Honey as an antimicrobial agent against Pseudomonas aeruginosa

isolated from infected wounds

Vishnu Prasad Shenoy1, Mamatha Ballal2, PG Shivananda3, Indira Bairy4

1
Department of Microbiology, Kasturba Medical College, Manipal University, Manipal, India
2
Department of Clinical Microbiology and Immunology, KMC International Center, Manipal,
India
3
Chair Microbiology and Incharge Virology Laboratory, Manipal University, Manipal, India
4
Department of Microbiology, Melaka Manipal Medical College, Manipal Campus Manipal
University, Manipal, India

Abstract

Background: As natural products garner attention in the medical field due to emergence of
antibiotic resistant strains of bacteria, honey is valued for its antibacterial activity. Objective:
Fifty strains of Pseudomonas aeruginosa isolated from infected wounds were evaluated for their
antibacterial action using honey in comparison with different antibiotics and Dettol.
Methodology and Results: All the strains were found to be sensitive to honey at a minimum
inhibitory concentration of 20% in comparison with Dettol at 10% using agar dilution method.
In the second step, the time kill assay was performed on five isolates of P. aeruginosa to
demonstrate the bactericidal activity of honey at different dilutions of honey ranging from 20%
to 100% at regular time intervals. All the isolates of P. aeruginosa tested were killed in 12-24 h
depending on the dilutions of the honey tested. Thus, honey could prevent the growth of P.
aeruginosa even if it was diluted by deionized water by fivefolds in vitro. Honey had almost
uniform bactericidal activity against P. aeruginosa irrespective of their susceptibility to
different classes of antibiotics. Conclusion: Honey which is a natural, non-toxic, and an
inexpensive product has activity against the P. aeruginosa isolated from infected wounds may
make it an alternative topical choice in the treatment of wound infections.

Keywords: Antibacterial activity, Honey, P. aeruginosa

How to cite this article:

Shenoy VP, Ballal M, Shivananda P G, Bairy I. Honey as an antimicrobial agent against
Pseudomonas aeruginosa isolated from infected wounds. J Global Infect Dis 2012;4:102-5

How to cite this URL:

Shenoy VP, Ballal M, Shivananda P G, Bairy I. Honey as an antimicrobial agent against
Pseudomonas aeruginosa isolated from infected wounds. J Global Infect Dis [serial online]
2012 [cited 2018 Nov 27];4:102-5. Available
from: http://www.jgid.org/text.asp?2012/4/2/102/96770
 Introduction

Honey whose medicinal uses date from ancient times has been lately rediscovered as therapy for
wounds. The antimicrobial effect of honey has been reported by a number of workers it is
commonly used as a base for ointments and has very successfully been applied in surgical
dressings for open wounds and burns to avoid septic infections. [1] The current prevalence of
antibiotic-resistant microbial species has led to a re-evaluation of the therapeutic use of ancient
remedies, including honey. [2] Strong solution of honey or sugar and sugar pastes inhibits
microbial growth due to high osmolarity but when used as dressings this action ceases. [3] But
such wounds are rapidly rendered sterile by honey because of its additional antimicrobial
activity. [4],[5] It has been traditionally used in treatment of burn wound infection in rural India
and the study has shown that it is superior to silver sulfadiazine. [6]

Indiscriminate use of antibiotics has led to the emergence of drug-resistant strains which have a
significant impact on patient's morbidity and mortality. [7] To date, there are many publications
on studies performed both in vitro and in vivo on the therapeutic properties of manuka honey,
and have confirmed its activity against a wide range of medically important bacteria. [8] Honey
is produced from many floral sources and its antimicrobial activity varies markedly with its
origin and processing. [9],[10],[11] This variation can be due to difference in the enzymatic action
and in the presence of additional antibacterial components derived from the floral source. [12] As
the potential role for honey as a topical agent to manage surgical site or wound infections is
increasingly acknowledged [13] other honeys need to be assessed and evaluated.

The present study was to evaluate the antimicrobial activity of honey native to India at various
concentrations against Pseudomonas aeruginosa causing wound infection and its comparison
with antibiotics and Dettol.

Materials and Methods

A total of 50 strains of P. aeruginosa isolated from different types of wound infection including
burns wound were used in the study. The isolation and identification of P. aeruginosa was done
using standard methods. [14] The antibiotic-sensitivity patterns of the isolates were studied by
Kirby Bauer's disc diffusion method using commercially available antibiotic discs (Hi-Media
labs, Mumbai India) gentamicin (10 μg), amikacin (30 μg), ceftazidime (30 μg), ciprofloxacin
(5 μg), netillin (30 μg), cefotaxime (30 μg), piperacillin (100 μg), and imipenem (10 μg) as per
the clinical and laboratory standards institute (CLSI) standards.

Antibacterial effect of honey

Agmark grade honey (Dabur India, Capital overseas), a polyfloral honey with yellowish brown
color, was used in the study. It had 100% purity and each 100 g of honey contains 80 g natural
sugars, sodium 17 mg, potassium 138 mg, calcium 13 mg, iron 1.5 mg, and phosphorus 5 mg;
sterilized by ultrafiltration and have the floral source from Himalayas, Nilgiris, and Sunderbans
of India.

The minimum active dilution of honey against P. aeruginosa isolates was determined by agar
dilution methods. [3] Double strength nutrient agar was used for the study, measured out into 10
ml aliquots and autoclaved. To prepare the plates it was melted and maintained at a temperature
of 50 °C water-bath until poured. Solutions of the honey samples (at a concentration of 50%
v/v) were prepared in sterile de-ionized water immediately prior to performing an assay.
Appropriate concentrations of the stock and deionized water (total 10 ml) were dispensed
aseptically into 10 ml sterile double strength nutrient agar before pouring into Petri dish More
Details
es to produce a dilution series (5-25%) from concentrations required in a volume of 20 ml.
The various agar honey mixtures were then poured into triplicate Petri dishes. Antibacterial
action of honey was compared with Dettol, (Reckitt Benckiser India Ltd, Capital Overseas) at a
concentration similar to honey which contains an aromatic chemical compound chloroxylenol
(C 8 H 9 ClO) (4.8% of the total Dettol mixture), which is the key ingredient exhibiting unique
antiseptic property. Subcultures of the P. aeruginosa isolates were grown overnight in 10 ml
peptone water. The turbidity was adjusted to 0.5 Mc Farland and 10 μl of culture was spot
inoculated on to the surface of the medium. The plates were incubated at 37°C for 24 h before
visual assessment of the growth. The tests were performed in triplicates. Control plates of plain
nutrient agar were included in each susceptibility assay to confirm the viability and density of
the cultures. P. aeruginosa american type culture collection (ATCC) strain 27853 was
inoculated on each plate for comparison.

