This study evaluated responses of the systemic endocrine stress (cortisol) and growth (IGF-I, GH) axes, as well as those of inflammatory mediators (prostaglandin E2 [PGE2] and tumor necrosis factor alpha [TNFalpha]), to active infection with Salmonella typhimurium. Eighteen crossbred barrows were penned individually with ad libitum access to feed and water. After an acclimation period, jugular catheters were placed in all animals. Control pigs received sterile broth orally (CON, n = 7), whereas the treated pigs (S.TYP, n = 11) received 3 x 10(9) cfu of S. typhimurium orally. Plasma was collected at 6-h intervals from -48 to 120 h. Body weights, feed intake, and rectal temperatures also were monitored. Rectal temperatures were elevated in S.TYP pigs (P < .01) relative to CON pigs by 12 h, peaked at 42 h (P < .001), and remained elevated throughout the remainder of the study. Feed intake was reduced maximally in S.TYP pigs at 48 h (P < .001) and remained reduced through 120 h after the challenge. Daily body weight gain also was reduced during the 2 wk following infection (P < .001). Plasma cortisol concentrations increased (P < .05) at 18 h after the challenge in S.TYP pigs and remained elevated generally until 60 h after infection. A marked suppression of plasma IGF-I occurred in S.TYP pigs beginning at 30 h after infection (P < .001), and it remained lower through 108 h. Plasma GH was not affected consistently by treatment, nor did infection alter plasma TNFalpha and PGE2. Taken together, the results reveal that infectious processes produce profound alterations in the endocrine stress and the somatotropic axis, and this may occur in the absence of significant changes in systemic proinflammatory mediators.