Bacteroides Infection

Updated: Oct 27, 2022
Author: Itzhak Brook, MD, MSc; Chief Editor: Michael Stuart Bronze, MD 



This article describes infections caused by the Bacteroides fragilis[1]  group and other anaerobic gram-negative bacilli (AGNB) that were previously included in the Bacteroides genus but are now included in the Prevotella and Porphyromonas genera. In addition, many new genera and several new species have been created to accommodate pathogens such as Bilophila wadsworthia, Sutterella wadsworthensis,Centipeda periodontii, and Anaerobiospirillum thomasii. Infections due to AGNB are common, yet the specific identification of AGNB in these infections is difficult.

Bacteroides species are anaerobic bacteria that are predominant components of the bacterial florae of mucous membranes[2] and are therefore a common cause of endogenous infections.[1]  Bacteroides infections can develop in all body sites, including the CNS, the head, the neck, the chest, the abdomen, the pelvis, the skin, and the soft tissues. Inadequate therapy against these anaerobic bacteria may lead to clinical failure.

Because of their fastidiousness, they are difficult to isolate and often are overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.[3] Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,[4] and the polymicrobial synergistic nature of the infection.[5]

Bacteroides spp. possess virulence factors or special characteristics to compete successfully for microbial niches, including pili and fimbriae and adhesins (which enhance adherence), hemagglutination, enzymes (collagenase, phospholipase A, hemolysin, peroxidase, protease, fibrolysin, heparinase, neuraminase, superoxide dismutase), toxins, and lipopolysaccharide endotoxin, and capsular polysaccharide (which enhance invasion and evasion from host phagocytosis).[1, 6]

Bacteroides spp possess important immunomodulatory effects and the body’s energy balance. B fragilis’ polysaccharide A enhances homeostatic immune function both in the gut and systemically and balances T-cell subset population size and function.[1, 6]

The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides ovatus, Bacteroides thetaiotaomicron,Parabacteroides distasonis (previously Bacteroides distasonis),[7] and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae[2] and predominate in intra-abdominal infections and infections that originate from those florae (eg, perirectal abscesses, decubitus ulcers). Enterotoxigenic B fragilis (ETBF) is also a potential cause of diarrhea.[8]

Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which were previously called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris) are part of the normal oral and vaginal florae and are the predominant AGNB isolated from respiratory tract infections and their complications, including aspiration pneumonia, lung abscess, chronic otitis media, chronic sinusitis, abscesses around the oral cavity, human bites, paronychia, brain abscesses, and osteomyelitis. Prevotella bivia and Prevotella disiens (previously called Bacteroides) are important in obstetric and gynecologic infections.


Although AGNB perform beneficial functions as part of the GI flora, they are also consummate opportunistic pathogens that can cause serious infections, typically in synergistic infections in combination with other anaerobic as well as aerobic bacteria. Most infections due to AGNB originate from the endogenous mucosal membrane florae. Knowledge of the common mode of distribution allows for a logical choice of antimicrobial therapy for infections in these sites.

AGNB infections are generally polymicrobial. The number of isolates can reach 5-10 organisms. The type of copathogens depends on the infection site and the circumstances of the infection. Antimicrobial therapy should be directed at all major aerobic and anaerobic pathogens. AGNB promote infection through synergy with their aerobic and anaerobic counterparts and with each other.

An indirect pathogenic role of AGNB is their ability to produce the enzyme beta-lactamase, which allows them to protect themselves and other penicillin-susceptible organisms from the activity of penicillins.



United States

The exact frequency of AGNB infection is difficult to calculate because of inappropriate methods of collection, transportation, and cultivation of specimens. AGNB are more commonly found in chronic infections. The rate of recovery of anaerobic bacteria in blood cultures is 5-15% and is higher among immunocompromised patients and those who have predisposing conditions.


The frequency of these infections appears to be higher in developing countries, where therapy is often inadequate or delayed. However, because of difficulties in isolation of these and other anaerobic bacteria, their role is underestimated.


Mortality has decreased over the past 4 decades because of early recognition, medical and surgical intervention, and the initiation of proper prophylactic and therapeutic antimicrobial therapies.


AGNB infections can occur in patients of all ages; however, the frequency of upper respiratory tract and head and neck infections is higher in children than in adults.




