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module menu icon Pathophysiology

A number of control pathways regulate the vomiting centre in the medulla oblongata in the brain. Neurotransmitter feedback includes:18

·       the gastrointestinal system via the vagus nerve of the autonomic nervous system with 5-hydroxytryptamine/serotonin (5-HT3);

·       the cortex and thalamus (through pain or fear);

·       the vestibular region (motion sickness) with histamine and acetylcholine;

·       the chemoreceptor trigger zone (also in the medulla oblongata) which responds to circulating drugs or hormones using the neurotransmitters dopamine, substance P through NK1 neurokinin receptors, and mu and kappa opioids.

In infectious gastroenteritis, pathogenic bacteria can release plasmids, discrete, self-replicating capsules of DNA which express enterotoxins and other substances. These can bind to specific cells and receptors in the GI system, directly stimulating 5-HT3 release in the gut ANS. They can also stimulate release of histamine from mast cells, along with leukotrienes and substance P, adding to vomitory triggers.19,20,21

Enterotoxins binding to antigens can also stimulate an inflammatory response in the intestinal mucosa resulting in diarrhoea.19,20

Enterotoxins released by pathogenic bacteria into food before it is ingested can still cause gastric effects as enterotoxins can resist heat and stomach acid beyond levels that destroy the bacteria, and are also resistant to the gut’s proteolytic enzymes.

Viruses invade host gastric cells to produce enterotoxin and gut antigens giving them similar actions to pathogenic bacteria. Rotavirus and its enterotoxins stimulate enterochromaffin cells in the gut wall which ordinarily are involved in gastric acid and histamine release. The stimulated cells cause 5-HT3 messaging along the vagus nerve ultimately to the vomiting centre.22

Investigations into norovirus have shown it can change intestinal cell structures and also reduce enzymatic activity at the brush border level of gut microvilli, resulting in diarrhoea. The virus also slows gastric emptying and reduces gastric motility, which may trigger nausea and vomiting.13

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