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Biology subjects

Karen F Steward

Publications and source records attributed to Karen F Steward.

2 recordsLinked to original sources

Genomic dissection of an Icelandic epidemic of equine respiratory disease

The native horse population of Iceland has remained free of major infectious diseases. Between May and July 2010 an epidemic of respiratory disease swept through the population. Initial microbiological investigations ruled out known equine viral agents as the cause of the infections, but identified the opportunistic pathogen Streptococcus zooepidemicus as being frequently isolated from diseased animals. This diverse bacterial species has a broad host range and is usually regarded as a commensal of horses. By genome sequencing S. zooepidemicus recovered from horses during the epidemic we show that although multiple clones of S. zooepidemicus were present in the population, one particular clone, ST209, was responsible for the epidemic. Concurrent with the epidemic, ST209 caused zoonotic infections, highlighting the pathogenic potential of this clone. Phylogenetic analysis suggests that the original ST209 strain entered Iceland in late 2008 or early 2009. Epidemiological investigation revealed that the incursion of this strain into a training yard that utilized a submerged treadmill between the 5th and 19th of February 2010 was a critical trigger for the ensuing epidemic of disease, provided a nidus for the infection of multiple horses, and subsequent distribution of these animals to multiple sites in Iceland.

Microbiology

Genome specialization and decay of the strangles pathogen, Streptococcus equi, is driven by persistent infection

Strangles, the most frequently diagnosed infectious disease of horses worldwide, is caused by Streptococcus equi. Despite its prevalence, the global diversity and mechanisms underlying the evolution of S. equi as a host-restricted pathogen remain poorly understood. Here we define the global population structure of this important pathogen and reveal a population replacement in the late 19th or early 20th century, contemporaneous with a spate of global conflicts. Our data reveal a dynamic genome that continues to mutate and decay, but also to amplify and acquire genes despite the organism having lost its natural competence and become host-restricted.\n\nThe lifestyle of S. equi within the horse is defined by short-term acute disease, strangles, followed by long-term carriage. Population analysis reveals evidence of convergent evolution in isolates from post-acute disease samples, as a result of niche adaptation to persistent carriage within a host. Mutations that lead to metabolic streamlining and the loss of virulence determinants are more frequently found in carriage isolates, suggesting that the pathogenic potential of S. equi reduces as a consequence of long term residency within the horse post acute disease. An example of this is the deletion of the equibactin siderophore locus that is associated with iron acquisition, which occurs exclusively in carrier isolates, and renders S. equi significantly less able to cause acute disease in the natural host. We identify several loci that may similarly be required for the full virulence of S. equi, directing future research towards the development of new vaccines against this host-restricted pathogen.

Microbiology