Abstract 1603 Poster Session II, Sunday, 5/2 (poster 103)
Introduction: Group B streptococci (GBS) are an important cause of early onset neonatal sepsis and infection-associated pulmonary hypertension. GBS hyaluronidase (HYL), which can degrade hyaluronan as well as unsulfated regions of chondroitin sulfate, is an extracellular GBS protein that may contribute to strain invasiveness and thereby virulence. Hypothesis: Strains of GBS which express HYL are more invasive in a neonatal animal model. Method: A strain of GBS expressing HYL (Wild type) was identified and a strain of GBS without HYL (mutant) was created by insertional mutagenesis. Neonatal rat pups (<24 hours) were intratracheally inoculated with either the wild type (n=17) or the mutant GBS (n=17) and sacrificed six hours later. Blood was collected and organs were weighted. Blood and homogenized organs were plated at logarithmic dilutions, and GBS colony counts were performed 24 hours after plating, as a semi-quantitative measure of GBS invasiveness.
Results: The GBS counts from the blood, lung, spleen, and kidney (adjusted for organ weight) did not differ in the rat pups receiving wild-type strain versus those receiving the mutant strain.
Conclusions: The presence or absence of hyaluronidase did not affect the dissemination of GBS in this neonatal rat pup model.
Speculation: If GBS hyaluronidase does, in fact, play a role in pathogenesis in human infants, our rat pup results suggest that it probably is not during the initial systemic invasion of the bacteria from the lungs into the circulation.
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Philips, J., Ambalavanan, N., Ware, J. et al. Group B Streptococcal Hyaluronidase Does Not Increase Systemic Bacterial Invasion in a Neonatal Rat Pup Model. Pediatr Res 45, 272 (1999) doi:10.1203/00006450-199904020-01620