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Scrapie is a naturally occurring fatal neurodegenerative disease of sheep and goats. Susceptibility to the disease is partly dependent upon the genetic makeup of the host. In a previous study it was shown that sheep intracerebrally inoculated with US scrapie inoculum (No. 13-7) developed terminal disease within an average of 19 months. We have since produced an inoculum, No. x124 from pooled brains of US-origin sheep scrapie, that results in incubations nearly threefold shorter. The present study documents clinicopathologic findings and the distribution of abnormal prion proteins (PrP(Sc)) by immunohistochemical (IHC) and Western blot (WB) techniques, in tissues of sheep inoculated with No. x124. All inoculated sheep developed clinical disease and were euthanatized within an average of 7.7 months postinoculation (MPI). Sheep that had valine/valine or alamine/valine at codon 136 of prion protein (PRNP) gene developed the disease faster and were euthanatized at an average of 4.3 and 5.6 MPI, respectively. Also, the inoculum was able to induce disease in a short time (7 MPI) in a sheep that was relatively resistant (QR at codon 171) to scrapie. This indicates that inoculum No. x124 appears to induce scrapie in shorter time than inoculum No. 13-7, especially in sheep homozygous or heterozygous for valine at codon 136.

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Leucomyelitis was the predominant feature in four North American adult sheep (cases 1-4) with ovine lentivirus (OvLV) infection. All four animals were OvLV-seropositive and a syncytogenic virus consistent with OvLV was isolated from the brain of case 3 and the lungs of case 4. Clinically, the sheep had dyspnoea and neurologic signs of varying severity. Changes in the central nervous system included asymmetrical meningoleucomyelitis with white matter degeneration in all four sheep and scattered foci of leucoencephalitis in periventricular, subependymal and other white matter areas of the brain of the three animals (cases 1, 2 and 4) for which the brain was examined. In the lungs of two sheep (cases 3 and 4), there was lymphoid interstitial pneumonia with marked lymphoid hyperplasia. The viral capsid antigen (p25) was detected by immunohistochemistry (IHC) in sections of lung, brain and spinal cord of the four sheep and OvLV RNA was detected by in-situ hybridization (ISH) in lung and spinal cord samples. The results confirm the usefulness of the IHC and ISH for differential diagnosis of visna.

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Separate groups of goats were used to determine drug depletion patterns in serum (n=10), tissue (n=20) and milk (n=8) following a single intramuscular (i.m.) dose of 20 mg/kg of a long-acting oxytetracycline (OTC) formulation (Liquamycin LA-200). Milk residues were also determined following a subcutaneous (s.c.) administration of the same product at the same dose. Serum samples were taken for 24 h post-treatment and tissues (fat, liver, kidney, muscle and injection site) collected at 4, 7, 14, 21 and 28 days following injection. Milk from lactating goats was collected every 12 h for 8 days following both the i.m. and s.c. treatments utilizing an intervening 5-week washout period. Residues in serum and tissue were measured using a microbial inhibition assay, while milk residues were measured using both a microbial inhibition assay and a validated HPLC method. The serum pharmacokinetic parameters of OTC in goats were determined, with a mean AUC=67.4 microg h/mL, mean terminal half-life=14.4 h, and apparent clearance=0.33 L/kg h. Tissue half-lives could not be determined with confidence because the collection times provided only two points at which residues could be measured for most tissues. Oxytetracycline residues in all goat tissue samples measured less then cattle tissue tolerance by 96 h postdosing. One-compartment model describing milk depletion data for i.m. and s.c. dosing had terminal slope half-lives of 20.1 and 36.1 h, respectively. By 96 h post-treatment none of the milk samples contained OTC residues in excess of the cattle milk tolerance (0.3 p.p.m.). For both milk and tissue, the upper-bound 99% confidence intervals for the samples taken from goats 96 h postdosing were lower than approved cow milk and tissue tolerances.

