About all

Natural treatment for staph infection: The request could not be satisfied

Содержание

6 Ways to Treat a Skin Infection Using Natural Remedies

The explosive growth of antibiotic-resistant bacteria has led to a resurgence of interest in the use of natural remedies, many of which have a rich history of use by our ancestors.

Read on for six ways to treat a skin infection naturally using medicinal herbs, honey, essential oils, and probiotics. I’ve also included three recipes you can try at home to start feeling better.

The Emergence of Drug-Resistant Infections

More and more adults are struggling with skin infections caused by antibiotic-resistant bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa. (1, 2, 3) And, perhaps because antibiotics are routinely prescribed by some pediatricians or because “antibacterial” soaps and other products are so widely used in homes and schools, this trend is also on the rise in children younger than 15 years of age. (4)

Drug-resistant skin infections pose a significant health risk at any age because they increase a person’s susceptibility to systemic infection. The growing problem of antibiotic resistance is causing many people to turn to natural substances for the treatment of skin infections.

Excitingly, an emerging body of research indicates that natural compounds, including botanical medicines, honey, and topical probiotics, have significant therapeutic value in the treatment of skin infections without the potential to cause antibiotic resistance. And these treatments don’t just work for MRSA. People with acne, ringworm, cutaneous Candida infections, and a host of other bacterial infections could also see positive results.

If you’re struggling with a skin infection—whether it’s acne, ringworm, or a bacterial infection—you can take your treatment into your own hands. Check out this article for six ways to treat it naturally, and get recipes for remedies you can make at home.

Six Ways You Can Treat a Skin Infection Naturally

While there are many natural compounds that have antimicrobial properties, a few stand out from the rest in their ability to combat antibiotic-resistant skin infections:

1.

Another Surprising Use for CBD Oil

Cannabis has received no shortage of attention from the medical community in recent years. A growing body of research indicates that it has an incredibly wide variety of health applications, including the treatment of skin infections. Cannabinoids may be a powerful ally in neutralizing the difficult-to-treat MRSA superbug, which often affects the skin. (5)

Cannabinoids may also make the skin more resistant to infection in the first place by upregulating the endocannabinoid system, a network of molecules and receptors that influences immunity, among many other effects. (6)

Topical CBD oil may be the best way to reap the antibacterial, skin-protective benefits of cannabinoids.

After extensive research on CBD products available today, Ojai Energetics Hemp Elixir is my top choice. It’s what I use myself and with my family, and what I recommend to most of my patients, because it’s effective, safe, and made from 100 percent organic ingredients.

2. Why Honey Is Liquid Gold

Honey, a sweet, viscous food derived from the nectar of flowers and produced most commonly by the European honey bee Apis mellifera, is truly “liquid gold” in the treatment of skin infections.

Topical application of natural, unprocessed honey reduces redness, swelling, and healing time in bacterial infections caused by Staphylococcus aureus and Klebsiella. Its effects are comparable to that of topical antibiotics. (7)

Natural honey also accelerates the healing of diabetic wounds and is useful in the treatment of ringworm, cutaneous Candida infections, and acne. (8, 9)

Manuka honey, a special type of honey produced in New Zealand by bees that pollinate the native manuka bush, has a broad spectrum of action, unlike any other known natural antimicrobial. It inhibits pathogenic bacteria that colonize the skin and wounds, including MRSA and Pseudomonas aeruginosa. (10) The powerful antimicrobial effects of manuka honey are due primarily to the presence of methylglyoxal (MGO), a naturally occurring phytochemical found in the nectar of Leptospermum flowers that damages bacterial DNA, RNA, and proteins.

When selecting manuka honey for medicinal uses, you need to consider the UMF, a quality trademark and grading system that rates the strength of the honey. (UMF stands for “unique manuka factor” and is an official designation granted only to authentic manuka honey produced and jarred in New Zealand.) (11) UMF 10+ is the minimum strength honey recommended for medicinal use; it is best for less serious infections such as acne. For more stubborn infections, I recommend UMF 15+ or 20+.

3. A Salve Made from

Cryptolepis Can Soothe Your Skin

Cryptolepis is a shrubby plant native to Africa that has traditionally been used to treat malaria. However, this plant also works as a broad-spectrum antimicrobial against pathogens implicated in skin infections, including MRSA, Pseudomonas aeruginosa, and Candida albicans. (12, 13)

Cryptolepis is best used as a salve. I recommend this salve from Woodland Essence.

4.

Sida acuta: Invasive Weed or Effective Treatment Option?

Sida acuta is a species of flowering plant in the mallow family that grows around the world and is often considered to be an invasive species or weed. Despite its lowly reputation, Sida acuta is a powerful treatment for skin infections. According to herbalist and author Stephen Harrod Buhner, it is active against Staphylococcus aureus, Pseudomonas aeruginosa, and Candida skin infections. (14)

5. Try Eucalyptus, Juniper Berry, or Another Essential Oil to Treat Your Skin

Essential oils are made by distilling the volatile oils from plants. They can be applied directly to the skin, either straight or diluted in a carrier oil (such as coconut or olive oil).

A wide variety of essential oils have antimicrobial properties that may neutralize skin pathogens, including:

  • Eucalyptus
  • Juniper berry
  • Lavender
  • Tea tree
  • Oregano
  • Sage
  • Thyme
  • Frankincense
  • Ylang-ylang
  • Cypress

Essential oils are often combined to produce synergistic effects. (15) One oil, for example, may be an effective antiseptic, while another works as an anti-inflammatory. Your best bet may be using a premade blend of essential oils intended for topical use in skin conditions.

6. Try Using Topical Probiotics

The health benefits of probiotics are not limited to the gut; they also have applications in the treatment of skin infections.

