Sucrose-independence of Streptococcus gordonii's failure to compete with Streptococcus mutans

Objective: We previously reported S. gordonii strain Challis's inability to compete with S. mutans for colonization of teeth in rats in the presence of a sucrose-rich diet. The data suggested that S. mutans' advantage was sucrose-dependent and associated with its synthesis of extracellular glucans and abundant metabolic acid. We also previously reported on complex relationships between the ability of S. gordonii to bind salivary-amylase and its amylase-binding protein A (AbpA) interaction with glucosyl transferases. We therefore tested whether the advantage of S. mutans over S. gordonii abpA+ and (abpA-) strains was independent of a high sucrose diet in rats. Methods: Six groups (n = 10/group) of weanling TAN:SPFOM(OMASF)BR rats free of indigenous mutans streptococci and amylase-binding bacteria, and eating a 56% cornstarch, sucrose-free powdered diet (2000CS), were inoculated simultaneously with 10⁹ of either of the following: S. mutans 10449S, S. gordonii Challis-KS1, its isogenic AbpA-defective mutant Challis-KS1 abpA-, or with S. mutans and either of the S. gordonii strains. Inoculation was done one day after provision of the diet to weanlings. One group of rats remained un-inoculated. Bacterial recoveries were quantified using selective and non-selective agars with appropriate antibiotic supplementation, both during the experiment and at euthanasia. Caries was scored by a blinded examiner. Results: Both S. mutans and S. gordonii strains colonized the rats well; however, when rats were doubly inoculated with S. mutans and either of the S. gordonii strains, the mutans streptococcus dominated the flora on the surface of the teeth. Caries scores were much lower, as expected, than in sucrose-diet-fed rats, but higher for the mutans-colonized animals than for the S. gordonii-colonized rats. Conclusion: S. mutans out-competes S. gordonii in rats fed a cornstarch, sucrose-free powdered diet. There is sucrose-independence of S. gordonii ability to compete with S. mutans in rats.

Supported by NIH DE-09838.