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Transmissible spongiform encephalopathies in humans and in animals are fatal neuro-degenerative diseases with long incubation times. The putative cause of these diseases is a normal host protein, the prion protein, that becomes altered. This abnormal prion protein is found mostly in the brains of infected individuals in later stages of the disease, but also can be found in lymphoid and other tissues in lower amounts. In order to eradicate this disease in animals, it is important to develop a system that can concentrate the abnormal prion protein and an assay that is very sensitive. The sensitivity that can be achieved with capillary electrophoresis makes it possible to detect the abnormal protein in blood. A peptide from the carboxyl terminal region, amino acid positions 218-232, was labeled with fluorescein during the synthesis of the peptide at the amino terminus. Antibodies that have been produced to this peptide were affinity purified and used in a capillary electrophoresis immunoassay. The amount of fluorescein labeled peptide in the capillary was 50 amol. Blood was obtained from normal sheep and elk, from sheep infected with scrapie and elk infected with chronic wasting disease. Buffy coats and plasma were prepared by a conventional method. After treatment with proteinase K, which destroys the normal protein but not the altered one, the blood fractions were extracted and tested in the capillary electrophoresis immunoassay for the abnormal prion protein. The abnormal prion protein was detected in fractions from blood from infected animals but not from normal animals. This assay makes a pre-clinical assay possible for these diseases and could be adapted to test for the abnormal prion protein in process materials that are used for manufacture of pharmaceuticals and products for human consumption.

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Two thousand Panama X Rambouillet ewes from a flock of 2,200 developed signs of acute toxicosis after being moved to a field that had been sprayed 16 hours earlier with elemental sulfur. Acute signs were lethargy, abdominal discomfort, and prostration. Two hundred six (10%) of the affected ewes died within 24 hours. Polioencephalomalacia that was unresponsive to thiamine treatment developed in another 40 (2%) of the ewes; 28 (70%) of the ewes with polioencephalomalacia recovered. Sulfur is converted to hydrogen sulfide in the rumen. Signs of sulfur toxicosis are a result of absorption of hydrogen sulfide and interaction with the cytochrome system and hemoglobin. Sulfide is detoxified in the RBC and by the liver.

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Two areas of drug needs in the sheep industry are reviewed. The first is the need for prolificacy drugs such as those used outside the country. These drugs would encourage out-of-season lambing, increased lambs/per ewe during the traditional lambing season and synchronize estrus for easier management of lambing and increased use of artificial insemination for faster genetic improvement. The other area is drugs to treat or prevent major causes of disease, specifically abortion, neonatal diarrhea, pneumonia and internal parasitism. Efficacious drugs for these diseases are either not now cleared for use in sheep at all; a safe, easy to administer product is not available; or not cleared for sheep at a dosage level which is effective. These are drugs which will have a positive impact on the industry by increasing production, reducing expenses, and helping the U. S. to be able to compete with other sheep producing countries in the U. S. markets.

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Concentration-time profiles and the rates of absorption, extent of distribution and half-lives of sulfamethazine (SMZ), administered intravenously, orally as a water solution and as a sustained-release formulation (CalfSpan) were determined in 10 healthy sheep. The geometric mean half-life of elimination of i.v. SMZ was 10.8 h, compared to 14.3 h for the sustained-release preparation (CalfSpan) and 4.3 h for the oral water solution. Blood levels of SMZ were at or above 50 micrograms/ml for more than 48 h for CalfSpan, for 24 h after i.v. SMZ (100 mg/kg body wt), and for less than 24 h after p.o. SMZ (100 mg/kg body wt). The mean bioavailability of the oral SMZ solution was 58.3% (AUCp.o./AUCi.v.). The estimated bioavailability of the CalfSpan preparation was 52.5%. The safety of the sustained-release preparation was tested by dosing sheep with multiples (one, three and five times) of the recommended dose (one tablet, 8 g SMZ, per 20 kg body wt), once a day for 3 days. Clinical blood chemistries showed a significant increase in serum iron, and a decrease in serum phosphorus in animals treated at the 3x and 5x dose levels. Necropsies of the 5x dose animals did not show any gross signs that could be attributed to SMZ, and histological examination of tissues from the 5x animals revealed no organ pathology. Residues of SMZ in liver, fat, kidney and skeletal muscle were measured in 20 animals that received one bolus per 20 kg body wt. The results indicate that SMZ residues are cleared rapidly, and are at or below the tolerance level of 0.1 mg/kg within 8 days after dosing so that the 18-day withdrawal time used in cattle would provide an appropriate margin of safety if used in sheep.

