Yoon Hang Kim, MD, MPH

Board-Certified in Preventive Medicine | Integrative & Functional Medicine Physician

⚕ Medical Disclaimer

This article is for educational and informational purposes only and does not constitute medical advice, diagnosis, or treatment. The strategies discussed should be implemented only under the guidance of a qualified healthcare provider. Always consult your physician before starting any new supplement or antimicrobial regimen. This content does not establish a provider–client relationship.

A Note on Evidence in This Article

Every citation in this article has been individually verified against the primary source. Where the evidence is weaker than commonly presented — or where it points in an unfavorable direction — that is stated plainly. Several widely circulated claims about botanical antimicrobials and probiotics for gut Pseudomonas do not survive scrutiny, and they are identified as such below.

Introduction

Pseudomonas aeruginosa is a gram-negative opportunistic pathogen with an outsized reputation in hospital settings. Its role in the gastrointestinal tract, however, is frequently misunderstood in outpatient integrative practice. When this organism turns up on a stool culture or a PCR-based GI panel, the clinical question is always the same: does this finding matter, and what — if anything — should I do about it?

For the majority of immunocompetent outpatients, the answer is: probably nothing. P. aeruginosa can colonize the GI tract transiently without causing disease, particularly after antibiotic exposure, proton pump inhibitor (PPI) use, GI surgery, or hospitalization. Colonization alone is not an indication for treatment.

This article covers the conventional framework for when GI Pseudomonas requires treatment, then examines — critically — the evidence for botanical antimicrobials and probiotics that are commonly recommended in integrative practice for this indication. A significant portion of that evidence turns out to be weaker, more conflicted, or more equivocal than it is usually represented. Clinicians deserve to know that before they prescribe.

Colonization Versus Infection

Not every positive culture demands a prescription. The distinction between colonization and infection is the first and most critical decision point.

When Treatment Is Warranted

Symptomatic enteritis or colitis attributable to Pseudomonas: New or worsening diarrhea, abdominal pain, fever, leukocytosis, and heavy Pseudomonas growth on stool culture — after exclusion of Clostridioides difficile, viral pathogens, and parasites — is the clearest indication for treatment.

Immunocompromised or critically ill clients: In neutropenic, transplant, and ICU populations, GI colonization with P. aeruginosa is a recognized reservoir for invasive infection. Intestinal carriage rates in hematology–oncology units have been reported in the range of roughly 12% to 37%, and extraluminal translocation is a well-described route to systemic infection in neutropenic patients.

Gut as suspected source of systemic infection: When blood cultures grow P. aeruginosa and the GI tract is the suspected portal of entry, decolonization strategies may be considered alongside systemic therapy.

When Treatment Is Not Indicated

Asymptomatic, low-level colonization in an immunocompetent client — particularly when found incidentally — does not require antibiotic treatment. Routine eradication of colonization is not supported by evidence and selects for resistance.

Risk Factors

Prior broad-spectrum antibiotics, GI obstruction or surgery, prolonged hospitalization or ICU stay, hypochlorhydria (including chronic PPI use), and immunosuppression all increase the likelihood that colonization becomes clinically relevant.

Why Pseudomonas Is Hard to Eradicate

LPS-driven inflammation: As a gram-negative organism, P. aeruginosa produces lipopolysaccharide, which activates TLR4 signaling and drives intestinal inflammation and permeability when the organism is present at high density.

Biofilm formation: P. aeruginosa is among the most efficient biofilm formers in clinical microbiology. Biofilms are up to roughly 1,000-fold less susceptible to antimicrobials than planktonic cells and shield the organism from immune clearance.

Quorum sensing: Virulence factor expression is coordinated through cell-density-dependent signaling systems (las, rhl, and pqs), which control elastase, pyocyanin, pyoverdine, rhamnolipids, and exotoxins.

Efflux pumps: The MexXY-OprM and related RND-type efflux systems actively extrude antibiotics and are a primary driver of aminoglycoside and multidrug resistance.

