Sindhu Mohandas, Michael J. Chusid
Anaerobic bacteria are among the most numerous organisms colonizing humans. Anaerobes are present in soil and are normal inhabitants of all living animals, but infections caused by anaerobes are relatively uncommon. Obligate anaerobes are markedly or entirely intolerant of exposure to oxygen. Facultative anaerobes can survive in the presence of environmental oxygen but grow better in settings of reduced oxygen tension. This chapter concentrates on conditions associated with obligate anaerobic bacterial infection.
Infections with anaerobes frequently occur adjacent to mucosal surfaces, often as mixed infections with aerobes. Conditions of reduced oxygen tension provide the optimal conditions for proliferation of anaerobes. Traumatized areas, devascularized areas, and areas of crush injury are all ideal sites for anaerobic infection. Frequently, both aerobic and anaerobic organisms invade devitalized areas, with local extension and bacteremia most often caused by the more virulent aerobes. Abscess formation evolves over days to weeks and generally involves both aerobes and anaerobes. Examples of such infections include appendicitis and periappendiceal, pelvic, perirectal, peritonsillar, retropharyngeal, parapharyngeal, pulmonary, and dental abscesses. Septic thrombophlebitis , as a consequence of appendicitis, chronic sinusitis, pharyngitis, and otitis media, provides a route for hematogenous spread of anaerobic infection to parenchymal organs such as the liver, brain, and lungs.
Anaerobic infection is usually caused by endogenous flora. Combinations of impaired physical barriers to infection, compromised tissue viability, ecologic alterations in normal flora, impaired host immunity, and anaerobic bacterial virulence factors contribute to infection with normal anaerobic inhabitants of mucous membranes. Bacterial virulence factors include capsules, toxins, enzymes, and fatty acids.
Anaerobic infections occur in a variety of sites throughout the body (Table 240.1 ). Anaerobes often coexist synergistically with aerobes. Infections with anaerobes are usually polymicrobial, including an aerobic component.
Table 240.1
Infections Associated With Anaerobic Bacteria
| SITE AND INFECTION | MAJOR RISK FACTORS | ANAEROBIC BACTERIA* |
|---|---|---|
| CENTRAL NERVOUS SYSTEM | ||
| Cerebral abscess |
Cyanotic heart disease Cystic fibrosis Penetrating trauma |
Polymicrobial Prevotella Porphyromonas Bacteroides Fusobacterium Peptostreptococcus |
| Epidural and subdural empyemas, meningitis | Direct extension from contiguous sinusitis, otitis media, mastoiditis, or anatomic defect involving the dura |
Bacteroides fragilis † Fusobacterium Peptostreptococcus Veillonella |
| UPPER RESPIRATORY TRACT | ||
| Dental abscess | Poor periodontal hygiene | Peptostreptococcus |
| Ludwig angina (cellulitis of sublingual-submandibular space) | Drugs producing gingival hypertrophy | Fusobacterium |
| Necrotizing gingivitis (Vincent stomatitis) |
Prevotella melaninogenica Fusobacterium |
|
| Chronic otitis-mastoiditis-sinusitis |
Tympanic perforation Tympanostomy tubes |
Prevotella Bacteroides Fusobacterium Peptostreptococcus |
|
Peritonsillar abscess Retropharyngeal abscess |
Streptococcal pharyngitis Penetrating injury |
Fusobacterium Prevotella Porphyromonas |
| Lemierre syndrome | Preexisting viral or bacterial pharyngitis | Fusobacterium |
| LOWER RESPIRATORY TRACT | ||
| Aspiration pneumonia | Periodontal disease |
Polymicrobial Prevotella Porphyromonas Fusobacterium Peptostreptococcus |
| Necrotizing pneumonitis | Bronchial obstruction | P. melaninogenica |
| Lung abscess |
Altered gag or consciousness Aspirated foreign body Sequestered lobe Vascular anomaly |