AGNB infections occur more often in chronic infections and in association with the predisposing conditions discussed below. However, they can also cause acute infections (ie, maxillary sinusitis associated with dental infections, intra-abdominal infections following perforation).[1, 9, 10]

CNS infections

AGNB can cause various intracranial infections, including brain abscess, subdural empyema, epidural abscess, and meningitis (usually from contiguous spread from adjacent foci of infection). Brain abscesses are commonly caused by adjacent chronic infections in the ears, the mastoids, the sinuses, the oropharynx, the teeth, or the lungs.

Hematogenous spread can occur after dental, oropharyngeal, pulmonary, or intra-abdominal infection. Rarely, bacteremia of another origin or endocarditis leads to such infection.[1, 11]

Head and neck infections

Anaerobes, including AGNB, are recovered from various infections, especially in their chronic form. Dental infections associated with various oral anaerobic bacteria, such as AGNB, include periodontal disease, gingivitis, pulpitis, acute necrotizing ulcerative gingivitis, localized juvenile periodontitis, adult periodontitis, pericoronitis, endodontitis, periapical and dental abscesses, and postextraction infection.

Head and neck infections include chronic otitis media[12] ; sinusitis[13] ; mastoiditis; tonsillar,[13] peritonsillar, and retropharyngeal abscesses; cervical lymphadenitis; all deep neck space infections; thyroiditis; odontogenic infections; and postsurgical and nonsurgical head and neck wounds and abscesses.[1, 14]

Deep neck space infections

These generally occur as a result of dental infections, and less often from pharyngeal or tonsillar infections. Ludwig angina and Lemierre syndrome are life-threatening deep neck infections.

Sinusitis is complicated by anaerobes, including AGNB, when it becomes chronic and oxygen levels decline. Anaerobes are isolated from 10% of patients with acute maxillary sinusitis (mostly secondary to odontogenic infection), but they are found in as many as 67% of chronic infections of the maxillary, ethmoid, frontal, and sphenoid sinuses.[15, 13] The infection may spread via anastomosing veins or contiguously to the CNS. Complications include orbital cellulitis, meningitis, cavernous sinus thrombosis, and epidural and subdural brain abscesses.

Tonsillitis, whether acute or chronic, may have AGNB involvement.[13, 16]  AGNB can also be involved with tonsillitis complications, including internal jugular vein thrombophlebitis, which often causes postanginal sepsis. Prevotella species and other anaerobes are recovered from tonsillar or retropharyngeal abscesses without any aerobic bacteria, and they are isolated in cases of Vincent angina.

Pleuropulmonary infections

Aspiration of oropharyngeal or gastric secretions and periodontal or gingival disease are risk factors for anaerobic pleuropulmonary infection due to AGNB and to other anaerobes. Aspiration may be a result of altered consciousness, dysphagia, or mechanical devices such as intubation equipment. Poor oral hygiene is associated with an increased anaerobic bacterial burden, and the presence of aerobes or necrotic tissue lowers pH, which, in turn, facilitates the growth of anaerobes. The infection can progress from pneumonitis to necrotizing pneumonia and lung abscess, with or without empyema.[17]

Anaerobes are involved in 90% of patients with community-acquired aspiration pneumonia and in about one third of patients with nosocomial aspiration pneumonia, empyema, lung abscess, and pneumonia associated with tracheostomy.

Intra-abdominal infections[18]

Anaerobes outnumber aerobes by 1000:1 in the large intestine; thus, they play an important role in almost all intra-abdominal infections.

Secondary peritonitis and abdominal abscesses generally occur after entry of enteric organisms into the peritoneal cavity through perforation of the intestine or other viscus as a result of obstruction, infarction, or trauma.

The more distal the perforation, the more numerous the types and number of organisms that gain access into the peritoneal cavity (ie, perforations in the descending colon are associated with spillage of more organisms than perforations in proximal parts of the colon).

Most visceral abscesses (eg, hepatic), chronic cholecystitis, perforated and gangrenous appendicitis, postoperative wound infections and abscesses, diverticulitis, and any infection associated with fecal contamination of the abdominal cavity involve both aerobes and anaerobes. Hepatic abscess was reported also in conjunction with COVID 19 infection.[19]

Enterotoxigenic B fragilis are considered an emerging enteropathogen-causing diarrhea.

