Objective To assess the efficacy of compounded cidofovir, famciclovir, and ganciclovir for the treatment of feline herpesvirus type 1 (FHV‐1) ocular surface disease. Animals studied 132 shelter‐housed cats qPCR positive for FHV‐1. Procedures A masked placebo‐controlled study design was utilized. Animals were enrolled in one of four treatment groups: topical ocular placebo + oral placebo (n = 32), compounded cidofovir 0.5% ophthalmic solution + oral placebo (n = 32), compounded famciclovir oral solution (90 mg/kg) + topical ocular placebo (n = 32), and compounded ganciclovir 0.15% ophthalmic solution + oral placebo (n = 36). Cats were treated with each medication twice daily for 7 days and were evaluated on Day 1 and Day 8 using an ocular scoring system, body weight, and qPCR for FHV‐1 viral load. Results Cidofovir significantly decreased viral load from Day 1 to Day 8 compared with placebo (p = .024). Neither famciclovir nor ganciclovir decreased viral load compared with placebo (p = .14, p = .41). There was no significant improvement of ocular scores for any drug group compared with placebo (p = .62). In all groups, 65%–75% of cats improved from Day 1 to Day 8. Juvenile cats had a significant increase in weight gain compared with placebo for cidofovir (p = .025) and ganciclovir (p = .023). All corneal ulcers in placebo animals failed to heal whereas 77% of ulcers in antiviral group animals healed. Conclusions Topical ophthalmic cidofovir significantly decreased ocular FHV‐1 viral shedding and increased weight gain in juvenile cats. Ganciclovir increased weight gain in juvenile cats. Compounded famciclovir demonstrated limited efficacy for the treatment of FHV‐1 ocular surface disease in shelter‐housed cats.
Feline herpesvirus type 1 (FHV-1) is endemic in captive cheetahs and sporadically causes devastating disease. Modified live vaccines (MLV), intended for use in domestic cats, are used in some captive cheetah populations and have been anecdotally linked to disease in certain subpopulations. Ten FHV-1 isolates from ten captive cheetahs and one isolate from an MLV used to inoculate four of the host animals were analyzed. Viral DNA was extracted for full-genome sequencing by Illumina MiSeq with viral genomes then used for phylogenomic and recombinational analyses. The FHV-1 shed by vaccinated cheetahs were almost identical to the MLV, with few variants among viral genomes. Eight cheetah FHV-1 isolates and the MLV were grouped in a clade along with FHV-1 isolates from domestic cats in the USA. The remaining two cheetah FHV-1 isolates (unknown host vaccine status) were not associated with a clade. The likely ancestral origin of these two isolates involves recombination events between Australian domestic cat and cheetah FHV-1 isolates. Collectively, these data suggest that the MLV is capable of causing clinical disease and viral shedding in some cheetahs and represents evidence of interspecies transmission of virus between domestic and wild cats.
Canid alphaherpesvirus 1 (CHV-1) is a widespread pathogen of dogs with multiple associated clinical signs. There has been limited prior investigation into the genomics and phylogeny of this virus using whole viral genome analysis. Fifteen CHV-1 isolates were collected from animals with ocular disease based in the USA. Viral DNA was extracted for Illumina MiSeq full genome sequencing from each isolate. These data were combined with genomes of previously sequenced CHV-1 isolates obtained from hosts in the UK, Australia and Brazil. Genomic, recombinational and phylogenetic analysis were performed using multiple programs. Two isolates were separated into a clade apart from the remaining isolates and accounted for the majority of genomic distance (0.09%): one was obtained in 2019 from a USA-based host (ELAL-1) and the other in 2012 from a host in Brazil (BTU-1). ELAL-1 was found to contain variants previously reported in BTU-1 but also novel variants in the V57 gene region. Multiple non-synonymous variants were found in USA-based isolates in regions associated with antiviral resistance. Evidence of recombination was detected between ELAL-1 and BTU-1. Collectively, this represents evidence of trans-boundary transmission of a novel form of CHV-1, which highlights the importance of surveillance for this pathogen in domestic dog populations.
Objective To determine whether wetting length of Schirmer tear test (STT) strips varies by commercial manufacturer of test. Animals Studied Ten normal female beagle cross‐breed dogs. Procedures Schirmer tear test strips from four commercial manufacturers were used to assess wetting lengths in‐vitro when exposed to a set volume of water over 1 minute. Digital photography was used to assess the total surface area of Schirmer strips from each manufacturer. Schirmer tear test type 1 was performed on normal dogs over 1 minute with STT strips from the same four commercial manufacturers in a randomized crossover design. ANOVA was used to detect differences between strips from different manufacturers. Results Significant differences in wetting length were found between STT strips from different manufacturers in‐vitro (P < .0001) and in‐vivo (P < .0001). STT wetting lengths for the in‐vitro experiments (mean ± SD) were 21.2 ± 0.8 mm (Amcon Laboratories), 27.8 ± 2.7 mm (Merck Animal Health), 30.0 ± 1.7 mm (HUB pharmaceuticals), and 31.5 ± 2.3 mm (Gulden Ophthalmics). STT wetting lengths for the experiments in live dogs (mean ± SD) were 17.5 ± 3.4 mm (Amcon Laboratories), 24.8 ± 3.9 mm (Merck Animal Health), 26.5 ± 3.7 mm (HUB pharmaceuticals), and 24.0 ± 3.9 mm (Gulden Ophthalmics). The surface area of STT strips were found to vary between different manufacturers. Conclusions Schirmer tear test type 1 results in dogs are affected by choice of STT strip commercial manufacturer. It is proposed that guidelines are created for the standardization of future STT strip production.
Feline herpesvirus type 1 (FHV-1) commonly causes ocular surface disease in cats and is treated with antiviral medications targeting viral DNA polymerase (UL30/42). Herein, we describe a method to assess the FHV-1 genome for mutation development and to assess the functional impact of mutations, if present. Fourteen shelter-housed domestic cats with FHV-1 ocular surface disease were assigned to one of four treatment groups: placebo (n = 3), cidofovir 0.5% ophthalmic solution (n = 3), famciclovir oral solution (n = 5), or ganciclovir 0.15% ophthalmic solution (n = 3). Swabs were collected before (day 1) and after (day 8) 1 week of twice-daily treatments to isolate viable FHV-1. Viral DNA was extracted for sequencing using Illumina MiSeq with subsequent genomic variant detection between paired day 1 and day 8 isolates. Plaque reduction assay was performed on paired isolates demonstrating non-synonymous variants. A total of 171 synonymous and 3 non-synonymous variants were identified in day 8 isolates. No variants were detected in viral UL23, UL30, or UL42 genes. Variant totals were not statistically different in animals receiving antiviral or placebo (p = 0.4997). A day 8 isolate from each antiviral treatment group contained a single non-synonymous variant in ICP4 (transcriptional regulator). These 3 isolates demonstrated no evidence of functional antiviral resistance when IC50 was assessed. Most (10/14 pairs) day 1 and 8 viral isolate pairs from the same host animal were near-identical. While functional variants were not detected in this small sample, these techniques can be replicated to assess FHV-1 isolates suspected of having developed resistance to antiviral medications.
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