may serve as a distinguishing clinical clue. Whereas patients with pneumococcal pneumonia often have the abrupt onset of symptoms accompanied by a shaking chill and a rapid progression of symptoms, these features are rare with an anaerobic pleuropulmonary infection. By contrast, these patients often present with weight loss, anemia, and chronic pulmonary complaints, all features that are relatively uncommon in pneumonia due to most aerobic bacteria other than mycobacteria. Nevertheless, pneumonia due to anaerobic bacteria may simulate pneumococcal pneumonia during the early stages [79].
Intra-abdominal infections — Infections within the abdominal cavity are usually polymicrobial and result in secondary peritonitis, which may be generalized or localized (phlegmon), or intra-abdominal abscess. Intra-abdominal infections are discussed in detail separately. (See "Antimicrobial approach to intra-abdominal infections in adults".)
Infections of the female genital tract — Nearly all infections of the female genital tract that are not caused by sexually transmitted pathogens are likely to involve anaerobic bacteria. The most common anaerobes are penicillin-resistant anaerobes, especially Prevotella bivia and, to a lesser extent, Prevotella disiens (formerly Bacteroides disiens). (See "Pelvic inflammatory disease: Pathogenesis, microbiology, and risk factors".)
Infections likely to involve anaerobic bacteria include:
●Bacterial vaginosis
●Bartholin gland abscess (see "Bartholin gland masses", section on 'Types of masses')
●Tubo-ovarian abscess (see "Epidemiology, clinical manifestations, and diagnosis of tubo-ovarian abscess")
●Pyometra, an accumulation of pus in the uterine cavity (see "Benign cervical lesions and congenital anomalies of the cervix")
●Endometritis (see "Postpartum endometritis")
●Adnexal abscess (see "Differential diagnosis of the adnexal mass", section on 'Tubo-ovarian abscess')
●Salpingitis (eg, pelvic inflammatory disease) (see "Pelvic inflammatory disease: Treatment in adults and adolescents")
●Pelvic cellulitis
●Amnionitis
●Septic thrombophlebitis of the pelvic veins (see "Septic pelvic thrombophlebitis")
●Wound infections after gynecologic surgery or obstetric procedures (see "Complications of gynecologic surgery", section on 'Infectious morbidity')
●Septic abortion after childbirth or gynecologic procedures, including medical abortion (see "Toxic shock syndrome due to Clostridium sordellii")
Bacterial vaginosis is a recent addition to this list [80], although the pathophysiology is poorly understood. The concept currently advanced is that of a polymicrobial disease in which the dominant bacteria in vaginal fluid from cases compared with controls are anaerobic bacteria (eg, Atopobium, Leptotrichia, Megasphaera, and Eggarthella) [81]. The anaerobic nature is supported by a clinical response when antibiotics directed against anaerobes are given (eg, metronidazole or clindamycin). (See "Bacterial vaginosis: Clinical manifestations and diagnosis".)
One of the great difficulties encountered in many of these infections is obtaining appropriate material for meaningful anaerobic culture. The problem of contamination by the normal genital tract flora may be obviated by using culdocentesis, laparoscopy, or quantitative cultures with telescoping catheters for transcervical sampling of the endometrium [7-9].
Soft tissue infections — Anaerobic bacteria are common pathogens in a diverse array of skin and soft tissue infections. Most involve the cutaneous flora, especially Peptostreptococcus, or the flora of adjacent mucosal surfaces. A relatively common feature of these infections is the low oxygen tension in tissues due to poor vascular supply; conditions in which this occurs include diabetes mellitus, injury (including surgery), and trauma. (See "Necrotizing soft tissue infections" and "Clostridial myonecrosis".)
Prosthetic devices — Cutibacterium (formerly Propionibacterium) is occasionally identified in infections involving prosthetic devices, especially shoulder devices [82-84]. The usual antibiotic treatment recommended is penicillin or a first-generation cephalosporin; clindamycin and vancomycin are alternatives.