Female genital tract infection

Various obstetric-gynecologic diseases involve anaerobes, including AGNB. These infections include bacterial vaginosis; soft tissue perineal, vulvar, and Bartholin gland abscesses; endometritis; pyometra; salpingitis; tubo-ovarian abscesses; adnexal abscess; pelvic inflammatory disease, which may include pelvic cellulitis and abscess; amnionitis; septic pelvic thrombophlebitis; vaginal cuff cellulitis; intrauterine device–associated infection; septic abortion; and postsurgical obstetric and gynecologic infections.[20]

Skin and soft tissue infections

Infections involving AGNB include superficial infections, such as infected cutaneous ulcers, cellulitis, secondary diaper rash, gastrostomy or tracheostomy site wounds, infected subcutaneous sebaceous or inclusion cysts, eczema, scabies or kerion infections, paronychia, hidradenitis suppurativa, and pyoderma.[21]

Subcutaneous tissue infections and postsurgical wound infections that may also involve the skin include cutaneous and subcutaneous abscesses, decubitus ulcers, infected diabetic (vascular or trophic) ulcers, breast abscesses, bite wounds,[22] anaerobic cellulitis and gas gangrene, bacterial synergistic gangrene, infected pilonidal cyst or sinus, Meleney ulcer, and burn wound infection.

Deeper anaerobic soft tissue infections include necrotizing fasciitis, necrotizing synergistic cellulitis, gas gangrene, and crepitus cellulitis. These infections can involve the fascia alone or also the muscle surrounded by the fascia, inducing myositis and myonecrosis.

Anaerobic infections, such as decubitus ulcers or diabetic foot ulcers, generally are polymicrobial and often are complicated by osteomyelitis or bacteremia.

Deep tissue infections, such as necrotizing cellulitis, fasciitis, and myositis, often involve clostridial organisms and Staphylococcus pyogenes. They may be polymicrobic; may contain gas and gray, thin, putrid pus; and are associated with bacteremia and mortality.[23]

Osteomyelitis and septic arthritis

Anaerobes are notable in oesteomyelitis of the long bones after trauma and fracture, osteomyelitis related to peripheral vascular disease, and decubitus ulcers and osteomyelitis of cranial and facial bones. Most of these infections are polymicrobial.[24]

Cranial and facial bone osteomyelitis generally is caused by spread from a contiguous soft-tissue source or from sinus, ear, or dental infection. Intestinal anaerobes originating from decubitus ulcers are involved in pelvic osteomyelitis. Osteomyelitis of long bones and septic arthritis are generally caused by hematogenous spread, trauma, or the presence of a prosthetic device.

Septic arthritis caused by anaerobic bacteria is uncommon and often is associated with hematogenous and contiguous spread of infection, trauma, and prosthetic joints. Most cases of septic arthritis caused by anaerobes are monomicrobial.


The prevalence of anaerobes, including AGNB, in bacteremia was once 5-15%. However, rates declined to 2-6% in the 1990s. Increased awareness of the importance of anaerobes and enhanced recognition of the types of clinical infection caused by these organisms, along with appropriate prophylaxis and treatment, have been proposed as explanations for the decreased incidence of anaerobic bacteremia from 1974–1988.[25] However, recent studies have reported a resurgence in anaerobic bacteremia. A study from the Mayo Clinic (Rochester, MN) has reported that the mean incidence of anaerobic bacteremia increased from 53 cases per year during 1993–1996 to 75 cases per year during 1997–2000 to 91 cases per year during 2001–2004 (an overall increase of 74%).[26]

The authors concluded that the sources of anaerobic bacteremia are now more varied than they once were, especially among immunosuppressed individuals and persons with complex underlying disease.

A study from Switzerland reported a decrease in the percentage of blood cultures yielding anaerobes over time; in 1997, 166 (1.8 %) of blood cultures grew anaerobes, compared with 70 (0.5 %) in 2006.[27]

Which organisms are involved depends on their portal of entry and the underlying disease. The common isolates are the B fragilis group (60-75% of isolates).[28]

Pigmented Prevotella, Porphyromonas, and Fusobacterium are associated with the oropharynx and a pulmonary source.

Fusobacterium species involve the female genital tract.

Propionibacterium acnes is associated with a foreign body.

Peptostreptococcus species are associated with all sources but especially with oropharyngeal, pulmonary, and female genital tract sources.

Predisposing factors include neoplasms; hematologic disorders; organ transplant; intestinal obstruction; decubitus ulcers; dental extraction; diabetes mellitus; postsplenectomy; use of cytotoxic agents or corticosteroids; total-body irradiation; and recent GI, obstetric, or gynecologic surgery.

Features typical of anaerobic bacteremia include metastatic lesions, hyperbilirubinemia, and suppurative thrombophlebitis.