Persister cells: A subpopulation of metabolically dormant cells tolerates antibiotic exposure without being genetically resistant, contributing to relapse after apparently successful treatment.

Conventional Antibiotic Treatment

When treatment is indicated, susceptibility-guided antibiotic therapy remains the standard of care.

Oral therapy (stable clients, susceptible isolates): Ciprofloxacin is the most reliable oral antipseudomonal agent when susceptibility is confirmed.

Severe disease or immunocompromised hosts: Antipseudomonal beta-lactams — piperacillin-tazobactam, cefepime, ceftazidime, or a carbapenem — form the backbone, often in combination with a fluoroquinolone or aminoglycoside.

Stewardship: Therapy should be susceptibility-guided. Fluoroquinolone monotherapy is discouraged in severe disease. Selective decolonization of asymptomatic carriers is not routinely supported and carries meaningful resistance risk.

Workup Before Treating

Confirm stool culture with heavy Pseudomonas growth and exclude other pathogens (C. difficile toxin/PCR, ova and parasites, viral panels). Assess host risk: immunocompromise, recent antibiotics, ICU stay, GI surgery or obstruction, PPI use. Look for systemic signs — fever, leukocytosis, hemodynamic instability — or bacteremia that would mandate IV therapy. Obtain susceptibilities before treating.

Botanical Antimicrobials: What the Evidence Actually Shows

Botanical antimicrobials are widely recommended in integrative practice for GI dysbiosis, including Pseudomonas overgrowth. The mechanistic rationale is genuinely attractive: many plant compounds target biofilm formation and quorum sensing — precisely the strategies that make P. aeruginosa difficult. But the strength of the evidence varies enormously by ingredient, and the gap between in vitro findings and achievable concentrations in the human gut is the central problem, not a footnote.

Biocidin® Liquid Formula: The Published Data

Biocidin® is a proprietary blend of 18 botanical extracts and essential oils — including bilberry, grape seed, shiitake, goldenseal root, noni, garlic bulb, white willow bark, milk thistle seed, Echinacea purpurea and E. angustifolia, raspberry, black walnut hull and leaf, lavender oil, oregano oil, galbanum oil, tea tree oil, fumitory, and gentian root — in a glycerin and ethanol base (under 5% alcohol in the final product). It contains walnut, an allergen. It has been commercially available since 1989.

The 2026 Frontiers in Antibiotics Biofilm Study

Mundanchira and colleagues tested Biocidin® against 5-day mature biofilms of E. coli, S. aureus, P. aeruginosa, K. pneumoniae, and C. albicans. The minimum inhibitory concentration against P. aeruginosa was 12.5%. A 4-hour bolus exposure at 25% or higher produced a greater than 2-log reduction in both biofilm and planktonic populations. Continuous 24-hour exposure at 50% drove P. aeruginosa, S. aureus, and E. coli biofilms below the limit of detection. Sub-inhibitory concentrations (5% and 10%) had no effect on biofilm viability, even after 5 days.

Two findings from this paper deserve more attention than they usually get. First, ciprofloxacin failed to kill P. aeruginosa biofilms at the concentrations tested in the same experiment — a useful reminder of how formidable biofilms are. Second, and far more consequentially, the authors state directly that 

⚠ The Central Caveat — Stated by the Study's Own Authors

"...the concentrations required for biofilm eradication in this study exceed those likely achievable within the gastrointestinal tract and other internal organs."

The concentrations that worked were 25–50% Biocidin by volume, sustained for 4–24 hours against a biofilm in a plastic well. Nothing resembling that exposure occurs in a human intestine after an oral dose of a tincture. The authors suggest the findings may be more applicable to localized oral or topical use. This does not mean Biocidin is useless in the gut — it means this particular study is not evidence that it eradicates Pseudomonas biofilms there.

