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Objective: To determine the effect of a commercial bioflavonoid antioxidant on acetaminophen-induced oxidative injury to feline erythrocytes., Design: Randomized controlled study., Animals: 45 healthy age-matched cats., Procedure: Cats were assigned to 3 experimental groups. Groups 1 and 3 received a bioflavonoid antioxidant (10 mg/d) orally for 2 weeks. Groups 2 and 3 received an oxidative challenge with acetaminophen (90 mg/kg [41 mg/lb] of body weight, PO) on day 7. Packed cell volume, percentage of erythrocytes with Heinz bodies, blood methemoglobin concentration, and blood reduced and oxidized glutathione concentrations were determined at various times during the 2-week study period., Results: Adverse effects were not associated with bioflavonoid antioxidant administration alone. Acetaminophen administration resulted in a significant increase in methemoglobin concentration in groups 2 and 3; differences were not detected between these groups. Heinz body concentrations in groups 2 and 3 increased after acetaminophen administration; however, the increase in cats that received the antioxidant was significantly less than in group-2 cats. Total blood glutathione concentrations did not change significantly in groups 2 and 3 after acetaminophen administration; however, ratio of reduced to oxidized glutathione concentration increased significantly after administration in group-2 cats, compared with group-3 cats., Conclusions and Clinical Relevance: Oral administration of bioflavonoid antioxidants to cats at risk for oxidative stress may have a beneficial effect on their ability to resist oxidative injury to erythrocytes.

Objective: To determine effects of intra-articularly administered 6alpha-methylprednisolone acetate (MPA) in exercised horses with carpal osteochondral fragmentation., Animals: 18 horses: 3 groups of 6 each., Procedure: An osteochondral (chip) fragment was created in 1 randomly chosen middle carpal joint of each horse. Polyionic fluid (PF) was injected into both middle carpal joints of horses in the control group. In horses of the MPA-control group, MPA was injected into the middle carpal joint without an osteochondral fragment; a similar volume of PF was injected into the contralateral middle carpal joint. In the MPA-treated group of horses, 100 mg of MPA was injected into the middle carpal joint containing the osteochondral fragment; a similar volume of PF was injected into the contralateral joint. Injections were administered on postsurgical days 14 and 28, and horses were exercised on a high-speed treadmill for 8 weeks, starting on postsurgical day 15., Results: Clinical improvement in degree of lameness was not associated with MPA administration. Joints that contained an osteochondral fragment and were treated with MPA had lower prostaglandin E2 concentration in synovial fluid, and lower scores for intimal hyperplasia and vascularity in synovial membrane, compared with PF-treated joints. However, articular cartilage erosion and morphologic lesions suggested possible deleterious effect of intra-articular MPA administration., Conclusions: Some beneficial effects of MPA administration on synovial fluid and synovial membrane were identified; however, the deleterious findings contrast with those associated with triamcinolone acetonide used in a similar model, but agree with other results of MPA administration in normal and abnormal joints.

Fifty clinically healthy llamas, 0.5-13 years of age (22 intact males, 10 neutered males, 18 females), with no biochemical evidence of liver disease or hematologic abnormalities, were selected to establish serum bile acid reference intervals. Serum samples submitted to the clinical pathology laboratory were analyzed using a colorimetric enzymatic assay to establish bile acid reference intervals. A nonparametric distribution of llama bile acid concentrations was 1-23 micromol/liter for llamas >1 year of age and 10-44 micromol/liter for llamas < or = 1 year of age. A significant difference was found between these 2 age groups. No correlation was detected between gender and bile acid concentrations. The reference intervals were 1.1-22.9 micromol/liter for llamas >1 year of age and 1.8-49.8 micromol/liter for llamas < or = 1 year of age. Additionally, a separate group of 10 healthy adult llamas (5 males, 5 females, 5-11 years of age) without biochemical or hematologic abnormalities was selected to assess the effects of feeding and time intervals on serum bile acid concentrations. These 10 llamas were provided fresh water and hay ad libitum, and serum samples were obtained via an indwelling jugular catheter hourly for 11 hours. Llamas were then kept from food overnight (12 hours), and subsequent samples were taken prior to feeding (fasting baseline time, 23 hours after trial initiation) and postprandially at 0.5, 1, 2, 4, and 8 hours. In feeding trials, there was no consistent interaction between bile acid concentrations and time, feeding, or 12-hour fasting. Prior feeding or time of day did not result in serum bile acid concentrations outside the reference interval, but concentrations from individual llamas varied within this interval over time.