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This article reviews lamb epididymitis and epididymitis caused by Brucella ovis. Pathogenesis, occurrence, signs and lesions, diagnosis, prevention, and treatment are discussed.

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History and syndromes of pneumonia, encephalitis, arthritis, and mastitis are reviewed. Occurrence, etiology, pathogenesis, transmission, diagnosis, treatment, and prevention of these diseases are discussed.

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An autogenous, multivalent, adjuvanted bacterin for epididymitis was tested in flocks of 700 to 800 Suffolk X white-faced lambs. Long-term feeding of low dosages of antibiotics also was tested in the Suffolk flock. Both methods appeared to reduce the incidence of the disease. The incidence of clinical epididymitis and the number of positive culture results from clinically affected rams were significantly reduced.

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A commercial flock of Suffolk and Suffolk-cross breeding rams was monitored for 5 years in an effort to control epididymitis caused by Brucella ovis. Scrotal palpation, semen evaluations, and vaccination against B ovis were used the first 3 years. Serologic evaluation (complement fixation and ELISA) was added the fourth year, and bacteriologic culturing was added to the program the fifth year. Semen culturing in the fifth year revealed 9 (37.5%) of 24 rams were actively excreting B ovis; 6 of those 9 rams were seronegative. Neither semen quality nor the presence of WBC in the semen were dependable criteria to detect these seronegative carriers. In spite of the high percentage of B ovis excretors, few clinical signs of epididymitis were detected in the flock during the last 3 years of the study. It was hypothesized that vaccination protected rams against the clinical disease but not the carrier state. The importance of culturing semen for assessment of a control program was emphasized.

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Fecal samples were taken at the time of pregnancy examinations and at parturition from two beef herds. They were also taken from sick calves at the onset of disease, and from 25% of the healthy calves at 15 days of age. All fecal samples were examined by electron microscopy for viruses.Four cows in herd A were detected excreting coronavirus, one at the time of the pregnancy examinations and three at parturition. The first cow was removed from the herd and the others calved at the end of the season. There were no sick calves.No cows in herd B were detected excreting virus at the time of pregnancy checks, but fourteen coronavirus and two rotavirus carrier cows were found at parturition. All but two calves sampled had large numbers of virus particles in their feces. Clinical illness was associated with dams shedding virus and with nightly low temperatures.

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Because of an episode of abortion caused by a tetracycline-resistant Campylobacter jejuni, lincomycin was mixed into a barley pellet and fed to 3,000 range ewes at a dosage of 225 mg/ewe/day. After the second feeding, a number of ewes were anorectic and diarrheic, and 6 were dead. Necropsies revealed congestion and hemorrhage of the entire gastrointestinal tract. The feeding of the medicated pellets was discontinued immediately. Sick ewes were treated with antihistamines and corticosteroids, but they did not recover, and many died during the next several weeks. Lambs born within the first 7 days after the incident were alert and vigorous. Dams did not produce milk and many died during or after parturition. Later, however, lambs were born dead or weak, and abortions of autolyzed lambs began. Affected ewes examined 3 weeks later had salmonellosis and/or toxic tubular nephrosis associated with an oxalate-like crystal. The flock had been grazed on range infested with Halogeton glomeratus just before treatment with lincomycin, and it also had a history of Salmonella-related abortions. The deaths finally ceased after a month. Approximately 2,000 ewes and 3,200 lambs were lost, resulting in an economic loss of $550,000.

