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模拟胃液消化过程中病原体存活的建模。

Modeling of pathogen survival during simulated gastric digestion.

机构信息

National Food Research Institute, 2-1-12 Kannondai, Tsukuba, Ibaraki 305-8642, Japan.

出版信息

Appl Environ Microbiol. 2011 Feb;77(3):1021-32. doi: 10.1128/AEM.02139-10. Epub 2010 Dec 3.

DOI:10.1128/AEM.02139-10
PMID:21131530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3028731/
Abstract

The objective of the present study was to develop a mathematical model of pathogenic bacterial inactivation kinetics in a gastric environment in order to further understand a part of the infectious dose-response mechanism. The major bacterial pathogens Listeria monocytogenes, Escherichia coli O157:H7, and Salmonella spp. were examined by using simulated gastric fluid adjusted to various pH values. To correspond to the various pHs in a stomach during digestion, a modified logistic differential equation model and the Weibull differential equation model were examined. The specific inactivation rate for each pathogen was successfully described by a square-root model as a function of pH. The square-root models were combined with the modified logistic differential equation to obtain a complete inactivation curve. Both the modified logistic and Weibull models provided a highly accurate fitting of the static pH conditions for every pathogen. However, while the residuals plots of the modified logistic model indicated no systematic bias and/or regional prediction problems, the residuals plots of the Weibull model showed a systematic bias. The modified logistic model appropriately predicted the pathogen behavior in the simulated gastric digestion process with actual food, including cut lettuce, minced tuna, hamburger, and scrambled egg. Although the developed model enabled us to predict pathogen inactivation during gastric digestion, its results also suggested that the ingested bacteria in the stomach would barely be inactivated in the real digestion process. The results of this study will provide important information on a part of the dose-response mechanism of bacterial pathogens.

摘要

本研究的目的是建立胃环境中病原菌失活动力学的数学模型,以进一步了解感染剂量反应机制的一部分。通过使用调整至不同 pH 值的模拟胃液,对主要的病原菌李斯特菌、大肠杆菌 O157:H7 和沙门氏菌进行了检验。为了与消化过程中胃内的各种 pH 值相对应,考察了改进的逻辑斯蒂微分方程模型和 Weibull 微分方程模型。各病原菌的特定失活动率成功地描述为 pH 的平方根模型的函数。将平方根模型与改进的逻辑斯蒂微分方程相结合,获得了完整的失活动力学曲线。对于每种病原菌,改进的逻辑斯蒂模型和 Weibull 模型都提供了高度精确的静态 pH 条件拟合。然而,尽管改进的逻辑斯蒂模型的残差图表明没有系统偏差和/或区域预测问题,但 Weibull 模型的残差图显示存在系统偏差。改进的逻辑斯蒂模型适当地预测了包括切碎生菜、金枪鱼末、汉堡和炒鸡蛋在内的实际食物在模拟胃消化过程中的病原菌行为。虽然所开发的模型使我们能够预测胃消化过程中的病原菌失活,但结果也表明,胃中的摄入细菌在实际消化过程中几乎不会失活。本研究的结果将为病原菌的剂量反应机制的一部分提供重要信息。

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