Introduction Infectious bovine rhinotracheitis (IBR) is an infectious disease of cattle caused by an herpesvirus (1, 2, 8) which also causes genital tract infection (infectious pustular vulvovaginitis) (9) conjunctivitis, encephalitis, rumenitis, and septicemia of young calves (4, 7, 8) and fetal infection (6). This case of encephalomyelitis in two heifers is reported because the syndrome produced could not be distinguished clinically from pseudorabies. It emphasizes the necessity of laboratory examination. History There were 525 cattle in a cow-calf and feedlot operation, of which 150 were feeders and the remainder the breeding herd. Several fences prevented direct contact between the breeding herd and the feedlot cattle. Most of the animals in the feedlot originated from the calf crop, but approximately 30% were purchased. All breeding herd additions were home raised heifers and were vaccinated against clostridial diseases and brucellosis routinely at four to five months of age. The three-yearold cattle were vaccinated for IBR as calves in 1970. However, the two affected heifers may not have received Brucella strain 19 and IBR vaccinations, as they did not have vaccination tags in their ears. The breeding herd was maintained under range conditions and no unusual health problems had occurred. Only one or two abortions had occurred over the last five years and pneumonia had been limited to the feedlot. Nutritional myopathy had been a continuing problem in newborn calves and animals were routinely treated and supplemented with selenium and vitamin E. A few heifers and cows confined for close observation in a calving paddock adjacent to the feedlot were in contact with two sows and their litters which had free access to the paddock. The owner reported they sometimes molested the cattle by nib'Veterinary Services Laboratory, Alberta Department of Agriculture, Edmonton, Alberta. CAN. VET. JOUR., vol. 16, no. 9, September, 1975

bling at their hindquarters while they lying down.


Clinical Findings A three-year old heifer became weak in the hind legs and knuckled at the fetlocks. Incoordination became more pronounced over 48 hours until the animal was unable to stand, her hind legs becoming rigid. The animal remained recumbent for five days and was then euthanized. One week later a second three-year old heifer began a similar clinical syndrome and within 24 hours she was unable to rise. The owner treated her with 500 ml of a calcium preparation subcutaneously, two injections of penicillin-dihydrostreptomycin, and one injection of a selenium preparation. The animal was referred to the Provincial Veterinary Laboratory by a practitioner for post mortem examination.

Flaccid paralysis of the hind quarters was the principal clinical sign with motor paralysis of the hind limbs and tail and partial sensory paralysis distal to the stifle joints. The forelimbs were unaffected. When the animal was unloaded she immediately and voraciously attacked her left side and flank area by biting the skin. A pronounced lesion had already been made by this action and hair and skin had been excoriated (Figure 1). She persisted frantically at this until euthanasia, but exhibited no other encephalitis signs.

Laboratory Findings Pathology - On post-mortem examination the only significant gross lesion was chronic interstitial nephritis in one kidney. Brain and spinal cord were removed for culture, histopathology, and animal inoculation. Bacteriological culture of brain and spinal cord did not yield any significant organisms, and fluorescent antibody examination for rabies was negative.1 Blood lRabies examination was performed by the Animal Diseases Research Institute (Western) using fluorescent antibody test. 569


FIGURE 3. Areas of demyelination, necrosis and hemorrhage at the junction of white and grey matter in spinal cord.

FIGURE 1. The paralyzed cow attempting to reach the red denuded lesion on the flank and stifle area. This localized unilateral lesion was made by licking and chewing.

FIGURE 4. IBR herpes type intranuclear inclusions in neurons of spinal cord.

FIGURE 2. Areas of malacia and hemorrhage in the grey matter lateral to the central spinal canal.

cholinesterase levels were within the normal range.

Histopathology - Microscopic lesions in the central nervous system decreased in severity from the cauda equina to the medulla. Lesions increased again in severity in the cerebellar peduncles, but did not progress further up the brain stem. The lesions were characterized by large focal areas of malacia and hemorrhage (Figure 2). Inclusions were found in numerous small neurons associated with necrotic lesions in both the brain and the spinal cord but were more numerous in the cerebellar peduncles (Figure 3). Blood vessels with the more intense areas of malacia had perivascular cuffing with macrophages and neutrophils. Neutrophils were infiltrating into some parts of the necrotic area. There was a mild gliosis and neurons involved in the necrotic area were undergoing severe chromatolysis (Figure 4). Animal Inoculations - Brain and spinal cord were removed as aseptically as possible. Portions were immediately frozen for virus isola-