In diseased animals, laboratory evaluations of erythrocytes, leukocytes, and hemostasis provide important information that contributes to either narrowing the list of potential diagnoses or to determining a specific diagnosis. To adequately interpret the results of these evaluations, normal erythrocyte and leukocyte kinetics and normal hemostatic function must be understood. In addition, knowledge of common diseases resulting in abnormalities of these laboratory tests and of typical changes in these tests caused by these diseases is vital. This article has reviewed normal erythrocyte and leukocyte kinetics and normal hemostatic functions that are clinically significant and has described the laboratory abnormalities expected in common diseases affecting these functions.

The PCV of a llama increased from 50.8 to 74.0% during a 19-month period. The llama remained clinically normal unless stressed, when it would become dyspneic and tachypneic. Thoracic auscultation revealed sounds consistent with pneumonia, but were probably attributable to pulmonary congestion resulting from polycythemia. A diagnosis of secondary absolute polycythemia was made on the basis of high serum erythropoietin concentrations and no evidence of hypoxia. Necropsy revealed congestion of the lungs and liver. Cause of the polycythemia was not determined. Polycythemia should be considered as a differential diagnosis in a llama with exercise intolerance and harsh bronchovesicular sounds.

Complete blood counts and sternal bone marrow aspirates were obtained from healthy adult llamas ranging in age from 2.5 to 8.4 years. Megakaryocyte numbers and erythroid and myeloid series maturation and morphology appeared similar to other mammalian species. The particles contained 50 to 75% marrow cells with the remainder composed of lipocytes and stromal cells. In samples with numerous particles and adequate cellularity, M/E ratios ranged from 0.9 to 2.9. Samples with higher white blood cell counts and fewer particles had higher M/E ratios. Eosinophils comprised 14.3% of the myeloid series which is higher than other domestic mammals. Hemosiderin granules were numerous in marrow particles.

Recent evidence concerning the pathogenesis of equine degenerative myeloencephalopathy indicated that low blood alpha-tocopherol values are a factor in the disease process. Variables that could be introduced by a veterinarian procuring, transporting, or storing samples were evaluated for effects on alpha-tocopherol concentration in equine blood. These variables included temperature; light; exposure to the rubber stopper of the evacuated blood collection tube; hemolysis; duration of freezing time, with and without nitrogen blanketing; and repeated freeze/thaw cycles. It was found that hemolysis caused the greatest change in high-performance liquid chromatography-measured serum alpha-tocopherol values, with mean decrease of 33% (P < 0.001). Lesser, but significant (P < 0.01) changes in serum alpha-tocopherol values were an approximate 10% decrease when refrigerated blood was left in contact with the red rubber stopper of the blood collection tube for 72 hours and an approximate 5% increase when blood was stored at 20 to 25 C (room temperature) for 72 hours. Repeated freeze/thaw cycles resulted in a significant (P < 0.05) 3% decrease in alpha-tocopherol values in heparinized plasma by the third thawing cycle. Freezer storage for a 3-month period without nitrogen blanketing resulted in slight (2%) decrease in mean serum alpha-tocopherol values, whereas values in serum stored for an identical period under nitrogen blanketing did not change. A significant (P < 0.001) mean decrease (10.3%) in alpha-tocopherol values was associated with freezer (-16 C) storage of nitrogen blanketed serum for 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma alpha-tocopherol (vitamin E) values were monitored serially in 9 foals sired by a stallion with equine degenerative myeloencephalopathy (EDM) and in 5 age-matched control foals (sired by a clinically normal stallion) raised in the same environment for the first year of life. Clinical evaluation determined that 8 of the 9 foals sired by the stallion with EDM had neurologic deficits consistent with the disease on one or more occasions during the study period, whereas control foals had normal gait. From 6 weeks to 10 months of age, plasma alpha-tocopherol values in foals with signs of EDM were significantly (P less than 0.001) lower than those in control foals. An oral vitamin E absorption test was performed, and results for 8 of the affected horses and the affected stallion were compared with results for 4 of the monitored control horses and 4 additional control horses. Significant differences were not evident in any of the absorption indices. On the basis of data from this study and supported by reported prophylactic and therapeutic benefits of supplemented vitamin E, low plasma concentration of vitamin E is concluded to be a factor in the development of EDM in the first year of life of hereditarily predisposed foals. It was also concluded that the significantly lower alpha-tocopherol values seen in the foals in this study did not reflect a primary gastrointestinal tract absorption problem.