⚠ Conflict of Interest Disclosure

This study was funded by Biocidin Botanicals. Two of the five authors are employed by Biocidin Botanicals. The senior and corresponding author served on the Biocidin Botanicals scientific board from 2022–2023 and is CEO of a biofilm company. The published disclosure states that the funder's involvement included "writing the manuscript and decision to publish."

This does not invalidate the data, and the work appears methodologically sound. But a clinician weighing this evidence should know that the manufacturer wrote the manuscript and decided whether it would be published. That is an unusually direct degree of sponsor involvement and it belongs in the assessment.

The Human Clinical Data: One Open-Label SIBO Study

The strongest human evidence for this formulation is an open-label study by Min and colleagues in Nutrients (2024). Adults with lactulose breath-test-confirmed SIBO received 10 weeks of Biocidin liquid plus GI Detox+, with Olivirex added for non-responders. The regimen produced favorable shifts in short-chain fatty acid producers (A. muciniphila +31.4%, F. prausnitzii +35.4%, C. eutactus +24.8%, R. faecis +48.7%) and a 20% reduction in facial erythema at week 10.

The limitations matter. This was open-label with no control group, so placebo and regression to the mean cannot be excluded. It was a combination regimen, so Biocidin's individual contribution is unknown. Critically, the intestinal permeability markers did not improve — there were no significant changes in plasma zonulin, DAO, histamine, or LPS immunoglobulin ratios, and LPS/IgG actually trended upward. And most relevant here: this study says nothing about Pseudomonas. It was a SIBO study. Extrapolating it to GI Pseudomonas is an inference, not a finding.

Claims That Should Be Retired

Two claims circulate widely in integrative literature and should be treated with skepticism. The first is a frequently cited "pilot study" at a Netherlands clinic reporting improvement in over 1,000 clients on Biocidin with preserved commensal flora. This appears only in manufacturer marketing material and practitioner blog posts; it has no traceable peer-reviewed publication and no accessible methods. It should not be cited as evidence. The second is the set of "unpublished university reports" on biofilm and Borrelia activity. The Borrelia work was in fact published (Karvonen and Gilbert, 2019), but in a journal with minimal visibility; the biofilm work has now been superseded by the 2026 study above. Citing unpublished internal reports as evidence is not defensible.

Ingredient-Level Evidence Against P. aeruginosa

Several individual constituents have genuinely good in vitro data against P. aeruginosa. This is the strongest part of the botanical case — with the persistent caveat that in vitro potency does not establish in vivo gut efficacy at oral doses.

Oregano Oil (Carvacrol / Thymol) — Strongest Ingredient Evidence

Lu and colleagues (Frontiers in Microbiology, 2018) tested oregano oil against 11 multidrug-resistant clinical isolates from combat casualties, including three P. aeruginosa strains. MICs ranged from 0.08 to 0.64 mg/mL. Oregano oil eradicated biofilms formed by all 13 pathogens tested at similar concentrations, and — notably — no resistance emerged after 20 consecutive passages at sublethal doses. In a mouse burn wound model, topical application reduced bacterial load by 3 log within one hour. Carvacrol and thymol disrupt membranes, interfere with quorum sensing, and inhibit biofilm formation.

Honest framing: This is strong data, but the in vivo component was topical application to a burn wound — not oral administration for gut colonization. A 2021 corrigendum corrected a figure error in this paper (the scientific conclusions were unchanged).

Berberine (from Goldenseal) — Real, But Not What Most People Think

Berberine's relationship with P. aeruginosa is more interesting and more limited than usually presented. As a direct antibacterial against P. aeruginosa, berberine is weak — Morita and colleagues report an MIC above 512 µg/mL, which is not a clinically meaningful antibacterial effect.

Its real value is as an efflux pump inhibitor. Morita et al. (Frontiers in Microbiology, 2016) showed berberine inhibits the MexXY-OprM system, restoring aminoglycoside susceptibility in MDR P. aeruginosa and enhancing amikacin–piperacillin synergy. Separately, Liu et al. (Microbial Pathogenesis, 2024) showed berberine hydrochloride inhibits biofilm growth by downregulating pslA and pelA, damages membranes, generates ROS, and depletes intracellular ATP, with minimal cytotoxicity.