Bacteroides intermedius Fusobacterium Peptostreptococcus Eubacterium B. fragilis Veillonella |
| Septic pulmonary emboli | Fusobacterium | |
| INTRAABDOMINAL | ||
| Abscess | Appendicitis |
Polymicrobial B. fragilis Bilophila wadsworthia Peptostreptococcus Clostridium spp. |
| Secondary peritonitis | Penetrating trauma (especially of the colon) |
Bacteroides Clostridium Peptostreptococcus Eubacterium Fusobacterium |
| FEMALE GENITAL TRACT | ||
| Bartholin abscess | Vaginosis | B. fragilis |
| Tuboovarian abscess | Intrauterine device | Bacteroides bivius |
| Endometritis | Peptostreptococcus | |
| Pelvic thrombophlebitis | Clostridium | |
| Salpingitis | Mobiluncus | |
| Chorioamnionitis | Actinomyces | |
| Septic abortion | Clostridium | |
| SKIN AND SOFT TISSUE | ||
| Cellulitis | Decubitus ulcers | Varies with site and contamination with oral or enteric flora |
| Perirectal cellulitis | Abdominal wounds | Clostridium perfringens (myonecrosis) |
| Myonecrosis (gas gangrene) | Pilonidal sinus |
Bacteroides Clostridium |
| Necrotizing fasciitis and synergistic gangrene |
Trauma Human and animal bites Immunosuppressed or neutropenic patients Varicella |
Fusobacterium Clostridium tertium Clostridium septicum Anaerobic streptococci |
| BLOOD | ||
| Bacteremia | Intraabdominal infection, abscesses, myonecrosis, necrotizing fasciitis |
B. fragilis Clostridium Peptostreptococcus Fusobacterium |
* Infections may also be from or may involve aerobic bacteria as the sole agent or as part of a mixed infection; brain abscess may contain microaerophilic streptococci; intraabdominal infections may contain gram-negative enteric organisms and enterococci; and salpingitis may contain Neisseria gonorrhoeae and Chlamydia trachomatis .
† Bacteroides fragilis is usually isolated from infections below the diaphragm except for brain abscesses.
Anaerobes account for approximately 5% of bloodstream bacterial isolates in adults, but this rate is lower in children. The most common blood isolates of anaerobic bacteria in children are Bacteroides fragilis group, Peptostreptococcus , Clostridium, and Fusobacterium spp.
Isolation of anaerobes from the blood is often an indication of a serious primary anaerobic infection. The lower gastrointestinal (GI) tract and wound infections are the 2 most common sources for bacteremia. Risk factors for anaerobic bacteremia include malignancy, hematologic disorders, solid-organ transplant, recent surgery (GI, obstetric, gynecologic), intestinal obstruction, decubiti, dental extraction, early infancy, sickle cell disease, diabetes mellitus, splenectomy, and chemotherapy or other immunosuppressive drug use.
As with certain aerobes, the cell wall of gram-negative anaerobes may contain endotoxins , which can be associated with the development of hypotension and shock when present in the circulatory system. Clostridia produce hemolysins , and the presence of these organisms in the blood can result in massive hemolysis and cardiovascular collapse.
Anaerobic meningitis is rare but can occur in neonates as a complication of ear or neck infections or from anatomic defects of meninges (dural sinus tracts). Anaerobic cerebrospinal fluid (CSF) shunt infections may occur when the distal end of the ventriculoperitoneal shunt perforates the intestinal tract.
Brain abscess and subdural empyema are usually polymicrobial, with anaerobes typically involved (see Chapter 622 ). Brain abscess usually occurs because of spread from infected sinuses, middle ear, or lung and rarely from endocarditis. Clostridium perfringens can cause brain abscess and meningitis after head injuries or after intracranial surgery. Brain abscesses may require surgical drainage combined with a prolonged course of antibiotic therapy.
