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To evaluate transabdominal ultrasound-guided amniocentesis for detection of equid herpesvirus 1 (EHV-1)-induced fetal infection in utero.


4 Welsh Mountain mares.


Pregnant mares were inoculated intranasally with EHV-1 during the ninth month of gestation. Amniocentesis was initiated on postinoculation day (PID) 12, and was performed at 2- to 3-day intervals in standing mares under deep sedation. Amniotic fluid samples were tested by virus isolation (VI), polymerase chain reaction (PCR), and immunoperoxidase cytologic examination (IC) for detection of EHV-1.


Exposure to EHV-1 in the ninth month of gestation resulted in nasal shedding of infective virus, establishment of cell-associated viremia, and seroconversion. Equid herpesvirus 1 was detected by VI, PCR, and IC in amniotic fluid collected on PID 14 from 1 mare and on PID 16 and 17 from a second mare. Specimens of amniotic fluid from a third mare were VI negative until PID 18, when collections ceased, although this mare subsequently aborted an EHV-1-infected fetus on PID 28. The fourth mare aborted an EHV-1 infected fetus on PID 14. The 2 mares with VI-positive amniotic fluid were each carrying an EHV-1 infected fetus in utero, confirmed by examination of the uterus, placenta, and fetus, using specific immunohistochemistry and in situ hybridization. Endothelial cells in the endometrium and allantochorion were often virus-infected, with accompanying vascular lesions. The fetus had been infected via the chorionic vasculature in the first and fourth mares, and by inhalation of infected amniotic fluid in the second mare.


Amniocentesis permits specific detection of EHV-1-induced fetal infection in utero.

Clinical Relevance

Amniocentesis may have a clinical role in the specific identification and isolation of mares carrying virus-infected fetuses during EHV-1- induced abortion epizootics. (Am J Vet Res 1997;58:997–1002)

Free access
in American Journal of Veterinary Research


Objective—To determine whether there was genetic linkage between the recurrent exertional rhabdomyolysis (RER) trait in Thoroughbred horse pedigrees and DNA markers in genes (the sarcoplasmic reticulum calcium release channel [RYR1] gene, the sarcoplasmic reticulum calcium ATPase [ATP2A1] gene, and the transverse tubule dihydropyridine receptor-voltage sensor [CACNA1S] gene) that are important in myoplasmic calcium regulation.

Animals—34 horses in the University of Minnesota RER resource herd and 62 Thoroughbreds from 3 families of Thoroughbreds outside of the university in which RER-affected status was assigned after 2 or more episodes of ER had been observed.

Procedures—Microsatellite DNA markers from the RYR1, ATP2A1, and CACNA1S gene loci on equine chromosomes 10, 13, and 30 were identified. Genotypes were obtained for all horses in the 4 families affected by RER, and data were used to test for linkage of these 3 loci to the RER phenotype.

Results—Analysis of the RYR1, CACNA1S, and ATP2A1 microsatellites excluded a link between those markers and the RER trait.

Conclusions and Clinical Relevance—It is likely that the heritable alterations in muscle contractility that are characteristic of RER are caused by a gene that is not yet known to cause related muscle disease in other species.

Full access
in American Journal of Veterinary Research