RESUMO
Vaccination is an effective tool to limit equine influenza virus (EIV H3N8) infection, a contagious respiratory disease with potentially huge economic impact. The study assessed the effects of antigenic change on vaccine efficacy and the need for strain update. Horses were vaccinated (V1 and V2) with an ISCOMatrix-adjuvanted, whole inactivated virus vaccine (Equilis Prequenza, group 2, FC1 and European strains) or a carbomer-adjuvanted, modified vector vaccine (ProteqFlu, group 3, FC1 and FC2 HA genes). Serology (SRH, HI, VN), clinical signs and viral shedding were assessed in comparison to unvaccinated control horses. The hypothesis was that group 2 (no FC2 vaccine strain) would be less well protected than group 3 following experimental infection with a recent FC2 field strain (A/equi-2/Wexford/14) 4.5 months after vaccination. All vaccinated horses had antibody titres to FC1 and FC2. After challenge, serology increased more markedly in group 3 than in group 2. Vaccinated horses had significantly lower total clinical scores and viral shedding. Unexpectedly, viral RNA shedding was significantly lower in group 2 than in group 3. Vaccination induced protective antibody titres to FC1 and FC2 and reduced clinical signs and viral shedding. The two tested vaccines provided equivalent protection against a recent FC2 EIV field strain.
RESUMO
Vaccination is one of the most effective tools for limiting the impact of equine influenza (EI). The humoral immunity established following a primary vaccination course can decrease significantly between the second (V2) and third immunisations (V3), leaving some horses insufficiently protected for several weeks. This so-called "immunity gap" poses a challenge to all EI vaccines. During this period, the EI infection of vaccinated animals may be followed by marked clinical signs and virus shedding. However, several EI vaccines have been shown to stimulate equine influenza virus (EIV)-specific cell-mediated immunity, which is likely to play a role in protection against EIV infection and/or mitigate the clinical and virological signs of EI. Reducing the interval between V2 and V3 has been shown to be counterproductive to longer-term immunity. Further research is needed to define and address the "immunity gap" in horses. This study aimed to measure the level of protection induced by a whole inactivated, ISCOMatrix adjuvanted, EI and tetanus vaccine (Equilis Prequenza-Te) when challenged during the immunity gap (i.e., immediately before the recommended boost immunisation, more than 5 months after V2) using infection with a recent heterologous Florida Clade 2 (FC2) equine influenza virus (EIV) strain. This vaccine was tested in a Welsh mountain pony model. A group of seven ponies was vaccinated twice, 4 weeks apart. The protective antibody response was measured and ponies were challenged, along with 5 unvaccinated control ponies, by experimental infection with the FC2 A/eq/Northamptonshire/1/13 EIV strain, 158 days (around 5.2 months) after V2 and their clinical signs and virus shedding were monitored. EI serology was measured by single radial haemolysis (SRH) and haemagglutination inhibition (HI). Clinical signs and virus shedding (measured by qRT-PCR and hen's egg titration) were compared with controls. All vaccinates had detectable, low SRH antibody titres and most had detectable, low HI titres. Significant clinical and virological protection was observed in vaccinates (p < 0.05), supporting the good performance of this vaccine against a recent EIV strain. In this study, the impact of the immunity gap in ponies was limited after primary vaccination with this whole inactivated, ISCOMatrix adjuvanted EI and tetanus vaccine (Equilis Prequenza-Te) when infected several months after V2 with a recent FC2 strain, which is representative of EIV circulating in the EU.
RESUMO
This prospective, multicentre, non-blinded, open study followed 46 cats with diabetes mellitus during treatment with porcine lente insulin (also known as porcine insulin zinc suspension, Caninsulin, Intervet) for 16+/-1 weeks (stabilization phase), with additional monitoring of some cats (n=23) for a variable period. At least three of the following were present at initial presentation: appropriate history of clinical signs consistent with diabetes mellitus, glucosuria, blood glucose greater than 15 mmol/l and fructosamine greater than 380 micromol/l. Insulin treatment was started at a dose rate of 0.25-0.5 IU/kg body weight twice daily, with a maximum starting dose of 2 IU/injection. Twenty-eight of the cats were classed as reaching clinical stability during the study, in 23 of these cats this was during the stabilization phase. Seven cats went into remission during the stabilization phase and one of the cats in week 56. Clinical signs of hypoglycaemia, significantly associated with a dose of 3 units or 0.5 IU/kg or more per cat (twice daily), were observed in nine of the 46 cats during the stabilization phase and concomitant biochemical hypoglycaemia was recorded in most cases. Biochemical hypoglycaemia, recorded in 6% of the blood glucose curves performed during the stabilization phase, was significantly associated with a dose rate of 0.75 IU/kg or more twice daily. This further highlights the need for cautious stepwise changes in insulin dose. The protocol used in the present study is suitable for and easy to use in practice. This study confirmed the efficacy and safety of porcine lente insulin (Caninsulin) in diabetic cats under field conditions.