The respiratory tract is colonized by both aerobes and anaerobes. Anaerobic bacteria are involved in chronic sinusitis, chronic otitis media, peritonsillar infections, parapharyngeal and retropharyngeal abscesses, and periodontal infections. The predominant organisms involved are Prevotella, Porphyromonas, Bacteroides, Fusobacterium, and Peptostreptococcus spp.
Anaerobic periodontal disease is most common in patients with poor dental hygiene or who are receiving drugs that induce gingival hypertrophy. Vincent angina, also known as acute necrotizing ulcerative gingivitis or trench mouth, is an acute, fulminating, mixed anaerobic bacterial-spirochetal infection of the gingival margin and floor of the mouth. It is characterized by gingival pain, foul breath, and pseudomembrane formation. Ludwig angina is an acute, life-threatening cellulitis of dental origin of the sublingual and submandibular spaces. Infection spreads rapidly in the neck and may cause sudden airway obstruction.
Lemierre syndrome, or postanginal sepsis, is a suppurative infection of the lateral pharyngeal space, of increasing prevalence, that often begins as pharyngitis (see Chapter 409 ). It may complicate Epstein-Barr virus or other viral and bacterial infections of the pharynx. It usually manifests as a unilateral septic thrombophlebitis of the jugular venous system with septic pulmonary embolization. Patients present with prolonged pharyngitis, neck pain and fever. Clinical signs include unilateral painful cervical swelling, trismus, and dysphagia, culminating with signs of sepsis and respiratory distress. Fusobacterium necrophorum is the most commonly isolated organism, although polymicrobial infection may occur. Metastatic infections involving muscles, bones, internal organs (often lungs), and the brain can occur as a complication of Lemierre syndrome.
Anaerobic lung abscess, empyema, and anaerobic pneumonia are most often encountered in children who have disordered swallowing or seizures or in whom an inhaled foreign body is occluding a bronchus. Infections are usually polymicrobial. Children and adults can aspirate oral or gastric contents during sleep, seizure, or periods of unconsciousness. In most cases, lung cilia and phagocytes clear particulate matter and microbes. If the aspiration is of increased volume or frequency or a foreign body blocks normal ciliary clearance, normal pulmonary clearance mechanisms are overcome and infection ensues. Appropriate cultures need to avoid specimen contamination with oral flora through use of bronchoalveolar lavage, lung biopsy, or thoracentesis.
In unusual cases, particularly in patients with poor dental hygiene, aspirated mouth contents may contain the anaerobe Actinomyces israelii , resulting in pulmonary actinomycosis (see Chapter 216 ). Anaerobic pneumonitis associated with this microorganism is remarkable for the ability of the infection to traverse tissue planes. Affected patients often develop fistulas on their chest walls overlying areas of intrathoracic infection. These may extrude distinctive, pathognomonic particles composed of bacterial colonies, called “sulfur granules.”
The entire digestive tract is heavily colonized with anaerobes. The density of organisms is highest in the colon, where anaerobes outnumber aerobes 1,000 : 1. Perforation of the gut leads to leakage of intestinal flora into the peritoneum, resulting in peritonitis involving both aerobes and anaerobes. Secondary sepsis caused by aerobes often occurs early. As the peritoneal infection is walled off, an abscess containing both aerobes and anaerobes often evolves. The predominant aerobic organisms are Escherichia coli and Streptococcus spp. (including Enterococcus spp.), and the anaerobes are the B. fragilis group, Peptostreptococcus , Clostridium, and Fusobacterium spp.
Secondary hepatic abscesses may then develop as complications of appendicitis, intestinal perforation, inflammatory bowel disease, or biliary tract disease. In children with malignancy receiving chemotherapy, the intestinal mucosa is often damaged, leading to translocation of bacteria and focal invasion of bowel wall. Typhlitis is a mixed infection of the gut wall in neutropenic patients, usually located in the ileocecum and characterized by abdominal pain, diarrhea, fever, and abdominal distention. Similarly, a mixed aerobic-anaerobic infection of the intestinal wall and peritoneum may develop in a small infant as a complication of necrotizing enterocolitis , believed to be a result of the relative vascular insufficiency of the gut and hypoxia (see Chapter 123.2 ).
