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Title: Experimental induction of malignant catarrhal fever in pigs with ovine herpesvirus 2 by intranasal nebulization

Author
item Li, Hong
item BROOKING, A - Washington State University
item Cunha, Cristina
item Highland, Margaret
item O'TOOLE, D - University Of Wyoming
item Knowles Jr, Donald
item Taus, Naomi

Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/12/2012
Publication Date: 4/18/2012
Citation: Li, H., Brooking, A., Cunha, C.W., Highland, M.A., O'Toole, D., Knowles Jr, D.P., Taus, N.S. 2012. Experimental induction of malignant catarrhal fever in pigs with ovine herpesvirus 2 by intranasal nebulization. Veterinary Microbiology. 159(3-4):485-489. doi:10.1016/j.vetmic.2012.04.016.

Interpretive Summary: Establishing a cost-effective experimental animal model for MCF viral infection and disease is a key step toward the development of a successful vaccine and for disease studies. The lack of a cell culture system to grow OvHV-2, the causative virus for sheep-associated MCF (SA-MCF), has constrained the research for decades. However, the ability to generate an infectious OvHV-2 pool from nasal secretions of shedding sheep has made it possible to establish a method of infection and induction of SA-MCF by intranasal aerosolization of cell-free virus, which most closely mimics the natural route of transmission. SA-MCF has been induced experimentally by this method in cattle, American bison and rabbits, but all three species have limitations as a model for research. The purpose of this study was to determine whether domestic pigs are experimentally susceptible to SA-MCF and assess their suitability as an animal model. The results showed that seven of twelve intranasally challenged pigs became infected with OvHV-2. Five of these seven, all in higher dose groups, developed SA-MCF. The characteristics of lesions in the pigs with experimentally induced SA-MCF are reminiscent of SA-MCF in cattle and bison, and are consistent with naturally occurring MCF in pigs. The relationship between dose and incubation period and between dose and time to a rise in viral DNA copy number in blood of clinically affected pigs are similar to those in bison with experimentally induced SA-MCF. The data indicate that pigs can be a useful natural host model for SA-MCF research.

Technical Abstract: Malignant catarrhal fever (MCF), a frequently fatal herpesviral disease, has been sporadically reported in pigs. All cases of naturally-occurring porcine MCF reported to date have been linked to ovine herpesvirus 2 (OvHV-2), a gammaherpesvirus in the genus Macavirus carried by sheep. Experimental induction of MCF by aerosolization of the virus in nasal secretions collected from infected sheep has been successful in bison, cattle and rabbits. The goals of this study were to determine the susceptibility of pigs to MCF following experimental intranasal inoculation of OvHV-2, and to characterize the disease. Twelve pigs in four groups were nebulized with OvHV-2 from 100,000 to 100,000,000 DNA copies in sheep nasal secretions. Three control pigs were nebulized with nasal secretions from uninfected sheep. Three additional pigs were inoculated intravenously with 10,000,000 DNA copies of OvHV-2 to evaluate this route of infection with cell-free virus. Seven of twelve intranasally challenged pigs became infected with OvHV-2. Five of these seven, all in higher dose groups, developed MCF. Lesions resembled those reported in natural cases of porcine MCF. The most striking and consistent histological lesions were in trachea, lung, kidney and brain, and comprised interstitial pneumonia, necrotizing arteritis-periarteritis, and nonpurulent meningoencephalitis. No infection was established in the intravenously-challenged or control groups. The study showed that MCF can be experimentally induced in pigs by aerosol challenge using sheep nasal secretions containing OvHV-2. Domestic pigs are a natural clinically-susceptible host for sheep-associated MCF and represent a useful, cost-effective model for MCF research.