Bovine respiratory syncytial virus infection

Bovine respiratory syncytial virus infection

M VAN VUUREN

Introduction

Infection with bovine respiratory syncytial virus (BRSV) is inapparent in the majority of animals, but in some it does cause mild to severe12 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.14 Evidence for the existence of a respiratory syncytial virus (RSV) affecting horses has been reported.13

The virus was first isolated from cattle in Switzerland in 197026 and has subsequently been found in North America, Europe and Japan. Its prevalence and importance in Africa is largely unknown, although antibody to it is widespread in feedlot cattle in South Africa.37

A review of BRSV by Sharma and Woldehiwet has been published.30

Figure 52.1 Pleomorphic form of bovine respiratory syncytial virus

Figure 52.2 Filamentous form of bovine respiratory syncytial virus

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 52.1), and up to 5 microns in length for filamentous forms (Figure 52.2). The elongated nucleocapsid is helically coiled and tortuous and contains single-stranded RNA.

The envelope contains surface projections, 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 is susceptible to infection with BRSV, including those prepared from most bovine tissue types, as well as kidney cells of pigs, hamsters, monkeys and humans.23 Cytopathic effects are characterized by multinucleate giant cell formation, intracytoplasmic inclusions and necrosis.

Bovine respiratory syncytial virus is antigenically related to human respiratory syncytial virus (HRSV),26 but the two viruses are distinct.32 Results from RNase A mismatch cleavage analysis suggest that ovine RSV may be distinct from BRSV and HRSV, whereas caprine RSV may be more closely related to BRSV.11

The genome of respiratory syncytial viruses codes for 10 polypeptides and the complete nucleotide sequence has been determined for the 10 genes.24

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, 9, 10, 19, 21, 28

Although respiratory disease caused by BRSV infection usually occurs in 3- to 12-month-old calves, it may also affect adult cattle. Infection has been reported in feedlot animals, in extensive beef farming operations, and in housed dairy calves.8 The disease has also been reported as an epidemic in adult cattle.12 Spread of the infection, probably by respiratory aerosols, can be rapid. Respiratory disease in cattle in the northern hemisphere caused by BRSV occurs in late autumn, winter and early spring, although outbreaks have also been reported in the summer.

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.5 Some strains are significant primary pathogens of young cattle because, acting alone, they are capable of causing severe damage to the lower respiratory tract.7, 25, 29 However, the virus more frequently predisposes the respiratory tract of cattle to the pathogenic effects of secondary bacterial infections.4

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.6 The virus also depresses opsonization and phagocytosis by alveolar macrophages. 23, 35 Depressed mucociliary clearance resulting from a loss of cilia is responsible for the accumulation of fluid and tissue debris in the airways and alveoli, which provides an ideal environment for the growth of bacterial opportunists.

It has been proposed that the lesions which result from BRSV infection can be a hypersensitivity reaction in which an initial sensitizing infection induces the production of reaginic antibody (IgE), while subsequent infection induces the development of an immediate hypersensitivity reaction characterized by acute bronchiolitis, lung oedema and emphysema. 4, 16 This hypothesis has been forwarded because recently weaned calves, in particular, after showing evidence of respiratory infection, show signs of partial recovery followed, after two to three days, by severe respiratory disease. However, dietary factors cannot be ruled out as possible causes of this condition, as fasting or a change in ration early in the course of the disease may have a beneficial effect;16 mortality is often highest in calves on a high plane of nutrition.15

Clinical signs

Although most infections are subclinical, some infected animals show mild to severe disease8, 12 after...

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