Human toxocariasis is a neglected tropical disease, which is actually global in distribution and has a significant impact on global public health. The infection can lead to several serious conditions in humans, including allergic, ophthalmic and neurological disorders such as epilepsy. It is caused by the common roundworm species Toxocara canis and Toxocara cati, with humans becoming accidentally infected via the ingestion of eggs or larvae. Toxocara eggs are deposited on the ground when infected dogs, cats and foxes defecate, with the eggs contaminating crops, grazing pastures, and subsequently food animals. However, transmission of Toxocara to humans via food consumption has received relatively little attention in the literature. To establish the risks that contaminated food poses to the public, a renewed research focus is required. This review discusses what is currently known about food-borne Toxocara transmission, highlighting the gaps in our understanding that require further attention, and outlining some potential preventative strategies which could be employed to safeguard consumer health.

Seroprevalence data illustrate that human exposure to Toxocara is frequent. Environmental contamination with Toxocara spp. eggs is assumed to be the best indicator of human exposure, but increased risk of exposure has also been associated with many other factors. Reported associations are inconsistent, however, and there is still ambiguity regarding the factors driving the onset of Toxocara antibody positivity. The objective of this work was to assess the validity of our current conceptual understanding of the key processes driving human exposure to Toxocara. We constructed an agent-based model predicting Toxocara antibody positivity (as a measure of exposure) in children. Exposure was assumed to depend on the joint probability of 3 parameters: (1) environmental contamination with Toxocara spp. eggs, (2) larvation of these eggs and (3) the age-related contact with these eggs. This joint probability was linked to processes of acquired humoral immunity, influencing the rate of antibody seroreversion. The results of the simulation were validated against published data from 5 different geographical settings. Using simple rules and a stochastic approach with parameter estimates derived from the respective contexts, plausible serological patterns emerged from the model in nearly all settings. Our approach leads to novel insights in the transmission dynamics of Toxocara.