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the majority of pet owners are unaware that their animals could be susceptible to an infection that is sometimes life threatening. it is not widely understood that the use of antibiotics in agricultural animals, which end up as meals for both humans and pets, is compounding the threat of mrsa. the situation is already worrying. there are voices of reason trying to educate government, medical personnel and the public about the correct use of antibiotics. in 1997, an alliance, ruma,2 was formed to ‘promote the highest standards of food safety, animal health and human health as well as ensure minimal damage to the environment.’ their mantra, on the use of antimicrobials, is ‘use as little as possible but as much as needed.’ cats and dogs companion animals, mainly cats and dogs, can act as a reservoir, or carrier, for mrsa. this was observed in a geriatric hospital ward where mrsa was prevalent amongst the patients. a ward cat was good company for the elderly patients and was considered to be helpful in their recovery, but the problem of mrsa became persistent. the ward staff were swabbed and found to be carriers of mrsa in their nostrils. the cat, also swabbed, was found to be heavily colonised with mrsa. after its removal, and in tandem with infection control measures, the mrsa rate amongst the geriatric patients began to decline. in 2005, a study of mrsa isolates from companion animals revealed that 93.5% were the same as mrsa isolates from epidemic mrsa commonly found in uk healthcare settings. according to information gathered by the royal veterinary college3 the early incidence of mrsa in companion animals was noted as follows: 1999 eleven dogs in uk, usa and korea 2003 one dog in the netherlands; 95 isolated incidents of mrsa recorded at one uk laboratory4 2004 seven dogs and five cats in uk 2005 since 2005 there have been more than 50 papers written on mrsa in pets.

mrsa in animals 43 in 2009 an analysis of swabs taken, over a period of years, from mrsa infected cats and dogs in europe was as follows: epidemic strain emrsa-15 95.4% epidemic strain emrsa-16 1.6% other mrsa 3.0% in 2004, in the uk, the first recorded death of a dog from the human form of mrsa spurred its owner to set up an educational foundation5 in order to create awareness of the dangers of mrsa infections in veterinary clinics and hospitals. within weeks of the website going live, emails were pouring in from pet owners, veterinary and human health practitioners, journalists, wildlife animal keepers and farmers, all wanting to know more about the risks of cross-infection of mrsa between humans and animals. from 2005 to the present day, the ongoing educational campaign is resulting in improved hygiene of veterinary practices6 and better barrier nursing of mrsa-infected pets in veterinary establishments on both sides of the atlantic. if your cat or dog has a wound that refuses to heal, and if you have recently been in hospital and have been treated for mrsa, then it is advisable to inform your vet so that they can have blood samples analysed to see if your pet’s problem is mrsa colonising the wound, and preventing healing from taking place. conversely, if you have been treated for mrsa and have been sent home with a clean bill of health, but can’t quite seem to regain full health, it is possible that your pet is a carrier of mrsa. even though the pet doesn’t seem to be affected by mrsa, every time you stroke him/her you may be unknowingly becoming re- infected. you need to tell your vet of your recent illness and say that you suspect your animal could be a carrier. have some tests carried out, so that both you and your pet can be decolonised. people with chronically infected wounds and/or colonised areas of the body, could potentially colonise their pets. a study conducted in the early 2000s has shown that pets can become colonised and their wounds can become infected with mrsa when the owners are themselves affected. both pet and owner need to be treated.

cross-infection between pet owners and pets is now a fact of life. if a wound is not healing up and you have a pet, it is advisable to take your animal to the vet for swabs to be taken. your vet will then send the swabs to a diagnostic laboratory and if results show that your pet is carrying mrsa on its coat or in its nostrils, it is important to have the animal treated with antimicrobials so that you are not re-contaminated with mrsa. similarly, if you have a pet with a wound that is not healing up, and you work in a hospital, nursing home or correctional facility, or are a visitor to a hospital, then you should consider having yourself swabbed and diagnosed, as you may be carrying mrsa which is being transferred to your animal. in the uk, it may be difficult, if not impossible, to persuade your doctor to take a swab, as the uk healthcare services are underfunded and this diagnostic procedure would not be considered as critical. it may be necessary to contact a private laboratory7 so that you can have swabs taken and analysed for your mrsa status. although the cost is not insignificant, it may in the long run save you money on continuing veterinary fees. within the uk it is widely believed that ca-mrsa is not as yet, and will not become, a problem in companion animals, but in the usa, researchers have detected pvl toxin in 23 animal isolates of mrsa.8 they say, ‘this is the first study to demonstrate the presence of the pvl toxin genes in mrsa strains isolated from companion animals.’ the results are noteworthy in that mrsa strains that produce the pvl toxin have been shown in many studies to cause pneumonia, necrotising dermatitis and other primary diseases in humans, and that these conditions were mirrored in animals. it would seem that the mrsa situation in the usa, in both humans and animals, is pointing towards ca-mrsa, with the addition of the pvl toxin in a significant number of cases. in the uk, the current status of mrsa, in both humans and animals, is predominantly ha-mrsa. key points • if you have an infected wound that won’t clear up – suspect your dog or cat! ask your vet to take swabs and send them off to a diagnostic laboratory. your vet should get the results within a

mrsa in animals 49 • in the united states a group of epidemiologists18 conducted studies on a large pig farm by taking and analysing swabs from the pigs’ noses. it was found that 70% of the pigs were colonised with mrsa. swine workers were found to be colonised when tested in a later research programme.19 • the infectious diseases society of america (idsa)20 has stated, ‘infectious disease physicians and public health advocates are greatly concerned about the growing body of scientific evidence demonstrating that antimicrobial drug use in livestock and poultry contributes to the spread of drug-resistant bacteria to people.’ • a comprehensive study of mrsa in animals, covering companion animals, horses, and livestock, both poultry and mammals, has been published by the soil association.21 it contains a vast amount of information on the emerging international problem of mrsa in domestic and agricultural animals. ‘organic farming methods are beneficial for the environment but they also reduce the need for antibiotics as young animals are allowed to stay with their mother until weaned. farmed pigs, for example, are weaned early before their immune systems are mature and are therefore vulnerable to infections and consequently antibiotics are routinely added to the feed of farmed swine.’ • the use of antibiotics in farmed animals differs greatly from country to country. the uk allows the prophylactic, or disease prevention, use of antibiotics in animal feed, whereas holland imposes fines on vets who do this. • in 2005, the united states food and drug administration announced a ban on the use of the antibiotic enrofloxacin in poultry because it was in the same antibiotic class as ciprofloxacin, used to treat people who have contracted ca-mrsa. one us pharmaceutical company22 produces both antibiotics. zoonotic legacy even though we may never have heard of the word ‘zoonotic’ before, we now need an awareness of the potential transfer of mrsa between humans and animals. we can’t turn back time to

prior to the development of penicillin in the 1940s, s. aureus infections could result in serious and often fatal disease. most strains of s. aureus were sensitive to penicillin, and remarkable recoveries were achieved, but it was soon noted that resistant strains were emerging. by the late 1950s, about nine out of every ten s. aureus strains isolated from infected patients were penicillin resistant. a modified form of penicillin called methicillin (also called meticillin), was introduced to treat penicillin-resistant strains, but it needed to be injected and could cause kidney damage, so antibiotics such as oxacillin or flucloxacillin were developed. resistance to methicillin was first recorded in the 1960s, but did not become a major problem in hospitals until the 1990s. how did antibiotic resistance develop in s. aureus? penicillin, and other antibiotics in the same class, kill s. aureus by stopping the synthesis of a compound which is an integral part of the bacterial cell wall. this cell wall compound, called peptidoglycan, maintains cell wall integrity, especially in the ‘gram-positive’ bacteria. the beta-lactam core of the antibiotic binds to specific sites on the bacterial cell wall, named penicillin-binding proteins, causing disruption of cell wall synthesis. this causes the cell walls to leak or collapse, resulting in death of the bacterium. antibiotic resistance develops because there are countless different strains of bacteria. if one has a genetic mutation which gives it a survival advantage, such as being resistant to an antibiotic, it will survive, and eventually most strains will carry the resistance genes. there are two mechanisms by which the bacteria develop resistance to penicillin, methicillin and other beta-lactam antibiotics. some strains produce an enzyme known as penicillinase, which breaks open the ring structure of the antibiotic, rendering it ineffective. other strains alter their own proteins so that antibiotics are unable to bind to them and bacterial cell walls are not disrupted. the evolution of mrsa resulted in strains resistant to penicillin and all beta-lactam antibiotics. mrsa also became resistant to members of the beta-lactam sub-group of antibiotics known as the cephalosporins. recently, strains of mrsa are showing resistance or reduced susceptibility to vancomycin, a member of the glycopeptide class of antibiotics.3

the evolution of mrsa 53 since glycopeptide antibiotics are now the drug of choice for severe mrsa infections, the possibility of vancomycin resistance has raised serious concerns regarding successful treatment of multi- drug-resistant staphylococcus aureus. mrsa as a superbug the world we live in is full of bacteria, the vast majority of which are harmless, although some are more dangerous than others. s. aureus is just one of more than 40 species of a large genus of bacteria, and is one of the few staphylococci that can cause disease. like some other species of staphylococci, it is a common commensal of humans, that is, it comprises part of the body’s normal bacterial flora, but without causing disease. staphylococci frequently live on the skin, especially in folds such as the armpit and groin, in the nose and less commonly in the throat.4 the main mode of transmission from one person to another is via the hands, especially those of healthcare workers. hands can become contaminated by contact with infected or colonised patients and their wounds, via medical devices, and objects and surfaces contaminated with blood or body fluids containing s. aureus or mrsa. some strains of s. aureus can be very resilient and survive for hours, days or longer on dry surfaces and fabrics. the superbug status of mrsa is further enhanced as several strains have become resistant to many of the disinfectants and antiseptics used in hospitals to clean surfaces, sterilise instruments and decontaminate skin. mrsa strains give rise to the same diseases and conditions as those caused by antibiotic-sensitive strains, and are usually no more aggressive or infectious. they are only more serious than other s. aureus infections because they do not respond to antibiotic treatment. mrsa infections can become more severe than they may otherwise have been if the cause of the infection is not diagnosed early enough, or if prescribed antibiotics do not work. certain strains of mrsa, particularly those classified as epidemic strains emrsa-15 and emrsa-16 (also referred to as st22 and st36 respectively), are easily transmissible between patients and hospital staff, and have the capacity to cause serious disease. these strains represent nearly half of the s. aureus bloodstream infections

(bacteraemia) in england, and about 95% of all bloodstream infections attributed to mrsa. s. aureus, including mrsa, may cause symptomless colonisation in humans, but is the same bacteria responsible for more serious and potentially life threatening conditions, including bloodstream infections (bacteraemia), endocarditis, pneumonia, scalded skin syndrome, toxic shock syndrome and necrotising fasciitis. s. aureus can also cause septic arthritis, intravenous line infections, heart-valve infections, urinary tract infections, and some strains are responsible for a type of food poisoning. in severe infections, symptoms can include high fever, raised white blood cell count, rigors (shaking), disturbance of blood clotting with a tendency to bleed into tissue, and the failure of vital organs, often resulting in death. most of the serious consequences of s. aureus infections are a result of one or more virulence factors produced by the bacteria. these include the exotoxins secreted by the bacteria, which act on cell membranes. other toxins produced by s. aureus include exfoliative toxins which cause peeling of the skin, observed with scalded skin syndrome, and enterotoxins, which cause a form of food poisoning. in some strains the golden pigment, staphyloxanthin, acts as a virulence factor, destroying the white blood cells targeting the bacteria. treatment of mrsa infections is difficult. many strains remain sensitive to the antibiotic fusidic acid, but because resistance to it develops easily, it must be used in combination with another antimicrobial for the treatment of serious mrsa infections. for skin infections, topical ointments containing the antibiotic mupirocin are often used, but resistance to this can develop. mupirocin is bacteriostatic at low doses and bactericidal at high concentrations, and works by inhibiting the synthesis of proteins and rna (ribonucleic acid), and to a lesser extent, dna as well as cell wall formation. to treat mupirocin-resistant strains, oral antibiotics such as clindamycin, or a combination of trimethoprim and co- trimoxazole, are being used.5 resistance to these antibiotics has led to the use of new broad-spectrum anti-gram-positive antibiotics such as the oral drug linezolid6 and daptomycin.7 intravenous vancomycin has become the last resort to treat serious mrsa infections, but it is toxic and drug levels in the bloodstream need regular monitoring. the drug was developed originally for

the evolution of mrsa 55 the treatment of infections caused by gram-positive bacteria such as s. aureus, but its side effects outweighed the benefits. vancomycin still has use in a clinical setting, as many strains remain susceptible to it, but vancomycin-intermediate s. aureus (visa) and vancomycin- resistant s. aureus (vrsa) strains have been reported.8,9 what is community-associated mrsa (ca-mrsa)? although mrsa infections were predominantly found in the hospital or clinical setting (ha-mrsa), there are now an increasing number of outbreaks of mrsa in community settings, in people who were otherwise healthy, and this has led to the term community- associated mrsa (ca-mrsa) being used. these outbreaks appear to be linked to strains that have some unique properties not seen with ha-mrsa strains. they are usually more virulent and spread more easily, cause skin and soft-tissue infections, but are commonly less resistant to antibiotics and easier to treat than ha-mrsa. some strains of mrsa produce the panton-valentine leukocidin (pvl) toxin, which can cause very serious infections.10 pvl is frequently detected in isolates of ca-mrsa obtained from infections in previously healthy children and young adults.11 the toxin destroys white blood cells and tissues, causing extensive tissue necrosis and spreading infection. recent research has demonstrated that overproduction of substances termed phenol-soluble modulins (psms) could be the main virulence factor in certain strains of ca- mrsa.12 psms are bacterial proteins that can cause a potentially fatal immune reaction called a cytokine storm, which rapidly kills white blood cells and immune cells. the main criteria differentiating ha-mrsa infections from ca-mrsa infections are that the latter are acquired by persons who have not been hospitalised within the past year, nor undergone invasive medical procedures such as dialysis, surgery, venous or urinary catheterisation. ca-mrsa is most often seen as skin or soft-tissue infections (sstis) such as boils or abscesses, but can cause more serious health problems, such as bloodstream infections or pneumonia. patients often describe having had what looked like a ‘spider bite’ before becoming ill. the involved site is red, swollen and painful and may produce yellow pus. the wound may break open or fail to heal and may develop into an abscess. in some cases,