The risk of mortality is 15-30% and improves with early appropriate antimicrobial therapy and resolution of the primary infection.[29]


Conditions that predispose to AGNB and other anaerobic infections include the exposure of sterile sites to a high inoculum of indigenous mucous membrane florae; use of antibiotics that are ineffective against AGNB; reduced blood supply; and tissue necrosis, which lowers the oxidation-reduction potential and favors the growth of anaerobes. Conditions that lower the blood supply include trauma, foreign body, malignancy, surgery, edema, shock, colitis, and vascular disease.[1, 9, 10]

Infection with aerobic bacteria can make the local tissue conditions more favorable for the growth of anaerobes. The host defenses can become impaired by anaerobic conditions and anaerobic bacteria.

Anaerobic infection often manifests as suppuration, thrombophlebitis, abscess formation, and gangrenous destruction of tissue associated with gas.

Anaerobes, including AGNB, are common in chronic infections. Therapy with antimicrobials, such as aminoglycosides, trimethoprim-sulfamethoxazole, and older quinolones, frequently fails to eradicate anaerobes.

Certain infections that often involve anaerobes include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia, lung abscesses, amnionitis, endometritis, septic abortions, pelvic inflammatory disease, tubo-ovarian abscess, peritonitis following viscus perforation, abscesses in and around the oral and rectal areas, and pus-forming necrotizing infections of soft tissue or muscle.[9, 10]

Some tumors, such as colonic, uterine, and bronchogenic carcinomas and necrotic tumors of the head and the neck, can become infected with anaerobes.



Laboratory Studies

Collection of specimens of anaerobic bacteria is important because documentation of an anaerobic infection is through culture of organisms from the infected site. Appropriate documentation of anaerobic infection requires proper collection of appropriate specimens, expeditious transportation, and careful laboratory processing.[1]

Specimens must be obtained free of contamination. Inadequate techniques or media can lead to missing the presence of anaerobic bacteria or the assumption that only aerobic organisms are present in a mixed infection.

Because anaerobes are present on skin and mucous membranes, even minimal contamination with normal florae can be misleading.

Unacceptable or inappropriate specimens can yield normal florae and, therefore, have no or little diagnostic value.

Appropriate materials should be obtained by using techniques that bypass the normal florae.

Direct-needle aspiration is the best method of obtaining a culture; the use of swabs is much less desirable.

Specimens obtained from normally sterile sites, such as blood or spinal, joint, or peritoneal fluids, are collected after thorough skin decontamination. Two approaches are used to culture the maxillary sinus by aspiration following sterilization of the canine fossa or the nasal vestibule, via either the canine fossa or the inferior meatus. Urine is collected by percutaneous suprapubic bladder aspiration.

Other specimens can be collected from abscess contents, from deep aspirates of wounds, and via special techniques, such as transtracheal aspirates or direct lung puncture.

Specimens of the lower respiratory tract are difficult to obtain without contamination with indigenous florae. Double-lumen catheter bronchial brushing and bronchoalveolar lavage, cultured quantitatively, can be useful.

Culdocentesis fluid obtained after decontamination of the vagina is acceptable.

Transportation of specimens should be prompt unless transport devices are available. Transport devices generally contain oxygen-free environments provided by a mixture of carbon dioxide, hydrogen, and nitrogen, plus an aerobic condition indicator. Specimens should be placed into an anaerobic transporter as soon as possible.

Liquid or tissue specimens are always preferred to swabs. Liquid specimens are inoculated into an anaerobic transport vial or a syringe and a needle. All air bubbles are expelled from the syringe. Insertion of the needle tip into a sterile rubber stopper is no longer recommended. Because air gradually diffuses through the plastic syringe wall, specimens should be processed in less than 30 minutes.

Swabs are placed in sterilized tubes that contain carbon dioxide or prereduced anaerobically sterile Carey and Blair semisolid media.

Tissue specimens can be transported in an anaerobic jar or in a sealed plastic bag rendered anaerobic.

Gram stain of a smear of the specimen provides important preliminary information regarding the types of organisms present, helps determine appropriate initial therapy, and serves as a quality control.

Cultures should be immediately placed under anaerobic conditions and should be incubated for 48 hours or longer. An additional 36-48 hours is generally required for species- or genus-level identification by using biochemical tests. Kits that contain these tests are commercially available.[3]

A rapid enzymatic test enables identification after only 4 hours of aerobic incubation.

Gas-liquid chromatography of metabolites is often used.

Nucleic acid probers and polymerase chain reaction methods are also being developed for rapid identification.[30]

Detailed procedures of laboratory methods can be found in microbiology manuals.[3]

Antimicrobial susceptibility testing of AGNB has become less predictable because their resistance to several antimicrobials has increased.[31] Screening of AGNB isolates for beta-lactamase activity may be helpful.[16, 32] However, occasional strains may resist beta-lactam antibiotics through other mechanisms.

