Polymorphonuclear cells have a critical role in the pathogenesis of bovine mastitis. We have documented that experimentally induced Staphylococcus aureus mastitis is associated with cyclic increase and decrease in the quantity of viable bacteria shed in the milk. Concomitant with this cycling of bacteria is an inverse cycling of the hosts cells within the milk. Such somatic cells were determined to be greater than or equal to 95% polymorphonuclear cells. The quality of these cells was evaluated by measuring their relative efficiency of bacterial killing and phagocytosis at various times during an infection. Host polymorphonuclear cells had as much as 10,000-fold variation in the bactericidal failure rate for staphylococci during cell cycling. The most efficient bactericidal effect was observed at or near the peak of the somatic cell count (SCC). The ability of these cycling cells to ingest fluorescent beads was also quantitated by use of flow cytometry. The percentage of phagocytic polymorphonuclear cells that ingested fluorescent latex beads ranged from 15 to 80% of the total cell population during cell cycling, and tended to be optimal at or near peak SCC. In addition, the average number of beads ingested varied between 1 and 2 particles/polymorphonuclear cell, with as many as 17% of the phagocytic cells ingesting 4 or more beads at maximal efficiency. Polymorphonuclear cells from quarters infected with S aureus varied quantitatively (total SCC) and qualitatively (bactericidal activity and phagocytic ability) during the course of an infection. Not only is the quantity of host's phagocytic cells in the mammary gland central to the defense mechanism against infection, but the biological activation state appears to be equally important. The role of these cells in the pathogenesis of a cycling infection is presented in a model to explain the cyclic nature of mastitis.

Periosteal autograft were used for repair of large osteochondral defects in 10 horses aged 2 to 3 years old. In each horse, osteochondral defects measuring 1.0 X 1.0 cm2 were induced bilaterally on the distal articular surface of each radial carpal bone. Control and experimental defects were drilled. Periosteum was harvested from the proximal portion of the tibia and was glued into the principal defects, using a fibrin adhesive. Control defects were glued, but were not grafted. Sixteen weeks after the grafting procedure, the quality of the repair tissue of control and grafted defects was assessed biochemically. Total collagen content and the proportion of type-II collagen were determined. Galactosamine and glucosamine contents also were determined. From these measurements, contents of chondroitin and keratan sulfate and total glycosaminoglycan, and galactosamine-to-glucosamine ratio were calculated. All biochemical variables were compared with those of normal equine articular cartilage taken from the same site in another group of clinically normal horses. Total collagen content was determined on the basis of 4-hydroxyproline content, using a colorimetric method. The proportions of collagen types I and II in the repair tissue were assessed by electrophoresis of their cyanogen bromide-cleaved peptides on sodium dodecyl sulfate slab gels. Peptide ratios were computed and compared with those of standard mixtures of type-I and type-II collagens. Galactosamine and glucosamine contents were determined by use of ion chromatography. In general, the biochemical composition of repair tissue of grafted and nongrafted defects was similar, but clearly differed from that of normal articular cartilage. Total glycosaminoglycan content, galactosamine and glucosamine contents, and galactosamine-to-glucosamine ratio of grafted and nongrafted defects were all significantly (P < 0.05) less than corresponding values in normal equine articular cartilage. By contrast, total collagen content of neocartilaginous tissues of grafted and nongrafted defects was greater than that of normal articular cartilage, although the difference was not significant. The proportion of type-I and type-II collagens in repair tissue in grafted and nongrafted defects was 70 and 30%, respectively. The fibrous nature of the repair tissue reported in a companion morphologic and histochemical study was substantiated by the biochemical results. We concluded that use of periosteal autograft did not improve the healing of osteochondral defects.

Bovine herpesvirus type 1 (BHV-1) isolates are classified into 3 subtypes by use of restriction endonuclease analysis. Isolates from aborted fetuses have been either subtype 1 or 2a, whereas subtype 2b viruses have not been associated with abortion. We assessed the abortifacient property of isolates representing each of the 3 BHV-1 subtypes by IV inoculation of heifers with the virus 25 to 27 weeks after breeding. Three heifers were given Cooper (subtype 1) isolate, 3 heifers were given FI (subtype 2a) isolate, and 5 heifers were given K22 (subtype 2b) isolate. All heifers developed fever and viremia 2 to 5 days after inoculation. Heifers given Cooper or FI isolate aborted between 17 and 85 days after inoculation. The 5 heifers given K22 isolate delivered full-term calves. Placenta was obtained from 4 of the 5 heifers, and K22 virus was isolated from each placenta. Four calves had BHV-1 neutralizing antibody in precolostral serum, with titer ranging from 1:4 to 1:512.

