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Streptococcus, Enterococcus, and Similar Organisms CHAPTER 15 251

TABLE 15-2 Pathogenesis and Spectrum of Diseasecontd

Organism Virulence Factors Spectrum of Diseases and Infections


Enterococcus spp. Little is known about virulence; adhesions, Most infections are nosocomial and include
cytolysins, and other metabolic capabilities urinary tract infections, bacteremia,
may allow these organisms to proliferate as endocarditis, mixed infections of abdomen and
nosocomial pathogens; multidrug resistance pelvis, wounds, and occasionally, ocular
also contributes to proliferation infections; CNS and respiratory infections are
rare
Abiotrophia spp. (nutritionally variant Unknown Endocarditis; rarely encountered in infections of
streptococci) other sterile sites
Leuconostoc spp., Lactococcus spp., Unknown; probably of low virulence; Whenever encountered in clinical specimens,
Globicatella sp., Pediococcus opportunistic organisms that require impaired these organisms should first be considered as
spp., Aerococcus spp., Gemella host defenses to establish infection; intrinsic probable contaminants; Aerococcus urinae is
spp., Helcococcus sp. resistance to certain antimicrobial agents (e.g., notably associated with urinary tract infections
Facklamia spp. Leuconostoc spp. and Pediococcus spp.
Ignavigranum ruoffiae resistant to vancomycin) may enhance survival
Dolosigranulum pigrum of some species in the hospital setting
Dolosicoccus paucivorans
Alloiococcus sp. Unknown Chronic otitis media in children

mediated by antigen-antibody complexes that deposit in polysaccharide capsule is associated with the organisms
glomeruli, where they initiate damage. virulence. There are more than 90 different serotypes of
The organism adheres and invades the epithelial cells encapsulated strains of S. pneumoniae. Nonencapsulated
through the mediation of various proteins and enzymes. strains are avirulent. The organism may harmlessly
Internalization of the organism is believed to be impor- inhabit the upper respiratory tract with a 5% to 75% car-
tant for persistent and deep tissue infections. Additional riage rate in humans. S. pneumoniae is capable of spread-
virulence factors are included in Table 15-2. ing to the lungs, paranasal sinuses, and middle ear. In
S. pyogenes is also a powerful modulator of the host addition, this organism accesses the bloodstream and
immune system, preventing clearance of the infection. the meninges to cause acute, purulent, and often life-
The M protein is able to bind beta globulin factor H, a threatening infections.
regulatory protein of the alternate complement pathway S. pneumoniae is capable of mobilizing inflammatory
involved in the degradation of C3b. The M protein also cells mediated by its cell wall structure, including pepti-
binds to fibrinogen blocking complement alternate doglycan, teichoic acids, and a pneumolysin. The pneu-
pathway activation. In addition, all strains produce a C5a molysis activates the classical complement pathway. The
peptidase, which is a serine protease capable of inactivat- pneumolysin mediates suppression of the oxidative burst
ing the chemotactic factor for neutrophils and mono- in phagocytes providing for effective evasion of immune
cytes (C5a). clearance. In addition, the organism contains phosphor-
S. agalactiae, group B, infections usually are associated ylcholine within the cell wall, which binds receptors for
with neonates and are acquired before or during the platele- activating factor in endothelia cells, leukocytes,
birthing process (see Table 15-2). The organism is known platelets, and tissue cells of the lungs and meninges pro-
to cause septicemia, pneumonia, and meningitis in new- viding for entry and spread of the organism.
borns. Although the virulence factors associated with the The viridans (greening) streptococci and Abiotrophia
other beta-hemolytic streptococci have not been defini- spp. (formally known as nutritionally variant strepto-
tively identified, groups C, G, and F streptococci cause cocci) are a heterogenous group consisting of alpha
infections similar to those associated with S. pyogenes (i.e., hemolytic and nonhemolytic species generally consid-
skin and soft tissue infections and bacteremia) but are ered to be opportunistic pathogens of low virulence. The
less commonly encountered, often involve compromised organisms colonize the gastrointestinal and genitouri-
patients, and do not produce postinfection sequelae. nary tract. These organisms are not known to produce
any factors that facilitate invasion of the host. However,
when access is gained, a transient bacteremia occurs and
STREPTOCOCCUS PNEUMONIAE AND endocarditis and infections at other sites in compro-
VIRIDANS STREPTOCOCCI mised patients may result.
S. pneumoniae contains the C polysaccharide unrelated to
the Lancefield grouping and is still one of the leading
causes of morbidity and mortality. The organism is the ENTEROCOCCI
primary cause of bacterial pneumonia, meningitis, and Enterococci, previously classified as group D strepto-
otitis media. The antiphagocytic property of the cocci, commonly colonizes the gastrointestinal tract.

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