Beyond Repair: Mold Toxicity, Lyme, and Coinfections

How to Test, Treat, and Tell Them Apart

Patients with chronic fatigue, brain fog, tingling, joint pain, mood changes, and weird “nobody can figure this out” symptoms often get told two totally different stories: “You have mold toxicity,” or “You have chronic Lyme.” Sometimes they’re told they have both. Clinically, the overlap is real — and the consequences of getting it wrong are huge. (Campbell, 2004; Campbell, 2019).

This post breaks down:

1. How mold toxicity (mycotoxicosis) presents and how we test for it.

2. How Lyme disease and its common coinfections (Babesia, Bartonella) present and how we test for them.

3. Why advanced antibody testing like multi-peptide ELISA (MPE) and comprehensive mycotoxin testing are changing the standard of care.

4. First-line treatment principles, including the role of itraconazole, antibiotics like doxycycline/minocycline, and why “3 weeks and done” is not always the full story in persistent cases. (Campbell, 2019; ImmunoSciences Lab, 2025).

Mold toxicity (mycotoxicosis): what it does to the body

Indoor water damage allows molds to colonize drywall, subfloor, HVAC, etc., and those molds release mycotoxins — biologically active toxins small enough to be inhaled, absorbed through skin, and swallowed in dust (Campbell, 2004; Campbell, 2019).

Dr. Andrew Campbell describes mold-related illness as a “great masquerader” of the 21st century because the symptom profile looks like neurology, rheumatology, psychiatry, and chronic fatigue all at once (Campbell, 2019).

Reported findings include:

• Cognitive changes: slowed processing, poor word recall, trouble with multitasking.

• Mood changes: anxiety, irritability, depressive symptoms.

• Peripheral neurologic complaints: numbness, tingling, burning, muscle weakness.

• Immune dysregulation: recurrent sinus or respiratory infections, chemical sensitivity, histamine-type reactivity.

• Generalized fatigue and body pain that can mimic fibromyalgia, MS, lupus, or even early neurodegenerative disease. (Campbell, 2004; Campbell, 2019).

  
  

Campbell and others have shown that patients exposed to indoor molds and mycotoxins often demonstrate measurable neurocognitive deficits on formal testing and immune dysregulation consistent with chronic inflammatory activation. Those changes correlate with exposure level, suggesting that this is not “in their head,” but a biologically plausible neurotoxic and immunotoxic process (Campbell, 2004).

Lyme disease and coinfections: what they do to the body

Lyme disease is caused primarily by Borrelia burgdorferi in North America, but related Borrelia subspecies (e.g., B. garinii, B. afzelii, B. miyamotoi) and coinfections like Babesia and Bartonella are clinically important. These organisms are transmitted by ticks and can disseminate into joints, nerves, endothelium, and brain tissue (ImmunoSciences Lab, 2025).

Typical early Lyme symptoms after a tick bite can include fever, headache, fatigue, migrating joint pain, and sometimes the classic erythema migrans rash. But here’s the problem:

• Not everyone remembers a tick bite.

• Not everyone shows the rash.

• Symptoms can emerge weeks to months later and may present as neuropathy, cognitive impairment, POTS-like dizziness, or inflammatory arthritis. (Campbell, 2019; ImmunoSciences Lab, 2025).

Coinfections matter:

• Babesia is a malaria-like protozoa. Think fevers, air hunger, night sweats, and profound fatigue out of proportion to physical exam.

• Bartonella can trigger neuropathic pain (burning soles, electric zaps), vascular inflammation, anxiety/irritability, and tender subcutaneous nodules or stretch-mark-like streaks that are not actually stretch marks.

• Ehrlichia/Anaplasma may cause fever, low white count, elevated liver enzymes. (ImmunoSciences Lab, 2025).

Clinically, Babesia and Bartonella symptoms are often what keep people disabled even after standard Lyme treatment, which is why testing for coinfections up front (not months later) actually changes care plans (ImmunoSciences Lab, 2025).

Why mold illness and Lyme get confused

Here’s why clinicians struggle:

• Both mold toxicity and Lyme/coinfections can produce crushing fatigue, brain fog, neuropathy, migrating joint pain, mood changes, and autonomic dysregulation. (Campbell, 2004; Campbell, 2019).