ca-mrsa can rapidly lead to widespread and potentially fatal infection. a number of ca-mrsa strains have been found in the united states; the three most common are named usa-100, usa-300 and usa-400. ca-mrsa strain usa-300 has also been found in england and wales since at least 2002, where it is called st8- sccmec iva. there is some evidence to suggest that the usa- 300 strain is more virulent than other ca-mrsa as it produces the pvl toxin13 and is commonly found in hiv-infected patients. the usa-300 strain is genetically related to an ha-mrsa strain, which emerged in the 1960s in europe, after the introduction of methicillin. both of these strains are thought to be descendants of a methicillin-susceptible ancestral strain.14 mrsa and biofilms bacteria and other micro-organisms can attach to the surface or interface of inanimate objects and develop highly complex structures called biofilms, composed of sticky polymers produced by the bacteria. it has been estimated that biofilms are responsible for more than 80% of all infections, many of which are of nosocomial origin, meaning that they were acquired in a hospital or clinical setting.15 a common example of a biofilm is the tartar plaque found on teeth. the bacteria within the biofilm matrix interact and function as a unit rather than as individual cells, and chemical signalling processes attract other bacteria. biofilms offer a protective shield for the microbes, and bacteria in this state are more able to resist antibiotic therapy. biofilms are a significant problem with catheters, prosthetics, pacemakers, artificial heart valves, dentures and contact lenses. many chronic infections caused by s. aureus and mrsa are aided by their ability to adhere to medical devices and form a biofilm. when s. aureus grows in a biofilm it undergoes an adaptive response. genetic analysis has identified 48 genes that are induced (switched on) and 84 genes that were repressed (switched off,) during biofilm growth compared to planktonic (free-floating) growth.16 experiments on the polysaccharide polymers produced by mrsa indicate that biofilm development involves a protein, regulated by genes involved in the adaptive response. concentrations of carbon

the evolution of mrsa 57 dioxide, oxygen and glucose appear to be triggers for biofilm development, although different mechanisms of biofilm production have been recorded in mssa (methicillin-sensitive) and mrsa clinical isolates.17 can mrsa be controlled? the emergence and increasing occurrence of mrsa and other antibiotic-resistant bacteria have encouraged the exploration of novel methods of treatment.18 laboratory trials with emulsions of nanoparticles coated with a novel, non-water soluble antibiotic have shown potent activity against mrsa.19 pharmaceutical companies are exploring the use of modified versions of older antibiotics and ‘cocktails’ of antibiotics in the quest to stay one step ahead of the evolving superbug. laboratory trials of some new antibiotics show promise and there are also attempts to develop immuno-therapies and vaccines specifically against mrsa. the implementation of screening tests to detect mrsa in patients prior to admission for elective surgery has led to a reduction in hospital infection rates.20 mrsa in animals not only is mrsa causing a huge problem to human health but it has also spread to animals. it is rare for a disease to cross the species barrier but mrsa can be spread from humans to animals and from animals to humans, and the collective term, zoonosis, has been adopted. the first report of mrsa being isolated from animals was in 1972,21 and since then, studies suggest that humans were the source of this zoonotic disease, as the isolates are generally the healthcare-associated epidemic strains, emrsa-15 and emrsa-16.22 mrsa has mostly been isolated from dogs and horses, and in some cases, the people associated with the animals. although the significance of this zoonotic disease in relation to public health has not been fully assessed, there is concern over the increase in the pvl toxin seen in animal-derived s. aureus isolates.23 tracking the changes mrsa is developing at a very fast rate, with mankind desperately trying to catch up, and there is clearly a need for systematic study

and vigilance in order to gain control over infection. one initiative, in place since the late 1990s, is a sophisticated surveillance system, under which specialist laboratories in the uk, the usa and europe collect data on suspected outbreaks of mrsa. this information helps to distinguish between ha-mrsa and ca-mrsa strains, between colonising and infecting isolates, and between new episodes and relapses of infection.24 each country forwards its data to a central unit in order for the collective data to be accessible by government departments tracking the spread and evolution of mrsa.

• antifungal agents (for fungal infections), e.g. nyastatin • antiparasitic agents (for parasite infections), e.g. quinine these antimicrobial agents act on specific target sites within the micro-organism and because many of those sites are unique to the micro-organism and not to a human cell, they can be relatively non- toxic. this is why these antimicrobial agents can be used within the body without causing too many side effects. some people may be allergic or intolerant to antimicrobial compounds, including antibiotics. there are other groups of antimicrobial agents that have a more general use to prevent or treat infection, inhibit growth or reduce the numbers of micro-organisms. these are disinfectants, antiseptics and preservatives. • disinfectants can be toxic to human cells so are only used in the environment to reduce the numbers of micro-organisms on surfaces. the most commonly used, cost-effective home disinfectant is chlorine bleach. • preservatives are natural or synthetic substances that are added to products such as pharmaceuticals, paints, foods, wood, etc. to prevent decomposition by micro-organisms. natural substances such as salt, sugar and vinegar are used as traditional preservatives in food products, whereas highly toxic compounds of arsenic, copper and petroleum-based chemical compounds are used in wood preservation. • antiseptics are substances that can be applied to living tissue or skin to prevent and treat less severe or non-life threatening infections. many are used for the prevention or treatment of malodour and skin infections. antiseptics can kill all major groups of micro-organisms when used at appropriate concentrations, depending upon the properties of the micro- organism, the presence of organic matter, the temperature and the time involved. essential oils are nature’s antiseptics. their ability to kill micro- organisms has been well-documented over the centuries.

the minimum bactericidal concentration (mbc) is then determined by sub-culturing the tubes where no growth is observed. a loopful (a standard laboratory measurement) of the broth is sub-cultured onto fresh culture media by streaking across the surface of a nutrient agar plate. the concentration where no growth is observed following sub-culture is called the mbc. when using essential oils the mic and the mbc are often the same. once the mbc has been determined, the time taken to kill the micro-organism can then be ascertained. the mbc is created in a broth and known numbers of the micro-organism added, at time denoted 0 hours. at set time intervals, usually 15 minutes, 30 minutes, 1 hour, 2 hours, 4 hours, 8 hours and 24 hours, a sample is taken and the numbers of micro-organisms accurately counted. the time taken to reduce the numbers to nil is known as the killing time or the time-kill. it is also important to be aware of the numbers of micro-organisms added to the test system, as the initial concentration of the numbers of micro-organisms can affect the efficiency of killing. the standard methods for these tests can be found in the british standard testing methods or the european standard testing methods.1 reported antimicrobial activity of essential oils in a study carried out by hammer and carson in 2000, the mic/mbc of tea tree oil (melaleuca alternifolia) was compared to prescribed antifungal agents ketoconazole, miconazole and econazole, which are used to treat the fungus malassezia spp. that causes a skin condition known as psityrias versiculor. tea tree oil, at a range of 0.12–0.25% was comparable to ketoconazole. other studies have shown that tea tree oil can inhibit a wide range of bacteria, some of which are resistant to commonly used antibiotics. the analysis of tea tree oil has shown that the major terpenes/ sesquiterpines are terpinen-4-ol (38%), gamma-terpinene (20%), alpha-terpinene (10%), 1,8-cineole (4%) and alpha-pinene (5%). these are also the major antimicrobial components. these individual components that make up the whole essential oil can be antimicrobial in their own right. sometimes, they are

microbiology explained 65 more active than the parent essential oil but, individually, are often more toxic than when combined in the parent oil. the two major components from tea tree oil, 1,8-cineole (eucalyptol) and terpinen- 4-ol, both have very good antimicrobial properties. how do essential oils work as antimicrobial agents? tea tree oil, as an example, disrupts the cell membrane of the bacterium, causing a loss of potassium ions from the cell. the lipophilic (lipid loving) monoterpenes integrate with the phospholipids in the membrane and leakage occurs. antimicrobial essential oils have also been known to cause inhibition of glucose- dependent respiration in s. aureus, e. coli and c. albicans. some common essential oils with antiseptic properties are: • tea tree oil (melaleuca alternifolia) • geranium oil (pelargonium graveolens) • lavender oil (lavandula angustifolia). antimicrobial activity in vaporised form one of the most noticeable things about essential oils is their aroma. some of the fragrant parts of the essential oil are also antimicrobial. the vapours released from essential oils have been proven to be highly antimicrobial. a recent study has shown that mrsa and clostridium difficile have been killed in the laboratory by a blend of vapours released from a variety of dispersion devices. the most efficient system is the use of ‘venturi technology’ where air is forced over the surface of essential oil blends and antimicrobial vapours are released into the atmosphere, killing bacteria in the air as well as on the surface. this use of essential oils is extremely exciting for reducing the spread of airborne healthcare-associated infections.

part two antimicrobial essential oils this part of the book looks specifically at those essential oils scientifically proven to possess antibacterial activity, and aims to relay this information in a simple way. a vast amount of microbiology research over the last few decades has been able to show which oils will inhibit growth of bacteria (bacteriostatic) and which are able to kill bacteria (bactericidal).

tea tree 69 manuka honey. a commercially available jellybush honey is being marketed as tea tree honey, but jellybush is not a melaleuca. it is leptospermum polygalifolium, one of the 79 species of leptospermum in australia. all are overshadowed by their famous new zealand relative, manuka. habitat over 300 varieties of melaleuca grow throughout australia and the most well-known is melaleuca alternifolia, which thrives naturally in the north-eastern region of new south wales. there, the tea trees growing in the swampy area of bungawalbyn creek have been harvested for over 60 years. this product is known as bush oil. today the majority of tea tree oil is grown in plantations. tea trees require a lot of moisture and plantations have to be very well irrigated. m. alternifolia is a small, 5–7 metre tall, tree or shrub, with needle-like leaves similar to cyprus or rosemary. it grows prolifically across south-eastern australia. the aroma-chemistry changes from the south to the north of its natural habitat. trees in the south produce high levels of 1,8-cineole and good levels of terpinen-4- ol. trees in the north produce high terpinen-4-ol with lower levels of 1,8-cineole. tea trees produce tiny white flowers in the spring. essential oil is produced in the summer season, which in australia is between december and may. there is rapid growth during the summer months and less in the winter months. the essential oil is a pale yellow-green or clear liquid with a distinctive aroma: warm, spicy and camphoraceous. melaleuca linariifolia, also called ‘snow in summer’, is a native of eastern australia. as with m. alternifolia, it grows near watercourses or swamps, but can reach heights of up to 10 metres. its bark is like paper, which is why it is known as one of the australian ‘paper bark’ trees. melaleuca dissitiflora, commonly known as creek tea tree, is another paper bark. it grows to a height of 5 metres and is a native of western australia, south australia, northern territory and queensland.

the plant and its products the tea tree is valued for its essential oil. in order to keep up with industry demand, a great many tea tree plantations have been set up in several areas of the country. at the end of the twentieth century, australia was producing between 300 and 400 tonnes a year, and planning to increase output to 1000 tonnes, but in the early part of the twenty-first century chinese tea tree became commercially available. this has had a negative effect on australian tea tree production as many growers were unable to compete with the lower chinese prices and switched to growing other crops. the benefits of tea tree have been known to the indigenous aboriginals for many hundreds of years, but the myriad of uses for its essential oil, and the potential of tea tree oil as a commercial product, has been recognised for barely a century. tea tree is known to be antiseptic, antibacterial, antifungal, antiviral and anti- inflammatory. tea tree essential oil is analysed and graded before being offered for sale. • superior grade is the highest priced tea tree oil and is incorporated into medicinal products for human and animal use. it must offer a minimum terpinen-4-ol content of 35% and contain a maximum of 5% cineole. one pharmaceutical preparation with tea tree is an emergency dressing for burns. it comes in sterile packs ready for use by ambulance crews. • standard grade has a slightly different ratio of aroma-chemistry, containing between 30% and 35% terpinen-4-ol and up to 8% cineole. • industrial grade tea tree oil contains lower levels of terpinen-4-ol and variable levels of cineole and is used for disinfectants and detergents. chemistry of tea tree the chemical make-up of tea tree essential oil varies considerably depending on its habitat. as far back as the 1930s, researchers1 had analysed the aroma-chemicals and made a declaration that trees producing high levels of cineole, in the 20% to 40% range, were of less importance than trees with high terpinen-4-ol and low cineole levels. cineole was considered to be inactive, even though

tea tree 71 it is a normal component of tea tree, and had been employed for its germicidal activity since 1925. tea tree oil is a complex mixture of terpenes and terpene-alcohols. a typical batch analysis would show over a hundred components, with 90% of the oil content made up of the following: terpinen- 4-ol, 1,8-cineole, alpha-terpineol, terpinolene, alpha-terpinene and gamma-terpinene. the main antimicrobial component, and therefore the most valued, is the terpinen-4-ol. over the years, most australian commercial plantations have made the decision to cultivate tea trees with 1,8-cineole levels ranging from 4% to 10% and with terpinen-4-ol levels within a 30% to 40% ratio. this is in keeping with the current australian government standard which specifies that tea tree oil should contain not more than 15% 1,8-cineole, and that the major active ingredient, terpinen-4-ol, must be at least 30%. when these ratios were set it was believed that cineole inhibited the antimicrobial action of terpinen-4-ol. australian standard in 1985, the australian standard stated that the name of melaleuca alternifolia could be given to a tea tree oil provided that it met their parameter of at least 30% of terpinen-4-ol and a maximum of 15% cineole and that any of the 300 tea tree varieties could be included in the mix. the standard of 1997, which replaced the 1985 standard, specified that three main tea trees should be used – melaleuca alternifolia, melaleuca linariifolia and melaleuca dissitiflora – and that the resultant blend could still be called tea tree with the inci name of melaleuca alternifolia, as long as the minimum/maximum levels of the key components are met. this means that even when a tea tree oil is labelled as ‘organic’ it could still be a blend of the three melaleucas, as long as each of them are grown organically. there are also tea tree plantations producing tea tree oil exclusively from cloned melaleuca alternifolia. the 1997 australian standard (iso 4730: 1996, which was subsequently followed by iso 4730: 2004) states that terpinen- 4-ol type, tea tree oil ‘may be obtained by steam distillation of the foliage and terminal branchlets of:

• melaleuca alternifolia • melaleuca linariifolia • melaleuca dissitiflora • other species of melaleuca provided that the oil obtained conforms to the requirements given in this international standard.’ in 1993, research2 to determine the optimum ratio of aroma- chemicals in tea tree produced some interesting end results. the experiment was to show whether or not cineole, in excess of the specified maximum levels of 15%, would inhibit the antimicrobial action of terpinen-4-ol. the research team carried out a series of tests with staphylococcus aureus, and other microbes, using tea tree oil with added cineole, and with blending cineole with terpinen-4- ol in varying ratios. the addition of cineole in concentrations of up to 30% was seen to be synergistic rather than antagonistic, as long as the terpinen-4-ol levels did not fall below 30%. there was a decrease in antimicrobial effectiveness but only when terpinen-4-ol levels fell below 30%. the conclusion was ‘that greater antimicrobial activity for tea tree oil is not achieved by increasing terpinen-4-ol concentrations above 40%, nor by decreasing cineole levels below 40%, provided that terpinen-4- ol remains at approximately 30% to 45%. consequently optimal bioactivity can be achieved with cineole present at 20% to 40% as long as terpinen-4-ol is maintained at 25% to 40%.’ with all of its documented germicidal and healing properties, tea tree has, over the past few years, been accused of being a skin irritant. research3 has been conducted with skin patch testing. results showed that less than 1% of volunteers reported any negative effects. possible theories for the slight irritancy are that fresh tea tree does not cause any problems but that oxidised tea tree is potentially problematic. according to one commercial manufacturer of tea tree products,4 it is the para-cymene content of tea tree that creates skin irritancy in a small number of users. this chemical can be present in tea tree between 2% and 12%. para- cymene is documented as being non-toxic, but is known to be a mild to moderate skin irritant. the company uses a tea tree strain

tea tree 73 that is low in para-cymene for its skincare products. these facts have been backed up by research5 published in contact dermatitis. microbiology research with tea tree oil tea tree is one of the most-researched essential oils. studies over several years have looked at its efficacy against a number of micro- organisms. research into the antimicrobial status of tea tree goes back to 1923 when dr penfold6 looked at the way tea tree oil killed bacteria and declared that tea tree oil was 13 times stronger as a bactericide than carbolic acid. he presented his findings in 1925, to the royal society of new south wales. more recent investigation7 looked into the level of antimicrobial activity of each of the major components of tea tree oil and concluded that it was the alcohols such as terpinen-4-ol that were the most antimicrobial. the research also compared terpinen-4-ol extracted from tea tree oil with tea tree oil, and found that against staph aureus they were equally efficient. the researchers realised that when it comes to killing off staph aureus in laboratory tests, it is the wide range of components in tea tree oil that contributes to the antimicrobial activity, and that a higher level of terpinen-4-ol may not necessarily increase the oil’s antimicrobial activity. one microbiology study8 looked at the antimicrobial activity of several australasian essential oils: tea tree, australian lavender, new zealand manuka, lemongrass and eucalyptus. tea tree was found to occupy the middle position in order of antimicrobial activity. when individual aroma-chemicals were compared to tea tree in zone of inhibition tests with staph aureus the results were as follows: linalool 16.0mm tea tree 15.0mm terpinen-4-ol 14.0mm lavender 12.5mm linalyl acetate 4.5mm

tea tree 75 and that alpha-terpineol had an important synergistic influence on the antimicrobial effects of tea tree oil. in zone of inhibition tests, they found terpinen-4-ol to have a kill zone of 6.9mm and that the kill zone for tea tree was 7.9mm. an independent researcher,10 working with tea tree as an antimicrobial agent, found that increasing the level of terpinen-4- ol above a certain level did not enhance the antimicrobial effects. researchers in a london hospital11 carried out time-kill studies with the standard tea tree oil (30% terpinen-4-ol) and tea tree oil with increased concentrations of terpinen-4-ol (superior tea tree oil) in order to determine whether one was any more effective than the other. both tea tree oils were tested against a wide range of micro- organisms, isolated from bacteria taken from hospital patients. amongst the micro-organisms were methicillin-sensitive staph aureus (mssa) and methicillin-resistant/vancomycin-tolerant mrsa. a 5% concentration of each tea tree oil was used. it was found that mrsa isolates were killed more slowly than the mssa isolates and that the standard tea tree oil was less effective than the superior oil. clinical trials with tea tree oil since the turn of the new century several clinical trials have been undertaken to prove that tea tree oil is an effective agent in decolonising mrsa. other trials have been set up to disprove the prevailing conception that tea tree oil is a skin irritant. in perth, australia, the australian society for microbiology hosted ‘2001: a microbial odyssey’.12 the conference had speakers on various aspects of microbial control and included talks on viral conditions such as herpes, the fungal condition candida, as well as presentations from tea tree researchers who had been instrumental in the setting up of clinical trials. they had compared the effect of tea tree oil with the standard mupirocin treatment used for clearing mrsa from carriers. one speaker13 from the university of western australia said, ‘a pilot study of 30 mrsa carriers comparing routine mupirocin nasal ointment and triclosan skin wash with tea tree oil ointment and wash, showed one third were completely cleared by tea tree but only 13% by conventional treatment.’

in 2003, a study was set up in a sydney institute14 to assess the risk of dermatitis occurring amongst people using tea tree oil. patch testing was carried out using varying concentrations of tea tree oil in several different bases. dilutions tested were 5%, 25% and 100% and test sites were assessed every 48 hours to determine whether sensitisation had occurred. at the end of the trial period it was found that out of 300 people, only three had experienced an allergic reaction. the overall results were zero allergic reactions at a 5% tea tree dilution and 0.25% allergic reactions at 100% tea tree oil. further research to compare tea tree oil with the standard topical antibiotic mupirocin was published in 2003.15 the purpose was to compare two methods of eliminating mrsa from the nose, where it can be carried by hospital patients who could then infect themselves, and from body sites where mrsa bacteria can be harboured. the standard treatment was a 2% mupirocin nasal cream used in conjunction with a triclosan body wash. the tea tree regimen used a 4% tea tree oil ointment for use in the nose plus a body wash with 5% tea tree oil. at the end of the trial period the researchers concluded, ‘the tea tree oil products appeared to work as well as the standard hospital treatments’. in 2004, a paper16 was published on a clinical trial carried out in the uk. the randomised control trial compared the efficacy of tea tree preparations to a standard hospital regimen for the eradication of mrsa colonisation. the standard regimen comprised the topical antibiotic mupirocin in a 2% dilution, for nasal treatment, along with chlorhexidine and a silver-infiltrated cream for cleansing colonised body sites. the tea tree regimen consisted of a 10% tea tree cream and 5% tea tree in a body wash. one hundred people were involved in the five-day trial with the standard regimen, and by the end 49% were cleared. a similar number of people were treated with the tea tree products and 47% were cleared. the trial conclusion was that whilst the topical antibiotic was more effective at clearing nasal carriage of mrsa, the tea tree products worked better at clearing the colonised body sites. in 2005, a paper was published17 into the efficacy of using tea tree oil in hand-cleansing formulations. the activity of

tea tree 77 different concentrations of tea tree oil, a hygienic hand wash, an alcoholic hygienic skin wash and an alcohol-based hand rub were investigated. staph aureus and three other bacteria were significantly reduced within one-minute contact time. a three-year trial, which started in 2007 and completed in 2010, was reported in a uk medical journal18 under the title ‘doctors test tea tree oil body wash for mrsa.’ the trial was set up to see if tea tree oil in a body wash could be used to prevent critically ill, hospitalised adults from becoming infected with mrsa. a 5% tea tree preparation was used daily for washing patients in intensive care units, whilst baby soap was used for daily washing of patients in the control group. the trial concluded by stating, ‘in our study, tto body wash was applied and rinsed off the skin; had it been left on the skin for a period of time it may have been more effective. however, the consequences of not rinsing the body wash are unknown and may be detrimental.’ ‘the findings of this study show that washing critically ill patients daily with a 5% tto body wash had no significant effect on the incidence of mrsa colonisation compared with baby soap.’ contraindications • tea tree oil should not be taken internally as some of the naturally occurring aroma-chemicals can exert a depressant effect. (tea tree contains aroma-chemicals which are also found in eucalyptus leaves, the staple diet of the permanently intoxicated koala.) • in a minority of cases tea tree oil may induce irritation of the skin. if this happens, its use should be discontinued and an alternative, replacement essential oil found. • it is best to avoid using the neat oil during pregnancy and lactation, although products containing small amounts of tea tree oil, for body/hair care or for localised treatment of cuts and scratches, etc. are considered safe. • some cat owners have reported adverse effects on their pets from the use of tea tree products. however, veterinary practitioners knowledgeable in the use of essential oils regularly use tea tree oil with good results.

manuka 79 composition is unique. there is a visual similarity between kanuka and manuka as both plants produce flowers with five white petals surrounding a dark red centre. manuka flowers are spaced singly on their stems, whilst kanuka flowers grow in clusters along theirs. the size of the blossom varies too, manuka being 8mm to 12mm in diameter whilst kanuka are much smaller, at 3mm to 5mm in diameter. the chemical composition of the two plants also sets them apart, with kanuka plants containing none of the triketones found in manuka. the aroma-chemistry of kanuka does have antibacterial properties but it has been found to be significantly less potent than manuka. manuka grows prolifically right across new zealand, from coastal areas to the upper regions of the hills. it is a fast growing plant with an average height of 4 metres, but varies from a ground level shrub to an 8 metre tall tree. manuka plants are subject to seasonal variations in temperature. throughout new zealand the flowering times fall between september and february with the peak flowering time between november and january. after the flowering season is over and the bees have returned to their hives to make honey, the harvesting of leaves and small branches begins. these parts of the shrub contain a valuable essential oil. the cut material is allowed to wilt before being distilled with high- pressure steam passing through the distillation vessels. according to the new zealand crop and food research centre manuka oil takes between two and six hours to distil, as the aroma-chemicals (sesquiterpenes) in manuka are heavier than the aroma-chemicals found in the majority of aromatic plants, including kanuka, which contains mostly monoterpenes. manuka and its products the essential oil of manuka has a yellow to light brown colour with a taste and aroma described as honey-like, with a sharp but earthy flavour. the oil is widely used in the perfume and toiletries industries. manuka honey is an important industry to new zealand. a great deal of research has already been done, and continues to be done, in order to regulate the describing and naming of the varying grades of manuka honey.

medicinal grade manuka honey is incorporated into wound dressings and topical agents and these are increasingly being used to heal chronic wounds in hospitals around the world. chemistry of manuka oil and how it changes with location the essential oil distilled from manuka plants varies in aroma, chemical constituents and antibacterial potency according to where the plant was grown. researchers in new zealand have grouped manuka essential oils into three main chemotypes, and the following information is courtesy of the new zealand crop and food research centre. • a high pinene content is to be found in the northern end of the north island. • a high triketone content is to be found in the east cape area of the north island and also in the marlborough sounds area of the south island. triketones are the three ketones: leptospermone, iso-leptospermone and flavesone. • a complex mix of aroma-chemicals is to be found in manuka plants growing over the rest of new zealand. research has demonstrated that the triketones in manuka are responsible for its high antibacterial action, which is why the geographical area is of so much interest. across new zealand it has been found that the important triketone chemistry falls roughly as follows, although even plants in one area can vary in composition. triketones east cape of north island 20–33% malborough sounds area of south island 15–20% east cape (north island) and marlborough sounds 10-15% marlborough sounds and most of the north island 5–10% most of south island 5% or less

manuka 81 research with manuka oil since the mid-1990s, a considerable amount of microbiology research has gone into looking at the potential of manuka essential oil as an effective antibacterial and possible substitute for antibiotics. it is interesting to see conflicting, yet useful, results. this is possibly due to researchers using manuka oils with varying levels of triketones. in 1994, researchers1 investigated the action of manuka and kanuka oils. they used 15 strains of staph aureus, a selection of gram- positive and gram-negative bacteria, as well as other organisms. results showed manuka to have the highest activity against gram- positive organisms, recorded at approximately 20 times that of tea tree. kanuka was similar in its action to tea tree. when tested against gram-negative bacteria, kanuka and manuka were similar in their action, both two to three times less effective than tea tree. research in 1998,2 conducted to compare the antibacterial properties of australian tea tree, australian lavender, new zealand manuka, lemongrass and eucalyptus oils, found that the outcome depended on the bacteria under review. although each essential oil had some antimicrobial properties, the activity varied according to which micro-organisms were tested. manuka oil from the east cape, high in triketones, was found to have the strongest antimicrobial action against the gram-positive mrsa. in 1999, research3 was undertaken to compare the antimicrobial effects of australian tea tree with a selection of australasian essential oils from the myrtaceae family: cajeput, eucalyptus, kanuka, manuka and niaouli. overall, the highest antimicrobial activity was with tea tree oil, with the exception of the gram-positive bacteria, for which a higher activity was recorded with manuka. research4 in 2000 looked at the antimicrobial action of essential oils from a range of ‘tea trees’: australian tea tree, cajuput, niaouli, kanuka and manuka, along with the b-triketone complex isolated from manuka. results once again showed that manuka oil had the best overall effect against gram-positive bacteria. however, in 2001, research5 concluded that ‘kanuka and manuka oils as well as the b-triketone complex (the active principle of manuka) lacked any bactericidal properties. their high effectiveness against gram-positive bacteria can be explained by

their bacteriostatic effects.’ it was observed that the oils tested proved to inhibit bacterial growth, but had not actively killed the bacteria. an extract of manuka oil, composed mainly of triketones, when blended with tea tree oil, had the most powerful bactericidal effect, prompting further research. in the same year, 2001, a larger team of researchers6 took the active aroma-chemicals, b-triketone complex from manuka oil, and mixed them with tea tree oil. they then made a mix of niaouli (melaleuca viridiflora) with the b-triketone complex. against four different bacteria, including staph aureus, both blends achieved a complete kill within 240 minutes. further research7 in 2001 looked at the antibacterial effect of a blend of australian tea tree and new zealand manuka essential oils. when the blend had more manuka than tea tree, the mixture was more effective against gram-positive organisms such as staph aureus. conversely, when the mixture had a higher proportion of tea tree to manuka, the mixture was more effective against gram-negative organisms such as e. coli. although the majority of manuka research has been with honey, the triketone research findings show how potent the essential oil can be against staphylococcus aureus and mrsa. honey honey is a saturated solution of sugars and has been used to heal wounds for hundreds of years. the presence of honey in a deep wound enables the wound to stay open, yet filled with honey, bacteria are prevented from getting in, and healing can take place from the inside out. healing of a wound can only occur when the infection has been eliminated, and by using honey, bacterial growth can be inhibited whilst the body repairs the damaged flesh. honey consists of water and sugars, with approximately 15% water to 85% sugars. it is well known that bacteria can readily breed in water, but not easily in honey. honey is similar to salt, in that it has the ability to draw water to itself by osmosis, and therefore by drawing water from a wound it draws bacteria with it. honey is acidic with a ph value range of 3.2 to 4.5. this is a contributing factor to honey’s antimicrobial action on the skin, which has a ph of 5.

