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Previous reports demonstrate that synthetic peptides corresponding to the amino acid region 174-187 of G glycoprotein from subgroups A and B human respiratory syncytial virus (HRSV), containing a Cys-->Ser substitution at position 186, confer complete resistance to immunized BALB/c mice against infection with the respective virus. In this report, we show that a Cys186-->Ser substituted peptide (BG/174-187) representing the corresponding region of the bovine (B) RSV G glycoprotein conferred complete protection of mice against BRSV challenge, suggesting that the 174-187 region of RSV G glycoproteins constitutes a dominant protective epitope which has been maintained throughout evolution. Furthermore, immunization of calves with peptide BG/174-187 efficiently induced the production of antibodies capable of recognizing both the parental G glycoprotein and peptide BG/174-187. Following challenge with live BRSV, although none of the animals were protected from upper respiratory tract disease, there were little or no gross pneumonic lesions in the four peptide-immunized calves. In contrast, moderate to extensive pneumonic lesions were observed in 2 out of 3 calves in the control group. Our results thus suggest that peptide BG/174-187 efficiently prevented BRSV-associated pneumonia in the natural host. The use of this system as a model is quite promising with regard to the development of a human synthetic vaccine.

Cloned cultures of 16 strains, representing nine different species of Mycoplasma and Acholeplasma, were inoculated intratracheally into gnotobiotic calves. Strains of M bovirhinis, M canadense, M verecundum, A axanthum and A modicum did not produce visible pneumonic lesions and were not reisolated from the lungs. Strains of M alkalescens and M arginini colonised the lower respiratory tract but failed to produce visible pneumonia. M bovigenitalium (strain M991/70) and M dispar (strain Gri226) both colonised the respiratory tract and induced pneumonic lesions estimated to involve up to 8 per cent (M bovigenitalium) and 17 per cent (M dispar) of the lung. Histologically M bovigenitalium produced a cuffing pneumonia and M dispar produced a interstitial alveolitis.

In a detailed microbiological and pathological study of eight outbreaks of calf pneumonia, which included the inoculation of respiratory material into 18 gnotobiotic calves, a total of five viruses, four species of mycoplasma and 19 species of bacteria were identified. The only microorganism not previously associated with bovine respiratory disease was a coronavirus. The experimental disease produced in the majority of the gnotobiotic calves by the intratracheal inoculation of unpassaged respiratory material, closely resembled the natural disease. However statistical analysis of the results could not ascribe the disease seen to a single microorganism or to a particular combination of microorganisms. Assuming therefore that no microorganisms were missed in the study, it was concluded that the microbiological cause of the experimental disease lay amongst the organisms already found and that one or more of three other factors, discussed in the paper, accounted for the experimental disease produced.

Five calves were inoculated intravenously with 10(8) colony forming units (cfu) of Pasteurella haemolytica A1; the mean score for pneumonic consolidation 3 days post-inoculation was 28%, and the mean clinical score was 7.8. Five calves inoculated intratracheally with 10(9) cfu of the same strain of P. haemolytica had comparable scores (34% and 8.8). Histological lesions of fibrinous pneumonia were similar in all calves. P. haemolytica was recovered from all but one of the affected lungs. From one calf killed in extremis 3 hours after intravenous inoculation, numbers of bacteria recovered from lung were 1,000-fold greater than from liver and spleen. A similar difference in bacterial numbers was also obtained from a gnotobiotic calf killed in extremis, 12 hours after intravenous inoculation of 10(8) cfu P. haemolytica. Evidence from these experiments supports the hypothesis that the blood-borne route is important in the pathogenesis of bovine pneumonic pasteurellosis.

Two gnotobiotic calves were treated once with tilmicosin (20 mg kg-1) six hours before they were infected by the intratracheal route with Mycoplasma bovis and Pasteurella haemolytica serotype 1. This treatment prevented colonisation of the lungs by P haemolytica and considerably reduced colonisation by M bovis, and the clinical scores and the extent of pneumonic consolidation, compared with two untreated gnotobiotic calves, both of which had to be killed in extremis for humanitarian reasons within 24 hours of infection. In a second experiment, 10 conventionally reared calves were similarly exposed to infection and, at the onset of clinical disease, five were treated once with tilmicosin (20 mg kg-1). Colonisation by P haemolytica and M bovis, the clinical scores and extent of pneumonic consolidation were suppressed or greatly reduced in the treated compared with the untreated calves, one of which had to be killed in extremis two days after infection. It was concluded that tilmicosin had a beneficial effect.

Pasteurella multocida was isolated from the lungs of calves that died on a farm in the south of England. This organism was inoculated experimentally into 13 calves by the intratracheal route: in all but two of the calves mild clinical disease resulted and at necropsy, three or four days later, pneumonic consolidation involving up to 22 per cent of the lung was observed. P multocida was isolated from all but two of the lungs. Of two calves inoculated intravenously with P multocida, one showed mild clinical disease and slight pneumonic consolidation at necropsy and the other remained normal. Control calves inoculated intratracheally and intravenously with sterile broth showed no signs of illness and no pneumonic consolidation. Histologically the lung lesions comprised a fibrinous bronchopneumonia with variable sized areas of coagulative necrosis, extensive deposition of fibrin and massive dilatation and oedema of the interlobular and pleural lymphatics. It is concluded that P multocida should receive more recognition as a primary pathogen.

Experimental pneumonia was produced in calves by the endobronchial inoculation of pneumonic lung homogenates. Irradiated homogenates produced minimal pneumonia. Ampicillin treatment of the homogenates and the experimental calves reduced the extent of pneumonia. Treatment with tylosin tartrate prevented experimental pneumonia. These results suggest that the total pneumonia was due to organisms susceptible to tylosin tartrate and that the residual pneumonia remaining after ampicillin treatment was due to organisms susceptible to tylosin tartrate but not to ampicillin. Of the organisms isolated from the lungs, the ones in this latter category most likely to be responsible are Mycoplasma dispar and ureaplasmas (T-mycoplasmas).

Cloned cultures of Mycoplasma dispar and of Ureaplasma sp were inoculated endobronchially into gnotobiotic calves. The resulting pneumonia was estimated to involve 2 to 10 per cent of the lung although no clinical signs were observed. The histopathological lesions consisted of infiltration with mononuclear cells, cuffing (peribronchiolar lympho-reticular hyperplasia), catarrhal bronchiolitis and atelectasis. The results indicate that both M dispar and Ureaplasma sp are capable of causing sub-clinical cuffing pneumonia in calves.