A method of inducing Pasteurella haemolytica serotype 1 (Ph1) lung infection in goats, using low numbers of bacteria and without impairing host immunity, was developed. Two trials were conducted. Results of trial 1, using 10 principals (Ph1 agar beads) and 6 controls (agar beads alone), indicated that Ph1 organisms imbedded in agar beads could survive host lung defenses for 32 days. Results of trial 2 indicated that lung immunity in the inoculated goats (principals) was high and they were more protected than controls against a transthoracic challenge of Ph1 (1.18 X 10(7) colony-forming units) injected into lung of each goat on posttreatment day 35. When comparing challenge-exposed principals with controls, the controls developed rectal temperatures above normal for a longer time, duration of anorexia was longer, and sign of depression were seen. The controls developed large are of consolidated lung tissue, more Ph1 isolates were recovered from nasal turbinates and lung tissue, and higher Ph1 concentrations were found in the lungs. The serum Ph1 indirect hemagglutination antibody titers in the principals of both trials increased, compared with titer in controls. Principal goats in trial 2 had higher Ph1 indirect hemagglutination antibody titers after injection of Ph1-impregnated agar beads and less severe lung lesion after challenge exposure than did controls. The small pneumonic consolidated lesions in the principals, compared with extensive lesions in controls after Ph1 challenge exposure, indicated a high degree of immunity after exposure to Ph1 organisms imbedded in agar beads.

A prospective cohort study was undertaken in a farrow-to-farrow swine herd to describe patterns of pneumonia, and to identify host risk factors associated with the extent of pneumonic lesions in 2 weight groups of slaughter swine. The risk of coughing and pneumonic lesions increased with increasing age of pigs within the herd (P < 0.0001). The age-specific prevalence of pneumonic lesions was low (2.7%) in pigs < 16 weeks old at slaughter, but increased rapidly when pigs were between 16 and 22 weeks old (8.6 to 67.9%). After 22 weeks, the prevalence remained relatively constant at about 80%. Associations between possible risk factors and pneumonia were investigated by use of multiple-regression models. Age at weaning (< 24 days) and birth weight (< 1 kg) exerted small, but significant (P < 0.002), effects on the extent of pneumonic lesions in pigs slaughtered at 30 to 50 kg live weight. For pigs slaughtered at 90 to 110 kg, pneumonic lesions were more extensive (P = 0.007) in pigs sired by Yorkshire boars than pigs sired by non-Yorkshire sires (Duroc, Hampshire, Chester White, or American Spotted). Other host factor variables including weaning weight and clinical diseases (atrophic rhinitis, diarrhea, and arthritis) were not associated with pneumonia extent in either weight group. Higher pneumonia percentages were also associated with reduced growth rates in the grower/finisher phase. Pigs sired by Yorkshire boars grew significantly (P < 0.0001) more slowly from entry into shed 2 (mean, 38 kg) until about the time of exit (mean, 92 kg) than pigs sired by other breeds (747 g/d and 795 g/d, respectively).

The influence of recombinant bovine interferon gamma (rBOIFN-gamma) treatment on resistance of clinically normal and dexamethasone-treated calves to Haemophilus somnus infection was evaluated. Four groups of 6 calves each were treated with saline solution (controls), dexamethasone (0.04 mg/kg of body weight/for 3 days), rBOIFN-gamma (2 micrograms/kg for 2 days), or dexamethasone and rBOIFN-gamma (aforementioned dosages). All treatments were started 24 hours before intrabronchial challenge exposure with 5 x 10(9) colony-forming units of H somnus. Rectal temperature and WBC count were monitored daily. Two of the dexamethasone-treated calves died of pneumonia 4 days after challenge exposure and were necropsied. All other calves were euthanatized and necropsied 7 days after challenge exposure. All calves had pneumonia of variable intensity. Dexamethasone-treated calves had increased volume of pneumonic lung (P < 0.05) and increased severity of pneumonia, compared with control calves. Recombinant bovine interferon gamma treatment resulted in reduction in pneumonic lung volume and severity of pneumonia in dexamethasone-treated calves (P < 0.05), although it did not influence severity of pneumonia in nondexamethasone-treated calves.

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P < 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia. The results indicated that young calves are susceptible to 3-methylindole-induced pulmonary injury and that nonciliated bronchiolar epithelial cells, type-I alveolar epithelial cells, and pulmonary endothelial cells are most susceptible to injury. The results failed to indicate that 3-methylindole pulmonary toxicosis significantly enhances respiratory disease induced by bovine respiratory syncytial virus.

A method of inducing Pasteurella haemolytica serotype 1 (Ph1) lung infection in goats, using low numbers of bacteria and without impairing host immunity, was developed. Two trials were conducted. Results of trial 1, using 10 principals (Ph1 agar beads) and 6 controls (agar beads alone), indicated that Ph1 organisms imbedded in agar beads could survive host lung defenses for 32 days. Results of trial 2 indicated that lung immunity in the inoculated goats (principals) was high and they were more protected than controls against a transthoracic challenge of Ph1 (1.18 X 10(7) colony-forming units) injected into lung of each goat on posttreatment day 35. When comparing challenge-exposed principals with controls, the controls developed rectal temperatures above normal for a longer time, duration of anorexia was longer, and sign of depression were seen. The controls developed large are of consolidated lung tissue, more Ph1 isolates were recovered from nasal turbinates and lung tissue, and higher Ph1 concentrations were found in the lungs. The serum Ph1 indirect hemagglutination antibody titers in the principals of both trials increased, compared with titer in controls. Principal goats in trial 2 had higher Ph1 indirect hemagglutination antibody titers after injection of Ph1-impregnated agar beads and less severe lung lesion after challenge exposure than did controls. The small pneumonic consolidated lesions in the principals, compared with extensive lesions in controls after Ph1 challenge exposure, indicated a high degree of immunity after exposure to Ph1 organisms imbedded in agar beads.

