1350 PART 5 Infectious Diseases

they can form abscesses as a protective measure, and they can act synergistically with other bacteria to better persist in the host.

Virulence factors associated with anaerobes typically confer the ability to evade host defenses, adhere to cell surfaces, produce toxins and/

or enzymes, or display surface structures such as capsular polysaccharides and lipopolysaccharide that contribute to pathogenic potential.

The ability of an organism to adhere to host tissues is often critical to

the establishment of infection. Some oral species adhere to the epithelium in the oral cavity. P. gingivalis, a common isolate in periodontal

disease, has fimbriae that facilitate attachment. In supragingival plaque,

many oral anaerobes are able to attach directly to aerobic bacteria (e.g.,

Streptococcus species) that are adherent to the tooth’s surface. F. nucleatum is a notable example of these secondary colonizers: it expresses

receptors to which almost all oral bacteria can bind and serves as an

important bridge between the primary colonizers and subsequent layers of bacteria. B. fragilis synthesizes pili, fimbriae, and hemagglutinins

that aid in attachment to host cell surfaces in the intestine.

Anaerobic bacteria produce a number of exoproteins that can

enhance the organisms’ virulence. P. gingivalis produces a collagenase

that enhances tissue destruction. Exotoxins produced by clostridial

species, including botulinum toxins, tetanus toxin, C. difficile toxins A

and B, and five toxins produced by Clostridium perfringens, are among

the most virulent bacterial toxins in mouse lethality assays. Anaerobic

gram-negative bacteria, such as B. fragilis, P. gingivalis, and Prevotella

intermedia, possess lipid A molecules (endotoxins) that are 100–1000

times less biologically potent than endotoxins associated with aerobic

gram-negative bacteria; these differences may relate to variations in

acylation status, length of fatty acids, and number of phosphate groups.

This relative biologic inactivity may account for the lower frequency

of disseminated intravascular coagulation and purpura in anaerobic

gram-negative bacteremia than in facultative and aerobic gramnegative bacillary bacteremia. An exception is the lipopolysaccharide

from Fusobacterium, which may account for the severity of Lemierre

syndrome (see “Complications of Anaerobic Head and Neck Infections,” below).

The most extensively studied virulence factor of the nonsporulating

anaerobes is the capsular polysaccharide complex of B. fragilis. This

organism is unique among anaerobes in its potential for virulence during growth at normally sterile sites. Although it constitutes only 0.5–1%

of the normal colonic microbiota, B. fragilis is the anaerobe most commonly isolated from intraabdominal infections and bacteremia. In an

animal model of intraabdominal sepsis, the capsular polysaccharide

was identified as the major virulence factor of B. fragilis; this polymer

plays a specific, central role in the induction of abscesses. A series of

detailed biologic and molecular studies of this virulence factor showed

that B. fragilis produces at least eight distinct capsular polysaccharides,

far more than the number reported for any other encapsulated bacterium. B. fragilis can exhibit distinct surface polysaccharides either

alone or in combination by regulating the expression of these different

capsules in an on–off manner through a reversible inversion of DNA

segments within the promoters for operons containing the genes

required for polysaccharide synthesis. Structural analysis of two of

these polysaccharides, PSA and polysaccharide B (PSB), revealed that

each polymer consists of repeating units with positively charged free

amino groups and negatively charged groups. This structural feature is

rare among bacterial polysaccharides, and the ability of PSA—and, to

a lesser extent, PSB—to induce abscesses in animals depends on this

zwitterionic charge motif. Intraabdominal abscess induction is related

to the capacity of PSA to stimulate macrophages to release cytokines

and chemokines—in particular, interleukin (IL) 8, IL-17, and tumor

necrosis factor α (TNF-α)—from resident peritoneal cells through a

Toll-like receptor 2–dependent mechanism. The release of cytokines

and chemokines results in the chemotaxis of polymorphonuclear neutrophils (PMNs) into the peritoneum, where they adhere to mesothelial

cells induced by TNF-α to upregulate their expression of intercellular

adhesion molecule 1 (ICAM-1). PMNs adherent to ICAM-1-expressing

cells probably represent the nidus for an abscess. PSA also activates

T cells to produce certain cytokines, including IL-17 and interferon γ,

that are necessary for abscess formation.