Eighteen healthy dogs were allotted to 3 groups (n = 6 dogs each). All dogs were evaluated at the beginning of the study by complete physical examination; total and differential WBC counts; serum biochemical analysis (alanine transaminase and alkaline phosphatase activities and bilirubin and albumin concentrations); sulfobromophthalein excretion, ammonia tolerance, and glucagon response testing; portal and intraparenchymal pressure determinations; operative mesenteric portography; and histologic assessment of hepatic biopsy specimens. The left hepatic vein was ligated completely in dogs of groups 1 and 2. Group-3 (control) dogs had a ligature placed loosely around the left hepatic vein. Dogs of groups 1 and 3 were reevaluated 24 hours after surgery by use of the aforementioned hematologic and biochemical tests. Group-1 dogs were reevaluated by use of portal and intraparenchymal pressure determinations, jejunal vein portography, and complete necropsy at 48 hours after surgery. At 4 weeks after surgery, dogs of groups 2 and 3 were reevaluated by use of all aforementioned tests. Results indicated transient hepatic congestion, which resolved by the fourth postoperative week. Longstanding effect on hepatic structure, circulation, or function was not found. We concluded that left hepatic vein ligation in clinically normal dogs does not cause severe or permanent liver damage.

To test the effect of a parasite control program for cattle, 2 groups of similar composition were grazed on separate, but equivalent, improved pastures. Cattle in 1 group were treated with fenbendazole at 5.0 mg/kg of body weight at the time they were turned out on pasture in the spring and again at midsummer, when the cattle were moved to a new pasture. The control group was not treated. Parasite egg counts were significantly (P < 0.04) lower in the treated group. Trichostrongyle-type eggs were the most prevalent throughout the, year, except in the month of May, when Strongyloides papillosus eggs were predominant. The number of worms recovered from tracer calves was lower for those on pastures where the treated group grazed than for those on- the control group's pasture. The most consistently recovered parasite was Ostertagia ostertagi, and hypobiosis was observed.

The toxicity of zinc ethylene-bis-dithiocarbamate (zineb), a widely used fungicide, was studied in four 4-week-old Friesian calves with immature rumen function. Calves were first subjected to liver biopsy, and thereafter, 3 of them were orally administered 200 mg of zineb/kg of body weight daily for 80 days, whereas the fourth calf served as control and remained untreated. Clinical, hematologic, and pathologic (including ultrastructural) findings were recorded. The distribution in body fluids and tissues of the parent compound and one of its main metabolites, ethylenethiourea (ETU), also was examined. Treated calves had unthrifty appearance and reduction in weight gain. They also had remarkable impairment of thyroid function, as reflected by reduction in serum concentrations of triiodothyronine and thyroxine and increase in weight of the thyroid gland associated with epithelial vacuolization and foci of hyperplasia. Moderate increase in liver glycogen content and impairment in maturation of germ cells were recorded consistently. Whereas zineb was widely distributed in body tissues, ETU accumulated mainly in the liver and the thyroid gland, although noticeable concentrations also were attained in muscle. Data were consistent with involvement of ETU mainly in the pathogenesis of thyroid gland lesions, and indicate that unweaned calves given zineb develop a clinicopathologic syndrome that does not differ qualitatively from that already described in adult cattle exposed to zineb.

Assay procedures for determining serum haptoglobin concentration and ceruloplasmin oxidase activity in dogs were validated, and reference values were established. Serum haptoglobin concentration is reported as milligrams per deciliter of cyanmethemoglobin binding capacity, whereas serum ceruloplasmin oxidase activity was determined by use of p-phenylenediamine as substrate. Both assays were used to analyze serum samples from 288 dogs. In each dog's case record, clinical history and final diagnosis were evaluated to determine whether the dog had an inflammatory condition. Complete blood cell counts were performed in 265 dogs, using simultaneously collected blood samples. Plasma fibrinogen concentration was determined for 161 dogs. A positive correlation (P < 0.01) was found for serum haptoglobin concentration and for ceruloplasmin oxidase activity, compared with WBC counts, segmented neutrophil and band neutrophil counts, and plasma fibrinogen concentration. Ceruloplasmin oxidase activity and haptoglobin concentration were up to 6 times more sensitive than fibrinogen concentration or leukocyte counts in detecting inflammation. Specificity of ceruloplasmin oxidase activity was comparable to fibrinogen concentration and leukocyte counts, whereas haptoglobin concentration was found to be slightly less specific. Specificity of haptoglobin concentration improved slightly (from 0.82 to 0.88) when dogs with a history of glucocorticoid administration were excluded from analysis. Predictive value of a negative test result (haptoglobin concentration < 125 mg/dl; ceruloplasmin oxidase activity < 20 IU/L) and predictive value of a positive test result for haptoglobin concentration and ceruloplasmin activity were comparable to or better than fibrinogen concentration or various oxidase leukocyte counts in detection of inflammation in a variety of disease conditions. We concluded that serum haptoglobin and ceruloplasmin oxidase assays could be used as adjuncts for diagnosis of the inflammation in dogs.

