Bacteroides Infection Clinical Presentation

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