Staphylococcus aureus: a key factor in the pathogenesis of schizophrenia

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Dear Editor,
This is an odd title for a response to a comprehensive article on schizophrenia, written by experts, in which the bacterial pathogen Staphylococcus aureus is not mentioned. But the time has passed in which S. aureus can be ignored.

The biopsychosocial model of disease is taught as fact to medical students. The model, a powerful concept, is based on complexity. Multiple factors interact to cause disease. The specificity of disease lies in this interaction and there are no single causes for complex diseases. Every disease, and schizophrenia is no exception, has psychological, sociological and physical causes. In the last two decades we have come to realise that one constant physical factor is chronic inflammation [1 - 4].

The very height of complexity is the interaction between the microbiome and the human genome [4]. Multiple bacteria line the epithelial surfaces of the body and keep the pathogens at bay. But a sub-optimal microbiome (dysbiosis) allows some pathogens to enter the body and establish an intra-mucosal microbiota. The pathogens that enter include S. aureus and the gram-negative anaerobic cocci that cause periodontitis. Many strains of S. aureus secrete superantigens (toxic shock syndrome toxin and enterotoxins) which cause inflammation. Indeed, the commonest cause of chronic inflammation is S. aureus.

Dysbiosis leads to chronic inflammation and chronic inflammation increases the risk of most disease including ischaemic heart disease, dementia, cancer, depression, obesity and type 2 diabetes mellitus. It is doubtful that schizophrenia is an exception. Schizophrenia is associated with periodontitis, which is a clinical marker of dysbiosis. Toxin laden extracellular vesicles, produced by S. aureus, are a plausible explanation for the neuropathological changes in patients with schizophrenia.

The argument linking bacterial toxins and schizophrenia has been made before, and the evidence has built with time. It should not be difficult to test the hypothesis and to see if carriage of S. aureus and chronic inflammation can be reduced by simple dietary measures.

There are those who wish to emphasise psychological and sociological causes of schizophrenia. They are right to do so. But it might be quicker to switch the nation to regular yoghurt consumption [5]. It could be that creating social equality will take longer.

References

1. Morris JA. Schizophrenia, bacterial toxins and the genetics of redundancy. Medical Hypotheses 1996; 46: 362 – 366.
2. Morris JA. Information theory: a guide in the investigation of disease. J BioSci 2001; 26: 15 – 23
3. Morris JA, Rigby RJ, Wray M, Taylor AM. The microbiome and the entropy paradox: an evolutionary perspective. Food & Nutrition Journal 2024; 9: 294 DOI: 10.29011/2575-7091.100194
4. Morris JA, Wray M, Nicholls K, Rigby RJ. Mucosal tissue dysbiosis induced inflammation interacts with psychological factors and genetic factors to cause schizophrenia. World Journal of Psychiatry and Mental Health Research, 2023; 6: 1036
5. Morris JA. Optimise the microbial flora with milk and yoghurt to prevent disease. Medical Hypotheses 2018; 114: 13 – 17. https://doi.org/10.1016/j.mehy.2018.02.031

No competing Interests: YesThe following competing Interests: Electronic Publication Date: Thursday, September 17, 2026 - 10:49AI use: No, I have not used AIHighwire Comment Subject:

Schizophrenia: advances in pathophysiology, management, and precision medicine

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Staphylococcus aureus: a key factor in the pathogenesis of schizophrenia

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Schizophrenia: advances in pathophysiology, management, and precision medicine

Check this box if you would like your letter to appear anonymously:: Last Name: MorrisFirst name and middle initial: JamesEmail:

jamorris@doctors.org.uk

Address: Carnforth, Lancs , UKOccupation: consultant pathologist (retired)Affiliation: Carnforth, Lancs , UKBMJ: Additional Article Info: Rapid response