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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #176341
Title: EVALUATION OF DIETARY LACTOSE ON THE MICROBIAL ECOLOGY IN POULTRY WITH NECROTIC ENTERITIS

Author
item McReynolds, Jackson
item Byrd Ii, James - Allen
item Duke, Sara
item Kubena, Leon
item Nisbet, David

Submitted to: Conference on Gastrointestinal Function
Publication Type: Abstract Only
Publication Acceptance Date: 2/1/2005
Publication Date: 4/11/2005
Citation: McReynolds, J.L., Byrd II, J.A., Duke, S.E., Kubena, L.F., Nisbet, D.J. 2005. Evaluation of dietary lactose on the microbial ecology in poultry with necrotic enteritis [abstract]. Conference on Gastrointestinal Function. p. 19.

Interpretive Summary:

Technical Abstract: The commercial poultry industry uses a wide variety of management tools to control pathogens including antibiotics, vaccines, and competitive exclusion cultures. The industry has used growth promoting antibiotics (GPA) to target gram-positive organisms which are associated with lower levels of performance and health. One target organism controlled with GPA is Clostridium perfringens, the etiologic agent of Necrotic Enteritis (NE). Due to increasing consumer pressure to remove GPA from the market, our laboratory is currently evaluating the effects of dietary lactose on the microbial populations of the GI tract in the disease condition of NE. Four populations of bacteria along with clinical signs were evaluated to determine the effects of the dietary lactose. Day-of-hatch broilers were assigned to one of the following groups containing 45 birds/treatment: Negative control (0 %), 1, 1.5, 2.0, 2.5, 3.0, 3.5, 4.0, and 4.5% dietary lactose; fed from day one until termination of the experiment (d 21). Clostridium perfringens (10**7 cfu/mL) was administered once daily via oral gavage to the birds for three consecutive days starting on day seventeen. In the control group, 100% of the birds showed clinical signs of NE compared to the 1, 1.5, 2.0, and 2.5% lactose treatment groups whose clinical signs were significantly reduced (P < 0.05, N=10) to 66, 66, 50, 22% for the respective groups. Lactobacilli, E. coli, Clostridia, and Enterococcus were monitored, but there was no significant association between these bacteria and NE in this model. It is our conclusion that a 2.5% lactose dietary additive is optimal in reducing the clinical signs of NE. With further research, this technology could provide the industry with a viable alternative that can immediately be used in current commercial production operations in reducing the clinical infection of Necrotic enteritis.