The bactericidal effect of honey was studied by time kill assay. [15] Honey was used undiluted
and at different dilutions. With each experiment saline control of the organism was also used.
Two milliliters each of undiluted and different dilutions of the honey were taken in sterile test
tubes and inoculated with 20 μl of broth culture of the test bacterium in an initial concentration
of approximately 5×10 5 CFU/ml. All the tubes were incubated at 37°C and the viable count of
bacteria in each tube was determined at an interval of 4 h up to 24 h by the surface plate
method. [16] Viable count of bacteria in both test and control tubes at each time interval was
noted by performing plate culture on nutrient agar without honey.

Results

A total of 50 strains of P. aeruginosa isolated from infected wounds were studied over a period
of 2 years. The antibiotic susceptibility patterns of the P. aeruginosa isolates are shown in
[Figure 1], where the y axis indicates the percentage of the isolates susceptible to various
antibiotics plotted on the X axis. Multidrug resistance was a common feature among most of
these isolates 41 (82%) and the remaining 9 (18%) isolates were pan sensitive. Among the
antibiotics tested against P. aeruginosa isolates in this study imipenem 50 (100%) being highly
effective followed by piperacillin 39 (78%), amikacin 38 (76%) netillin 32 (64%), ceftazidime
28 (56%), gentamicin 23 (46%), cefotaxime 23 (46%), and ciprofloxacin 20 (40%),
respectively.
 Figure 1: Percentage of susceptibility pattern to different class of
antibiotics to Pseudomonas aeruginosa isolates used in the study

Click here to view

The effects of honey on all the isolates of P. aeruginosa were studied by the determination of
minimum inhibitory concentration (MIC), indicating the highest dilution of honey in the culture
medium which inhibits the growth of P. aeruginosa isolates. The MIC of all the 50 strains
(100%) to honey was found to be 20%, of which 19 strains (38%) were having an MIC of 15%
including the standard strain of P. aeruginosa ATCC 27853. Honey concentrations ranging
from 5% to 10% were found to be ineffective as shown in [Figure 2]. The Y axis indicates the
number susceptible percentage of isolates to honey and Dettol at various concentrations (5-
25%) plotted on the X axis.

Figure 2: MIC of Pseudomonas aeruginosa isolates towards honey

and Dettol at different concentrations

Click here to view

The time kill assay for the bactericidal effect was tested on five isolates of P. aeruginosa so as
to understand the time required to kill the bacterial population irrespective of their antibiotic
susceptibility patterns as isolates varying in their susceptibility pattern were used. Honey at
concentrations of 20%, 25%, 50% could bring out complete destruction in 24 h, whereas
concentration of honey at 75% and 100% could bring about complete destruction of P.
aeruginosa in 12 h [Table 1]. The lowest concentration of the honey which showed bactericidal
activity was at 20% for all the five isolates tested in time kill assay. The antibacterial activity of
honey was concentration dependent for all the 50 isolates tested at a concentration below 20%
using agar dilution methods [Figure 2]. The antibacterial effect of 50% honey on P. aeruginosa
with number of hours and percentage of survival rate was calculated. The average percentages
of survival rate for five P. aeruginosa isolates after 4 h, 8 h, 12 h, and 24 h were found to be
22.3, 5.2, 1.1, and 0 respectively as shown in [Table 2].
Table 1: Time kill assay of honey against the wound isolates of
Pseudomonas aeruginosa

Click here to view

Table 2: Antibacterial effect of 50% honey on P. aeruginosa wound
isolates

Click here to view

 Discussion

The present study shows the bactericidal activity of honey against P. aeruginosa strains. As
honey is considered as a natural antiseptic in the management of wound infections, its efficacy
was compared with Dettol. It was observed that these organisms were more or less susceptible
to honey and Dettol at 20% and 10% irrespective to their antibiotic sensitivity patterns. Dettol
antiseptic liquid contains chloroxylenol which is proved to kill a wide variety of microbes and is
widely used for cleansing wound. The antibacterial action is due to disruption of the cell
membrane potentials and blocking the production of adenosine triphosphate. [17] The
antibacterial effect of honey was concentration dependent and bactericidal effect was observed
at concentration of 20% or more for P. aeruginosa isolates tested. Since P. aeruginosa are
recalcitrant to antibiotic therapy the ability to inhibit test isolates irrespective of their antibiotic
sensitivity patterns has important clinical applications. [10] This property may make honey useful
in the treatment of drug-resistant infections.