• Both can present as chronic, relapsing, “mystery illness” after a known stressor (water damage at home vs. outdoor exposure to ticks).

• Both can inflame the endothelium and the nervous system, which means similar neurocognitive testing abnormalities and similar inflammatory markers.

Campbell argues that one of the biggest clinical errors is locking onto “it’s Lyme” or “it’s mold” too early and failing to check for the other, leading to partial treatment and long-term disability (Campbell, 2019).

How we test: standard vs advanced

Traditional Lyme testing

The CDC-endorsed algorithm is 2-tiered: first an ELISA (enzyme-linked immunosorbent assay) for Borrelia antibodies, then, if positive or equivocal, a confirmatory Western blot looking for defined IgM or IgG bands (Cleveland Clinic Journal of Medicine, 2019; Global Lyme Alliance, 2025).

Limitations:

• These are indirect tests. They don’t look for the organism. They look for your immune response to it.

• Antibodies can take weeks to mature, so very early Lyme can still test negative. False negatives in early infection are common, with estimates that standard ELISA screening alone can miss a substantial portion of clinically positive cases (Global Lyme Alliance, 2025).

• Western blot interpretation is rigid and was designed for surveillance, not nuanced chronic presentations. (Cleveland Clinic Journal of Medicine, 2019).

Multi-Peptide ELISA (MPE) and ImmunoSciences Lab

Dr. Campbell and collaborators highlight an alternative/improved method: multi-peptide ELISA (MPE). Instead of relying on one crude Borrelia lysate and then a yes/no Western blot, MPE measures IgG and IgM antibodies against multiple purified Borrelia antigens and peptides simultaneously, including outer surface proteins (OspA, OspB, OspC, OspE), C6, and variable major proteins. It also separately reports antibodies to multiple Borrelia subspecies (burgdorferi sensu stricto, garinii, afzelii, miyamotoi) and to common coinfections like Babesia and Bartonella in the same panel. (ImmunoSciences Lab, 2025; Campbell, 2019).

Why this matters:

• Borrelia changes its outer surface proteins (“antigenic variation”) to hide from the immune system and to survive in joints, nerves, and other low-drug-penetration tissues (Campbell, 2019).

• A single-antigen ELISA can miss those shifts. A multi-antigen/MPE approach increases sensitivity because it’s looking for a broader immune signature rather than “one handshake only.” (ImmunoSciences Lab, 2025).

• Including coinfection antigens up front helps explain persistent fevers, air hunger, neuropathic pain, or psychiatric/cognitive symptoms that don’t respond to standard Lyme antibiotics, because the real driver might be Babesia or Bartonella, not Borrelia alone. (ImmunoSciences Lab, 2025).

  
  

In short: Campbell stresses that clinicians should pair symptoms + physical exam + the most sensitive lab method available, which in his view includes multi-peptide ELISA and Western blot together, not Western blot alone (Campbell, 2019; ImmunoSciences Lab, 2025).

Mycotoxin testing

For mold, the modern approach is not just “Did you have water damage?” It’s:

• Test the environment (air/dust or building materials) for mold species and mycotoxins.

• Test the patient (often urine mycotoxin panels) to identify and quantify specific mycotoxins associated with pathogenic molds; these are interpreted in the context of symptoms and exposure history. (Campbell, 2019; MyMycoLab, 2025).

Campbell points out that mycotoxins are biologically active at extremely low concentrations and can cross into neural tissue, so documenting exposure with a validated lab strengthens the medical case, supports targeted detoxification strategies, and can guide legal/occupational accommodations when housing or workplace remediation is needed (Campbell, 2004; Campbell, 2019).

First-line treatment: where conventional medicine starts

Acute / early Lyme

Standard guidance for early Lyme borreliosis is typically a tetracycline-class antibiotic such as doxycycline for about 14–21 days, sometimes extended to ~28 days depending on presentation. Minocycline is an alternative in some cases. The goal here is rapid kill of Borrelia before it disseminates into joints, nervous tissue, or endothelium (Cleveland Clinic Journal of Medicine, 2019).

That “3-week doxy” approach works well in straightforward early Lyme with classic symptoms and documented recent tick exposure (Cleveland Clinic Journal of Medicine, 2019).

