Significant Shift in Median Guinea Pig Infectious Dose Shown by an Outbreak-Associated<i>Listeria monocytogenes</i>Epidemic Clone Strain and a Strain Carrying a Premature Stop Codon Mutation in<i>inlA</i>

Stelten, A. Van; Simpson, J. M.; Chen, Y.; Scott, Virginia N.; Whiting, Richard C.; Ross, William H.; Nightingale, Kendra K.

doi:10.1128/aem.02626-10

Cited by 32 publications

(44 citation statements)

References 49 publications

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“…Nonsense mutations in inlA are reported to be at least partially responsible for an attenuated invasion phenotype (7,24,(39)(40)(41). These mutations may have accumulated as a result of selection for environmentally adapted ecotypes with reduced virulence, which do not require a fulllength InlA protein for ecological success (22).…”

Section: Discussionmentioning

confidence: 99%

“…L. monocytogenes isolates belonging to lineage I serotypes 1/2b and 4b are the predominant causes of listeriosis in humans. Molecular epidemiology studies have identified three highly clonal lineage I serotype 4b strains, termed epidemic clones I, Ia, and II, which have been associated recurrently with outbreaks of the disease globally (7). Lineage II isolates, which are predominantly serotype 1/2a, have also been implicated in a number of recent outbreaks of listeriosis (9)(10)(11)(12).…”

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confidence: 99%

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Listeria monocytogenes Associated with New Zealand Seafood Production and Clinical Cases: Unique Sequence Types, Truncated InlA, and Attenuated Invasiveness

Cruz

Pitman

Harrow

et al. 2014

Appl Environ Microbiol

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bListeriosis is caused by the food-borne pathogen Listeria monocytogenes, which can be found in seafood and processing plants. To evaluate the risk to human health associated with seafood production in New Zealand, multi-virulence-locus sequence typing (MVLST) was used to define the sequence types (STs) of 31 L. monocytogenes isolates collected from seafood-processing plants, 15 from processed foods, and 6 from human listeriosis cases. The STs of these isolates were then compared with those from a collection of seafood isolates and epidemic strains from overseas. A total of 17 STs from New Zealand clustered into two lineages: seafood-related isolates in lineages I and II and all human isolates in lineage II. None of the New Zealand STs matched previously described STs from other countries. Isolates (belonging to ST01-N and ST03-N) from mussels and their processing environments, however, were identical to those of sporadic listeriosis cases in New Zealand. ST03-N isolates (16 from mussel-processing environments, 2 from humans, and 1 from a mussel) contained an inlA premature stop codon (PMSC) mutation. Therefore, the levels of invasiveness of 22 isolates from ST03-N and the three other common STs were compared using human intestinal epithelial Caco-2 cell lines. STs carrying inlA PMSCs, including ST03-N isolates associated with clinical cases, had a low invasion phenotype. The close relatedness of some clinical and environmental strains, as revealed by identical MVLST profiles, suggests that local and persistent environmental strains in seafood-processing environments pose a potential health risk. Furthermore, a PMSC in inlA does not appear to give L. monocytogenes a noninvasive profile.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Listeria monocytogenes Associated with New Zealand Seafood Production and Clinical Cases: Unique Sequence Types, Truncated InlA, and Attenuated Invasiveness

Cruz

Pitman

Harrow

et al. 2014

Appl Environ Microbiol

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“…(19)(20)(21)(22) Therefore, point mutations in the inlA gene can lead to virulence attenuation of L. monocytogenes strains. (16,23,24) New data are also available regarding the variability in susceptibility among individuals with different predisposing conditions such as pregnancy, old age, or other underlying conditions. (25)(26)(27)(28) The relative risk of listeriosis for pregnant women, for example, has been estimated to be approximately 100 times higher than that for nonpregnant women.…”

Section: Introductionmentioning

confidence: 98%

Listeria monocytogenes Dose Response Revisited—Incorporating Adjustments for Variability in Strain Virulence and Host Susceptibility

Pouillot¹,

Hoelzer²,

Chen³

et al. 2014

Risk Analysis

110

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Evaluations of Listeria monocytogenes dose-response relationships are crucially important for risk assessment and risk management, but are complicated by considerable variability across population subgroups and L. monocytogenes strains. Despite difficulties associated with the collection of adequate data from outbreak investigations or sporadic cases, the limitations of currently available animal models, and the inability to conduct human volunteer studies, some of the available data now allow refinements of the well-established exponential L. monocytogenes dose response to more adequately represent extremely susceptible population subgroups and highly virulent L. monocytogenes strains. Here, a model incorporating adjustments for variability in L. monocytogenes strain virulence and host susceptibility was derived for 11 population subgroups with similar underlying comorbidities using data from multiple sources, including human surveillance and food survey data. In light of the unique inherent properties of L. monocytogenes dose response, a lognormal-Poisson dose-response model was chosen, and proved able to reconcile dose-response relationships developed based on surveillance data with outbreak data. This model was compared to a classical beta-Poisson dose-response model, which was insufficiently flexible for modeling the specific case of L. monocytogenes dose-response relationships, especially in outbreak situations. Overall, the modeling results suggest that most listeriosis cases are linked to the ingestion of food contaminated with medium to high concentrations of L. monocytogenes. While additional data are needed to refine the derived model and to better characterize and quantify the variability in L. monocytogenes strain virulence and individual host susceptibility, the framework derived here represents a promising approach to more adequately characterize the risk of listeriosis in highly susceptible population subgroups.

