Multistate Outbreak of Listeria monocytogenes Associated with Mexican-Style Cheese Made from Pasteurized Milk among Pregnant, Hispanic Women
ABSTRACT Listeriosis is a severe infection caused by Listeria monocytogenes. Since 2004, the Centers for Disease Control and Prevention has requested that listeriosis patients be interviewed using a standardized Listeria Initiative (LI) questionnaire. In January 2009, states and the Centers for Disease Control and Prevention began investigating a multistate outbreak of listeriosis among pregnant, Hispanic women. We defined a case as an illness occurring between October 2008 and March 2009 with an L. monocytogenes isolate indistinguishable from the outbreak strain by pulsed-field gel electrophoresis. We conducted a multistate case-control study using controls that were selected from L. monocytogenes illnesses in non-outbreak-related pregnant, Hispanic women that were reported to the LI during 2004 to 2008. Eight cases in five states were identified. Seven of these were pregnant, Hispanic females aged 21 to 43 years, and one was a 3-year-old Hispanic girl, who was excluded from the study. Seven (100%) cases but only 26 (60%) of 43 controls had consumed Mexican-style cheese in the month before illness (odds ratio, 5.89; 95% confidence interval, 1.07 to ∞; P = 0.04). Cultures of asadero cheese made from pasteurized milk collected at a manufacturing facility during routine sampling by the Michigan Department of Agriculture on 23 February 2009 yielded the outbreak strain, leading to a recall of cheeses produced in the plant. Recalled product was traced to stores where at least three of the women had purchased cheese. This investigation highlights the usefulness of routine product sampling for identifying contaminated foods, of pulsed-field gel electrophoresis analysis to detect multistate outbreaks, and of the LI for providing timely exposure information for case-control analyses. Recalls of contaminated cheeses likely prevented additional illnesses.
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ABSTRACT: The aim of this study was to analyze the changing patterns of Listeria monocytogenes contamination in a cheese processing facility manufacturing a wide range of ready-to-eat products. Characterization of L. monocytogenes isolates included genotyping by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST). Disinfectant-susceptibility tests and the assessment of L. monocytogenes survival in fresh cheese were also conducted. During the sampling period between 2010 and 2013, a total of 1284 environmental samples were investigated. Overall occurrence rates of Listeria spp. and L. monocytogenes were 21.9% and 19.5%, respectively. Identical L. monocytogenes genotypes were found in the food processing environment (FPE), raw materials and in products. Interventions after the sampling events changed contamination scenarios substantially. The high diversity of globally, widely distributed L. monocytogenes genotypes was reduced by identifying the major sources of contamination. Although susceptible to a broad range of disinfectants and cleaners, one dominant L. monocytogenes sequence type (ST) 5 could not be eradicated from drains and floors. Significantly, intense humidity and steam could be observed in all rooms and water residues were visible on floors due to increased cleaning strategies. This could explain the high L. monocytogenes contamination of the FPE (drains, shoes and floors) throughout the study (15.8%). The outcome of a challenge experiment in fresh cheese showed that L. monocytogenes could survive after 14days of storage at insufficient cooling temperatures (8 and 16°C). All efforts to reduce L. monocytogenes environmental contamination eventually led to a transition from dynamic to stable contamination scenarios. Consequently, implementation of systematic environmental monitoring via in-house systems should either aim for total avoidance of FPE colonization, or emphasize a first reduction of L. monocytogenes to sites where contamination of the processed product is unlikely. Drying of surfaces after cleaning is highly recommended to facilitate the L. monocytogenes eradication.International Journal of Food Microbiology 08/2014; 189C:98-105. DOI:10.1016/j.ijfoodmicro.2014.08.001 · 3.16 Impact Factor
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ABSTRACT: It has been possible to determine the genotype diversity of Listeria monocytogenes in the actual cheese lots of acid curd cheese that caused a multinational outbreak between 2009 and 2010. Following product recall in January 2010 all lots were investigated. A total of 422 L. monocytogenes isolates were characterized by genotyping. In a first approach the PCR serogroups were defined by multiplex-PCR assays. Subsequently, the isolates were subtyped by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST). Sequence types were assigned by submitting the DNA sequences to the Listeria MLST database at the Institute Pasteur. The serogroup PCR resulted in a homogeneous 1/2a – 3a (genetic linage II) cluster. The generated PFGE patterns divided the strains into two clusters (type 1 and 2) diverging at a homogeneity level of 74%. PFGE-type 2 was predominant, accounting for 98.3% (n = 415/422) of the isolates and was isolated during the whole period of acid curd cheese processing (01.12.2009–13.01.2010). 1.7% of all tested L. monocytogenes isolates (n = 7/422) belonged to PFGE-type 1 and were isolated from 28% of all cheese lots (n = 5/18) produced between the time span of 08.12.2009 to 13.01.2010. Furthermore, PFGE-type 1 and 2 showed the same PFGE patterns as the human outbreak strains (clone 1 and clone 2).Food Microbiology 05/2014; 39:68–73. DOI:10.1016/j.fm.2013.11.006 · 3.37 Impact Factor
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ABSTRACT: The foodborne pathogen Listeria monocytogenes has the capacity to survive and grow in a diverse range of natural environments. The transition from a food environment to the gastrointestinal tract begins a process of adaptation that may culminate in invasive systemic disease. Here we describe recent advances in our understanding of how L. monocytogenes adapts to the gastrointestinal environment prior to initiating systemic infection. We will discuss mechanisms used by the pathogen to survive encounters with acidic environments (which include the glutamate decarboxylase and arginine deiminase systems), and those which enable the organism to cope with bile acids (including bile salt hydrolase) and competition with the resident microbiota. An increased understanding of how the pathogen survives in this environment is likely to inform the future design of novel prophylactic approaches that exploit specific pharmabiotics; including probiotics, prebiotics, or phages.Frontiers in Cellular and Infection Microbiology 02/2014; 4:9. DOI:10.3389/fcimb.2014.00009 · 2.62 Impact Factor