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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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For 119 days, 36 cattle, allotted to 6 treatment groups, were fed a balanced growth diet containing 0, 5, 10, 15, 20, or 25% cull onions on a dry-matter basis. Cattle performance was comparable to that associated with barley-base non-onion diet; statistical differences were not observed among treatments. During the first 28 days of the study, reduction in numbers of RBC, hemoglobin concentration, and PCV was observed in all cattle fed onions, but clinical anemia was not seen in any individual animal. After onion feeding was discontinued at 119 days, RBC numbers, hemoglobin concentration, and PCV returned to baseline values within 30 days. Heinz bodies were detected in erythrocytes of all cattle fed onions, and the percentage was proportional to the amount of onions consumed. Addictive onion consumption was prevented by mixing chopped or crushed onions in a total balanced ration.

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Serum ionized calcium (ICa) concentration was determined in 141 clinically normal dairy cattle by use of a direct-measuring calcium ion-selective electrode instrument. Mean serum ICa concentration 2 hours after blood withdrawal was 4.59 mg/dl; range varied from 3.79 to 5.25 mg/dl. Regression analysis indicated a high degree of correlation between ICa and serum total calcium concentrations if serum stored at 23 C was analyzed within 12 hours after blood withdrawal. Abnormal ICa concentration was detected in 19 of 85 dairy cows that were affected with various pathologic conditions. All 19 cows had hypocalcemia (n = 13 with parturient hypocalcemia, 4 with hypomagnesemic tetany, and 2 with renal disease). In all cases, the ICa concentration clearly related to the clinical manifestation of disease and the functional status of the cow's calcium metabolism.

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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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Adult cows from an Anaplasma marginale-infected herd that were negative to the A marginale rapid card agglutination (RCA) and complement fixation (CF) tests for 1 to 4 years developed acute anaplasmosis after inoculation with 0.5 ml of blood from an A marginale carrier cow. The test cattle were as susceptible as the control cattle of similar ages. Also, 2 cows that had seroconverted from RCA/CF-positive to RCA/CF-negative status naturally were fully susceptible to anaplasmosis when they were experimentally infected. Results of the study indicated that indigenous seronegative cattle in anaplasmosis-enzootic regions probably do not have acquired or natural immunity to A marginale infection.

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The role of ticks and carrier cattle in epizootics of bovine anaplasmosis was further clarified by demonstrating unequivocally, for the first time, that male ticks fed on a chronic carrier cow naturally infected with Anaplasma marginale can transmit this parasite intrastadially and biologically when subsequently fed on susceptible cattle. These data indicate that field epizootics of acute anaplasmosis may be initiated by males of tick vector species that feed on carrier cattle and subsequently transfer to susceptible cattle.

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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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The prevalance of Anaplasma marginale-infected cows, as determined by use of the modified rapid card agglutination (MRCA) test, was measured during a 4-year period (1980-1983). The prevalence of A marginale-infected cows, defined as positive reactors on the MRCA test, remained constant (31%-37%). The apparent incidence of A marginale transmission to susceptible cows was approximately 7% from 1980 to 1981, 8% from 1981 to 1982, and no transmission from 1982 to 1983. The occasional MRCA-positive cow became negative on the MRCA test, and 1 cow was determined to be free of A marginale infection by subinoculation of 100 ml of the cow's blood into a susceptible, splenectomized calf. Dermacentor andersoni, a known vector of A marginale, was often found on the cattle and in their environment. However, A marginale was not transmitted to susceptible, splenectomized calves, using collected ticks. Of 56 calves born to MRCA-positive cows, 82% were MRCA-positive within the first 3 months of life. These calves converted to MRCA-negative status and were determined to be free of A marginale infection by subinoculation of their blood into susceptible, splenectomized calves, indicating the passive transfer of colostral antibodies.

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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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The mean urea nitrogen concentration in vitreous humor (VUN) in 97 healthy steers after death was 15.7 mg/dl. The mean serum urea nitrogen concentration in the same cattle was 20.0 mg/dl. The mean vitreous creatinine (VC) concentration was 0.7 mg/dl, and the serum creatinine value was 1.5 mg/dl. The VUN and VC were both significantly lower than serum urea nitrogen and serum creatinine, respectively, but varied in a consistent, predictable manner. In tests with 10 cows, postmortem intervals as long as 36 hours and ambient temperatures up to 30 C had no significant effects on VUN and VC. Evaluation of 8 animals with uremia confirmed that the vitreous humor is a stable fluid compartment after death, usable as an indicator of serum urea nitrogen and creatinine.

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The range for postmortem vitreous humor Mg2+ concentration in 97 healthy cattle was 1.8 mg/dl to 2.72 mg/dl at 23 C for a 48-hour postmortem interval. The postmortem vitreous Mg2+ concentration closely paralleled the antemortem serum Mg2+ concentration at 23 C. Low environmental temperature (4 C) had no effect on postmortem vitreous concentration. However, high environmental temperatures (30 C) significantly (P less than 0.05) reduced postmortem vitreous Mg2+ concentration at the 36-hour postmortem interval. It was concluded that postmortem vitreous humor Mg2+ determination could be a useful diagnostic aid in cattle for detecting Mg2+ imbalances for at least 48 hours after death, provided the postmortem environmental temperature did not exceed 23 C after 24 hours.