These virulence factors not only promote persistence of the anaerobe that produces them but also aid in the survival of bystander organisms and result in bacterial synergies. Clinically, these synergies are

evidenced by the fact that anaerobic infections typically involve three

to six different organisms. Examples of this synergistic pathogenesis

include creation of a favorable environment for growth (e.g., establishment and maintenance of an anaerobic environment by facultative

organisms), inhibition of host defenses (e.g., production of short-chain

fatty acids and succinic acid that inhibit the ability of phagocytes to

clear facultative organisms), provision of necessary growth factors for

other organisms (e.g., oral diphtheroids that produce vitamin K, which

is needed by P. melaninogenica), and creation of tissue damage that

promotes spread of the infection. In these ways, facultative and obligate

anaerobes synergistically potentiate abscess formation.

APPROACH TO THE PATIENT

Infections Due to Anaerobic Bacteria

The physician must consider several points when approaching the

patient with a possible infection due to anaerobic bacteria.

1. The organisms colonizing mucosal sites are commensals, very

few of which typically cause disease. When these organisms do

cause disease, it often occurs in proximity to the mucosal site

they colonize.

2. For anaerobes to cause tissue infection, they must spread beyond

the normal mucosal barriers.

3. Conditions favoring the propagation of anaerobic bacteria, particularly a lowered oxidation-reduction potential, are necessary.

These conditions exist at sites of trauma, tissue destruction,

compromised vascular supply, and necrosis.

4. Frequently, a complex array of infecting microbes can be found,

occasionally with >10 different species isolated from a suppurative site.

5. Anaerobic organisms tend to be found in abscess cavities or

in necrotic tissue. The failure of an abscess to yield organisms

on routine culture is a clue that the abscess is likely to contain

anaerobic bacteria. Often smears of this “sterile pus” are found to

be teeming with bacteria when Gram’s stain is applied. Although

some facultative organisms (e.g., Staphylococcus aureus) are also

capable of causing abscesses, abscesses in organs or deeper body

tissues should call anaerobic infection to mind.

6. Gas is found in many anaerobic infections of deep tissues but is

not diagnostic because it can be produced by aerobic bacteria

as well.

7. Although a putrid-smelling infection site or discharge is considered diagnostic for anaerobic infection, this manifestation

usually develops late in the course and is present in only 30–50%

of cases.

8. Some species (the best example being the B. fragilis group) require

specific therapy. However, many synergistic infections can be

cured with antibiotics directed at some but not all of the organisms involved. Antibiotic therapy, combined with debridement

and drainage, disrupts the interdependent relationship among the

bacteria, and some species that are resistant to the antibiotic do

not survive without the co-infecting organisms.

9. Manifestations of severe sepsis and disseminated intravascular coagulation are unusual in patients with purely anaerobic

infection.

■ EPIDEMIOLOGY

Difficulties in the performance of appropriate cultures, contamination

of cultures by components of the normal microbiota, and the lack of

readily available, reliable culture techniques have made it challenging

to obtain accurate data on the incidence or prevalence of anaerobic

infections. However, anaerobic infections are encountered frequently,

with anaerobes comprising 7–8% and 13–15% of bacteria isolated

from inpatients and outpatients, respectively. Bacteremia and soft

1351CHAPTER 177 Infections Due to Mixed Anaerobic Organisms

Head and neck

Lung

Abdomen

Soft tissue and joints

Bacteremia

Catheter-related

Surgical site infection

FIGURE 177-2 Distribution of types of infection from which anaerobic organisms

were cultured at a single hospital over a 7-year period. Head and neck infections

included sinusitis, otitis media, and retropharyngeal abscess; abdominal infections

included liver abscess, biliary tract infection, bowel obstruction, and intraabdominal

abscess; catheter-related infections included those related to peritoneal dialysis

catheters and ventriculoperitoneal shunts. (Data from Y Park et al: Clinical features

and prognostic factors of anaerobic infections: A 7-year retrospective study. Korean

J Intern Med 24:13, 2009.)

tissue infections are the most common types of anaerobic infection

(Fig. 177-2). Typically, anaerobic bacteria account for <1% of all cases

of bacteremia.