Alveolar macrophages were collected at necropsy from pigs inoculated with Mycoplasma hyopneumoniae or Actinobacillus pleuropneumoniae or both and were tested for phagocytic capabilities, using in vitro techniques. Macrophages from noninoculated littermates were used as controls. Alveolar macrophages from pigs inoculated with either M hyopneumoniae or A pleuropneumoniae had significantly (P < 0.05 to P < 0.0025) higher phagocytic capacity than that of noninoculated controls. Macrophages from A pleuropneumoniae-inoculated pigs were comparatively more stimulated than were those from M hyopneumoniae-inoculated pigs. Pigs inoculated with M hyopneumoniae and then challenge-exposed with A pleuropneumoniae 2 and 4 weeks later had greatly reduced phagocytosis. Infection with M hyopneumoniae or A pleuropneumoniae caused stimulation of alveolar macrophage functions, and M hyopneumoniae infections may have suppressed phagocytic responses when pigs were challenge-exposed with a secondary pathogen (A pleuropneumoniae). This potential suppression may represent a prediposition of the host by M hyopneumoniae to secondary bacterial infections.

An immunoperoxidase technique was used to study the relationship between the necrotic lesions and causative bacteria found in lungs of 53 calves that had naturally acquired pneumonia. Four types of necrotic lesions were identified on the basis of morphologic characteristics as follows: type 1 had coagulation necrosis surrounded by a dense zone of numerous degenerated leukocytes; type 2 was similar to type 1, but the central area of the lesions was severely affected, had no alveolar architecture remaining, and was surrounded by a thin, sparse layer of degenerated leukocytes; type 3 had small swirling accumulation of degenerated leukocytes; and type 4 had necropurulent lesions resembling abscesses. By use of the immunoperoxidase technique, Pasteurella haemolytica serovar 1 antigen was confirmed to be associated with the necrotic lesions in many cases of type 1 and in some cases of types 2 and 3. Although some lesions were induced by other bacteria (Haemophilus somnus or Actinomyces pyogenes), the pneumonic lesions associated with P haemolytica could be differentiated from other pneumonic lesions in calves by use of the immunoperoxidase technique.

Cellular and humoral immune responses of pigs inoculated with Mycoplasma hyopneumoniae were investigated at postinoculation weeks (PIW) 2, 4, and 6. The response of blood lymphocytes (BL) and bronchial lymph node lymphocytes (LNL) to stimulation by M hyopneumoniae antigens was evaluated by a lymphocyte-stimulation test. Specific antibodies in serum and lung washing samples were assayed by ELISA. Immunoglobulin-positive cells in lungs and bronchial lymph nodes were identified by indirect fluorescent antibody test, using isotype-specific monoclonal antibodies. At PIW 0 to 6, BL from control and M hyopneumoniae-inoculated pigs were stimulated by M hyopneumoniae cells; however, BL from inoculated pigs generally had higher stimulation indices, especially at PIW 6. The response of LNL was influenced by previous exposure to M hyopneumoniae, as indicated by higher stimulation indices (P < 0.01) of LNL from inoculated pigs killed at PIW 2 and 6. Specific ELISA antibodies to M hyopneumoniae in lung washings from inoculated pigs consisted mainly of IgG and IgA isotypes. Examination of lung sections by indirect immunofluorescence revealed that cells producing IgM and IgA were in controls as well as M hyopneumoniae-inoculated pigs, but IgG-positive cells were only in lungs of inoculated pigs. Resolution of pneumonia appeared to correlate with development of increased sensitization of BL, as well as development of marked increases in immunoglobulins, particularly IgG in lung washings at PIW 6.

Experimental pneumonia caused by Pasteurella haemolytica was induced in 2-week-old gnotobiotic (n = 4) and conventional (n = 6) calves by endobronchial inoculation into the right caudal lung lobe of 7.9 X 10(10) +/- 0.6 X 10(10) (mean +/- SD) colony-forming units of P haemolytica in the 6-hour log phase of growth. The calves were studied for 24 hours or less. Regression lines for the relationship between clinical index and time for the gnotobiotic group and conventional group of calves were compared, and the clinical index was found to be significantly (P less than or equal to 0.005) more rapid in the gnotobiotic group. There was also a significant difference in the preinoculation, absolute segmented neutrophil count (P less than or equal to 0.05), and in the total serum protein, albumin, and globulin values (P less than or equal to 0.05). Comparison of the preinoculation and post inoculation blood cell and blood chemical values revealed a significant increase (P less than or equal to 0.05) in the numbers of band neutrophils and fibrinogen in conventional calves, and a significant decrease (P less than or equal to 0.05) in the total WBC count in gnotobiotic calves. Necropsy of both groups of calves revealed a circular to oblong lesion that was congested, edematous, and firm, and which occupied 20% to 100% of the right caudal lung lobe and involved the remaining lung lobes to a more minor degree. When mean lesion scores of the 2 groups of calves were compared, no significant difference (P less than or equal to 0.05) was found. Microscopic examination of the lungs revealed edema of the perivascular and interlobular septa and hemorrhage in the alveoli of both groups, although the conventional group had more fibrinopurulent inflammation.