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Title: EFFECTS OF RUMINAL AND POST-RUMINAL INFUSION OF STARCH HYDROLYSATE OR GLUCOSE ON THE MICROBIAL ECOLOGY OF THE GASTROINTESTINAL TRACT IN GROWING STEERS

Author
item Van Kessel, Jo Ann
item NEDOLUHA, PATTI
item Williams Campbell, Anisha
item Baldwin, Ransom - Randy
item McLeod, Kyle

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/16/2002
Publication Date: 11/1/2002
Citation: VAN KESSEL, J.S., NEDOLUHA, P.C., WILLIAMS CAMPBELL, A.M., BALDWIN, R.L., MCLEOD, K.R. EFFECTS OF RUMINAL AND POST-RUMINAL INFUSION OF STARCH HYDROLYSATE OR GLUCOSE ON THE MICROBIAL ECOLOGY OF THE GASTROINTESTINAL TRACT IN GROWING STEERS. JOURNAL OF ANIMAL SCIENCE. 2002. pp. 3027-3034.

Interpretive Summary: Several outbreaks of Escherichia coli O157:H7 infections in humans have been associated with consumption of beef and dairy products. Cattle have also been implicated as the source in outbreaks due to contaminated water supplies. Post-harvest remediation is effective at reducing pathogens, but reduction of pathogen shedding by cattle is preferred. Dietary effects on E. coli shedding are contradictory. Our goal is to develop a model system for determining conditions under which pathogenic bacteria proliferate or are inhibited in cattle. In the current experiment, we determined the effects of site of carbohydrate supply on the indigenous bacteria of the gastrointestinal tract of steers. Forty steers were surgically fitted with catheters and we compared basal diets with diets that were supplemented with starch or glucose that were infused into the rumen or abomasum. Increasing the supply of energy (with starch or glucose) to the large intestine reduced pH and therefore altered the microbial profile. Changes in the total anaerobic and total aerobic populations were observed; however, there was no affect on the concentration of fecal coliforms or E. coli. In order for pathogenic organisms to infect humans, they must be able to survive the acidic conditions of the stomach. In this study, the fecal E. coli were highly acid-sensitive, even when fecal pH was neutral. More information is needed in order to accurately predict the response of specific bacterial species (i.e., pathogenic E. coli) to changes in dietary composition.

Technical Abstract: Forty steers were fitted with ruminal and abomasal catheters and assigned randomly to one of 8 groups. Treatments included: 1.) a pelleted basal ration fed at 0.163 Mcal ME ú (kg BW.75)-1 ú d-1 (LE), 2.) the basal ration fed at 0.215 Mcal ME ú (kg BW.75)-1 ú d-1 (HE), 3.) the basal ration fed at 0.163 Mcal ME . (kg BW.75)-1 . d-1 plus ruminal infusion of starch hydrolys s(SH) (RSH), 4.) the basal ration fed at 0.163 Mcal ME ú (kg BW.75)-1 ú d-1 plus abomasal infusion of SH (ASH), and 5.) the basal ration fed at 0.163 Mcal ME ú (kg BW.75)-1 ú d-1 plus abomasal infusion of glucose (AG). Glucos and SH were infused at 14.35 and 12.64 g/kg BW.75/d, respectively. Ruminal, intestinal, and fecal samples were obtained on d 36. Ruminal pH was low (5.79) in LE steers and unaffected (P > 0.10) by increased energy intake or carbohydrate infusions. Intestinal and fecal pH were 6.93 and 7.00, respectively for LE steers. Energy intake (P < 0.10) and carbohydrate infusions (P < 0.01) decreased intestinal and fecal pH compared with LE. Abomasal carbohydrate infusion had no affect (P > 0.10) on ruminal counts of anaerobic bacteria in LE steers. However, ASH and AG steers had 1.5 Log10 cells/g higher (P < 0.01) intestinal and fecal anaerobic populations. Ruminal, intestinal, and fecal aerobic counts were 40, 22, and 23%, respectively, lower than anaerobic counts. Aerobic counts response was similar to anaerobic response. In all sites, less than 1% of the anaerobic bacteria were coliforms, and 97% of the coliforms were Escherichia coli. Carbohydrate infusions resulted in only numerical increases in fecal coliform and E. coli concentrations (P > 0.10). Fecal E. coli were highly acid-sensitive in all steers. This suggests that intestinal or fecal pH is not a good indicator of acid-resistance.