In this study, we found that Indian origin honey have activity against P. aeruginosa wound
isolates comparable to Tualang and Manuka honey as reported in previous studies. [18] Lusby et
al. [19] reported that any honey can have equivalent antibacterial activity against some bacteria
compared with other pharmaceutical honeys, whereas Basson et al. [20] found no such high
antimicrobial activity for honeys native to South Africa. Orla et al. [21] compared the activity of
Ulmo90 and Manuka honey and reported similar activity against the P. aeruginosa at a
concentration of 12.5%, better than the results from our study. Results from these studies
confirm that honeys from different countries and regions may have wide variations in their
antimicrobial activity. It has been shown that honey may have antimicrobial action ranging from
lesser than 3% to 50% and higher concentrations. [22] Honey has been successfully used in the
treatment of surgical wounds, [23],[24] burns wound, [6] and decubitus ulcers. [25] It has also been
shown as a good medium to store skin grafts [26] and honey has antileishmanial effect also. [27]

The mechanisms of antibacterial action of honey remain speculative. Honey may inhibit
bacterial growth due to a number of different mechanisms. High sugar concentration, low pH,
hydrogen peroxide generation, proteinaceous compounds, or other unidentified components
present in the honey may all provide antimicrobial activity. [28] Shrinkage and disruption of the
bacteria may be due to its osmotic effect, low pH, and also due to the presence of antibacterial
substance such as inhibine. [29],[30] Several components may contribute to the non-peroxide
activities of honey, such as the presence of methyl syringate and methylglyoxal, which have
been extensively studied in Leptospermum honeys. [31] Besides its antimicrobial properties,
honey can clear infection in a number of ways in vivo, like boosting the immune system, anti-
inflammatory, and antioxidant activities and via stimulation of cell growth. [32] After reviewing
the literature it has been found that apart from Mulai et al., [33] no other Indian study has been
carried out exclusively on antibacterial activity of honey against P. aeruginosa in vitro. As there
is lack of scientific research and documentation, still the medicinal properties of Indian honeys
remain in the dark. Further studies on human subjects are required in vivo to understand the
efficacy of Indian honeys in eliminating bacteria from wounds. As this study presents the
findings of in vitro antibacterial activity of honey against planktonic bacteria this should not be
related to chronic wound environment where indeed biofilms of P. aeruginosa may be present
and the characteristic of bacteria can change; hence, future studies in this direction will pave the
way in establishing the medicinal importance of Indian honey against the sessile forms of P.
aeruginosa.

Conclusion

As honey is easily available in the market and is inexpensive its antibacterial activity was
comparable to other medicinal honeys. All strains of P. aeruginosa including both resistant
phenotypes and sensitive strains were inhibited at 20% antibacterial honey concentrations in
vitro. This intriguing observation may have important clinical implications and could lead to a
new approach for treating multidrug resistant P. aeruginosa infected wounds using honey of
Indian origin.

References

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4. Molan PC, Cooper RA. Honey and sugar as a dressing for wound and ulcers. Trop Doct
2000;30:249-50.

5. Cooper RA, Molan PC. Honey in wound care. J Wound Care 1999;8:340.

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Microbiology. 14 th ed. New york: Churchill Livingstone; 1996. p. 845.

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19. Lusby PE, Coombes AL, Wilkinson JM. Bactericidal activity of different honeys against
pathogenic bacteria. Arch Med Res 2005;36:464-7.

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21. Orla S, Anthony D, Rahma A, Alice P, Georgina G, Seamus C, et al. Comparison of the
antimicrobial activity of Ulmo honey from Chile and Manuka honey against methicillin-
resistant Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa. BMC
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22. Wilkinson JM, Cavanagh HM. Antibacterial activity of 13 honeys against Escherichia coli
and Pseudomonas aeruginosa. J Med Food 2005;8:100-3.

23. Greenwood D. Honey for superficial wounds and ulcers. Lancet 1993;341:90-91.

24. Chiriife J, Searmato G, Herszage L. Scientific basis for use of granulated sugar in treatment
of infected wounds. Lancet 1982;1:560-1.

25. Blomfield R. Honey for decubitus ulcers. JAMA 1973;224:905.

26. Subramanyam S. Storage of skin grafts in honey. Lancet 1993;341:63-4.

27. Zeina B, Zohra BI, Al-assad S. The effects of honey on leishmania parasites: An in vitro
study. Trop Doct 1997;27 Suppl 1:36-8.

28. Mundo MA, Padilla-Zakour OI, Worobo RW. Growth inhibition of foodborne pathogens
and food spoilage organisms by select raw honeys. Int J Food Microbiol 2004;97:1-8.

29. White JW Jr, Subers MM, Scheparts AI. The identification of inhibine, the antibacterial
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Inhaling Essential Oils
4/20/2014

68 Comments

I have some wonderful things to report after several weeks of self-experimentation. I've been
inhaling essential oils since late February, and after seven weeks I feel like I have enough
of consistent results to report my findings (I am a scientist, after all).

First of all, before I started inhaling essential oils I had just gotten off of oral antibiotics
(minocycline and bactrim) and was planning on going into the hospital for some IV vancomycin
to treat my MRSA infection. Fate brought me a snow storm that prevented me from getting to the
hospital, and instead I decided to test out the eucalyptus essential oil I had bought the day before.
I am so glad things worked out the way they did, or I would never had made these radical
discoveries!

Why Use Essential Oils?

It's been on my mind for many months now that I should begin inhaling essential oils. In
herbalism school we talk a lot about plant constituents, and that those herbs that are the most
antimicrobial (antibacterial, antifungal, antiviral, etc.) contain a high amount of volatile oils.

Volatile oils from plants have been used for millennia in folk medicine to treat infections, to
reduce muscle and GI spasms, and to calm the nervous system. But in recent years, the scientific
interest in essential oils (a concentrated extract of the volatile oils from particular plant species)
has grown significantly as antibiotic-resistant superbugs (like the MRSA I've got in my lungs
right now) are proving themselves to be beyond the control of the conventional pharmaceutical
approach. Essential oils can be very effective against antibiotic-resistant bacteria, and there have
been many in vitro studies testifying to this effect.

I also got in touch with several other CFers who had experimented with essential oils with great
results, and this further encouraged me. My lung infections are so bad now that I feel horrible
anytime I'm not on antibiotics. I know how bad antibiotics are for my body (i.e. disrupt gut flora,
cause liver and kidney stress, weird side effects, etc.) so I of course want to avoid them as much
as possible. But in the last few years I've become dependent on them just in order to get through
the day, and I hate that. So I've been looking for a long time for something natural and less-
stressful on my body that can be as effective as antibiotics.

In this article, I will first discuss my experiments and their results. Secondly, I will present the
scientific research on how essential oils work as well as the physiological actions and
characteristics of the oils that I've used in my experiments.

