Written and medically reviewed by Dr. Diane Mueller, ND, LAc, DAOM, founder of MyLymeDoc. Last reviewed September 16, 2026.
Mycoplasma is real, and its connection to Lyme disease is not what most articles claim. If you are already working through a co-infection workup, this is one organism worth understanding accurately before deciding whether to test for it. Several pages online state flatly that ticks transmit Mycoplasma, with no source behind the claim. The one published review that actually addresses transmission says the opposite for the species most often named: it spreads through respiratory droplets between people, not through a tick bite. What does hold up is something different and, in a way, more useful: chronically ill patients, including many with Lyme disease, show elevated rates of Mycoplasma on PCR testing, and that pattern deserves attention even though it does not mean what the tick-transmission claim implies.
What makes Mycoplasma different from most bacteria you have heard of? It has no cell wall, a single biological fact that explains almost everything else worth knowing about how it behaves and how it is treated.
Mycoplasma is a genus of bacteria without a rigid outer cell wall, which makes it smaller and structurally simpler than most bacteria, and which changes which antibiotics can actually kill it.
Mycoplasma organisms are described in the scientific literature as “lacking cell wall components, requiring cholesterol for membrane function and growth.” Most bacteria rely on a rigid cell wall for structure, and most antibiotics, including the penicillin family, work by attacking that wall. Mycoplasma does not have one, which means those antibiotics have nothing to target. This is settled, uncontested microbiology, not a point of debate.
The published literature does not support tick transmission for Mycoplasma pneumoniae, the species most often named in Lyme-adjacent content, and several competing sources online state the opposite without any citation. This is the single most important accuracy point in this entire topic.
A narrative review on chronic Lyme disease and co-infections classifies Mycoplasma pneumoniae’s transmission route as “droplet infection, humans,” categorizing it as an other co-infection, specifically not tick-borne, in direct contrast to Bartonella henselae, which the same paper documents as genuinely tick-transmitted. In plain terms, this species most commonly spreads the way a cold or respiratory infection does, person to person through the air, not through a tick bite. When you see a page claim ticks transmit Mycoplasma with no study cited behind it, that claim is not supported by the one review that actually addresses the question directly.
The real connection is not tick co-transmission. It is that chronically ill patients, across several diagnoses, show elevated rates of Mycoplasma on PCR testing, and that pattern is documented in real research, just not research done specifically in Lyme-diagnosed populations. This distinction matters more than it sounds like it should.
Among 261 chronic fatigue syndrome patients tested in one study, “179, or 68.6 percent, were infected by at least one species of Mycoplasma, compared to two out of 36, or 5.6 percent, in the control sample.”
A separate study of 200 CFS patients found 52 percent Mycoplasma PCR-positivity. The authors’ conclusion was carefully hedged: “a large subset of CFS patients show evidence of bacterial and/or viral infection(s).” These infections, they wrote, “may contribute to the severity of signs and symptoms.”
Multiple infections were common in a third study, examining 91 mycoplasma-positive patients with chronic fatigue and fibromyalgia: “multiple mycoplasmal infections were found in 48 of 91 patients, with double infections being detected in 30.8% and triple infections in 22%.”
Those are real, PCR-based findings with striking positivity rates. They were studied in chronic fatigue syndrome populations, not in people specifically diagnosed with Lyme disease. The relevance to Lyme patients comes from symptom overlap and shared immune dysregulation, not from a study that directly tested Lyme patients for Mycoplasma and compared the results.
Mycoplasma pneumoniae and Lyme disease can produce a similar-looking skin presentation, which creates real diagnostic confusion in individual cases. A 2025 case report describes a patient whose rash mimicked erythema migrans, the classic Lyme bullseye rash, but whose lab results told a different story.
Seroconversion is the point at which a person’s immune system has produced enough detectable antibodies against a specific infection for a blood test to register as positive, usually appearing days to weeks after the infection begins.
Lyme serology “still showed only positive IgM antibodies” while Mycoplasma testing showed seroconversion, with positive IgG. The rash eventually traced to Mycoplasma, not active Lyme infection.
