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 could 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 United Kingdom.

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 could 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.

CONTACT: John Timoney, MVB, PhD, DSc, MRCVS—859/218-1106——University of Kentucky Maxwell H. Gluck Equine Research Center

This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd's, London, brokers, and their Kentucky agents.

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Equine Disease Quarterly

Equine Disease Quarterly is a quarterly equine disease research newsletter published by the University of Kentucky's Gluck Equine Research Center, and funded by underwriters at Lloyd's of London, brokers, and their agents.

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