tion studies. Fresh preparations of normal saline suspension of brain were inoculated subcutaneously into a rabbit. Later a saline suspension of frozen brain and spinal cord was inoculated into a second rabbit. No lesions or symptomatology was produced. Virology - One gram of frozen brain and cord tissue was emulsified with 10 ml of phosphate buffered saline. The supernatant was inoculated onto bovine embryonic kidney monolayer tissue culture cells. Within 48 hours cytopathic effects were evident. Supernatant derived from freezing and thawing second passage monolayer cultures containing 100 TCD50 virus was neutralized by a 1:20 dilution of IBR antisera prepared in rabbits that were inoculated with standard reference IBR virus supplied by National Animal Disease Laboratory in Ames, Iowa (NADL). Standard neutralization technique was followed (5). Fluorescent antibody test was performed on bovine embryonic kidney cells grown on cover slips and infected with 100 TCDro of isolated virus. Twenty-four hours after infection cover slips were stained with commercially obtained



anti IBR conjugate and antipseudorabies conjugate (NADL). Specific fluorescence was found with IBR but not pseudorabies. Discussion A diagnosis of pseudorabies is suggested when clinical signs of severe localized pruritis and a short fatal disease course occurs and when confirmation is obtained by rabbit transmission and virus neutralization tests (3). The differential diagnosis of pseudorabies includes nervous acetonemia, the furious form of Rabies, and acute lead poisoning. The main clinical differential feature of these diseases from pseudorabies is the absence of local pruritis (2). In the present disease most of the clinical features of pseudorabies were present including close association with swine, involvement of more than one animal, short clinical course, paralysis and intense local pruritis in the flank area. One exception was the absence of maniacal behavior commonly associated with pseu-

dorabies. Comparison of the histological changes in this case with those of pseudorabies (3) gave the impression of wider distribution of lesions with equal severity of necrosis in the brain and spinal cord. The malacia and tissue destruction seemed more intense in this case than in pseudorabies, although the type of inflammatory reaction elicited was similar. The diagnosis of IBR was based on histological lesions with herpes type inclusions, isolation of the IBR virus in tissue culture, and identification by serum neutralization and fluorescent antibody test. Additional diagnostic criteria were the lack of response in the inoculated rabbit and the presence of more severe lesions than those usually associated with pseudorabies. Summary A clinical syndrome is described in two heifers. Severe neurological lesions were present in one animal and the infectious bovine rhinotracheitis virus was isolated from the brain and cord. This syndrome was clinically indistinguishable from pseudorabies in cattle.



L'auteur decrit un syndrome qu'il a observe chez deux taures. L'une d'elles presentait des lesions nerveuses marquees et on isola le virus de la rhino-tracheite infectieuse bovine, du cerveau et de la moelle epiniere de cet animal. Cliniquement, il s'avera impossible d'etablir une diff6rence entre ce syndrome et la pseudorage bovine. Acknowledgments To Dr. G. Weir of the Weir Veterinary Clinic, Lloydminster for submitting this case to the Alberta Provincial Veterinary Laboratory, and to Miss Emma Barager for the virus isolation and identification and Mrs. Shirley Rawluk for animal

inoculation studies.

References 1. ANSPAUGH, V. Infectious bovine rhinotracheitis - a review. Vet. Med. small Anim. Clin. 65: 1171-1176. 1970. 2. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine. Fourth Edition. London: Bailliere Tindall. 1974. 3. Dow, C. and J. B. McFERRAN. The pathology of Aujeszky's in cattle. J. comp. Path. 72: 337-347. 1962. 4. EDINGTON, N., G. J. CHRISTOFINIs and A. 0. BETTS. Meningoencephalitis in two gnotobiotic calves infected intranasally and orally with infectious bovine rhino-tracheitis virus. Res. vet. Sci. 13: 292-293. 1972. 5. LENErrE, E. H. and N. J. SCHMIDT. Diagnostic Procedures for Viral and Rickettsial Diseases. 3rd Edition. pp. 120-121. American Public Health Association. 6. McKERCHER, D. G. and E. M. WADA. The virus of infectious bovine rhinotracheitis as a cause of abortion in cattle. J. Am. vet. med. Ass. 144: 136-142. 1964. 7. REED, D. E., E. J. BICKNELL and R. J. BuRY. Systemic form of infectious bovine rhinotracheitis in young calves. J. Am. vet. med. Ass. 163: 753-755. 1973. 8. ROSNER, S. F. Infectious bovine rhinotracheitis: Clinical review, immunity and control. J. Am. vet. med. Ass. 153: 16311638. 1968. 9. STRAUB, 0. C. Bovine rhinotracheitis and coital exanthema. Vet. Med. Rev., Leverkusen 2/3: 246-256. 1967.

Infectious bovine rhinotracheitis encephalomyelitis in cattle and its differential diagnosis.

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