Microbiology — S. aureus and S. pyogenes are commonly viewed as the dominant pathogens in soft tissue infections, although anaerobic bacteria account for a major portion. Cutaneous abscesses above the waist usually involve S. aureus or Peptostreptococcus spp; abscesses below the waist are more likely to involve anaerobic bacteria and often reflect the bacterial flora of the colon [10]. Similarly, anaerobes are the predominant isolates in infected sebaceous (epidermal) cysts, infected pilonidal cysts [12], paronychia [13], wound infections after surgery [14,15], bite wounds [16], diabetic foot ulcers [85], and decubitus ulcers [86]. Quantitative cultures of diabetic foot ulcers show anaerobes to be the numerically dominant microbes [87], and osteomyelitis secondary to decubitus ulcers or diabetic foot ulcer is also likely to involve anaerobes [88]. Detection of putrid odor from the wound is considered diagnostic of anaerobic infection at the anatomic site [89]. (See "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities".)
Deep soft tissue infections likely to involve anaerobic bacteria include necrotizing fasciitis, synergistic necrotizing cellulitis, crepitant cellulitis, and gas gangrene. These infections involve the fascia, the muscle compartment formed by the enveloping fascia, or both. Major pathogens in these deep infections comprise a short list: group A beta-hemolytic streptococci, clostridia, and combinations of aerobic and anaerobic bacteria. (See "Necrotizing soft tissue infections" and "Clostridial myonecrosis".)
Human bites and, to a lesser extent, animal bites often involve anaerobic bacteria. These types of infections can arise from the oral flora of the biter or from the flora of the adjacent skin of the bite recipient. The clenched fist injury is the equivalent of a human bite in the sense that the infection involves the flora of the mouth of the person struck or the skin flora of the person delivering the punch. Eikenella corrodens and aerobic and microaerophilic streptococci from the oral flora are frequent pathogens in human bite wounds; S. aureus from the skin at the site of the injury may also be involved. (See "Human bites: Evaluation and management" and "Animal bites (dogs, cats, and other animals): Evaluation and management".)
Breast abscesses, particularly recurrent breast abscesses, sometime involve anaerobes. (See "Primary breast abscess", section on 'Microbiology'.)
Abscesses — Anaerobic bacteria are particularly common in abscesses at most anatomical sites, including cerebral abscess, dental abscess, perimandibular space abscess, cutaneous abscess, perirectal abscess, intra-abdominal abscess, pelvic abscess, and prostatic abscess (table 1). A series of studies in a rodent model with an intra-abdominal challenge using stool to simulate intra-abdominal sepsis showed B. fragilis (and possibly other anaerobes) was the dominant component in subsequent intraabdominal abscesses; abscess formation could be prevented with antibiotics directed against B. fragilis [90-92]. Further, abscesses could be produced with a monomicrobial challenge with B. fragilis and could also be reproduced with just the capsular polysaccharide of the B. fragilis. These data show the somewhat unique pathologic potential of B. fragilis, and presumably other anaerobes, to produce abscesses.
Bacteremia — Anaerobes have accounted for 2 to 5 percent of blood culture isolates from patients with clinically significant bacteremia. The rate decreased from the 1970s through the early 1990s, reflecting the frequent use of bowel preparations prior to abdominal surgery and of anti-anaerobic antibiotics [18,88,93-95]. An exception was Cutibacterium, which is a common isolate but almost invariably represents a skin contaminant rather than a true pathogen.
However, a report from the Mayo Clinic suggests that this trend is reversing [96]. The number of cases of anaerobic bacteremia per year increased from 53 during 1993 to 1996 to 75 during 1997 to 2000 to 91 during 2001 to 2004, which represents an overall increase of 74 percent. During this period, the frequency of anaerobes as a percentage of all organisms causing bacteremia increased from 5.4 to 10.4 percent. A presumed contributor was the increasing proportion of patients with complex underlying diseases.
A different experience was reported from Switzerland, in which the percentage of blood cultures yielding anaerobes has decreased over time; in 1997, 166 (1.8 percent) of blood cultures grew anaerobes compared with 70 (0.5 percent) in 2006 [97].
