In this review, the major steps used in the formulation of a health risk assessment for Listeria monocytogenes in foods are discussed. Data is given on the numbers of human listeriosis cases reported in Canada along with the current Canadian regulatory policy on L. monocytogenes. Four major steps in the health risk assessment of this organism in foods, namely, hazard identification, hazard characterization, exposure assessment and risk characterization, were examined. For hazard characterization, since it is known that no direct human dose response data is available for L.monocytogenes, a flexible dose response model called the Weibull-Gamma model was evaluated. For the exposure assessment, pâté and soft cheese, both high-risk foods in terms of listeriosis infection, were used as prototypes in some of the models that were used. Using disappearance data for cheese and 100 g as a typical serving, the data suggested an average of 102 servings per capita, per year in Canada. As a rough approximation, for L. monocytogenes, reference ID10 and ID90 dose levels of response for both normal and high risk populations were given as 10(7) and 10(9) for normal individuals, and 10(5) and 10(7) for high-risk people. The corresponding dose response models were graphically displayed. These models exhibited a higher degree of susceptibility and less host/pathogen heterogeneity for the higher risk group. The range of doses between the ID10 and ID90 reference values corresponded roughly to levels associated with cases of listeriosis. In the risk characterization stage, dose response data was combined with some predictive growth modeling data of L. monocytogenes on pâté, assuming an initial exposure of a single cell for food stored at 4 degrees and 8 degrees C. Storage of pâté at 4 degrees C for more than 35 days resulted in a rapidly increasing risk for the high risk population, while storage at 8 degrees C produced a similar risk after about 13 days. In addition, an equation, used to calculate the average probability of acquiring human listeriosis in Canada from soft and semi-soft cheese consumption, was formulated. Computations derived from this equation indicated a substantial level consistency between reported data and assumptions of the risk assessment model. An important part of risk characterization or possibly risk management is characterizing the economic and social consequences of estimated risks. The total annual estimated cost of listeriosis illnesses and deaths in Canada was estimated to be between 11.1 and 12.6 million dollars.
As a leading cause of death from a foodborne pathogen, Listeria monocytogenes continues to cause sporadic cases and outbreaks of illness. The most recent of these outbreaks in the United States involved consumption of hot dogs, with 101 cases of illness and 21 deaths reported to the Centers for Disease Control and Prevention for the years 1998-1999. Epidemiologic analysis determined that contamination levels in hot dogs were remarkably low (0.3 CFU [colony-forming units] L monocytogenes serotype 4b/g). That same year, manufacturers of hot dogs and luncheon meats collectively recalled more than 500,000 pounds of product owing to possible Listeria contamination. This article, through focus on issues such as reexamination of zero-tolerance policies, improvements in detection and enumeration procedures, the impact of epidemiologic innovations, and measures needed to further reduce the incidence of listeriosis will highlight why L monocytogenes remains a continuing challenge for the food industry.
The present situation regarding Listeria monocytogenes and ready-to-eat (RTE) seafood is discussed. An updated regulatory policy on L. monocytogenes directs inspection and compliance action to those RTE foods capable of supporting growth of the organism and is based on a combination of inspection, environmental sampling and product testing. The incidence of L. monocytogenes in imported seafood products in 1996-1997 and 1997-1998 was 0.88 and 0.3%, respectively. With respect to domestic products, an analysis of 347 RTE foods in 1997-1998 and 1998-1999, at one of the large fish inspection labs in the Maritimes, revealed an absence of L. monocytogenes. The only seafood product linked to suspect cases of listeriosis in Canada was imported.
