This work was an attempt to develop an in vitro adherence model for Mycoplasma hyopneumoniae, using monolayers of human and porcine lung fibroblasts and porcine kidney cells. Mycoplasma hyopneumoniae grown in Friis mycoplasma broth was radiolabeled with 35[S]-methionine, washed, concentrated, and inoculated on the monolayers. After 15 minutes of centrifugation to facilitate adherence, monolayers were washed 3 times, dissolved with 0.1N NaOH, and suspended in scintillation liquid, and the radioactivity was determined in a liquid scintillation counter. Adherence, measured as a percentage of counts added, varied according to the mycoplasma strain and the cell line used. Comparison of strains J, 144L, and 232 of M hyopneumoniae revealed 7.5 +/- 5.9, 31.9 +/- 13, and 9.6 +/- 5% adherence to porcine kidney cells, respectively. Slightly different, but proportionally the same relationships were obtained with swine or human fibroblasts. Adherence was decreased slightly by repeated washings of the mycoplasma-treated cell monolayers; however, a plateau was reached, indicating irreversibility of the adherence process. Pretreatment of cell monolayers with nonlabeled organisms substantially blocked adherence by labeled organisms. Dilution of labeled organisms resulted in an increased proportion adhering. Therefore, it appears that the adherence was a receptor-dependent event. Treatment of the mycoplasmas with trypsin prior to the inoculation of monolayers resulted in a marked reduction in adherence. Treatment of the mycoplasmas with hyperimmune swine serum against M hyopneumoniae or normal swine serum resulted in 80 to 90% reduction of adherence; however, no inhibition occurred when mycoplasmas were treated with purified IgG from the hyperimmune serum.

A mucosal lesion was created in the center of each test sinus of 6 mature, healthy, nonlactating Holstein cows by resecting a circumferential band of mucosa. Each lesion was then treated by implantation of strip grafts of autogenous oral mucosa, temporary silastic tube implant, or a combination of strip grafts and temporary silastic tube implant. All teats were evaluated for patency 6 weeks after treatment, and tube implants were removed through a second thelotomy incision. All teats were reevaluated for gross and radiographic patency 12 weeks after treatment, and teats were collected for histologic evaluation of lesions. All 4 teats treated with grafts only were obstructed at 6 and 12 weeks after treatment. Incomplete coverage of the lesion with mucosa was observed in all 4 teats. The major source of obstruction was proliferation of epithelium and keratin into the lumen. All 8 teats treated with temporary silastic tube implants alone were patent at 6 weeks after treatment, but were obstructed at 12 weeks after treatment. Foci of mucosa at the lesion site were detected in only 2 of the 8 teats. Obstruction resulted from proliferation of granulation tissue into the lumen. All 12 teats treated with grafts and a temporary tube implant were patent at 6 weeks after treatment and 11 of 12 were patent at 12 weeks after treatment, although marked luminal narrowing was evident in 9 of 11 teats. Partial to complete coverage of the lesion with mucosa was seen in all teats. Proliferative granulation tissue, epithelium, and keratin contributed to luminal narrowing in 10 of 11 patent teats. Bacteriologic culture of quarters from 6 of the 11 teats patent at the final evaluation yielded pathogens.

To investigate the cardiopulmonary effects of positive end-expiratory pressure (PEEP), values of 10, 20, and 30 cm of H2O, were applied to anesthetized, dorsally recumbent, ventilated ponies. After IV induction of general anesthesia, PEEP was superimposed on controlled ventilation with 100% oxygen, and changes in gas exchange and cardiac function were measured. Increasing values of PEEP in these ponies caused a linear increase in the mean (+/- SEM) functional residual capacity, from a control value (zero end-expiratory pressure) of 1.7 +/- 0.24 L to 2.2 +/- 0.31, 2.9 +/- 0.32 and 3.4 +/- 0.3 L at PEEP of 10, 20, and 30 cm of H2O, respectively (P < 0.05). Paralleling these changes, intrapulmonary shunt fraction decreased significantly (P < 0.05) from a control value of 12.9 +/- 0.5%, to 7.5 +/- 1.1 and 2.1 +/- 0.6%, at PEEP of 20 and 30 cm of H2O, respectively. Cardiac output was decreased by increasing values of PEEP, from control value of 11.7 +/- 1.56 L/min to 9.9 +/- 1.51, 8.8 +/- 1.33 and 5.62 +/- 0.56 L/min at PEEP of 10, 20, and 30 cm of H2O, respectively. Related to decreasing cardiac output, tissue oxygen delivery also decreased as PEEP was increased, from control value of 2.0 +/- 0.09 L/min to 1.8 +/- 0.07, 1.6 +/- 0.06, and 1.03 +/- 0.04 L/min at PEEP of 10, 20, and 30 cm of H2O, respectively. Thus, the effects of increasing values of PEEP in these ponies included increased functional residual capacity and arterial oxygenation, but marked reduction in cardiac output, resulting in no improvement or decrease in total oxygen delivery. Although PEEP is useful for improving arterial oxygenation, the deleterious cardiovascular effects should be anticipated or ameliorated by use of volume loading and/or inotrope administration.

