capsule formation by strep pyogenes is said to be genotypic character, reason
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In her early studies of group A streptococci (Streptococcus pyogenes), Rebecca Lancefield noted an association between virulence and a distinctive appearance of the bacterial colonies on solid media. Isolates that were highly virulent for mice and that grew well in fresh human blood typically formed large colonies with a translucent, liquid appearance (mucoid) or an irregular, collapsed appearance (matte). By contrast, avirulent isolates that grew poorly in human blood formed compact, opaque colonies (glossy). Strains that grew as mucoid or matte colonies usually produced large amounts of M protein, which was given the designation “M” by Lancefield because of this association with colony morphology (1, 2). Later work by Armine Wilson demonstrated that the mucoid or matte appearance of such strains was in fact due to elaboration of capsular polysaccharide, not M protein (3). Wilson showed that the mucoid or matte colony type was converted to a nonmucoid or glossy colony by growth on medium containing hyaluronidase which digested the hyaluronic acid capsule, whereas growth on medium containing trypsin, which digested M protein, had no such effect. Furthermore, while many strains that produced abundant capsular polysaccharide also were rich in M protein, expression of the two surface products was not always linked; certain mucoid or highly encapsulated strains produced little or no M protein, and certain strains rich in M protein produced little or no capsule (1, 4).
Both M protein and capsule have since been shown to contribute independently to S. pyogenes virulence. The association of mucoid strains of S. pyogenes with both invasive infection and acute rheumatic fever suggested a role for the capsular polysaccharide in virulence. Anecdotal observations that linked the capsule to pathogenesis of streptococcal disease were supported by a study that characterized the colony morphology of more than 1,000 S. pyogenes clinical isolates received by a streptococcal reference lab in the 1980s. In that study, only 3% of S. pyogenes isolates from patients with pharyngitis had a mucoid colony morphology, whereas 21% of isolates from patients with invasive disease syndromes such as bacteremia, necrotizing fasciitis, or streptococcal toxic shock syndrome and 42% of isolates associated with acute rheumatic fever were mucoid (5). The overrepresentation of mucoid strains among isolates associated with invasive infection and rheumatic fever suggested that the capsule contributes to enhanced virulence. The occurrence of outbreaks of acute rheumatic fever associated with mucoid strains of S. pyogenes at several locations in the United States in the 1980s supported the same inference (6–8). These clinical and epidemiologic observations implicating the capsule in pathogenesis have been corroborated by extensive experimental studies that have demonstrated a definite role of the hyaluronic acid capsule as a virulence factor in S. pyogenes infection.
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