Pelvic inflammatory disease and tuboovarian abscesses are frequently caused by mixed aerobic-anaerobic infection. Vaginitis can be caused by overgrowth of anaerobic flora. Anaerobes frequently contribute to chorioamnionitis and premature labor and may result in anaerobic bacteremia of the newborn. Although these bacteremias are often transient, anaerobes occasionally cause invasive disease in the newborn, including central nervous system (CNS) infection.
Anaerobic skin infections occur in the setting of bites, foreign bodies, and skin and tissue ulceration because of pressure necrosis or lack of adequate blood supply. Animal bites and human bites inoculate oral and skin flora into damaged and hypoxic cutaneous tissue. The extent of the infection depends on the depth of the bite and the associated crush injury to the tissues. In immunocompromised patients, unusual oral anaerobes such as Capnocytophaga canimorsus can cause life-threatening infection.
Clostridial myonecrosis, or gas gangrene, is a rapidly progressive infection of deep soft tissues, primarily muscles, associated with Clostridium perfringens. Necrotizing fasciitis is a more superficial, polymicrobial infection of the subcutaneous space with acute onset and rapid progression that has significant morbidity and mortality (see Chapter 685.2 ). Group A streptococcus, known in the lay press as the “flesh-eating bacteria,” and Staphylococcus aureus are occasionally the causative pathogens. Typically, necrotizing fasciitis is produced by combined infection of S. aureus or gram-negative bacilli and anaerobic streptococci, termed synergistic gangrene . This infection is often seen as a complication of varicella following secondary infection of a cutaneous vesicle. Diabetic patients may develop a particularly aggressive and destructive synergistic gangrene of the inguinal area and adjacent scrotum or vulva known as Fournier gangrene . Early recognition with aggressive surgical debridement and antimicrobial therapy is necessary to limit disfiguring morbidity and mortality.
Occasionally, the bone adjacent to an anaerobic infection becomes infected by direct extension from a contiguous infection in cranial and facial bones or by direct inoculation associated with trauma to tubular bones. Anaerobic septic arthritis is rare, and risk factors include trauma and prosthetic joints. Most infections are monomicrobial, and the organism isolated is related to the route of infection. Peptostreptococcus and P. acnes are isolated in prosthetic joint infections, B. fragilis and fusobacteria in hematogenous infections, and clostridia following trauma.
Anaerobic infections of the kidneys (renal and perirenal abscesses) and heart (pericarditis) are rare. Enteritis necroticans (“pigbel”) is a rare but often fatal GI infection that can follow ingestion of a large meal in a chronically starved child or adult. It is associated with the consumption of pork and is believed to be caused by Clostridium welchii type C (an organism not usually present in the human intestine), the organism being transmitted by contaminated pig meat. Anaerobic osteomyelitis , particularly of fingers and toes, can complicate any process capable of producing hypoxic necrosis, including diabetes, neuropathies, vasculopathies, and coagulopathies.
The diagnosis of anaerobic infection requires a high index of suspicion and the collection of appropriate and adequate specimens for anaerobic culture (Table 240.2 ). Culture specimens should be obtained in a manner that protects them from contamination with mucosal bacteria and from exposure to ambient oxygen. Swab samples from mucosal surfaces, nasal secretions, respiratory specimens, and stool should not be sent for anaerobic culture because these sites normally harbor anaerobic flora. Aspirates of infected sites, abscess material, and biopsy specimens are appropriate for anaerobic culturing. Specimens should be protected from atmospheric oxygen and transported to the laboratory immediately. Anaerobic transport medium is used to increase the likelihood of recovery of obligate anaerobes. Gram staining of abscess fluid from suspected anaerobic infections is useful because even if the organisms do not grow in culture, they can be seen on the smear.
