Infections

Depending on the infection and the person, the mental health symptoms linked to infection include:

• Depression, anxiety, psychosis, cognitive impairment and fatigue Arbune, M., Nicolcescu, P., Ciubară, A., Bogdan, P.M., Vlase, C.-M. and Arbune, A.-A. (2026) ‘Toward a unified neuroimmune framework for infection-associated psychiatric disorders’, Diseases, 14(8), article 290. 
• Sleep problems, which are common in people with long COVID Seighali, N., Abdollahi, A., Shafiee, A., Amini, M.J., Teymouri Athar, M.M., Safari, O. et al. (2024) ‘The global prevalence of depression, anxiety, and sleep disorder among patients coping with post COVID-19 syndrome (long COVID): a systematic review and meta-analysis’, BMC Psychiatry, 24(1), article 105. 
• Sudden-onset obsessive-compulsive symptoms, tics or restricted eating in children, with anxiety, emotional instability, irritability and school deterioration, in paediatric acute-onset neuropsychiatric syndrome Grandinetti, R., Mussi, N., Pilloni, S. et al. (2024) ‘Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: a Delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up’, Frontiers in Immunology, 15, article 1420663. Available at: https://doi.org/10.3389/fimmu.2024.1420663.
• Cognitive impairment, depression, suicidal thoughts and psychotic-like symptoms in Lyme disease Delaney, S.L., Murray, L. and Fallon, B.A. (2022) ‘Neuropsychiatric symptoms and tick-borne diseases’, in Current Topics in Behavioral Neurosciences, vol. 61. Cham: Springer, pp. 279–302.
• Depression, anxiety, post-traumatic stress and delirium after sepsis Li, D., Zhang, X., Lu, Y., Liang, J., Hu, H., Song, Y., Wu, S. and Zhu, W. (2024) ‘Post-sepsis psychiatric disorder: pathophysiology, prevention, and treatment’, Neurological Sciences, 45(7), pp. 3093–3105. 
• Brain fog, poor concentration and word-finding difficulties, which are commonly reported across several of the infections on this page

Infections can influence the brain without the pathogen itself entering it. Signals from an activated immune system can cross or disrupt the blood–brain barrier and switch on the brain’s own immune cells, microglia and astrocytes. Arbune, M., Nicolcescu, P., Ciubară, A., Bogdan, P.M., Vlase, C.-M. and Arbune, A.-A. (2026) ‘Toward a unified neuroimmune framework for infection-associated psychiatric disorders’, Diseases, 14(8), article 290. Martins, D., Beckman, D., Loggia, M.L., Costanza, A. and Borsini, A. (2026) ‘Understanding neuroinflammation in post-COVID-19 syndrome: biological mechanisms, diagnostic biomarkers, and therapeutic prospects’, Translational Psychiatry. In post-COVID-19 syndrome, sustained microglial and astrocyte activation, blood–brain barrier disruption and abnormal cytokine signalling are central features, along with changes in cerebral blood flow and oxygen use. Martins, D., Beckman, D., Loggia, M.L., Costanza, A. and Borsini, A. (2026) ‘Understanding neuroinflammation in post-COVID-19 syndrome: biological mechanisms, diagnostic biomarkers, and therapeutic prospects’, Translational Psychiatry.

Other proposed routes include molecular mimicry, in which antibodies made against a microbe cross-react with the body’s own tissue, essentially causing the immune system to mistake healthy tissue for the infection it was fighting. This has been proposed for streptococcal infection Grandinetti, R., Mussi, N., Pilloni, S. et al. (2024) ‘Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: a Delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up’, Frontiers in Immunology, 15, article 1420663. and for Lyme disease.Delaney, S.L., Murray, L. and Fallon, B.A. (2022) ‘Neuropsychiatric symptoms and tick-borne diseases’, in Current Topics in Behavioral Neurosciences, vol. 61. Cham: Springer, pp. 279–302. Overactivity of the body’s stress-hormone system may also play a part, for example after sepsis. Li, D., Zhang, X., Lu, Y., Liang, J., Hu, H., Song, Y., Wu, S. and Zhu, W. (2024) ‘Post-sepsis psychiatric disorder: pathophysiology, prevention, and treatment’, Neurological Sciences, 45(7), pp. 3093–3105. Infection can also divert tryptophan metabolism into the kynurenine pathway, which is described in more detail on our Metabolism page. Arbune, M., Nicolcescu, P., Ciubară, A., Bogdan, P.M., Vlase, C.-M. and Arbune, A.-A. (2026) ‘Toward a unified neuroimmune framework for infection-associated psychiatric disorders’, Diseases, 14(8), article 290.

