Effect of mild heat stress and mild infection pressure on immune responses to an E. coli infection in chickens

Abstract

Outdoor or organic farming demands robust chickens that are able to combat common infections before they spread to the flock. Priming the immune system of the chickens early in life with micro-organisms that they will encounter later in life prepares chickens to a life in environments where they are subjected to a more natural level of infection pressure. Also, exposure to non-infectious stressful situations may prepare the immune system to combat infectious challenges. The present study investigated whether the immune system could be primed by applying small doses of infective material to the chicken flock or by exposure to short-term non-infectious stimulation, and whether the effect of those stimuli would depend on the genetic material chosen. The effect of the stimulations was examined on selected immunological variables in two chicken strains, using small amounts of manure and litter from other chickens or short-term heat stress, respectively. After 6 weeks of treatment, all chickens were subjected to an Escherichia coli infection and followed for another 3 weeks. Measures of body weight gain, chicken mannan-binding lectin (cMBL), percentage of CD41 and MHCII1 lymphocytes, mean fluorescence intensity (m.f.i.) of CD4 on CD41 cells and MHCII on MHCII1 cells and antibody titres to E. coli were taken. In conclusion, the chickens redistribute lymphocyte populations in peripheral blood in response to potentially infectious agents as well as to stressful non-infectious treatments. Responses to stress situations were dependent on the frequencies of stress exposures and on the chicken breed. This may reflect the superiority of one breed over another in adapting to treatments or in discriminating whether a treatment is harmless or dangerous. However, the differences did not influence the disease resistance to infection with a mixture of E. coli O2, O11 and O78 in the present study.

High Incubation Temperature and Threonine Dietary Level Improve Ileum Response Against Post-Hatch Salmonella Enteritidis Inoculation in Broiler Chicks

“…It has been suggested that exposition to non-infectious stressful situations might prepare the immune system to fight against infectious challenges [ 16 , 17 ] and protection mediated by heat shock proteins against inflammatory and infectious processes occurs due to the suppression of inflammatory mediators [ 23 ]. Indeed, lower stress response with reduction in the levels of corticosterone has been reported in three-old-chicks previously treated with heat between D16 and D18 [ 24 ].…”

“…Since the stress response is non-specific, thermotolerance induction might also improve resistance to other kinds of stresses. In fact, non-infectious stress situations may prepare the immune system to fight against infectious challenges [ 16 , 17 ]. Although the consequences of thermal manipulation during incubation on the performance and meat quality of broiler chickens have been widely assessed, the responses of birds to other types of stresses have not been addressed to date.…”

Immune response in Eimeria sp. and E. coli challenged broilers supplemented with amino acids

“…When the immune system is activated, there are physiological and metabolic changes in their organism, which alter food intake and consequently weight gain and feed conversion ratio. In commercial broiler breeding, environmental stress factors such as overcrowding, humidity, low quality of the air and the presence of infectious and stressing agents may alter their metabolism and nutrient absorption (Norup et al 2008).…”

Factors Modulating the Avian Immune System

“…The mechanism by which heat stress modulates immunity is in part due to the extent of induction of heat shock proteins in lymphocytes, heterophils, and macrophages [77], while cold stress suppresses plasma corticosterone levels and enhances thyroid hormone levels [81]. Even mild heat stress can cause a redistribution of lymphocytes and immune system changes, although these changes may have minimal impact on resistance to some disease challenges [82].…”