Table 240.2
Clues to Presumptive Diagnosis of Anaerobic Infections*
|
Infection contiguous to or near a mucosal surface colonized with anaerobic bacteria (oropharynx, intestinal-genitourinary tract) Severe tissue necrosis, abscesses, gangrene, or fasciitis Gas formation in tissues (crepitus on exam or visible on plain radiograph) Failure to recover organisms using conventional aerobic microbiologic methods, despite the presence of mixed pleomorphic organisms on smears Failure of organisms to grow after pretreatment with antibiotics effective against anaerobes Failure of clinical response to antibiotic therapy poorly effective against anaerobic bacteria (e.g., aminoglycosides) “Sulfur granules” in discharges caused by actinomycosis Toxin-mediated syndromes: botulism, tetanus, gas gangrene, food poisoning, pseudomembranous colitis Infections associated with anaerobic bacteria (see Table 240.1 ) Septicemic syndrome with jaundice or intravascular hemolysis Typical appearance on Gram stain: Bacteroides spp.—small, delicate, pleomorphic, pale, gram-negative bacilli Fusobacterium nucleatum —thin, gram-negative bacilli with fusiform shape, pointed ends Fusobacterium necrophorum —pleomorphic gram-negative bacilli with rounded ends Peptostreptococcus —chained, gram-positive cocci similar to aerobic cocci Clostridium perfringens —large, short, fat (boxcar-shaped) gram-positive bacilli |
* Suspicion of anaerobic infection is critical before specimens are sampled for culture, to ensure optimal microbiologic techniques and prompt, appropriate therapy.
Antimicrobial resistance among anaerobes has consistently increased over time, and the susceptibility of anaerobic agents to antimicrobial agents has become less predictable. A rapid and simple screening test for antibiotic susceptibility can be used to detect β-lactamase production and presumptive penicillin resistance. More detailed susceptibility testing, available at reference laboratories, is recommended for isolates recovered from sterile body sites or those that are clinically important and are known to have variable or unique susceptibilities.
Recent advances in direct detection of anaerobes from clinical samples include 16S ribosomal RNA (16S rRNA) gene-based methods, DNA hybridization, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), multiplex PCR, and oligonucleotide array technologies. MALDI-TOF MS has been used as a rapid method to identify infectious agents, including many anaerobes. 16S rRNA gene sequencing can be used for isolates whose identification by MS is unreliable.
Treatment of anaerobic infections usually requires adequate drainage and appropriate antimicrobial therapy. Antibiotic therapy varies depending on the suspected or proven anaerobe involved. Many oral anaerobic bacterial species are susceptible to penicillins, although some strains may produce a β-lactamase. Drugs that are active against such strains include metronidazole, penicillins combined with β-lactamase inhibitors (ampicillin-sulbactam, ticarcillin-clavulanate, piperacillin-tazobactam), carbapenems (imipenem, meropenem, doripenem, ertapenem), clindamycin, tigecycline, linezolid, and cefoxitin. Penicillin and vancomycin are active against the gram-positive anaerobes.
Increasing resistance to antimicrobials has been noted among anaerobes, particularly with Bacteroides spp. Clindamycin is no longer recommended in the empirical treatment of abdominal infections due to increasing resistance among Bacteroides. Aerobes are usually present with the anaerobes, necessitating broad-spectrum antibiotic combinations for empirical therapy. Specific therapy is based on culture results and clinical course.
For soft tissue infections , providing adequate perfusion to the area is critical. At times, a muscle flap or skin flap procedure is needed to ensure that nutrients and antimicrobial agents are brought to the affected area and adequate oxygen tension is maintained. Drainage of infected areas is often necessary for cure. Bacteria may survive in abscesses because of high bacterial inoculum, lack of bactericidal activity, and local conditions that facilitate bacterial proliferation. Aspiration is sometimes effective for small collections, whereas incision and drainage may be required for larger abscesses. Extensive debridement and resection of all devitalized tissue are needed to control fasciitis and myonecrosis. Adjunctive hyperbaric oxygen (HBO) therapy has been found to be beneficial in a few uncontrolled studies. However, it should be recognized that surgical treatment is critical and should never be delayed for the provision of HBO therapy.
