Skip to main content
ARS Home » Pacific West Area » Pullman, Washington » Animal Disease Research » Research » Publications at this Location » Publication #223202
Title: Experimental infection of rabbits with ovine herpesvirus 2 from sheep nasal secretions

Author
item Gailbreath, Katherine
item Taus, Naomi
item Cunha, Cristina
item Knowles Jr, Donald
item Li, Hong

Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/25/2008
Publication Date: 9/22/2008
Citation: Gailbreath, K.L., Taus, N.S., Cunha, C.W., Knowles Jr, D.P., Li, H. 2008. Experimental infection of rabbits with ovine herpesvirus 2 from sheep nasal secretions. Veterinary Microbiology. 132:65-73.

Interpretive Summary: Malignant catarrhal fever (MCF) is a generally fatal disease that primarily occurs in ruminants and is caused by a group of herpesviruses. Outside of Africa, MCF is mainly caused by ovine herpesvirus 2 (OvHV-2) which is carried by sheep. Although sheep remain healthy when infected, cattle, bison and other ruminants develop severe, usually fatal disease when infected. Infection occurs when susceptible species breath in viral particles shed in the nasal secretions of infected sheep. In the past, experimental infection involved transfer of blood or tissue from MCF affected animals but recently a new method that involves intranasal nebulization with sheep nasal secretions containing infectious virus has been developed. Because rabbits are smaller and easy to handle, and they develop MCF-like disease when inoculated, they represent a good animal model for this disease. However, the intranasal method of inoculation has not been previously attempted in rabbits. This paper reports the results of a study involving intranasal nebulization of rabbits with sheep nasal secretions containing OvHV-2 and subsequent evaluation of infection status, clinical signs, and lesions. Five out of eight rabbits inoculated by the intranasal nebulization method showed evidence of infection, clinical signs of MCF and developed histologic lesions similar to those in rabbits infected by other methods. Intraperitoneal injection of sheep nasal secretions containing infectious virus did not result in clinical disease or histologic lesions. The study demonstrates that intranasal nebulization of rabbits can be used as an experimental model for OvHV-2 induced MCF that mimics that natural route of infection.

Technical Abstract: Malignant catarrhal fever (MCF) is a generally fatal disease that primarily occurs in ruminants and is caused by a group of gammaherpesviruses. Outside of Africa MCF is mainly caused by ovine herpesvirus 2 (OvHV-2) which is carried subclinically by sheep. Cell-free virus is present in nasal secretions of shedding sheep and aerosol is the primary mode of transmission. Although OvHV-2 has never been propagated in vitro, experimental infection involving intranasal nebulization with nasal secretions from shedding sheep has been used to induce MCF in cattle and bison. This method of inoculation has never been tested in rabbits, which are the primary small animal model. The objectives of this study were to determine whether rabbits become infected with OvHV-2 after intranasal nebulization with cell-free virus from sheep nasal secretions and whether they develop MCF with consistent gross and histologic lesions. Five of eight rabbits became infected, showed clinical signs and developed histologic lesions typical of MCF including multisystemic vasculitis and perivascular lymphoid accumulation. These lesions are similar to those reported in rabbits infected by intravenous injection with tissues from clinically affected animals containing cell-associated virus. Viral DNA and mRNA transcripts of a structural viral protein were present in tissues from affected rabbits suggesting that viral replication was occurring. This work demonstrates that OvHV-2 infection of rabbits by intranasal nebulization is a potentially useful model that mimics the natural route of infection and may be used to study viral replication and pathogenesis.