⚠ Correction to a Commonly Repeated Claim

The often-cited goldenseal "synergy" finding — flavonoids (sideroxylin and desmethyl-sideroxylins) potentiating berberine via efflux pump inhibition, with a fractional inhibitory concentration of 0.375 — is against Staphylococcus aureus and the NorA efflux pump. S. aureus is gram-positive. This finding does not transfer to Pseudomonas aeruginosa, which is gram-negative and uses entirely different RND-family pumps. (Junio et al., J Nat Prod 2011; Ettefagh et al., Planta Med 2011.)

Berberine's relevance to Pseudomonas is real, but it rests on the MexXY work — not on this synergy data.

Garlic / Allicin — Good Quorum-Sensing Evidence

Allicin is an anti-virulence agent rather than a bactericide. Xu and colleagues (Canadian Journal of Microbiology, 2019) demonstrated that allicin attenuates elastase, pyocyanin, pyoverdine, and rhamnolipid production by suppressing the rhl and pqs quorum-sensing systems. Lihua and colleagues (Polish Journal of Microbiology, 2013) showed allicin inhibits early adhesion and reduces extracellular polysaccharide secretion in P. aeruginosa biofilms. Harjai and colleagues (FEMS Immunology & Medical Microbiology, 2010) found garlic attenuated P. aeruginosa virulence in an experimental UTI model, and Bjarnsholt and colleagues (Microbiology, 2005) showed garlic promoted clearance of pulmonary P. aeruginosa in mice.

Honest framing: The models are urinary and pulmonary, not intestinal. Anti-virulence is not eradication — quorum-sensing inhibition disarms the organism without killing it, which may be clinically desirable but is a different endpoint than clearing colonization.

Black Walnut / Juglone

Juglone, the principal naphthoquinone in black walnut hull, inhibits P. aeruginosa colony formation at approximately 35 µg/mL through membrane damage, biofilm blockage, and gene expression inhibition (Molecules, 2021). This work was conducted in a food-safety context, and oral bioavailability of juglone in the human gut at antimicrobial concentrations has not been established.

Tea Tree Oil

Tea tree oil has demonstrated anti-biofilm activity against cystic fibrosis-associated P. aeruginosa, and — unusually — was effective at lower concentrations against biofilms than against planktonic cells. However, P. aeruginosa is known to display intrinsic tolerance to tea tree oil mediated by its outer membrane and energy-dependent efflux, and commercial tea tree oil products vary substantially in composition and potency. Tea tree oil is not recommended for ingestion in most clinical contexts.

Ingredients With Weak or Absent Anti-Pseudomonas Evidence

Several constituents of multi-botanical formulas are frequently listed as if they contribute anti-Pseudomonas activity when the evidence does not support it. Grape seed extract has demonstrated antimicrobial activity, but gram-positive organisms are consistently more susceptible than gram-negatives, and reported inhibitory concentrations against P. aeruginosa are high. Echinacea is primarily immunomodulatory; direct antibacterial activity against P. aeruginosa is modest, and P. aeruginosa has been noted as an exception to Echinacea's antimicrobial spectrum in at least one study. Shiitake (lentinan) and milk thistle (silymarin) contribute immune and barrier support respectively, but neither has meaningful direct anti-Pseudomonas data. Bilberry, noni, raspberry, lavender, galbanum, fumitory, and gentian have general antimicrobial literature but essentially no Pseudomonas-specific evidence. Gentian's plausible contribution is as a bitter that supports gastric acid secretion — an upstream risk factor — not as an antimicrobial.

Probiotics for GI Pseudomonas: A Necessary Correction

Probiotics are routinely recommended for Pseudomonas dysbiosis. The in vitro literature is encouraging. The in vivo literature is not uniformly so, and there is a safety signal that is rarely mentioned in integrative sources. This section presents both.