The inflammatory-messenger (cytokine) profiles seen after viral infections such as influenza, herpes simplex virus, cytomegalovirus, Epstein-Barr virus, rubella, HIV and SARS-CoV-2 overlap with those seen in psychiatric disorders. Interleukin-6 and tumour necrosis factor-alpha are raised in depression, bipolar disorder and schizophrenia, and interleukin-8 together with interleukin-10 is associated with psychotic symptoms. The cytokine profile after influenza closely resembles the pattern seen in schizophrenia and first-episode psychosis. Lorkiewicz, P. and Waszkiewicz, N. (2024) ‘Viral infections in etiology of mental disorders: a broad analysis of cytokine profile similarities – a narrative review’, Frontiers in Cellular and Infection Microbiology, 14, article 1423739.This overlap is one reason researchers increasingly think of some psychiatric symptoms as, in part, an immune phenomenon rather than a purely psychological one.

Mental health problems are common among people with long COVID (post-COVID-19 syndrome), with depression, anxiety and sleep disorder all frequently reported, and sleep disorder the most common of the three. Seighali, N., Abdollahi, A., Shafiee, A., Amini, M.J., Teymouri Athar, M.M., Safari, O. et al. (2024) ‘The global prevalence of depression, anxiety, and sleep disorder among patients coping with post COVID-19 syndrome (long COVID): a systematic review and meta-analysis’, BMC Psychiatry, 24(1), article 105.  Severe COVID-19, particularly cases requiring hospitalisation or intensive care, is linked to a higher risk of new neurological problems. This risk is similarly raised after hospitalisation for other severe respiratory infections, suggesting that serious infection in general, rather than this virus specifically, can leave a mark on the nervous system. Grønkjær, C.S., Christensen, R.H.B., Kondziella, D. and Benros, M.E. (2023) ‘Long-term neurological outcome after COVID-19 using all SARS-CoV-2 test results and hospitalisations in Denmark with 22-month follow-up’, Nature Communications, 14(1), article 4235.

Several interacting drivers of long COVID have been proposed, including reactivation of Epstein-Barr virus, molecular mimicry, persistence of virus in tissue reservoirs, autoantibodies and mitochondrial dysfunction. Ponnachan, P., Dhawlarker, A., Yasmin, H., Shah, A., Malhotra, A., Shastri, A., Al-Ramadi, B.K. and Kishore, U. (2026) ‘Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination’, Frontiers in Immunology, 17, article 1710777. Vaccination before infection appears to lower the risk of developing long COVID. Ponnachan, P., Dhawlarker, A., Yasmin, H., Shah, A., Malhotra, A., Shastri, A., Al-Ramadi, B.K. and Kishore, U. (2026) ‘Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination’, Frontiers in Immunology, 17, article 1710777. Mitochondrial dysfunction is covered on our Mitochondrial dysfunction page, and helps explain why long COVID so often includes profound fatigue alongside mood and cognitive symptoms.

Herpesviruses, including herpes simplex virus (HSV), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and varicella-zoster virus (VZV, which causes chickenpox and shingles), remain dormant in the body for life after the first infection and can reactivate later, particularly at times of stress or reduced immunity. Reactivation of herpesviruses, particularly EBV and HSV-2, is linked to depression in both directions: reactivation can contribute to depression, and depression appears to make reactivation more likely. Shafiee, A., Nakhaee, Z., Amini, M.J., Esmailpur Abianeh, F., Goodarzi, M., Parvizi Omran, S. et al. (2025) ‘Bidirectional relationship between human herpes virus reactivation and depression: a systematic review and meta-analysis’, Journal of NeuroVirology, 31(2), pp. 145–153. A