My First Experiment
First, I began inhaling Eucalyptus radiata oil twice a day. I would put 2 mL of hypertonic saline
(essentially half of a plastic 4 mL vial) in my Pari nebulizer cup and put in two drops of
eucalyptus oil (EO). I'd shake it a little to break up the big globs of oil that float on top, then start
the nebulizer. It takes about 5-10 minutes to nebulize. I nebulized the EO at the end of my
morning and evening treatments at the time when you would usually inhale an antibiotic like
Tobi or Cayston.

At first, the EO was kinda irritating and it made me cough up a good amount of mucus. Over the
next week or so I developed a tolerance to it so that the irritated coughing subsided. The irritating
cough was really not so bad because it made my cough more productive, and the menthol-like
feeling of the EO soothed my throat and ultimately reduced my spasms. I also believe that since I
started out this experiment mixing the EO with hypersal, part of this productive cough was a
reaction to the hypersal. In my later experiments I used normal saline.

The Results
After stopping my oral antibiotics and before inhaling EO, I had been having my usual spasmy
morning cough (an annoying asthmatic-like hacking for 20-30 minutes), chest tightness,
shortness of breath, tons of mucus, and a feeling of chronic inflammation and irritation in the
lungs. I had also been getting night sweats and would often wake up at 3 am to cough with a
scary feeling like I had woken up from sleep apnea. My energy throughout the day was lower
than when on antibiotics. My ever-present low-grade fever required one acetaminophen every
morning at 9 am.

After only two treatments of inhaled EO I immediately felt a huge effect. The EO stopped my
spasmy cough that first day and it has not returned since. EO is bronchodilating, a counter-
irritant, antispasmodic, and anti-inflammatory, so almost immediately made my lungs felt more
open, less inflamed, and more resilient. After only a few days I was able to take in deep breaths
where I could feel air moving all the way down to the lower parts of my lungs, something that I
can rarely do except when on vancomycin. My shortness of breath was gone. My cough was less
spasmodic but more productive, as if each cough was more efficient at getting mucus up. After a
week I noticed a decrease in the amount of mucus I was coughing up, and that amount decreased
still in the following weeks. The oil seemed to be getting more effective with time. My night
sweats left and never came back. I could sleep through the night again without waking up from
sleep apnea to then hack up mucus. My lungs felt open and clear throughout the night and even
when waking up. My morning cough was minimal enough that I could eat a small breakfast
before starting my morning treatments, something not usually possible when off antibiotics (I
usually cough too much to get food into my mouth). I still had my daily low-grade fevers, which
I control with the morning acetaminophen, but my energy had improved. My sinuses cleared up
after about 2 weeks, and the only stuff that comes out is clear snot, no more green plugs. The
coating on my tongue (an important diagnostic tool in Chinese Medicine) had shifted from my
usual coating of thick white-yellow-brown gunk to almost nothing at all.

Needless to say, I was really excited about all this. It was pretty much revolutionary. I could feel
great and not be dependent on antibiotics?! With no impact on my gut flora. No side effects at
all. But the real test was the results of my FEV1. After 3 weeks of EO treatment my FEV1 was
up 8% from what it was 2 months before! It was now at the same level that it was after my last
10 day course on IV vancomycin in December! I had even caught a cold the week before my test
(kicked it in a record-breaking 3 days!) and still my numbers were high. Pretty amazing. In
addition to being antibacterial, EO is also antiviral and antifungal, so I assume inhaling it made
me recover from the cold quicker and prevented it from moving into my lungs. During the cold I
had also added a drop of EO to my sinus rinse bottle, which really helped reduce mucus build up
and inflammation.

Further Experimentation
Eucalyptus worked so well that I thought I would experiment with other oils to see if all essential
oils are as effective, or if not, which ones are more effective for me than others. After 4 weeks of
nebulizing EO I decided to stop it and try pine oil (Pinus sylvestris, a.k.a Scotch Pine) alone. I
decided to try it alone to be more "scientific" about it. After five days of only pine oil it became
clear that it was nowhere near as effective as EO. I began to notice an increase in my mucus load
and my lungs became a bit more irritated in the mornings. The spasmy cough did not return, but I
felt my lung capacity begin to decline very slowly and my shortness of breath/ diaphragm
tightness returned. After five days of this trend I decided the experiment was over (I planned to
do a two-week trial but the results were clear enough after 5 days - not worth dropping my FEV1
for science's sake!).

For the next three days I mixed 2-3 drops of pine with 1 drop of EO in 2 mL hypersal and
nebulized twice a day. Things improved somewhat. My shortness of breath went away and my
diaphragm relaxed again. My morning coughs became less irritated.

For the next two days I added cinnamon leaf oil to EO (1 drop and 1 drop) and also tried
cinnamon leaf by itself. It was really intense! I wanted to try cinnamon because the scientific
literature has said that cinnamon oil, with its high levels of cinnamaldehyde, is essentially the
strongest antibacterial essential oil out there [3]. It may be really bactericidal but it burned my
throat and numbed my mouth and was so irritating that I think it actually worsened my shortness
of breath. So after a few days of that I decided the pain wasn't worth it, and I needed to move on.