An oral vitamin E absorption test used in human beings was modified for use in horses. The most appropriate techniques with which to measure gastrointestinal tract absorption of vitamin E (alpha-tocopherol) in horses were developed. Vitamin E was administered orally, and serum values of alpha-tocopherol were measured by use of high-performance liquid chromatography at 0, 3, 6, 9, 12, and 24 hours after vitamin E administration. Variables included comparison of 2 dosages (45 and 90 IU/kg of body weight), routes of administration, and absorption dynamics of 3 preparations of dl-alpha-tocopherol. Absorption of the 2 doses of dl-alpha-tocopherol acetate indicated a dose response; the area under the curve at 24 hours (AUC24) was 4.3 micrograms.h/ml for the 45-IU/kg dose and 32.2 micrograms.h/ml (P less than 0.01) for the 90-IU/kg dose. Maximal absorption was apparent when vitamin E was naturally consumed in grain, compared with administration of identical preparations by stomach tube or paste. In the same horses, dl-alpha-tocopherol and dl-alpha-tocopherol acetate plus polyethylene glycol had statistically similar absorption curves and both had significantly greater AUC24, compared with dl-alpha-tocopherol acetate; values for the 3 compounds were 23.6, 25.8, and 12.6 micrograms.h/ml, respectively. The AUC24 varied between individual horses, but time of peak value was consistently observed between 6 and 9 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

A clinical, viral, hematologic , and genetic study was conducted over a 4-year period on a family of Appaloosas with high incidence of clinical ataxia and pathologic features of equine degenerative myeloencephalopathy. Marginal to deficient serum vitamin E (alpha-tocopherol) and blood selenium values were the only other consistent antemortem abnormalities in the affected horses. Members of this family were all descendants of a clinically normal mare and were raised in 3 separate environments with variable quality of feed. All horses had access to pasture grasses. Normal chromosomal karyotypes were found in 11 affected and/or related horses examined. Equine herpesvirus type 2 was isolated from 4 of the horses, but evidence for a role of this virus in the pathogenesis of the disease was not found. The role of antioxidant deficiency in the pathogenesis of neurologic dysfunction in this equine family and in others reported to be affected with equine degenerative myeloencephalopathy remains speculative.

A syndrome characterized by anemia, erythrocyte dyscrasia, low body weight, and hypothyroidism was observed in 8 llamas (Lama glama). At initial examination (1 to 23 months of age; median, 7.5 months), llamas (3 males, 5 females) were markedly underweight (29 to 55 kg; median, 36 kg) and anemic (PCV, 12.9 to 25.5% [median, 19%]). Five of the llamas became progressively more anemic over time; in 2 of them, PCV decreased to less than 10%. Erythrocyte changes included severe poikilocytosis, anisocytosis, asymmetric distribution of hemoglobin within the cytoplasm, and cytoplasmic extensions from one or both poles. Six llamas had moderate to severe valgus deformities of the carpus. All llamas had low baseline serum thyroxine concentration and diminished response to thyrotropin administration. Baseline and post-thyrotropin triiodothyronine concentrations did not have consistent patterns. Five llamas were hypophosphatemic and 7 had low serum iron concentration (iron concentration was not determined in 1 llama). Orally administered iron supplementation did not induce clinical improvement. Because 3 of the affected llamas were full sisters, a genetic basis for the problem has to be considered. It was not possible to evaluate the familial relationship of the other 5 affected llamas. Although the underlying cause of the problem was not established, the prognosis for affected llamas is guarded to poor.

Between 1983 and 1989, we examined 586 fetuses and dead lambs submitted to a diagnostic laboratory in Oregon. Toxoplasmosis was diagnosed in 74 (12.6%), campylobacteriosis in 89 (15.2%), chlamydiosis in 75 (12.8%), miscellaneous infections in 153 (26.1%), noninfectious causes in 37 (6.3%), and undetermined causes in 158 (27.0%). Detection of Toxoplasma gondii agglutinating antibodies (greater than or equal to 20) in body fluids or heart serum was considered specific for the diagnosis of toxoplasmosis in ovine fetuses or lambs. Toxoplasma gondii antibody titers (reciprocal) in 285 fluids from fetuses or dead lambs were less than 20 (64.5%), 20 (4.5%), 40 (1.7%), 80 (0.7%), 160 (2.1%), 320 (1.7%), 640 (4.9%), 1,280 (2.8%), 2,560 (4.5%), 5,120 (3.8%), 10,240 (2.1%), and greater than or equal to 20,480 (6.3%).

