Chickens were subjected to the sound produced by banging on a metal pail (104 decibels) for 30 seconds. Heterophil/lymphocyte (H/L) ratios began to rise 18 hours later, reaching their maximum value (0.62) in 20 hours and returning to pre-stress values after 30 hours. Neither resistance to Escherichia coli challenge infection nor antibody response were altered.

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The concept of nonspecific cellular defense of the respiratory system of poultry against respiratory pathogens by "preventive activation" of avian respiratory phagocytes (ARPs) was tested in an in vivo protection trial. Chickens were stimulated intratracheally by Pasteurella multocida Choloral vaccine strain. Seven hours later, these and mock-inoculated control chickens were challenged with pathogenic Escherichia coli via the air-sac route. Stimulated chickens had a 25-fold-elevated number of ARPs compared with mock-inoculated control chickens. The proportion of active phagocytes and the phagocytic capacity of these cells was higher in the ARP populations of stimulated chickens than in the ARP populations of control chickens. In vivo protection against E. coli air-sac infection was demonstrated by reduction of morbidity and mortality rates, diminished weight loss, and lower scores of gross and histopathological lesions of P. multocida-stimulated chickens compared with mock-inoculated controls.

Chickens from lines selectively bred for either a high-antibody (HA) or low-antibody (LA) response to sheep erythrocytes were injected intravenously with Mycobacterium avium while being held in low, medium, or high levels of social stress for 5 days (first environment). During the remaining 6 weeks, they were held under either low or medium levels of social stress (second environment). Infection led to lesions consisting of granulomas, some of which had necrotic centers. There was a positive correlation between numbers of lesions with necrotic centers and M. avium cells recovered from livers. The numbers and nature of lesions were influenced by both genetic and environmental factors. Numbers of necrotizing lesions increased with stressfulness of the first environment. Total numbers of lesions were reduced by the medium-stress second environment, and the total number of necrotizing lesions was reduced among LA chickens in the low-stress second environment.