■ CLINICAL MANIFESTATIONS

Although anaerobes can cause infection anywhere in the body, certain clinical findings and characteristics are commonly found. These

include abscess formation, putrid purulence (due to volatile fatty acid

by-products), septic thrombophlebitis, tissue necrosis, and failure

to respond clinically to broad-spectrum antibiotics that lack activity

against anaerobes.

Anaerobic Infections of the Mouth, Head, and Neck

Anaerobic bacteria are commonly involved in infections of the mouth,

head, and neck (Chap. 35). The predominant isolates are components

of the normal microbiota of the upper airways—mainly Prevotella species, P. asaccharolytica, Fusobacterium species, peptostreptococci, and

microaerophilic streptococci.

OROFACIAL INFECTIONS The most common oral infections are

odontogenic and include dental caries and periodontal disease (gingivitis and periodontitis). While dental caries usually manifest with pain,

sensitivity, and discoloration of the tooth, periodontal disease involves

inflammation of the gums and underlying tissue. In its more severe

forms, periodontitis can result in difficulty chewing, loose teeth, and

occasionally tooth loss. Severe orofacial infections typically develop as

a consequence of dental infection, and the infection can spread from

the tooth to different anatomic areas that provide the least resistance,

resulting in periapical, periodontal, or pericoronal infections. If the

dental surface is completely breached, an endodontic infection (pulpitis) can occur. In late stages of pulpitis, the tooth is generally very sensitive to heat, but cold stimuli may provide relief. Left untreated, pulpitis

can progress to invade the alveolar bone and develop into a periapical

abscess. The abscesses, particularly those involving the second and

third molars, can occasionally extend into the submandibular, sublingual, and submental spaces (Ludwig’s angina). This infection results in

marked local swelling of tissues, with pain, trismus, and superior and

posterior displacement of the tongue. Submandibular swelling of the

neck and obstruction by the tongue can impair swallowing and cause

respiratory obstruction. In some cases, tracheotomy is lifesaving.

Microbiologically, dental caries begin with the binding of Streptococcus mutans and Streptococcus sanguis to the tooth surface, with

subsequent further colonization by anaerobes. In contrast, periodontitis is typically associated with P. gingivalis, Tannerella forsythensis,

Aggregatibacter actinomycetemcomitans, and Treponema denticola.

Fusobacterium, Actinomyces, Peptostreptococcus, and Bacteroides species (other than B. fragilis) are the organisms most commonly isolated

from periapical abscesses.

ACUTE NECROTIZING ULCERATIVE GINGIVITIS Gingivitis may

become a necrotizing infection (trench mouth, Vincent’s stomatitis).

The onset of disease is usually sudden and is associated with painful

bleeding gums, foul breath, and a bad taste. The gingival mucosa,

especially the papillae between the teeth, becomes ulcerated and may

be covered by a yellowish-white or gray “pseudomembrane,” which is

removable with gentle pressure. Patients may become systemically ill,

developing fever, malaise, cervical lymphadenopathy, and leukocytosis.

The infection can sometimes extend into the pharynx, resulting in an

extremely sore throat, foul breath, and tonsillar pillars that are swollen,

red, ulcerated, and covered by a pseudomembrane. Prevotella, Treponema, and Fusobacterium species have been implicated.

In some cases, acute necrotizing gingivitis can rapidly progress to

noma (cancrum oris), a gangrenous infection that destroys the soft and

hard tissues related to the oral cavity. Noma occurs most frequently

in young children (1–4 years of age) who have immune dysfunction

related to malnutrition and endemic infections (particularly measles).

This infection occurs worldwide but is most common in sub-Saharan

Africa, where the incidence is 1–7 cases per 1000 children. Although

the pathogenesis is not fully understood, infections with F. necrophorum and P. intermedia are thought to be key drivers of this disease.

Without treatment, the mortality rate is 70–90%.

PERIPHARYNGEAL SPACE INFECTIONS These infections arise from

the spread of organisms from the upper airways to potential spaces

formed by the fascial planes of the head and neck. The etiology is

typically polymicrobial and represents the normal microbiota of the

mucosa of the originating site.

