Bacteroides Infection: Background, Pathophysiology, Epidemiology (original) (raw)

Background

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 therefore are 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) also is a potential cause of diarrhea. [8]

Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which previously were called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris, Prevotella. bivia) 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.

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Pathophysiology

Although AGNB perform beneficial functions as part of the GI flora, they also are 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 generally are 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.

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Epidemiology

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. 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.

International

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

Mortality/Morbidity

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.

Age

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.

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Author

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, The Society of Federal Health Professionals (AMSUS), Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Jeffrey D Band, MD, FACP, FIDSA Professor of Medicine, Oakland University William Beaumont School of Medicine; Health System Chair, Healthcare Epidemiology and International Medicine, Beaumont Health System; Former Chief of Infectious Diseases, Beaumont Hospital; Clinical Professor of Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.