Bug of the Month: Streptococcus equi
This post was written by guest author Dr. John Prescott, Professor, Department of Pathobiology, University of Guelph.
April’s "bug of the month" is Streptococcus equi subspecies equi, the cause of equine strangles, specifically strain 4047. This is the first strangles strain to have its entire genome (i.e. all of its DNA, including every gene) sequenced. The March 2009 issue of the open-access journal Pathogens, published by the Public Library of Science (PLoS), describes how British scientists think the strangles organism evolved to be such a scourge of horses, by comparing its genome to that of the first equine Streptococcus equi subspecies zooepidemicus strain to also have its genome sequenced, strain H70. It is believed that S. zooepidemicus was the ancestor of the S. equi that causes strangles.
Like all evolution, the story involves both loss and gain. As far as loss is concerned, the strangles organism has more genes that have been "turned-off" (inactivated genes) than does S. zooepidemicus. These genes were turned off by a large number of extra pieces of DNA called insertion sequences which S. equi picked up over time. These sequences get inserted in many different places within the bacterium's DNA (its genome) leading to inactivation or loss of various genes. Loss of genes in this manner can often result in bacteria becoming restricted to a particular type of host - S. equi essentially only infects horses and other equids, while S. zooepidemicus still has a broader host range.
What S. equi lost by becoming restricted to equids, it gained by becoming a nastier bug. It did this by becoming "infected" by four unique bacterial viruses. (Bacterial viruses are viruses that only infect bacteria. Some of these viruses "transmit" (transfer) genes to the bacteria they infect but leave the bacteria alive. Other bacterial viruses can kill bacteria after infecting them). Most bacteria have anti-viral defense mechanisms to protect themselves from these viruses, but S. equi's defenses may have been damaged or turned-off by insertion sequences. Being infected by these four bacterial viruses gave S. equi many genes not found in S. zooepidemicus. One of these viruses is thought to be capable of leaving S. equi and killing S. zooepemidicus in the horse’s throat - a useful trick for S. equi to wipe out the competition in this area so it can move in more easily and cause infection. A second virus gives the strangles organism a phospholipase enzyme which is known to be involved in the bacterium's ability to cause disease. The third and fourth viruses each donated two different superantigen genes – these genes help S. equi to cause inflammation and impair the ability of the immune system to fight off the bacteria. A unique additional piece of “foreign” DNA that S. equi acquired is associated with the ability to capture iron. This allows S. equi to grow better in infections than S. zooepidemicus, because the body of the infected host will often try to bind up as much iron as possible so the bacteria can’t use it to grow. The scientists speculate that this iron-capturing gene was the key to starting S. equi on its evolutionary spiral to becoming a major horse pathogen.
A final thought is that the bacterial viruses that made S. equi what it is today have many similar DNA sequences to bacterial viruses found in Streptococcus pyogenes, a major human bacterial pathogen. Humans might have had an unwitting hand in creating this pathogen from one of their own.
More information on strangles can be found on the equIDblog Resources page.
