Microbiota present a promising and underexploited source of novel neuroactive compounds for the treatment of neurological and psychiatric diseases in humans. However, due to the diverse and complex interactions that they have with each other and the host nervous system, identifying causal microbes and the molecules they produce remains a difficult challenge. Here, I address this challenge in the nematode worm, Caenorhabditis elegans, as it is a small bacterivore with a simple nervous system, yet it displays a variety of behavioural responses to bacteria that are observable in the laboratory and governed by conserved neural signalling pathways. I perform phenotypic screening and use custom animal tracking software to investigate worm behaviour in response to a library of Escherichia coli single- gene deletion mutants. I find that bacterial strains with disrupted iron import or respiratory chain function elicit an acute arousal behaviour in C. elegans. Subsequent experiments reveal a novel neural sensorimotor mechanism for arousal in C. elegans that is modulated by oxidative stress from its bacterial diet. Oxidative stress damage is known to contribute to the development of neurodegenerative diseases in humans, and the principal metabolic machinery and oxidative stress mechanisms involved are highly conserved in lower eukaryotes such as C. elegans. Further research using C. elegans as a model to understand how microbiota affect host oxidative stress mechanisms and alter host behaviour could lead to important therapeutic discoveries for the treatment of these diseases.