Routine susceptibility testing is time-consuming and often unnecessary. Poor quality control of in-vitro susceptibility testing and the difficulty to obtain results in a reasonable time make testing less useful. However, testing the susceptibility of isolates recovered from sterile body sites and/or those that are clinically important (ie, blood cultures, bone, CNS, serious infections) and have variable susceptibilities, especially those isolated in pure culture from properly collected specimens, is important.[4] Antimicrobial testing is recommended, however, to monitor local hospital and geographic susceptibility profiles and to determine the activity of new antimicrobials.

Antibiotics that should be tested include penicillin, a broad-spectrum penicillin, a penicillin plus a beta-lactamase inhibitor, clindamycin, chloramphenicol, a second-generation cephalosporin (eg, cefoxitin), tigecycline, newer quinolones (eg, moxifloxacin), chloramphenicol, metronidazole, and a carbapenem. The recommended methods include agar microbroth and macrobroth dilution. Newer methods include the E-test and the spiral gradient end point system.

Imaging Studies

Radiologic or imaging studies and scans (ie, computed tomography and magnetic resonance imaging) are helpful. Abscesses are a common complication of Bacteroides infections. The presence of gas in the infected site is highly suggestive of anaerobic infection.[1]



Medical Care

The patient's recovery from anaerobic infection depends on prompt and proper management according to the following 3 principles:

  • Toxins produced by anaerobes must be neutralized.

  • The environment must be changed to prevent local bacterial proliferation.

  • The spread of bacteria must be limited.

The environment is controlled by debriding necrotic tissue, draining pus, improving circulation, alleviating obstruction, and increasing tissue oxygenation.

Certain types of adjunctive therapy, such as hyperbaric oxygen therapy, may be useful but remain unproven.

In many cases, antimicrobial therapy is the only form of therapy required, but it can also be used as an adjunct to a surgical approach.

Because anaerobic bacteria are generally recovered mixed with aerobic organisms, the appropriate choice for antimicrobial agents should provide adequate treatment of both groups of pathogens.

When choosing antimicrobials for the treatment of mixed infections, consider their aerobic and anaerobic antibacterial spectrum and their availability in oral or parenteral form.

Some antimicrobials have a limited range of activity. For example, metronidazole is active only against anaerobes and cannot be administered as a single agent in mixed infections. Others, such as imipenem, have wide spectra of activity against aerobes and anaerobes.

Because culture results are often not available, many patients are treated empirically.[1, 6]

Antimicrobial resistance patterns may vary.[33, 34] Some anaerobes have become, or may become, resistant to antimicrobials. Resistance rates vary among different geographic regions and institutions, and some antibiotic regimens that were used in the past are no longer considered adequate for empiric therapy. The major increase in antimicrobial resistance for AGNB is of clindamycin, cefoxitin, and cefotetan. The B fragilis group is almost uniformly susceptible to metronidazole, carbapenems, chloramphenicol, and combinations of a penicillin and beta-lactamase inhibitors. Resistance to other agents varies.

Multidrug antimicrobial resistance (MDR) in anaerobes including AGNB is increasing.[1, 35]  Bacteroides fragilis group isolates have numerous resistance determinants such as multidrug efflux pumps and cfiA and nimB genes and activating insertion sequences; some isolates exhibited extensive drug-resistant patterns. MDR rates in B fragilis group were from 1.5 to >18% and up to >71% in cfiA and nimB positive isolates carrying insertion sequences. MDR was found in Prevotella spp. (in ≤10% of isolates), and Finegoldia magna.[35]

Recent reports of multidrug-resistant B fragilis[36, 37] underscore the need for improved antibiotic stewardship. Although B fragilis has long been considered reliably susceptible to a number of broad-spectrum antianaerobic drugs,[4] these cases suggest clinicians should no longer rely on cumulative susceptibility data from surveys alone to direct treatment and should consider requesting susceptibility testing when treating serious infections caused by B fragilis.

Aside from susceptibility patterns, other factors that influence the choice of antimicrobials include their pharmacokinetics, their toxicity, their effect on the normal florae, their bactericidal activity, and their ability to penetrate into sites of infection.

Although identification of organisms and their susceptibility is needed for optimal therapy, the clinical setting and the Gram stain results from the specimen are often helpful.

