Capsular hyaluronic acid of equine isolates of Streptococcus zooepidemicus is upregulated at temperatures below 35°C.

This research investigates how temperature variation influences the expression of a certain bacterial capsule, specifically in Streptococcus zooepidemicus, a bacterium causing respiratory and other infections in horses.

Research Objective

• The main purpose of this study was to comprehend the molecular basis of increased expression of the bacterial capsule from the equine isolates of the Streptococcus zooepidemicus bacteria at temperatures below 35 degrees Celsius.

Methodology

• An observational study was conducted where the capsule production of equine S. zooepidemicus strains was determined at various temperatures – 23, 30, 35, and 37 degrees Celsius.
• Further, Hyaluronidase or HylC (an enzyme capable of breaking down hyaluronic acid) at temperatures of 23 and 37 degrees Celsius was measured using a quantitative enzyme-linked immunosorbent assay.
• The expressions of genes, hasA and hylC, at temperatures 23 and 37 degrees Celsius were quantified using quantitative reverse transcriptase-PCR.
• The covRS genes present in the S. zooepidemicus were sequenced and examined for mutations.

Results

• Temperature shift to 23°C resulted in S. zooepidemicus strains becoming mucoid or exhibiting a noticeable increase in colony mucoidy.
• The expression of hasA was found to be 45 to 700 times greater at 23°C than at 37°C, while hylC transcription was 2.5 to 200 times higher at 23°C compared to 37°C.
• Despite higher transcription of hylC at lower temperatures, enzyme concentrations in cultures were significantly higher at 37°C, indicating post-transcriptional regulation of HylC production.
• The research found no mutations in the covRS genes in S. zooepidemicus similar to Streptococcus pyogenes strains with increased capsule production at 25°C.

Conclusions

• The findings suggest that while sensitivity of capsule expression to temperature is higher above 35°C, it is not required for prolonged colonisation or opportunist invasion, indicating that the bacterial capsule might not be necessary.
• Low-temperature capsule production might reflect the bacteria’s adaptation to life on skin and mucosal surfaces, where the hyaluronic acid capsule contributes to adhesion and dehydration resistance.
• It is proposed that the pathogenicity of S. zooepidemicus following opportunist invasion may depend on factors other than the capsule, potentially co-regulated with HylC.