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Quantitative molecular viral loads in 7 horses with naturally occurring equine herpesvirus‐1 infection
Author(s) -
Estell K. E.,
Dawson D. R.,
Magdesian K. G.,
Swain E.,
Laing S. T.,
Siso S.,
Mapes S.,
Pusterla N.
Publication year - 2015
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/evj.12351
Subject(s) - viral load , medicine , horse , population , genotype , histopathology , gastroenterology , virology , virus , pathology , biology , paleontology , biochemistry , environmental health , gene
Summary Reasons for performing study Data associating quantitative viral load with severity, clinical signs and survival in equine herpesvirus‐1 myeloencephalopathy ( EHM ) have not been reported. Objectives To report the clinical signs, treatment, and temporal progression of viral loads in 7 horses with naturally occurring EHM and to examine the association of these factors with survival. Study design Retrospective case series. Methods The population included 7 horses with EHM presented to the University of C alifornia, D avis W illiam R . P ritchard Veterinary Medical Teaching Hospital from M ay to S eptember 2011. Horses were graded using a neurological grading scale. Daily quantitative PCR was performed on nasal secretions and whole blood. Treatment, survival, outcome and histopathology were reported. Results A t presentation, one horse was neurological grade 5/5 , 3 were grade 4/5 and 3 were grade 3/5 . All were treated with anti‐inflammatory drugs, valacyclovir and management in a sling if necessary. All were infected with equine herpesvirus‐1 of DNA polymerase D 752 genotype. Peak viral load in nasal secretions and blood of 5 survivors ranged from 6.9 × 10 3 to 2.81 × 10 5 (median 5.11 × 10 4 ) and from 143 to 4340 gB gene copies/million eukaryotic cells (median 3146), respectively. The 2 nonsurvivors presented with grade 3/5 neurological signs and progressed to encephalopathy. Peak viral load was higher in nonsurvivors, with levels in nasal secretions of 1.9 × 10 9 and 2.2 × 10 9 and in blood of 2.05 × 10 4 and 1.02 × 10 5 gB gene copies/million eukaryotic cells. Case fatality was 2/7. Conclusions Nonsurvivors had viral loads 1000‐fold higher in nasal secretions and 10‐fold higher in blood than survivors. There was no relationship between severity of clinical signs at presentation and survival. Thus, encephalopathy and high viral load were negatively associated with survival in this population. Further research should be performed to determine whether high viral loads are associated with encephalopathy and poor prognosis. The Summary is available in Chinese – see Supporting information .