AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

This article describes infections caused by the Bacteroides fragilis 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. 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 membranes¹ and are therefore a common cause of endogenous infections. 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 are often overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.² Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,³ and the polymicrobial synergistic nature of the infection.⁴

The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides distasonis, Bacteroides ovatus, Bacteroides thetaiotaomicron, and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae¹ 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.⁵

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.

Pathophysiology

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.

Frequency

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. Their rate of recovery in blood cultures is 2-5% and higher with patients who have predisposing conditions.

International

The frequency of these infections appears to be higher in developing countries, where therapy is often inadequate or delayed.

Mortality/Morbidity

The mortality rate has decreased over the past 3 decades because of early recognition and initiation of proper prophylactic and therapeutic antimicrobial therapies.

Age

AGNB infections can occur in patients of all ages; however, the frequency of head and neck infections is higher in pediatric patients than in other patients.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

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).^{6, 7}

• 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 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.⁸
• Head and neck infections: Anaerobes, including AGNB, are recovered from various infections, especially in their chronic form. Head and neck infections include chronic otitis media⁹; sinusitis¹⁰; mastoiditis; tonsillar,¹⁰ peritonsillar, and retropharyngeal abscesses; cervical lymphadenitis; all deep neck space infections; thyroiditis; odontogenic infections; and postsurgical and nonsurgical head and neck wounds and abscesses.¹¹
• • 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.^{12, 10} 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, 10} 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. The infection can progress from pneumonitis to necrotizing pneumonia and lung abscess, with or without empyema.¹⁴
• Intra-abdominal infections¹⁵
• • 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).
  • Enterotoxigenic B fragilis are considered an emerging enteropathogen-causing diarrhea.
• Female genital tract infection: 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; intrauterine device–associated infection; septic abortion; and postsurgical obstetric and gynecologic infections.
• 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.
  • 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,¹⁶ 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, are generally polymicrobial and are often 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.¹⁷
• Osteomyelitis and septic arthritis: Osteomyelitis in the long bones and the cranial and facial bones is frequently polymicrobic and may be associated with anaerobes in patients with peripheral vascular disease and decubitus ulcers.¹⁸
• Bacteremia
• • 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 1974–1988.¹⁹ 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%).²⁰
  • 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.
  • 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).⁸ The B fragilis group and clostridial organisms are associated with a GI source.
  • 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.

Causes

• Conditions that predispose to AGNB 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.^{6, 7}
• 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-sulfamethazine, 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.^{6, 7}
• Some tumors, such as colonic, uterine, and bronchogenic carcinomas and necrotic tumors of the head and the neck, can become infected with anaerobes.

WORKUP

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab 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.
• • 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 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.²
• 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.
• Detailed procedures of laboratory methods can be found in microbiology manuals.²
• Antimicrobial susceptibility testing of AGNB has become less predictable because their resistance to several antimicrobials has increased.²¹ Screening of AGNB isolates for beta-lactamase activity may be helpful.^{13, 22} However, occasional strains may resist beta-lactam antibiotics through other mechanisms.
• Routine susceptibility testing is time-consuming and often unnecessary. 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.³
• • 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, 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 are helpful. The presence of gas in the infected site is highly suggestive of anaerobic infection.

TREATMENT

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.
• • Antimicrobial resistance patterns may vary. Some anaerobes have become, or may become, resistant to antimicrobials.
  • 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.
• 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:²³
• • Penicillins
  • • 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, carbenicillin, ticarcillin, piperacillin, and mezlocillin have good activity against gram-negative enterics and most anaerobes; however, they are not completely resistant to beta-lactamase.
  • Cephalosporins
  • • The B fragilis group, Prevotella species, and Porphyromonas species are resistant to first-generation cephalosporins by virtue of cephalosporinase production.
    • 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.
  • Carbapenems: These agents, including imipenem, meropenem, doripenem (recently approved by the FDA for the treatment of complicated intra-abdominal infections), and ertapenem have excellent activity against a broad spectrum of aerobic and anaerobic bacteria.
  • Chloramphenicol: 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.
  • Clindamycin: This antimicrobial is effective against anaerobes and has good activity against aerobic gram-positive cocci. Resistance of the B fragilis group is 5-25%. Antibiotic-associated colitis due to Clostridium difficile, although associated with most antimicrobials, was first described following clindamycin therapy.
  • Metronidazole: 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) is often necessary.
  • Tigecycline: 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. Tigecycline was recently approved by the FDA for the treatment of complicated skin and skin-structure infections and complicated intra-abdominal infections.
  • Quinolones: Trovafloxacin, moxifloxacin, and gatifloxacin yield low minimum inhibitory concentrations (MICs) against most groups of anaerobes. Moxifloxacin was recently approved by the FDA for the treatment of complicated skin and skin-structure infections and complicated intra-abdominal infections. 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.
• When surgical drainage is not used, the infection may persist and serious complications may develop.

MEDICATION

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Clinical judgment, personal experience, safety, and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. 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) 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.

