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Strains of Streptococcus ferus isolated from the oral cavities of wild rodents inhabiting sucrose-rich and sucrose-poor environments have many traits in common with the "mutans" streptococci. Thus, S. ferus HD3 and 8S1, like cariogenic S. sobrinus 6715-13, from adherent, alpha (1 leads to 3) glucopyranosyl-glucose linkage-rich, plaquelike deposits in vitro and in vivo through the action of constitutive glucosyltransferase(s) enzymes on sucrose, produce and degrade intracellular polysaccharide, produce short-chain fatty acids from the catabolism of mono- and disaccharides, carry the c antigen of S. mutans, and penetrate, persist, and proliferate in a sucrose-augmented fashion in the oral cavities of specific-pathogen-free rodent caries models. However, unlike infection with common S. mutans, infection with tested S. ferus strains does not cause caries. This avirulence appeared to result more from the reduced aciduricity of S. ferus than from differences in glucosyltransferase complements. Studies showed that despite generally similar growth rates and extracellular glucan syntheses, the acidogenic metabolism of S. ferus was more inhibited by declining environmental pH than was cariogenic S. sobrinus 6715-13 and that, in vitro, less hydroxyapatite was solubilized by S. ferus metabolic end products. The physiology of these S. ferus strains demonstrated that, in addition to plaque formation and acid production, acid tolerance was crucial to the carious process.

Physiology of "mutans-like" Streptococcus ferus from wild rats