When Psychiatric Symptoms Have Inflammatory Roots

Why brain health and mental health cannot be separated

When anxiety, depression, obsessive thoughts, rage, or even psychosis appear, we tend to sort them immediately into a psychiatric category. The symptoms are real, and psychiatric care can be lifesaving. But the label does not necessarily tell us why the symptoms developed.

The brain is an organ. Like every other organ, it is affected by immune signals, circulation, oxygen delivery, metabolic stress, and microbes. When inflammation changes how the brain functions, the result may not look like a fever or a swollen joint. It may look like panic, irritability, loss of motivation, intrusive thoughts, cognitive decline, emotional volatility, or a profound change in personality.

This is why brain health and mental health cannot be separated. Sometimes what appears to be a purely psychiatric illness may also have inflammatory roots, and in some patients that inflammation may be driven or sustained by stealth pathogens.

A Study That Asks a Difficult Question

A 2026 paper in Parasites & Vectors examined postmortem samples from six chronically ill young people, ages 14 to 30, who had died by suicide, pursued medical aid in dying, or lived with severe suicidal thinking before dying from another inflammatory illness.

Their histories included much more than psychiatric symptoms. Across the cases were combinations of:

• Disabling fatigue and pain
• Gastrointestinal dysfunction
• Cognitive problems and sleep disruption
• Autonomic dysfunction
• Skin changes, shortness of breath, and weight changes

Their psychiatric diagnoses included depression, anxiety, obsessive-compulsive disorder, bipolar disorder, schizoaffective disorder, psychosis, PANS, and PANDAS. Many had received extensive medical and psychiatric treatment, yet their illnesses continued to progress.

The researchers tested blood, urine, cerebrospinal fluid, and tissues for molecular evidence of Babesia, Bartonella, and Borrelia. DNA sequencing confirmed Babesia, Bartonella, or both in five of the six individuals. Bartonella henselae was confirmed in two. Three Babesia species were identified among four individuals, and two of those individuals carried more than one Babesia species.

Those findings do not prove that the pathogens caused suicide. This was a very small, highly selected case series with inconsistent specimen availability, and there was no comparison group. It cannot tell us how frequently these pathogens occur in people with psychiatric illness, whether they were incidental findings, or how much they contributed to each person's symptoms. The authors appropriately describe their conclusion as a hypothesis requiring further study.

But the findings should not be dismissed either. Detecting DNA from stealth pathogens in postmortem samples from five of six profoundly ill young people is a signal worth investigating, especially when their psychiatric symptoms occurred alongside complex, multisystem illness.

How Inflammation Can Change the Mind

The connection between immune activity and behavior is not a new idea. Most of us have experienced a mild version during an infection: we become tired, withdrawn, foggy, unmotivated, and less interested in things we usually enjoy. These behavioral changes are partly produced by inflammatory signals acting on the brain.

When immune activation becomes persistent, those same pathways may remain engaged. Cytokines can:

• Alter neurotransmitter production and signaling
• Affect the stress-response system
• Disturb sleep and change energy production
• Influence the permeability of the blood-brain barrier

Inflammation can also affect the brain's microglia, the immune cells that continuously monitor and respond to changes within the nervous system.

The Basal Ganglia and Limbic System

The basal ganglia and limbic system are especially relevant. These regions help regulate motivation, reward, movement, fear, emotion, and behavior. Inflammatory cytokines can reduce dopamine signaling in the basal ganglia, contributing to fatigue, slowed thinking, loss of pleasure, and depression.

In one person described in the study, PET imaging showed hypermetabolism consistent with inflammation in the basal ganglia and limbic system, along with reduced metabolism in other cortical regions. Later imaging showed improvement in cortical metabolism after prolonged treatment, although inflammation in the basal ganglia persisted.

This does not mean that every psychiatric symptom is caused by brain inflammation. It means that inflammation is one biologically plausible pathway through which a physical illness can change mood, thinking, perception, and behavior.

Why Stealth Pathogens Are Easy to Miss

Babesia and Bartonella are sometimes described as stealth pathogens because they can persist while evading a straightforward immune response.