manuka 83 the first indication that the antimicrobial activity of honey was not just an osmotic effect was in a report published in 1919.8 researchers observed that the antibacterial potency was increased by limited dilution of honey. two decades later, research9 led to the identification of an antibacterial factor which was named ‘inhibine’. this term was used in research literature for the next 26 years until the antibacterial factor was identified as hydrogen peroxide.10 this is formed when the bee injects an enzyme (glucose oxidase) into the nectar it has collected during the process of making honey. the glucose oxidase is damaged when honey is heated and the honey loses much of its antibacterial properties. honey is sensitive to heat and light and must be carefully stored to avoid loss of its glucose oxidase activity. more recent findings by professor molan, leading expert in the field of honey and manuka research, are included in a book11 published in 2009, ‘the clearance of infection by honey may involve more than the antibacterial activity of honey, as research findings with leukocytes in cell culture indicate that honey may also work by stimulating the activity of the immune system.’ and ‘the use of hydrogen peroxide as an antiseptic has been discouraged because it is cytotoxic, but at the low levels that form in honey this is not a problem. many antiseptics in common use, including silver, are cytotoxic and slow the healing process. honey is not only non- toxic but stimulates the growth of cells involved in wound healing.’ as most honeys contain spores of clostridium botulinum, there is some concern about using honey in wounds. for this reason, honey used for commercially manufactured, impregnated dressings for topical use is always sterilised, not by heat but by gamma- irradiation. honey is a potent remedy for treating infected wounds because of its levels of acidity, its osmolarity and its hydrogen peroxide activity which increases when it comes into contact with fluid in the wound. manuka honey has all these antibacterial qualities, but in addition, it has unique manuka factor (umf), differentiating manuka from other honeys.

manuka honey manuka honeys are classified by their strength against bacteria. it was waikato university in new zealand that first discovered that manuka honey had an antibacterial agent in addition to the hydrogen peroxide activity. the discovery was made by an msc student12 in 1982, but it was not until 1988, after much further investigation by professor molan and a team of researchers that a scientific paper was published13 on the non-peroxide activity of manuka honey. this research concluded, ‘it was found that in the honeys with high antibacterial activity, a larger part of this activity was due to a factor other than hydrogen peroxide. the test micro-organism used, staphylococcus aureus, was not inhibited by the osmolarity or the acidity of the honey. the association of high antibacterial activity with particular floral sources suggests that the non-peroxide antibacterial activity is of floral origin.’ umf – unique manuka factor unique manuka factor rating is set by the active manuka honey association (amha). in a microbiology laboratory, batches of manuka honey are challenged with staphylococcus aureus and the results compared with similar tests using phenol, a carbolic acid once used as a disinfectant. it is a powerful germicide and was the active ingredient found in traditional antiseptics such as tcp, commonly used for disinfecting cuts and scrapes. the number that follows the trade mark umf is equal to the concentration of phenol used, indicating that the same strength of antibacterial activity is present in the honey. so, a manuka honey with a umf 10 rating would be equal to a 10% dilution of phenol, whilst a umf 20 rating would be equal to a 20% dilution of phenol, which would be twice as strong. the umf standard was established to identify and set apart from other manuka honey those manuka honeys which had the mysterious ‘non-hydrogen peroxide’ antibacterial activity. such honey can be diluted ten-fold or more and still completely inhibit the usual wound-infecting micro-organisms. where honey is diluted by body fluid, the acidity of honey makes a minor contribution to antibacterial activity. it is the other

manuka 85 antibacterial components that are primarily responsible for control of infection when honey is used therapeutically. some phenolic acid components of manuka honey have been identified, but these comprise just 4% of its non-hydrogen peroxide antibacterial activity. the unusual antibacterial activity in manuka honey is fully effective, even when it is undiluted. manuka honey manufacturers analyse every batch of honey as it comes from bee-keepers in each of the manuka honey producing areas, and then blend the batches together, in specific ratios, in order to produce ‘industry standard’ manuka umf 10, manuka umf 15, manuka umf 20 and higher. these high-potency honeys are often used for the treatment of mrsa infected wounds, even though the honey is not irradiated. the recommendation is to use ce regulated medical honey products to treat mrsa-infected wounds. honey that is umf 5 is not considered powerful enough to treat mrsa. outside of new zealand, an entirely different method of establishing and measuring the antibacterial activity of manuka honey was discovered by german researchers in 2006.14 since that time there has been much interest in the measurement of methyl-glyoxal. it is naturally produced in humans, animals and plants during the conversion of glucose and is believed to attack the nucleophilic centres of the bacterial cell’s dna molecule. this renders the cell unable to produce new proteins and contributes to a breakdown of the cell. methylglyoxal content methylglyoxal (mg) in manuka honey has been shown to originate from di-hydroxy-acetone (dha), present in varying amounts in the nectar of manuka flowers. freshly produced manuka honey contains low levels of mg and high levels of dha. researchers found that storage of these honeys at 37°c led to a decrease in the dha content and a related increase in methylglyoxal. very low, but measurable, levels of mg, sometimes written as mgo, are found in most honeys. manuka honey has been shown to have levels several hundred times greater. the 2006 german discovery, with research14 published in 2008, showed that naturally occurring methylglyoxal is the

dominant constituent in manuka honey, responsible for much of its antibacterial properties. mg levels in manuka honey varied from 30mg per kg to 700mg per kg. a minimum mg level of 100mg per kg was needed in order to effectively inhibit the growth of staphylococcus aureus. further, there was an indication that the umf-value, the commercially used parameter to rate the antibacterial activity of manuka honey, is directly related to the content of mgo. it was unambiguously demonstrated for the first time that mgo is directly responsible for the antibacterial activity of manuka honey, but the story is not yet fully told. as professor henle’s paper states, ‘at present, only speculations can be made concerning the origin of mgo in manuka honey’. the paper concluded, ‘with the present investigation, the occurrence of high amounts of mgo in new zealand manuka honey was demonstrated. mgo was identified as a bioactive compound responsible for the antibacterial activity of these honey samples. studies in order to clarify the pathways for the biochemical formation of mgo in manuka plants and honey are underway in our laboratory.’ umf and mg/mgo in regards to the antibacterial rating system for manuka honey the consensus seems to be: • methylglyoxal is responsible for the antibacterial activity of manuka honey and equates to the unique manuka factor (the non-peroxide antibacterial activity). • umf equates to the antibacterial power of phenol dilutions with umf 10 being equal to a 10% phenol solution. • methylglyoxal is measured in grams: mg 100 or mgo 100 = 100 grams methylglyoxal in 1kg honey. • umf 10 is comparable to mgo 100. a minimum level of mgo 100 or umf 10 is needed to inhibit the growth of staphylococcus aureus, and because there is a different rating system for mgo and umf it could be a little confusing, as the following demonstrates:

manuka 87 • umf 20 is twice as potent as umf 10 • but mgo 400 is twice as potent as mgo 100 • so umf 10 = mgo 100 but umf 20 = mgo 400. see under ‘manuka honey’ in the ‘resources: products’ section at the end of the book for more information on ratings. further research into the detection and measurement of methylglyoxal has taken place in new zealand,15 with several papers and articles being published. ongoing university research in both hemispheres of the world is trying to come to a definitive conclusion as to why the nectar of manuka flowers creates an antibacterial honey. relationship of plant, essential oil and honey in 2007, a team of researchers16 in new zealand obtained dozens of honey samples in order to identify variations in methylglyoxal levels and to try to find out why the variations occurred. they did this by isolating different fractions of manuka honey and analysing each component by high performance liquid chromatography (hplc) and concluded, ‘methyl-glyoxal levels in some plants increase significantly, from two to six fold, in response to salinity, drought and cold stress. much of the manuka honey comes from areas deemed too marginal for farming. it is possible that the soil and climatic conditions in these areas are contributing high stress levels to the plant. the excess methyl-glyoxal produced is then transferred to the honey.’ according to a 2008 article in the new zealand beekeeper,17 professor molan and his team analysed manuka honey and essential oil of manuka profiles and had this to say: ‘…tree populations in central north island and east coast represented leptospermum scoparium var. myrtifolium and an unnamed variety of manuka. the latter, growing principally on the east coast, contains triketones in the essential oil, giving the oil antibacterial activity.’ the 200915 new zealand research looking for the origin of methylglyoxal in manuka honey said, ‘we conclude that the methylglyoxal in nz manuka honey is derived by the non-enzymatic conversion of di-hydroxyacetone which occurs at high levels in the nectar for reasons which are as yet unknown.’ when looking at the

manuka 89 for wound healing, burns and various skin conditions, and to potentially have a role within cancer care.’ researchers20 at the university of wales in 2009 conducted research with three commercially available wound dressings, each impregnated with manuka honey. epidemic strain emrsa-15 was the bacteria used across all test materials. results showed that all three products had an ability to kill off the bacteria. at the end of six hours, two had reduced the bacteria to negligible levels. the third reduced the bacterial load by a smaller amount within the same timeframe. medical grade manuka honey in order for a manuka honey to achieve the status of a medicinal honey and be used in wound dressings, it must hold the european conformity (ce) mark and have regulatory approval as a sterile medical device. medical grade manuka honey products are gaining acceptance in hospitals and clinics for the treatment of wounds, burns and skin ulcers. there is a reduction in inflammation, and both swelling and pain are reduced. infected wounds give off a bad odour which is eliminated by the regular use of manuka products. the consistency and properties of manuka honey make it easier for wounds to heal. dead tissue is drawn into the honey, and because honey always retains its moisture, this facilitates the painless removal of dressings without damaging new skin tissue. this results in quicker healing, less scarring and significantly less distress for the patient when dressings are changed. several companies are now producing manuka-impregnated wound dressings as well as creams for topical application. excellent results are being obtained on infected wounds which were not responding to standard antibiotic and antiseptic therapy. reports from medical personnel already utilising manuka honey in a hospital environment are that umf 10 is adequate for treating leg ulcers, but to treat a more serious bacterial infection it is recommended to use umf 15 or higher. manuka honey with a quality assured level of antibacterial activity is used by the companies marketing manuka honey products for wound care. every product has to conform to strict guidelines set down by the european regulatory agencies.

contraindications manuka honey and products containing manuka honey should not be used by: • anyone with a known sensitivity to bees • babies under the age of one year: honey sometimes contains spores of clostridium botulinum • some hay fever sufferers • vegans, as honey is produced by hard working bees and is the hive’s winter foodstore. diabetics are advised not to consume manuka honey, although it is safe to treat a wound with a manuka honey wound dressing, as the sugars in honey cannot be absorbed through the skin. however, a diabetic person with a wound should in the first instance seek medical attention.

habitat and how it alters the chemistry the thyme plant is polymorphous. polymorphism means that within the plant chemical changes occur, many times over, depending on the environment in which it is growing. so, for example, if several identical common thyme plants (thymus vulgaris) were to be planted in different locations and altitudes, and furthermore, that each was subject to differing soil types, levels of sunshine, exposure to or protection from wind and early morning frosts, then the individual thymes would vary in their mix of aroma-chemicals. researchers1 in the south of france carried out such an experiment in and around a valley. the results of chemical analysis demonstrated the thyme plant’s ability for adaptive variation. charles darwin first noted this process of natural selection among thyme plants. some of the numerous thymus vulgaris sub-species have been deliberately cloned in order to produce a plant with a specific chemotype. for example, a plant rich in thymol will be of significant importance to some, whereas a thyme rich in linalool may be of great interest to others. thyme oil is universally recognised as being one of the most powerful of aromatic plants. authors of books promoting the use of essential oils advise caution when using thyme oil. it is useful to have some comprehension of thyme’s polymorphous qualities, as it goes some way towards explaining why some thymes are too powerful to use on the skin of healthy adults whilst other thymes can be safely used on children. thyme and its products the cultivation of thyme is split between the fresh herb for culinary use, the whole plant for garden use, the dried herb for culinary/ food industry use, the dried herb from which a tincture is obtained for medicinal use and the essential oil which is mainly sold to the food industry, but increasingly to the pharmaceutical, aromatherapy and natural cosmetics industries. thyme oil from spain is usually red when distilled, and is sold as ‘red thyme’. the red colour is caused by a reaction between the thymol content of the plant and the iron in the field stills. ‘white thyme’ is not a separate species of thyme, but is rectified red thyme oil. what this means is that the red thyme oil is distilled for a

thyme 93 second time in stainless steel equipment. white thyme has a high thymol content as the rectification process causes a loss of some of the more volatile aromatic compounds. thyme essential oil of the variety of thymes under cultivation for their essential oil, the five species of greatest economic importance are: thymus vulgaris, thymus zygis, thymus capitatus, thymus serpyllum and thymus mastichina. of the aroma-chemicals found within the plants, the most widely used compounds are thymol and carvacrol, followed by linalool. both thymol and carvacrol are phenols, which can be irritating to the skin. for this reason some thyme growers have sought to clone the linalool and geraniol chemotypes for the aromatherapy and toiletries market, as the phenol content of these chemotypes is greatly reduced. thymes with high levels of thymol and carvacrol have been found to be the most antimicrobial and are used in the food industry to extend the shelf life of meats and processed food. thyme essential oil and thymol are acquired by the pharmaceutical industry for use in cough medicines and for oral hygiene products. commercially available thyme oil is generally labelled as ‘red thyme’ or ‘white thyme’. red thyme oil is the crude product of common thyme, whereas white thyme oil, as mentioned, is rectified red thyme. chemistry of thyme within thyme plants there are dozens of different aromatic compounds. the 20 most common are listed in order of the quantity obtained: 1. thymol 2. carvacol 3. linalool 4. para-cymene 5. gamma-terpinene 6. borneol 7. 1,8-cineole 8. geraniol 9. alpha-terpinene 10. alpha-terpineol 11. beta-caryophyllene 12. geranyl acetate 13. camphor 14. linalyl acetate 15. citral 16. myrcene 17. terpinen-4-ol 18. trans-sabinene 19. alpha-pinene 20. camphene

other minor constituents added together contribute to a small percentage of the entire oil. typical chemistry of common thyme (thymus vulgaris) phenols thymol 66.95% + carvacrol 3.73% = 70.73% alcohols linalool 2.51% + terpinen-4-ol 0.72% = 3.23% terpenes total combined terpenes* = 20.49% *para-cymene 10.83%, gamma-terpinene 5.23%, alpha-pinene 0.43%, camphene 0.22%, myrcene 0.84%, alpha-terpinene 0.69, limonene 0.35%, beta-caryophyllene 1.9% research with thyme oil thyme oil has been used as a fumigant in sick rooms and places of worship by many ancient civilisations. since 1887,2 thyme was recognised as having antibacterial properties, although it wasn’t until the 1980s that it became the subject of scientific interest. the majority of microbiology research into thyme’s ability to kill bacteria has been published in food journals. one of the many bacteria responsible for food decay is staphylococcus aureus, so it is the common staph bacterium and not mrsa that has been the subject of most of the microbiology research with thyme oil. along with some other essential oils, thyme oil is widely recognised as a reliable preservative for the food industry. another strand of research has been with the plaque-inhibiting properties of thyme oil and thymol (the plant’s major constituent) which has led to thyme oil being widely used as a treatment for, and deterrent against, gum disease. it is found in over-the-counter oral hygiene products. however, the use of thyme in the pharmaceutical industry has remained small in comparison to its use in the food industry. there has been little enthusiasm for the employment of thyme for topical use as the chemical make-up of most thymes includes significant levels of phenols, which can be an irritant to the skin. many species of thyme contain in excess of 50% phenols (a combination of thymol and carvacrol), with some thymes containing 80% phenols. in the 1990s, researchers3 established that thymol

similar (to each other) levels of antimicrobial activity, but one of the thymes appeared to be more efficient…in particular against staph aureus and four other bacteria.’ this thyme oil contained the highest concentrations of phenols, at 67.5%. in 2007, researchers7 in spain looked at three species of thyme (some with chemotypes) growing in murcia, as antimicrobial agents for the food industry. there are ten micro-organisms of significant importance in the food industry and each was assessed against the thyme oils. the strain of staph aureus tested was cect 239. results against staph aureus total phenols zoi thymus zygis chemotype – thymol 71.6% 25.0mm chemotype – 39% linalool 0.5% 18.3mm chemotype – 82% linalool 2.2% 18.6mm thymus vulgaris chemotype – thymol 61.8% 45.0mm thymus hyemalis chemotype – carvacrol 48.4% 35.0mm chemotype – thymol/linalool 18.0% 32.3mm chemotype – thymol 43.9% 38.6mm mic and mbc tests showed that the most antimicrobial thymes were t. hyemalis (thymol and carvacrol chemotypes), t. zygis (thymol chemotype) and t. vulgaris (thymol chemotype). ‘in our study, most of the antimicrobial activity in essential oils from the thymus genus appears to be associated with the phenolic compounds: thymol and carvacrol.’ however, the authors concluded that minor compounds could play an important part in the antimicrobial potency of the oil: ‘results suggest that it could be a synergistic action among phenolic compounds and cited compounds.’