The Veterinary Diagnostic Laboratory at Oregon State University received 172 aborted ovine fetuses during the 1985-1987 lambing seasons; from 120 of these, body fluids were evaluated for IgG levels. Fifty-two (43%) of the fetal fluids had immunoglobulin G (IgG) levels greater than 15 mg/dl. Forty-five (87%) of the fluids with elevated IgG levels were confirmed or presumed toxoplasma or chlamydia abortions. A mean fetal fluid IgG concentration of 111.5 +/- 78 mg/dl was found for the 26 toxoplasma abortions; for the 19 chlamydia abortions, a mean IgG concentration of 109 +/- 91 mg/dl was found. Antibody titers equal to or greater than 1:40 against Toxoplasma gondii were detected in 23 fetal fluids. Fetal fluid IgG concentration less than 15 mg/dl was found to be associated with bacterial organisms (i.e., Campylobacter sp.) as the confirmed or presumed cause of abortion. These results suggest that measurement of fetal fluid IgG concentration is a useful, supportive diagnostic test in determining the cause of ovine abortion, and should be included as a routine laboratory procedure for ovine abortion diagnosis.

Thirty pigs, weighing 17 to 24 kg, were exposed to lead or sodium acetate orally or intraperitoneally (IP) 6 days each week for 13 weeks. These pigs were extremely tolerant of lead. Only mild clinical signs of lead toxicosis were observed in orally lead-exposed pigs despite blood lead concentrations of up to 290 micrograms/dl. Four IP lead-exposed pigs died, but eight other IP lead-exposed pigs survived the exposure period despite blood lead concentrations up to 14,300 micrograms/dl. Lead exposure caused marked decreases in blood delta-aminolevulinic acid dehydratase activities of all pigs and moderate decreases of blood hemoglobin concentrations, hematocrit percentages, mean corpuscular volumes, mean corpuscular hemoglobin concentrations, and mean corpuscular hemoglobins in IP lead-exposed, but not in orally lead-exposed pigs. Basophilic stippling was observed in erythrocytes of lead-exposed pigs, but not in those of control pigs.

The Activated Coagulation Time (ACT) was determined on 10 normal cows. Duplicate samples were taken from each cow. The mean ACT was 145 seconds with a range of 120-180 seconds. Standard deviations were 18 and 13 for the first and second sampling, respectively. Repeatability of the ACT was acceptable.

Blood samples were collected on nonracing days from 57 racing Greyhounds at 2 weeks, 8 weeks, 13 weeks, and 16 weeks after the beginning of the racing season. Hematologic and biochemical tests were performed to detect marked changes induced by stress of racing. In general, these Greyhounds were healthy. Rhabdomyolysis was detected in one dog. In several other dogs, possible subclinical muscle injury was identified by increased serum creatine kinase activities. Mean serum Ca concentrations tended to decrease during the racing season. None of the tests was a good predictor of racing performance. Mean values for several hematologic and biochemical tests were different from those of other breeds of dogs.

Fluctuations of serum vitamin E (alpha-tocopherol), cholesterol, and total lipids were monitored in 12 horses at 3-hour intervals for 72 hours. Mean coefficients of variation were 12, 5, and 15%, respectively. Statistical analyses were used to conclude that instrumentation error was accountable for only a small portion of the vitamin E variation. Results indicated that a single serum sample assay is an unsatisfactory indicator of vitamin E status in horses. These data have clinical application in the evaluation of horses suspected to be affected with equine degenerative myeloencephalopathy. The large variance of serum total lipids and the lack of correlation of it with serum vitamin E over time preclude the use of vitamin E/serum total lipids ratio in assessing vitamin E status.

Fifteen clinical biochemical measurements were done on serum from 64 clinically healthy adult llamas (26 males and 38 females). Values for several of these tests were different from those reported for llamas and from reference values for other domesticated ruminants. Comparison of values between males and females revealed significant differences for several tests. Clinical biochemical values reported in the present study can serve as reference values for adult llamas.

