Serum concentrations of iodine were determined after cattle were given ethylenediamine dihydriodide (EDDI) orally at dosages ranging from 0.0 (placebo) to 0.77 mg/kg of body weight/day. The serum iodine concentration was correlated with the dosage of EDDI. A rate of 0.11 mg EDDI/kg/day was correlated with serum iodine concentrations (20 to 80 micrograms/dl) previously found to be effective in preventing foot rot in cattle. A linear dose-response curve that was generated could be helpful in predicting dosage of EDDI if the serum iodine concentration is known.

A study on erythrocyte distribution was performed on 10 healthy, nonstressed adult white Pekin ducks. Results indicated 2 populations of erythrocytes, with average mean corpuscular volumes of 128.37 fl/cell and 308.50 fl/cell. Variations in erythrogram patterns were evident over time, when comparing specimens from different ducks or the same duck. There were 5 patterns of cell number/volume distribution observed between the 2 cell populations when all ducks were studied. Females had a greater change than did males when population density and volume percentage comparisons were made on erythrocyte compartments.

Concurrent bacteriologic culture of feces and agar gel immunodiffusion (AGID) testing was performed on all cows and bred heifers over 14 months old in 10 dairy herds during a 32-month period to determine the effectiveness of the AGID test for the detection of subclinical paratuberculosis. Herds were sampled 5 times and, when possible, culled animals were tested again at slaughter. During 5 herd-wide samplings, Mycobacterium paratuberculosis was isolated from 139 fecal specimens obtained from 109 cattle. Results of the AGID test were simultaneously positive 40 of 139 times (28.8%). Thirty-six of the 109 cattle (33.0%) determined to be infected had a positive AGID test result at some point during the 5 herd-wide samplings. When results of tests performed at time of slaughter were included, 117 cattle were identified as infected by culture methods; 55 of these (47.0%) were AGID test-positive at some point during the study. The upper limit of the maximal false-positive rate for the AGID test was 2.1%. On the basis of colony counts from cultures, subclinically infected cows shedding higher numbers of M paratuberculosis in the feces were more likely to have positive AGID test results (P less than 0.0001). In known infected cattle, neither the culture nor AGID test results were consistently positive on repeated testing. Of 48 official calfhood paratuberculosis vaccinates tested as adults, 3 had positive AGID test results and in 1 of these, M paratuberculosis was also isolated from the feces, indicating that the rate of false-positive AGID test results in calfhood vaccinates is low.

Hereford heifer calves were experimentally infested with Psoroptes ovis. Histologic examination of skin specimens was conducted at weekly intervals before and after treatment with ivermectin on postinfestation week 7. Electron microscopy revealed numerous degranulating mast cells in the skin of infested but not in control calves. Many active, as well as degenerate, neutrophils were in the scab on infested calves. Microscopic epidermal ulcers developed on infested calves when live mites were present but not after treatment. Numbers of dermal neutrophils and plasma cells decreased and numbers of circulating neutrophils increased 1 week after treatment. Numbers of dermal eosinophils and mast cells in calves with eosinophilia increased for several weeks after treatment. Statistical analysis indicated significant correlations (P less than 0.05) among numbers of dermal inflammatory cells, hemogram values, and changes in dermal thickness. Seemingly, mite-induced epidermal damage was the key pathogenic event in psoroptic scabies in calves. Mast cell degranulation contributed to the pathogenesis of the dermatitis, and neutropenia was caused by sustained, poorly compensated efflux of neutrophils into the scab through mite-induced breaks in the epidermis.

Capsular polysaccharide (CP) of Pasteurella haemolytica (type A1) was first deposited by fiberoptic bronchoscopy in the lungs of sheep to examine lesions and changes in bronchoalveolar lavage cell populations and, later, was mixed with pulmonary surfactant to investigate alterations in physical properties or surface tension. At 22 hours after deposition, minimal lesions were seen in the lungs only at and contiguous to the site of CP deposition in 2 of 4 sheep. Microscopically, alveoli and interlobular septa were filled with edema fluid. Terminal airways and alveoli contained a moderate amount of neutrophils that varied between sheep. Significant differences in number or type of bronchoalveolar lavage cells were not observed in the weekly lavages between each group or among sheep within each group, either before or after deposition of CP or physiologic saline solution. After 6 hours of incubation at 37 C, CP-surfactant mixtures were examined with a surface tensiometer and centrifuged in sucrose gradients. The CP bound to surfactant, resulting in formation of a precipitate with a surface tension of 31.6 +/- 0.1 dynes/cm and a density of 1.07 to 1.08 g/ml. Lipopolysaccharide of P haemolytica, used as a control, also bound to surfactant, resulting in a complex with a surface tension of 57.7 +/- 0.4 dynes/cm and a density of 1.06 to 1.10 g/ml. Surfactant alone had a surface tension of 32.6 +/- 0.2 dynes/cm and density of 1.05 to 1.06 g/ml. The CP appears by itself not to be a direct major factor in the lung damage that develops in cases of pneumonic pasteurellosis. However, the precipitation of surfactant by CP may be a lectin reaction that would allow the attachment of the organism to the lining of the alveolus and become established during an infection.

Sensory nerve conduction velocity was measured in the lateral palmar nerve of 8 horses. The limb temperature was manipulated by external means and monitored. Alterations in the nerve conduction velocity related to limb temperature variation were identified at both increased and decreased temperatures. These were quantified and a mean value of 2.15 +/- 0.2 m/s/degree Celsius was determined. The effect of altered limb temperature should be considered in nerve conduction velocity determinations.