Another observation in the Mayo Clinic study is that 34 percent of cases were not in typical settings in which anaerobic infections are seen [96]. This is potentially important because some have suggested that blood cultures for anaerobic infection should be performed in selected settings, not routinely. However, this approach has not been adopted in adults [98].
The most common blood culture isolates among anaerobes are the B. fragilis group, which account for 35 to 80 percent [95,97]. A review of the suspected portal of entry for 855 episodes of bacteremia involving anaerobes indicated an intra-abdominal source in 52 percent, the female genital tract in 20 percent, the lower respiratory tract in 6 percent, the upper respiratory tract in 5 percent, and soft tissue infections in 8 percent [95].
Although anaerobic bacteremia accounts for a small percent of clinically significant bacteremia, B. fragilis group bacteremia contributes significantly to morbidity and mortality. The attributable mortality of bacteremia associated with the B. fragilis group was examined in a matched case-control study [99]. Patients with B. fragilis group bacteremia were matched to control patients without bacteremia but with the same principal diagnosis or the same major surgical procedure. Patients with B. fragilis group bacteremia had a significantly higher mortality rate compared with control patients (28 compared with 9 percent) and an attributable mortality rate of 19 percent (95% CI 8 to 30 percent).
SUMMARY AND RECOMMENDATIONS
●Antimicrobial selection – Antimicrobial agents are usually chosen empirically for the treatment of anaerobic infections without the benefit of in vitro susceptibility tests. This is due to inadequate anaerobic culture techniques, poor quality control of in vitro susceptibility results, and difficulty in obtaining test results within a useful time frame. (See 'Antimicrobial selection' above.)
●Antimicrobial resistance – Antibiotic resistance of the Bacteroides fragilis group is an increasing problem. (See 'Antimicrobial resistance' above.)
●Sites of infection – Anaerobes have been encountered in infections at virtually all anatomic sites, although the frequency of recovery is highly variable and the bacteriologic patterns depend largely upon the flora at adjacent mucocutaneous sites (table 1).
•Central nervous system – Pyogenic intracranial infections that commonly involve anaerobic bacteria include cerebral and epidural abscess and subdural empyema. (See 'Central nervous system infections' above.)
•Upper airways – Anaerobic bacteria are involved in a variety of infections of the oral cavity and adjacent structures. Organisms isolated in oral infection reflect the contiguous normal oral flora. (See 'Infections of the upper airways' above.)
•Lower respiratory tract and pleura – Anaerobic bacteria are relatively common in pleuropulmonary infections usually arising from aspiration of oral and dental secretions that results in aspiration pneumonitis or lung abscess. (See 'Pleuropulmonary infections' above.)
•Abdomen – Infections within the abdominal cavity are usually polymicrobial and include peritonitis, which may be generalized or localized, and intra-abdominal abscess. (See 'Intra-abdominal infections' above and "Antimicrobial approach to intra-abdominal infections in adults".)
•Female genital tract – Infections of the female genital tract that are not caused by sexually transmitted pathogens are likely to involve anaerobic bacteria. (See 'Infections of the female genital tract' above.)
•Soft tissue – Anaerobic bacteria are common pathogens in skin and soft tissue infections including abscesses, necrotizing fasciitis, and decubitus or diabetic foot ulcers. Most involve the cutaneous flora, especially Peptostreptococcus, or the flora of adjacent mucosal surfaces. (See 'Soft tissue infections' above.)
●Management – The management of anaerobic infections involving other sites is discussed separately. (See "Treatment and prognosis of bacterial brain abscess" and "Complications, diagnosis, and treatment of odontogenic infections" and "Deep neck space infections in adults" and "Ludwig angina" and "Aspiration pneumonia in adults" and "Lung abscess in adults" and "Management and complications of tubo-ovarian abscess" and "Postpartum endometritis" and "Clostridial myonecrosis" and "Necrotizing soft tissue infections".)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge John G Bartlett, MD, who contributed to an earlier version of this topic review.