After these two unsuccessful experiments, I came up with a combo that I think is pretty effective,
and I've been using it for the last two weeks. In the morning I am nebulizing 1 drop EO, 1 drop
tea tree oil (TTO), and 1 drop lemongrass mixed in normal saline. I remembered that I had a box
of normal saline syringes left over from my home-IV treatments in December, so I decided it
would be less irritating to use normal saline instead of hypersal as my substrate. I nebulize the
EO and TTO together in 2 mL saline, then the lemongrass (LG) by itself in 2-3 mL saline. I neb
the LG by itself because it is pretty irritating (similar to cinnamon, spicy, but a little milder, and
does not cause me shortness of breath) and I have to inhale it with my mouth open, unsealed
around the neb cup or else my throat will burn. I don't want to waste any TTO or EO, so I neb
the LG separately this way. I recently began to use LG in combo with 1 drop of pine oil (a much
more mild oil), which seems to reduce the irritating effects of LG a little bit so that I can inhale it
without my throat burning as much. Then, at the end of this treatment, I add in another 1/2 mL of
saline and neb that to make sure I get every last morsel of essential oil left in the neb cup. I don't
want to waste any of it. I put up with the irritation of the LG because I feel that it is effective, as
in the last two weeks my mucus production has declined to be even less than what it was in my
first experiment with EO, and LG has been shown to be particularly effective against MRSA in
the literature (which I will discuss later). In the evening I nebulize 1 drop EO, 1 drop TTO, and 1
drop pine oil together in 3 mL saline. This seems to be a soothing combo that lets me sleep better
through the night, versus when I neb LG before bed it can sometimes cause me a bit of irritation
that can make me wake up with a dry cough at 3 am, but not always.

The Science
There have been numerous in vitro studies on the bactericidal (i.e. bacteria-killing) effects of
essential oils on bacteria, viruses, and fungi in the last decade or so. Interestingly, because the
pharmaceutical-industrial complex dominates modern Western medicine in America and Europe
to the point where almost all research is done for the development of multi-billion dollar
blockbuster drugs, some of the most innovative and groundbreaking research on the use of herbs
and non-patentable nutraceuticals to fight disease is coming out of Asia, the Middle East, and
Eastern Europe. There are a few studies coming out of research universities in the US, Australia,
and Europe as well. I find it fascinating that countries that are less obsessed with ultra-capitalism
or are less financially stable are finding cheap, safe, and innovative ways to make people
healthier, often times by rediscovering natural medicine.

Anyway, there is a growing body of evidence from in vitro studies, clinical experience, and case
studies that essential oils are an incredibly useful tool as we move into a post-antibiotic era
dominated by antibiotic-resistant superbug infections. Essential oils can be as effective or more
effective than many of our strongest antibiotics, yet the risk of developing bacterial resistance is
significantly less because essential oils are complex cocktails of many chemical constituents
(sometimes over 100) working synergistically to fight infection. In fact, when scientists isolate
single constituents from essential oils (like 1,8 cineole from eucalyptus oil) and apply these to
bacteria, they generally have weaker activity against bacteria than the whole oil, or than multiple
oils applied together in a formula. This is because whole oils contain many different constituents
that can be antimicrobial, immunomodulating, antioxidant, as well as antispasmodic,
bronchodilating, analgesic (pain killing), anti-inflammatory, or have several other effects that
work together synergistically [1][6]. In addition to essential oils' direct inhibitory effects against
microbes, they also commonly contain constituents that stimulate the immune system to mount a
more efficient and effective immune response to invading pathogens. Thus, applying modern
Western medicine's reductionist approach to the use of essential oils may not be as helpful as
using whole oils.

Using whole oils with their varying combinations of many different constituents will also help
prevent bacterial resistance to these oils. The chemical makeup of plants high in volatile oils is
constantly shifting depending on weather, the season, the climate, soil composition, and many
other environmental factors. Even oils from two plants of the same species planted side by side
may have slightly different chemical profiles, or the oils harvested in spring may differ
significantly from those harvest from the same plant in autumn [2]. This can make it difficult to
"standardize" the chemical composition of an essential oil for therapeutic use, but I like to think
of this in a positive light - it further reduces the risk of bacterial resistance if we're constantly
changing the rules of the game on them. The main reason why bacteria so easily develop
resistance to pharmaceutical antibiotics is that they mainly consist of only one chemical
constituent, and when a bacteria figures out a way around it, the antibiotic is made useless. Some
antibiotics are used in combination, like the common anti-Pseudomonas combo of IV Tobi and
ceftazidime when going in for a hospital "clean out", or oral Bactrim (a combo
of sulfamethoxazole and trimethoprim) because of this emergence of resistant bacteria.

Furthermore, it's been found in preliminary research (and through several CFers personal
experiences) that using formulas made of a mixture of different essential oils (like the formulas
sold by Young Living) are even more effective against pathogens at smaller concentrations than
single oils [6]. Studies have shown that certain plant constituents, when used together make each
other more effective at killing bacteria, such as 1,8-cineole and terpenine in tea tree oil. We call
this synergism. A study by Weber University and Young Living found that blended oil formulas
were more effective than any of their single oils alone, and even more effective than the
strongest of the single oils (i.e. lemongrass). In fact, their most bactericidal formula, R.C., was a
combination of 11 oils, none of which by itself was particularly bactericidal. It's been found that
essential oils and their constituents can work synergistically with antibiotics as well [6].

Choosing Oils
All plants have different chemical constituents and different energetic signatures that make their
oils more or less effective against certain microorganisms and more or less helpful for certain
kinds of people. All oils are at least somewhat antimicrobial because they are made of lipids (i.e.
volatile oils), and many kinds of microorganisms (especially gram-positive bacteria, viruses, and
fungi) have cell membranes that are made up of oils and are "lipophilic". Lipophilic means "fat
loving"; that fats bind well to the cell membrane. As very small oil-like constituents, essential
oils can bind to membranes of microbes and disrupt the lipid molecules in their cell membranes,
essentially ripping a hole in them. In addition, their chemical constituents, being fat-soluble, can
bind to the microbial cell membranes and insert themselves inside those cells, doing damage to
the organelles or DNA on the inside. Gram-positive bacteria (i.e. MRSA,
all Staph, mycobacteria) viruses, and fungi are especially vulnerable to essential oils because
they are protected on the outside by a lipid-based membrane. Gram-negative bacteria
(i.e. Pseudomonas) have lipophobic (fat-fearing)/hydrophilic cell membranes that are covered in
a barrier of polysaccharide chains. This means that volatile oils and fat-soluble chemical
constituents are going to have a harder time killing gram-negative bacteria [3]. So while studies
have shown essential oils are very effective against gram-positive, viral, and mold/yeast
infections, they are less effective against the CF's arch-nemesis, Pseudomonas. However, it
doesn't mean they're completely ineffective. Tea tree oil has been proven to be mildly effective
against multi-resistant Pseudomonas [4].

