Bovine respiratory syncytial virus infection

Previous authors: M VAN VUUREN

Current authors:
J L MCGILL - Assistant Professor, MS, PhD, Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, 1907 Christensen Drive, VMRI Building 5, Iowa, 50011, United States of America
RE SACCO - Research Microbiologist/Immunologist /Lead Scientist, PhD, Ruminant Diseases and Immunology Research Unit, National Animal Disease Center/USDA/ARS, 1920 Dayton Avenue, Ames, Iowa, IA 50010, United States of America

GENERAL INTRODUCTION: PARAMYXOVIRIDAE AND PNEUMOVIRIDAE

Introduction

Infection with bovine respiratory syncytial virus (BRSV) is inapparent in the majority of animals, but in some it does cause mild to severe²³ respiratory tract disease characterized by fever, coughing, serous nasal and ocular discharges, dyspnoea and, in some animals, subcutaneous emphysema. It is one of several viruses that are primary pathogens in the bovine respiratory disease complex (see Pneumonic pasteurellosis in cattle). Respiratory syncytial virus also infects sheep and goats and may cause rhinitis in sheep.²⁵ Evidence for the existence of a respiratory syncytial virus (RSV) affecting horses has been reported.²⁴

The virus was first isolated from cattle in Switzerland in 1970⁴⁰ and has subsequently been found worldwide. Its prevalence and importance in Africa is largely unknown, although antibody to it is widespread in feedlot cattle in South Africa.⁶¹

Several reviews on BRSV have been published.^{3, 7, 28, 36, 44, 46, 59}

Aetiology

The virus is classified as a member of the genus Pneumovirus in the family Paramyxoviridae. Virions are pleomorphic, enveloped and measure 80 to 500 nm in diameter for the round and pleomorphic forms (Figure 1), and up to 5 microns in length for filamentous forms (Figure 2). The elongated nucleocapsid is helically coiled and tortuous and contains single-stranded RNA.

The envelope contains transmembrane surface glyoproteins, but, in contrast to ortho- and paramyxoviruses, pneumoviruses lack neuraminidase and haemagglutinin. Virions mature by budding from the cytoplasmic membrane.

A wide range of cell cultures are susceptible to infection with BRSV, including those prepared from most bovine tissue types, as well as kidney cells of pigs, hamsters, monkeys and humans.³⁸ Cytopathic effects are characterized by multinucleate syncytial cell formation, intracytoplasmic inclusions and necrosis.

Bovine respiratory syncytial virus is antigenically related to human respiratory syncytial virus (HRSV),⁴⁰ but the two viruses are distinct.⁴⁸ It has been proposed that ruminant RSVs can be divided into 2 subgroups, BRSV and ovine RSV, with caprine RSV more closely related to BRSV.²⁰

The genome of respiratory syncytial viruses is approximately 15.2 kb and is transcribed into 10 major subgenomic mRNAs encoding 11 proteins, because M2 mRNA contains two overlapping reading frames, which encode 2 proteins, M2-1 and M2-2.¹⁶

Figure 1 Pleomorphic form of bovine respiratory syncytial virus

Figure 2 Filamentous form of bovine respiratory syncytial virus

Epidemiology

Cattle are probably the principal reservoirs of the virus. Sheep and goats may also be infected but their role in the epidemiology is not clear, and inapparent infections are common in these species.^{2, 15, 19, 20, 32, 37, 43}

Since the initial isolation of BRSV in Switzerland in 1970, the virus has been detected worldwide in cattle herds, with rates of infection impacted by multiple factors. In some countries, it has been estimated that frequency of BRSV exposure exceeds 50 per cent in some dairy and beef herds.²⁸ Respiratory disease due to BRSV is most severe in calves less than 6 months of age, and infection can occur in the presence of maternal antibody. In some geographic areas, by 12 months of age, exposure of calves to BRSV may exceed 70 per cent.⁵⁸ Reinfection in calves is common, likely as a result of reintroduction of BRSV into herds.³⁶ Spread of the infection may result from direct contact with or aerosol droplets from infected animals, or indirectly from contaminated surfaces.²⁹ Respiratory disease in cattle in the northern hemisphere caused by BRSV occurs mainly in late autumn, winter and early spring, although outbreaks have also been reported in the summer. In addition to a role for fluctuations in temperature, risk of BRSV infections can be impacted by stresses associated with weaning, transport, handling, crowding, and mixing of cattle from different sources.

Pathogenesis

The severity of clinical disease caused by BRSV is dependent on the age and immune status of the calf, the route of infection, and the strain of the virus.⁸ Some strains are significant primary pathogens of young cattle because, acting alone, they are capable of causing severe damage to the lower respiratory tract.^{12, 39, 45} However, the virus more frequently predisposes the respiratory tract of cattle to the pathogenic effects of secondary bacterial infections.⁶

The virus replicates in epithelial cells of the nasal cavity, pharynx, trachea, bronchi and bronchioli, and in type II pneumocytes and alveolar macrophages. It induces cytopathic changes characterized by loss of cilia and/or necrosis of bronchial and bronchiolar epithelial cells.¹¹ The virus also alters opsonization and phagocytosis by alveolar macrophages.^{38, 56}  Reduced mucociliary clearance resulting from a loss of cilia is...