thyme 97 canadian researchers8 evaluated 28 essential oils for their antibacterial properties against four bacteria prevalent in the food industry. staphylococcus aureus was one of the four. of the essential oils tested, the most effective were thyme oils. thymus vulgaris (chemotype thymol), thymus serpyllum, and thymus satureioides, each having significant levels of thymol and carvacrol, were found to be the most effective against the four bacterial pathogens responsible for outbreaks of food poisoning. other varieties of thyme: thymus mastichina, thymus vulgaris (chemotype thuyanol), thymus vulgaris (chemotype linalool), were still effective but required a higher dosage to inhibit bacterial growth. the most effective essential oil was a close relative of thyme, spanish oregano (thymus capitatus), containing 76% carvacrol and 5% thymol. in canada alone, the cost of treating foodborne disease due to contamination with bacteria is estimated to be $500 million a year. the above results bear out those of numerous other researchers: that thyme oils with high levels of phenols are very effective agents against staphylococcus aureus and other bacteria, and are perfectly suited for use in the food industry. very little research has been carried out into the bacteriostatic properties of thyme oil against mrsa. there is some published mrsa research that includes mention of white thyme oil being used in tandem with manufactured antimicrobials such as quaternary ammonium. in 1997, research9 compared the efficacy of thyme oil against the essential oils of tea tree, lavender, mint and juniper, after each had been challenged with 15 strains of mrsa isolates taken from hospital in-patients. results showed that tea tree was the most bactericidal/bacteriostatic. ‘tea tree oil was the most potent of the five oils…these results are identical to those reported previously for strains isolated in both the uk and australia.’ in laboratory studies, us researchers10 compared three different pharmaceutical compounds against four strains of mrsa. the compounds were: neomycin + polymyxin, polymyxin + gramicidin, benzethonium chloride (a quaternary ammonium) + tea tree + white thyme oil. this last blend had the most rapid action.

in summary out of several hundred species of thyme, only a few have been used in microbiology research, and often without an analysis of the oil’s chemistry. primarily the research has centred on common thyme, and its major compounds, as a food preservative. to date, when thyme has been used in mrsa research, it has either been in combination with other antimicrobials or, when it comes under comparison with other essential oils, it has been found to be less effective than tea tree oil. thyme vs mrsa: new microbiology research in 2003, i began my own studies into mrsa. i was looking for an essential oil, or blend of essential oils, powerful enough to kill the evolving superbug. i had already studied and written about tea tree oil and was impressed with its pedigree. however, as two of my three children are unable to tolerate tea tree oil on their skin, and a small percentage of users, worldwide, are estimated to have experienced similar problems, i was hoping to find a viable alternative. in 2005, i began working with scientists at the university of brighton11 to try to find an effective essential oil, or blend of essential oils, that would be safe to use whilst having the ability to kill epidemic strains emrsa-15 and emrsa-16. common thyme oil was not included in tests, as its skin irritant factor is well known, but i did include a sub-species of thyme – a thyme linalool – which produced good results against both epidemic strains as well as two strains of mssa (methicillin-sensitive staphylococcus aureus). a search was then made to find a consistently available source of the right sort of thyme oil, as without a secure supply chain the research would remain academic. eventually i began working with a distiller of essential oils with a vast knowledge of essential oil chemistry, in order to find the perfect combination of thyme oils. several different thymes were investigated, resulting in a blend of four thymes which gave a thyme linalool with a slightly higher thymol content than is normally found in a thyme linalool. with a further round of university microbiology tests already scheduled, i sent through the thyme blend, which became known as ‘oil b’ in testing. this round of tests challenged epidemic strains emrsa-15

further research with essential oils 105 antiseptic with additional antifungal and insect repellent properties. the essential oil is a pale yellow/green colour, with a camphor- like, almost medicinal aroma. chemistry when analysed by gas chromatography-mass spectrometry (gsms), lelechwa was identified as being composed of: fenchol 15.90% 1,8-cineole 14.30% eucalyptol 13.90% alpha-terpineol 6.51% alpha-pinene 6.87% trans-pinene hydrate 6.51% terpinen-4-ol 4.74% camphene 3.76% + beta-pinene, delta-2-carene, alpha-phellandrene, limonene, gamma- terpinene, terpinolene, fenchone, trans-caryophyllene, bergamotene, delta-cadinene and alpha-curcumene microbiology microbiology research has been undertaken in order to support a patent5 application for the use of lelechwa in medicated products, with its use against mrsa being one of the main ‘inventions’. one of the claims is that ‘compositions of the invention can be used…in the control of airborne infection and for routine protection against antibiotic-resistant bacteria such as, for example, mrsa.’ in 2005, an international team of scientists6 conducted microbiological tests with lelechwa against a range of micro- organisms. the essential oil was screened for antimicrobial activity against both gram-positive (which included staphylococcus aureus) and gram-negative bacteria, as well as a pathogenic fungus. with the exception of one of the gram-negatives that showed resistance, lelechwa oil had pronounced antibacterial and antifungal activities. agonis (taxandria fragrans) agonis fragrans is a fairly new essential oil to the commercial market in comparison to tea tree and eucalyptus oils, which have been exported from australia for decades. research into the uses of agonis is in its infancy; it belongs to the myrtaceae family along with tea tree, eucalyptus, manuka and myrtle. this shrub has undergone

a few name changes7 in just over a decade. since 1998, it has been known as agonis sp. coarse tea tree, agonis sp. coarse agonis and agonis fragrans but since 2007 it has been called taxandria fragrans by western australian flora, although agonis fragrans is still in use. it is sometimes referred to as fragrant ti-tree. geographical location the agonis tree is native to the south-west corner of western australia, but is now being grown commercially across western australia, notably between perth and albany. habitat the shrub grows up to 2 metres tall, flowering between february and may. the flowers are clustered toward the end of stems/ branches and resemble manuka flowers with small white petals surrounding a dark red centre. it likes waterlogged soil and can be found in swampy areas and along waterways. the distilled oil is pale yellow. the aroma is described variously as: citrusy, spicy- cinnamon and sweet balsamic. commercial production of agonis began in the 1990s, with the establishment of plantations in the south-western corner of western australia.8 a particular clone is now being marketed internationally for the treatment of minor ailments and for use in cosmetic products. chemistry analysis9 of the high cineole agonis shows the proportion of aroma- chemicals across five essential oil samples to be between: 1,8-cineole 28.3–34.1% alpha-pinene 13.7–28.0% linalool 3.3–14.7% alpha-terpineol 5.2–5.9% myrtenol 1.7–5.5% terpinen-4-ol 2.9–3.9% para-cymene 2.4–2.8% myrcene 1.6–2.7% gamma-terpinene 1.9–2.4% beta-pinene 1.4–1.9% + minor aroma-chemicals across all five oils tested ranged from 0–3.8%

further research with essential oils 109 antimicrobial vapours to be released into the atmosphere. testing showed that the single oils produced little or no inhibition of the bacteria, whereas some of the combinations had good zones of inhibition. the research paper16 concluded, ‘essential oils have a huge potential for exploitation in the healthcare setting over the forthcoming years. many of the bacteria we now see routinely in hospitals are resistant to most antibiotics and alternative treatments have to be found. essential oils offer a whole new concept to prevention and treatment of infectious disease in the future.’ more research with antimicrobial essential oils united states utah research conducted in 2008, at a utah university,17 looked at the inhibitory effects of 91 single essential oils and 64 blends of essential oils on the growth of staphylococcus aureus. the bacterium used was an mrsa staph atcc 700699,18 tested on agar plates at a non-specified inoculum. of the 91 single oils tested, the zone of inhibition results demonstrated that the majority had inhibitory properties. the essential oils with a zone of inhibition of 50mm or larger were: lemon myrtle, lemongrass, melissa, mountain savoury, cinnamon bark, cumin, lemon scented eucalyptus and common thyme. of the blends, a handful had inhibition zones of 50mm or more. zone of inhibition tests are used for first stage research to ascertain the minimum inhibitory concentration. united kingdom ayrshire the antimicrobial activity of a selection of essential oils was investigated in a scottish college19 in 1999. the essential oils under consideration were: black pepper, clove, geranium, nutmeg, oregano and common thyme. each oil was tested against 25 bacteria, which included staph aureus. components with the widest spectrum of activity were found to be, in descending order: thymol, carvacrol, alpha-terpineol, terpinen-4-ol, eugenol and linalool, followed by those exhibiting lesser activity.

the researchers found, ‘the volatile oils exhibited considerable inhibitory effects against all the organisms under test while their major components demonstrated various degrees of growth inhibition’ and concluded, ‘the plant extracts clearly demonstrate antibacterial properties, although the mechanistic processes are poorly understood. these activities suggest potential use as chemotherapeutic agents, food preserving agents and disinfectants. their volatility would be a distinct advantage in lowering microbial contamination in air and on difficult to reach surfaces.’ india bhubaneswar india is a country where aromatic plants grow in abundance. many are commercially grown, not only for food spices, but also for their essential oils. researchers20 in india looked into the antimicrobial properties of ten essential oils, two of them not widely available. of the eight oils of general interest, each was tested for antibacterial activity against 22 bacteria, which included staphylococcus aureus. the essential oils were: citronella, eucalyptus, geranium, lemongrass, orange, palmarosa, patchouli and peppermint. the overall inhibitory results were as follows: lemongrass, eucalyptus, peppermint and orange oils were effective against all the 22 bacterial strains. palmarosa oil inhibited 21 bacteria, patchouli inhibited 20, citronella 15 strains and geranium oil was inhibitory to 12 bacterial strains. the mic of the oils varied widely, with some essential oils working at very low dilution and others requiring more than a hundred-fold stronger dilution before they were effective at inhibiting growth of the bacteria. chennai a team of microbiologists21 in chennai set up a research programme to evaluate the antibacterial activity of 21 plant essential oils against six bacterial species. the objective was to determine the minimum levels of each essential oil needed in order to prevent growth of bacterial culture. six micro-organisms were obtained22 including staphylococcus aureus atcc 25923. results revealed that the selected essential oils exhibited antibacterial activity with varying magnitudes: 19 showed activity

further research with essential oils 111 against one or more bacteria. cinnamon, lime, geranium, rosemary, orange, lemon and clove showed maximum activity against all the bacterial species tested, whereas aniseed, eucalyptus and camphor failed to inhibit any of the tested strains. both gram-positive and gram-negative bacteria were sensitive to the essential oils, with staph aureus sensitive to 14 oils. in general, cinnamon oil showed significant inhibitory effect against bacteria giving a zone of inhibition of 20.8mm. moderate effects were seen in lime, clove and lemon oils. based on the zone of inhibition screening, seven of the original 21 essential oils: cinnamon, clove, geranium, lemon, lime, orange and rosemary that had been identified as having antibacterial activity then had their minimum inhibitory concentrations determined. mics for the seven oils revealed that cinnamon oil had the greatest antibacterial activity, with mic values ranging from 0.8% to 3.2%, followed by clove oil with mic values ranging from 1.6% to 6.4%. the other oils showed moderate mic values. in this study cinnamon, clove, geranium, lemon, lime, orange and rosemary oils exhibited the strongest activity against selected bacterial strains. it is interesting to note that lemon oil produced good results in this study, in marked contrast to results obtained by other researchers. bulgaria micro-organisms of interest to the veterinary industry in bulgaria,23 12 essential oils were tested for their inhibitory activity against 14 micro-organisms of veterinary interest. the specified essential oils they tested were: • common thyme (thymus vulgaris) • clove (syzygium aromaticum) • cinnamon (cinnamomum aromaticum) • marjoram (origanum marjorana) • tea tree (melaleuca alternifolia) • clary sage (salvia sclarea) • peppermint (mentha piperita)

• lemon (citrus limonum) • lemongrass (cymbopogon citratus) • grapefruit (citrus paradisi) • oregano (origanum vulgare) • mandarin (citrus reticulata var. madurensis). the 14 micro-organisms used included staphylococcus aureus atcc 25923. the researchers noted interesting inhibitory effects against the bacterial and yeast isolates taken from animals. mics varied from 0.8% to 2%. zones of inhibition varied from 12mm to more than 20mm. thyme, cinnamon, peppermint, lemongrass and oregano oils inhibited all organisms at 2.0%. good antimicrobial activities were exhibited by lemongrass, clary sage and peppermint oils. lemon, grapefruit and mandarin oils did not show antimicrobial activity against the micro-organisms. the researchers concluded, ‘in our study cinnamon, oregano, lemongrass and thyme exhibit the strongest activity against the selected strains with veterinary interest.’ for further information hundreds of research papers have been published on the antimicrobial activity of essential oils and readers wishing to know more can do an internet search by going to google scholar and typing ‘antimicrobial essential oils for mrsa’ into the search bar. the abstracts are always free; occasionally the entire paper is also free, but usually the publisher charges for the research article.