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 clindamycin, metronidazole, chloramphenicol, cefoxitin, a penicillin (ie, ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (ie, clavulanic acid, sulbactam, tazobactam), tigecycline, and the carbapenems (eg, imipenem, meropenem, doripenem, ertapenem).²³

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.

Drug Category: Antimicrobials

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

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Deterrence/Prevention

• In areas where AGNB and other anaerobes predominate, early and aggressive treatment of acute infection can prevent them from becoming chronic.
• 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 eMedicine's Bites and Stings Center and Ear, Nose, and Throat Center. Also, see eMedicine's patient education articles Human Bites and Tonsillitis.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to promptly and properly institute the following 3 principles:
• • Neutralization of toxins produced by anaerobes
  • Prevention of local bacterial proliferation by changing the environment
  • Limitation of bacterial spread

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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2. Jousime-Somers H, Summanen P, Citron DM. Belmont, Calif. Wadsworth-KTL Anaerobic Bacteriology Manual. 6^th ed. Star Publishing; 2002.
3. Wexler HM, Finegold SM. Current susceptibility patterns of anaerobic bacteria. Yonsei Med J. Dec 1998;39(6):495-501. [Medline].
4. Brook I. Enhancement of growth of aerobic and facultative bacteria in mixed infections with Bacteroides species. Infect Immun. Dec 1985;50(3):929-31. [Medline].
5. Durmaz B, Dalgalar M, Durmaz R. Prevalence of enterotoxigenic Bacteroides fragilis in patients with diarrhea: a controlled study. Anaerobe. Dec 2005;11(6):318-21. [Medline].
6. Brook I. Treatment of anaerobic infection. Expert Rev Anti Infect Ther. Dec 2007;5(6):991-1006. [Medline].
7. Finegold SM. Anaerobic Bacteria in Human Disease. Orlando, Fla: Academic Press; 1977.
8. Brook I. Anaerobic bacterial bacteremia: 12-year experience in two military hospitals. J Infect Dis. Dec 1989;160(6):1071-5. [Medline].
9. Brook I. Prevalence of beta-lactamase-producing bacteria in chronic suppurative otitis media. Am J Dis Child. Mar 1985;139(3):280-3. [Medline].
10. Nord CE. The role of anaerobic bacteria in recurrent episodes of sinusitis and tonsillitis. Clin Infect Dis. Jun 1995;20(6):1512-24. [Medline].
11. Brook I. The role of anaerobic bacteria in upper respiratory tract and other head and neck infections. Curr Infect Dis Rep. May 2007;9(3):208-17. [Medline].
12. Brook I, Thompson DH, Frazier EH. Microbiology and management of chronic maxillary sinusitis. Arch Otolaryngol Head Neck Surg. Dec 1994;120(12):1317-20. [Medline].
13. Brook I. The role of beta-lactamase-producing bacteria in the persistence of streptococcal tonsillar infection. Rev Infect Dis. Sep-Oct 1984;6(5):601-7. [Medline].
14. Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect Dis. Jun 1993;16 Suppl 4:S248-55. [Medline].
15. Bohnen JM. Antibiotic therapy for abdominal infection. World J Surg. Feb 1998;22(2):152-7. [Medline].
16. Goldstein EJ. Current concepts on animal bites: bacteriology and therapy. Curr Clin Top Infect Dis. 1999;19:99-111. [Medline].
17. Brook I, Frazier EH. Clinical and microbiological features of necrotizing fasciitis. J Clin Microbiol. Sep 1995;33(9):2382-7. [Medline].
18. Lewis RP, Sutter VL, Finegold SM. Bone infections involving anaerobic bacteria. Medicine (Baltimore). Jul 1978;57(4):279-305. [Medline].
19. Dorsher CW, Rosenblatt JE, Wilson WR, Ilstrup DM. Anaerobic bacteremia: decreasing rate over a 15-year period. Rev Infect Dis. Jul-Aug 1991;13(4):633-6. [Medline].
20. Lassmann B, Gustafson DR, Wood CM, Rosenblatt JE. Reemergence of anaerobic bacteremia. Clin Infect Dis. Apr 1 2007;44(7):895-900. [Medline].
21. Aldridge KE, Ashcraft D, Cambre K, Pierson CL, Jenkins SG, Rosenblatt JE. Multicenter survey of the changing in vitro antimicrobial susceptibilities of clinical isolates of Bacteroides fragilis group, Prevotella, Fusobacterium, Porphyromonas, and Peptostreptococcus species. Antimicrob Agents Chemother. Apr 2001;45(4):1238-43. [Medline].
22. Nakano V, Padilla G, do Valle Marques M, Avila-Campos MJ. Plasmid-related beta-lactamase production in Bacteroides fragilis strains. Res Microbiol. Dec 2004;155(10):843-6. [Medline].
23. Brook I. Treatment of anaerobic infection. Expert Rev Anti Infect Ther. Dec 2007;5(6):991-1006. [Medline].
24. Brook I. Anaerobic Infections. Diagnosis and Management. In: Informa Healthcare USA, Inc. 4th Ed. New York, NY: 2007.

Article Last Updated: Jun 20, 2008