The neurophysiological response of an animal to stress involves the production of a number of stress-related neurochemicals including the catecholamines norepinephrine and epinephrine. It is generally believed that such neurochemicals belong exclusively to the animal kingdom and that any role such neurochemicals play in the infective process is largely confined to host physiology and immunology-related parameters. This, however, is wholly incorrect as many of the bacterial species that are known to cause infections possess the capacity to not only recognize neuroendocrine hormones produced by the host in response to stress, but also synthesize the very same neurochemicals. Given this, infectious microorganisms are capable of directly responding to the neurochemical outflow resulting from a stress event and initiating pathogenic processes. Although the neuroendocrine environment of the lung following a stress event is not fully understood, it most likely possesses abundant levels of stress-related neurochemicals due to its rich blood supply and rich noradrenergic tissue innervation. The ability of microorganisms to recognize and produce neurochemicals that can influence the host, known as microbial endocrinology, provides for a mechanistic basis with which to examine the ability of stress to influence health and susceptibility to disease.

The feed efficiency of ruminant meat and dairy livestock can be significantly influenced by factors within their living environments. In particular, events perceived by the animals as stressful (such as parturition, transport or handling) have been found to affect susceptibility to infection. It has been well documented that even minor stress such as weighing can result in an increase in colonisation and faecal shedding of enteric pathogens such as Salmonella enterica and Escherichia coli O157:H7. Such infections affect both ruminant overall health and therefore performance, and are a particular problem for the meat production industries. Prior explanations for stress enhancing the likelihood of infection is that activation of the sympathetic nervous system under stress leads to the release of neuroendocrine mediators such as the catecholamine stress hormones noradrenaline and adrenaline, which may impair innate and adaptive immunity. More recently, however, another equally compelling explanation, viewed through the lens of the newly recognised microbiological discipline of microbial endocrinology is that the myriad of bacteria within the ruminant digestive tract are as responsive to the hormonal output of stress as the cells of their host. Work from our laboratories has shown that enteric pathogens have evolved systems for directly sensing stress hormones. We have demonstrated that even brief exposure of enteric pathogens to physiological concentrations of stress hormones can result in massive increases in growth and marked changes in expression of virulence factors such as adhesins and toxins. Happy, less stressed ruminants may therefore be better-nourished animals and safer sources of meat. This article reviews evidence that stress, as well as affecting nutrition, in ruminants is correlated with increased risk of enteric bacterial infections, and examines the molecular mechanisms that may be at work in both processes.