Although all essential oils are somewhat bactericidal, some are much more powerful than others.
This has a lot to do with their chemical constituents. Certain classes of chemical constituents,
such as aldehydes and phenols, are more antimicrobial than other chemicals that are more
weakly bactericidal, such as alcohols, ketones, or ethers [3]. In addition, essential oils' direct
antimicrobial actions are not their only actions, so we should not be myopic when it comes to
choosing oils based on their bactericidal capacities only. Many oils have other actions as well,
such as anti-inflammatory, antispasmodic, mucolytic (thins mucus), nervine (calms the mind),
bronchodilating, and immunomodulating, among others. For example, eucalyptus is not the most
bactericidal oil on the block, but it is a powerful oil for helping respiratory function in many
ways, as I will describe below, so I make sure to include eucalyptus in my formula for all of its
benefits, not just because it kills bacteria.

Eucalyptus
Eucalyptus is a genus of trees that includes over 500 species native to Australia, Tasmania, and
nearby islands [5]. A handful of these species have been extensively studied for their medicinal
applications, especially Eucalyptus globulus, or the Blue Gum tree. The major constituent in
most eucalyptus species' oils is 1,8-cineole, also called eucalyptol. There has been a lot of
scientific study on this constituent, especially concerning its effect on the respiratory and
immune systems. Eucalyptus oil has been found to increase phagocytosis by the white blood
cells of the innate immune system without increasing cytokine production. In other words, EO
stimulates a better immune response without increasing inflammation, especially in the airways.
In fact, in-vitro studies have shown that EO actually reduces cytokine production in already-
irritated cells, which would explain why it helps me so much when I feel inflamed. It is thought
that 1,8-cineole is the main reason for the ability for EO to reduce inflammation. In fact, one
study on asthmatics found that 1,8-cineole reduced inflammation and allergic response so much
that they were able to reduce their dose of prednisone, even after treatment with 1,8-cineole had
stopped. It is also thought that this constituent can control airway mucus hypersecretion,
reducing respiratory exacerbations in asthma, sinusitis, and COPD [1], which also means it
would be similarly effective in CF. Human and animal studies have shown that 1,8-cineole
significantly reduces symptoms of chronic bronchitis, sinusitis, and COPD.

Although 1,8-cineole is great and there has been a lot of research on it, it may not be as effective
against microbes as the whole oil. One study showed that although 1,8-cineole is a major
component of many eucalyptus species oils, its strongest antibacterial constituent may be alpha-
terpineol, which is found in smaller quantities in the oils [3]. To me, this is further proof that we
should not follow the conventional reductionistic thinking patterns in the use of essential oils or
herbs in general. Whole plants containing synergistic cocktails of constituents are often more
powerful than their chemical isolates, even if those isolates can be delivered at higher doses.

Out of 18 essential oils tested against Candida albicans, E. globulus was the most effective
followed by peppermint, ginger grass, and clove. E. globulus was found to be more effective
than fluconazole (a commonly used anti-fungal drug for yeast infections), and peppermint oil
was found to be as effective as fluconazole [1]. One study found E. globulus to be not as
effective against Staph as tea tree oil, but it is the most effective thing out of anything (including
pharmaceutical drugs and synthetic chemicals) against dental cavities and plaque, and that is why
many toothpastes now include eucalyptus as an ingredient. EO is also effective against MRSA,
depending on the species. In one study on essential oils' effect against MRSA, E. citriodora was
found to have the largest zone of inhibition (i.e. the radius of bacteria death upon exposure to the
oil) of the eucalyptus species (50 mm) with E. radiata second (25 mm). E. globulus was
ineffective. E. citriodora was moderately effective when compared to the most effective oils in
this study: lemongrass (zone of inhibition = >83 mm = complete eradication), lemon myrtle (65
mm), mountain savory (62.5 mm), cinnamon bark (Cinnamomum verum) and melissa (60 mm),
and thyme (Thymus vulgaris) at 57 mm [6]. In another study, zones of inhibition for EO against
14 strains of MRSA were comparable to that of vancomycin [10]!

There are so many amazing things about EO and so much science backing it up that I couldn't
possibly go into it all here, but if you're interested I suggest you read the paper at the link in
footnote 1.

The only possible drawback I could find in the use of EO is that it is mildly anti-tussive in large
doses, meaning that it may suppress a cough. It does this by reducing movement of the cilia
(little hairs) lining the airways of our lungs and sinuses [1]. It is not known how strongly an
effect this has on humans (studies have only been done on this subject in-vitro) but I have
noticed in myself a slight reduction in my urge to cough, even when I feel there may be mucus in
my lower airways. I mentioned this to my CF doctor and she didn't seem that concerned about it.
She said that what matters more is how I feel (i.e. great!), how I sound under the stethoscope (i.e.
clear!), and my PFTs (i.e. improved!). This effect may vary from person to person, but it's a good
thing to watch out for and keep in mind.

Tea Tree Oil

The tea tree (Melaleuca alternifolia) is also a native tree of Australia and has several similar
chemical actions and constituents to eucalyptus. It is highly antimicrobial and is kind of a "go to"
oil in the herbal first aid kit for its antiseptic properties. It is now commonly used in antiseptic
hand washes and cosmetics. It is considered to be more antibacterial than many eucalyptus
species, but does not have EO's immunomodulating effects. Although it has a small amount of
1,8-cineole, its main constituent is terpinen-4-ol, which is credited as giving TTO most of its
antimicrobial effects [7]. Research has proven it to be effective against 27 bacterial and 24 fungal
strains, as well as some viruses and protozoa [1]. In one study it was shown to have powerful
antibacterial effects on biofilm-grown MRSA [12]. There have been several case reports of
prolonged tuberculosis infections (a type of mycobacterium) being cured by inhaling several
days of TTO by steam inhalation. As was previously mentioned, TTO is one of the few oils
effective against multi-resistant Pseudomonas [4] and other gram-negative bacteria. In one study,
tea tree oil was moderately effective against MRSA with a zone of inhibition of 45 mm
(compared to E. citriodora at 50 mm, or lemongrass at >83 mm) [6].

