Primary infection, latency, and reactivation of bovine herpesvirus type 5 in the bovine nervous system.
Bovine herpesvirus type 5 (BHV-5) infection in calves causes meningoencephalitis, a fatal disease highly prevalent in South America. To study the pathogenesis of BHV-5 infection in cattle, 12 calves (group 1: acute infection) and 11 calves (group 2: latent infection) were intranasally inoculated with an Argentinean BHV-5 isolate at 10(8) and 10(4.7) tissue culture infective doses, respectively; six calves (control group) were mock infected. At 3 months postinoculation, all of the calves in group 2 and three calves in group 3 were given dexamethasone to reactivate the virus. The animals were euthanatized between days 6 and 17 postinoculation (group 1) and between days 6 and 16 postreactivation (group 2). Seventy-five percent and 91% of animals in groups 1 and 2, respectively, excreted BHV-5 in nasal and ocular discharges. Following dexamethasone administration, 45% of calves shed virus in both types of secretions. Spontaneous virus reactivation and shedding was observed in one calf. Neurologic signs consisting of circling, teeth grinding, ptyalism, jaw chomping, tongue protrusion, and apathy were observed in two animals in group 1 and, during the reactivation period, in four animals in group 2. Macroscopic findings consisted of softening of the cerebral tissue, meningeal hemorrhages and swelling, and edema and hemorrhages of prescapular, retropharyngeal and submandibular lymph nodes. Histologic lesions consisted of meningitis, mononuclear perivascular cuffing, neuronophagia, satellitosis, gliosis, hemorrhage, and necrosis and edema. Lesions in anterior cerebral cortex, medulla, and pons were consistently seen in all the animals of group 1. In the acutely infected animals, lesions in the diencephalon appeared at day 10 postinoculation, whereas in the latently infected calves these lesions were observed as early as at day 6 postreactivation. Latently infected animals developed lesions simultaneously in anterior cortex, medulla, pons, and diencephalon, showing a remarkable difference from the acutely infected group. Trigeminal ganglionitis appeared relatively early in animals of both groups (day 7 postinoculation in group 1 and day 8 postreactivation in group 2).
Estación Experimental Agropecuaria Balcarce, Instituto Nacional de Tecnología Agropecuaria, Bulcarce, Argentina.
S E
SE
Perez
G
G
Bretschneider
M R
MR
Leunda
E A
EA
Osorio
E F
EF
Flores
A C
AC
Odeón
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000378:metabolism; D000914:Antibodies, Viral / Q000097:blood; D001118:Argentina; D002417:Cattle; D002418:Cattle Diseases / Q000473:pathology / Q000821:virology*; D002540:Cerebral Cortex / Q000473:pathology / Q000821:virology; D003588:Cytopathogenic Effect, Viral; D003907:Dexamethasone / Q000378:metabolism; D018792:Encephalitis, Viral / Q000134:cerebrospinal fluid / Q000473:pathology / Q000662:veterinary* / Q000821:virology; D006566:Herpesviridae Infections / Q000134:cerebrospinal fluid / Q000473:pathology / Q000662:veterinary* / Q000821:virology; D025881:Herpesvirus 5, Bovine / Q000472:pathogenicity*; D008590:Meningoencephalitis / Q000134:cerebrospinal fluid / Q000473:pathology / Q000662:veterinary* / Q000821:virology; D009297:Nasal Mucosa / Q000821:virology; D009500:Neutralization Tests / Q000662:veterinary; D011897:Random Allocation; D012668:Trigeminal Ganglion / Q000473:pathology / Q000821:virology; D014775:Virus Activation; D017735:Virus Latency; D017201:Virus Shedding
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000914:Antibodies, Viral; D003907:Dexamethasone