bacteriophages (phages) are viruses that specifically target bacteria and cannot infect mammalian cells. each phage is specific to a particular bacterium, so there will be a phage to kill staphylococcus aureus, a phage to kill e. coli, phages that kill streptococci, phages that kill salmonellae, and so on. as each phage is specific to one particular bacterium, it means that the body’s good bacteria, the intestinal flora, are not damaged. this is of great benefit to a sick person as the immune system remains intact. the unique quality of using phages over antibiotic therapy is that only the targeted bacterium is killed. there is little possibility of resistance being transferred to surviving bacteria, as happens when antibiotics are used, as there are no survivors. if we were to think of different bacteria as having a specific colour and that e. coli was, for example, the colour ‘orange’ then once the e. coli phage was administered it would seek out and destroy only the ‘orange’ bacteria, leaving all the other colours of bacteria intact. phages multiply at the site of infection, which in the case of e. coli would be the intestinal tract. once in place the phages multiply until all targeted bacteria have been killed. from a single bacterial cell, in excess of a hundred new phage virus particles may be liberated and each of these is able to go on to attack a new bacterial cell. these infection cycles have the potential to continue until all susceptible bacterial cells have been killed. phage therapy would seem to offer the prospect of a cure for bacterial infections that are currently outwitting antibiotic therapy, and without any of the side effects, such as diarrhoea, which often accompanies antibiotic treatment. however, the downside, according to thomas hausler, author of a book on phage therapy,3 is that they are more difficult to administer than antibiotics as the physician needs special training in order to correctly prescribe and use phages. a precise diagnosis must be obtained in advance of prescribing phage therapy. a ‘broad-spectrum’ phage to completely replace broad-spectrum antibiotics does not exist at present. however, in georgia, home of phage therapy, a cocktail of phages, known as a ‘pyophage’ is being used with success to treat a wide range of pathogens.4 one of their most important phages is a highly virulent monoclonal staphylococcal bacteriophage active against 80% to 95% of staph aureus strains, including mrsa. this phage mixture, which is effective against staphylococci, streptococci, p. aeruginosa, and

to its biological activity and the antibacterial activity10 of garlic extracts against mrsa. silver crude silver was used to heal infections as far back as 69 bc, as even then it was known to control the spread of infection and to prevent meat from spoiling. silver was used throughout the greco- roman empire, and hippocrates, the father of medicine, taught his students that silver healed wounds and controlled disease. the healing properties of silver nitrate were described in the physicians’ pharmacopoeia of the time. although a popular form of medicine, one side effect from the treatment can be discolouration of the skin, as the overuse of silver can cause a condition known as agyria. the name is taken from the chemical symbol for silver, ag. once the skin turns a blue-grey colour, the process cannot be reversed. in the late 1800s, a chemist11 found that silver could be diffused through a liquid to make a solution. he coined the term ‘colloidal’ for it, from the greek word ‘kolla’ which means glue-like, although as it was not a true solution, it became known as a ‘sol’. a few years later, a swiss botanist12 working with soft metals such as silver, found them to be antimicrobial when in the form of a hydrosol, and he coined the term oligodynamic. several researchers during the first half of the twentieth century increased the understanding of silver’s capability and created many medicinal silver-based products. millions of people around the world, notably within the united states, were treated with silver ions. this trend continued until the widespread introduction of antibiotics in 1940. fresh research into the use of silver as a biocidal agent began in 1970, under the direction of nasa. university scientists13 were able to achieve a significant biocidal effect, with kill rates within four hours, when working with silver ions. now, in the twenty-first century, silver is being re-evaluated as an antimicrobial in the light of increasing numbers of antibiotic-resistant infections. silver can be chemically bonded to a doorknob, or painted surface, so that when bacteria are detected, the silver compound releases silver ions, killing all microbes that come into contact with it. silver has been used in several innovative ways:

other ways to combat mrsa 117 • as a paint additive providing a non-toxic, silver-based coating for hospital air ducts so that when bacteria are detected, the silver compound releases silver ions to the surface, killing microbes for the life of the product • in hand soap and washing powder • as a coating for washing-machine drums • for wound dressings. silver research with mrsa as silver is an inorganic material, it has withstood the bacterial resistance that has dogged antibiotics, and as silver is a natural material it does not cause problems in the environment when discharged from the body, unlike antibiotics and many other medications which are not environmentally neutral. one us research team14 says, ‘silver kills microbes by interacting with multiple binding sites that are unlike those used by organic antibiotics; the use of silver is therefore unlikely to promote antibiotic resistance.’ from the emerging realisation that antibiotics were unable to overcome the problem of bacterial resistance, and in particular mrsa, silver has regained some respect from the scientific and medical professions. by the end of the first decade of the twenty-first century there were several pharmaceutical companies producing wound dressings that incorporated silver ions/nanoparticles. in 2007, a team of researchers15 conducted microbiology trials with several bacteria including staphylococcus aureus, where zone of inhibition tests were carried out using a nanocrystalline silver and a commercially available silver dressing. the objective was to determine the antimicrobial activity of silver-containing dressings on wounds affected by biofilm. results varied between dressings and microbes, with zone of inhibition for the staphylococcus aureus being 2.6mm to 6mm. further research in 2007,16 looked at whether there was any danger of silver, when utilised as a wound dressing, leading to bacterial resistance. the researcher evaluated other people’s research procedures and measurements, and noted that different silver products released silver at different rates. he concluded, ‘the clinical incidence of silver resistance remains low, and emergence of

other ways to combat mrsa 119 a death sentence, nor should it be now. back then many natural products were found to be effective. what differentiates the two eras is that we now have laboratory evidence to prove why and how these products work against bacteria, whereas in the pre-antibiotic era there was scant scientific evidence. in general, antimicrobial products were used empirically, as knowledge of observable effects was passed down from generation to generation, or written up in herbals and medical compendiums. then, as now, the key to a successful outcome was to treat early, not to wait for the bacterial growth to reach critical mass and invade the bloodstream. once in the bloodstream mrsa is so much more difficult to treat, needing intravenous antibiotic treatment in order to save the life of the patient. seventy years ago the old saying ‘a stitch in time saves nine’ would have been quoted. today we would interpret this as ‘prevention is better than cure’.

europe-wide levels of mrsa resistance by end of 2010 malta 55% uk 30% cyprus 55% other european countries 29% greece 40% norway 0%+ ireland 33% holland 0%+ mrsa strains in the united states type number usa 100 usa 200 usa 300 usa 400 usa 500 usa 600 usa 700 usa 800 usa 900 usa 1000 usa 1100 usa 1200 brazilian* iberian* *these two clones are also responsible for 90% of mrsa outbreaks at the largest teaching hospital in portugal. similarity of different mrsa strains in north america usa 300 and usa 500 similar usa 400 and usa 700 similar usa 400 and usa 800 similar usa 1100 and usa 200 similar usa 100 unique, lacking in similarity to any other strain usa 600 unique, lacking in similarity to any other strain research into ca-mrsa strain typing was undertaken at diversilab, durham, north carolina, usa. analysis of animal mrsa from dogs and cats in europe epidemic strain emrsa-15 95.4% epidemic strain emrsa-16 1.6% other mrsa 3.0%

reasons for antibiotic resistance 127 or wards by employing routine prophylaxis use of antibiotics on uninfected patients “just in case”…this results in excessive antibiotic use and is certainly counter productive.’1 when antibiotics are freely available there is no control over the purchase of antibiotics in many developing countries, where they can be bought as easily as sweets or cigarettes. poorer citizens of the united states, unable to afford to visit a doctor, may opt to purchase the cheapest available antibiotic from an internet company when they, or a family member, are unwell. antibiotic use in agricultural animals antibiotics were routinely fed to cattle, pigs and other livestock in order to increase growth and prevent disease: disease often caused by unsanitary factory farming methods. although many countries have banned the use of antibiotics to promote growth and have created laws whereby only a vet can prescribe antibiotics for specific reasons, others continue to feed massive amounts of antibiotics to animals as a prophylactic. this allows them to legally add antibiotics to the animal feed. animals have been given the very same antibiotics that are needed by humans to combat disease. a serious consequence of the bad practice of feeding antibiotics to animals means that human consumers are eating meat containing traces of antibiotics. whatever is consumed ends up in the waterways and is eventually piped into people’s homes. almost all the water we drink, use for cooking, shower or bathe in, contains traces of antibiotics. evolutionary intelligence bacteria have evolved, and in doing so, developed not only clever defence mechanisms against being killed by antibiotics, but have also developed sophisticated means of attack, like the pvl strains of mrsa that attack and kill leukocytes, a vital part of the human immune system. recent research with phenol soluble modulins (psms) is pointing to another evolutionary step: that ca-mrsa with psms can cause a cytokine storm, where a fatal immune response is triggered.

risk factors 129 infections result in a longer hospital stay for the patient, the number of infected patients on any one day will be closer to one in ten. elderly and frail the elderly of many developed countries are often required to move back and forth from their nursing home to a hospital. nursing homes take care of the elderly with chronic health conditions, but when an acute problem presents, such as a fall or influenza, the elderly person will usually be admitted to hospital. for many elderly citizens these transfers happen on a regular basis. ha- mrsa moves effortlessly from hospital to nursing home and back again to hospital. mrsa has been found in the oral cavity of several age groups, but most frequently in people of 70 years or older, with dentures also found to be colonised. a risk factor for oral carriage of mrsa among older people in long-term care is related to repeated antibiotic use and poor nutrition. babies and young children when young children are hospitalised it is generally because of a serious health problem and/or a need for surgery. the immune system will be challenged by the illness itself, the surgery, the anaesthesia and prescribed drugs; any one of these can weaken the immune system making the young patient more vulnerable to becoming infected with mrsa. broken skin other risk factors include having a break in the skin where bacteria may enter, and this includes anyone suffering from eczema, as they could contract mrsa whilst visiting an elderly relative in a nursing home just as easily as when they are in hospital as an in-patient. community-associated mrsa outside of healthcare facilities, mrsa mainly manifests in the form of skin infections, causing swelling or growth, from a small pimple to a lump the size of a chicken’s egg. occasionally it causes a flesh eating disease in which tissue begins to die off, necessitating surgery to remove the decayed flesh. the amputation of an arm or

leg may become necessary to prevent infection spreading to other parts of the body. what to look for a bump or infected area on the skin that may be: • red • warm to the touch • swollen • painful • full of pus or other drainage. if you or someone in your family has these signs, especially with a fever, cover the area with a bandage and see your doctor.1 a number of conditions and situations appear to increase the risk of contracting ca-mrsa infections and the following lists have been taken from advisory organisations. the usa currently experiences the highest number of ca-mrsa cases, and many of the following risk factors, at the moment, are specific to the us. ca-mrsa is on the increase in europe. risk factors for ca-mrsa in no particular order: • participation in contact sports. most at risk are football players, wrestlers and basketball players, both professional and student. • sharing of towels or razors in sports facilities. • sharing of hot tubs. • busy gyms, particularly locker rooms, where there is a moist, sweaty atmosphere. moist, warm areas are a perfect breeding ground for bacteria. • shared exercise equipment, unless wiped down between users. • living in overcrowded conditions such as prisons. • military bases: cramped living quarters. • day care centres for the elderly.

risk factors 131 • poverty: people forced to live in cramped conditions and who suffer lack of hygiene. • day surgery: which could include circumcision or cosmetic surgery. • dentistry: tooth extraction. • tattoos. • childbirth, as bacteria could be on the hands of midwife/ gynaecologist. • having a weakened immune system: for example, a person living with hiv/aids, anyone receiving chemotherapy, transplant patients. • living with chronic ailments such as diabetes, severe asthma or eczema. • intravenous drug users. • a severe attack of influenza can leave a person vulnerable to bacterial invasion. ca-mrsa pneumonia appears to occur most commonly following an influenza-like illness and may have special relevance given the emergence of swine flu (h1n1 influenza). most worrying is that more children than adults are affected by flu-mrsa. flu-mrsa cases are often fatal. • highest infection rate is in people of 65 years or more. • african americans are affected at twice the rate of other americans. • native americans and pacific island peoples show raised vulnerability. • although swimming in the ocean is not classified as a risk factor, a team of researchers in florida have determined that bacteria can survive in the waters off florida, as skin cells are shed whilst swimming, and that mrsa could potentially be picked up by bathers. • travelling on public transport comes with risks as mrsa bacteria can live on floors, doorknobs, handles, seats and benches; it is easy for the superbug to spread.

risk for our animals researchers in the uk have assessed risk factors for mrsa in dogs and cats as: • contact with human carriers • surgical implants • admission to veterinary clinic for two days or longer • having had at least three courses of antibiotics.

• do not allow your wounds or vulnerable sites to be attended to whilst cleaning is being done, nor within one hour of its completion. dust carries germs and should be allowed to settle before your wounds are uncovered. • never allow your wounds to be left uncovered even for the briefest time. the longer they are exposed the greater the chance of infection getting in. • the most vulnerable areas of skin prone to bed sores and consequent infection are the buttocks, elbows and heels. at the slightest hint of soreness insist on the area being sanitised and treated as a matter of urgency. do not delay, as this is a major entry point for infection. • never put bare feet on the ward floor. • do not allow visitors to sit on your bed. • paper may harbour infection. politely decline another patient’s offer of the use of their reading matter; avoid offence by explaining why. • ask your relatives to take laundry home in a secure plastic bag and wash separately in a hot wash above 65ºc, or with a disinfectant. mrsa can live in fabric for approximately 60 days and withstand lower washing temperatures. • it is recommended that you wash with antibacterial soap and shampoo for at least three days before admission, especially prior to surgery, as this may prevent you being a carrier and infecting yourself and others. make sure that the groin area, between the toes and any other folds of skin are thoroughly cleansed and dried. • take a supply of antibacterial soaps and antiseptic wipes into hospital with you. use these until you are discharged. • there are many proprietary antibacterial preparations which may well add to your safety and may prevent the spread of infection. be aware, however, that use of these preparations may offer a modicum of protection but will not prevent you from contracting a hospital infection, as in order for them to be totally effective it is necessary for everyone in the hospital to adhere to high hygiene standards.