• Babesia is a protozoan parasite that lives inside red blood cells.
• Bartonella species can involve red blood cells and the cells lining blood vessels.

Both can affect multiple organ systems, and both may be difficult to detect consistently when the number of organisms in a particular sample is low or fluctuates over time.

That matters because a negative test does not always settle the question. Several people in the case series had negative or inconclusive testing during life, followed by molecular evidence in other samples or after death. Testing limitations do not mean that every negative result is false, nor do they justify assuming an infection is present. They do mean that laboratory results must be interpreted alongside the clinical pattern, exposure history, physical findings, and the strengths and limitations of the specific test used.

The larger lesson extends beyond Babesia and Bartonella. Persistent microbes may act as upstream triggers that keep the immune system activated. The downstream symptoms can then be neurological, psychiatric, autonomic, gastrointestinal, musculoskeletal, or some combination of all of them. Once those symptoms are divided among separate specialties, the unifying process can become hard to see.

The False Divide Between Physical and Psychiatric Illness

Patients with complex illness are often sent down one of two paths. If testing reveals a clear structural or laboratory abnormality, the illness is considered physical. If routine testing is unrevealing and the most visible symptoms involve mood or behavior, the illness may be treated as psychiatric.

Biology does not respect that divide. A person can need psychiatric support and still have an infection-associated inflammatory illness. An antidepressant, mood stabilizer, antipsychotic, therapy, sleep support, or hospitalization may reduce suffering and protect life while the underlying drivers are investigated. These approaches should not be framed as competing explanations.

At the same time, psychiatric treatment alone may be incomplete when there is a sudden or dramatic personality change, new obsessive-compulsive symptoms, cognitive decline, hallucinations, rage, severe sleep disruption, or suicidality accompanied by unexplained physical illness. In that setting, it is reasonable to broaden the medical evaluation rather than assuming that every symptom originates solely within the traditional psychiatric framework.

Clues That May Justify a Broader Evaluation

No single symptom proves that inflammation or a stealth pathogen is involved. The pattern matters.

The goal is not to test every person with anxiety or depression for every possible microbe. It is to remain curious when the clinical story does not fit neatly into one box. A thoughtful evaluation may consider infectious, immune, metabolic, endocrine, nutritional, toxic, medication-related, neurological, and psychosocial contributors. Often there is more than one layer.

Treat the Person While Investigating the Roots

The most important message is not that psychiatric diagnoses are wrong. It is that they are descriptive. They tell us what a person is experiencing, but not always what is driving it.

For some patients, psychiatric symptoms may be downstream expressions of an immune system responding to persistent biological stress. When stealth pathogens are part of that stress, treatment may need to address both the immediate psychiatric danger and the deeper inflammatory process. Because antimicrobial treatment can sometimes temporarily intensify inflammatory and neuropsychiatric symptoms, this work requires careful pacing, close monitoring, and coordination among clinicians. It should never replace urgent psychiatric care when safety is at risk.

We will understand mental illness more fully when we stop treating the brain as if it exists apart from the body. Mood, thought, perception, memory, and behavior all emerge from biology. Brain health is mental health, and protecting it requires us to consider the whole person.

A Note About Immediate Safety

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References

1. Breitschwerdt EB, Robveille C, Maggi RG, Lindner HH, Harris BT, Kingston E. Postmortem evidence of Babesia and Bartonella infections in chronically ill suicidal young people. Parasites & Vectors. 2026;19:376. doi:10.1186/s13071-026-07541-8
2. Felger JC, Miller AH. Cytokine effects on the basal ganglia and dopamine function: the subcortical source of inflammatory malaise. Frontiers in Neuroendocrinology. 2012;33:315–327. doi:10.1016/j.yfrne.2012.09.003
3. Bransfield RC, Mao C, Greenberg R. Microbes and mental illness: past, present, and future. Healthcare. 2024;12:83. doi:10.3390/healthcare12010083
4. Fallon BA, Madsen T, Erlangsen A, Benros ME. Lyme borreliosis and associations with mental disorders and suicidal behavior: a nationwide Danish cohort study. American Journal of Psychiatry. 2021;178:921–931. doi:10.1176/appi.ajp.2021.20091347