Coronavirus and Pasteurella infections in bovine shipping fever pneumonia and Evans' criteria for causation

Citation
J. Storz et al., Coronavirus and Pasteurella infections in bovine shipping fever pneumonia and Evans' criteria for causation, J CLIN MICR, 38(9), 2000, pp. 3291-3298
Citations number
37
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Microbiology
Journal title
JOURNAL OF CLINICAL MICROBIOLOGY
ISSN journal
00951137 → ACNP
Volume
38
Issue
9
Year of publication
2000
Pages
3291 - 3298
Database
ISI
SICI code
0095-1137(200009)38:9<3291:CAPIIB>2.0.ZU;2-J
Abstract
Respiratory tract infections with viruses and Pasteurella spp. were determi ned sequentially among 26 cattle that died during two severe epizootics of shipping fever pneumonia. Nasal swab and serum samples were collected prior to onset of the epizootics, during disease progression, and after death, w hen necropsies were performed and lung samples were collected. Eighteen nor mal control cattle also were sampled at the beginning of the epizootics as well as at weekly intervals for 4 weeks. Respiratory bovine coronaviruses ( RBCV) were isolated from nasal secretions of 21 and 25 cattle before and af ter transport. Two and 17 cattle nasally shed Pasteurella spp. before and a fter transport, respectively. RBCV were isolated at titers of 1 x 10(3) to 1.2 x 10(7) PFU per g of lung tissue from 18 cattle that died within 7 days of the epizootics, but not from the lungs of the remaining cattle that die d on days 9 to 36. Twenty-five of the 26 lung samples were positive for Pas teurella spp., and their CFU ranged between 4.0 x 10(5) and 2.3 x 10(9) per g. Acute and subacute exudative, necrotizing lobar pneumonia characterized the lung lesions of these cattle with a majority of pneumonic lung lobes e xhibiting fibronecrotic and exudative changes typical of pneumonic pasteure llosis, but other lung lobules had histological changes consisting of bronc hiolitis and alveolitis typical of virus-induced changes. These cattle were immunologically naive to both infectious agents at the onset of the epizoo tics, but those that died after day 7 had rising antibody titers against RB CV and Pasteurella haemolytica. In contrast, the 18 clinically normal and R BCV isolation-negative cattle had high hemagglutinin inhibition antibody ti ters to RBCV from the beginning, while their antibody responses to P, haemo lytica antigens were delayed. Evans' criteria for causation were applied to our findings because of the multifactorial nature of shipping fever pneumo nia. This analysis identified RBCV as the primary inciting cause in these t wo epizootics. These viruses were previously not recognized as a causative agent in this complex respiratory tract disease of cattle.