When Princess Bajrakitiyabha — known to many as Princess Bha — died in June 2026 after more than three years of unconsciousness following her collapse in December 2022, I found myself returning to a question that has troubled me for some time. Why was this case so quickly settled, publicly, around a single explanation?
The official account held that she suffered a severe arrhythmia linked to cardiac inflammation following Mycoplasma infection. On the surface, that is medically possible. Mycoplasma pneumoniae is a recognised bacterial pathogen. It usually affects the lungs. It can, rarely, involve the heart. It can be associated with myocarditis.
But medicine is not meant to stop at what is possible. Medicine is meant to ask what is probable, what fits the pattern, and what else should be considered.
That is where this case becomes important.
I am not approaching this from a position of certainty. I do not have her medical records. I cannot confirm her vaccination timeline, laboratory findings, imaging, or histology. What I can do is examine the reasoning and ask whether the publicly accepted explanation is strong enough to exclude other possibilities.
My concern is that it is not.
Who She Was Matters
Before discussing the medicine, it is worth remembering who Princess Bha was. She was the eldest daughter of the King of Thailand — a lawyer, diplomat, and public servant who championed justice, human rights, and the welfare of women prisoners through the UN Bangkok Rules. She was not simply a name in a medical story. She was a deeply respected figure, and her death carried enormous significance.
That is precisely why this case deserves careful thought.
She reportedly collapsed while training dogs in December 2022. She suffered a cardiac arrest or severe arrhythmic event, was resuscitated, remained unconscious, and never recovered. The public explanation became Mycoplasma-associated myocarditis.
The question is not whether Mycoplasma can cause myocarditis. The question is whether that explanation is sufficient given how abruptly this occurred.
Professor Bhakdi claimed that Princess Bajrakitiyabha had received a third COVID injection before her collapse, saying she was “perfectly well” earlier that day and then suffered cardiac arrest later. He described meeting Thai contacts after arriving in Thailand on 31 December 2022, including people he characterised as close to the royal family and government, and argued that the public diagnosis of Mycoplasma myocarditis did not make clinical sense to him. His central point was that he believed Mycoplasma myocarditis could not plausibly develop within hours and cause sudden cardiac arrest, whereas he considered vaccine-associated myocarditis a more plausible explanation
What Mycoplasma Usually Looks Like
Mycoplasma pneumoniae is often called “walking pneumonia” because many people remain active while infected — managing a dry cough, fever, fatigue, or mild chest symptoms while continuing their daily lives. It is fundamentally a respiratory illness, and most people recover without complication.
Rarely, it can involve other systems: skin, blood, nervous system, and heart. When cardiac involvement occurs, myocarditis becomes possible. I am not dismissing that. The condition exists, and dismissing it would be medically wrong.
But there is an important clinical distinction to hold in mind. In most severe cases with extra-pulmonary complications, the patient is already significantly unwell. Heart involvement tends to be part of a broader systemic picture, not a sudden isolated event in someone apparently healthy enough to be outdoors training dogs.
That is a different clinical pattern. Not impossible — medicine humbles anyone who speaks in absolutes — but not the cleanest fit either.
The Case Report That Raises the Real Issue
To understand the problem more precisely, I looked at a published case report of Mycoplasma myocarditis involving a 29-year-old man who presented with sustained supraventricular tachycardia and acute heart failure.
At first glance, this appeared to validate the Mycoplasma-myocarditis connection. But looking more closely, it raised more questions than it answered.
This man had experienced palpitations and abdominal fullness for four days before attending hospital. He was breathless, hypoxic, tachycardic, with basal crackles and pulmonary oedema on imaging. His heart was enlarged. The echocardiogram showed an ejection fraction of 30%, moderate valve regurgitation, and regional wall motion abnormalities.
That last finding matters. A significantly dilated left ventricle does not usually appear overnight. Those findings may fit myocarditis, but they can equally suggest a prior or underlying cardiac process that has then decompensated under the stress of an acute illness.
