Molecular characterization of Streptococcus pyogenes isolates collected during periods of increased acute rheumatic

Lonnie J Miner1, Susan J Petheram, Judy A Daly

  • 1Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, UT, USA.

Abstract

Insights

Specific Streptococcus pyogenes strains, including emm3 and emm18.1, were linked to rheumatic fever (RF) resurgence in Salt Lake City during peak activity years. These strains were absent during periods of reduced RF incidence.

Area of Science:

  • Infectious Diseases
  • Microbiology
  • Epidemiology

Background:

  • Salt Lake City has experienced a persistent increase in rheumatic fever (RF) cases since 1985.
  • Understanding the specific microbial factors driving RF resurgence is crucial for public health interventions.

Purpose of the Study:

  • To investigate the emm genotypes of Streptococcus pyogenes associated with periods of high and low rheumatic fever activity in Salt Lake City.
  • To determine if specific emm types or clones correlate with RF resurgence.

Main Methods:

  • emm genotyping and multilocus sequence typing were performed on Streptococcus pyogenes isolates.
  • Isolates were collected from periods of increased and decreased RF activity in Salt Lake City.
  • Genotypic data was analyzed to identify correlations between emm types and RF incidence.

Main Results:

  • Multiple emm genotypes were detected during peak RF years (1985, 1998) and a low-activity year (1992).
  • emm3 and emm18.1 were prevalent in peak RF years but absent in the low-activity year.
  • emm12 and emmL28 showed significant elevation during a peak RF year compared to a non-peak year, and emm3/emm18.1 isolates demonstrated clonality.

Conclusions:

  • Specific emm genotypes, notably emm3 and emm18.1, were associated with increased rheumatic fever activity.
  • The absence of emm3 and emm18.1 during low RF activity periods suggests their critical role in resurgence.
  • Clonality of emm3 and emm18.1 indicates specific strains are driving RF outbreaks, with emm12 and emmL28 potentially contributing to RF persistence.

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