Eucalyptus — Antimicrobial & Wound Care

Long before modern microbiology gave us a name for Staphylococcus aureus or MRSA, Australian Aboriginal peoples were applying the sticky red kino resin from eucalyptus trees to cuts, burns, and sores — an effective wound antiseptic with tens of thousands of years of empirical use. Modern in-vitro work has demonstrated broad-spectrum antibacterial activity for Eucalyptus globulus essential oil against both Gram-positive and Gram-negative pathogens, including methicillin-resistant Staphylococcus aureus (MRSA) at minimum inhibitory concentrations of 0.125–1.0% v/v, plus key respiratory pathogens (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis) and oral biofilm organisms (Streptococcus mutans, Porphyromonas gingivalis, Fusobacterium nucleatum). The antimicrobial mechanism is multi-target — cineole, alpha-pinene, limonene, p-cymene, and globulol all integrate into bacterial cell membranes, disrupting the proton motive force and quorum-sensing biofilm signals — which is why bacteria struggle to develop resistance to essential oils the way they do to single-compound antibiotics. This page walks through the in-vitro evidence, the dental and oral applications (eucalyptol is a Listerine active ingredient), the Aboriginal kino tradition, the surgical antiseptic history dating to Joseph Lister, and the modern wound-dressing research.

Table of Contents

1. Australian Aboriginal Kino Tradition
2. Multi-Target Antibacterial Mechanism
3. MRSA and Antibiotic-Resistant Pathogens
4. Activity Across Gram-Positive and Gram-Negative
5. Biofilm and Quorum-Sensing Disruption
6. Oral and Dental Antimicrobial Use (Listerine)
7. Wound Care and Topical Antiseptic
8. Lister and the Surgical Antiseptic Era
9. Synergy with Conventional Antibiotics
10. Preparations and Topical Dilution
11. Cautions
12. Key Research Papers
13. Connections

Australian Aboriginal Kino Tradition

The earliest documented medicinal use of eucalyptus is in Australian Aboriginal pharmacopoeia, where the genus has played a central role for tens of thousands of years — predating any written medical tradition by a wide margin. The signature preparation is kino, the dark red, astringent gum-resin that exudes from wounds in the bark of certain eucalyptus species (particularly Eucalyptus citriodora, E. resinifera, and E. camaldulensis). Kino is rich in polyphenolic tannins, kinotannic acid, and pyrocatechin — compounds that astringe tissues, precipitate bacterial surface proteins, and form a temporary protective barrier over wounds.

Aboriginal healers applied freshly harvested kino directly to cuts, burns, abscesses, ulcers, sores, and the umbilical stumps of newborns. The astringent precipitation of mucus and surface protein creates a localized antimicrobial environment, and the tannins themselves have direct bacteriostatic activity against many skin and wound pathogens. Aboriginal women across many Australian language groups also chewed kino for sore throats and chewed eucalyptus leaves for the same purpose, recognizing the same active properties that we now call essential-oil terpenoids.

Eucalyptus leaves themselves were processed in several ways: chewed for mouth and throat infections, made into infusions for fevers and respiratory congestion, pounded into pastes and applied to wounds, and burned in smoking ceremonies that simultaneously purified living spaces of biting insects and respiratory pathogens. The smoke ceremonies, sometimes carried out at the entrance to dwellings during epidemic illness, have a clear modern parallel in air-disinfection research: vaporized eucalyptus essential oil at concentrations of 0.05–0.1 mL per cubic metre of air produces 40–70% reductions in airborne bacterial colony counts after sixty minutes.

The pharmacological sophistication is striking. Aboriginal communities distinguished among the hundreds of Eucalyptus species and selected specific ones for specific purposes — species rich in kino resin for wound work, species rich in volatile oil for respiratory steam ceremonies, and species with particular taste and bitterness for digestive complaints. This was not random foraging; it was a knowledge system passed orally across generations that mapped chemotype to clinical effect long before any chemist isolated a single terpene.

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Multi-Target Antibacterial Mechanism

The antibacterial potency of Eucalyptus globulus essential oil derives from a complex terpenoid mixture, with each component contributing through distinct biochemical mechanisms. Unlike single-target pharmaceutical antibiotics — penicillin binds penicillin-binding proteins; ciprofloxacin inhibits DNA gyrase — eucalyptus attacks bacterial cells on several fronts at once.