Immunoturbidimetric determination of serum IgG concentration in foals was compared with the reference methods of single radial immunodiffusion and serum protein electrophoresis. High positive correlations were discovered when the technique was compared with either of these reference methods. The zinc sulfate turbidity test for serum IgG estimation was also evaluated. Although a positive correlation was discovered when the latter method was compared with reference methods, it was not as strong as the correlation between reference methods and the immunoturbidimetric method. The immunoturbidimetric method used in this study is specific and precise for equine serum IgG determination. It is rapid and, thus, is advantageous when timely evaluation of critically ill foals is necessary. The technique should be adaptable to various spectrophotometers and microcomputers for widespread application in veterinary medicine.

T-cell-mediated and humoral immune responses were measured in chickens infected with standard and variant strains of infectious bursal disease virus. One-day-old and 3-week-old chickens were infected with these viruses and then given sheep RBC, killed Brucella abortus strain 19, and Newcastle disease virus. Appropriate serologic tests were used to monitor the primary and secondary responses to the antigens. Lymphoblast transformation assays were performed weekly. The response to the infectious bursal disease virus was determined by virus neutralization tests, microscopic examination of bursas, and bursal to body weight ratios. One-day-old chickens had T-cell-mediated and humoral immune suppression with both strains of virus, compared with controls. The lymphoblast transformation responses indicated that the variant strain was significantly (P < 0.05) more suppressive than the standard strain. Three-week-old chickens had humoral immune suppression with the standard strain, but not with the variant strain. The lymphoblast transformation response was transiently suppressed at this age by the variant strain only. During the first week of infection, 1-day-old and 3-week-old chickens had lower neutralizing antibody titers to the variant strain than to the standard strain.

The development of Anaplasma marginale was studied in Dermacentor andersoni nymphs after they had fed on a calf with ascending Anaplasma infection. Gut tissues were collected on day 4 of tick feeding, from newly replete (fed) nymphs and on postfeeding days (PFD) 5, 10, 15, 20, and were processed for light and electron microscopy to determine density of A marginale colonies. Homogenates of gut tissues were prepared from nymphs collected on the same days and inoculated into susceptible, splenectomized calves to test for infectivity. Anaplasma colonies were detected in gut cells on PFD 5, 10, 15, and 20. Although colony density appeared to be higher on PFD 10 and 15, differences were not significant. Nymphal type-1 colonies were detected in highest numbers on PFD 5 and 10, transitional colonies were seen in highest numbers at PFD 10 and 15, and nymphal type-2 colonies were observed only on PFD 20. Gut homogenates that were collected from ticks at 4 days of feeding, when newly replete, and on PFD 20 caused anaplasmosis when injected into susceptible calves, but homogenates made from ticks collected on PFD 5, 10, and 15 were not infective. The data indicate that of the colony types of A marginale that develop in replete nymphs, nymphal type-1 and transitional colonies may contain organisms that are not infective for cattle.

Streptococcal species isolated from dairy cows with clinical mastitis were obtained from mastitis research workers in Florida, Louisiana, New York, Vermont, Washington, and West Virginia. Seventy-one streptococcal isolates were tested, including 39 strains of Streptococcus agalactiae, 21 strains of S dysgalactiae, and 11 strains of S uberis. The minimal inhibitory concentration of erythromycin, lincomycin, oxytetracycline, penicillin, spectinomycin, streptomycin, and tetracycline was determined for each isolate. Differences were not detected among strains with respect to geographic origin. None of the strains was resistant to penicillin. Lincomycin was the next most effective antimicrobial, with only 2 resistant strains of each streptococcal species. There were no differences among the streptococcal species with respect to resistance to either penicillin or lincomycin. Streptococcus uberis was more likely to be resistant to erythromycin than were S agalactiae and S dysgalactiae (P < 0.02). Streptococcus agalactiae and S uberis had similar distributions for resistance to oxytetracycline, tetracycline, spectinomycin, and streptomycin. Strains of S dysgalactiae were more likely to have intermediate resistance to oxytetracycline and streptomycin than were strains of S agalactiae and S uberis, which were highly resistant to oxytetracycline and streptomycin (P < 0.001). Differences were not detected among the streptococcal species with respect to resistance to spectinomycin. Resistance to multiple antimicrobials was observed in all streptococcal species tested. Although S dysgalactiae appeared to have a greater percentage of strains (73%) that were resistant to multiple antimicrobials than did S agalactiae (31%) or S uberis (45%), differences were not statistically significant.