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Sentinel steers were placed with 3 beef herds on irrigated pastures in southern Idaho for 1-month periods from May until November 1982 to determine the transmission pattern of Fasciola hepatica. Transmission was found to increase through the pasture season, reaching a peak during November. Overwintering of metacercariae or snail-borne stages was not found to contribute to infections in the year under study. A variety of species of Lymnaea were found to be available in southern Idaho as potential intermediate hosts. The enzyme-linked immunosorbent assay was found to be a good serologic indicator of light infections with F hepatica. The serum gamma-glutamyltransferase activity was not diagnostically significant when the degree of fluke infection was low.

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The prophylactic efficacy of a long-acting oxytetracycline formulation was determined in 36 susceptible cows experimentally inoculated with Anaplasma marginale. Each of 10 cows in 3 treatment groups (T2, T3, T4) were given IM injections of 20 mg of oxytetracycline/kg of body weight once, twice, or three times during the prepatent period. The T2 group was treated once at 1 week after experimental inoculation, the T3 group was treated 2 times (at 1 and 2 weeks) after exposure, and the T4 group was treated 3 times (at 1, 2, and 3 weeks) after exposure. Six cows comprising group T1 served as nonmedicated controls. Treatment of cattle in the prepatent period with the long-acting oxytetracycline formulation produced significantly fewer clinical anaplasmosis cases. This reduction in frequency was proportional to the number of weekly treatments given. In cattle which developed clinical disease, only 1 IM injection of 20 mg of oxytetracycline/kg was necessary to induce recovery. The prepatent period in the treated cattle was extended approximately 30 days beyond the prepatent period of the control cattle after their final treatment. Humoral rapid card agglutinating and complement fixing antibodies regularly were present in the cows 10 days after they were inoculated; however, neither the presence of antibody nor that of the antibiotic was sufficient to prevent establishment of the carrier state in the principals.

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Blood samples from 16 anaplasmosis complement-fixation (CF) positive sheep from a flock near Cambridge, Idaho, were inoculated into 3 intact sheep and 3 splenectomized calves. The 3 sheep became CF positive, and 2 developed parasitemia. None of the 3 calves had signs of anaplasmosis, but all became ill when they were subsequently challenge exposed with blood from known carriers of Anaplasma marginale. After a 75-day observation period, blood from the recipient intact sheep was subinoculated into 3 splenectomized sheep. These splenectomized sheep developed clinical anaplasmosis and became CF positive. In only 1 sheep was there a positive rapid card agglutination test. Therefore, the rapid card agglutination test was not considered to be diagnostic for anaplasmosis carrier status in sheep. Electron microscopic studies were performed on infected sheep erythrocytes to determine the morphologic structure of the organism involved. The causative organism was determined to be Anaplasma ovis.

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Acute Halogeton glomeratus poisoning occurred in 16 of 680 range cattle during and following a trail drive. Signs of toxicosis included posterior ataxia, recumbency, coma, and death. Histopathologically, abundant, refractile calcium oxalate crystals were seen in renal tubules. Inasmuch as the plant is generally unpalatable for cattle, poisoning in this case was enhanced by a preceding period of food deprivation.

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We measured serum carnitine in groups of patients with various diseases. The concentration was frequently above normal in patients with renal insufficiency. The clinical significance of such an increase in renal insufficiency may be analogous to that of increases in urea nitrogen, creatinine, or uric acid in the serum.

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Villonodular synovitis was diagnosed as the cause of lameness in 14 horses. The diagnosis was based on the history, clinical signs, and arthrographic findings. Treatment consisted of surgical excision and radiation therapy. The response to treatment was favorable in 13 horses.

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A bovine fecal Chlamydia, isolated from a clinically normal cow, had pathogenic capabilities and antigenic structure similar to those of a chlamydial agent of epizootic bovine abortion (EBA). Intravenous inoculation of the fecal chlamydia into a pregnant heifer caused abortion and lesions in the fetus indistinguishable from those of experimentally induced EBA. In serotests with species-specific complement fixation antigens, the intestinal agent was similar to the EBA agent.

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Pathologic findings in mature dogs with old dog encephalitis were compared with the findings in multiple sclerosis, subacute sclerosing panencephalitis and neuromyelitis optica in man. Fluorescent antibody studies in animal and human tissues were compared. Optic neuritis in dogs with chronic distemper shows changes similar to those in the optic tract of human patients with severe demyelinating disease. The pathologic changes in multiple sclerosis, such as perivascular infiltration with lymphocytes, plasma cells and demyelination are similar to those seen in old dog encephalitis. Demyelination in old dog encephalitis is usually diffuse. The findings strongly support a possible relationship of old dog encephalitis to multiple sclerosis, subacute sclerosing panencephalitis, and neuromyelitis optica.

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