Peritonsillar abscess (quinsy) is the most common peripharyngeal

infection and occurs as a complication of acute tonsillitis. Consistent

with its association with tonsillitis, adolescents are most commonly

affected. Patients present with a sore throat, dysphagia, peritonsillar

swelling, muffled voice, and uvular deviation to the contralateral side.

The abscess material typically grows group A Streptococcus in conjunction with obligate anaerobes (e.g., Bacteroides, Prevotella, and Peptostreptococcus species) (Chap. 35). Retropharyngeal abscesses typically

occur in children 2–4 years of age, although they can occur at any age.

Although a suppurative infection of the retropharyngeal lymph nodes

is the usual precursor to these abscesses in children, foreign-body

ingestion and/or local trauma is more commonly the inciting factor in

adults. The clinical presentation shares many features with peritonsillar

abscesses, but difficulty extending the neck and torticollis are more

common with retropharyngeal abscesses. The etiologic agents are the

same as in peritonsillar abscesses, with additional aerobic organisms

(e.g., S. aureus, viridans streptococci) also playing a role.

SINUSITIS AND OTITIS Anaerobic bacteria have been implicated

in chronic sinusitis but play little role in acute sinusitis. Numerous

studies related to the microbiology of chronic sinusitis have been conducted; on average, anaerobic bacteria have been found in two-thirds

of patients, with many studies demonstrating their presence in >90%

of patients. Anaerobic bacteria represent ~40% of all bacteria cultured,

with Peptostreptococcus, Prevotella, and Porphyromonas species the

most commonly isolated anaerobes. S. aureus and Enterobacteriaceae

are the aerobes most commonly recovered in chronic sinusitis. Anaerobic bacteria have been isolated in ~60% of cases of chronic suppurative

otitis media in children, but they are not involved in acute otitis media.

COMPLICATIONS OF ANAEROBIC HEAD AND NECK INFECTIONS Direct

extension of these infections into contiguous areas can result in additional disease manifestations. Cranial spread of these infections can result

in osteomyelitis of the skull or mandible or in intracranial infections,

such as brain abscess and subdural empyema. Caudal spread can produce

mediastinitis or pleuropulmonary infection. Hematogenous complications can also result from anaerobic infections of the head and neck.

Bacteremia, which occasionally is polymicrobial, can lead to endocarditis or other distant infections. Lemierre’s syndrome (Chap. 35), which

is usually due to F. necrophorum, is an acute oropharyngeal infection with secondary septic thrombophlebitis of the internal jugular

vein and frequent septic emboli, most commonly to the lung. This

infection typically begins with pharyngitis, which is followed by local

invasion in the lateral pharyngeal space, with resultant internal jugular

vein thrombophlebitis.

1352 PART 5 Infectious Diseases

Central Nervous System (CNS) Infections CNS infections

associated with anaerobic bacteria are brain abscess, epidural abscess,

and subdural empyema, in which anaerobes are recovered in up to 30,

20, and 10% of cases, respectively. The frequency with which anaerobes

are recovered depends in large part on the underlying reason for the

infection. For example, brain abscesses are typically due to hematogenous seeding, contiguous spread, penetrating head trauma, or recent

surgical intervention. Anaerobic bacteria are most commonly associated with brain abscesses resulting from contiguous spread (related

to otogenic, odontogenic, and sinus infections), and the pathogens

recovered are the same as in these antecedent infections. Facultative or

microaerophilic streptococci and coliforms are often part of a mixed

infecting flora in brain abscesses. The location of the abscess may also

provide insight into the pathogens. Abscesses in the frontal lobe (often

associated with sinusitis) are due to anaerobes, streptococci, and staphylococci; temporal lobe and cerebellar abscesses are often related to the

oral microbiota and middle-ear pathogens.

Obligate anaerobes rarely cause meningitis. Only one obligate

anaerobe was identified in a seminal study of 188 bacterial meningitis

isolates, and a U.S. national surveillance study of 18,642 such isolates

collected between 1977 and 1981 found only five obligate anaerobes.