Uncomplicated infections caused by anaerobic organisms are generally treated for 2-4 wk. Some infections, including osteomyelitis and brain abscess, may need longer treatment of 6-8 wk.
Strains of Clostridium cause disease by proliferation and often by production of toxins. Of the >60 species that have been identified, only a few cause infections in humans. The most frequently implicated Clostridium spp. are C. difficile (Chapter 239 ), C. perfringens , C. botulinum (Chapter 237 ), C. tetani (Chapter 238 ), C. butyricum, C. septicum, C. sordellii, C. tertium, and C. histolyticum.
Clostridia can cause unique histotoxic syndromes produced by specific toxins (e.g., gas gangrene, food poisoning) as well as nonsyndromic infections (e.g., abscess, local infections, sepsis).Based on the clinical syndrome produced, clostridial species are categorized into 3 groups: histotoxic (C. perfringens , C. ramosum , C. novyi , C. septicum , C. bifermentans , and C. sordellii ), enterotoxigenic (C. perfringens and C. difficile ), and neurotoxic (C. tetani and C. botulinum ).
C. perfringens produces a variety of toxins and virulence factors. Strains of C. perfringens are designated A through E. Alpha toxin is a phospholipase that hydrolyzes sphingomyelin and lecithin and is produced by all strains. This toxin causes hemolysis, platelet lysis, increased capillary permeability, and hepatotoxicity. Beta toxin , produced by strains B and C, causes hemorrhagic necrosis of the small bowel. Epsilon toxin is produced by B and D strains and injures vascular endothelial cells, leading to increased vascular permeability, edema, and organ dysfunction. Iota toxin, produced by E strains, causes dermal edema. An enterotoxin is produced by type A and some type C and D strains. Hemolysins and a variety of enzymes are produced by many C. perfringens strains.
Clostridia can be involved in various other polymicrobial pediatric infections: arthritis, osteomyelitis, skin and soft tissue infections (often after trauma or foreign body penetration), intraabdominal, pulmonary, intracranial, and pelvic infections; abscesses; and panophthalmitis.
Clostridial species invade the bloodstream shortly before, during, or just after death, leading to contamination of tissues that may be donated for transplantation. A large outbreak of Clostridium infections in tissue graft recipients was reported in 14 patients who received musculoskeletal grafts processed at a single tissue bank. Because of this outbreak, recommendations for tissue processing now include a processing method that kills bacterial spores.
Clostridium perfringens is the major etiologic cause of myonecrosis, a rapidly progressive anaerobic soft tissue infection. Gas gangrene usually affects muscles compromised by surgery, trauma, or vascular insufficiency that become contaminated with C. perfringens spores, usually from foreign material or a medical device. Wounds can be contaminated by C. perfringens spores from the skin, dirt, soil, and clothing, especially wounds in the lower trunk.
In immunocompromised persons, especially patients receiving cancer chemotherapy, C. septicum is a classic cause of rapidly fatal gas gangrene. A clue to the diagnosis of gas gangrene is pain out of proportion to the clinical appearance of the wound. Infection progresses rapidly with edema, swelling, myonecrosis, and sometimes crepitation of soft tissues. Hypotension, mental confusion, shock, and renal failure are common. A characteristic sweet odor is present in the serosanguineous discharge. The exudate reveals gram-positive bacilli but few leukocytes. Early and complete debridement with excision of necrotic tissue is key to controlling the infection. Repeated, frequent assessment of tissue viability in the operating room is required. High-dose penicillin (250,000 units/kg/day divided every 4-6 hr [q4-6h] intravenously [IV]) or clindamycin (25-40 mg/kg/day divided q6-8h IV) can be employed in pure clostridial infections. If, as is often the case, a mixed bacterial infection is suspected, broader antibiotic coverage is warranted, with an agent such as piperacillin-tazobactam (300 mg/kg/day divided q6hr IV) or meropenem (60 mg/kg/day divided q8h IV). Addition of clindamycin or vancomycin is warranted if staphylococcal or streptococcal co-infection is suspected.