Antimicrobials useful in anaerobic infection are as follows[31] :


Penicillin G is still the drug of choice against most non–beta-lactamase–producing AGNB. However, in addition to the B fragilis group, which is resistant to penicillin, other AGNB show increased resistance. These include pigmented Prevotella and Porphyromonas species, P bivia, P disiens, Bilophila wadsworthia, and Bacteroides splanchnicus.

The combination of beta-lactamase inhibitors (eg, clavulanic acid, sulbactam, tazobactam) with a beta-lactam antibiotic (eg, ampicillin, amoxicillin, ticarcillin, piperacillin) can overcome these beta-lactamase–producing AGNB.

In high concentrations, ticarcillin, piperacillin, and mezlocillin have good activity against gram-negative enteric bacilli and most anaerobes; however, they are not completely resistant to beta-lactamase.

Anaerobes manifest 3 major mechanisms of resistance to beta-lactam antibiotics: inactivating enzymes, mainly beta-lactamases, which include penicillinases and cephalosporinases; low-affinity penicillin-binding proteins (PBPs); and decreased permeability through alterations in the porin channel.[4]


The B fragilis group, Prevotella species, and Porphyromonas species are resistant to first-generation cephalosporins by virtue of cephalosporinase production.[38]

Cefoxitin is the most effective cephalosporin against the B fragilis group, although 5-15% may be resistant. Cefoxitin is inactive against most clostridial organisms, except Clostridium perfringens. Other second-generation cephalosporins, such as cefotetan and cefmetazole, have a longer half-life than cefoxitin and are as effective as cefoxitin against B fragilis; however, they are less efficacious against other members of the B fragilis group.


These agents, including imipenem, meropenem, doripenem, and ertapenem have excellent activity against a broad spectrum of aerobic and anaerobic bacteria. Two recent reports have noted the development of some carbapenem resistance among anaerobes,[31, 39]  ranging from 1.1 to 2.5% in a multicenter US survey, but with a higher rate for a small number of isolates from Taiwan.[40]


This agent shows excellent in vitro activity against most anaerobic bacteria, and resistance is rare; however, the development of less-toxic newer agents has limited their use. The drug has a somewhat unique property of lipid solubility to permit penetration across lipid barriers and achieves high concentrations in the CNS, even in the absence of inflammation.

Macrolides (erythromycin, azithromycin, and clarithromycin)

The macrolides have moderate-to-good in vitro activity against anaerobic bacteria other than the B fragilis group strains and fusobacteria.[4] Macrolides are active against pigmented Prevotella and Porphyromonas species and microaerophilic streptococci, gram-positive non–spore-forming anaerobic bacilli, and certain clostridia. They are less effective against Fusobacterium and Peptostreptococcus species.[41] They show relatively good activity against Clostridium perfringens and poor or inconsistent activity against AGNB. The emergence of erythromycin-resistant organisms during therapy has been documented and reached up to 50% in recent studies.[42, 43]


This antimicrobial is effective against aerobic gram-positive cocci. Although the patterns differ by region, B fragilis resistance to clindamycin is increasing worldwide. Resistance of the B fragilis group in some centers in the United States and Europe recently reached about 40%.[44] Up to 10% resistance was noted for Prevotella,Fusobacterium, Porphyromonas, and Peptostreptococcus species, with higher rates for some Clostridium species (especially C difficile).[45] This agent therefore can not be used as empiric therapy. Antibiotic-associated colitis due to C difficile, although associated with most antimicrobials, was first described following clindamycin therapy.


This has excellent activity against anaerobes, including AGNB; however, this efficacy is limited to anaerobes. Microaerophilic streptococci, P acnes, and Actinomyces species are often resistant; therefore; adding an antimicrobial that is effective against these organisms (eg, penicillin) often is necessary. Only 9 strains of the B fragilis group were ever reported to be clinically resistant and associated with therapeutic failure.[4, 46] Aerobic and facultative anaerobes, such as coliforms, are usually highly resistant.


Tetracycline, once the drug of choice for anaerobic infections, is presently of limited usefulness because of the development of resistance to it by virtually all types of anaerobes, including Bacteroides and Prevotella species. Resistance to P acnes has been related to previous use.[47] Only about 45% of all B fragilis strains are susceptible to this drug.[4] The newer tetracycline analogs doxycycline and minocycline are more active than the parent compound.

Because of the significant resistance to these drugs, they are useful only when susceptibility tests can be performed or in less severe infections in which a therapeutic trial is feasible. Doxycycline is effective against chlamydial and mycoplasmal infections and is added to most regimens when treating pelvic infections. The use of tetracycline is not recommended in patients younger than 8 years because of the adverse effect on teeth.