This low incidence may be due, in part, to the fact that many clinical

microbiology laboratories do not routinely culture cerebrospinal fluid

(CSF) for anaerobes.

Pleuropulmonary Infections The lungs are constantly seeded

with organisms from the oral microbiota via subclinical microaspiration that normally occurs in all people. Even though the lung is the site

of oxygen exchange and is therefore an overwhelmingly aerobic environment, the organisms most abundant in the lower respiratory tract

(as assessed by culture-independent methods) include anaerobes such

as Prevotella and Veillonella species, with oral microaerophilic streptococcal species (e.g., the Streptococcus milleri group) also present in

significant abundances. In patients who have impaired bacterial clearance (due to decreased cough, dysfunctional mucociliary transport, or

alcohol intoxication) and/or increased rates of aspiration (due to neurologic disorders, impaired consciousness, or swallowing dysfunction),

these anaerobic bacteria can establish an infection and result in aspiration pneumonia, lung abscess, or empyema. These anaerobic infections

have an indolent course that may serve as a clinical clue differentiating

them from conditions with other etiologies (e.g., chemical pneumonitis, pneumococcal pneumonia) that often present more acutely.

ASPIRATION PNEUMONIA Bacterial aspiration pneumonia must be

distinguished from two other clinical syndromes associated with

aspiration that are not of bacterial etiology. One syndrome results

from aspiration of food or, rarely, other foreign bodies. Obstruction of

major airways typically results in difficulty breathing, atelectasis, and

moderate nonspecific inflammation. Therapy consists of removal of

the foreign body. The second aspiration syndrome relates to chemical

pneumonitis caused by inhalation or aspiration of alveolar irritants.

Perhaps the most common cause of chemical pneumonitis is Mendelson syndrome, which results from regurgitation and aspiration of

acidic gastric juices. Pulmonary inflammation—including the destruction of the alveolar lining, with transudation of fluid into the alveolar

space—occurs with remarkable rapidity. This syndrome typically

develops within 4–6 h, often following anesthesia when the gag reflex is

depressed. The patient becomes tachypneic, tachycardic, and hypoxic,

often in the absence of fever. The leukocyte count may rise, and the

chest x-ray may evolve from normal to a complete bilateral “whiteout”

within 8–24 h. Sputum production is minimal. The pulmonary signs

and symptoms often resolve quickly with symptom-based therapy,

but this condition can culminate in respiratory failure due, in part, to

pulmonary edema. Antibiotic therapy is not indicated unless bacterial

superinfection occurs.

In contrast to these syndromes, bacterial aspiration pneumonia

develops over a period of several days or weeks rather than hours.

The pathogenesis includes some combination of an increased bacterial

burden, increased virulence of the organisms aspirated, and potential

airway damage related to aspiration of gastric fluid. Patients generally

report fever, malaise, and sputum production. In some patients, weight

loss and anemia reflect a more chronic process. Usually the history

reveals factors predisposing to aspiration, such as significant alcohol

consumption or neurologic impairment due to a previous stroke.

Severe dental disease is often associated with aspiration pneumonia,

but it is not clear whether this association relates to an increased number of oral microbes and/or the presence of organisms with increased

virulence. Sputum characteristically is not malodorous unless the

process has been ongoing for at least a week. Chest x-rays show consolidation in dependent pulmonary segments: in the basilar segments of

the lower lobes if the patient has aspirated while upright and in either

the posterior segment of the upper lobe (usually on the right side, given

that the right mainstem bronchus has a more vertical orientation) or

the superior segment of the lower lobe if the patient has aspirated while

supine.

A mixed bacterial population with many PMNs is evident on Gram’s

staining of sputum. Expectorated sputum is unreliable for anaerobic cultures because of inevitable contamination by the normal oral microbiota.

Reliable specimens for culture can be obtained by transtracheal or transthoracic aspiration—techniques that are rarely used at present. Although

the culture of protected-brush specimens or bronchoalveolar lavage fluid

obtained by bronchoscopy is controversial, more recent data suggest that

these approaches can be used without oropharyngeal contamination and

can recover anaerobic organisms from the lower respiratory tract in a

site-directed manner. Further research is needed to determine how these

approaches compare with the previous gold standards.