What the In Vitro Data Show

Lactobacillus acidophilus and L. plantarum: Drumond and colleagues (Frontiers in Pharmacology, 2023) tested cell-free supernatants from four lactic acid bacteria against two P. aeruginosa strains. L. acidophilus supernatant at 18–22% completely inhibited growth of both strains; L. plantarum required 46–48%. Antibiofilm activity ranged from 40% to 80% across pre-coated, co-incubated, and preformed biofilm conditions.

Lactobacillus plantarum in vivo: Valdéz and colleagues (Clinical Microbiology and Infection, 2005) showed L. plantarum inhibited P. aeruginosa colonization in infected burn wounds in animals, with improved tissue repair and enhanced phagocytosis. This is a topical burn wound model, not a gut model.

L. rhamnosus GG: Bianchi and colleagues (International Journal of Molecular Sciences, 2024) showed L. rhamnosus culture filtrates killed P. aeruginosa persister cells — including those surviving high-dose tobramycin and ciprofloxacin — in artificial sputum medium. This is a cystic fibrosis lung model using cell-free filtrates, not oral probiotics in the gut.

⚠ The Mechanism Is Mostly Just pH

Chappell and Nair (npj Biofilms and Microbiomes, 2020) characterized how L. plantarum and L. rhamnosus GG inhibit P. aeruginosa and found the activity was dependent on the low pH generated during culture — the inhibitory effect was abolished when the supernatant was buffered to neutral pH.

This matters enormously. The colon is buffered and near-neutral. An in vitro effect that disappears at neutral pH is unlikely to reproduce in the large intestine. The impressive 85% biofilm degradation in that paper came from genetically engineered lactobacilli secreting a pathogen-derived enzyme (PelAh) — not from any commercially available probiotic.

The Human Trial: More Modest Than Usually Reported

Forestier and colleagues (Critical Care, 2008) conducted the only randomized, double-blind, placebo-controlled trial of a probiotic against P. aeruginosa — 102 probiotic and 106 placebo ICU patients receiving Lactobacillus casei rhamnosus Lcr35.

The result is often cited as showing prevention of Pseudomonas infection. It did not. Ventilator-associated pneumonia due to P. aeruginosa occurred in 2.9% of the probiotic group versus 7.5% of placebo — a difference that was not statistically significant. What the trial showed was a delay in respiratory tract colonization (adjusted hazard ratio 3.2 for absence of probiotic, 95% CI 1.1–9.1). The authors themselves cautioned against generalizing, noting it was a single strain in a single mixed ICU. It was also a respiratory outcome, not a gut eradication outcome.

The Safety Signal Integrative Sources Rarely Mention

🚨 Probiotics Worsened Gut-Derived Pseudomonas Sepsis in an Animal Model

Huang FC and Huang SC (Biomedicines, 2024) — the same research group that produced the favorable in vitro IL-8 / human beta-defensin-2 findings for LGG and Bifidobacterium longum — tested those same two probiotics in vivo in mice with chemotherapy-induced, gut-derived P. aeruginosa sepsis.

The probiotics made it worse. LGG and B. longum amplified inflammatory gene expression, increased colitis severity on histology, DECREASED antimicrobial peptide expression, REDUCED tight junction protein staining (zonulin, claudin-2), and INCREASED bacterial translocation to the liver, spleen, and bloodstream.

The authors' own words: they were "astonished," and concluded that "we must be prudent when using probiotics in mice receiving chemotherapy complicated with gut-derived sepsis."

This is an animal model and should not be over-extrapolated. But it is a direct in vivo test of the exact organisms, the exact probiotics, and the exact clinical scenario — immunocompromised host with gut-derived Pseudomonas — in which integrative practitioners are most tempted to intervene. The in vitro benefit did not survive contact with a living immunocompromised host.