Campylobacter jejuni was inoculated intravenously into pregnant ewes on gestation days 114 and 123 to reproduce ovine abortion. All ewes aborted 7-12 days post-inoculation. High numbers of C. jejuni were isolated from ewe tissues (caruncle, bile, cecal feces), fetal tissues, and placenta. C. jejuni colonies were identified in caruncles and placenta by light microscopy and immunoperoxidase techniques. Histologically, inoculated ewes had a severe purulent endometritis with vasculitis. Placentas from inoculated ewes and field cases showed necrosis and purulent inflammation; however, placentas from inoculated ewes had large numbers of bacterial colonies compared to few bacteria found in field cases. Histologically, only one fetus from the inoculated ewes showed lesions (purulent bronchopneumonia), whereas all fetuses from field cases had a distinct bronchopneumonia, and one fetus showed multifocal hepatic necrosis. These results suggest that C. jejuni (serotypes Penner 1 and Lior 2) is an important abortifacient organism for sheep.

Neutralizing antibodies against equine herpesvirus 1 were measured in serum and cerebrospinal fluid of 16 horses and ponies from a closed herd both before and after vaccination with modified live equine herpesvirus 1. These titers were also measured in 22 neurologically normal and 15 neurologically abnormal horses at a teaching hospital. Animals from the closed herd had prevaccination serum titers up to 1:8 and postvaccination serum titers up to 1:128. Horses from the teaching hospital had serum titers up to 1:64. Cerebrospinal fluid titers were not detected in the vaccinated horses or the neurologically normal horses but a low titer (1:8) was noted in one neurologically abnormal horse. This titer probably resulted from hemorrhage into the cerebrospinal fluid following trauma.

Dried tansy ragwort containing pyrrolizidine alkaloids was fed as 2.5% of a complete (control) diet to Hereford steers, with and without (basal) a mixture of additives. The additives provided a dietary supplement equivalent to 0.1% ethoxyquin, 1% methionine hydroxy analog, 2% MgO, 2.7 mg of vitamin B6/kg of diet, 50 micrograms of vitamin B12/kg of diet, 0.45 g of folic acid/kg of diet, and 0.2 g of cobalt/kg of diet. The additives did not alter tansy ragwort toxicity substantially, as assessed by liver histologic changes, sulfobromophthalein clearance rate, and serum gamma-glutamyl transpeptidase activity. After 281 days, 1 of 4 steers fed the basal diet was alive, whereas 3 of 4 steers in the basal plus additives group were alive, suggesting some protective activity. The chronic lethal dose of tansy ragwort in steers was 3.6% of initial body weight.

A conifer twig was responsible for severe fibrinopyogranulomatous adhesive pleuritis and pneumonia in a horse. At necropsy, the twig was found in a terminal bronchus and extended into the lung parenchyma, through the pleura, and into the accumulated exudate. Inhalation of plant material may be a more common cause of pleuritis than previously recognized. Meticulous examination at necropsy would be necessary to make the diagnosis.

The effect of oral subclinical lead exposure on the susceptibility of swine to Salmonella choleraesuis var kunzendorf was studied in two experiments. In experiment 1, 18 pigs were exposed to lead acetate and 18 pigs were exposed to sodium acetate for 1, 2, or 3 weeks and then challenge exposed intraperitoneally. In experiment 2, 8 pigs were exposed to lead chloride for 2 weeks, 8 pigs were exposed to lead chloride for 1 week, and 8 pigs were exposed to sodium chloride for 2 weeks. These pigs were then challenge exposed orally. Only one pig (sodium acetate-exposed) died during experiment 1, but clinical signs were more severe in sodium acetate-exposed than in lead acetate-exposed animals. In experiment 2, 93.6% of the lead-exposed pigs died, whereas control pigs had 50.0% mortality. In experiment 2, clinical signs were more severe in lead-exposed pigs, and bacteria were more widespread in the tissues of these animals. Significant reductions of beta- or gamma-globulin concentrations or of agglutinating antibody titers were not observed in lead-exposed pigs in either of the trials. Possible mechanisms of the increased susceptibility in lead-exposed pigs of experiment 2 are discussed.

Five days after treatment with chlorpyrifos, a 1.5-year-old male llama was unable to stand, had saliva flowing from its mouth, and had constricted pupils, hyperglycemia, a metabolic acidosis, and a plasma pseudocholinesterase activity of 111 IU/L. Mean (+/- 1 SD) plasma pseudocholinesterase activity of 29 healthy llamas was 233.76 +/- 51.55 IU/L. Five to 8 days after topical application of chlorpyrifos (25 mg/kg of body weight) to 3 healthy llamas, the pseudocholinesterase activity decreased to 38% to 62% of pretreatment (base-line) activity and returned to within 90% of base-line activity by the 36th to 48th day after treatment.