This is a single case report, the lowest tier of evidence, and it illustrates something worth knowing regardless: serology between these two infections can overlap in confusing ways, and a rash that looks like Lyme is not automatically Lyme.
Testing for Mycoplasma is genuinely harder than testing for many other infections, because culturing it is notoriously unreliable. PCR testing and antibody titers are the practical options used in clinical practice, and treatment relies on antibiotic classes that do not depend on attacking a cell wall. Our co-infection testing guide covers how PCR and antibody panels get ordered and interpreted for the co-infections with stronger evidence behind them, and the same testing logic applies here.
Because Mycoplasma has no cell wall, penicillin-class antibiotics are ineffective against it. Macrolides, tetracyclines including doxycycline, and fluoroquinolones are the standard classes used instead, the same logic that shapes treatment for other cell-wall-deficient organisms.
The current mainstream infectious-disease guideline for Lyme disease addresses co-infection testing for two specific organisms, and Mycoplasma is not one of them. This is worth stating plainly for transparency, even though it complicates the narrative some content pushes.
The 2020 IDSA, AAN, and ACR guideline, summarized by the American Academy of Family Physicians, recommends co-infection testing specifically for “Anaplasma phagocytophilum and Babesia microti” under defined clinical circumstances. Mycoplasma does not appear anywhere in that guidance. Routine Mycoplasma co-infection testing in the context of Lyme disease is a practice specific to Lyme-literate and functional medicine, not a mainstream infectious-disease recommendation. That does not make it wrong. It means it sits outside standard guidelines, and that context belongs in any honest conversation about whether to test for it.
A statistic putting Mycoplasma co-infection at 15 percent of Lyme cases circulates widely. One patient-advocacy source lists “Mycoplasma (15%)” among reported co-infections, citing a patient-reported survey published in the peer-reviewed journal PeerJ. The distinction that matters here is not peer review, the survey did go through peer review, it is that the data is self-reported by patients rather than confirmed through lab testing. Self-report and lab-confirmed diagnosis are different kinds of evidence, and the two should not be presented as interchangeable. Our co-infection symptom comparison chart covers Mycoplasma’s symptom picture against the tick-borne co-infections that do have lab-confirmed data behind them.
If you are dealing with chronic Lyme symptoms that have not resolved with standard treatment, Mycoplasma is a reasonable consideration alongside other co-infections, framed accurately rather than as a settled tick-borne diagnosis. Our page on Bartonella co-infection, by contrast, covers an organism that genuinely is tick-transmitted, a useful comparison for seeing why that distinction matters clinically.
A co-infection treatment overview walks through how antibiotic selection changes once more than one organism is in play.
In our practice, we consider Mycoplasma as one piece of a full clinical picture, not a default assumption for every chronically ill patient. If your symptoms have not improved and your workup has not looked at this possibility, book a consultation to talk through whether it belongs in your evaluation.
The published literature does not support this for Mycoplasma pneumoniae, the species most often discussed. The one review that directly addresses transmission classifies it as droplet-spread between people, not tick-transmitted, in contrast to genuinely tick-borne organisms like Bartonella.
Fatigue, joint pain, and cognitive symptoms are commonly reported, overlapping heavily with Lyme disease symptoms. This overlap is part of why the two get discussed together, even though the transmission route differs.
PCR testing and antibody titers are the practical options. Culturing Mycoplasma is notoriously difficult because of its unusual biology, so culture is rarely used in practice.
Not entirely. Mycoplasma lacks a cell wall, so penicillin-class antibiotics do not work against it. Macrolides, tetracyclines, and fluoroquinolones are the standard treatment classes, some of which overlap with Lyme treatment and some of which do not.
No. Current guidelines from the IDSA, AAN, and ACR address co-infection testing specifically for Anaplasma and Babesia. Mycoplasma testing in the Lyme context is a functional-medicine practice, not part of mainstream infectious-disease guidance.
Because it lacks a cell wall, the structure that penicillin-class drugs target. Antibiotics that work through a different mechanism, such as macrolides and tetracyclines, remain effective.
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