This glycylcycline has effective in vitro activity against both gram-positive and gram-negative anaerobes, as well as against gram-positive aerobic strains such as methicillin-resistant staphylococci, streptococci, and enterococci. Resistance of members of the B fragilis group varied from 3.3% to 7.2%.[31] Tigecycline was approved by the FDA for the treatment of complicated skin and skin-structure infections and complicated intra-abdominal infections.


Trovafloxacin, moxifloxacin, and gatifloxacin yield low minimum inhibitory concentrations (MICs) against most groups of anaerobes. Moxifloxacin was approved by the FDA for the treatment of complicated skin and skin-structure infections and complicated intra-abdominal infections. However, up to 50% of Bacteroides isolates are resistant to moxifloxacin.[48, 49] The use of the quinolones is restricted in growing children and pregnancy because of their possible adverse effects on the cartilage.

Surgical Care

In most cases, surgical therapy is of critical importance. Surgical therapy includes draining abscesses, debriding necrotic tissues, decompressing closed-space infections, and relieving obstructions.[1, 18]

When surgical drainage is not used, the infection may persist and serious complications may develop.



Medication Summary

Clinical judgment, personal experience, safety, and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents.[1] When choosing antimicrobials for the therapy of mixed infections, their aerobic and anaerobic antibacterial spectrum and their availability in oral or parenteral form should be considered. Some antimicrobials have a limited range of activity. For example, metronidazole is active only against anaerobes and therefore cannot be administered as a single agent for the therapy of mixed infections. Others (ie, carbapenems and the combination of penicillin and a beta-lactamase inhibitor) have wide spectra of activity against aerobes and anaerobes.

Aside from susceptibility patterns, other factors that influence the choice of antimicrobial therapy include the pharmacologic characteristics of the various drugs, their toxicity, their effect on the normal florae, and their bactericidal activity. Although identification of the infecting organisms and their antimicrobial susceptibility may be needed for selection of optimal therapy, the clinical setting and Gram-stain preparation of the specimen may indicate the types of anaerobes present in the infection and the nature of the infectious process.[1]

Although the duration of therapy for anaerobic infections is generally longer than for aerobes and facultative infections, the duration of treatment must be individualized, depending on the response. In some cases, treatment may require 6-8 weeks, but therapy may be shortened with proper surgical drainage. An anti–gram-negative enteric agent is generally added to treat Enterobacteriaceae when treating intra-abdominal infections.

The available parenteral antimicrobials for most infections include metronidazole, a penicillin (ie, ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (ie, clavulanic acid, sulbactam, tazobactam), tigecycline (approved only for intra-abdominal and skin and soft tissue infections), and the carbapenems (eg, imipenem, meropenem, doripenem, ertapenem).

An agent effective against gram-negative enteric bacilli (ie, aminoglycoside) or an antipseudomonal cephalosporin (ie, cefepime) is generally added to clindamycin, metronidazole, and, occasionally, cefoxitin when treating intra-abdominal infections to provide coverage for these bacteria.

Penicillin can be added to metronidazole in the therapy of intracranial, pulmonary, or dental infections to cover microaerophilic streptococci and Actinomyces species.

A macrolide (ie, erythromycin) is added to metronidazole for upper respiratory tract infections to treat Staphylococcus aureus and aerobic streptococci.

Penicillin is added to clindamycin to supplement its coverage against Peptostreptococcus species and other gram-positive anaerobic organisms.

Penicillin is still the drug of choice for bacteremia caused by non–beta-lactamase producers. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producers.

For Chlamydia and Mycoplasma species, doxycycline is added to most regimens when treating pelvic infections.

Oral therapy is often substituted for parenteral therapy. The agents available for oral therapy include clindamycin, amoxicillin and clavulanate, and metronidazole.

Antibiotics, Other

Class Summary

Empiric antimicrobial therapy must cover all likely pathogens in the context of this clinical setting.

Penicillin G (Pfizerpen)

Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms (beta-lactam).

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond.


Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Dosage and route of administration depend on condition of patient, severity of infection, and susceptibility of causative organism.

Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.

Amoxicillin and clavulanate (Augmentin)

Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. Addition of clavulanate inhibits beta-lactamase–producing bacteria.

Good alternative antibiotic for patients allergic to or intolerant to macrolides. Usually is well tolerated and provides good coverage for most infectious agents. Not effective against Mycoplasma and Legionella species. Half-life of oral dosage form is 1-1.3 h. Has good tissue penetration but does not enter cerebrospinal fluid.

