From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 X 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus. Age at puberty was similar between gilts exposed to low or moderate concentration of ammonia (208 vs 205 days; SEM, 1.3 days), even though weight at puberty was less (P < 0.03) for gilts exposed to low concentration of ammonia than for gilts exposed to moderate concentration of ammonia (109.7 vs 118.2 kg; SEM, 4.5 kg).

Hematologic and rheologic changes were examined in 49 Thoroughbreds before and after competitive racing. Mean postrace values for RBC count, hemoglobin concentration, and PCV increased by 58 to 61%, whereas blood viscosity increased 2 to 3 times. Postrace echinocyte numbers were 162% greater than prerace values. Smaller, but statistically significant, changes were found for mean corpuscular hemoglobin concentration, red cell distribution width, plasma total protein concentration, total WBC count, neutrophil count, and lymphocyte count. Variables measured did not predict whether a horse was a bleeder not treated with furosemide, a bleeder treated with furosemide, or a nonbleeder.

Pulmonary lavage samples were collected from 90- to 130-day-old calves before and 6 days after aerosol inoculation with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI3) virus. Alveolar lining material was separated from lavage fluids by high-speed centrifugation and phospholipids were extracted from alveolar lining material and analyzed by high-performance liquid chromatography. Phosphatidylcholine and phosphatidylethanolamine were 74.2 +/- 6.5% and 13.3 +/- 2.8%, respectively, of the total phospholipid content in the surfactant obtained from calves before virus inoculation. Other phospholipids were represented by substantially lower percentages. Infection with either of the 2 viruses caused a significant (P < 0.05) decrease in the percentage of phosphatidylcholine to 66.0 +/- 8.0% and 65.1 +/- 10.8% in the calves inoculated with BHV-1 and PI3 virus, respectively. A significant (P < 0.05) increase in the percentage of phosphatidylethanolamine to 18.1 +/- 2.2% and 17.8 +/- 4.5% developed in calves inoculated with BHV-1 and PI3 virus, respectively. Infection with BHV-1 also induced an increase (not significant) in the percentage of phosphatidylinositol from 5.5 +/- 2.8% to 7.8 +/- 2.2%. A similar, but not significant, increase in the percentage of phosphatidylinositol was also seen in the calves inoculated with PI3 virus. Less substantial changes in the percentage of other phospholipids were detected after virus infection.

Twenty-one mixed-breed pony foals, reared and maintained under parasite-free conditions, were used to test the efficacy of ivermectin in oral drench and paste formulations (200 microgram/kg) against 11-day-old migrating larvae of Parascaris equorum. Three replicates of 4 foals and 3 replicates of 3 foals were formed on the basis of age. Foals in replicates of 4 were randomly allocated to be indicators, or to receive vehicle (control) or ivermectin paste or ivermectin liquid. Foals in replicates of 3 were randomly allocated to receive vehicle or ivermectin paste or ivermectin liquid. The recovery of larvae from the lungs, liver, and small intestines of the indicator foals showed that 99.9% of the larvae were in the lungs 11 days after inoculation (day 0 of treatment). The recoveries of larvae from lungs and small intestines of controls at 25 days after inoculation indicated that all larvae had migrated to the small intestine by this time. The mean length of larvae recovered from the lungs (11 days after inoculation) was 0.87 mm; the mean length of those recovered from the small intestine (25 days after inoculation) was 3.65 mm. Using larvae recovered from small intestinal contents for calculations, ivermectin in both formulations was 100% effective against 11-day P equorum (P less than 0.01, compared with control group geometric mean of 1498.4).

In a search of viral agents in pulmonary macrophages of horses with chronic pulmonary disease, equine herpesvirus 2 was found to be unique. In 8 of 9 horses with chronic pulmonary disease, antigens of equine herpesvirus 2 were detected by indirect immunofluorescence staining of scattered foamy macrophages immediately after harvesting by bronchoalveolar lavage and fractionation on metrizamide gradients. In a healthy horse, antigens were not found. After 1 week of cultivation of bronchoalveolar lavage cells from a second group of 9 horses with chronic pulmonary disease, viral antigens were detected in 90% of the adherent pulmonary macrophages. In 2 of 3 healthy horses, viral antigens also were found in 90% of the adherent pulmonary macrophages. Antigens of equine herpesvirus 1, equine herpesvirus 4, parainfluenza virus 3, or adenovirus were not detected. Antigens of the 5 investigated viruses also were not detected in lung tissue slices from a third group of 14 horses, 4 healthy; 7 with varying degrees of bronchiolitis, 2 of which also had chronic intestitial pneumonia; 2 with eosinophilic bronchitis; and 1 with pulmonary hemorrhage. The exclusive presence of equine herpesvirus 2 in pulmonary macrophages was confirmed qualitatively by isolation of infective virus by cocultivation. In a fourth group of 12 horses with chronic pulmonary disease, infective virus could be isolated from pulmonary macrophages of 3 horses and from mixed-blood leukocytes of 5 horses. Virus isolations from 2 healthy horses were not successful from pulmonary macrophages, whereas 1 isolation was obtained from mixed-blood leukocytes. Other viruses were not detected by cocultivation.

