Application of colicin E1 as a prefabrication intervention strategy.

Colicin E1 (ColE1) is a bacteriocin produced by and effective against Escherichia coli and related species. The current study examined ColE1 as a potential intervention strategy for controlling E. coli O157:H7 contamination on beef carcasses. Untrimmed beef round roasts were cut into sample sizes of 5.08 by 2.52 by 5.08 cm, with an adipose layer covering an entire surface of lean beef. Samples were placed on sterile metal hooks and inoculated with E. coli O157:H7 at a level of 5 log CFU/ml in sterile tryptic soy broth. After inoculum attachment, ColE1 in doses of 0, 100 microg, 500 microg, and 1 mg/ml of 10 mM Tris, pH 7.6, was sprayed on the samples for a period of 10 min. Samples were evaluated at 0 and 30 min, 1, 2, 3, 4, and 5 days post-spraying at 10 degrees C for E. coli O157:H7 inhibition. Treating samples with 500 microg and 1 mg of ColE1 effectively inhibited E. coli O157:H7 growth. When these doses were applied to samples inoculated with E. coli WS 3331, E. coli contamination was reduced by 4 and 7 log CFU/cm2, respectively, compared with the untreated control samples. In strain WS 3331, treatment with 1 mg ColE1 significantly inhibited growth of E. coli O157:H7 compared with the untreated control during the entire study. ColE1 provided powerful reduction of E. coli O157:H7 as a beef carcass spray intervention.

Inhibitory activity of colicin E1 against Listeria monocytogenes.

Colicins are gram-negative bacteriocins produced by and effective against Escherichia coli and related species. Colicin E1 (ColE1) is composed of three functional domains, which collectively have a pore-forming effect on targeted bacteria. ColE1 binding and translocation domains are highly specific in contrast to the pore-forming domain, implying that ColE1 could be broadly effective. In this study, the activity of ColE1 against Listeria monocytogenes was evaluated in broth and on surfaces of ready-to-eat products. Individual strains of L. monocytogenes were examined in broth containing ColE1 at 0, 0.1, 1, or 10 microg/ml. Although strain differences in sensitivity to ColE1 existed, growth was significantly reduced in all strains at doses as low as 0.1 microg/ml. Sterilized ham slices were submerged in a five-strain L. monocytogenes cocktail (either 7 or 4 log CFU/ ml) and placed in vacuum packages containing 0, 1, 5, 10, 25, or 50 microg of ColE1. Ham slices were then stored at 4 or 10 degrees C, and samples were removed and examined for L. monocytogenes after 1, 3, 7, and 14 days. Reduction of L. monocytogenes by ColE1 was dependent on initial inoculum concentration and storage temperature. For slices stored at 4 degrees C, treatment with 25 microg reduced Listeria growth below detection limits for the slices inoculated with 4 log CFU/ml for the entire 14 days, whereas for the 7-log CFU/ml slices, growth was detected at 7 days postinoculation. For slices stored at 10 degrees C, 10 microg/ml ColE1 significantly inhibited growth of L. monocytogenes for up to 3 days for both inoculation groups. These data indicate that ColE1 is highly effective against Listeria.

Effects of atrazine on sexual maturation in female Japanese quail induced by photostimulation or exogenous gonadotropin.

The herbicide atrazine has gained recent attention for its reported effects on reproduction in amphibians. The present study examined the putative effects of atrazine during sexual maturation in the photostimulated female Japanese quail. Furthermore, the effects of atrazine on birds administered exogenous gonadotropin (pregnant mare serum gonadotropin [PMSG]) were investigated. Atrazine was administered up to 1,000 ppm in the diet to female quail undergoing photoperiodically induced sexual maturation. At high dietary concentrations, atrazine exhibits signs of overt toxicity with reductions in growth, feed intake, and liver weights, but these effects were dependent on the timing of treatment administration. Atrazine did not influence the weights of reproductive tissues (ovary and oviduct) or circulating concentrations of luteinizing hormone (LH). However, high concentrations of atrazine depressed circulating concentrations of estradiol. Treatment with atrazine for four weeks during sexual maturation inhibited growth but did not affect any other parameter assessed (feed intake, liver, ovary, or oviduct weights or the circulating concentrations of LH and estradiol). In birds receiving daily injections of PMSG, atrazine reduced growth, feed intake, and liver weights. However, PMSG-induced gonadal and oviduct growth was not affected by atrazine. The present results suggest that dietary atrazine exhibits limited reproductive toxicity in female quail during sexual maturation and only at concentrations above ecological relevance.

Atrazine and the hypothalamo-pituitary-gonadal axis in sexually maturing precocial birds: studies in male Japanese quail.

The herbicide atrazine is a putative endocrine disruptor. The present studies investigated the effects of atrazine in male Japanese quail during sexual maturation. Atrazine was administered for two weeks in the diet or systemically to birds under long photoperiods. Atrazine had no effect on mortality but depressed both feed intake and growth (average daily gain [ADG] in g/day) at dietary concentrations of 1000 ppm. Atrazine in the diet at 10 ppm, but at no other concentrations, increased testes weight and gonadal-somatic-index and decreased the seminiferous tubule diameter-to-testis weight ratio. However, there were no effects on absolute tubule diameter, relative stage of testicular development, or the presence of a lumen. Atrazine in the diet at 1000 ppm increased circulating concentrations of testosterone but this effect was not observed consistently in all studies. Dietary atrazine at 10 ppm increased circulating concentrations of estradiol. Moreover, in one study, atrazine at 1000 ppm in the diet decreased circulating concentrations of luteinizing hormone. Atrazine administered systemically exerted no effect on indices of growth or reproduction. Atrazine did not mimic the effects of either estradiol or tamoxifen in male quail; thus, atrazine did not exhibit overt estrogenic or anti-estrogenic activity. Conversely, atrazine augmented the effects of testosterone and estradiol on testis regression, presumably by increasing the negative-feedback effects of these sex-steroids on follicle stimulating hormone secretion. It is concluded that atrazine up to 1000 ppm in the diet may exert some effects on reproductive development in sexually maturing male birds, but these are inconsistent and modest.