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Title: A PROLONGED SURGE IN CORTISOL IS EVOKED IN PIGS INFECTED WITH ACTINOBACILLUS PLEUROPNEUMONIAE

Author
item RAMANATHAN, B - KANSAS STATE UNIVERSITY
item WRIGHT, K - KANSAS STATE UNIVERSITY
item TURNER, J - KANSAS STATE UNIVERSITY
item HILL, C - KANSAS STATE UNIVERSITY
item DRITZ, S - KANSAS STATE UNIVERSITY
item FENWICK, B - KANSAS STATE UNIVERSITY
item Carroll, Jeffery - Jeff Carroll
item MINTON, J - KANSAS STATE UNIVERSITY

Submitted to: Journal of Animal Science Supplement
Publication Type: Abstract Only
Publication Acceptance Date: 7/21/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Bacterial lipopolysaccharide (LPS) has been used experimentally to model infectious processes. However, the fever, anorexia, and neuroendocrine responses to LPS are limited to a few hours post-challenge. Yet, the febrile response to bona fide infectious processes is more prolonged, suggesting that LPS challenge models have limitations for modeling infection. The current study was designed to assess activation of the hypothalamic-pituitary-adrenal (HPA) axis in pigs in response to Actinobacillus pleuropneumoniae (APP) infection. Weaned pigs were housed in individual pens in environmentally controlled rooms, with free access to feed and water. Jugular catheters were inserted nonsurgically into all pigs about 7 d prior to challenge. Serum was collected at frequent intervals from -12 to 72 h relative to infection for serum cortisol analysis. Feed intake also was assessed at 12-h intervals during this time eto mark the clinical course of the disease. At infection, pigs were given 5 X 10**8 CFU APP intranasally (n=6), or a similar intranasal volume of sterile growth media (n=6). Feed intake was reduced to the greatest extent in the first 12 h following infection (P<.0001), and also was reduced at 24 to 36 (P<.001), 48 to 60 (P=.053), and 60 to 72 (P<.05) h post-infection. Serum cortisol was increased by 3 h post-infection (P<.001), peaking at 12 h, before gradually returning to control concentrations at 30 h post-treatment. A second surge in cortisol was evident in the latter portion of the sampling period at 36 (P=.056), 42 (P<.001), and 60 (P=.056) h. Thus, bacterial infection evokes a surge in serum cortisol that is sustained to a much greater extent than that stimulated by sublethal doses of LPS.