Coronavirus and Pasteurella Infections in Bovine Shipping Fever Pneumonia and Evans' Criteria for Causation

Author:

Storz Johannes1,Lin Xiaoqing1,Purdy Charles W.2,Chouljenko Vladimir N.1,Kousoulas Konstantin G.1,Enright Frederick M.3,Gilmore William C.4,Briggs Robert E.5,Loan Raymond W.6

Affiliation:

1. Department of Veterinary Microbiology and Parasitology, School of Veterinary Medicine, Louisiana State University, 1 and

2. Conservation and Production Research Laboratory, USDA, Agricultural Research Service, Bushland, 2

3. Department of Veterinary Science, LSU Agricultural Center, Baton Rouge, 3 Louisiana;

4. Texas Veterinary Diagnostic Laboratory, Amarillo, 4 and

5. National Animal Disease Center, Ames, Iowa 5

6. Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, 6 Texas; and

Abstract

Respiratory tract infections with viruses andPasteurella spp. were determined 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, when necropsies were performed and lung samples were collected. Eighteen normal 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 after transport. Two and 17 cattle nasally shed Pasteurella spp. before and after transport, respectively. RBCV were isolated at titers of 1 × 103to 1.2 × 107 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 died on days 9 to 36. Twenty-five of the 26 lung samples were positive for Pasteurella spp., and their CFU ranged between 4.0 × 105 and 2.3 × 109 per g. Acute and subacute exudative, necrotizing lobar pneumonia characterized the lung lesions of these cattle with a majority of pneumonic lung lobes exhibiting fibronecrotic and exudative changes typical of pneumonic pasteurellosis, but other lung lobules had histological changes consisting of bronchiolitis and alveolitis typical of virus-induced changes. These cattle were immunologically naive to both infectious agents at the onset of the epizootics, but those that died after day 7 had rising antibody titers against RBCV andPasteurella haemolytica. In contrast, the 18 clinically normal and RBCV isolation-negative cattle had high hemagglutinin inhibition antibody titers to RBCV from the beginning, while their antibody responses to P. haemolytica antigens were delayed. Evans' criteria for causation were applied to our findings because of the multifactorial nature of shipping fever pneumonia. This analysis identified RBCV as the primary inciting cause in these two epizootics. These viruses were previously not recognized as a causative agent in this complex respiratory tract disease of cattle.

Publisher

American Society for Microbiology

Subject

Microbiology (medical)

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