Experimental inoculations with Ostertagia ostertagi or exposure to artificial illumination alter peripheral cortisol in dairy calves (Bos taurus).

A series of experiments were conducted on dairy calves (Bos taurus) to assess, by way of circulating cortisol, the impact of a parasitic infection as a systemic stressor. The first study was designed to assess the effects of chronic stress on dairy calves resulting from a large bolus inoculation of the nematode parasite, Ostertagia ostertagi. Peripheral cortisol concentrations and adrenal cortical competency to adrenocorticotropic hormone (ACTH) challenge were utilized as indicators of chronic stress for 5 weeks. Calves were cleared of nematodes by anthelminthic treatment after the third week of infection. Calves were challenged with ACTH on weeks 0 and 2, and blood samples were obtained at a 12 x 10-min bleeding schedule. Cortisol concentrations were significantly higher (P < 0.05) in the infected calves than in the uninfected calves. The maximal response level to the ACTH challenge was also higher while the calves were infected. Two additional experiments were conducted to investigate the effects of experimental procedures that became evident during Experiment 1. Firstly, calves that had previously been fitted with jugular cannulae were sampled from 3 hr predawn until 5 hr after dawn under red- or white-light incandescent illumination. Calves under red lights had lower initial cortisol concentrations but increased to the concentrations in calves under white lights, indicating a compounding effect of lighting with the procedures of blood-sample acquisition. Secondly, 12 calves were inoculated with 10,000, 100,000, or 200,000 third-stage, infective larvae of O. ostertagi. Blood samples were obtained similarly to the regimen in Experiment 1. Cortisol concentrations were elevated only in the 200,000-dose group during week 3, correlating with the period immediately after emergence of the young adult parasites from the gastric glands. Continuous emergence of these parasites might induce chronic hyperadrenocorticism and the concomitant negative consequences on metabolic and immunological processes.