Tea tree oil does have anti-inflammatory properties as well. Studies have shown that it
downregulates the production of pro-inflammatory cytokines (chemicals produced by a certain
part of the immune system) and reduces inflammatory oxidation in animal studies when inhaled
[7]. Furthermore, TTO is highly antifungal and very effective against Candida yeast infections,
inhibiting its ability to mutate from yeast to hyphae form. TTO has also been shown to be
bactericidal against MRSA biofilms [7].

Lemongrass
Lemongrass is actually a genus (Cymbopogon) of 45 species of grasses native to southern Asia.
It has been used as a medicinal and culinary herb for centuries, and can also be used to repel
insects (citronella grass is a species within this genus). In folk medicine, lemongrass is used not
just as an antiseptic but also to calm the mind, reduce anxiety, and improve mental
clarity. Cymbopogon citratus is the most commonly used species for its oil. The species are
differentiated by their chemotypes, meaning that they are categorized by their dominant chemical
constituents, which can vary significantly between lemongrass species. Its most prevalent
chemical constituents are citral and geraniol [9]. Lemongrass oil (LG) is strongly antimicrobial,
especially against bacteria but also against fungi, viruses, and even parasitic worms (i.e.
helminths). One study found that out of 14 different essential oils tested including some of the
strongest like cinnamon and thyme, lemongrass oil was the most effective against the H.
influenzae (flu) virus [3]. LG has been shown to have anti-cancer and anti-inflammatory effects
as well. It is also effective against Aspergillus and Candida fungal (mold and yeast) infections.
LG has extraordinarily high antioxidant powers [9].

In a study comparing the antibacterial power of essential oils against drug-resistant bacteria, LG
had the strongest bactericidal effect against MRSA compared to eucalyptus and TTO.
Interestingly, all three essential oils were more bactericidal against these drug-resistant bacteria
than both 70% ethanol (alcohol) and chlorhexidine (a commonly-used chemical antiseptic) [4].
Furthermore, lemongrass oil proved to be more antibacterial against all bacteria tested (including
two strains of Staphyloccocus aureus) than any of its isolated constituents (citral, geraniol, and
myrcene), proving once again that whole oils are more powerful than chemical isolates. This
study also showed that LG is effective against Staph biofilms [8], which is an incredibly
important distinction to make, since the chronic infections that we CFers get in our lungs become
intractable precisely because of the development of bacterial biofilms. Many in-vitro studies only
test effectiveness of antibacterial substances against planktonic bacteria, but biofilm-inhabiting
bacteria is a whole different beast, and biofilms are what make chronic infections so resistant to
antibiotics. All this said, lemongrass seems to me one of the most powerful oils against the bug
that most bugs me (MRSA), and while it is pretty irritating it is less so than several of the other
oils that have similarly powerful antibacterial effects (i.e. cinnamon and thyme).

Other Oils
As I mentioned, I tried cinnamon leaf oil but it was too irritating for me to continue. I gave it to
my sister to use when she gets cuts on her hands (she's a dirty farmer and gets infected cuts a
lot). I was interested in cinnamon because several studies have shown that cinnamon
(Cinnamomum verum and several other species within Cinnamomum genus) and its major
constituent, cinnamaldehyde, are extraordinarily antimicrobial. While I do not think inhaling
cinnamon is a good idea because it's so irritating, I do think it has a place in the treatment of skin
and external tissue infections, when properly diluted in other oils (like coconut or olive oil) to
prevent skin irritation. For infected wounds (especially with antibiotic-resitant bacteria) or
MRSA infections of the skin, this may be just the ticket. It may also be safe to diffuse it into the
air of a room using an aromatherapy diffuser or oil burner, especially if there is any risk of
passing pathogens back and forth in a particularly well-populated room (like at a party or
something).

One study showed that cinnamon bark oil was the most effective oil at the lowest concentrations
against Staph and several other bacteria compared to clove, cardamom, and cumin oils [11].
Another in-vitro study that created a model of essential oil inhalation showed that out of 14 oils
tested, cinnamon and thyme oils were the strongest antimicrobial oils, especially
against Staph and the flu virus [3]. Cinnamaldehyde in cinnamon and thymol in thyme are
considered to be some of the strongest bactericidal constituents in essential oils.

Thyme oil is another very promising essential oil, and it is probably the next one I will
experiment with. There are about 350 species within the Thymus genus native to Europe, North
Africa, and Asia. In the scientific literature, there has been significant study on a handful of these
species and their major constituents. There have been several studies on Thymus vulgaris,
Thymus zygis, and Thymus serpylum, but most research has been done on specific chemotypes
of T. vulgaris. The major constituents of thyme that are the most well-studied are thymol,
geraniol, eugenol, carvacrol, and linalool. Thymol, carvacrol, and eugenol have very strong
effects against MRSA [6]. Thymol chemotypes of thyme are the strongest antimicrobial oils that
I have read about in the scientific literature [3], and are stronger than vancomycin against MRSA
[10].

I have been hesitant to try inhaling thyme because I have been warned by multiple herbalists that
although thymol is a very effective antibacterial constituent, it is toxic to the kidneys in high
doses. Inhaling a few drops a day would likely not cause any adverse effects, but it is something
important to keep in mind (especially since I've had kidney troubles caused by IV antibiotics in
the past). A solution to this problem is to choose chemotypes of thyme that do not have much
thymol in them, and instead have more linalool, geraniol, or alpha-terpineol. There is some
research being conducted currently by a well-known aromatherapist, Maggie Tisserand, on the
use of a specially formulated thyme blend called "benchmark thyme" for therapeutic use against
MRSA infections. Benchmark thyme oil is unique because it harvests certain chemotypes of
thyme at certain times of the year to ensure a specific balance of chemical constituents that are
effective against MRSA [2]. Thyme may be irritating to inhale, or so I have heard, but
benchmark thyme is formulated to be as gentle as possible while still maintaining its bactericidal
powers, so it has obviously attracted my attention in the last few weeks. In the near future I will
give it a try and report back my findings.