Herpesviruses have also been linked to a higher risk of dementia, and antiviral treatment for shingles is associated with a lower risk of dementia. Drinkall, N.J., Siersma, V., Lathe, R., Waldemar, G. and Janbek, J. (2025) ‘Herpesviruses, antiviral treatment, and the risk of dementia – systematic review and meta-analysis’, Alzheimer’s Research & Therapy, 17(1), article 201. Recurrent shingles is linked to a higher dementia risk than a single episode, while shingles vaccination is linked to a lower risk of dementia. Polisky, V., Littmann, M., Triastcyn, A., Horn, M., Georgiou, A., Widenmaier, R. et al. (2025) ‘Varicella-zoster virus reactivation and the risk of dementia’, Nature Medicine, 31(12), pp. 4172–4179. EBV infection has also been linked to a substantially higher risk of multiple sclerosis, and HSV-1 infection has been detected in the years before an Alzheimer’s diagnosis. Zheng, H. and Savitz, J. (2024) ‘Herpesviruses and neuropsychiatric disorders: overlooked adversaries or innocent bystanders?’, Neuropsychopharmacology, 49(1), pp. 313–314. Early research in concussed athletes suggests that neuroinflammation after brain injury may trigger CMV reactivation. See our TBI/Trauma page for the link with head injury. Zheng, H. and Savitz, J. (2024) ‘Herpesviruses and neuropsychiatric disorders: overlooked adversaries or innocent bystanders?’, Neuropsychopharmacology, 49(1), pp. 313–314.

EBV and HSV-1 seropositivity, meaning evidence of past infection detected in the blood, are also more common in people with schizophrenia and bipolar disorder than in the general population, alongside raised inflammatory markers. Akgül, Ö., Demirel, Ö.F., Tosun, İ., Kavla, Y., Kırpınar, M.M., Sapmaz, B., Şenyiğit, G., Çalışkan, R. and Öner, Y.A. (2025) ‘Unveiling the interplay of EBV, HSV-1, and inflammatory biomarkers in psychiatric disorders’, Journal of Clinical Medicine, 14(19), article 6730. Because these viruses are so widespread, most people carry one or more of them without ever developing mental health problems, but they appear to be one contributing piece of a much larger picture.

Hepatitis B and C are viral infections of the liver, and active infection is linked to a higher likelihood of depressive symptoms. Yang, G., Zhang, S., Wang, Y., Han, B. and Sun, D. (2025) ‘Association between viral hepatitis and depressive symptoms: National Health and Nutrition Examination Survey (NHANES) 2007–2018’, BMC Public Health, 25(1), article 3161.  This connection may relate both to the direct effects of infection and inflammation on the brain, and to the wider physical and emotional burden of living with a chronic liver condition.

PANDAS (paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections) describes the abrupt onset of obsessive-compulsive disorder, tics or food restriction linked in time to infection with group A streptococcus, the bacterium responsible for common childhood illnesses such as strep throat. PANS (paediatric acute-onset neuropsychiatric syndrome) is a broader category triggered by a range of infectious or environmental factors. Diagnosis relies on a sudden, dramatic onset of obsessive-compulsive disorder or restricted eating together with other neuropsychiatric symptoms, after other causes have been excluded; there is currently no confirmatory biomarker. Grandinetti, R., Mussi, N., Pilloni, S. et al. (2024) ‘Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: a Delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up’, Frontiers in Immunology, 15, article 1420663.

The proposed mechanisms include molecular mimicry, in which antibodies against streptococcal proteins cross-react with proteins in the basal ganglia (a group of brain structures involved in movement and habit), antibodies against dopamine receptors, altered complement activity, and changes in gut bacteria with neuroinflammation. Treatment typically involves treating the underlying infection alongside cognitive behavioural therapy and SSRIs, with steroids, immunoglobulin and plasma exchange reserved for severe cases. Grandinetti, R., Mussi, N., Pilloni, S. et al. (2024) ‘Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: a Delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up’, Frontiers in Immunology, 15, article 1420663.  Parents who notice a sudden, dramatic change in a child’s behaviour shortly after a throat infection are encouraged to seek medical assessment.

Lyme disease is a bacterial infection spread by ticks. It can cause cognitive impairment, depression, suicidal thoughts and psychotic-like presentations, and a meaningful proportion of people continue to have symptoms after antibiotic treatment (post-treatment Lyme disease syndrome). Delaney, S.L., Murray, L. and Fallon, B.A. (2022) ‘Neuropsychiatric symptoms and tick-borne diseases’, in Current Topics in Behavioral Neurosciences, vol. 61. Cham: Springer, pp. 279–302. Molecular mimicry and antibodies that react with nerve tissue are among the possible mechanisms. Delaney, S.L., Murray, L. and Fallon, B.A. (2022) ‘Neuropsychiatric symptoms and tick-borne diseases’, in Current Topics in Behavioral Neurosciences, vol. 61. Cham: Springer, pp. 279–302. The neuropsychiatric aspects of Lyme disease are often overlooked, and diagnosis can be difficult, particularly when blood tests are negative. Anyone with suspected tick-borne infection, particularly if there was a known tick bite, rash or flu-like illness beforehand, should seek medical assessment. Delaney, S.L., Murray, L. and Fallon, B.A. (2022) ‘Neuropsychiatric symptoms and tick-borne diseases’, in Current Topics in Behavioral Neurosciences, vol. 61. Cham: Springer, pp. 279–302.

