J. Anim Sci.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J. Anim Sci. 2007. 85:1161-1167. doi:10.2527/jas.2006-482
© 2007 American Society of Animal Science

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jas.2006-482v1
85/5/1161    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fraser, J. N.
Right arrow Articles by Minton, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fraser, J. N.
Right arrow Articles by Minton, J. E.

Effects of feeding Salmonella enterica serovar Typhimurium or serovar Choleraesuis on growth performance and circulating insulin-like growth factor-I, tumor necrosis factor-{alpha}, and interleukin-1ß in weaned pigs1

J. N. Fraser, B. L. Davis, K. A. Skjolaas, T. E. Burkey2, S. S. Dritz, B. J. Johnson and J. E. Minton3

Department of Animal Sciences and Industry, Weber Hall, Kansas State University, Manhattan 66506-0201

3 Corresponding author email: eminton{at}ksu.edu

The most common Salmonella serovars causing clinical disease in pigs are Salmonella enterica serovars Typhimurium (Typhimurium) and Choleraesuis. Given that the swine host-adapted serovar Choleraesuis has been reported to cause systemic disease, a different disease outcome from that of Typhimurium, our working hypothesis was that this serovar would likely engage systemic immune-inflammatory mechanisms, resulting in elevated systemic cytokine secretion. Forty-eight weaned pigs were blocked by BW and sex, and randomly allotted to 1 of 3 treatments in a 14-d study. Each treatment had 8 replicates (pens), with 2 pigs/pen. The treatments consisted of a negative control and pigs repeatedly fed 108 cfu of Typhimurium or Choleraesuis. On d 0, the pigs were fed Choleraesuis or Typhimurium in dough balls, and the bacteria were refed twice weekly throughout the experiment. Control pigs received dough balls without bacteria. All pigs were housed in temperature-controlled rooms under constant lighting and were fed a standard corn-soybean meal-based nursery diet. Pig BW and feed disappearance were used to determine ADG, ADFI, and G:F. Rectal temperatures were obtained daily from 1 pig/pen beginning 2 d before the first bacterial feeding through d 7 using rapid-response digital thermometers. Serum was collected on d 0, 7, and 14 from a single pig/pen for analysis of IGF-I, tumor necrosis factor-{alpha} , and IL-1ß. There was no change in the rectal temperature of the control or the Typhimurium-challenged pigs (compared with d 0) or when comparing Typhimurium-challenged pigs with control animals. In contrast, pigs fed Choleraesuis had increased rectal temperatures beginning on d 2 and continuing through d 7 (P < 0.05), with the greatest elevation on d 3 (P < 0.001) compared with the control pigs. Average daily gain and ADFI of pigs challenged with Typhimurium did not differ from those of the control animals. Pigs fed Choleraesuis had a 25% reduction in ADG (P < 0.0001) and ADFI (P < 0.002) compared with the control pigs. On d 7, pigs fed Choleraesuis had reduced serum IGF-I compared with control (P < 0.01) or Typhimurium-challenged pigs (P = 0.01). Bacterial feeding did not affect serum tumor necrosis factor-{alpha} or IL-1ß compared with control pigs at any time throughout the experiment. We conclude that repeated exposure of weaned pigs to Choleraesuis reduced growth performance in the absence of changes in systemic inflammatory cytokines.

Key Words: insulin-like growth factor-I • interleukin-1ß • Salmonella enterica • swine • tumor necrosis factor-{alpha}


1 Contribution no. 06-316-J from the Kansas Agricultural Experiment Station. The authors thank C. M. Hill for technical assistance in the laboratory. The authors gratefully acknowledge partial support from USDA under section 1433 of Public Law 95-113.

2 Current address: 206f Animal Sciences, University of Nebraska, PO Box 830908, Lincoln, NE 68583-0908.




This article has been cited by other articles:


Home page
J ANIM SCIHome page
J. A. Carroll
Bidirectional communication: Growth and immunity in domestic livestock
J Anim Sci, April 1, 2008; 86(14_suppl): E126 - E137.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the American Society of Animal Science.