Outbreaks of food-borne listeriosis have often involved strains of serotype 4b. Examination of multiple isolates from three different outbreaks revealed that ca. 11 to 29% of each epidemic population consisted of strains which were negative with the serotype-specific monoclonal antibody c74.22, lacked galactose from the teichoic acid of the cell wall, and were resistant to the serotype 4b-specific phage 2671.
Cites: Appl Environ Microbiol. 1999 Nov;65(11):4793-810543788
Cites: MMWR Morb Mortal Wkly Rep. 1999 Jan 8;47(51-52):1117-89921730
Cites: N Engl J Med. 1983 Jan 27;308(4):203-66401354
Cites: J Biochem. 1983 May;93(5):1401-96411698
Cites: N Engl J Med. 1985 Feb 14;312(7):404-73918263
Cites: J Biochem. 1986 Feb;99(2):315-273084460
Cites: N Engl J Med. 1988 Sep 29;319(13):823-83137471
Cites: JAMA. 1989 Mar 3;261(9):1313-202492614
Cites: Appl Environ Microbiol. 1991 Apr;57(4):969-751905523
In February 1999, an outbreak of listeriosis caused by Listeria monocytogenes serotype 3a occurred in Finland. All isolates were identical. The outbreak strain was first isolated in 1997 in dairy butter. This dairy began delivery to a tertiary care hospital (TCH) in June 1998. From June 1998 to April 1999, 25 case patients were identified (20 with sepsis, 4 with meningitis, and 1 with abscess; 6 patients died). Patients with the outbreak strain were more likely to have been admitted to the TCH than were patients with other strains of L. monocytogenes (60% vs. 8%; odds ratio, 17.3; 95% confidence interval, 2.8-136.8). Case patients admitted to the TCH had been hospitalized longer before cultures tested positive than had matched controls (median, 31 vs. 10 days; P=.008). An investigation found the outbreak strain in packaged butter served at the TCH and at the source dairy. Recall of the product ended the outbreak.
An outbreak of listeriosis in Sweden, consisting of nine cases, was investigated by means of molecular typing of strains from patients and strains isolated from suspected foodstuffs, together with interviews of the patients. Listeria monocytogenes was isolated from six of the patients, and all isolates were of the same clonal type. This clonal type was also isolated from a "gravad" rainbow trout, made by producer Y, found in the refrigerator of one of the patients. Unopened packages obtained from producer Y were also found to contain the same clonal type of L. monocytogenes. Based on the interview results and the bacteriological typing, we suspect that at least six of the nine cases were caused by gravad or cold-smoked rainbow trout made by producer Y. To our knowledge, this is the first rainbow trout-borne outbreak of listeriosis ever reported.
Public health authorities place a high priority on investigating listeriosis outbreaks, and these epidemiological investigations remain challenging. Some approaches have been described in the literature to address these challenges. This review of listeriosis clusters and outbreaks investigated in the Province of Quebec (Quebec) highlights investigative approaches that contributed to identifying the source of these outbreaks.
The Laboratoire de Santé Publique du Québec (LSPQ) implemented pulsed-field gel electrophoresis (PFGE) molecular subtyping in 1997 to identify Listeria monocytogenes clusters among isolates from invasive listeriosis cases identified throughout Quebec. A cluster was defined as three cases or more with the same or similar PFGE profiles (=3 band difference) occurring over a 4-month period. An investigation was initiated if the epidemiologic indicators suggested a common source. Listeriosis data from LSPQ's database were reviewed to identify and describe clusters detected from 1997 to 2011, including those that led to an outbreak investigation. Epidemiological reports prepared following each outbreak were also reviewed.
Eleven clusters were identified in the province by LSPQ between 1997 and 2011. Outbreak investigations were initiated for six clusters, four of which involved more than 10 cases. Factors that contributed to identifying the source for three of these outbreaks highlighted the value of (1) making all stakeholders (food safety and inspection services, public health authorities, and laboratories) aware of any ongoing investigation and sharing relevant information even if the source is not yet identified; (2) promptly collecting food samples identified and considered as possible vehicles of infection identified during the interview of a Listeria case; (3) collecting food items and/or environmental samples in locations reported in common by cases in the same cluster.
Multiple approaches should be considered when investigating L. monocytogenes clusters. Networks to facilitate continuous exchange of human and food data between public health and food safety partners should be encouraged.
