The relationship of serum complement activity and bacteriostatic activity was investigated in male guinea pigs given aflatoxin and/or rubratoxin. In experiment 1, guinea pigs were given 0.6 mg of aflatoxin/kg of body weight, PO, once. In experiment 2, guinea pigs were given 0.02 mg of aflatoxin/kg, PO, and/or 8 mg of rubratoxin, PO, 11 times. Aflatoxin (0.02 mg/kg) had no effect given alone, but potentiated the effect of rubratoxin. In both experiments, changes in complement activity were accompanied by similar but not always significant (P less than 0.05) changes in bacteriostatic activity of serum. Guinea pigs given 0.06 mg of aflatoxin/kg had significant (P less than 0.05) changes in complement titers and in serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase activities. Guinea pigs given repeated oral doses of aflatoxin and/or rubratoxin had changes in complement titers, bacteriostasis, and alkaline phosphatase and aspartate aminotransferase activities, but not in alanine aminotransferase activities. Significant differences were detected only when average values for all guinea pigs given rubratoxin or rubratoxin with aflatoxin were compared with average values for guinea pigs not given rubratoxin.

Thirty-eight tracheobronchial aspirates (TBA) were collected from twenty 1 to 6-month-old foals, which were free of clinical signs of respiratory tract or other infectious disease. We collected TBA from 9 of the foals 3 times when they were approximately 8, 16, and 24 weeks old. Aspirates were examined cytologically after staining with modified Wright-Giemsa, Gram, toluidine blue, and prussian blue stains. Aerobic bacterial culturing was performed on all aspirates. Of the 20 initial TBA, 4 (20%) were normal cytologically on the basis of previously defined criteria for TBA from clinically normal horses, 6 (30%) had a high percentage of eosinophils (> 5%), 8 (40%) were classified as indicative of subacute inflammation, and 2 (10%) were classified as indicative of acute inflammation. Nine (45%) were positive for mast cells and none were positive for hemosiderin-laden macrophages (hemosiderophages). Of the 9 foals from which samples were collected at 16 and 24 weeks of age, results were similar, except for an increase in the number of TBA classified as indicative of chronic inflammation (33% and 22% respectively) and the number positive for hemosiderophages (33% and 88%, respectively). One TBA was considered nondiagnostic because of pharyngeal contamination. Culturing of 12 of the 37 aspirates (32%) yielded a potential microbial pathogen. Only 2 were positive cultures from the same foal. The following organisms were isolated: beta-hemolytic Streptococci spp (4), Actinobacillus/Pasteurella spp (4), Rhodococcus equi (2), unidentified nonenteric Gram-negative rod (1), and Escherichia coli (1). Thirty-four of the 37 aspirates (92%) yielded light growth of various organisms considered to be nonpathogenic and normal inhabitants of the upper respiratory tract. It was concluded that the presence of inflammatory cells, eosinophils, and mast cells in the tracheobronchial aspirates from clinically normal foals is a common finding. These cytologic findings were consistent in the samples collected from foals at 8, 16, and 24 weeks of age. It was also concluded that bacteria with recognized pathogenicity can be isolated from TBA from clinically normal foals and were most frequently isolated from 1- to 2-month-old foals or those with cytologic evidence of inflammation, even in the absence of clinical signs of respiratory tract disease.

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.

Salivary glands from males of 3 Dermacentor species (D andersoni, D variabilis and D occidentalis) that were infected with either the Virginia or Idaho isolate of Anaplasma marginale as nymphs or adults were examined for colonies of A marginale by use of light and electron microscopy. Prior to dissection of salivary glands, exposed ticks were held at 25 C for 15 to 18 days, followed by a 3-day incubation at 37 C. Ticks of 2 species transmitted A marginale to calves; the third tick species was confirmed infected by demonstration of typical colonies in tick gut cells, but transmission was not attempted; Colonies of A marginale were seen with light microscopy in salivary glands of all 3 species of ticks; they were located in acinar cells that contained simple granules. Colonies varied morphologically from small, compact ones to larger structures that contained distinct organisms and often were adjacent to the host cell nucleus. Electron microscopy confirmed that the colonies were rickettsial organisms. Morphologic features of A marginale varied and included reticulated forms, forms with electron-dense centers, and small particles; these various forms were similar to those described previously in midgut epithelial cells of ticks. We believe that the organism seen within tick salivary glands may replicate in the glands before its transmission to the vertebrate host.

