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首页> 外文期刊>Food microbiology >Behavior of Listeria monocytogenes in the presence or not of intentionally-added lactic acid bacteria during ripening of artisanal Minas semi-hard cheese
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Behavior of Listeria monocytogenes in the presence or not of intentionally-added lactic acid bacteria during ripening of artisanal Minas semi-hard cheese

机译:李斯特里亚单核细胞增生在手工山半硬奶酪成熟期间有意添加的乳酸菌存在的行为

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摘要

The fate of Listeria monocytogenes during ripening of artisanal Minas semi-hard cheese, as influenced by cheese intrinsic properties and by autochthonous (naturally present) or intentionally-added anti-listerial lactic acid bacteria (LAB) was modeled. Selected LAB strains with anti-listerial capacity were added or not to raw or pasteurized milk to prepare 4 cheese treatments. Counts of LAB and L. monocytogenes, pH, temperature and water activity were determined throughout cheese ripening (22 days, 22 ± 1°C). Different approaches were adopted to model the effect of LAB on L. monocytogenes: an independent approach using the Huang primary model to describe LAB growth and the linear decay model to describe pathogen inactivation; the Huang-Cardinal [pH] model using the effect of pH variation in a dynamic tertiary approach; and the Jameson-effect with N_(max tot) model which simultaneously describes L. monocytogenes and LAB fate. L. monocytogenes inactivation occurred in both treatments with added LAB and inactivation was faster in raw milk cheese (-0.0260 h~(-1)) vs. pasteurized milk cheese (-0.0182 h~(-1)), as estimated by the linear decay model. Better goodness-of-fit was achieved for the cheeses without added LAB when the Huang primary model was used. A faster and great pH decline was detected for cheeses with added LAB, and the Huang-Cardinal [pH] model predicted higher pathogen growth rate in cheese produced with raw milk, but greater L. monocytogenes final concentration in pasteurized milk cheese. The Jameson-effect model with N_(max tot) predicted that LAB suppressed pathogen growth in all treatments, except in the treatment with pasteurized milk and no LAB addition. The Huang-Cardinal [pH] model was more accurate in modeling L. monocytogenes kinetics as a function of pH changes than was the Jameson-effect model with N_(max tot) as a function of LAB inhibitory effect based on the goodness-of-fit measures. The Jameson-effect model may however be a better competition model since it can more easily represent L. monocytogenes growth and death. This study presents crucial kinetic data on L monocytogenes behavior in the presence of competing microbiota in Minas semi-hard cheese under dynamic conditions.
机译:根据奶酪内在特性和通过自加密(天然存在)或有意添加的抗脑卒中乳酸菌(实验室)的熟练迷住期间的李斯特菌米纳斯半硬乳酪中李斯特氏菌半硬化乳酪的命运。选择具有抗脑卒中能力的所选实验室菌株或不加入生物或巴氏杀菌牛奶,以制备4个奶酪处理。在整个奶酪成熟(22天,22±1°C)中测定实验室和L.单核细胞元,pH,温度和水活性的计数。采用不同的方法来模拟实验室对L.单核细胞增生的影响:使用黄初级模型描述实验室生长和线性衰变模型的独立方法来描述病原体灭活; Huang-Cordinal [pH]模型使用pH变异在动态三级方法的影响;和N_(MAX TOT)模型的JAMESON效应,其同时描述L.单核细胞元和实验室命运。 L.单核细胞增生在含有额外的实验室和灭活的治疗中发生的灭活(-0.0260h〜(-1))与杀菌牛奶奶酪(-0.0182h〜(-1))更快,如线性估计腐烂模型。使用Huang初级模型时,没有添加实验室的奶酪达到了更好的健康状况。对于奶酪,奶酪和黄色基团[pH]模型预测奶酪中的奶酪中的病原体生长速度较快,Huang-Condinal含量较高,但在巴氏杀菌乳奶酪中更大的L.单核细胞生成的最终浓度。 JAMESON效应模型与N_(MAX TOT)预测,除了用巴氏杀菌牛奶治疗和没有实验室添加外,实验室抑制了所有治疗的病原体生长。黄态[pH]模型在将L.单核细胞增生动力学建模中更准确地作为pH变化的函数,而不是JAMESON效应模型与N_(MAX TOT)的函数,作为基于良好的实验室抑制效果的函数适合措施。然而,Jameson效果模型可能是更好的竞争模型,因为它可以更容易地代表L.单核细胞生成和死亡。本研究介绍了在动态条件下在Minas半硬质奶酪中竞争微生物群的L单核细胞生成的关键动力学数据。

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