Viral-Bacterial Synergistic Interactions/Pathogenesis in Cattle

Abstract

Animals are constantly exposed to microorganisms present in the environment, especially in aerosols which easily enter the respiratory tract, yet pneumonia is a relatively rare event. In fact many organisms associated with lower respiratory tract disease can be part of the commensal bacterial flora of the upper respiratory tract. The normal defence mechanisms of healthy animals maintains the homeostasis between the host and the microorganisms. This implies that very effective defense mechanisms are present to eliminate the vast majority of microorganisms before they establish themselves in the lower respiratory tract and cause clinical disease. However, if there is a disruption of the normal lung defenses, animals fail to clear the infection. Although a number of “stressors” might be involved in disrupting homeostasis, viruses clearly can be critical to enhancing bacterial colonization. It is estimated that individuals suffering from a severe respiratory viral infection have a 40% chance of developing bacterial pneumonia (Jakab, 1982). In cattle, shipping fever or bovine pneumonic pasteurellosis is considered to be one of the major causes of economic loss to the cattle producer. These losses are estimated to be as high as one billion dollars annually. This disease is thought to be caused by the interaction of stressors (management) and infection by viruses and bacteria acting synergistically. Based on these observations a number of viral-bacterial models have been used to reproduce “shipping fever” and to study the interaction between viruses and bacteria in respiratory disease (Babiuk and Acres, 1984). Our laboratory has focused our studies on a bovine herpesvirus-1 (BHV-1) model wherein seronegative animals are infected with an aerosol of BHV-1 followed four days later by an aerosol of Pasteurella haemolvtica (Yates et al., 1983; Bielefeldt Ohmann and Babiuk, 1985). Results from this model will be presented to indicate how viral infection of the respiratory tract by BHV-1 alters the respiratory tract environment to allow Pasteurella haemolvtica to establish itself and cause pneumonia. These events are summarized in Figure 1. Briefly, in addition to altering the epithelial environment, by infecting and causing cell death, BHV-1 also influences host specific and nonspecific defense mechanisms. For example, BHV-1 has been shown to infect macrophages/monocytes and thereby alter their function, even if cell death does not occur.