This is where clinical reasoning becomes essential. If a patient has Mycoplasma markers and myocarditis simultaneously, it is tempting to join the dots and call it Mycoplasma myocarditis. But correlation is not causation. Mycoplasma may have been the primary driver. It may equally have been a trigger, an association, or simply the stress that pushed an already vulnerable heart over the edge.
That distinction is being missed.
The Missing Differential
In medicine, we use differential diagnosis because symptoms rarely arrive with labels attached.
If a patient is breathless, we do not immediately assume infection. We work through heart failure, pulmonary embolism, arrhythmia, anaemia, metabolic derangement, and more. The differential is not a formality — it is the mechanism by which we protect ourselves from premature closure.
That is why I found it significant that in this 2024 case report, vaccination status was not discussed. That omission matters. The case occurred in the post-pandemic era, after widespread COVID vaccination and repeat boosters. I am not asserting that vaccination caused that man’s myocarditis. I am saying it should have appeared in the differential.
A more complete clinical question would be: could prior myocardial injury, immune-mediated inflammation, or vaccine-associated myocarditis have left the heart vulnerable, with Mycoplasma then acting as the stressor that tipped the patient into failure? That possibility makes more clinical sense to me than assuming a previously normal heart became severely dilated and regionally dysfunctional within days on the basis of Mycoplasma alone.
The same reasoning applies to Princess Bha. If she had received a recent booster — and I stress I cannot confirm that — then vaccine-associated myocarditis should not be dismissed from the differential. Not because it is proven. Because it is medically relevant.
The Pathology We Are Not Doing
There is another piece of this picture that I believe is critical.
A Japanese autopsy study examined patients who had died from unexplained cardiac arrest and found multiple tiny scars distributed throughout the myocardium. What stood out was the observation that across decades of clinicopathological conference experience, this pattern of multiple micro-scars outside the context of myocardial infarction had not previously been seen.
That is extraordinary.
If we are encountering unexplained arrhythmias and sudden cardiac deaths, and if post-mortem histology is revealing an unusual pattern of micro-scarring, the scientific response should be immediate and intense. We should be asking whether this is new, whether it is related to infection, immune dysregulation, vaccination, reinfection, microvascular injury, or some combination. Instead, that research sits quietly in the background, barely discussed.
That is not acceptable.
When someone dies after an unexplained cardiac arrest — particularly in this era — histology matters. The pattern of inflammation or scarring in the myocardium matters. Without it, we are left with assumptions dressed as conclusions.
Koizumi, Tomomi, and Masao Ono. "Cardiac Multiple Micro-Scars: An Autopsy Study." Case Reports 30.5 (2025): 103083.
Why This Matters Beyond One Case
The broader issue extends well beyond Princess Bha. Her case is important because it exposes a structural weakness in the current scientific posture.
We are living through a period in which infection, reinfection, immune dysregulation, vaccine exposure, endothelial injury, and inflammatory cardiac disease may all intersect. If our diagnostic process refuses to place all of those possibilities on the table, we will not understand what is happening.
The risk is not simply that one case may be misclassified. The risk is that a whole pattern may be missed.
When someone dies from sudden cardiac arrest in this era, families should be asking for histology where possible. They should be asking whether myocarditis was present, whether micro-scars were found, whether the pattern resembled infarction, immune injury, or something that does not fit any prior category. If the scientific establishment will not pursue those questions systematically, families may find themselves having to ask them alone.
That is a terrible position to be in. But it is where we are.
The Question I Am Left With
I do not claim to know what caused Princess Bha’s collapse. Mycoplasma myocarditis is possible. Vaccine-associated myocarditis is possible if the timing supports it. A mixed process is possible. A pre-existing vulnerability unmasked by infection is possible.
What I object to is the absence of visible diagnostic rigour.
I object to the idea that identifying Mycoplasma closes the question.
The right question is not, “Can Mycoplasma cause myocarditis?” It can. The right question is, “Was Mycoplasma the primary cause in this specific case, and what evidence excludes other plausible contributors?”
Until that is answered transparently, the case remains medically unresolved.
And that is the real problem. If we do not demand better answers now, we will spend the next decade slowly discovering what we should have investigated from the beginning.
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