In an upcoming article in Equine Veterinary Journal, which is available online at Wiley.com, John Timoney, MVB, PhD, DSc, MRCVS, and Sridhar Velineni, PhD, are co-authors on a study that looks at whether Streptococcus zooepidemicus can “up-regulate” at lower temperatures below 35°C (95°F). The study is titled “Capsular hyaluronic acid of equine isolates of Streptococcus zooepidemicus is up-regulated at temperatures below 35°C.” There is an article by Timoney at the end of this research report that gives more information about Streptococcus zooepidemicus.
Reasons for Performing Study
“Streptococcus zooepidemicus (Sz) causes opportunist respiratory and other infections in the horse. Capsule expression is highly variable and known to affect resistance to phagocytosis. Most clinical isolates producing small dry colonies at 37°C produce mucoid colonies at temperatures below 35°C.”
“The aim was to understand the molecular basis of increased capsule expression by equine isolates of Sz at temperatures less than 35°C.”
"Capsule production by groups of equine Sz strains was determined at 23, 30, 35 and 37°C. Hyaluronidase (HylC) at 23 and 37°C was measured by quantitative ELISA. hasA and hylC expression at 23 and 37°C were measured by qRT-PCR. covRS in representative Sz were sequenced and checked for mutations.”
“Colonies of randomly selected Sz strains became mucoid or showed marked increase in colony mucoidy following temperature shift to 23°C. hasA expression at 23°C was 45 to 700-fold greater than at 37°C. Transcription of hylC at 23°C was 2.5 to 200-fold greater than at 37°C yet enzyme concentrations in cultures were significantly higher at 37°C (p<0.05) suggesting production of HylC is post-transcriptionally regulated. The covRS gene in Sz was not mutated as seen in isolates of S. pyogenes with increased capsule production at 25°C.”
“Sensitivity of capsule expression to temperature above 35°C, but not hyaluronidase by the general population of equine Sz, indicates capsule is not required for extended colonization nor for opportunist invasion. Instead capsule production at lower than body temperature may reflect adaptation to life on skin and mucosal surfaces where hyaluronic acid contributes to adhesion and resistance to desiccation. Pathogenicity of Sz following opportunist invasion is possibly dependent on factors other than capsule that may be co-regulated with hyaluronidase.”
Sridhar Velineni, PhD, and John F. Timoney, MVB, PhD, DSc, MRCVS, of the University of Kentucky’s Gluck Equine Research Center.
Article from Equine Disease Quarterly
Timoney also published the following article on Streptococcus zooepidemicus in the Gluck Equine Research Center’s Equine Disease Quarterly in July 2013.
Streptococcus zooepidemicus – Only an Opportunist?
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.
Despite the diversity of equine isolates of S. zooepidemicus, emerging experimental evidence indicates that immune responses 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.