This finding is consistent with a broader and long-standing concern: probiotics in critically ill and immunocompromised populations have an uneven safety record. The PROPATRIA trial in severe acute pancreatitis famously showed increased mortality in the probiotic arm. Lactobacillus and Saccharomyces bacteremia and fungemia are documented, particularly in patients with central venous catheters or compromised gut barriers.

What This Means for Practice

For immunocompetent outpatients with incidental Pseudomonas on stool testing: There is no evidence that probiotics eradicate GI Pseudomonas, and none is needed, because there is no evidence that eradication is warranted. Probiotics may reasonably be used for general dysbiosis, symptom management, and post-antibiotic recovery — indications for which they have far better evidence — without any claim that they are targeting Pseudomonas specifically. This is an honest and defensible position.

For immunocompromised clients, clients on chemotherapy, or clients with a compromised gut barrier: Given the Huang and Huang findings, caution is warranted, and reflexive probiotic supplementation is not appropriate. This population is precisely where the theoretical benefit is most appealing and where the available in vivo evidence points toward harm. Decisions here should be individualized, made in coordination with the treating oncology or infectious disease team, and should not be driven by in vitro data.

Saccharomyces boulardii: Frequently recommended on the grounds that, as a yeast, it survives concurrent antibacterial therapy. That is true, and its evidence base for antibiotic-associated diarrhea and barrier support is genuinely strong (Huang et al., Gut Microbes, 2025; Kelesidis and Pothoulakis, 2012). But its commonly cited direct anti-Pseudomonas activity traces to a single old observation about inhibiting growth in an enteral feeding solution, which I could not verify to a primary source. S. boulardii is reasonable as an adjunct for antibiotic-associated diarrhea and microbiome preservation. It should not be presented as an anti-Pseudomonas agent. It also carries a documented fungemia risk in immunocompromised clients and those with central lines.

Supportive Measures With Better Evidence

The interventions with the most defensible rationale in GI Pseudomonas dysbiosis are the ones that address upstream drivers rather than attempting eradication.

Restore gastric acid. Hypochlorhydria is a well-established risk factor for enteric pathogen colonization. Evaluate and, where clinically appropriate, deprescribe unnecessary PPIs. This is likely the single highest-yield intervention available and it is frequently overlooked.

Antibiotic stewardship. Prior broad-spectrum antibiotic exposure is the dominant modifiable risk factor. Not prescribing an unnecessary antibiotic prevents more Pseudomonas colonization than any supplement will treat.

Diet. Low-FODMAP and low-histamine approaches where SIBO/IBS or histamine intolerance overlap; adequate fermentable fiber to support short-chain fatty acid production and colonization resistance.

Address the actual symptom burden. In most outpatients, the Pseudomonas is an incidental finding and the symptoms have another cause. Chasing the organism can delay the correct diagnosis.

Evidence Grading

Established: Conventional antibiotic management of symptomatic Pseudomonas enteritis/colitis. The pathophysiology of P. aeruginosa biofilm formation, quorum sensing, efflux, and persistence. The role of hypochlorhydria and prior antibiotics as risk factors. That asymptomatic colonization in immunocompetent hosts should not be treated.

Reasonably supported (in vitro): Anti-Pseudomonas activity of oregano oil, allicin (anti-virulence), juglone, and berberine (as an efflux inhibitor). Anti-Pseudomonas activity of Lactobacillus cell-free supernatants — with the caveat that this is substantially a pH effect.

Weak or unestablished: That any of the above translates to eradication of Pseudomonas from the human gut at achievable oral doses. This is the crux, and it is not established for a single agent discussed in this article. The Biocidin biofilm study's own authors say the effective concentrations exceed what is achievable in the gut.

Evidence pointing the other way: Probiotic supplementation (LGG, B. longum) worsened outcomes in an in vivo model of gut-derived Pseudomonas sepsis in immunocompromised mice.

Not evidence at all: Unpublished manufacturer reports, uncontrolled clinic case series without accessible methods, and in vitro findings from gram-positive organisms extrapolated to gram-negatives.

