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The viridans streptococci are genetically diverse organisms that share the propensity to colonize humans and occasionally penetrate local barriers to cause life-threatening disease. Their importance as the predominant cause of endocarditis in children and adults has been known for decades. Improvements in identification and classification led to the recognition that these organisms are a significant cause of other infections as well, including septicemia and infection of the central nervous system. In this chapter, Abiotrophia and Granulicatella (formerly nutritionally variant streptococci [NVS]) and Streptococcus bovis group organisms are considered together with viridans streptococci. S. bovis is not uniformly classified within the viridans streptococci but shares significant clinical similarities with this group of organisms.
As is the case with all streptococci, viridans streptococci are gram positive and do not produce catalase. Most are facultative anaerobes; however, some (including the S. anginosus group) are capnophilic and others are microaerophilic. Viridans streptococci derive their name from the Latin word viridis, meaning green, because most isolates cause α-hemolysis on sheep blood agar, producing a ring of greenish discoloration surrounding the colonies. This pattern of hemolysis is predominantly the result of red blood cell damage mediated by hydrogen peroxide, which is released from the organism when it is grown in the presence of oxygen. Notably, many viridans organisms are nonhemolytic when grown in oxygen, and most are nonhemolytic when grown under anaerobic conditions. Although nucleotide sequence homology places S. pneumoniae among the viridans streptococci, this species generally is considered separately because of its unique virulence potential. S. pneumoniae is differentiated from other viridans streptococci by its optochin susceptibility and bile solubility. Most viridans streptococci fail to react with the Lancefield antisera, but a number of exceptions exist. For example, the S. anginosus group contains minute, colony-forming β-hemolytic organisms that may react with the antisera of Lancefield groups A, C, F, and G.
Speciation of the viridans streptococci has been the subject of considerable confusion. Nucleotide sequencing of the 16S ribosomal RNA (rRNA) genes and whole genome sequencing have helped considerably in the classification of these organisms. The viridans streptococci are now classified into five groups, distinguished from S. bovis and the pyogenic streptococci (see Fig. 117.1 ). In the clinical laboratory, viridans streptococcal species are differentiated on the basis of biochemical reactions and patterns of hemolysis ( Table 121.1 ). (The term viridans streptococci is preferred to Streptococcus viridans because it avoids the misconception that these organisms belong to a single species or taxon.)
Organism | Hemolysis | Voges-Proskauer Test | Hydrolysis of | Acid Production From | |||||||
---|---|---|---|---|---|---|---|---|---|---|---|
Esculin | Arginine | H 2 O 2 | Mannitol | Sorbitol | Lactose | Trehalose | Inulin | Raffinose | |||
S. mutans | α, β, γ | + | + | − | − | + | + | + | + | + | + |
S. mitis | α | − | − | − | + | − | − | + | v | − | v |
S. oralis | α | − | − | − | + | − | − | + | v | − | v |
S. sanguis | α | − | v | + | + | – | v | + | + | + | v |
S. gordonii | α | − | + | + | + | − | − | + | + | + | v |
S. cristatus | α | − | − | v | + | − | − | V | + | − | − |
S. salivarius | α | + | + | − | − | − | − | V | v | V | + |
S. vestibularis | α | v | v | − | + | − | − | V | v | − | − |
S. parasanguis | α | − | v | + | + | − | − | + | v | − | + |
S. anginosus | α, β, γ | + | + | + | v | v/− | − | + | + | − | v |
S. intermedius | α, γ | + | + | + | V | v/− | − | + | + | − | − |
S. bovis group | γ | NA | + | − | NA | + | − | + | + | + | + |
Gemella morbillorum | α, γ | NA | − | − | NA | − | − | − | − | − | − |
Nutritionally variant streptococci originally were believed to be mutant forms of S. mitis. Biochemical testing and genetic sequence analysis dispelled this notion, and these organisms are now classified as either Abiotrophia or Granulicatella species. They are fastidious organisms that require pyridoxine (vitamin B 6 ) or thiol supplementation for growth. Because these requirements can be fulfilled by the metabolic byproducts of other bacteria, Abiotrophia and Granulicatella grow in culture as satellite colonies around other bacterial species, including Staphylococcus aureus.
The automated biochemical identification systems commonly used in clinical microbiology laboratories can lead to incorrect species assignment of viridans streptococcal isolates. Advanced techniques such as 16S rRNA sequencing or matrix-assisted laser desorption ionization time of flight (MALDI-TOF) generally are more accurate but still have difficulty distinguishing S. pneumoniae from S. mitis and S. oralis .
Nonenterococcal group D organisms comprise the S. bovis group and are an uncommon cause of disease in children. This group previously was classified into two biotypes, I and II, which were subdivided into subtypes II/1 and II/2. The current classification defines distinct species and subspecies: S. gallolyticus (also known as S. gallolyticus subsp. gallolyticus [formerly S. bovis biotype I]); S. pasteurianus (also known as S. gallolyticus subsp. pasteurianus [formerly S. bovis biotype II/2]); S. lutetiensis (also known as S. infantarius subsp. coli ); and S. infantarius (also known as S. infantarius subsp. infantarius ]). The species S. lutetiensis and S. infantarius formerly were classified as S. bovis biotype II/1.
Among the S. bovis group, S. gallolyticus accounts for the majority of invasive infections in children, and S. pasteurianus accounts for most of the remaining pediatric cases. Clinical microbiology laboratories might not be capable of identifying these organisms to the species or subspecies level, an undertaking that can require sequencing of the 16S rRNA gene. In addition, in some parts of the literature these organisms still are referred to simply as S. bovis , leading to inconsistency and further confusion.
Viridans streptococci lack the classic virulence factors that other streptococci have, such as streptolysin O, streptolysin S, deoxyribonuclease B (DNAase B), adhesion-promoting M and F proteins, and pyrogenic exotoxins. The absence of such factors likely accounts for the low pathogenic potential of these organisms in healthy people. However, some viridans species have a notable predilection for causing endocarditis, a characteristic that appears to correlate with the production of extracellular dextran. S. mutans, S. sanguis, S. mitis, and—to some extent— the S. bovis group most often are implicated in endocarditis, and all produce dextran. Dextran exopolysaccharide might play a dual role in the pathogenesis of endocarditis, mediating bacterial adherence to heart valves and also rendering organisms relatively resistant to penicillin. S. mutans plays an important role in dental caries, at least in part due to adherence to dental enamel, which is mediated by glucan exopolysaccharides. S. anginosus has an enhanced propensity to cause localized infections, such as dental and intra-abdominal abscesses. In contrast to other viridans streptococci, S. anginosus produces hydrolytic enzymes (e.g., hyaluronidase, DNAase, and chondroitin sulfatase) and can produce neuramidase. The role of these enzymes in the pathogenesis of disease remains unclear. Many viridans organisms produce an immunoglobulin (Ig) A protease that presumably attenuates the local immune response and enables the organisms to persist in the mouth.
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