Data at admission and at surgery were collected on 458 cows with right displacement of the abomasum or abomasal volvulus, to derive multiple logistic regression models for predicting postsurgical outcome (productive, salvaged, or terminal). The derived models contained few and easily obtained variables. The weight associated with each variable was determined objectively. Three admission variables (heart rate, base excess, and plasma chloride concentration), and 5 surgical variables (heart rate, base excess, diagnosis, method of decompression used, and appearance of abomasal serosa) were used in the final models. Predicted outcomes that used the admission and surgical models were closely related with actual outcomes. Total correct classification for satisfactory (productive) versus unsatisfactory outcome (salvaged and terminal) was 78.2% for the admission model and 82.7% for the surgical model. Combining data on cows with productive and salvaged outcomes as satisfactory outcome, and terminal as unsatisfactory outcome, total correct classification was 90.7% for the admission model and 93.2% for the surgical model. Using predicted probabilities, the market value of productive and salvaged cows, and the medical and surgical costs, one can calculate the expected economic value of each outcome. Treatment can be justified if the sum of the expected value of productive and salvaged outcome exceeds the sum of the medical and surgical costs and the expected salvaged value of the cow that was not treated surgically.

The balance of coagulation and fibrinolysis was studied in 15 horses during the prodromal stages of acute laminitis induced by carbohydrate overload. Progression of the disease was stopped 12 to 24 hours before the expected onset of lameness in trial 1 (8 horses) and at the onset of lameness in trial 2 (7 horses). The end points in each trial were identified by specific changes in blood pressures (trial 1) and by changes in pulse, rectal temperature, and arterial pressure (trial 2) that were anticipated on the basis of original description of the experimental model. Blood samples for hemostasis evaluation were collected before and after carbohydrate overload in trial 1 and after carbohydrate overload in trial 2. Significant changes were not detected in platelet count, mean platelet volume, prothrombin time, activated partial thromboplastin time, fibrinogen concentration, plasminogen concentration, alpha-2-antiplasmin, antithrombin III, protein C, thromboxane B2, or fibrin(ogen) degradation product concentration. We concluded that an imbalance in coagulation and fibrinolysis is not pathogenic in the onset of experimentally induced equine acute laminitis. Because several test methods used to evaluate hemostasis in these horses were new, reference values for 34 healthy adult horses were established.

Changes in clotting time (CT) and fibrinolytic activity (FA) were evaluated in 6 mature, female horses during exercise. Two trials were performed on consecutive days, using a randomized crossover design. Each mare was assigned to either an exercise trial or a control trial on the first day, and to the alternate trial 24 hours later. Mares exercised for 20 minutes on a treadmill at an elevation of 2 degrees and a velocity of 5 m/s. Venous blood samples were collected immediately before exercise, at 4, 8, 12, 16, and 20 minutes during exercise, and 15 minutes after cessation of exercise. Blood was placed into plain glass tubes for determination of CT, and into chilled, citrated tubes for determination of FA, plasminogen/plasmin complex activity (PLG), one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), and antithrombin-III (AT-III) activity. There were significant differences (P < 0.05) between the control and exercise groups for CT, FA, and PLG. During exercise, clotting time decreased from 21.5 +/- 1.6 minutes to 9.9 +/- 1.6 minutes (mean +/- SD; P < 0.05), without significant changes in OSPT, APTT, or AT-III. Fibrinolytic activity and PLG increased (P < 0.05) during exercise. Changes in CT, FA, and PLG were significant at 4 minutes of exercise, remained altered until the end of exercise, and returned to baseline values by 15 minutes of recovery. Clotting time, OSPT, APTT, FA, AT-III, and PLG did not change (P > 0.05) during control trials.