equine herpesvirus Flashcards
EHV-1 and EHV-4 introduction
AKA rhinopneumonitis, seen primarily in young horses at the time of weaning and beginning of training, 80-90% of horses are exposed to the virus by the age of 2, majority of horses run a mild respiratory disease (like a common cold), disease is acute, treatment is palliative (ban amine, fluids etc.) and prognosis is favorable, natural transmission happens by contact with another infected horse, aerosolized respiratory secretions or virus-contaminated fomites
types of EVH
EHV 1-5 infect horses, EHV 6-9 infect wild horses and zebras, EHV 1 and 4 are the most important, closely related but antigenically distinct with different disease profiles
distinguishing features of EHV 1 and EHV 4
EHV 1 infects a variety of cell types: respiratory, epithelial, endothelial, neuronal, lymphoid cells, EHV 1 is more virulent and can cause neurologic disorders, abortion (due to vasculitis), neonatal death, ocular disease and death
EHV 4 is more commonly isolated from mild respiratory cases and prognosis is favorable
similarities of EHV 1 and 4
both are enveloped viruses that make them highly susceptible to destruction by common disinfectants
main reservoir of EHV 1 and 4
latently infected horses (horse that is carrying the virus and begins shedding it due to stress), at stud farms foals acquire the virus from adult mares that shed the virus asymptomatically
How is EHV spread?
lives in the environment an average of 7 days, spread through direct horse to horse contact and indirect contact (fomites, personnel), very contagious, morbidity can reach 100%
risk factors for EHV outbreaks
overcrowding, heavy parasite burden, poor nutritional state, climatic extremes, concurrent disease and the intermingling of animals from different social groups (separate animals based on age/use), even if you have a closed herd, you can still have outbreaks
EHV latency
large majority of recovered horses carry a latent EHV infection for life in the t lymphocytes and the neurons of the trigeminal ganglia (cranial nerve that aids in feeling/movement of jaw), reactivation of the virus occurs after transport, rehousing, weaning, inclement weather, surgery, corticosteroid administration etc., reactivation is not accompanied by respiratory clinical signs, but the shedding of virus particles may infect other horses, reactivation may cause abortion due to destruction of blood vessels or endothelial cells in uterus
EHV 1 pathogenesis
replicates in upper respiratory tract, infects endothelial cells, lymphocytes and monocytes, viremia (virus reaches the blood stream and goes all over the body including the uterus and CNS), causes vasculitis and ischemia in the CNS and uterus, resulting in late term abortionthe virus reaches the trigeminal neurons 48 hours after infection and establishes latency
EHV 4 pathogenesis
replicates in the upper respiratory tract, has low affinity for endothelial cells, does not establish viremia so it does not cause abortion or neurologic disease, respiratory disease that may have started with EHV (1 or 4) predisposes the affected horses to opportunistic bacterial infections leading to bacterial pneumonia
EHV 4 clinical signs
mild respiratory disease but may lead to secondary bacterial pneumonia, young animals have a more serious disease-depression, anorexia, biphasic fever (days 1-2 and 6-7), nasal discharge and ocular discharge
older animals or previously exposed show very mild respiratory disease or no sign of disease
EHV 1 clinical signs
uncommon to cause clinically apparent respiratory disease, except for very young foals infected with a highly virulent strain, mares abort, but without previous signs of respiratory disease
incubation period of EHV
up to 10 days
EHV vs flu clinical signs
in EHV cough is not a major clinical sign, except if horse is kept in unclean environment or is not rested from training/performance activities
diagnosis
laboratory: virus isolation, CSF, serology
very difficult to detect latently infected horses
