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Title:   Author  item
                                            MCREYNOLDS, JACKSON - TX A&M UNIVERSITYitem
                                            Byrd Ii, James

                                                         - *Allen*item
                                            Anderson, Robinitem
                                            KNAPE, KOYLE - TX A&M UNIVERSITYitem
                                            Moore, Randleitem
                                            Kubena, Leonitem
                                            Nisbet, David
  Submitted to: Poultry Science
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 8/12/2002
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: Clostridium perfringens (Cp), the etiologic agent of necrotic enteritis is an economically important pathogen of the poultry industry; causing significant morbidity and mortality in commercial flocks worldwide.  As pressure mounts to discontinue the use of antibiotics in the agriculture industry, it is important to develop new strategies to combat this costly enteric pathogen.  Previous reports have shown that some facultative bacteria utilize the nitrate reductase enzymatic pathway to reduce chlorate to a toxic chlorite ion.  Unlike most anaerobes, Cp possesses a respiratory nitrate reductase pathway, thus this anaerobe may be susceptible to an experimental chlorate product (ECP).  In the present investigation, an in vitro assay was developed to determine the effects ECP on Cp.  Briefly, a mixed gut culture was obtained from SCWL laying hens and diluted (1:1) with thioglycollate enrichment medium.  The suspension was then divided into six 10 ml aliquots comprising the following experimental groups: negative control, ECP with a 5 mM chlorate ion equivalent, and ECP with a 10 mM chlorate ion equivalent (n=2 per groups). The effects of ECP were evaluated in vitro over several different time intervals, 0 h, 1 h, 2 h, and 3 h.  The initial Cp measurement showed that there was a log value of 5.57.  At the 1 h time interval there was no difference between the control (6.05 Log10), 5 mM ECP (5.43 Log10), and 10 mM ECP (5.50 Log10) treatment groups.  However, there was a significant reduction (P< .05) of Cp in both of the experimental groups at the 2 h time point when compared to the control (5.46 Log10), 5 mM ECP (5.13 Log10), and 10 mM ECP (4.93 Log10).  There was also a significant reduction (P< .05) at the 3h time point between the experimental groups, 5 mM ECP (3.88 Log10), and 10 mM ECP (3.29 Log10), and control (5.51 Log10).  In the present investigation the use of ECP reduced the number of recoverable Cp at the 2 h and 3 h time points.  Further research is needed in order to determine the effects of chlorate products in an in vivo model.


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