For children >3 mo, base dosing protocol on amoxicillin content. Because of different ratios of amoxicillin to clavulanic acid in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.

Ticarcillin and clavulanate potassium (Timentin)

Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes. Contains 4.7-5.0 mEq of Na+/g.


Binds to 50S bacterial ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Imipenem and cilastatin (Primaxin)

Carbapenem used for treatment of multiple organism infections in which other agents do not have wide-spectrum therapeutic activity or are contraindicated because of potential toxicity.

Meropenem (Merrem)

Broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis and has bactericidal activity. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared with imipenem. Also less likely to cause seizures compared with imipenem.

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for C difficile enterocolitis).

Ertapenem (Invanz)

Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.

Moxifloxacin (Avelox)

Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.

Tigecycline (Tygacil)

A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit and blocks entry of amino-acyl tRNA molecules in ribosome A site. Indicated for complicated skin and skin structure infections caused by E coli, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible and -resistant isolates), S agalactiae, S anginosus group (includes S anginosus, S intermedius, and S constellatus), S pyogenes, and B fragilis.




In areas where AGNB and other anaerobes predominate, early and aggressive treatment of acute infection can prevent them from becoming chronic.[1]

When the risk of anaerobic infections (eg, intra-abdominal and wound infection following surgery) is high, proper antimicrobial prophylaxis may reduce the risk.

Preventing oral florae aspiration by improving neurologic status, suctioning oral secretions, improving oral hygiene, and maintaining lower stomach pH can reduce the risk of aspiration pneumonia and its complications.

Irrigation and debridement of wounds and necrotic tissue, drainage of pus, and improvement of the blood supply help prevent skin and soft tissue infections.

Patient Education

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center and Ear, Nose, and Throat Center. Also, see eMedicineHealth's patient education articles Human Bites and Tonsillitis.


Questions & Answers


What is Bacteroides (AGNB) infection?

What is the pathophysiology of Bacteroides (AGNB) infection?

What is the prevalence of Bacteroides (AGNB) infection in the US?

What is the global prevalence of Bacteroides (AGNB) infection?

Which factors have reduced the mortality of Bacteroides (AGNB) infection?

Which age groups have the highest prevalence of Bacteroides (AGNB) infection?


Which clinical history findings are characteristic of Bacteroides (AGNB) infection?

What are the signs and symptoms of CNS Bacteroides (AGNB) infection?

What are the signs and symptoms of head and neck Bacteroides (AGNB) infection?

What are the signs and symptoms of deep neck space Bacteroides (AGNB) infection?

What are the signs and symptoms of pleuropulmonary Bacteroides (AGNB) infection?

What are the signs and symptoms of intra-abdominal Bacteroides (AGNB) infection?

What are the signs and symptoms of female genital tract Bacteroides (AGNB) infection?

What are the signs and symptoms of skin and soft tissue Bacteroides (AGNB) infection?

Which clinical history findings are characteristic of osteomyelitis and septic arthritis due to Bacteroides (AGNB) infection?

Which clinical history findings suggest bacteremia due to Bacteroides (AGNB) infection?

What causes Bacteroides (AGNB) infection?


What is the role of lab testing in the workup of Bacteroides (AGNB) infection?

What is the role of antimicrobial susceptibility testing in the workup of Bacteroides (AGNB) infection?

What is the role of imaging studies in the workup of Bacteroides (AGNB) infection?


Which factors affect the recovery from a Bacteroides (AGNB) infection?

How is a Bacteroides (AGNB) infection treated?

What is the role of penicillin in the treatment of Bacteroides (AGNB) infection?

What is the role of cephalosporins in the treatment of Bacteroides (AGNB) infection?

What is the role of carbapenems in the treatment of Bacteroides (AGNB) infection?

What is the role of chloramphenicol in the treatment of Bacteroides (AGNB) infection?

What is the role of macrolides in the treatment of Bacteroides (AGNB) infection?

What is the role of clindamycin in the treatment of Bacteroides (AGNB) infection?

What is the role of metronidazole in the treatment of Bacteroides (AGNB) infection?

What is the role of tetracyclines in the treatment of Bacteroides (AGNB) infection?

What is the role of tigecycline in the treatment of Bacteroides (AGNB) infection?

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Which medications are used in the treatment of Bacteroides (AGNB) infection?

Which medications in the drug class Antibiotics, Other are used in the treatment of Bacteroides Infection?


How are Bacteroides (AGNB) infections prevented?