• 1,8-Cineole (eucalyptol). The dominant compound at 60–90% of E. globulus oil. Lipophilic ether that partitions into the bacterial phospholipid bilayer, expanding membrane volume, increasing permeability, and disrupting membrane-embedded protein function. Independent bactericidal activity in standard broth-microdilution assays.
• Alpha-pinene. 2–10% of the oil. Bicyclic monoterpene with independent antibacterial action against both Gram-positive and Gram-negative bacteria, and an important second function as a membrane-permeabilizing agent that enhances penetration of cineole and other co-occurring actives.
• Limonene. 1–8%. Cyclic monoterpene that disrupts membrane integrity and has been shown to enhance the activity of conventional antibiotics when used in combination — particularly relevant to the antibiotic-synergy work discussed below.
• p-Cymene. 1–5%. Aromatic monoterpene with modest direct antibacterial activity but a strong membrane-targeting role. p-Cymene inserts into the phospholipid bilayer, expanding and destabilizing it, opening the membrane to the more potent actives.
• Globulol. 0.5–4%. A sesquiterpene alcohol largely unique to eucalyptus species. Lower volatility than the monoterpenes, so globulol persists on surfaces and in tissues longer, providing sustained antibacterial activity. Particular potency against Staphylococcus aureus.

The mechanistic upshot: bacteria exposed to eucalyptus essential oil suffer simultaneous membrane permeabilization, leakage of ions and small molecules, collapse of the transmembrane proton gradient (which powers ATP synthesis and most active transport), and disruption of membrane-anchored signaling proteins. Electron microscopy of eucalyptus-treated bacteria shows visible morphological damage: membrane blebbing, cytoplasmic condensation, and at higher doses complete cell lysis.

Because each component compound hits a slightly different molecular target, evolving resistance requires simultaneous mutations in multiple bacterial systems — statistically vanishingly unlikely on the timescales over which antibiotic resistance normally develops. This is the same logic behind combination antiretroviral therapy for HIV: three drugs hitting three different targets defeat any single-mutation escape.

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MRSA and Antibiotic-Resistant Pathogens

The single most striking finding in modern eucalyptus antimicrobial research is its retained activity against methicillin-resistant Staphylococcus aureus (MRSA). MRSA is defined by resistance to the beta-lactam antibiotic class (penicillins, cephalosporins, carbapenems) via the mecA-encoded modified penicillin-binding protein PBP2a. Because eucalyptus oil does not act on penicillin-binding proteins at all — it disrupts the membrane upstream of any wall-synthesis machinery — the resistance mechanism is completely irrelevant to its activity.

Reported minimum inhibitory concentration (MIC) values for E. globulus oil against MRSA clinical isolates fall in the 0.125–1.0% (v/v) range, depending on the specific oil chemotype, the MRSA strain, and the assay method. Minimum bactericidal concentration (MBC) is typically within one to two dilutions of MIC, indicating rapid killing rather than mere growth arrest. These concentrations are easily achievable in topical formulations and on a per-volume basis are actually competitive with chlorhexidine, the gold-standard hospital antiseptic.

Eucalyptus oil retains activity against other resistant pathogens of clinical importance:

• Vancomycin-resistant Enterococcus (VRE) — inhibited at 1–5% in surface-disinfection studies
• Extended-spectrum beta-lactamase (ESBL)-producing E. coli — inhibited at concentrations similar to non-ESBL strains
• Carbapenem-resistant Pseudomonas aeruginosa — moderate direct activity, strong biofilm-disrupting activity
• Multidrug-resistant Acinetobacter baumannii — reported activity in in-vitro panels

The clinical translation is not that essential oils replace IV vancomycin for systemic MRSA bacteremia — they cannot achieve therapeutic plasma levels and are not formulated for parenteral use. The translation is that for topical and surface applications — wound care, skin colonization eradication, hospital surface disinfection, dental biofilm management — eucalyptus oil is a viable adjunct that does not select for the same resistance phenotypes as conventional antibiotic agents.

For more on staphylococcal infection, see our Staphylococcus aureus page.

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Activity Across Gram-Positive and Gram-Negative

Gram-positive bacteria (single thick peptidoglycan cell wall, single plasma membrane) are generally more susceptible to essential oils than Gram-negative bacteria (additional outer membrane with lipopolysaccharide barrier). Eucalyptus oil follows that general pattern but retains useful activity across both groups.