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“…The virulence factor internalin A (InlA; encoded by inlA) facilitates the crossing of the host intestinal barrier, which enables subsequent establishment of a systemic infection by L. monocytogenes (20). L. monocytogenes isolates carrying a PMSC in inlA produce a truncated form of InlA that is secreted rather than anchored to the bacterial cell wall; these strains have been shown to be virulence attenuated in a guinea pig model (17,(21)(22)(23). A number of studies specifically indicate that lineage II strains carry an inlA PMSC more frequently than lineage I strains (18,23,24).…”

mentioning

confidence: 99%

Prevalence and Distribution of Listeria monocytogenes inlA Alleles Prone to Phase Variation and inlA Alleles with Premature Stop Codon Mutations among Human, Food, Animal, and Environmental Isolates

Manuel

Stelten

Wiedmann

et al. 2015

Appl Environ Microbiol

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cIn Listeria monocytogenes, 18 mutations leading to premature stop codons (PMSCs) in the virulence gene inlA have been identified to date. While most of these mutations represent nucleotide substitutions, a frameshift deletion in a 5= seven-adenine homopolymeric tract (HT) in inlA has also been reported. This HT may play a role in phase variation and was first identified among L. monocytogenes lineage II ribotype DUP-1039C isolates. In order to better understand the distribution of different inlA mutations in this ribotype, a newly developed multiplex real-time PCR assay was used to screen 368 DUP-1039C isolates from human, animal, and food-associated sources for three known 5= inlA HT alleles: (i) wild-type (WT) (A 7 ), (ii) frameshift (FS) (A 6 ), and (iii) guanine interruption (A 2 GA 4 ) alleles. Additionally, 228 DUP-1039C isolates were screened for all inlA PMSCs; data on the presence of all inlA PMSCs for the other 140 isolates were obtained from previous studies. The statistical analysis based on 191 epidemiologically unrelated strains showed that strains with inlA PMSC mutations (n ‫؍‬ 41) were overrepresented among food-associated isolates, while strains encoding full-length InlA (n ‫؍‬ 150) were overrepresented among isolates from farm animals and their environments. Furthermore, the A 6 allele was overrepresented and the A 7 allele was underrepresented among food isolates, while the A 6 allele was underrepresented among farm and animal isolates. Our results indicate that genetic variation in inlA contributes to niche adaptation within the lineage II subtype DUP-1039C. Listeria monocytogenes is a food-borne pathogen and the etiological agent of listeriosis, a severe invasive disease that can affect both humans and animals (1). More than 99% of human listeriosis cases are estimated to be transmitted through food (2). Despite its presence in a wide range of environments and foods, the majority of human listeriosis infections appear to be linked to consumption of contaminated ready-to-eat (RTE) foods (3) that support L. monocytogenes growth. Numerous studies have indicated that not all L. monocytogenes strains are equally associated with invasive disease. For example, McLauchlin reported that three (1/2a, 1/2b, and 4b) of the 13 serotypes of L. monocytogenes were responsible for 90% of 1,363 listeriosis cases from the United Kingdom (4). Additionally, multiple studies using both DNA band-based and sequence-based subtyping methods have shown that L. monocytogenes forms a structured population composed of at least four divergent lineages (I, II, III, and IV), which in a number of studies have been suggested to differ in their associations with different sources and in their pathogenic potentials (5-9). The majority of L. monocytogenes isolates belong to lineages I and II, which contain the serotypes most commonly associated with human clinical cases; serotypes 1/2b and 4b group into lineage I, while serotypes1/2a and 1/2c group into lineage II. Lineage III and IV strains are rare and usually isolated from ...

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Significant Shift in Median Guinea Pig Infectious Dose Shown by an Outbreak-AssociatedListeria monocytogenesEpidemic Clone Strain and a Strain Carrying a Premature Stop Codon Mutation ininlA

Cited by 32 publications

References 49 publications

Listeria monocytogenes Associated with New Zealand Seafood Production and Clinical Cases: Unique Sequence Types, Truncated InlA, and Attenuated Invasiveness

Listeria monocytogenes Associated with New Zealand Seafood Production and Clinical Cases: Unique Sequence Types, Truncated InlA, and Attenuated Invasiveness

Listeria monocytogenes Dose Response Revisited—Incorporating Adjustments for Variability in Strain Virulence and Host Susceptibility

Prevalence and Distribution of Listeria monocytogenes inlA Alleles Prone to Phase Variation and inlA Alleles with Premature Stop Codon Mutations among Human, Food, Animal, and Environmental Isolates

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