Systemic and pulmonary antibody responses of calves to Pasteurella haemolytica were evaluated by measuring immunoglobulin production in blood for 9 days and in pulmonary lavage fluid for 7 days after intrapulmonary inoculation. Clinical signs, pulmonary lesions, pulmonary and systemic inflammatory response, and amount of antigen in lavage fluid were used to evaluate the response of calves to challenge with P haemolytica. The pulmonary response consisted of production of IgG, IgE, and IgM antibodies to P haemolytica antigens and a 17- to 68-fold increase of cells in lavage fluid 8 hours after inoculation, with a gradual decrease toward normal. Antibodies of the IgM isotype to P haemolytica were demonstrated as early as 8 hours through 7 days after inoculation in 3 of 3 calves. Of the anti-P haemolytica isotypes, IgM was found in the highest concentration. In all of the inoculated calves, IgE was found 1 to 2 days after inoculation, and IgG was found in 2 of 3 inoculated calves from day 1 through 7 after inoculation. Detection of IgG correlated with smaller pulmonary lesions. Immunoglobulin A was not detected in lavage fluid. Serum was evaluated for IgG and IgM antibody response to P haemolytica. Specific IgM was detectable 5 days after inoculation, and IgG was detectable 7 days after inoculation. Pasteurella haemolytica antigens were not detected in serum or plasma. A transient increase in neutrophil count was found 8 hours after inoculation, with return to baseline values by 24 hours after inoculation. Antigen was detected in lavage fluid by use of monoclonal antibodies against selected P haemolytica capsular antigen, outer membrane antigens, and leukotoxin in all inoculated calves 8 hours after inoculation. The monoclonal antibody specific for P haemolytica capsule provided the best detection of antigen. The other monoclonal antibodies detected antigen, but were less consistent.

Efficacy of sulbactam, a beta-lactamase inhibitor, in combination with ampicillin, was evaluated for treatment of experimentally induced pneumonia caused by beta-lactam-resistant Klebsiella pneumoniae. Infection was experimentally induced in 18 healthy weanling foals that were randomly allocated to 3 treatment groups: sulbactam plus ampicillin (S/A, 3.3 and 6.6 mg/kg of body weight, respectively), ampicillin (6.6 mg/kg), or vehicle only. Foals were treated daily for 7 days; the observer was unaware of treatment status. Compared with ampicillin and vehicle, treatment with S/A resulted in a statistically significant (P < 0.05) decrease in severity of pneumonia, with regard to bronchoalveolar lavage cytologic findings (decreased total cell and neutrophil numbers, and increased lymphocyte numbers) and extent of macroscopic lesions in lung tissue of the noninoculated regions. Marked trends toward improvement of S/A-treated foals were observed for quantitative results of bacteriologic culture of bronchoalveolar lavage fluid samples (P < 0.07), macroscopic pathologic features of the whole lung (P < 0.1), and histopathologic variables (P < 0.07), compared with ampicillin- and vehicle-treated foals. Treatment effects were not observed for radiographic, hematologic, and blood gas abnormalities that resulted from infection. In conclusion, the combination of sulbactam plus ampicillin was found to have synergistic effects in vivo, to reduce the extent and severity of experimentally induced grain-negative lung infection in foals.

The role of endotoxin in the pathogenesis of acute pneumonic pasteurellosis is uncertain. Recently, we reported that Escherichia coli-derived endotoxin given by airway inoculation fails to induce lung injury in calves. Because Pasteurella haemolytica-derived endotoxin may differ substantially from E coli in its pathogenicity, we repeated these studies with Pasteurella endotoxin. Intratracheal inoculation of P haemolytica endotoxin caused hypoxemia and increased the alveolar-arterial oxygen differences without causing hypercarbia or changes in lung mechanical properties and volumes. In contrast, IV inoculation of endotoxin caused systemic hypotension, leukopenia, gas exchange impairment, increased total pulmonary resistance, and decreased dynamic compliance. Both routes of inoculation increased serum endotoxin concentrations and were associated with areas of pulmonary hemorrhage, edema, and acute inflammation. We concluded that P haemolytica-derived endotoxin is pathogenic by IV and airway routes of inoculation, and therefore differs from E coli endotoxin in its ability to induce lung lesions in calves.