Gram-positive susceptibility (typical MICs 0.125–1% v/v):

• Staphylococcus aureus (including MRSA) — the most-studied target
• Streptococcus pneumoniae — community-acquired pneumonia, otitis media, meningitis pathogen
• Streptococcus pyogenes — group A streptococcus, strep throat and skin infection
• Streptococcus mutans — primary dental-caries pathogen
• Enterococcus faecalis and E. faecium — including VRE strains
• Listeria monocytogenes — foodborne pathogen
• Bacillus cereus, B. subtilis — environmental and foodborne sporeformers

Gram-negative susceptibility (typical MICs 1–5% v/v):

• Haemophilus influenzae — respiratory pathogen, particularly susceptible due to mucoid environment
• Moraxella catarrhalis — respiratory pathogen, among the largest inhibition zones in standardized testing
• Escherichia coli (including ESBL) — UTI, GI infection
• Pseudomonas aeruginosa — opportunistic, biofilm-forming
• Klebsiella pneumoniae — nosocomial pneumonia, UTI
• Salmonella species — foodborne enteric pathogens

For more on respiratory bacterial infection, see our Pneumonia page; for urinary infection, see Urinary Tract Infections.

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Biofilm and Quorum-Sensing Disruption

The greatest clinical advantage of eucalyptus oil over many conventional antibiotics is its activity against bacterial biofilms. Biofilms are structured communities of bacteria embedded in a self-produced extracellular matrix of polysaccharides, proteins, and DNA. Biofilm-embedded bacteria are 100 to 1,000 times more resistant to conventional antibiotics than the same species in planktonic (free-floating) form. Many chronic infections — chronic sinusitis, otitis media with effusion, chronic prostatitis, diabetic foot ulcers, venous leg ulcers, indwelling-catheter colonization, prosthetic-joint infection — are biofilm-driven and notoriously resistant to systemic antibiotic therapy.

Eucalyptus oil disrupts biofilms through two distinct mechanisms:

• Quorum-sensing interference. Bacteria coordinate biofilm formation, virulence-factor expression, and stress responses through quorum-sensing — the secretion and detection of small signaling molecules (acyl-homoserine-lactones in Gram-negatives, autoinducing peptides in Gram-positives). Cineole has been shown to interfere with both AHL- and AIP-class quorum-sensing systems, preventing bacteria from coordinating the cooperative behaviors needed for biofilm establishment.
• Matrix penetration. Once a biofilm is established, the lipophilic terpenoid mixture in eucalyptus oil penetrates the extracellular matrix where many hydrophilic antibiotics cannot. The dispersed cineole and globulol then act on the resident bacteria, exposing them to immune clearance and any concurrently administered systemic antibiotic.

The dental application is the most evidence-supported real-world example: dental plaque is a polymicrobial biofilm, and the essential-oil mouthwashes (most prominently Listerine, which combines eucalyptol with thymol, menthol, and methyl salicylate) demonstrably reduce plaque mass, gingival inflammation, and total oral bacterial counts compared to control rinses. The mechanism is the same biofilm-matrix-penetration logic operating on a smaller scale.

The chronic-wound application is less clinically developed but actively studied. In-vitro work has shown eucalyptus oil penetrates and disrupts S. aureus and P. aeruginosa biofilm cultures grown on wound-relevant substrates. Clinical case series have reported improved healing outcomes when eucalyptus-based dressings are part of a comprehensive wound-care protocol, though high-quality randomized controlled trials remain limited.

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Oral and Dental Antimicrobial Use (Listerine)

The most universally familiar antimicrobial application of eucalyptol is the mouthwash. Eucalyptol is one of the four active essential-oil compounds in Listerine, alongside thymol (from thyme), menthol (from mint), and methyl salicylate. Together these four actives at concentrations of approximately 0.092% (eucalyptol), 0.064% (thymol), 0.042% (menthol), and 0.060% (methyl salicylate) produce the characteristic flavor and the documented oral-antimicrobial effect of Listerine and its generic equivalents.

Clinical-trial evidence is extensive. Six-month and twelve-month controlled trials comparing essential-oil mouthwash to placebo or to mechanical-hygiene-only controls have shown:

• 20–35% reduction in plaque accumulation
• 30–45% reduction in gingivitis severity scores
• 40–60% reduction in salivary bacterial counts
• Significant reduction in volatile sulfur compound production (halitosis)

Comparison to chlorhexidine, the prescription gold-standard mouthwash, is the more interesting trial design. Chlorhexidine is more potent on a per-rinse basis for short-term plaque suppression, but it has two real-world disadvantages that eucalyptol-containing mouthwashes do not share: it causes brown tooth staining with chronic use, and it produces a temporary taste disturbance that many patients find intolerable. For long-term daily use, the essential-oil class is generally preferred for adherence reasons.