Bottom Line

Most GI Pseudomonas found on outpatient stool testing in immunocompetent clients is incidental and should not be treated. The strongest available intervention is often restraint, plus correction of upstream risk factors — particularly unnecessary PPI and antibiotic use.

When treatment is genuinely indicated — symptomatic enteritis/colitis, or an immunocompromised host with a documented reservoir — susceptibility-guided antibiotics are the standard of care, and integrative measures are adjunctive at best.

The botanical evidence is mechanistically genuine and in vitro robust for several ingredients, most convincingly oregano oil. But the concentrations that work in a microtiter plate are not concentrations achievable in a human colon after an oral dose, and the authors of the best study on the leading commercial formulation say so explicitly. Clinicians who use these products should do so with clear eyes about what is and is not established, and should disclose that the pivotal biofilm study was funded and co-written by the manufacturer.

The probiotic evidence is weaker than commonly presented, is substantially a pH artifact in vitro, failed to reach significance in the only human RCT, and — in the one in vivo model that tested the exact clinical scenario of concern — pointed toward harm in immunocompromised hosts. Probiotics remain reasonable for general dysbiosis and post-antibiotic recovery. They should not be marketed to clients as an anti-Pseudomonas therapy, and they warrant real caution in immunocompromised and oncology populations.

Integrative medicine is at its best when it is more rigorous than the alternative, not less. On this particular question, rigor means acknowledging that the honest answer to "how do I treat GI Pseudomonas naturally?" is frequently: you probably shouldn't be treating it at all — and if you should, botanicals and probiotics are not yet shown to do it.

References

All references below were individually verified against the primary source. Claims that could not be verified to a primary source have been removed from the text.

1. Mundanchira AV, Wong A, Klos-Maki K, Strand J, Marques CNH. Activity of Biocidin® against microbial biofilms. Frontiers in Antibiotics. 2026;4:1692653. doi:10.3389/frabi.2025.1692653. [Funded by Biocidin Botanicals; two authors are company employees; funder involved in manuscript writing and decision to publish.]

2. Min M, Nadora D, Chakkalakal M, Afzal N, Subramanyam C, Gahoonia N, Pan A, Thacker S, Nong Y, Chambers CJ, Sivamani RK. An oral botanical supplement improves small intestinal bacterial overgrowth (SIBO) and facial redness: results of an open-label clinical study. Nutrients. 2024;16(18):3149. doi:10.3390/nu16183149.

3. Lu M, Dai T, Murray CK, Wu MX. Bactericidal property of oregano oil against multidrug-resistant clinical isolates. Frontiers in Microbiology. 2018;9:2329. doi:10.3389/fmicb.2018.02329. [Corrigendum: Front Microbiol. 2021;12:713573.]

4. Morita Y, Nakashima K, Nishino K, Kotani K, Tomida J, Inoue M, Kawamura Y. Berberine is a novel type efflux inhibitor which attenuates the MexXY-mediated aminoglycoside resistance in Pseudomonas aeruginosa. Frontiers in Microbiology. 2016;7:1223. doi:10.3389/fmicb.2016.01223.

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6. Junio HA, Sy-Cordero AA, Ettefagh KA, Burns JT, Micko KT, Graf TN, Richter SJ, Cannon RE, Oberlies NH, Cech NB. Synergy-directed fractionation of botanical medicines: a case study with goldenseal (Hydrastis canadensis). Journal of Natural Products. 2011;74(7):1621–1629. [Synergy demonstrated against S. aureus / NorA pump — not P. aeruginosa.]

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8. Xu Z, Zhang H, Yu H, Dai Q, Xiong J, Sheng H, Qiu J, Jiang L, Peng J, He X, Xin R, Li D, Zhang K. Allicin inhibits Pseudomonas aeruginosa virulence by suppressing the rhl and pqs quorum-sensing systems. Canadian Journal of Microbiology. 2019;65(8):563–574. doi:10.1139/cjm-2019-0055.

