| dc.description.abstract | Streptococcus equi subsp. equi (SEE) is the bacterium that causes the equine respiratory disease known as strangles. Strangles is endemic worldwide among horses. Despite its apparent prevalence and costs to equine agriculture, limited data exist regarding the molecular epidemiology of SEE from the United States (US). Thus, we conducted a series of genomic studies of SEE isolates from the US. First, we showed that mutations are rare in the genomes of SEE from an outbreak, and that some US isolates are closely related to SEE strains from other countries. Collectively, these data improved our understanding of phenotypic and genotypic variation of isolates within an outbreak, and the international distribution of SEE. Next, we compared the genomes and methylomes of US isolates of SEE with its multi-host ancestor Streptococcus equi subsp. zooepidemicus (SEZ) to identify a molecular basis for the host-specificity of SEE. We identified mobile genetic elements and methylation of genes that differed between SEE and SEZ, and are thus candidates for further investigation for their role in host-specificity of SEE. Because SEE does not survive in the environment for an extended period and has no known biological vectors, and because most horses develop prolonged immunity following recovery from disease, the persistence of strangles must be attributable to survival in horses that shed the bacterium without showing clinical signs (a.k.a. carrier horses). Thus, we examined the genomes of SEE isolates from carrier horses from the US and Europe. Whole genome sequencing of carrier and clinical SEE isolates from Pennsylvania and Sweden revealed neither significant nor consistent differences in the genomes or methylomes between carrier and clinical strains, and RNA sequencing of SEE isolates from Pennsylvania demonstrated no differentially expressed genes between clinical and carrier isolates of SEE. These results indicate that pathogen-adaptations of SEE are unlikely to explain the carrier state. Together, our findings indicate that genetic changes occur among isolates within outbreaks and within individual hosts, and that host factors are most likely to drive the carrier state. The host-specificity of SEE might have arisen from acquisition of mobile genetic elements or differential methylation of specific genes. | en |