Sepsis is a life-threatening response to infection, in which the body’s own immune response causes widespread inflammation and organ dysfunction. Depression, anxiety, post-traumatic stress disorder and delirium are common complications, affecting a substantial proportion of survivors in the years after discharge; depressive symptoms after sepsis are also linked to higher long-term mortality. Li, D., Zhang, X., Lu, Y., Liang, J., Hu, H., Song, Y., Wu, S. and Zhu, W. (2024) ‘Post-sepsis psychiatric disorder: pathophysiology, prevention, and treatment’, Neurological Sciences, 45(7), pp. 3093–3105. Proposed biological mechanisms include blood–brain barrier disruption, overactivation of the body’s stress-hormone system, neuroinflammation, oxidative stress and impaired neuroplasticity. Li, D., Zhang, X., Lu, Y., Liang, J., Hu, H., Song, Y., Wu, S. and Zhu, W. (2024) ‘Post-sepsis psychiatric disorder: pathophysiology, prevention, and treatment’, Neurological Sciences, 45(7), pp. 3093–3105. Anyone recovering from sepsis or a period of critical illness should be aware that psychological after-effects are common and treatable, not a sign of personal weakness.

Most research looks at one infection at a time, but people often experience several over the years, whether that is recurrent colds, urinary infections or other everyday illnesses. Emerging research suggests that having a greater number of infections is linked to a higher risk of later developing a mental health disorder, a finding that is still being investigated and may reflect a cumulative burden on the immune system and the brain over time. Kramer, A., Weinstein, O., Givon-Lavi, N. et al. (2026) ‘Community-based infections and its association with mental disorder onset: a nationwide matched cohort study’, Translational Psychiatry.

Toxoplasma gondii is a parasite, often picked up from undercooked meat or contact with cat faeces, that has long been investigated in relation to schizophrenia, and maternal infection during pregnancy has also been implicated in schizophrenia risk. Hall, M.B., Willis, D.E., Rodriguez, E.L. and Schwarz, J.M. (2023) ‘Maternal immune activation as an epidemiological risk factor for neurodevelopmental disorders: considerations of timing, severity, individual differences, and sex in human and rodent studies’, Frontiers in Neuroscience, 17, article 1135559. Toxoplasma infection has been linked to raised cortisol levels in people with severe mental illness, although the overall relationship with psychiatric symptoms is complex and not yet fully understood. Andreou, D., Steen, N.E., Jørgensen, K.N., Nerland, S., Ueland, T., Wortinger, L.A. et al. (2025) ‘Toxoplasma gondii associated with psychotic symptom load and cortisol in severe mental illness’, Schizophrenia, 11(1), article 80. Most people who carry the parasite have no symptoms at all, so a positive test result should always be interpreted by a doctor in the context of a person’s wider health.

Interest in fungi and mental health has grown alongside research on the gut microbiome. Disturbed gut fungal communities (the mycobiome) have been linked to schizophrenia, depression, bipolar disorder, autism spectrum disorder and Alzheimer’s disease. The yeast Candida albicans, which normally lives in the gut in small amounts, features prominently, with overgrowth linked in some studies to more severe psychiatric symptoms, chronic inflammation and increased gut permeability, sometimes referred to as “leaky gut”. Sellami, H., Hadrich, I., Turki, M. et al. (2025) ‘Gut mycobiome and neuropsychiatric disorders: insights and therapeutic potential’, Frontiers in Cellular Neuroscience, 18, article 1495224. Proposed mechanisms include neuroinflammation, altered serotonin and dopamine pathways, and a weakened intestinal barrier. Sellami, H., Hadrich, I., Turki, M. et al. (2025) ‘Gut mycobiome and neuropsychiatric disorders: insights and therapeutic potential’, Frontiers in Cellular Neuroscience, 18, article 1495224.

This is still an early and evolving area of research, so it is wise to be cautious about claims that yeast overgrowth alone explains mental health symptoms in an individual, without proper testing and medical guidance. See our Gut dysbiosis page.