Bovine pulmonary artery cells in cell culture were exposed to lipopolysaccharide (LPS) purified from Pasteurella haemolytica serotype A1. This resulted in severe membrane damage, which caused a time- and dose-dependent release of lactate dehydrogenase that was first detected 4 hours after exposure and reached a maximal mean release of 67% after 24 hours of exposure to 1 microgram of LPS/ml. Mean release of 51chromium followed by a similar pattern and reached a maximum of 61% following 24 hours of exposure to 10 micrograms of LPS/ml. Morphologically, endothelial cells responded to LPS by marked cell membrane retraction, the formation of numerous cytoplasmic blebs, and ruffling of the cell membrane. Subsequently, the cells became round and detached. Cell detachment reached a mean of 95% following 8 hours of exposure to 1 microgram of LPS/ml. These studies demonstrated that P haemolytica LPS is capable of causing direct damage to bovine pulmonary arterial endothelial cells, which may be important in the pathogenesis of bovine pneumonic pasteurellosis.

Blood and urine chemical values at parturition in clinically normal Holstein cows (n = 12) were compared with the same values in Holstein cows developing udder edema (n = 12). There was no statistically significant mean difference between the 2 groups for the serum and urine chemical data. Furosemide (500 mg) given IV caused a significant increase in serum calcium and sodium, urine chloride, potassium, and sodium, and fractional excretional ratio of chloride, potassium, and sodium. There was a significant mean decrease in the serum potassium, urine creatinine, osmolality, pH, and specific gravity. Hydrochlorothiazide (250 mg) given IV caused a significant mean increase in serum chloride, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride, potassium, and sodium. There was a significant mean decrease in serum potassium and sodium, urine osmolality, pH, and specific gravity. Acetazolamide (500 mg) given IV caused a significant mean increase in blood urea nitrogen, serum chloride and glucose, urine sodium, and fractional excretion ratio of sodium, while causing a significant mean decrease in serum potassium, sodium, and phosphorus, and urine creatinine. Dextrose (500 g) given IV as a 50% solution caused a statistical mean increase in serum glucose, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride and potassium. A statistical mean decrease occurred in the packed cell volume, blood urea nitrogen, serum calcium, potassium, sodium, and phosphorus, urine creatinine, osmolality, and pH.

A controlled anthelmintic trial was conducted to determine the efficacy of febantel paste (45.5%) at dosages of 2.5, 5.0, 7.5, and 10.0 mg/kg in calves harboring natural gastrointestinal nematode infections. Dosages of 5.0, 7.5 and 10.0 mg of febantel/kg of body weight were greater than 96% effective in removing adults of Haemonchus contortus, Ostertagia spp, Cooperia spp, and Oesophagostomum radiatum. The 2.5 mg/kg dosage was considered suboptimal because of low efficacy against Ostertagia and Cooperia spp. Efficacies against Trichostrongylus axei, Trichuris spp, Bunostomum phlebotomum, and Strongyloides papillosus were difficult to determine because fewer numbers of these nematodes were recovered. Efficacies of febantel paste against immature bovine parasites ranged from 83.62% to 97.72%.

Anthelmintic efficacy of levamisole against induced infections with 7- and 21-day-old Haemonchus contortus, Ostertagia circumcincta, Trichostrongylus axei, and T colubriformis was evaluated as an oral drench in goats. Group 1 (n = 8) was not treated, group 2 (n = 8) was given 3.96 mg of levamisole/kg of body weight, group 3 (n = 8) was given 7.92 mg of levamisole/kg, and group 3 (n = 7) was given 11.88 mg of levamisole/kg. Efficacy against all worms was low in goats given 3.96 mg of levamisole/kg, but was high against adult H contortus (99%) and adult T colubriformis (99.7%) in goats given 7.92 mg of levamisole/kg. Although efficacy against adults of all species was high in goats given 11.88 mg of levamisole/kg, some immature worms of all species remained in the abomasa of goats.

Protein profiles of whole homogenates of anconeus (slow twitch) and biceps femoris (fast twitch) muscles of clinically normal dogs and of Labrador Retrievers with hereditary myopathy (HM) were resolved on flat bed polyacrylamide isoelectric-focusing gels. Three methods of sample solubilization were performed. The solubilization buffer, with high concentrations of urea, precipitated the zwitterionic detergent, but use of the buffer containing 3% NP-40, 9.2M urea, and 0.1M arginine resulted in better resolution and stability of pH gradient. Gels of anconeus muscle from clinically normal dogs contained 2 protein bands specific to anconeus muscle, whereas gels of biceps femoris muscle from clinically normal dogs contained 3 protein bands amplified in biceps femoris muscle that were barely detectable in anconeus muscle. The staining intensity of protein bands in biceps femoris muscles from Labrador Retrievers with HM was decreased, relative to controls. The quantitative analysis of peak height ratios of biceps femoris muscle revealed significant (P less than 0.05) differences between profiles of clinically normal dogs and Labrador Retrievers with HM.