Pneumonia in young horses is a difficult problem to face whether you have hundreds of foals each year or only a couple. Pneumonia often have cultures taken to determine the causative bacteria and put the youngster on an antibiotic to which the bacteria is susceptible. In this article from the University of Kentucky’s Gluck Equine Research Center, John Timoney, MVB, MRCVS, MS, PhD, talks about how Streptococcus species invade and move around in the horse.
The good news is that despite the diversity of equine isolates of S. zooepidemicus found in young horses with pneumonia, emerging experimental evidence indicates that immune responses that are cross-protective for different strains can be generated. This discovery will be a significant asset in the development of effective vaccines to combat Streptococcal respiratory infections.
The association of a Streptococcus sp. with cases of equine fibrinous pneumonia was first reported in 1887 by the German bacteriologist J. W. Schultz. Now known as S. zooepidemicus, this organism is the most frequently isolated bacterial pathogen of the respiratory tract of weanling and yearling horses. Many of these infections are secondary to respiratory viral infections or to transportation of extended duration.
Although different genetic and serologic variants (serovars) of S. zooepidemicus co-colonize the tonsillar complex of most healthy horses, only a single Streptococcal clone is usually found in disease of the lower respiratory tract, a clone being isolates of a bacterial species that are indistinguishable in genotype. The invading clone varies from foal to foal in a group, although the same clone may affect more than one foal in that group. Genetic testing for specific genes in bacterial isolates can provide a valid, cost-effective approach to epidemiologic studies based on sequencing.
Most equine respiratory infections associated with S. zooepidemicus appear to be endogenous involving expansion of a clone similar to those in that animal’s tonsillar complex. Nevertheless, outbreaks of respiratory disease involving specific clonal genotypes transmitted in a geographic area over an extended time period have been observed in recent years. Each outbreak was associated with a different sequence type of S. zooepidemicus, a phenomenon similar to that observed with increasing frequency in dog shelters in North America, South Korea and the UK.
The enhanced virulence/transmissibility of epidemic Streptococcal clones is probably explained by genetic rearrangement or acquisitions that affect expression of virulence factors or increase their ability to proliferate and damage respiratory tissue or avoid innate immune defenses. For instance, acquisition of sequence that encodes a binding site for plasminogen in a virulence protein would create sites on the bacterial surface with plasmin-associated proteolytic activity for host cell or plasma components. Rapid proliferation accompanied by shedding of large numbers of streptococci from the respiratory tract would favor onward transmission of the clone.
The extreme diversity of S. zooepidemicus of equine origin and evidence that it has acquired DNA by lateral horse-to-horse transfer from other streptococci suggest emergence of novel clones may be a frequent event. The mechanism and site of these transfers are unknown. However, DNA elements that can mediate genetic transfer to recipient strains of S. agalactiae are present in the chromosomes of some strains of S. zooepidemicus. Another potential mechanism involves direct uptake and exchange of DNA, an extremely efficient process between co-colonizing strains of S. pneumoniae in the human nasopharynx, an environment, that physically at least, closely mimics that of the equine tonsillar crypt.