Key result
Equine influenza virus challenge in yearling ponies did not significantly increase cardiac troponin I concentrations compared to unexposed controls, showing no evidence of severe myocardial necrosis.
Why the study?
Does equine influenza virus challenge cause myocardial damage detectable by increased cTnI in ponies?
Does equine influenza virus challenge cause myocardial damage detectable by increased cTnI in ponies?
Absolute Event Rate: 13% vs 0%
Equine influenza virus challenge in ponies does not cause severe myocardial necrosis, though transient cTnI increases suggest possible mild myocardial damage.
Reduces concern for severe myocardial necrosis in equine influenza models; leaves open mild or transient injury in natural infections.
BACKGROUND: Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence. HYPOTHESIS/OBJECTIVES: We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations. ANIMALS: Twenty-nine influenza-naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 10⁸ EID₅₀ EIV A/eq/Kentucky/91 6 months after vaccination. Six age-matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls. METHODS: Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi-square, or clustered regression analyses were used to identify relationships between each group and cTnI. RESULTS: All EIV-infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was < 0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups. CONCLUSIONS AND CLINICAL IMPORTANCE: This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 10⁸ EID₅₀ EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur.
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Durando et al. (2011) studied Equine influenza virus infection (n=29). Equine influenza virus (EIV) challenge vs. Healthy, unvaccinated, unexposed controls was evaluated on Plasma cardiac troponin I (cTnI) concentrations. Equine influenza virus challenge in yearling ponies did not significantly increase cardiac troponin I concentrations compared to unexposed controls, showing no evidence of severe myocardial necrosis.
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