Where it gets controversial is persistent or relapsing neurologic, rheumatologic, or autonomic symptoms after standard therapy. Campbell notes that Borrelia can alter its surface antigens and occupy low-drug-penetration niches, which may help explain why some patients remain symptomatic even after a textbook course (Campbell, 2019). Because of that, many clinicians now (1) reassess for coinfections like Babesia and Bartonella and (2) reassess for parallel drivers like mold toxicity, instead of just repeating the exact same antibiotic for the exact same duration.

Babesia

Babesia acts like a blood parasite. When it’s clinically significant — high fevers, night sweats, air hunger, fatigue — standard care often requires antiparasitic / antiprotozoal combinations (e.g., atovaquone plus azithromycin or clindamycin plus quinine in classical guidelines). Babesia will not clear with doxycycline alone because it’s not a bacterium in the same sense; so if a patient “failed doxy,” but no one ever treated Babesia, that’s a diagnostic miss, not proof that “Lyme is incurable.” (ImmunoSciences Lab, 2025).

Bartonella

Bartonella species are intracellular and can require combination or sequential antimicrobial therapy, sometimes including tetracyclines, macrolides, or rifamycins in integrative/infectious disease practice patterns. Persistent neuropathic pain, neuropsychiatric agitation, and microvascular/angiogenic skin findings push you to think “Bartonella,” especially if Lyme-focused antibiotics didn’t solve it (ImmunoSciences Lab, 2025).

Treating mold toxicity

Mold/mycotoxin treatment generally has three pillars in Campbell’s model:

• Source control / remediation

  You must get the patient out of the exposure. If the home, office, school, or gym is actively producing mycotoxins, no pill will fix that. (Campbell, 2019).

• Bind / mobilize / excrete

  After exposure stops, many clinicians use targeted binders, antioxidants, glutathione support, mitochondrial support, and anti-inflammatory protocols to help the patient lower total toxic load and calm neuroinflammation. Campbell reports measurable neurologic and cognitive improvement once ongoing exposure stops and toxin burden drops (Campbell, 2004; Campbell, 2019).

• Treat secondary fungal colonization when appropriate

  If a patient has evidence of fungal colonization (for example, in sinuses) or systemic fungal burden, azole antifungals like itraconazole are sometimes used. Itraconazole has broad activity against many pathogenic molds and yeasts and is part of published therapeutic strategies in mold-associated illness under supervision of a qualified clinician because it has liver and drug–drug interaction considerations (Campbell, 2019). The intent is not “kill every mold spore in the body,” but rather reduce persistent fungal load enough that the immune system stops firing 24/7

  
  

Practical clinical algorithm

Step 1. History + environment.

• Water-damaged building? Visible mold? Musty odor? Co-workers or family sick in the same place? Think mold/mycotoxins.

• Outdoor tick exposure, hiking, pets with ticks, new onset fever + joint pain or neurologic symptoms? Think Lyme and coinfections. (Campbell, 2019).

  
  

Step 2. Symptom clusters.

• Air hunger/night sweats → screen for Babesia.

• Burning soles/vascular streaks/anxiety surges → screen for Bartonella.

• Cognitive slowdown with chemical sensitivity, chronic sinusitis and/or migraines in a known water-damaged space → screen for mycotoxins. (Campbell, 2004; ImmunoSciences Lab, 2025).

  
  

Step 3. Order targeted labs early.

• Use high-sensitivity multi-peptide ELISA + Western blot panels that look at Borrelia subspecies AND Babesia/Bartonella antibodies up front, not months later. (ImmunoSciences Lab, 2025; Campbell, 2019).

• Run urine/environmental mycotoxin testing to document exposure and guide treatment. (Campbell, 2019; MyMycoLab, 2025).

  
  

Step 4. Treat what is actually there.

• Early Lyme → appropriate antibiotic course such as doxycycline or minocycline for ~3–4 weeks is still standard first-line. (Cleveland Clinic Journal of Medicine, 2019).

• Babesia and Bartonella require their own targeted regimens; if you don’t address them, symptoms labeled “chronic Lyme” may persist. (ImmunoSciences Lab, 2025).

• Mold toxicity → remove exposure, support detoxification and inflammation control, and consider antifungals like itraconazole when colonization is documented and benefits outweigh risks (Campbell, 2019).

Step 5. Rebuild, don’t just suppress.

