Foodborne disease as a result of raw milk consumption is an increasing concern in Western countries. Quantitative microbial risk assessment models have been used to estimate the risk of illness due to different pathogens in raw milk. In these models, the duration and temperature of storage before consumption have a critical influence in the final outcome of the simulations and are usually described and modeled as independent distributions in the consumer phase module. We hypothesize that this assumption can result in the computation, during simulations, of extreme scenarios that ultimately lead to an overestimation of the risk. In this study, a sensorial analysis was conducted to replicate consumers' behavior. The results of the analysis were used to establish, by means of a logistic model, the relationship between time-temperature combinations and the probability that a serving of raw milk is actually consumed. To assess our hypothesis, 2 recently published quantitative microbial risk assessment models quantifying the risks of listeriosis and salmonellosis related to the consumption of raw milk were implemented. First, the default settings described in the publications were kept; second, the likelihood of consumption as a function of the length and temperature of storage was included. When results were compared, the density of computed extreme scenarios decreased significantly in the modified model; consequently, the probability of illness and the expected number of cases per year also decreased. Reductions of 11.6 and 12.7% in the proportion of computed scenarios in which a contaminated milk serving was consumed were observed for the first and the second study, respectively. Our results confirm that overlooking the time-temperature dependency may yield to an important overestimation of the risk. Furthermore, we provide estimates of this dependency that could easily be implemented in future quantitative microbial risk assessment models of raw milk pathogens.
Foodborne infection is a result of exposure to complex, dynamic food systems. The efficiency of foodborne infection is driven by ongoing shifts in genetic machinery. Next-generation sequencing technologies can provide high-fidelity data about the genetics of a pathogen. However, food safety surveillance systems do not currently provide similar high-fidelity epidemiological metadata to associate with genetic data. As a consequence, it is rarely possible to transform genetic data into actionable knowledge that can be used to genuinely inform risk assessment or prevent outbreaks. Big data approaches are touted as a revolution in decision support, and pose a potentially attractive method for closing the gap between the fidelity of genetic and epidemiological metadata for food safety surveillance. We therefore developed a simple food chain model to investigate the potential benefits of combining ‘big’ data sources, including both genetic and high-fidelity epidemiological metadata. Our results suggest that, as for any surveillance system, the collected data must be relevant and characterize the important dynamics of a system if we are to properly understand risk: this suggests the need to carefully consider data curation, rather than the more ambitious claims of big data proponents that unstructured and unrelated data sources can be combined to generate consistent insight. Of interest is that the biggest influencers of foodborne infection risk were contamination load and processing temperature, not genotype. This suggests that understanding food chain dynamics would probably more effectively generate insight into foodborne risk than prescribing the hazard in ever more detail in terms of genotype.
1 November 2017 in International Journal of Food Microbiology
Toxoplasma gondii is recognized as a widely prevalent zoonotic parasite worldwide. Although several studies clearly identified meat products as an important source of T. gondii infections in humans, quantitative understanding of the risk posed to humans through the food chain is surprisingly scant. While probabilistic risk assessments for pathogens such as Campylobacter jejuni, Listeria monocytogenes or Escherichia coli have been well established, attempts to quantify the probability of human exposure to T. gondii through consumption of food products of animal origin are at early stages. The biological complexity of the life cycle of T. gondii and limited understanding of several fundamental aspects of the host/parasite interaction, require the adoption of numerous critical assumptions and significant simplifications. In this study, we present a hypothetical quantitative model for the assessment of human exposure to T. gondii through meat products. The model has been conceptualized to capture the dynamics leading to the presence of parasite in meat and, for illustrative purposes, used to estimate the probability of at least one viable cyst occurring in 100g of fresh pork meat in England. Available data, including the results of a serological survey in pigs raised in England were used as a starting point to implement a probabilistic model and assess the fate of the parasite along the food chain. Uncertainty distributions were included to describe and account for the lack of knowledge where necessary. To quantify the impact of the key model inputs, sensitivity and scenario analyses were performed. The overall probability of 100g of a hypothetical edible tissue containing at least 1 cyst was 5.54%. Sensitivity analysis indicated that the variables exerting the greater effect on the output mean were the number of cysts and number of bradyzoites per cyst. Under the best and the worst scenarios, the probability of a single portion of fresh pork meat containing at least 1 viable cyst resulted 1.14% and 9.97% indicating that the uncertainty and lack of data surrounding key input parameters of the model preclude accurate estimation of T. gondii exposure through consumption of meat products. The hypothetical model conceptualized here is coherent with current knowledge of the biology of the parasite. Simulation outputs clearly identify the key gaps in our knowledge of the host-parasite interaction that, when filled, will support quantitative assessments and much needed accurate estimates of the risk of human exposure.