Recent food-borne outbreaks of human listeriosis as well as numerous sporadic cases have been mainly caused by Listeria monocytogenes serovar 4b strains. Thus, it was of interest to find out whether a certain clone or a certain few clones were responsible for these cases and especially for outbreaks. We used pulsed-field gel electrophoresis of large chromosomal DNA restriction fragments generated by ApaI, SmaI, or NotI to analyse 75 L. monocytogenes strains isolated during six major and eight smaller recent listeriosis outbreaks. These strains could be divided into 20 different genomic varieties. Thirteen of 14 strains isolated during major epidemics in Switzerland (1983-1987), the United States (California, 1985) and Denmark (1985-1987) demonstrated indistinguishable DNA restriction patterns. In contrast, strains responsible for the outbreaks in Canada (Nova Scotia, 1981), the United States (Massachusetts, 1983), France (Anjou, 1975-1976), New Zealand (1969), and Austria (1986) and some smaller outbreaks in France (1987, 1988, 1989) were each characterized by particular combinations of DNA restriction patterns. Seventy-seven percent of the tested strains could be classified into the previously described ApaI group A (Brosch et al. 1991), demonstrating a very close genomic relatedness. Because 49% of the epidemic strains selected for this study belonged to phagovar 2389/2425/3274/2671/47/108/340 or 2389/47/108/340, fifty-six additional strains of these phagovars, isolated from various origins, were also typed to determine whether differences in DNA restriction profiles between epidemic and randomly selected strains of the same phagovars could be pointed out. Variations in DNA patterns appeared more frequently within randomly selected strains than within epidemic strains.
Human listeriosis outbreaks in Canada have been predominantly caused by serotype 1/2a isolates with highly similar pulsed-field gel electrophoresis (PFGE) patterns. Multilocus sequence typing (MLST) and multi-virulence-locus sequence typing (MVLST) each identified a diverse population of Listeria monocytogenes isolates, and within that, both methods had congruent subtypes that substantiated a predominant clone (clonal complex 8; virulence type 59; proposed epidemic clone 5 [ECV]) that has been causing human illness across Canada for more than 2 decades.
Canadian cases and outbreaks of illness caused by Listeria monocytogenes between 1995 and 2004 were assessed. Isolates (722 total) were characterized by serotyping, and pulsed-field gel electrophoresis (PFGE) was performed to provide a means of detecting case clusters. Rates of listeriosis remained fairly consistent during the period of study, and patient characteristics were similar to those seen in studies of other populations. Most isolates were obtained from blood and cerebrospinal fluid, although during some outbreak investigations isolates were also obtained from stools. Serotype 1/2a predominated in isolates from patients in Canada, followed by serotypes 4b and 1/2b. Outbreaks caused by L. monocytogenes that occurred during the period of study were caused by isolates with serotypes 1/2a and 4b. A retrospective analysis of PFGE data uncovered several clusters that might have represented undetected outbreaks, suggesting that comprehensive prospective PFGE analysis coupled with prompt epidemiological investigations might lead to improved outbreak detection and control.
Food and clinical isolates of Listeria monocytogenes recovered from four different outbreaks of listeriosis were analyzed by their PCR-based randomly amplified polymorphic DNA (RAPD) patterns to verify their causal relationships. The generation of DNA fingerprints by PCR-based RAPD analysis is a fast and sensitive method for the epidemiological tracking and identification of bacteria implicated in food poisoning outbreaks. The L. monocytogenes strains used in the study were obtained from the following four outbreaks: California, 1985, Mexican-style cheese; Canadian Maritime Provinces, 1981, coleslaw; Canada, 1989, brie cheese; and Canada, 1989, alfalfa tablets. RAPD profiles were generated by using random 10-mer primers for at least one food and one clinical isolate recovered from each outbreak. Identical profiles for 20 different primers were observed for each pair of food and clinical isolates from two of the four outbreaks. Isolates from the outbreak involving alfalfa tablets exhibited identical patterns for 19 primers; however, primer OPA-1 produced one additional 1.8-kb fragment, designated OPA-1-1.8, that was found in the food isolate but not in the corresponding clinical isolate. Hybridization analysis revealed that the absence of the OPA-1-1.8 polymorphic fragment in the clinical isolate was due to a deletion of at least 1.8 kb. Loss of the OPA-1-1.8 polymorphic fragment could not be induced by infective passage of the L. monocytogenes isolate from the alfalfa tablet through a mouse or by growth of this isolate under selective conditions. This suggests that the isolate recovered from the food was not identical to the isolate recovered from the patient. The ability to produce unique RAPD patterns allows for the discrimination between isolates even if they are of the same serotype and multilocus enzyme electrophoretic type.
Cites: Appl Environ Microbiol. 1992 Feb;58(2):709-121610193
Cites: Appl Environ Microbiol. 1991 Aug;57(8):2324-311662932
Cites: Res Microbiol. 1992 Jun;143(5):499-5051448625
Cites: Res Microbiol. 1992 Jun;143(5):507-121448626