Both chronic tickborne infection and chronic mycotoxin exposure can dysregulate mitochondria, immune tolerance, and the endothelial/vascular lining. Campbell emphasizes that full recovery often requires nutrition, sleep repair, autonomic stabilization, mitochondrial support, and gut repair — not only killing microbes or binding toxins (Campbell, 2004; Campbell, 2019).

Key takeaways for patients (and for providers)

• Mold toxicity and Lyme are not mutually exclusive. You can have both. In fact, many very sick patients do. (Campbell, 2019).

• “Normal Lyme test” does not always mean “no Lyme,” especially if only a basic ELISA was run early. More sensitive multi-peptide ELISA plus Western blot that screens Borrelia subspecies and coinfections gives a fuller picture. (ImmunoSciences Lab, 2025).

• “We remediated the house” is not enough if the patient still has elevated mycotoxins on testing and ongoing neurologic symptoms; you still have to lower body burden and calm inflammation. (Campbell, 2004; Campbell, 2019).

• A simple 3-week course of doxycycline or minocycline is appropriate for straightforward early Lyme, but if disabling symptoms remain, you must reassess for Babesia, Bartonella, and mold toxicity — not just repeat the same antibiotic. (Cleveland Clinic Journal of Medicine, 2019; ImmunoSciences Lab, 2025; Campbell, 2019).

Further Discussion:

Dr. Campbell also cautions against the overuse or misuse of toxin binders such as cholestyramine, activated charcoal, and bentonite clay as “standalone cures.” While these agents may bind certain lipid-soluble toxins in the gastrointestinal tract, they do not neutralize mycotoxins already distributed in tissue or circulating within the central nervous system (Campbell, 2019).

According to Campbell, true recovery from mold and mycotoxin exposure requires a systemic approach—not just binding agents:

1. Remove the source of exposure (home, office, or school).

2. Stabilize the immune and nervous systems before initiating detoxification.

3. Repair mitochondrial and cellular damage caused by oxidative stress.

4. Introduce binders or antioxidants only when the body’s elimination pathways are supported and the patient can tolerate mild toxin mobilization.

Campbell emphasizes that the use of binders without medical guidance can lead to constipation, dehydration, nutrient depletion, or the false assumption that detoxification is complete while underlying inflammation persists, but rather these basic supplements are necessary for mitochondria and cellular support.

When we approach these problems like systems engineers — exposure source, immune response, pathogen load, toxin load, mitochondrial cost — patients stop being “mystery cases” and start getting better. If you suspect you have Lyme/mold toxicity why wait? Get started today and test yourself today!

References

Campbell, A. W. (2004). Mold and mycotoxins: Effects on the neurological and immune systems in humans. Advances in Applied Microbiology, 55, 375–406. PubMed

Campbell, A. W. (2019). Lyme disease and mycotoxicosis: How to differentiate between the two. Alternative Therapies in Health and Medicine, 25(4), 8–11. Today's Practitioner

Campbell, A. W. (2019). Lyme disease and mycotoxicosis: How to differentiate between the two. Alternative Therapies in Health and Medicine, 25(4), 8–11.

Campbell, A. W., & Weinstock, S. (2022). Molds, mycotoxins, the brain, the gut, and misconceptions. ResearchGate Preprint. https://www.researchgate.net/publication/358749321_Molds_Mycotoxins_the_Brain_the_Gut_and_Misconceptions

Campbell, A. W. (2022). Mold Treatment Protocol. Clinical handout, cited in HAWK Recorder Protocol Archive.

Cleveland Clinic Journal of Medicine. (2019). Appropriate laboratory testing in Lyme disease. Cleveland Clinic Journal of Medicine, 86(11), 751–759. Cleveland Clinic Journal of Medicine

Global Lyme Alliance. (2025). Lyme disease testing: ELISA, Western blot, and test effectiveness. Global Lyme Alliance. Global Lyme Alliance

ImmunoSciences Lab. (2025). Immunoserology of Lyme disease by multi-peptide ELISA (MPE) and Western blot: Borrelia subspecies and coinfection antibody panel (Panel B). ImmunoSciences Lab. Immunosciences Lab, Inc.+1

MyMycoLab. (2025). Mycotoxin testing for environmentally acquired mold illness. MyMycoLab. MyMycolab