ANAEROBIC LUNG ABSCESSES (See also Chap. 127) These abscesses

result from subacute anaerobic pulmonary infection. The clinical

presentation typically involves a history of constitutional signs and

symptoms (including malaise, weight loss, fever, night sweats, and

foul-smelling sputum) that have typically persisted for 1–3 weeks

prior to hospitalization. Patients who develop lung abscesses often, but

not always, have an antecedent dental infection. Abscess cavities may

be single or multiple and generally occur in dependent pulmonary

segments (Fig. 177-3). The differential diagnosis for lung abscesses

includes pneumonia (including necrotizing pneumonia), a purulent

pleural effusion with a bronchopleural fistula, and a pneumatocele. Of

note, infection with some aerobic organisms, particularly S. aureus,

can develop into a lung abscess without an anaerobic component.

Approximately 90% of cases have an anaerobe identified—usually

three to six isolates per sample—if careful attention is paid to handling

and processing of the abscess sample. The most common isolates

include peptostreptococci, Prevotella and Porphyromonas species,

and F. nucleatum. An important finding is that ~90% of cultures also

demonstrate the presence of aerobic organisms, such as S. aureus,

Streptococcus pneumoniae, and Klebsiella pneumoniae. Consistent with

the notion that anaerobes are contributing to disease, patients often

do not improve clinically until they receive an antibiotic regimen that

includes anaerobic coverage.

EMPYEMA Empyema is a manifestation of long-standing anaerobic

pulmonary infection and manifests with thick, purulent material in

the pleural space, often in association with a bronchopleural fistula.

Alternatively, a subdiaphragmatic infection may extend into the pleural

space and similarly result in an empyema. The clinical presentation

resembles that of other anaerobic pulmonary infections and may

include foul-smelling sputum, pleuritic chest pain, and marked chestwall tenderness. This disease process must be differentiated from a

parapneumonic effusion resulting from more routine causes of pneumonia (e.g., S. pneumoniae). In the latter instance, the fluid is a thin

exudate that has a mean white blood cell (WBC) count of ~5000 cells/

mL, a lactate dehydrogenase level of >200 IU/L, and a pH of ~7.4. In

contrast, empyema is characterized by foul-smelling thick pus with a

mean WBC count of ~55,000 cells/mL, a lactate dehydrogenase level

of >1000 IU/L, and a pH of <7.2 as well as loculations and a thick

pleural peel on imaging. Drainage and occasionally decortication of the

visceral and parietal pleura are required. Defervescence, a return to a

feeling of well-being, and resolution of the process may require several

months, particularly in the absence of surgical intervention.

1353CHAPTER 177 Infections Due to Mixed Anaerobic Organisms

Intraabdominal Infections Breach of the gut mucosal surface

(e.g., due to trauma, intestinal perforation, or malignancy) allows

members of the microbiota to enter the normally sterile peritoneum.

Accordingly, the offending organisms reflect the microbiota in the

affected intestinal region. For example, recovery of Candida species

from intraabdominal infections should prompt evaluation of the

stomach and proximal small bowel for potential perforation. Furthermore, a study of patients with perforated and gangrenous appendicitis

demonstrated that virtually all samples yielded E. coli and members of

the B. fragilis group; peptostreptococci and Bilophila wadsworthia—

additional components of the appendiceal and colonic microbiota—

were also recovered from >50% of samples. Notably, some studies

have identified an average of 10 different bacterial species, with an

anaerobe-to-aerobe ratio of ~3:1. Given that >1000 bacterial species

are present in the colonic microbiota, the dominance of such a limited

repertoire of bacterial genera and species recovered in intraabdominal

infections reflects a combination of two factors: the increased propensity of these organisms to result in intraabdominal abscesses and the

difficulty faced by clinical microbiology laboratories in culturing the

diverse organisms present in these samples. See Chap. 132 for a complete discussion of intraabdominal infections.

