Misleading chronic infection screening in autoimmune disease

Infectious disease serology

Infectious disease serology are laboratory studies ordered by your physician to support the suspicion that an infectious burden is present. One example would be Epstein Barr Virus (EBV), which causes mono.

Your physician might consider this test in a young adult with sudden onset of disabling fatigue, fever, sore throat, swollen lymph nodes and an enlarged liver or spleen.

In the test we look for the presence of two classes of antibodies made by certain lymphocytes that target the EBV… IgGs and IgMs specific to different components of the virus.  The classes present and the degree to which they are present tell us whether an infection is or was present.

Removed from acute issues and looking for the root cause

Screening for chronic infectious is a trail clinicians in the integrative and functional sphere often steer towards in trying to figure out what the actual cause of your chronic inflammatory disease is.

There’s a large body of evidence incriminating different bacteria and viral infections in the pathogenesis of many different autimmune conditions. Unfortunately, deeper investigation has provided inconsistent results in terms of pegging specific infectious agents to ongoing disease. 

Still, recent development in the understanding of the pathophysiology behind different chronic inflammatory conditions make it an attractive avenue for continued investigation. And rather than wait for medical science to advance, some clinicians are taking advantage of tools out there in going deeper with diagnosing what the problem actually is.

But we need to understand the limitations of screening for infections.

When things aren’t working right

The interpretation of infectious serology is complicated in generally healthy individuals. But in folks with autoimmune disease, there’s an extra layer of complexity. 

Autoimmune disease essentially means you have dysregulation of the immune system. Dysregulation is a very broad term, and there’s hundreds of specific hiccups that we could zoom in on in further study, but then you’d miss the forest for the trees. Basically you have miscommunication that results in the less of tolerance to yourself, and your immune system no longer tolerates you.

There’s also miscommunication among your cells that make antibodies. B Cells are a type of lymphocyte that under certain instructions, create antibodies that go out and tag invaders for destruction.

During active autoimmune disease or flares, sometimes B cells get the wrong message. They could get text messages from other members and components of the immune system that tell them to release Epstein Barr Virus antibodies when no infection is present, and interestingly, when no infection was EVER present. More on this later.


Antibodies don’t necessarily mean you have a chronic infection.

Recall the explanation above of the unspecific B-Cell response to an autoimmune disease flare. Here’s an example of this:

There’s this case of a young gal who was diagnosed with Rheumatoid arthritis in her late teens. Part of her long drawn out workup that eventually led to the diagnosis included serology for:





H Pylori


Epstein Barr


Various Herpes Viruses

And several others

Every test for potential infectious disease came back positive.

Was she infected with every one of these bugs?

Most certainly not.

The rheumatologist involved in her care referred to this as an “immunologic convulsion.” What a fitting description. Essentially your plasma cells spaz out firing off all sorts of IgG and IgM antibodies creating these false positive lab tests.

Your immune system has a filing cabinet for all sorts of dietary, bacterial, viral, fungal and other antigens. The file folders residing in that cabinet can be inappropriately accessed during disease flares.

These unspecific and erratic B-cell responses have the potential to mislead you and your clinician in the management of your case.

My experience with a patient diagnosed and treated with Lyme’s disease

There was a patient I saw who was diagnosed with Hashimotos thyroiditis suffering from a probable seronegative polyarthropathy who had been treated for Lyme disease… REPEATEDLY.

She would get a little bit better after each treatment, but whose to say it was even the antibiotics? Looking at her records it was clear she had the whole kitchen sink thrown at her.

It was a tough one to deal with, because she kept returning to the idea of the Lyme disease and there was this psychosomatic component of being entrenched in this illness identity for so long.


“Oh, the antimicrobial regimen was…”

“Oh the co infections are now…?”

“Oh [this and that]…”

Jesus christ, maybe it’s not even lyme.

I remember brainstorming with the group and writing every treatment on the board she had been through.

What was really obvious was the basics weren’t in place, and they never were. We addressed the basics and her symptoms improved dramatically.

We dropped her expensive IV treatments, left the idea of treating heavy metals behind and discontinued most of her supplements.

“Well what about the lyme?”

“Who cares,” was my response.

A more balanced perspective

That’s not to say infections don’t play a role, because they do.

Again, investigators haven’t been able to consistently find any bugs in the synovium or the tissues peripherally involved in these autoimmune arthritides, but some times the criminals aren’t at the most obvious crime scene.

Dispensing with the idea that chronic infection could be perpetuating your illness would be foolish (which is the stance in most conventional settings). But all the more reason we want to look at each case carefully and proceed with the individual context in mind. And then we also want to remember that things can be really wacky in autoimmune disease when it comes to laboratory findings.


Dr. Mitchell is a physician practicing rheumatology in Gilbert, Arizona. His interests include clinical nutrition, autoimmune disease and environmental medicine.

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