The anti-viral effect of valacyclovir was evident in the study horses, as viremia decreased from 42% at onset of treatment to 0% within 7 days

The anti-viral effect of valacyclovir was evident in the study horses, as viremia decreased from 42% at onset of treatment to 0% within 7 days. EHV-1 in blood and/or nasal secretions via qPCR, while subclinically infected horses had detectable EHV-1 mainly in nasal secretions. The majority of infected horses showed a rise in antibody titers to EHV-1 Silvestrol aglycone during the outbreak. All 31 horses were treated with valacyclovir, while clinically infected horses further received flunixin meglumine and sodium heparin. This investigation highlights various relevant aspects Silvestrol aglycone of an EHV-1 outbreak caused by a new H752 genotype: (i) importance of early detection of EHV-1 infection; (ii) diagnostic challenge to assess H752 genotype; (iii) apparent benefit of valacyclovir use in the early stage of the outbreak; and (iv) weekly testing of blood and nasal secretions by qPCR in order to monitor individual infection status and lift Rabbit Polyclonal to CDX2 quarantine. gene, while the genotype assays were unable to differentiate between D752 and N752. The unusual molecular results and lack of systemic clinical signs at the exception of fever prompted the investigation of this outbreak. In the following 35 days, each of the 31 horses was monitored daily for abnormal physiological parameters, blood and nasal secretions were collected once weekly for the qPCR detection of EHV-1 and blood was collected 35 days apart to measure specific antibodies to EHV-1. The horse population was composed of 14 geldings and 17 mares, aged 1 to 27 years (median 4 years). Various breeds were represented, including Warmblood (24 horses), Welsh pony (4), Thoroughbred (2), and Thoroughbred/draft horse cross (1). Twenty-seven horses were kept in the main barn and 4 horses were stabled in a shed row barn located 30 m from the entrance to the main barn. Throughout the 35-day observation period, 26/31 horses developed fever with peak temperatures ranging from 38.7 C to 41.0 C (median 39.3 C, Table Silvestrol aglycone 1). The fever lasted from 1 to 8 days (median 2.5 days). Additional clinical signs reported included anorexia (7 horses), distal limb edema (3), and mild neurological deficits such as ataxia, weakness and proprioceptive deficits (4). Twenty-one horses developed abnormal clinical signs during the first week of the outbreak, while 2 and 3 horses developed abnormal clinical signs during the second and third week of the outbreak, respectively. Five horses did not develop any abnormal clinical signs during the entire observation period. Table 1 Clinical, molecular and serological results from 31 horses involved in an EHV-1 outbreak. target genes/million cells. Table 2 EHV-1 qPCR viral load results in nasal secretions and blood from 31 horses involved in an EHV-1 outbreak. target genes per million cells. Treatment of the study horses consisted of the administration of valacyclovir (Camber Pharmaceuticals, Piscataway, NJ, USA) in all horses, and flunixin meglumine (Merck Animal Health, Madison, NJ, USA) and sodium heparin (Sagent Pharmaceuticals, Schaumburg, IL, USA) in all febrile horses (Table 3). All horses treated with valacyclovir experienced a strong decline in EHV-1 viral load in nasal secretions and all horses had no detectable EHV-1 by qPCR in blood on day 7. However, susceptibility to EHV-1 in horses remained, as exemplified by five horses that showed clinical and molecular evidence of EHV-1 infection after the valacyclovir treatment was discontinued. Table 3 Treatment administered to 31 horses involved in an EHV-1 outbreak. gene. Sequencing was performed since all EHV-1 qPCR positive horses tested only positive when targeting the gene and could not be further characterized into either a D752 or a N752 genotype. The 663 bp product of the gene showed 100% homology among the five individual horses. A single nucleotide polymorphism, cytosine, was found at position 2254, translating into histidine at position 752 of the amino acid sequence (H752). The origin of the outbreak could not be determined with certainty. However, one month prior Silvestrol aglycone to the onset of the outbreak, a mare was referred to a local hospital for an elective procedure. The mare returned to the performance horse barn, where she stayed for 2 weeks before leaving for another barn. On the two-week recheck (end of February), the mare appeared in good health and displayed normal physical findings. In early March, the local hospital reported on a hospitalized horse that Silvestrol aglycone was diagnosed with EHM and was euthanized within hours of admission. The diagnosis of EHM was further confirmed on necropsy. DNA of this horse was available for the gene sequencing. Two days later, one additional horse, stabled in the adjacent state of Maryland, was diagnosed with EHM.. This horse was already recumbent when seen on emergency by the ambulatory service and was euthanized. It had direct contact to a horse that came back from the local hospital about 3 weeks earlier, but had exhibited hind limb edema and discomfort thought to be laminitis-related about 1 week prior to becoming acutely recumbent. DNA from the second EHM.