before going into hospital 137 forget that using soap and water is still a valid way of removing bacteria. we are constantly becoming contaminated when we touch items that are also touched by other people, for example lift buttons, door handles and shopping trolley handles, but basic hand hygiene allows us to decontaminate. however, anyone with a heavy build up of bacteria, occurring most often at any one of the following sites, will be classified as being colonised. body areas where swabs will be taken to check mrsa status inside the nose use 1% dilution of essential oil in jojoba (a liquid wax) or a seed/nut oil twice a day. this is especially important before going to bed as bacteria and other microbes have a perfect opportunity to multiply whilst we are asleep. throat gargle with aromatic water. spit out. do not swallow. armpits wash with aromatic water. after drying the area with clean paper towels/tissues, use a 1% essential oil dilution to gently spread over the area. leave on the skin for one hour before wiping off excess and putting on clothes. during that hour only wear a loose fitting bath robe. groin as for armpits. perineum as for armpits. hair wash hair with a tea tree shampoo at least three days prior to admission. alternatively make your own antimicrobial essential oil shampoo. taking a bath with one of the antibacterial essential oils will help to lessen bacteria on the skin, but the concentration of essential oil to a bath of water is not strong enough to kill mrsa. as bacteria are known to double in number every 24 hours, use diluted essential oils every day on each of the specified body areas where swabs will be taken to ascertain mrsa status. most of the university trials with mrsa bacteria used a 5% dilution of essential oil but as these were in vitro tests, and did not take into account the possibility of skin irritation, my recommendation is to use a 1% dilution. all of the essential oils in the trials described in part two of this book inhibited the growth of bacteria, whilst a few showed a

do not be afraid to ask and do not be afraid to complain • do not be afraid to monitor what is happening to you and around you, and speak up if you are concerned that something is not right. • contaminated dressings and cotton swabs should be immediately bagged up and safely disposed of by clinical staff. you should avoid contact with such items. • before a doctor uses a stethoscope on your bare skin you can ask that it be wiped with an antiseptic. the same applies to blood pressure cuffs: if it is going onto your bare skin you have a right to request that it be sanitised. you might like to keep your own antiseptic wipes at hand to enable fast and efficient sanitising of these items. • when a dressing is being changed and the clinician is not wearing a mask, it is prudent to request that they refrain from speaking whilst in close contact with your open wound. • drips (cannula) should not be left in place for more than three days. each time the integrity of the skin is breached there is an opportunity for invasion by pathogenic organisms and intravenous cannulation is the most common invasive procedure amongst hospitalised patients. guidelines5 stating that cannulae be removed/re-sited every 72 hours are not mandatory. this means that individual hospital trusts can choose whether or not to implement the guidelines. alert staff if you notice any redness or soreness at drip sites. every hospital has an infection control team: ask to speak to a team member if you have concerns. their job is to minimise the risk of infection. • always remember that should you fall ill with an mrsa infection whilst in hospital or within days of returning home, you may not get any sympathy from hospital management. it is extremely difficult for an mrsa victim to bring a successful lawsuit against a hospital. post-operative patients are now routinely sent home after a couple of days, which is in sharp contrast to procedures a generation ago when patients were kept in hospital for seven to ten days. a wound may not show signs of inflammation until four days after an operation, and

before going into hospital 141 this makes it easier for hospital management to claim that the surgical site became infected in the patient’s home environment. long, long ago joseph lister, known as the father of antiseptic surgery, insisted on the use of carbolic acid to clean hospitals as it was a powerful phenol that killed germs. he had noticed that people often survived the trauma of an operation but died of what was known as ‘ward fever’. lister had read about louis pasteur’s work with microbes and believed it was these microbes carried in the air that caused diseases to be spread in wards. people who had been operated on were especially vulnerable as their bodies were weak, their skin had been cut open, and germs were able to get into the body with more ease. lister then developed his idea further by devising a machine that pumped out a fine mist of carbolic acid into the air of the theatre during operations. post-operative deaths due to sepsis fell from 50% to 15%. lister’s protocol has been replaced by aseptic techniques in operating rooms and the prophylactic use of antibiotics. although surgery is now safer than in lister’s day, with regards to ward hygiene there is much scope for improvement.

essential oils 147 from the very wide range of essential oils available to the public, i have selected a few of those with antimicrobial activity referred to in part two. whichever essential oil is chosen it needs to be correctly diluted. recommended antimicrobial essential oils for wound care • tea tree • thyme linalool • manuka recommended essential oils for wound cleansing • lavender • manuka • geranium • tea tree • clary sage • agonis fragrans • lelechwa • thyme linalool recommended essential oils for washing colonised body areas: armpits, groin, perineum • lavender • manuka • geranium • tea tree • clary sage • agonis fragrans • lelechwa • thyme linalool essential oils for general bathing • lavender • bergamot • geranium • manuka • clary sage • agonis fragrans • lelechwa • thyme linalool

essential oils for spritzing or vaporising and that are not for use on the skin • cinnamon • orange • lemongrass • lemon • grapefruit • thyme linalool • or use any of the oils recommended in above lists essential oils for making an antimicrobial shampoo • tea tree • geranium • thyme linalool • manuka • lavender • or any of the citrus oils essential oils recommended for nose or throat • manuka • agonis fragrans • tea tree • clary sage jojoba oil, although more expensive than fatty oils such as sweet almond and sunflower, is my preferred choice for application of dilute essential oil to the inside of the nose, as it coats the surface, forming a barrier.

if a wound is not healing then it is being kept open by something, as it is the body’s natural urge to heal. that something could be a material item such as a surgical swab, but most commonly it will be a mixture of micro-organisms, including mrsa. anyone experiencing the inconvenience of a wound that will not close, and who has very recently been hospitalised, is quite likely to have an mrsa-colonised wound. when bacteria in a wound are killed, the body will close the wound: this is the innate healing capacity of the human body. antibiotics used to be able to facilitate this function, but increasingly, it is multi-drug-resistant bacteria that hold the balance of power, with wounds remaining open. a small amount of staph aureus in an acute wound is a good thing, as it acts as a guard against more dangerous bacteria getting in and causing problems whilst the immune system is mobilising its defenses. as a rule the immune system will take care of the micro-organisms as part of the healing process. bacteria in a wound become a threat to health when the immune system is unable to control the growth and the bacteria multiply to a dangerous level. my recommendation for anyone with a wound is to consult their doctor as soon as a problem is noticed, and not wait until the wound is causing pain, inflammation or malodour. this section of the book is for people who wish to tend to their own small wounds. large wounds should always be dealt with by a medically trained person. when taking care of your own wound the main points to consider are: • hygiene • removal of debris • use of an effective antibacterial agent • dressing the wound. items to have to hand • small plastic bags: sandwich bags are an ideal size. • a packet of cotton pads, the kind used for removing make-up. • paper kitchen towels or paper napkins. • individually wrapped dressings, available from pharmacies.

exercise caution when changing wound dressings. if the dressing has stuck to the wound do not force it off. soak the dressing with aromatic water. tea tree or lavender is recommended. if the wound is on the foot/ankle or lower arm you could soak the extremity in a bucket containing aromatic water. buy a plastic bucket specifically for wound care, and keep it sanitised. if the wound is somewhere on the body where it cannot be soaked in a bucket of water, then soak a clean washcloth in aromatic water and apply over the old dressing. leave in place for at least 30 minutes or until the old dressing can be easily removed. • daily care: | | cleanse wound with aromatic water. | | apply dilute essential oil. | | dress wound. • weekly care: | | debride if necessary. it is quite likely that medical personnel will be dismissive of/ frown upon a patient undertaking their own wound care. but i firmly believe that when it comes to the wellbeing of our own bodies we need to take more responsibility. there is a dearth of viable alternatives to topical antibiotics, and as a consequence many people are suffering the inconvenience and pain of living with a chronic wound caused by heavy mrsa colonisation.

health and to address inequalities.’ www.gov.uk/government/ organisations/public-health-england bsac the british society for antimicrobial chemotherapy exists to facilitate the acquisition and dissemination of knowledge in the field of antimicrobial chemotherapy. it sets standards for antimicrobial susceptibility testing and publishes the journal of antimicrobial chemotherapy (jac), one of the leading journals in the field. www. bsac.org.uk see also www.antibiotic-action.com for information on the resistance surveillance projects, see www. bscasurv.org ears-net the coordination of ears-net, the european antimicrobial resistance surveillance network (formerly earss), was transferred from the dutch national institute for public health and the environment (rivm) to the european centre for disease prevention and control (ecdc) in january 2010. it collects data from participating laboratories and hospitals in eu member states. results available from the european centre for disease prevention and control, www.ecdc.europa.eu ips the infection prevention society exists to promote the advancement of education in infection prevention and control for the benefit of the community as a whole, in particular by the provision of training courses, accreditation schemes, educational materials, meetings and conferences. www.ips.uk.net react action on antibiotic resistance is a coalition that links a range of individuals, organisations and networks around the world taking concerted action to respond to antibiotic resistance. the organisation campaigns for the appropriate use of antibiotics and for improved hygiene in hospitals to ensure better infection control. based in sweden. www.reactgroup.org

international agencies 159 united states idsa the infectious diseases society of america represents physicians, scientists and other healthcare professionals who specialise in infectious diseases. idsa’s purpose is to improve the health of individuals, communities and society by promoting excellence in patient care, education, research, public health and prevention relating to infectious diseases. www.idsociety.org the idsa supported the reintroduction of the staar (strategies to address antimicrobial resistance) act and it was reintroduced by us congress in 2009. www.idsociety.org/staaract.htm tfah trust for america’s health is a non-profit, non-partisan organisation dedicated to saving lives by protecting the health of every community, and working to make disease prevention a national priority. http://healthyamericans.org shea shea’s mission is to prevent and control healthcare-associated infections and advance the field of healthcare epidemiology. shea is dedicated to advancing the science and practice of healthcare epidemiology and preventing and controlling morbidity, mortality and the cost of care linked to healthcare-associated infections. shea signed the world alliance against antibiotic resistance (waaar) declaration against antibiotic resistance. www.shea-online.org cste the council of state and territorial epidemiologists is an organisation of member states and territories representing public health epidemiologists. cste works to advance public health policy and epidemiologic capacity and to establish more effective relationships among state and other health agencies. www.cste.org nmqf the national minority quality forum is a non-profit health research and educational organisation dedicated to the elimination of health disparities. the forum supports national and local efforts

international agencies 161 authorities and strengthens the agency’s ability to safeguard and advance public health an fda drug safety podcast, broadcast 16 august 16 2013, stated that label changes are required to warn of risk for possibly permanent nerve damage from antibacterial fluoroquinolone drugs taken by mouth or by injection. the fda advises that some fluroquinolones, a class of antibiotics often prescribed as ‘first choice’, should only be used with caution. cipro, for example, which used to be routinely prescribed, can produce many undesirable side effects. the list is extensive. the fda will continue to evaluate the safety of drugs in the fluroquinalone class and will communicate with the public again if additional information becomes available. international apua alliance for the prudent use of antibiotics. membership of this international group extends to more than a hundred countries. through communication and education, the organisation seeks to promote improved use of antibiotics in order to prolong their long- term efficacy. www.apua.org ific the international federation of infection control facilitates international networking in order to improve the prevention and control of healthcare-associated infections worldwide. www.theific.org who the world health organization publishes strategies for the containment of antimicrobial resistance. who strives to raise awareness of the overuse of antibiotics and issues guidelines to doctors. the site contains fact sheets on mrsa that are freely available to the public. www.who.int waaar in june 2014 more than 700 committed individuals from 55 countries signed up to the world alliance against antibiotic resistance declaration. search www.bsac.org.uk

resources products essential oils there are numerous websites supplying essential oils and many, though not all, carry a good quality range of essential oils for use by individuals and therapists. the following companies carry a high quality range of essential oils including benchmark thyme oil. for more information and direct links to distributors, visit the website. www.benchmark-thyme.com uk aromantic natural skin care 17 tytler street, forres, moray, iv36 1el, scotland phone: +44 (0)1309 696 900 fax: +44 (0)1309 696 911 email: info@aromantic.co.uk www.aromantic.co.uk canada green valley aromatherapy ltd 4988 north island highway, courtenay, bc v9n 9h9, canada phone: +1 250 334 4836 | toll free: 1 877 572 7662 (canada and us) fax: +1 250 338 4835 email: sales@57aromas.com www.57aromas.com usa ananda apothecary 2555 49th st, unit 3, boulder co 80301, usa phone: +1 303 440 3766 email: information@anandaapothecary.com www.anandaapothecary.com

products 163 aromatics international 9280 mormon creek road, lolo mt 59847, usa phone: +1 406 273 9833 www.aromaticsinternational.com earth sweet essential oils crystal baldwin, golden co 80403, usa fax: +1 303 642 3944 email: earthswt@aol.com www.earthsweetessentialoils.com indigo aromatics 1110 n. west end blvd, quakertown pa 18951, usa email: indigoaromatics.com www.indigoaromatics.com inshanti phone: +1 717 587 3990 email: info@inshanti.com www.inshanti.com nature’s gift 316 old hickory blvd., east madison tn 37115, usa phone: +1 615 612 4270 www.naturesgift.com stillpoint aromatics 415 juniper drive, sedona az 86336, usa phone: +1 928 301 8699 email: info@stillpointaromatics.com www.stillpointaromatics.com asia asia-pacific aromatherapy ltd. room 1001, 10/f, java commercial centre, 128 java road, north point, hong kong phone: +852 2882 2444 fax: +852 2882 5444 email: info@apagroup.com.hk www.aromatherapyapa.com

making products with essential oils before attempting to make products containing essential oils you need a good knowledge of essential oils and how to mix them with other ingredients. i recommend two excellent books written by kolbjorn borseth of aromantic skin care ltd: natural spa products – secrets of the cosmetic industry revealed and the aromantic guide to making your own natural skin, hair and body care products. www. aromantic.com essential oil therapy for animals knowledge and experience of using essential oils is of paramount importance before treating an animal, and remember that it is against the law to treat an animal other than your own. to find a vet with a working knowledge of essential oils, an internet search will provide hundreds of sites from the input ‘aromatherapy vets’. it is always advisable to speak with a vet if your pet is unwell. the guild of essential oil therapists for animals (geota) horsehay farm, duns tew rd, middle barton, oxon, ox7 7dq, uk phone: +44 (0)1869 349 955 fax: +44 (0)1869 340 969 email: info@geota.com the guild of essential oil therapists for animals (geota) is the self-regulatory governing body in essential oil therapy for animals. geota was set up to meet the overwhelming demand for people wanting to learn more about the use of essential oils with animals. geota hold training programmes and their website has a list of therapists ‘qualified to educate pet owners in the safe use of essential oils on their own pets.’ holistic aromatherapy for animals by kristen bell, findhorn, forres, scotland. an excellent book for pet owners on the safe use of essential oils.

products 165 other products allicin allicin international limited half house, military road, rye, east sussex, tn31 7ny, uk phone: +44 (0)1797 227 959 www.allicin.co.uk silver products • silvatec hand soap, incorporating silver ions, is available from several internet companies. the technical details can be found online. www.giltech.biz/silvatec • silver impregnated plasters are available from pharmacies, supermarkets and via the internet. • silver wound care dressings such as acticoat by smith and nephew are only available on prescription via a healthcare provider. • silverguard products provide antimicrobial protection for textiles. a range of products for use in washing machines, or sprayed directly onto textiles, can be found online. www. silverguard.co.uk manuka honey the internet has numerous sites selling manuka honey but for treating wounds it is advisable to purchase sterilised manuka wound dressings from a reliable company. comvita uk limited box 220, 5 high street, maidenhead, berkshire sl6 1jn, uk phone: +44 (0)1628 779 460 email: info@comvita.co.uk www.comvita.co.uk (uk) www.comvita.com (us) www.comvita.co.nz (nz) • medihoney: medical grade manuka honey products including medihoney apinate dressings that are only available online. • manuka honey: in three strengths: umf 10+, umf 15+, umf 20+.

