This study was performed to determine the effect of influenza virus challenge on circulating cardiac troponin I (cTnI) concentrations in ponies. In people, viral infections are a common cause of myocarditis. Similarly, myocardial damage/myocarditis is thought to occur secondary to viral respiratory infections in horses. However there is a lack of published information in the equine literature confirming a causal relationship between viral infections and myocarditis. The hypothesis was that influenza virus infection in ponies would cause myocardial damage, detectable by elevations in plasma cTnI. cTnI is a sensitive and specific biochemical marker for myocardial damage with utility in horses, and has been used to monitor viral-associated myocarditis in people and in experimental models.
The study included 29 influenza-naïve yearling ponies: 23 were part of an influenza vaccine study, with 11 unvaccinated ponies (UN) and 12 that received a primary vaccination series 6 months previously with RecbombitekTM (Merial) (VAC). These 23 ponies were challenged with 108 EID50 influenza virus A/eq/Kentucky/91 using a nebulizer. An additional 6 ponies, housed in a similar manner but not exposed to influenza, were used as controls (CON). Physical examinations and body weights were recorded, and heparinized blood collected from all groups 1 day prior to challenge, and on days 1, 3, 5, 7, 10, 14, 21, 24 and 28 after challenge. Repeated measures ANOVA, chi-square, and/or clustered regression analyses were used to evaluate possible relationships among the various treatment groups and cTnI. Significance was set at P<0.05.
All virus challenged ponies developed typical clinical signs of infection. All CON ponies had normal cTnI concentrations at all time points (mean±SD, 0.00±0.01 ng/ml). One VAC pony (0.32 ng/ml on day 5) and two UN ponies (0.46 ng/ml on day 28, and 0.13 ng/ml on day 14) had cTnI concentrations greater than our upper normal limit of 0.08 ng/ml. At all other sample times, cTnI concentrations were < 0.05 ng/ml. There were no significant associations between body weight, temperature or clinical event score (an indicator of severity of clinical disease) and cTnI (P = 0.34, 0.93, and 0.13, respectively). There were no significant differences in cTnI between groups (mean±SD; CON, 0.00±0.01, VAC, 0.01±0.03 and UN, 0.01±0.05 ng/ml; P = 0.16). When separated into abnormal vs normal cTnI, there were 0/6 abnormal in CON, 1/12 in the VAC, and 2/11 in UN, with no significant differences between groups (p = 0.49).
This study shows that acute myocardial damage does not commonly occur secondary to influenza virus infection in sedentary ponies, however, transient elevations in cTnI suggesting mild myocardial damage do occur. Possible relationships in active performance horses, as opposed to sedentary ponies, as well as time points beyond 28 days should be examined.