Specific oral pathogens hit by eucalyptol:

• Streptococcus mutans — primary dental-caries bacterium
• Porphyromonas gingivalis — key periodontal pathogen, marker of chronic gingivitis-to-periodontitis progression
• Fusobacterium nucleatum — bridge organism in oral biofilm maturation
• Aggregatibacter actinomycetemcomitans — associated with aggressive periodontitis
• Tannerella forsythia and Treponema denticola — periodontal red-complex organisms
• Prevotella intermedia — halitosis-producing

The volatile-sulfur-compound producers (P. gingivalis, P. intermedia, T. denticola) are the primary contributors to halitosis, and reduction in their populations explains why essential-oil mouthwash produces sustained breath improvement beyond the immediate masking effect of the menthol.

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Wound Care and Topical Antiseptic

Topical eucalyptus oil at appropriate dilution has documented antibacterial activity against wound-relevant pathogens (S. aureus, P. aeruginosa, Acinetobacter baumannii) and combined antibacterial-plus-anti-inflammatory effects that distinguish it from purely antiseptic agents.

Burns. Burn wounds are highly susceptible to bacterial colonization, particularly by S. aureus, P. aeruginosa, and A. baumannii. Animal burn-wound model studies have shown that topical eucalyptus oil at 2–5% dilution in a carrier reduces wound bacterial counts by 2–3 log units versus untreated controls and promotes faster epithelialization. The anti-inflammatory action reduces excessive inflammation in the burn bed, which can impede healing.

Chronic ulcers. Diabetic foot ulcers and venous leg ulcers represent a major clinical challenge due to persistent bacterial biofilm infection. The biofilm-disrupting properties of eucalyptus oil discussed above are particularly relevant. Eucalyptus has been formulated into hydrogels, nanofiber mats, chitosan films, and alginate dressings for sustained-release antibacterial delivery; in-vitro testing of these advanced dressings has shown inhibition of wound-relevant pathogen growth alongside maintained cytocompatibility with human fibroblasts and keratinocytes.

Insect bites and minor wounds. Diluted eucalyptus oil applied topically to insect bites provides both antibacterial protection against secondary infection and a local cooling-analgesic effect via TRPM8 activation (covered on the Pain & Joint Relief page). Aboriginal traditional use of kino on cuts and abrasions falls into the same category.

Important practical guidance. Undiluted eucalyptus essential oil is too irritating for direct application to a wound — dilute to 1–2% in a carrier oil (jojoba, coconut, sweet almond) or use a commercial preparation already formulated for topical use. For substantial burns, deep wounds, or chronic ulcers, consult a healthcare provider before topical application.

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Lister and the Surgical Antiseptic Era

Joseph Lister's 1867 introduction of antiseptic surgery using carbolic acid (phenol) is widely credited as the foundation of modern surgical practice — the breakthrough that turned operating theaters from charnel-house mortality factories into the survivable-procedure environments we expect today. What is less remembered is that eucalyptus oil rapidly joined carbolic acid as an alternative surgical antiseptic, particularly across the British Empire's tropical and Antipodean territories.

The Australian surgeon-naturalist Joseph Bosisto began commercial distillation of E. globulus oil at Dandenong (Victoria) in 1854, supplying medical-grade product to military and civilian hospitals across Australia and from there to Britain. By the 1880s, eucalyptus oil appeared in the British Pharmacopoeia and was listed in multiple colonial pharmacopoeias as an approved wound antiseptic. Australian military surgeons used eucalyptus-based antiseptic preparations extensively during the Boer War and World War I, with favorable wound-healing outcomes reported in dispatches.

Eucalyptus oil's advantage over carbolic acid was twofold: significantly less tissue toxicity at antimicrobial concentrations, and a more tolerable scent for both patient and surgical staff. Carbolic acid at the concentrations needed for reliable antisepsis caused chemical burns, cleaved skin proteins, and was systemically toxic if absorbed. Eucalyptus oil, while not bacteria-killing on the same per-volume basis as carbolic acid, produced sufficient bactericidal effect at concentrations the surrounding tissues tolerated well.

The eucalyptus-as-surgical-antiseptic era waned with the introduction of synthetic antiseptics (hexachlorophene, povidone-iodine, chlorhexidine) in the mid-20th century, which were standardizable to a precision impossible with natural essential oils. But the historical reputation cemented eucalyptus oil's position in the hospital pharmacy and in OTC topical preparations through to the present day.

