Administration of a DNA immunostimulant does not mitigate bovine herpesvirus-1 recrudescence in dexamethasone challenged beef cattle
Abstract: The study objective was to determine the effect of a DNA immunostimulant on recrudescence of bovine herpes virus-1 (BHV-1) after dexamethasone challenge. It was hypothesized that the DNA immunostimulant would mitigate stress-induced immunosuppression; thereby, reducing the incidence of BHV-1 recrudescence. Steers (n=10) and heifers (n=10) (initial BW = 489 kg ± 57 kg) were stratified by pre-existing BHV-1 antibody titer, sex and initial BW and randomly assigned to treatment (n=4 pens/treatment; 2 or 3 animals/pen). Calves were administered 40 mg of dexamethasone intravenously at 0600 h from d 0 to 2. On d 1 calves were administered 2 mL of DNA immunostimulant (Zelnate; ZEL) or sterile saline (CON) based on treatment assignment. Whole blood was collected for complete blood count (CBC) analysis and nasal swabs were collected to determine BHV-1 prevalence via virus isolation testing. A repeated measures mixed model was used to test the effect of treatment, day and their interaction for CBC variables. There was a treatment × day interaction for eosinophils (P = 0.02) and percent eosinophils (P = 0.03). Eosinophils were greater (P < 0.01) for ZEL on d 3 and 6 post-dexamethasone challenge. On d 11 and 12, eosinophils for CON rebounded such that their concentration was greater than ZEL (P < 0.01). Lymphocytes, neutrophil and monocyte concentration did not differ; however, a day effect (P < 0.01) existed such that each variable increased transiently after dexamethasone challenge. All cattle had BHV-1 present in a nasal swab sample on at least one sample day, with prevalence of BHV-1 in nasal swab samples being greatest on d 5 (80% positive virus isolation rate overall; P = 0.01). However, no treatment differences were detected for BHV-1 prevalence in this study. The DNA immunostimulant altered eosinophil concentrations but did not mitigate BHV-1 recrudesce after dexamethasone challenge.
Hannah A. Seiver*
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