9. Lihua L, Jianhuit W, Jialini Y, Yayin L, Guanxin L. Effects of allicin on the formation of Pseudomonas aeruginosa biofilm and the production of quorum-sensing controlled virulence factors. Polish Journal of Microbiology. 2013;62(3):243–251.

10. Harjai K, Kumar R, Singh S. Garlic blocks quorum sensing and attenuates the virulence of Pseudomonas aeruginosa. FEMS Immunology & Medical Microbiology. 2010;58(2):161–168. doi:10.1111/j.1574-695X.2009.00614.x.

11. Bjarnsholt T, Jensen PØ, Rasmussen TB, Christophersen L, Calum H, Hentzer M, et al. Garlic blocks quorum sensing and promotes rapid clearing of pulmonary Pseudomonas aeruginosa infections. Microbiology. 2005;151:3873–3880. doi:10.1099/mic.0.27955-0.

12. Juglone inactivates Pseudomonas aeruginosa through cell membrane damage, biofilm blockage, and inhibition of gene expression. Molecules. 2021;26(19):5854. doi:10.3390/molecules26195854.

13. Drumond MM, Tapia-Costa AP, Neumann E, Nunes ÁC, Barbosa JW, Kassuha DE, Mancha-Agresti P. Cell-free supernatant of probiotic bacteria exerted antibiofilm and antibacterial activities against Pseudomonas aeruginosa: a novel biotic therapy. Frontiers in Pharmacology. 2023;14:1152588. doi:10.3389/fphar.2023.1152588.

14. Chappell TC, Nair NU. Engineered lactobacilli display anti-biofilm and growth suppressing activities against Pseudomonas aeruginosa. npj Biofilms and Microbiomes. 2020;6:48. doi:10.1038/s41522-020-00156-6. [Wild-type LAB activity was pH-dependent; 85% biofilm degradation required engineered strains.]

15. Valdéz JC, Peral MC, Rachid M, Santana M, Perdigón G. Interference of Lactobacillus plantarum with Pseudomonas aeruginosa in vitro and in infected burns: the potential use of probiotics in wound treatment. Clinical Microbiology and Infection. 2005;11(6):472–479.

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17. Forestier C, Guelon D, Cluytens V, Gillart T, Sirot J, De Champs C. Oral probiotic and prevention of Pseudomonas aeruginosa infections: a randomized, double-blind, placebo-controlled pilot study in intensive care unit patients. Critical Care. 2008;12(3):R69. doi:10.1186/cc6907. [Reduction in VAP was not statistically significant; the finding was delayed respiratory colonization.]

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19. Huang FC, Huang SC. The hazards of probiotics on gut-derived Pseudomonas aeruginosa sepsis in mice undergoing chemotherapy. Biomedicines. 2024;12(2):253. doi:10.3390/biomedicines12020253. [LGG and B. longum EXACERBATED sepsis and increased bacterial translocation.]

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21. Kelesidis T, Pothoulakis C. Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders. Therapeutic Advances in Gastroenterology. 2012;5(2):111–125.

22. Karvonen K, Gilbert L. Effective killing of Borrelia burgdorferi in vitro with novel herbal compounds. General Medicine Open. 2019;2(6).

About Dr. Kim

Dr. Yoon Hang "John" Kim is board-certified in Preventive Medicine and Integrative & Functional Medicine, with over 20 years of clinical experience. He completed fellowship training at the University of Arizona under Dr. Andrew Weil (Osher Fellow) and holds additional certifications in preventive medicine, medical acupuncture, and integrative and holistic medicine. He specializes in low dose naltrexone (LDN), autoimmune conditions, chronic pain, integrative oncology, fibromyalgia, chronic fatigue syndrome, mast cell activation syndrome (MCAS), and mold toxicity. He is the author of three books and over 20 articles.

Professional: www.yoonhangkim.com  | 

Clinical: www.directintegrativecare.com