Data on the levels of bacteria and the amounts of food consumed in food-borne outbreaks provides an excellent opportunity to study the effects of exposure to Listeria monocytogenes. Between June 1998 and April 1999, an outbreak caused by L. monocytogenes serotype 3a in butter occurred in Finland. The majority of the cases were immunocompromised and hospitalized at the Helsinki University Central Hospital (HUCH), where 7-g butter packages produced by a dairy plant were used as the only butter brand. The butter had also been sold to 10 other central hospitals as well as to the retail market. Based on the data on hospital stay, butter consumption and the qualitative and quantitative analyses of L. monocytogenes in butter, the attack rates and exposure were estimated. Incubation studies on the naturally contaminated small butter packages showed that the levels found in the packages at the time of detection of the outbreak could reliably be used for these estimations. However, the levels of L. monocytogenes in 500-g packages increased. The attack rate among HUCH patients varied from 70 to 117 cases per 1000 patients at risk, depending on which estimate of the contamination level of butter (100-60%) was used. The highest single dose (7.7 x 10(4) CFU in one meal) could have been sufficient to cause the listeriosis cases at HUCH. However, this data also supports another hypothesis, according to which these listeriosis cases were caused by a prolonged daily consumption of contaminated butter during the hospital stay. The estimated daily dose, based on the hospital kitchen data or the highest detected level in a wholesale sample (11,000 CFU/g), would have varied from 1.4 x 10(1) to 2.2 x 10(3) CFU/day or from 2.2 x 10(4) to 3.1 x 10(5) CFU/day, respectively. The choice of the hypothesis has a crucial impact on the interpretation of this data for the dose-response estimations as well as for the discussion on Food Safety Objectives. Due to the susceptibility of hospital patients, special care must be taken in order to avoid even low levels of L. monocytogenes in food served.
An outbreak of febrile gastroenteritis affected consumers of on-farm manufactured dairy products from a summer farm in Sweden. Symptoms included diarrhoea, fever, stomach cramps and vomiting in 88, 60, 54 and 21% of cases identified. The median incubation period was 31 h. A cohort study with 33 consumers showed an attack rate of 52% and an association between the total amount of product eaten and illness (P=0.07). Twenty-seven of 32 (84%) stool samples cultured for Listeria monocytogenes tested positive, although there was no association between clinical disease and the isolation of L. monocytogenes. In addition, gene sequences for VTEC and ETEC were detected in 6 and 1 subjects, respectively. Bacteriological analysis of cheese samples revealed heavy contamination with L. monocytogenes and coagulase positive staphylococci in all of them and gene markers for VTEC in one of them. Molecular profiles for L. monocytogenes isolated from dairy products, stool samples and an abscess from 1 patient who developed septic arthritis were identical. Results of both microbiological and epidemiological analyses point to L. monocytogenes as the most likely cause of this outbreak. The finding of markers for VTEC in some humans and cheese samples means that a mixed aetiology at least in some cases cannot be conclusively ruled out.
Two hundred seventy-nine cases of human listeriosis (92 pregnancy-related cases and 187 non-pregnancy-related cases) caused by a serovar 4b and phagovar 2389:2425:3274:2671:47:108:340 strain were identified in France between March and December 1992. Epidemiological investigations included a case-control study (not described here) and microbiological analyses of foods. Results of the case-control study and characterization of food isolates identified pork tongue in jelly, a ready-to-eat meat product, as the major vehicle of this outbreak, and to a lesser extent, delicatessen products contaminated secondarily during handling in food stores. As far as serotyping, phage typing, DNA macrorestriction pattern analysis (obtained by pulsed-field gel electrophoresis [PFGE]), and ribotyping are concerned, this epidemic strain is phenotypically and genomically closely related to strains responsible for major outbreaks of listeriosis previously observed in Europe and North America. The epidemic strain sensu stricto as defined by PFGE (2/1/3) displayed the same serovar, phagovar, ribovar, and ApaI and NotI PFGE patterns as the epidemic strains from outbreaks in Switzerland, California, and Denmark, but it consistently showed differences in the SmaI PFGE profile. This information greatly contributed to the identification of the major food vehicle (pork tongue in jelly) and further allowed exclusion of other foods (cheese) as possible sources of this major listeriosis epidemic.
Among 504 clinical lineage II isolates of Listeria monocytogenes isolated during 1958-2010 in Sweden, 119 pulsed-field gel electrophoresis (PFGE) types (AscI) have been identified based on the number and distribution of all banding patterns in each DNA profile. In this study, these types were further divided into PFGE groups based on the configuration of small bands with sizes 145.5?kb.
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.