Neutropenic enterocolitis (typhlitis) involves marked thickening of

the bowel wall (typically >4 mm) in the setting of neutropenia, abdominal pain, and fever. This condition most commonly affects the cecum

and may extend to the neighboring terminal ileum and/or proximal

colon, but any intestinal region may be involved. Typhlitis generally

occurs after 1–2 weeks of chemotherapy-induced neutropenia associated with treatment of hematologic or, less commonly, solid tumor

malignancies, but it can occur regardless of the cause of neutropenia. At

least 5% of adults hospitalized for malignancy are thought to develop

typhlitis, but this is likely an underestimate. Although the right lower

quadrant is the most common location of abdominal pain and tenderness, these symptoms are absent in nearly half of cases; moreover, some

patients, particularly those taking glucocorticoids, may not experience

abdominal pain at all. Given the weakened integrity of the bowel wall

and the associated neutropenia, patients often develop bacteremia due

to one or more organisms related to the microbiota of the affected

intestinal segment. Patients who develop bacteremia due to Clostridium septicum often have relatively severe disease, and identification of

this organism is highly associated with the presence of malignancy—

notably, colon cancer. Medical management including bowel rest,

intestinal decompression, and broad-spectrum antibiotic administration is generally successful, although surgical intervention may be

required in cases of persistent intestinal bleeding, necrotic bowel, or

clinical deterioration suggestive of an ongoing intestinal process.

Pelvic Infections Anaerobes are frequently encountered in pelvic inflammatory disease, pelvic abscess, endometritis, tubo-ovarian

abscess, septic abortion, and postoperative or postpartum infections.

These infections are often of mixed etiology, involving both anaerobes

and coliforms; pure anaerobic infections without coliform or other

facultative bacterial species occur more often in pelvic than in intraabdominal sites. The major anaerobic pathogens in pelvic abscesses are

P. bivia, P. disiens, and the B. fragilis group, but many other anaerobes

have also been implicated. See Chap. 136 for a complete discussion of

pelvic inflammatory disease.

Anaerobic bacteria have been thought to be contributing factors

in bacterial vaginosis. This syndrome of unknown etiology is characterized by a profuse malodorous discharge and a change in bacterial

ecology that results in replacement of the Lactobacillus-dominated

normal microbiota with an overgrowth of anaerobic bacterial species.

Culture-based and culture-independent approaches have identified

numerous organisms, including Gardnerella vaginalis, peptostreptococci, genital mycoplasmas, and species within the genera Prevotella,

Mobiluncus, Atopobium, Leptotrichia, Megasphaera, and Eggerthella.

This wide array of implicated bacteria may reflect differences in the

overall disease spectrum of bacterial vaginosis and/or a shared physiologic response to these different organisms.

Skin and Soft Tissue Infections Similar to other anatomic sites,

skin or soft tissue injured by trauma, ischemia, or surgery creates a suitable environment for anaerobic infections. The infecting bacteria either

are introduced directly (e.g., wounds associated with intestinal surgery,

decubitus ulcers, or human bites) or originate in contiguous areas (e.g.,

cutaneous abscesses, rectal abscesses, and axillary sweat gland infections [hidradenitis suppurativa]). Anaerobes also are often cultured

from foot ulcers of diabetic patients. The most common locations for

anaerobic cellulitis include the neck, trunk, groin (including the genitalia), and legs. The deep soft tissue infections associated with anaerobic

bacteria are gas gangrene, synergistic cellulitis (both progressive and

necrotizing), necrotizing fasciitis, and myositis (Chaps. 129 and 154).

Gas gangrene (crepitus cellulitis) is most often due to C. perfringens,

although other clostridial species have been implicated as well. This

infection involves extensive gas formation in the tissue leading to

crepitus and a thin, dark, occasionally malodorous discharge. True gas

gangrene typically presents with fever and tenderness around the lesion

and can rapidly spread; in contrast, there are somewhat more indolent

FIGURE 177-3 Chest radiograph (left) and CT image (right) of a lung abscess. The patient aspirated while supine and developed an abscess in the posterior segment of

the right upper lobe. Cultures were pretreated and grew only Klebsiella pneumoniae. (Images provided by Gita N. Mody, MD, MPH, Division of Cardiothoracic Surgery,

Department of Surgery, The University of North Carolina at Chapel Hill.)