To test the acidifying ability of the distal portion of the nephrons in healthy dogs, 0.2 g of NH4Cl/kg of body weight was given PO. Samples for venous blood gas analysis and urine pH were taken hourly for 6 hours. Systemic acidemia developed, as evidenced by statistically significant (P less than 0.05) decrease in blood pH 1 hour after NH4Cl administration. Four hours after administration, mean urine pH decreased to a low of 5.16 +/- 0.1 and was less than 5.5 3 hours after administration. Changes in urine pH 2 hours after administration were statistically significant (P less than 0.05). In human beings, NH4Cl loading is used to detect patients with distal renal tubular acidosis (defective hydrogen ion secretion by the distal nephrons) and normal acid/base values. Distal renal tubular acidosis is diagnosed if urine pH fails to decrease to less than 5.5 after NH4Cl administration. On the basis of findings of this study, a similar value would be valid for dogs.

Fecal excretion of a particulate marker, ytterbium (Yb), was evaluated in 9 horses before surgery and 3 weeks, 3 months, and 6 months (4 trials) after sham-operation (group 1; n = 3) or extensive large colon resection (group 2; n = 6). Fecal excretion curves of total Yb excretion, log(e) Yb excretion, % Yb excretion, log(e) % Yb excretion, and cumulative % Yb excretion were evaluated, and kinectic analysis was performed on the log(e) Yb excretion curves to detect mixing pools and to calculate the fractional rate of particulate passage, turnover rate, and pool size. Calculations were performed to determined transit time, mean overall retention time, adjusted mean retention time, peak time, and disappearance time. Values were statistically analyzed to determine differences between groups and among trials (P less than 0.05). Group-2 horses had significantly shorter transit, peak, and mean overall retention times, compared with preoperative values and with values for group-1 horses. Two mixing pools were identified: a slower emptying pool of 5.7% hour-1 (k1) and a faster emptying pool of 12.3% hour-1 (k2). The rate of passage from the first pool (k1) was not altered by colon, resection, and was interpreted as being most influenced by the cecum. In further support of this interpretation, the capacity of the k1 pool approximated the capacity of the cecum (17 L). The capacity of the k1 pool significantly expanded by 6 months in the resected horses. The rate of passage from the second pool (k2) significantly increased initially after colon resection (3 weeks and 3 months), but returned to preoperative values by 6 months. This pool was affected by colon resection, and was therefore interpreted as being influenced by a portion of the colon. Despite these changes in rate of passage and capacity of the mixing pools, on all the trials, colon resection decreased intestinal transit time and overall mean retention time because of a decrease in the total large intestinal length or capacity. This decrease in particulate matter retention and transit time may partially or totally explain the decrease in fiber digestion reported in horses with extensive large colon resection.

Eight mature horses with no prior signs of joint disease or history of intra-articular therapy were treated with 8 weekly intra-articular injections of methylprednisolone acetate. Treatments were given at a dose of 120 mg/joint into the right radiocarpal and intercarpal joints, with the left joints as untreated controls. Articular cartilage samples were obtained at necropsy 1, 4, and 8 weeks after the last injection. Compared with controls, cartilage from injected joints had loss of hematoxylin basophilia and decreased intensity of staining in safranin O fast green dye. Chondrocyte necrosis and hypocellularity were observed in all samples of cartilage from treated joints. Proteoglycan content and its rate of synthesis were reduced. There was a progressive loss of proteoglycan content, whereas proteoglycan synthesis increased somewhat 4 and 8 weeks after treatment. Collagen content was unchanged, but its rate of synthesis was markedly inhibited. Collagen synthesis did not recover, but remained decreased at 5 to 15% of the values from untreated cartilage. Water percentage was increased, but fibronectin content was not significantly different. A single injection of methylprednisolone acetate was also given into the right metacarpophalangeal joints of 3 of the 8 horses in this group, with the left joints serving as untreated controls. Sixteen weeks after the treatment, cartilage of the treated joints had a loss of histochemical staining and proteoglycan content was reduced to 50% of control values. The mean rate of proteoglycan synthesis and mean fibronectin content were increased, but the differences were not statistically significant (P greater than 0.05). Other variables were essentially unchanged. For control studies, the right carpal joints of 2 additional horses were injected with the drug suspension vehicle. All measurements, compared with those of samples from untreated joints, were unchanged. On the basis of our findings, we concluded that the effects on cartilage of intra-articular injections of methylprednisolone acetate were not ameliorated at 8 weeks after 8 weekly injections or 16 weeks after a single injection. Cartilage remained biochemically and metabolically impaired.

Transstadial and transovarial transmission of Anaplasma marginale by Dermacentor variabilis were attempted with ticks exposed to the organism once by feeding as larvae or nymphs, and twice by feeding as larvae and nymphs. Typical colonies of A marginale were in gut tissues of adults that were infected as larvae, larvae and nymphs, and as nymphs; repeated exposure of ticks did not appear to result in an increase in the number of colonies in the gut of subsequently molted adults nor did it affect severity of the clinical disease that developed in cattle they fed on. In contrast, colonies of A marginale were not found in the midgut epithelium of unfed nymphs exposed as larvae, even though companion nymphs transmitted the parasite, causing severe clinical anaplasmosis in susceptible calves. The organism was not transmitted transovarially by F1 larvae or nymphs from the groups exposed as parent larvae, nymphs, larvae and nymphs, and as adults. Some of the calves fed on by F1 progeny had a few erythrocytic marginale bodies that looked suspiciously like A marginale, as well as postchallenge exposure prepatent periods that were longer than other calves in the transovarial transmission study. Sera from these calves were tested for antibody to A marginale, using a highly sensitive immunoblot technique. Antibodies were not detected in any of the sera.