New Data, Strategies, and Insights for Listeria monocytogenes Dose‐Response Models: Summary of an Interagency Workshop, 2011

Abstract

Listeria monocytogenes is a leading cause of hospitalization, fetal loss, and death due to foodborne illnesses in the United States. A quantitative assessment of the relative risk of listeriosis associated with the consumption of 23 selected categories of ready-to-eat foods, published by the U.S. Department of Health and Human Services and the U.S. Department of Agriculture in 2003, has been instrumental in identifying the food products and practices that pose the greatest listeriosis risk and has guided the evaluation of potential intervention strategies. Dose-response models, which quantify the relationship between an exposure dose and the probability of adverse health outcomes, were essential components of the risk assessment. However, because of data gaps and limitations in the available data and modeling approaches, considerable uncertainty existed. Since publication of the risk assessment, new data have become available for modeling L. monocytogenes dose-response. At the same time, recent advances in the understanding of L. monocytogenes pathophysiology and strain diversity have warranted a critical reevaluation of the published dose-response models. To discuss strategies for modeling L. monocytogenes dose-response, the Interagency Risk Assessment Consortium (IRAC) and the Joint Institute for Food Safety and Applied Nutrition (JIFSAN) held a scientific workshop in 2011 (details available at http://foodrisk.org/irac/events/). The main findings of the workshop and the most current and relevant data identified during the workshop are summarized and presented in the context of L. monocytogenes dose-response. This article also discusses new insights on dose-response modeling for L. monocytogenes and research opportunities to meet future needs.

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

“…A key-events approach to dose-response modeling (29) was identified as a promising though extremely challenging, data-intensive, and potentially unachievable framework for future microbial doseresponse models. (2) Current dose-response models linked to epidemiological data tend to agree that a low dose of L. monocytogenes leads to an average low probability of invasive listeriosis in the general population as well as in broadly defined populations with heightened susceptibility. (4,5,30) However, a more nuanced evaluation of L. monocytogenes dose response for L. monocytogenes strains with different virulence and for different human population subgroups at heightened risk of listeriosis is needed to adequately characterize the listeriosis risk in different population subgroups, including those with highest susceptibility.…”

“…(1) Derivations of L. monocytogenes dose-response relationships, though crucially important for risk assessment and risk management, are impaired by the difficulties of collecting adequate data from outbreak investigations or sporadic cases, by the lack of appropriate animal models, and by the inability to use volunteer studies due to ethical and practical concerns. (2,3) Two well-accepted L. monocytogenes doseresponse models have been developed by U.S. agencies (4) and an international expert panel, (5) both scaled to epidemiological data. In 2003, the Food and Drug Administration (FDA) of the U.S. Department of Health and Human Services and the Food Safety and Inspection Service (FSIS) of the U.S. Department of Agriculture published a joint risk assessment for L. monocytogenes in 23 selected categories of ready-to-eat (RTE) foods.…”

Closing gaps for performing a risk assessment on Listeria monocytogenes in ready‐to‐eat (RTE) foods: activity 2, a quantitative risk characterization on L. monocytogenes in RTE foods; starting from the retail stage

“…Recently, the background and relevant data for L. monocytogenes dose-response assessments were described together with the new insights in the light of recent advances in the understanding of L. monocytogenes pathophysiology or strain diversity (Hoelzer et al, 2013).…”

“…Serving size data are described by pointestimate values as well as probability distributions. It can also be deduced that frequency intake (servings/capita/year) was described according to the population group to whom the intended food was destined (Latorre et al, 2011;Chen et al, 2013).…”

“…Mechanistic models could be potentially more flexible since they are developed on a set of biologically plausible, mechanistic assumptions. Thus, they should account for the host-pathogen-food interaction (Hoelzer et al, 2013).…”