Mycoplasma Species: Stealth Pathogens Associated with CFS and Fibromyalgia

Author: Rohan Smith | Functional Medicine Practitioner | Adelaide, SA

For many people in Adelaide living with the invisible pain of fibromyalgia or the persistent exhaustion of chronic fatigue syndrome (CFS), standard investigations often fail to reveal a clear explanation. In some cases, underlying biological contributors may include persistent, difficult-to-detect infections. Mycoplasma species represent a unique class of bacteria capable of evading immune surveillance and altering cellular metabolism, potentially contributing to chronic multisystem illness.

Quick Answer: How Are Mycoplasma Species Associated with CFS and Fibromyalgia?

Mycoplasma species are among the smallest free-living organisms and are unique because they lack a cell wall (1,2). This allows them to live inside host cells, where they may evade immune detection and resist antibiotics that target cell-wall synthesis. In susceptible individuals, persistent Mycoplasma infection has been associated with chronic immune activation, mitochondrial stress, and molecular mimicry—processes that may contribute to fatigue, widespread pain, and cognitive symptoms seen in CFS and fibromyalgia (3,4,15).

The Biology of a Stealth Infection

Because Mycoplasma species such as M. pneumoniae, M. hominis, and M. fermentans lack a rigid cell wall, they are pleomorphic and capable of adapting their shape to infiltrate diverse tissues, including synovial fluid and the central nervous system (1,5).

• Metabolic parasitism: Mycoplasma species cannot synthesise cholesterol or fatty acids and must acquire these components from host cell membranes, potentially destabilising cellular structure and function (4,6).
• Mitochondrial interference: Competition for nutrients and oxidative byproducts may impair electron transport chain activity, contributing to reduced ATP availability and persistent fatigue (7,11).

Molecular Mimicry and Fibromyalgia Pain

Persistent exposure to Mycoplasma antigens has been associated with molecular mimicry, a process in which immune responses directed at microbial proteins cross-react with host tissues (3,8). In certain individuals, this immune cross-reactivity may contribute to:

• Neuro-inflammation: associated with cognitive dysfunction, sensory sensitivity, and “fibro-fog” (8,14).
• Central sensitisation: a state of heightened nervous system reactivity that amplifies pain perception (9,15).

Advanced Diagnostic Testing in Adelaide

Standard antibody-based testing may fail to detect persistent Mycoplasma infections due to immune evasion and variable antibody responses. In a functional medicine setting, additional markers may be considered when clinically appropriate:

• Advanced PCR testing: direct detection of microbial DNA to identify active or persistent infection (10,12).
• Cytokine profiling: assessment of inflammatory mediators such as IL-6 and TNF-α that may reflect chronic immune activation (11,13).
• Mitochondrial dysfunction assessment: functional markers used to evaluate downstream metabolic stress associated with chronic illness.

Supportive Botanical and Nutritional Strategies

Addressing persistent intracellular infections often involves more than antimicrobial suppression alone. Functional medicine approaches emphasise restoring host resilience alongside pathogen-targeted strategies. Supportive protocols may include:

• Biofilm support: enzymes and nutrients used clinically to assist in disrupting microbial protective matrices (12,15).
• Intracellular botanical support: herbs such as Isatis, Cryptolepis, and Houttuynia, supported by in vitro and preclinical research suggesting antimicrobial activity against Mycoplasma species (13,14).
• Mitochondrial support: targeted nutrients aimed at restoring membrane integrity and ATP production affected by chronic metabolic stress (7,15).

Frequently Asked Questions

Can Mycoplasma infections be treated with standard antibiotics?

Certain Mycoplasma species are conventionally treated with macrolide or tetracycline antibiotics. However, intracellular persistence and immune evasion may limit effectiveness in some chronic presentations, prompting consideration of adjunctive strategies (1,3).

Are Mycoplasma species contagious?

Many Mycoplasma species are common in human populations. Clinical relevance often depends on host factors such as immune resilience, environmental stressors, and overall immune system regulation (5,12).

How long does supportive care usually take?

Because intracellular infections may replicate slowly, supportive care is often implemented over several months, with duration guided by clinical response rather than fixed timelines (14,15).

Key Insights

• Mycoplasma species are cell-wall-deficient bacteria capable of intracellular persistence (1,2).
• They have been associated with mitochondrial stress and reduced ATP production in some individuals (4,7).
• Molecular mimicry may contribute to immune-mediated pain and neurological symptoms (3,8).
• Effective care focuses on immune balance, metabolic support, and host resilience rather than pathogen eradication alone.

Reclaiming Energy and Resilience

For individuals experiencing persistent fatigue or widespread pain without clear explanations, investigating contributory biological factors such as stealth infections may provide additional insight. A personalised, systems-based approach can help identify and address the physiological patterns underlying chronic illness.

References

1. Razin S, Yogev D, Naot Y. Molecular biology and pathogenicity of mycoplasmas. Microbiol Mol Biol Rev. 1998.
2. Baseman JB, Tully JG. Mycoplasmas: sophisticated, reemerging, and burdened by their notoriety. Emerg Infect Dis. 1997.
3. Nicolson GL, Nasralla M, Haier J, et al. Mycoplasmal infections in chronic fatigue syndrome, fibromyalgia, and autoimmune diseases. J Chronic Fatigue Syndr. 1998.
4. Rottem S. Interaction of mycoplasmas with host cells. Physiol Rev. 2003.
5. Waites KB, Talkington DF. Mycoplasma pneumoniae and its role as a human pathogen. Clin Microbiol Rev. 2004.
6. Razin S. The cell membrane of mycoplasma. Ann N Y Acad Sci. 1967.
7. Nicolson GL. Lipid replacement therapy: a natural medicine approach to replacing damaged lipids in cellular membranes. J Am Nutraceutical Assoc. 2003.
8. Vojdani A, Choppa PC, Tagle C, et al. Detection of Mycoplasma genus and species by PCR in patients with chronic fatigue syndrome. J Clin Lab Immunol. 1998.
9. Nijs J, Meeus M, De Meirleir K. Chronic fatigue syndrome: exercise performance related to immune dysfunction. Clin Rheumatol. 2006.
10. Endresen M. Mycoplasma blood infection in chronic fatigue syndrome and fibromyalgia. Lancet. 2003.
11. Lo SC, Wear DJ, Green SL, et al. Pathogenicity of Mycoplasma fermentans (incognitus strain). Am J Trop Med Hyg. 1991.
12. Waites KB, Xiao L, Liu Y, et al. Mycoplasma pneumoniae from the respiratory tract and beyond. Clin Microbiol Rev. 2017.
13. Feng J, Schiavon CR, He XY, et al. Identification of essential genes for Mycoplasma pneumoniae survival. Front Microbiol. 2019.
14. Naviaux RK. Metabolic features of the cell danger response. Mitochondrion. 2014.
15. Nijs J, Meeus M, Van Oosterwijck J, et al. Treatment of central sensitization in patients with chronic pain. Expert Opin Pharmacother. 2011.