Conclusion
In conclusion, the inhalation of essential oils has been a revolutionary discovery for me and it
has greatly helped me control my lung infections. They work better for me than oral antibiotics
and almost as well as IV antibiotics with no side-effects at all. They helped me clear a head cold
in only 3 days and prevented it from traveling down into my lungs. They are safe and easy to
use. There is a lot of in-vitro research on the antimicrobial effects of essential oils, but more
human trials need to be done to determine how whole oils benefit those with lung infections, like
CFers with Pseudo, Staph, or mycobacterium infections. If enough of us find positive results
from inhaling essential oils on our own and we inform our doctors of our progress, maybe
researchers will conduct more human trials, leading to the use of this as a commonplace therapy
in our toolbox against chronic CF lung infections.

At the present moment I am taking a break from inhaling essential oils to work on another
experiment, and I want to be scientific about it by reducing the number of variables. I also want
to give my body a rest from the oils for a few weeks, just to make sure my liver and kidneys can
process their metabolites and clear them out completely. In addition, although the risk of
bacterial resistance is probably thousands of times less than that associated with conventional
antibiotic usage, it's good to take a break once in a while to ensure my bacteria maintain
maximum sensitivity to the oils.

Update: May 2018

A lot of people ask me where they should source their essential oils from. This is a very
controversial subject because there are two companies that have been doing very deceptive and
dishonest marketing for years, spreading misinformation about the quality of their oils and how
they can be properly used: Young Living and doTerra. I encourage people to avoid both of these
companies. Instead, choose companies that source only from organic or unsprayed sustainably
wildcrafted plants. The company should also be testing every batch with GC/MS testing and
should be able to provide you with that information upon request. You should also be able to
acquire any information about the oil, such as where the plants were harvested, where the oil was
distilled, what processes they used, and when it was distilled. I have a local aromatherapist who
runs an excellent aromatherapy shop near me, so I source all of my oils from there because I trust
her expertise and the quality of her oils. But if you are not as lucky as I am, I recommend you
buy oils from a reputable company such as Aromatics International. In addition, if any company
recommends taking essential oils internally, that means they are a disreputable source. Certified
aromatherapists will tell you that taking essential oils internally is unsafe and can cause serious
side effects if done without supervision.

Update: October 2018

I wanted to give an extra precaution to the use of nebulized essential oils in people with a history
of pleurisy, pleural pain, or pneumothoraxes (lung collapses). I am now a person with a sensitive
pleura (and a history of multiple collapses) and I have tried several of times in the last two years
to do a course of nebulized essential oils like I have done in the past. I have found that each time
I have pleural pain in my lungs after nebulizing EOs for more than about 5 days, even though it
certainly helps clear up my infection and reduces my mucus burden. Though correlation does not
prove causation (because the pain could be coming from other things, like the infection itself), I
have reason to believe that nebbing EOs is no longer a good idea for me, since my pleura are
now so sensitive. I can, however, use an aromatherapy diffusor without issue, and use EOs in
other ways, like on the skin (in a carrier oil). I have not tried rectal suppositories since my first
rounds of experimentation, but I assume this would also be fine for me to do. Therefore, I want
to encourage people to take extra precaution if they have a history of pleural complications, and I
also recommend to stop nebbing oils immediately if you think they could be causing pleural
pain. Discuss this with a certified aromatherapist or herbalist (like me) if you want to explore this
issue further.

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Sources:
[1] Immune-modifying and antimicrobial effects of eucalyptus oil and simple inhalation devices.
<http://www.altmedrev.com/publications/15/1/33.pdf>
[2] The Thyme is Right. <http://www.benchmark-
thyme.com/userfiles/file/FHT%20Article%20Benchmark%20Oil%20APRIL%202011%20witho
ut%20cover.pdf>
[3] Antibacterial activity of essential oils and their major constituents against respiratory tract
pathogens by gaseous contact. <http://jac.oxfordjournals.org/content/47/5/565.full>
[4] The ongoing battle against multi-resistant strains: in-vitro inhibition of hospital-acquired
MRSA, VRE, Pseudomonas, ESBL E. coli and Klebsiella species in the presence of plant-derived
antiseptic oils. <http://www.ncbi.nlm.nih.gov/pubmed/23199627>
[5] http://www.britannica.com/EBchecked/topic/194767/Eucalyptus
[6] Inhibition of methicillin-resistant Staphylococcus aureus (MRSA) by essential oils.
<http://aromatherapyliving.com/docs/MRSA_Research_Young_Living_Weber_Univ.pdf>
[7] Tea Tree Oil. <http://www.sigmaaldrich.com/life-science/nutrition-research/learning-
center/plant-profiler/melaleuca-alternifolia.html>
[8] The effect of lemongrass oil and its major components on clinical isolate mastitus pathogens
and their mechanisms of action on Staphyloccocus aureus DMST 4745.
<http://www.ncbi.nlm.nih.gov/pubmed/21316719>
[9] Lemongrass. <http://www.sigmaaldrich.com/life-science/nutrition-research/learning-
center/plant-profiler/cymbopogon.html>
[10] Antibacterial effect of essential oils from two medicinal plants against
MRSA. <http://www.ncbi.nlm.nih.gov/pubmed/19576738>
[11] Antimicrobial activity of the bioactive components of essential oils from Pakistani spices
against Salmonella and other multi-drug resistant
bacteria. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853939/>
[12] In vitro activity of tea-tree oil against clinical skin isolates of meticillin-resistant and -
sensitive Staphylococcus aureus and coagulase-negative staphylococci growing planktonically
and as biofilms. <http://jmm.sgmjournals.org/content/55/10/1375.full>