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Three Targhee rams obtained from the Ohio Agricultural and Experimental Station had been identified as foot rot resistant on the basis of results of challenge exposure. In the first breeding trial, when rams were bred to 20 foot rot-susceptible ewes, the percentages of foot rot-resistant offspring from the 3 foot rot-resistant rams were 68, 82, and 100, compared with 55 and 60 for foot rot-resistant offspring from 2 known foot rot-susceptible rams. In the second year, the foot rot-resistant rams were mated with ewes of unknown foot rot status. The foot rot-resistant status of their lambs was compared with that of range-raised lambs whose parents' foot rot status was unknown. During the first year, challenge exposure to the disease consisted of confinement of the lambs in moist or wet pens with sheep affected with the naturally acquired disease. This protocol was repeated for lambs born during the second-year breeding trial. In addition, the right front foot of each lamb was inoculated with a broth culture of Bacteroides nodosus. During the second year, when data that included infected feet from all lambs were analyzed, 41% of the progeny of the foot rot-resistant rams and 17% of the offspring of parents of unknown foot rot status were unaffected by the disease. When the B nodosus-inoculated foot was not included in the analysis, however, 61% of the progeny of the foot rot-resistant rams and 29% of the others were unaffected. The resistance to foot rot undoubtedly is hereditary. The mechanism of resistance may be in the interdigital skin.(ABSTRACT TRUNCATED AT 250 WORDS)

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Four methods of treatment for ovine foot rot were evaluated: foot trimming and topical treatment (brief, daily foot bathing in 10% zinc sulfate); vaccination with an oil-alum adjuvanted, multivalent, Bacteroides nodosus bacterin, vaccination with the bacterin plus foot trimming and brief foot bathing, and 1-hour 10% zinc sulfate foot soaks. Compared with results of sheep in a nontreated control group, vaccination reduced the number of infected feet by 8%. Daily walk-through foot bathing reduced the number of infected feet by 16%, and vaccination and foot bathing reduced the number by 27%. In another experiment, treated but nonresponsive sheep were subjected to 2 one-hour foot soaks in 10% zinc sulfate. Compared with results in nontreated controls, the soaks reduced the number of affected sheep by 58%. Previously nontreated sheep responded with a 69% reduction of affected animals over controls.

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Copper disodium edetate in recommended doses was apparently responsible for the deaths of one calf and clinical signs of toxicosis in 5 others on one farm, and 7 deaths and clinical signs of toxicosis in a number of others on another ranch. Signs of hyperexcitability, hypermetria, hindlimb weakness, head pressing, depression, and opisthotonos occurred 6 to 24 hours after injections and preceded death by 1 to 2 days. Necropsy and histologic examination revealed massive liver necrosis. High blood concentrations of liver enzymes in affected cattle that did not die indicated that they had liver damage. High blood concentration of iron in cattle that died indicated possible interaction of copper and iron.

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A condition of firm udders in periparturient ewes, with little or no milk available at the teat, was associated with negative bacterial cultures of mammary tissue, isolation of ovine progressive pneumonia virus from mammary tissue, lymphocytic accumulations in mammary tissue, especially around ducts, and antibody to ovine progressive pneumonia virus in sera. Milk was present in the glands, but was not adequately transported through the duct system. The cull rate of ewes with this condition was reported by producers and veterinarians to be less than 5% in flocks where the condition was recognized, but approximately 10% of ewes were apparently affected in at least 1 flock.

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Six-month-old calves were inoculated with 200 metacercariae of Fasciola hepatica over a 72 day period. Their aspartic transaminase, alkaline phosphatase, arginase and gamma glutamyl transpeptidase (GGT) values were measured at two-week intervals. Infections with a final fluke count of 19 to 87 flukes did not result in an increase of serum alkaline phosphatase or arginase compared with those in control calves. Serum aspartic transaminase values were increased significantly (P less than 0.025) above those of controls but were not increased over reference values. Seemingly, measurement of these enzymes would not be useful in assessing the degree of fluke infestation. In contrast, serum values of GGT increased 56 days after preliminary inoculation and remained high for at least 83 days after infection. The initial rise coincided with the penetration of bile ducts by migrating flukes. This relationship may be useful in further studies of fluke-induced biliary damage.

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Campylobacter jejuni was isolated from a Wheaten Terrier bitch which had aborted (in southern Idaho). A Campylobacter of undetermined species also was isolated from aborted Poodle pups (in central Washington). It appears that persons may have been the source of infection in the Idaho event, but the source for the other was not speculated. These findings of perinatal death due to Campylobacter in dogs from widely separated areas indicate that pathologic evaluation of cases involving premature and aborted pups should include bacteriologic tests, using appropriate media and atmospheric conditions necessary for the cultivation of these organisms.

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