Enterococcus

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Chapter 179 Enterococcus

David B. Haslam

Enterococcus has long been recognized as a pathogen in select populations and over the past 2 decades has become a common and particularly troublesome cause of hospital-acquired infection. Enterococci were formerly classified with Streptococcus bovis and Streptococcus equinus as the Lancefield group D streptococci and are now placed in a separate genus. These organisms are notorious for their frequent resistance to antibiotics.

Etiology

Enterococci are gram-positive, catalase-negative facultative anaerobes that grow in pairs or short chains. Most are nonhemolytic (also called γ-hemolytic) on sheep blood agar, although some isolates have α- or β-hemolytic activity. Enterococci are distinguished from most Lancefield groupable streptococci by their ability to grow in bile and hydrolyze esculin. Enterococci are able to grow in 6.5% NaCl and hydrolyze L-pyrrolidonyl-β-naphthylamide (PYR), features used by clinical laboratories to distinguish them from group D streptococcus. Identification at the species level is enabled by differing patterns of carbohydrate fermentation.

Epidemiology

Enterococci are normal inhabitants of the gastrointestinal tract of humans and animals and are also often found in oral secretions and dental plaque, the upper respiratory tract, the skin, and the vagina. Enterococcus faecalis is commonly acquired in the 1st week of life and is nearly ubiquitous by adulthood. Enterococcus faecium colonization is less common, although approximately 25% of adults harbor this organism.

E. faecalis accounts for approximately 80% of enterococcal infections, and E. faecium is responsible for almost all of the remaining enterococcal infections. Only rarely are other species such as Enterococcus gallinarium and Enterococcus cassiliflavus associated with infection. Typically, the patient’s indigenous flora is presumed to be the source of enterococcal infection. Direct spread from person to person or from contaminated medical devices may occur, particularly within newborn nurseries and intensive care units. Nosocomial spread is an important source of hospital outbreaks.

Pathogenesis

Enterococci are not aggressively invasive organisms, usually causing disease only in children with damaged mucosal surfaces or impaired immune response. Their dramatic emergence as a cause of nosocomial infection is predominantly due to their resistance to antibiotics commonly used in the hospital setting. Aside from antibiotic resistance genes, few classic virulence factors have been described among enterococci. Adhesion-promoting factors, such as the surface protein Eps, likely account for the propensity of these organisms to cause endocarditis and urinary tract infections (UTIs). The ability to form biofilms likely facilitates the colonization of urinary and vascular catheters. Many isolates also produce a cytolysin that has a broad range of host cells and is released at high bacterial density in a process called quorum sensing. The cytolysin contributes to virulence in experimental models of endocarditis, peritonitis, and endophthalmitis. Other proposed virulence factors include aggregation substance, gelatinase, and extracellular superoxide.

Antimicrobial Resistance

Enterococci are highly resistant to cephalosporins and semisynthetic penicillins such as nafcillin, oxacillin, and methicillin. They are moderately resistant to extended-spectrum penicillins such as ticarcillin and carbenicillin. Ampicillin, imipenem, and penicillin are the most active β-lactams against these organisms. Some strains of E. faecalis and E. faecium demonstrate resistance to ampicillin and penicillin due to mutations in penicillin binding protein 5. In addition, occasional strains of E. faecalis produce a plasmid-encoded β-lactamase similar to that found in Staphylococcus. These isolates are completely resistant to penicillins, necessitating the combination of a penicillin plus a β-lactamase inhibitor or the use of imipenem or vancomycin. Any active drug may be insufficient if used alone for serious infections wherein high bactericidal activity is desired (Tables 179-1 and 179-2).

Table 179-1 INTRINSIC RESISTANCE MECHANISMS AMONG ENTEROCOCCUS

ANTIMICROBIAL MECHANISM
Ampicillin, penicillin Altered binding protein
Aminoglycoside (low level) Decreased permeability, altered ribosomal binding
Clindamycin Altered ribosomal binding
Erythromycin Altered ribosomal binding
Tetracyclines Efflux pump
Trimethoprim-sulfamethoxazole Utilize exogenous folate

Table 179-2 ACQUIRED RESISTANCE MECHANISMS AMONG ENTEROCOCCUS

ANTIMICROBIAL MECHANISM
Ampicillin, penicillin (high level) Mutation of PBP-5
Aminoglycoside (high level) Enzyme modification
Quinolones DNA gyrase mutation
Chloramphenicol Efflux pump
Glycopeptide Altered cell wall binding
Quinupristin/dalfopristin Ribosomal modification, efflux pump
Linezolid Point mutation
Daptomycin Unknown

All enterococci have intrinsic low-level resistance to aminoglycosides because these antibiotics are poorly transported across the Enterococcus

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