This study evaluated responses of the systemic endocrine stress (cortisol)
and growth (IGF-I, GH) axes, as well as those of inflammatory mediators (pr
ostaglandin E-2 [PGE(2)] and tumor necrosis factor alpha [TNF alpha]), to a
ctive infection with Salmonella typhimurium. Eighteen crossbred barrows wer
e penned individually with ad libitum access to feed and water. After an ac
climation period, jugular catheters were placed in all animals. Control pig
s received sterile broth orally (CON, n = 7), whereas the treated pigs (S.T
YP, n = 11) received 3 x 10(9) cfu of S. typhimurium orally. Plasma was col
lected at 6-h intervals from -48 to 120 h. Body weights, feed intake, and r
ectal temperatures also were monitored. Rectal temperatures were elevated i
n S.TYP pigs (P < .01) relative to CON pigs by 12 h, peaked at 42 h (P < .0
01), and remained elevated throughout the remainder of the study. Feed inta
ke was reduced maximally in S.TYP pigs at 48 h (P < .001) and remained redu
ced through 120 h after the challenge. Daily body weight gain also was redu
ced during the 2 wk following infection (P < .001). Plasma cortisol concent
rations increased (P < .05) at 18 h after the challenge in S.TYP pigs and r
emained 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 TNF alpha and PGE
(2). Taken together, the results reveal that infectious processes produce p
rofound alterations in the endocrine stress and the somatotropic axis, and
this may occur in the absence of significant changes in systemic proinflamm
atory mediators.