Experimental vesicular stomatitis in swine: effects of route of inoculation and steroid treatment.
An enzootic focus of vesicular stomatitis virus New Jersey serotype (VSV-NJ) exists on Ossabaw Island, Georgia. Many questions regarding the epizootiology of this virus at this focus still exist, but evidence suggests that the vector for this virus is a phlebotomine sand fly (Lutzomyia shannoni), with feral swine serving as a potential source of virus for the sand fly and for other swine via contact transmission. We conducted 2 experimental trials in domestic swine using VSV-NJ isolated from a sand fly from Ossabaw Island to determine if route of inoculation or immunosuppression via steroid administration affected the development of disease, viremia, viral shedding, or the neutralizing antibody response. In a third trial, we studied the potential for contact transmission among swine using this isolate. Virus isolations were made from nasal cavity or palatine tonsil of the soft palate, and VSV-NJ neutralizing antibodies developed when pigs were inoculated intradermally in the apex of the snout, ear, or coronary band, intravenously, intranasally, or via scarification of the apex of the snout or coronary band. Vesicles developed only in pigs inoculated in the apex of the snout or coronary band, and these vesicles were at the site of inoculation. Steroid treatment did not potentiate the development of secondary vesicles and did not prolong the period of virus shedding from VSV-NJ-infected swine. Contact transmission, as determined by shedding of virus from the tonsil of the soft palate and the development of VSV-NJ neutralizing antibodies, occurred in pigs in contact with animals inoculated in the apex of the snout but not in contact animals exposed to pigs inoculated intradermally in the coronary band or intranasally. These trials show that contact transmission can occur and VSV-NJ can be shed without the development of clinical disease (i.e., vesicle formation). Viremia was never detected in any of the experimental pigs, suggesting that swine may not be a good amplifying host for VSV-NJ.
Howerth
E W
EW
Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens 30602, USA.
Stallknecht
D E
DE
Dorminy
M
M
Pisell
T
T
Clarke
G R
GR
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000914:Antibodies, Viral / Q000097:blood; D000917:Antibody Formation; D002921:Cicatrix / Q000821:virology; D003907:Dexamethasone / Q000494:pharmacology*; D007165:Immunosuppression Therapy; D008213:Lymphocyte Activation; D009297:Nasal Mucosa / Q000821:virology; D014066:Palatine Tonsil / Q000821:virology; D018353:Rhabdoviridae Infections / Q000276:immunology* / Q000473:pathology / Q000635:transmission*; D012867:Skin / Q000821:virology; D013280:Stomatitis / Q000276:immunology / Q000473:pathology / Q000821:virology*; D013552:Swine; D018116:Vesiculovirus / Q000302:isolation & purification; D017201:Virus Shedding
D000893:Anti-Inflammatory Agents; D000914:Antibodies, Viral; D003907:Dexamethasone