More from the International Conference on Equine Infectious Diseases, this time from guest blogger and bacteriologist-extraordinaire, Dr. John Prescott of the University of Guelph:

Stellar work on understanding strangles and Streptococcus equi subspecies equi was presented at the Ninth International Equine Infectious Disease conference in Lexington, Kentucky. Researchers at the Animal Health Trust in Newmarket, United Kingdom (Andrew and Carl Robinson) are working with Matthew Holden at the Sanger Centre in Cambridge to use NextGen sequencing to understand better the strangles bacterium, and the impact of the carrier state on the pathogen as it lurks in the guttural pouch. The abstracts of their work are freely available through the conference web site, http://www.eidc2012.com/.

A novel quantitative PCR (qPCR) based on two unique genes of S. equi was was described that will identify S. equi within 2 hours, with a sensitivity of 93% and specificity of over 96%. Not only is it more sensitive than culture but it also overcomes the effects of non-S. equi contaminants which can interfere with culture. Another development reported was an ELISA based on two antigens unique to S. equi that together have a similar sensitivity and specificity to the qPCR. Current thoughts are that the ELISA could be used as a serological test in screening for carriers, with the qPCR then being used on guttural pouch aspirates to confirm the carrier state, which would then be treated.

The strangles (equi) subspecies of S. equi has been thought to be genetically and immunologically identical, but sequencing the M protein SeM gene has shown that there are over 100 strains. Holden and his colleagues have used high throughput sequencing to characterize the genomes of an astonishing 240 isolates from different countries, including one strain from Canada. They have found that genomic diversity is even higher than SeM sequencing had suggested. As a result of this work, they identified a “fitter” clone (ST151) now spreading through the UK population at the expense of an older clone (ST179).

Most interestingly, they have identified the genetic changes occurring as outbreak strains adapt to their different life in the guttural pouch, which is where the organism hangs out in carrier horses. The adaptation involves discarding some genes, stopping the expression of others, but also duplicating others. According to Holden, a Sanger Centre genome veteran, the S. equi genome is more dynamic than any of the other pathogens with which he has worked. The big question is of course the impact of this adaptation on virulence, and the extent and speed with which these genetic adaptations can be reversed if and when the “carrier“ strains revert to cause acute strangles. There is a horrible suspicion that some may be able to borrow back the deleted genes from other S. equi strains in the guttural pouch.

Because of both its species- and niche-adaptation, strangles has all the characteristics of a bacterial infection that can be eradicated. The superb work being done at the Animal Health Trust, all based on genomics, is drawing the noose ever tighter around this ancient scourge of the horse.

– John Prescott, Department of Pathobiology, University of Guelph