Infections during pregnancy can influence how a baby’s brain develops. Viral and bacterial infections in pregnancy, including rubella, influenza, cytomegalovirus, herpes simplex and urinary tract infections, are associated with later neurodevelopmental diagnoses such as autism and schizophrenia. Raised maternal inflammatory messengers are associated with these conditions even without overt infection, suggesting that the mother’s immune response, and not just the microbe itself, plays an important role. Hall, M.B., Willis, D.E., Rodriguez, E.L. and Schwarz, J.M. (2023) ‘Maternal immune activation as an epidemiological risk factor for neurodevelopmental disorders: considerations of timing, severity, individual differences, and sex in human and rodent studies’, Frontiers in Neuroscience, 17, article 1135559.

Timing and severity matter: second-trimester exposure appears particularly relevant for schizophrenia risk, and infections severe enough to require hospital admission carry a stronger association than infections managed at home. Hall, M.B., Willis, D.E., Rodriguez, E.L. and Schwarz, J.M. (2023) ‘Maternal immune activation as an epidemiological risk factor for neurodevelopmental disorders: considerations of timing, severity, individual differences, and sex in human and rodent studies’, Frontiers in Neuroscience, 17, article 1135559.  Most infections in pregnancy do not lead to any neurodevelopmental problem, but this research underlines the importance of preventing and promptly treating infection during pregnancy, through good hygiene, appropriate vaccination and timely medical care.

Good sleep supports the immune system’s ability to fight off infection. People who sleep five hours or less a night are more vulnerable to respiratory infections, and short sleep around the time of vaccination can reduce the strength and durability of the immune response. Garbarino, S., Lanteri, P., Bragazzi, N.L., Magnavita, N. and Scoditti, E. (2021) ‘Role of sleep deprivation in immune-related disease risk and outcomes’, Communications Biology, 4, article 1304. Prioritising sleep, especially during periods of stress or illness, is therefore a simple but meaningful way to support immune resilience.

Herpesviruses persist in the body after the first infection, and reactivation and depression appear to be linked in both directions. Shafiee, A., Nakhaee, Z., Amini, M.J., Esmailpur Abianeh, F., Goodarzi, M., Parvizi Omran, S. et al. (2025) ‘Bidirectional relationship between human herpes virus reactivation and depression: a systematic review and meta-analysis’, Journal of NeuroVirology, 31(2), pp. 145–153. It has also been proposed that brain injury can trigger CMV reactivation. Zheng, H. and Savitz, J. (2024) ‘Herpesviruses and neuropsychiatric disorders: overlooked adversaries or innocent bystanders?’, Neuropsychopharmacology, 49(1), pp. 313–314.

Recurrent shingles is linked to a higher risk of dementia in older adults, while shingles vaccination is linked to a lower risk. Polisky, V., Littmann, M., Triastcyn, A., Horn, M., Georgiou, A., Widenmaier, R. et al. (2025) ‘Varicella-zoster virus reactivation and the risk of dementia’, Nature Medicine, 31(12), pp. 4172–4179. The immune system naturally becomes less effective with age, which can make older adults more vulnerable both to new infections and to reactivation of dormant ones.

The more severe the infection, the greater the apparent effect on the nervous system and mental health. Neurological risk rises with the severity of COVID-19, Grønkjær, C.S., Christensen, R.H.B., Kondziella, D. and Benros, M.E. (2023) ‘Long-term neurological outcome after COVID-19 using all SARS-CoV-2 test results and hospitalisations in Denmark with 22-month follow-up’, Nature Communications, 14(1), article 4235. and psychiatric disorders are common after sepsis. Li, D., Zhang, X., Lu, Y., Liang, J., Hu, H., Song, Y., Wu, S. and Zhu, W. (2024) ‘Post-sepsis psychiatric disorder: pathophysiology, prevention, and treatment’, Neurological Sciences, 45(7), pp. 3093–3105.

Overgrowth of gut yeasts such as Candida, and altered fungal and bacterial balance more broadly, have been proposed as contributors to mental health symptoms. Sellami, H., Hadrich, I., Turki, M. et al. (2025) ‘Gut mycobiome and neuropsychiatric disorders: insights and therapeutic potential’, Frontiers in Cellular Neuroscience, 18, article 1495224.

Infection and inflammation during pregnancy can affect the developing baby’s brain, with timing and severity important. Hall, M.B., Willis, D.E., Rodriguez, E.L. and Schwarz, J.M. (2023) ‘Maternal immune activation as an epidemiological risk factor for neurodevelopmental disorders: considerations of timing, severity, individual differences, and sex in human and rodent studies’, Frontiers in Neuroscience, 17, article 1135559.

If you suspect an infection may be contributing to your symptoms, please speak to your doctor. Testing and treatment need to be tailored to the individual, and many of the conditions on this page respond well to appropriate medical care.