microbiology tests to determine carrier status following discharge from hospital after an mrsa infection, you may be concerned about being an mrsa carrier, perhaps because you have elderly relatives or have young children or grandchildren. or you may still feel unwell, months after returning home, and suspect that you may not be free of mrsa. you may wish to have swabs taken and analysed so that you will know your status. if your gp dismisses your concerns, or says that the practice does not have the necessary funds to undertake such analysis, you can have swabs taken privately. the tests have to be carried out in a clinic, as swabs need to be correctly taken and sent for laboratory analysis. the london clinic 20 devonshire place, london, w1g 9bw, uk phone: +44 (0)20 7935 4444 (ask for diagnostics department) www.thelondonclinic.co.uk the london clinic will take swabs from five body areas and give you a report. it is necessary to ring for an appointment and you would need a referral from your healthcare provider. at the moment there are no clinics outside of london offering this service in the uk. the cost, at the time of press, is under £100. wound healing chronic wounds that just won’t heal are commonplace in people throughout the uk; mrsa is one of the many bacteria that can prevent a wound from healing. sadly, there are no statistics being kept, which means that the numbers of sufferers are unknown. if mrsa is suspected, or if you have already been informed that your wound is colonised with mrsa bacteria and the prescribed treatment has not been effective, you can seek private assessment and treatment. the wound healing centre 43 gildredge road, eastbourne, bn21 4rl, uk phone: +44 (0)1323 735 588 fax: +44 (0)1323 737 132 www.woundhealingcentres.org

services and support 169 this clinic uses alternatives to antibiotics and has a high success rate, with wounds healing in approximately six weeks. they use a variety of effective, natural products. action against medical accidents (avma) freedom house, christopher wren yard, 117 high street, croydon, surrey, cr0 1qg, uk phone: 0845 123 2352 (10am–5pm mon–fri) fax: +44 (0)20 8667 9065 www.avma.org.uk avma personnel are available to give advice to anyone who has picked up hospital acquired mrsa. initial advice is given on a telephone helpline, but more intensive/specialist support is available if required. it is not a walk-in service, so ring for an appointment. they also offer advice to people who have been bereaved by mrsa. some of the services they offer are: • help with understanding medical terminology. • an explanation of the processes available to persons seeking answers/compensation after the death of a loved one. this allows the person to make an informed choice. • specialised advice about whether people have a legal case. legal cases are complex and expensive to instigate and pursue. very few win their case, which can increase distress at a difficult time. • a list of vetted, specialist solicitors. the uk sepsis trust www.sepsistrust.org mrsa is a major contributor to sepsis fatalities. this website is to raise awareness of sepsis and lists signs and symptoms to look for. pathogens other than mrsa can cause fatal sepsis. mrsa in animals the bella moss foundation (bmf) bella moss was the first recorded case of death from mrsa in a dog in the uk. the foundation was set up by jill moss to raise awareness of mrsa in animals and to promote new research into mrsa and other serious infections in companion animals. use your search engine to find latest news.

glossary agar plate: a petri dish containing a growth medium (typically agar + nutrients) used to culture micro-organisms. antagonist: something that reduces the activity of a substance. antibiotic classification: a broad-spectrum antibiotic can be used against a variety of bacteria/fungi as opposed to a narrow-spectrum antibiotic which is used to kill a specific micro-organism. antimicrobial: a substance that kills or inhibits the growth of micro- organisms such as bacteria, fungi or protozoans. bacteraemia: the presence of bacteria in the bloodstream. bactericide/bactericidal: a substance with the power to kill bacteria. bacteriostatic: a substance that is powerful enough to prevent the growth of bacteria, although not powerful enough to kill off the bacteria. barrier nursing: also known as ‘bedside isolation’ when caring for a patient known or thought to be suffering from a contagious or infectious disease. the aim is to erect a barrier to the passage of pathogenic organisms between the patient and other patients or staff in the hospital. biofilm: a collection of bacteria or other micro-organism in which they adhere to each other and/or a surface and then produce a slimy covering, effectively giving the bacteria a protective element against antimicrobials. broad­ spectrum: see antibiotic classification. ca-mrsa: community-associated mrsa. camphoraceous: smelling of camphor. canula/cannula: a needle is inserted into a vein on the arm or back of the hand, then pulled out leaving a flexible tube for the delivery of fluids. carrier/carriage: a person carrying mrsa is colonised without necessarily being affected by it.

glossary 171 cellulitis: skin infection caused by bacteria, triggering severe inflammation of the connective tissue. chemotype: predominance of one chemical compound, either naturally occurring or created by hybridisation. clone: a group of organisms, or cells, of the same genetic constitution as another, derived by asexual reproduction. chlorhexidine: a chemical antiseptic, both bactericidal and bacteriostatic, effective on gram-positive and gram-negative bacteria. clostridium botulinum: a bacterium that is sometimes found in honey. colloidal solution: where particles are mixed in such a way that they remain evenly distributed in a liquid. colonised: to be carrying the mrsa bacteria. common sites are: armpits, groin, perineum and inside the nostrils. commensal: common and benign bacteria living on and in humans. cytokine storm: cytokines are components of the immune system and include interferons that trigger inflammation as a response to infections. research is still being undertaken to accurately define a cytokine storm and it is thought that hormones are also involved. under normal response mode, the immune system mounts a defence to fight off an invading pathogen (e.g. influenza). a cytokine storm is an abnormally magnified/ multiplied action of the immune response, which not only kills the pathogen but overwhelms the normal balance (homeostasis) of the body and kills the host. cytotoxic: quality of being toxic to cells. can be either a product of the immune system or a chemical substance. emrsa: epidemic mrsa. in the uk most ha-mrsa infections are caused by epidemic 15 and 16. there are more than a dozen epidemic strains of mrsa in the united kingdom. by 2014 emrsa-16 was becoming less of a problem. endogenous: when a person with staphylococci spreads the bacteria from one part of their body to another part. endotoxin: poison produced by the death of bacteria, such as mrsa. in infected people, endotoxins cause fever and weaken capillaries, causing fluid to leak into surrounding tissues which can cause a sudden drop in blood pressure, resulting in toxic shock.

exogenous: when organisms are transferred from person to person by direct contact or via a contaminated environment or equipment. exotoxin: poison released by bacteria that enters the bloodstream and causes serious problems throughout the body. exotoxins are among the most poisonous substances known. faculative aerobe: an organism able to grow with or without the presence of oxygen. fusidic acid: an antibiotic that is used topically in creams and eye drops, but is only given internally in combination with other drugs. gram-negative/gram-positive: in 1884, a danish scientist called gram experimented with bacteria by adding a purple dye, leaving it overnight and then washing the bacteria with an inert liquid.the bacteria that stayed purple he called gram-positive.the ones that washed out he called gram- negative. all staphylococci are gram-positive, and all streptococci are gram- negative bacteria. h1n1: haemagglutinin, neuraminadase. swine flu is h1n1. ha-mrsa: hospital-associated mrsa. hcai: healthcare-associated infections. infections that are acquired as a result of healthcare interventions. holistic: in alternative/complementary medicine, refers to the treatment of an individual by taking into account all aspects of their wellbeing, disease state, lifestyle, diet, etc. and treating the person as a whole, rather than just treating the disease. holistic, in the medical world, refers to treating a disease with multiple drugs and/or topical antimicrobials such as fusidic acid/chlorhexidene simultaneously in order to bombard the infection and save the life of the patient. hydrosol: a colloidal solution. icu: intensive care unit. the same term is used in both the us and uk. inci: international nomenclature of cosmetic ingredients. inoculum/innoculum: the number of bacteria present on a petri dish at the beginning of a microbiology test, measured in logs. isolates: specific bacteria taken from patients’ wounds, urine, etc. for use in microbiology tests. la-mrsa: livestock-associated mrsa.

glossary 173 log: the short form of logarithm. bacteria are grown on an agar plate (petri dish) until the bacteria have multiplied to a required amount. log 3 would be a low inoculum of 1000 bacteria per ml, log 5 a medium inoculum of 100,000 bacteria per ml. log 10 would be a very high inoculum of 10,000,000,000 per ml. loopful: a loop is a laboratory tool used to apply bacteria to an agar plate. malodour: a bad smell. mbc: minimum bactericidal concentration, smallest amount of a substance needed to kill bacteria. mersa/mursa: us terms for mrsa. mic: minimum inhibitory concentration, smallest amount of a substance needed to halt the growth of bacteria. microbes: bacteria (staphylococcus and streptococcus), viruses (influenza virus, chicken pox), fungi (candida albicans). sometimes newspaper articles refer to mrsa as a virus but this is incorrect. monoclonal: a group of cells produced from a single ancestral cell by repeated cellular replication. morbidity: the condition of being diseased. mupirocin: pseudomonic acid, a fermentation product produced by pseudomonas fluorescens (ncib 10586), a standard treatment for the carriage of mrsa. nanocrystalline: in a vacuum chamber, pure silver is bombarded with positive ions to liberate individual atoms. these silver atoms are then re- formed into new high-energy nanocrystalline structures. nanoparticles: are sized between one and one hundred nanometres. a nanometre is equal to one billionth of a metre. narrow-spectrum: see antibiotic classification. nctc: national collection of type cultures, a library of micro- organisms. necrosis: the death of tissue cells, which is now becoming more common in ca-mrsa infections. the infection continues to spread through the body until all the infected tissue, or limb, is surgically removed. streptococcal bacteria can also cause this type of damage.

necrotising fasciitis (nf): commonly known as ‘flesh-eating disease’ is a rare infection of the deeper layers of skin and sub-cutaneous tissues. historically, streptococcus made up most cases but since 2001, it has been observed that staphylococcus aureus was a major source of the disease. without surgery and medical assistance, the infection rapidly progresses and eventually leads to death. nosocomial: healthcare-environment acquired condition. osmolarity/osmosis: ability of a substance, such as honey or salt, to draw water from an object. paradox: a statement that seems to be absurd or self-contradictory but may be true. pathogen/pathogenic: an infectious agent (or germ) such as a virus, bacteria, prion or fungus that causes disease to its host. perineum: area between the anus and the genitals. picc line: peripherally inserted central catheters, used to deliver intravenous chemotherapy or antibiotics. prophylaxis: another word for preventative. psm: phenol-soluble modulins, a family of protein toxins that are soluble in phenols and produced by ca-mrsa, and thought to be the cause of severe infections. non-methicillin-resistant bacteria are not found to produce psms. although the toxins are produced in all mrsa strains, the more virulent ca- mrsa strains have a higher number of toxins. pvl: panton-valentine leukocidin toxin was originally discovered in 1894, but named in 1932 after the two scientists, panton and valentine who found the connection between it and soft-tissue infections. the toxin kills leukocytes (white blood cells), an important part of our immune system. this particular toxin makes mrsa bacteria more deadly as it kills the leukocytes which would normally defend the body against bacteria. pvl mrsa: ca-mrsa with pvl toxins. polymorphic: occurring in several or many forms or appearing in varying forms in different developmental stages. polymorphism: diversity occurring within biological populations, determined genetically or by environment. purulent: something that creates pus is called suppurative, pyogenic or purulent.

glossary 175 quaternary ammonium: a powerful antimicrobial used in pre-operative disinfectants and soaps. also commonly used in swimming pools to prevent a build up of algae over the winter months. benzethonium chloride and benzalkonium fluoride are both quaternary ammoniums. sepsis: infection of a wound with bacteria resulting in localised pus. blood poisoning. septic shock: a life-threatening condition when there is a dramatic drop in blood pressure as a result of septicaemia. septicaemia: a life-threatening condition caused by a rapid build up of bacteria in the bloodstream which overpowers the immune system. sol: short form of hydrosol. solubilise: to make soluble, help to dissolve. an agent that increases the solubility of a substance. ssti: skin and soft-tissue infections. synergist: something that enhances the action of a substance, as when two or more essential oils produce a better result than any of the oils used singly. systemically: affecting the entire organism or bodily system. tcp: brand name of a liquid used for disinfecting cuts and scrapes of the skin. originally comprised the chemical tri-chloro-phenylmethyliodosalicyl (hence its name) but reformulated in the 1950s to a mixture of phenol and halogenated phenols. topically/topical: medication applied to body surfaces such as the skin, eyes or mucous membranes. turbidity: when something is turbid it is muddy, thick, not clear. tween 20: a surfactant used in microbiology labs as either an emulsifier or as a washing agent. venturi effect: a combination of air pressure and velocity that creates lift off (e.g. as when a plane takes off). zoi: zone of inhibition. zoonotic: a disease capable of jumping the species barrier. technically, the transfer of disease from human to animal is anthroponosis, and animal to human is zoonosis. the terms zoonosis and zoonotic have been adopted for both modes of transmission.

about the author maggie first became interested in alternative medicine back in the early 1970s when it was called ‘fringe medicine’. her involvement with essential oils began shortly afterwards and became the mainstay of her medicine chest during pregnancy, childbirth and the rearing of three children with all the usual childhood diseases. she was one of the earliest uk published writers on the subject of aromatherapy. her first book, aromatherapy for women, published in 1985, went on to become an international bestseller, selling in excess of 700,000 copies worldwide. four other books followed, commissioned by mainstream publishing houses. with the publication of aromatherapy for women in japan, her partners there successfully introduced aromatherapy to the japanese market. in 1989, maggie was the first to speak on the subject, returning many times to lecture in kyoto, osaka and tokyo. her essential oil and herbal essence products created and led the market in japan for more than ten years. she was also instrumental in setting up the company which sells tisserand oils but has not been involved since the late 80s. maggie has travelled extensively in pursuit of the best quality essential oils, working with growers on three continents. based on practical experience of using essential oils to overcome serious chest infections picked up in india, maggie began investigating the possibility that a combination of essential oils might be effective in combating multi-drug-resistant infections. this led to working with the mrsa support group and successful trials with volunteers. maggie was inspired to continue the research and worked with the university of brighton to investigate the antibacterial effects of essential oils against mrsa. maggie established benchmark oils ltd to raise investment for the long-term research and to help bring important laboratory discoveries into the public realm.

maggie was born in 1950. a single mother since 1984, she has managed to juggle work commitments, book writing and motherhood. she lives in dorset, south west england, has three children and three grandchildren. www.maggietisserand.com

also by maggie tisserand aromatherapy for women essential oils for lovers the 14-day aromabeauty plan stress: the aromatic solution the magic and power of lavender co-authored with monika junemann