A flow cytometric procedure was evaluated to measure the oxidative burst activity (hydrogen peroxide formation) of bovine neutrophils. The method involves measuring the oxidation of intracellular dichlorofluorescin to fluorescent dichlorofluorescein (DCF). Phorbol myristate acetate (PMA) was used to perturb the neutrophil plasma membrane. The sources of variation introduced into the DCF assay were also examined. The sources of variation were attributable to the isolation of neutrophils from blood, variation between duplicate assays and duplicate flow cytometric determinations of oxidative product formation, variation in neutrophil oxidative product formation among cows, and the variation (over repeated daily and weekly neutrophil isolations) in neutrophil oxidative product formation. A final objective was to determine effects of dexamethasone on oxidative product formation, and whether differences existed between blood and mammary neutrophils in oxidative product formation. There was an increasing trend in the formation of DCF with increasing time of incubation and with increasing PMA concentration. Increasing the concentration of PMA decreased lag time and increased the rate of oxidative product formation. The increase in DCF formation was statistically significant up to a PMA concentration of 10 ng/ml. This concentration was considered optimal for bovine neutrophils. Examination of the sources of variation indicated that (i) the neutrophil isolation technique was a major source of variation (17.2 to 28.4% of the total variation), and that more than one neutrophil isolation within a cow would be required to obtain an accurate estimation of DCF formation in neutrophils; (ii) duplicate assays and duplicate readings on the flow cytometer accounted for < 0.05% of the total variation and would not be necessary when performing the DCF assay; (iii) large variation (62.4 to 70.8%) existed among cows in neutrophil oxidative product formation, indicating that any treatment being compared should be done either within or preferably repeated across a large number of cows; and (iv) the variation over repeated daily (0.3%), but not weekly (19.6%) determinations of neutrophil oxidative product formation, were small enough to allow for the evaluation of major physiologic and environmental effects. Intramuscular administration of dexamethasone (50 microgram/ kg of body weight) resulted in an approximate 80% decrease in neutrophil oxidative product formation. Oxidative product formation was 75% less for neutrophils isolated from mammary secretions when compared with neutrophils from blood. These results indicated that the DCF procedure was responsive to factors known to interfere with oxidative metabolism of bovine neutrophils.

Enterotoxemia was induced in 4 lambs and 4 goat kids by continuous intraduodenal infusion of a whole culture of Clostridium perfringens type D. Clinical signs, hematologic values, biochemical alterations, and postmortem lesions in the lambs and goat kids were compared. The 4 lambs and 4 goat kids died within 25 hours of beginning the infusions. Lesions were not observed in the gastrointestinal tract of the 4 lambs; however, severe hemorrhagic enterocolitis was found in the 4 goat kids. This difference between the lambs and goat kids in the lesions caused by experimentally induced enterotoxemia may explain the discrepancies reported between sheep and goats in clinical signs, response to treatment, and efficacy of vaccination observed in naturally induced enterotoxemia in the 2 species.

Nine 115- to 180-kg, hay-adapted, Holstein steers were fed an experimental diet with added sodium sulfate that induces polioencephalomalacia (PEM). Five calves developed the disease. Thiamine concentrations in blood, CSF, brain, and liver were not indicative of thiamine deficiency. The odor of hydrogen sulfide in eructated rumen gas was associated with the onset of PEM. Sulfide concentrations in rumen fluid were measured 1 or 2 times a week by 2 techniques. Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced. The highest concentrations coincided with the onset of clinical signs of PEM and were significantly higher in the calves that developed PEM than in those that did not. This suggests that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.