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Synergy with Conventional Antibiotics

One of the most clinically promising areas of current eucalyptus research is the demonstration of synergistic interaction with conventional antibiotic drugs. Synergism — defined as a combined effect exceeding the sum of individual effects — allows lower doses of each agent to achieve equivalent or superior antibacterial activity. This is measured by the fractional inhibitory concentration index (FICI); FICI values below 0.5 indicate true synergism.

Documented synergistic combinations include:

• Eucalyptus oil + ampicillin against MRSA clinical isolates that are fully resistant to ampicillin alone. The proposed mechanism: cineole permeabilizes the bacterial membrane, increasing intracellular ampicillin concentration and allowing the antibiotic to reach its penicillin-binding-protein target despite the modified PBP2a.
• Eucalyptus oil + gentamicin against resistant Pseudomonas aeruginosa. Eucalyptus disrupts efflux-pump function, reducing the pseudomonad's ability to actively pump out the aminoglycoside.
• Eucalyptus oil + ciprofloxacin against resistant E. coli. Similar efflux-pump-disruption mechanism.
• Eucalyptus oil + chlorhexidine against biofilm-embedded oral pathogens. Reported in the Hendry 2009 JAC study.
• Eucalyptus oil + tea tree oil (terpinen-4-ol). Two membrane-disrupting essential oils together produce synergistic activity against MRSA with FICI values of 0.25–0.50.
• Eucalyptus oil + thyme oil (thymol, carvacrol). Phenolic-membrane attack from thyme plus terpenoid-ether attack from cineole produce 2–4-fold faster kill kinetics than either alone.

These synergistic combinations are an active area of research, with potential to restore the clinical effectiveness of older antibiotics against resistant pathogens. Sub-inhibitory concentrations of eucalyptus oil — below the level that would itself kill bacteria — appear to be enough to disable resistance mechanisms and resensitize bacteria to standard antibiotic therapy.

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Preparations and Topical Dilution

Topical dilution rules of thumb:

• General topical use (intact skin): 2–3% eucalyptus essential oil in carrier oil. Approximately 12–18 drops essential oil per 30 mL (1 oz) carrier.
• Wound care: 1–2% dilution near (not directly into) open wounds.
• Face wash or gentle skin antiseptic: 0.5–1% dilution.
• Oral rinse (homemade): 1–2 drops in a small glass of warm water; swish 30 seconds; do not swallow.

Commercial preparations:

• Listerine and generic essential-oil mouthwashes — the most widely-used delivery vehicle for eucalyptol antimicrobial activity. Use as directed on label (typically 20 mL twice daily).
• Eucalyptus-based wound salves — commercial preparations at 2–5% in beeswax or shea butter base; appropriate for minor cuts, scrapes, and abrasions on intact-margin wounds.
• Surgical-grade antiseptic preparations — still used in some traditional Australian medical practices and in tropical-medicine settings; check labeling for concentration.
• Dental gel adjuncts — some toothpaste and gum-care products contain eucalyptol at low percentage as adjunctive antimicrobial.

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Cautions

• Never apply undiluted essential oil to mucous membranes — including the mouth, nostrils, eyes, genital mucosa, or directly into an open wound. Cineole at full strength causes chemical burns.
• Never swallow undiluted eucalyptus oil. Ingestion of 3.5 mL has been fatal in pediatric case reports; 5 mL has caused serious adult toxicity. Mouthwash use involves swishing and spitting; do not ingest.
• Children under six. Eucalyptus essential oil should not be applied to the face, chest, or near the nose of children under six. Mentholated rubs near the airway can trigger laryngospasm and bronchospasm.
• Skin sensitivity. Some individuals develop contact dermatitis to eucalyptus oil. Perform a patch test on a small skin area 24 hours before broader use. Stop immediately if redness, itching, burning, or rash develops.
• Not a substitute for systemic antibiotics. Topical eucalyptus oil is appropriate adjunctive therapy for minor wound infection and oral biofilm management. It is not a substitute for IV vancomycin, oral cephalexin, or any other systemic antibiotic when one is indicated for cellulitis, bacteremia, deep tissue infection, or other serious bacterial syndromes.
• Drug interactions. Cineole induces CYP3A4 and CYP2B6, potentially affecting metabolism of warfarin, cyclosporine, tacrolimus, carbamazepine, phenytoin, and many statins. Confirm with pharmacist before regular use.
• Pregnancy. Topical eucalyptus at proper dilution is generally considered low-risk in pregnancy. Avoid concentrated essential-oil exposure or any oral cineole product.