Aggressive supportive care is essential, and amputation of affected limbs is often required. HBO therapy can reduce tissue loss and thus the extent of debridement and has been beneficial in a few studies. However, HBO should only be used as an adjunct to surgical treatment, which is primary.
The prognosis for patients with myonecrosis is poor, even with early, aggressive therapy.
Clostridium perfringens type A produces an enterotoxin that causes food poisoning. This intoxication results in the acute onset of watery diarrhea and crampy abdominal pain. The usual foods containing toxin are improperly prepared or stored meats and gravies. A specific etiologic diagnosis is rarely made in children with food poisoning. Therapy consists of rehydration and electrolyte replacement if necessary. The illness resolves spontaneously within 24 hr of onset. Prevention requires the maintenance of hot food at a temperature ≥74°C (165.2°F).
Bacteroides fragilis is one of the more virulent anaerobic pathogens and is most frequently recovered from blood cultures and cultures of tissue or pus. The most common B. fragilis infection in children occurs as a complication of appendicitis . The organism is part of normal colonic flora but is not common in the mouth or respiratory tract. B. fragilis is usually found as part of polymicrobial appendiceal and other intraabdominal abscesses and is often involved in genital tract infections such as pelvic inflammatory disease and tuboovarian abscess. Prevotella organisms are normal oral flora, and Prevotella infection typically involves gums, teeth, tonsils, and parapharyngeal spaces. Both B. fragilis and Prevotella may be involved in aspiration pneumonitis and lung abscess.
Strains of B. fragilis and Prevotella melaninogenica produce β-lactamase and are resistant to penicillins. Recommended treatment is with ticarcillin-clavulanate, piperacillin-tazobactam, cefoxitin, metronidazole, clindamycin, imipenem, or meropenem. Increasing rates of antimicrobial resistance has been seen in Bacteroides spp. over the last few decades. B. fragilis resistance to clindamycin is increasing worldwide and has reached 40% in some locales. Therefore, clindamycin is no longer recommended as empirical therapy for intraabdominal infections.
Because infections involving B. fragilis and P. melaninogenica are usually polymicrobial, therapy should include antimicrobial agents active against likely concomitant aerobic pathogens. Drainage of abscesses and debridement of necrotic tissue are often required for control of these infections.
Fusobacterium organisms inhabit the intestine, respiratory tract, and female genital tracts. These organisms, which are more virulent than most of the normal anaerobic flora, cause bacteremia and a variety of rapidly progressive infections. Lemierre syndrome , bone and joint infections, and abdominal and genital tract infections are most common. Some strains produce a β-lactamase and are resistant to penicillins, requiring therapy with drugs such as ampicillin-sulbactam and clindamycin.
Veillonella spp. are normal flora of the mouth, upper respiratory tract, intestine, and vagina. These anaerobes rarely cause infection. Strains are recovered as part of the polymicrobial flora causing abscess, chronic sinusitis, empyema, peritonitis, and wound infection. Veillonella spp. are susceptible to penicillins, cephalosporins, clindamycin, metronidazole, and carbapenems.
Peptostreptococcus spp. are normal flora of the skin, respiratory tract, and gut. These organisms are often present in brain abscesses, chronic sinusitis, chronic otitis, and lung abscesses. Such infections are often polymicrobial, and therapy is aimed at the accompanying aerobes as well as the anaerobes. Most of the gram-positive cocci are susceptible to penicillin, cephalosporins, carbapenems, and vancomycin.