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Key Research Papers

1. Mulyaningsih S, Sporer F, Zimmermann S, Reichling J, Wink M (2010). Synergistic properties of the terpenoids aromadendrene and 1,8-cineole from the essential oil of Eucalyptus globulus against antibiotic-susceptible and antibiotic-resistant pathogens. Phytomedicine 17(13):1061–1066. — PubMed
2. Hendry ER, Worthington T, Conway BR, Lambert PA (2009). Antimicrobial efficacy of eucalyptus oil and 1,8-cineole alone and in combination with chlorhexidine digluconate against microorganisms grown in planktonic and biofilm cultures. Journal of Antimicrobial Chemotherapy 64(6):1219–1225. — PubMed
3. Bachir RG, Benali M (2012). Antibacterial activity of the essential oils from the leaves of Eucalyptus globulus against Escherichia coli and Staphylococcus aureus. Asian Pacific Journal of Tropical Biomedicine 2(9):739–742. — PubMed
4. Cermelli C, Fabio A, Fabio G, Quaglio P (2008). Effect of eucalyptus essential oil on respiratory bacteria and viruses. Current Microbiology 56(1):89–92. — PubMed
5. Elaissi A, Rouis Z, Salem NAB, Mabrouk S, Salem YB, Salah KBH, Aouni M, Farhat F, Chemli R, Harzallah-Skhiri F, Khouja ML (2012). Chemical composition of 8 eucalyptus species' essential oils and the evaluation of their antibacterial, antifungal and antiviral activities. BMC Complementary and Alternative Medicine 12:81. — PubMed
6. Sharafati Chaleshtori R, Rokni N, Rafieian-Kopaei M, Drees F, Salehi E (2013). Antioxidant and antibacterial activity of basil (Ocimum basilicum L.) essential oil in beef burger. Journal of Agricultural Science and Technology 16(5):1109–1117 (eucalyptus comparator). — PubMed
7. Tyagi AK, Malik A (2011). Antimicrobial potential and chemical composition of Eucalyptus globulus oil in liquid and vapour phase against food spoilage microorganisms. Food Chemistry 126(1):228–235. — PubMed
8. Sharma R, Rao R, Kumar S, Mahant S, Khatkar S (2019). Therapeutic potential of citronella essential oil: a review (eucalyptus comparator data). Current Drug Discovery Technologies 16(4):330–339. — PubMed
9. Stoeken JE, Paraskevas S, van der Weijden GA (2007). The long-term effect of a mouthrinse containing essential oils on dental plaque and gingivitis: a systematic review. Journal of Periodontology 78(7):1218–1228. — PubMed
10. DePaola LG, Overholser CD, Meiller TF, Minah GE, Niehaus C (1989). Chemotherapeutic inhibition of supragingival dental plaque and gingivitis development (Listerine essential-oil mouthwash). Journal of Clinical Periodontology 16(5):311–315. — PubMed
11. Sherry E, Boeck H, Warnke PH (2001). Topical application of a new formulation of eucalyptus oil phytochemical clears methicillin-resistant Staphylococcus aureus infection. American Journal of Infection Control 29(5):346. — PubMed
12. Salari MH, Amine G, Shirazi MH, Hafezi R, Mohammadypour M (2006). Antibacterial effects of Eucalyptus globulus leaf extract on pathogenic bacteria isolated from specimens of patients with respiratory tract disorders. Clinical Microbiology and Infection 12(2):194–196. — PubMed
13. Trivedi NA, Hotchandani SC (2004). A study of the antimicrobial activity of oil of Eucalyptus. Indian Journal of Pharmacology 36(2):93–95. — PubMed

PubMed Topic Searches

• PubMed: Eucalyptus and MRSA
• PubMed: Biofilm disruption
• PubMed: Essential-oil mouthwash trials
• PubMed: Wound antiseptic use
• PubMed: Aboriginal kino tradition

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Connections

• Eucalyptus Overview
• Eucalyptus Benefits Hub
• Eucalyptus — Respiratory Health
• Eucalyptus — Pain & Joint
• Eucalyptus — Antifungal
• Tea Tree
• Thyme
• Oregano
• Antibacterial Herbs
• Staphylococcus aureus & MRSA
• Pneumonia
• Sinusitis
• Urinary Tract Infections
• Immune Boosting

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