Lactobacilli have antimicrobial activity against skin pathogens and prevent the formation of biofilm (a stubborn surface build-up of bacteria that is difficult to eradicate) when applied topically. (16) Lactobacillus plantarum also inhibits Pseudomonas aeruginosa colonization on the skin and enhances tissue repair in burn wounds. (17)

While a variety of probiotic-containing skincare products are emerging on the market, I am unaware of any that are explicitly intended for treating skin infections. However, one product line that may be worth a shot is Mother Dirt. The ammonia-oxidizing bacteria (AOB) in Mother Dirt skin care products replace essential bacteria lost by modern hygiene and lifestyles and may fortify the skin’s natural defenses against infection.

Why Natural Skin Infection Treatments Make Sense

Antibiotics have long reigned supreme in the field of dermatology, forming the cornerstone of treatment for skin infections. The practice of using one type of therapy to treat a disease, such as an antibiotic for a skin infection, is referred to as “monotherapy.”

Monotherapy is problematic because pathogens are highly adaptable organisms that quickly develop ways to evade the effects of single antimicrobial compounds.

Pathogens that successfully evade the impact of antibiotics pass their antibiotic resistance genes down to subsequent generations. Considering that some bacteria can go through a single generation in as little as 20 minutes, it is no surprise that antibiotic resistance has skyrocketed in our modern-day society!

Using natural compounds to treat a skin infection is an effective way to avoid the pitfalls of antibiotic monotherapy. In contrast to antibiotics, which contain a single active antimicrobial compound, botanical medicines and other natural substances contain many active compounds all in one package. The presence of multiple antimicrobial compounds makes it difficult for pathogens to adapt and evade the effects of the intervention, which reduces the risk of antibiotic resistance. Furthermore, in traditional herbal medicine, several plants are often administered together to treat infections. The synergistic effects produced by a combination of botanicals enhance the antimicrobial effects of the intervention and further reduce the risk of bacterial resistance. Using a natural remedy to treat your skin infection allows you to take a Functional Medicine approach to the problem—by addressing the root cause—without contributing to the rise of antibiotic-resistant pathogens.

Ready to Try It Yourself? Here Are Three Recipes to Get You Started

You don’t need to spend a lot of money to treat a skin infection naturally. In fact, you can make an herbal antibacterial wash, wound powder, and herbal oil for skin infections right in your kitchen. The recipes featured below are courtesy of Stephen Harrod Buhner’s excellent book Herbal Antibiotics: Natural Alternatives for Treating Drug-Resistant Bacteria.

If you’ve never made your own herbal oil before, don’t worry. These recipes are easy to follow, and you can find supplies at a number of online retailers. Look for a vendor that sells organic herbs.

General Antibacterial Wash

Ingredients:

  • 2 ounces antibacterial herbs such as Artemisia absinthium, Cryptolepis, or Sida acuta
  • 2 ounces echinacea (if you’re using Echinacea angustifolia, use the root; if it’s  Echinacea purpurea, use the flowers or seeds)
  • 2 ounces dried evergreen needles (any species)
  • 1 quart water, either filtered or distilled

Combine the herbs with water. Cover, bring to a boil, and simmer uncovered for 30 minutes. Let cool and strain. Rinse the affected skin liberally with the decoction four times daily.

Wound Powder

Ingredients:

  • 1 ounce Berberis root or bark
  • 1 ounce Cryptolepis root or Sida acuta, Bidens, or Alchornea leaf
  • 1 ounce echinacea root or seed
  • 1 ounce juniper leaf
  • 1 ounce Lomatium root
  • 1 ounce Usnea lichen

Powder all herbs as finely as possible. (Stephen recommends using a high-powered blender or food processor to get a semi-small grind and then transferring the blend to a nut or coffee grinder to make a finer powder.) Strain powder through a sieve. Use as needed. This formula can be sprinkled onto feet or into shoes and socks to treat athlete’s foot. It may also be used on babies for diaper rash.

Herbal Oil for Skin Infections

Ingredients:

  • 1 ounce dried Artemisia leaf (any species of Artemisia will work)
  • 1 ounce dried Berberis plant (such as barberry or Oregon grape)
  • 1 ounce dried Cryptolepis (or Sida acuta)
  • 1 ounce dried echinacea root or seed
  • 1 ounce dried evergreen needles (any species)
  • 1 quart extra virgin olive oil

Grind herbs as finely as possible with a high-powered blender or coffee grinder. Place ground herbs in a small, ovenproof glass dish or ceramic pot than can be covered; do not use a metal pot. Pour in enough olive oil to saturate the herbs, stir well, and then add extra oil to cover the herbs by one quarter inch. Heat the mixture, with the lid on, overnight in the oven for eight hours at a low temperature, between 150 and 200 degrees Fahrenheit. Let the mixture cool and then press the mixture through a cloth to extract the oil. Store the oil in a sealed glass container out of the sun.

Antibiotics and bioactive natural products in treatment of methicillin resistant Staphylococcus aureus: A brief review

Abstract

Infections caused by Staphylococcus aureus strains with Methicillin resistance are associated with increased mortality and morbidity, aggressive course, multiple drug resistance and hospital outbreaks. Several first and second line antibiotics are rapidly becoming ineffective for treatment due to emergence of resistance. Extracts of medicinal plants are rich source of unique phytochemicals. Plants used in traditional medicine have been reported to have significant anti-MRSA activity. The objective of this review is to provide a brief overview of antibiotics as well as anti-MRSA natural products and their future prospect.

Keywords: Methicillin resistant Staphylococcus aureus (MRSA), phytochemicals, plant extracts

INTRODUCTION

Staphylococcus aureus is one of the prominent medically important bacterial pathogen. Its potential to cause wide spectrum of pyogenic lesions involving several organs, hospital outbreaks and community acquired infections are well recognized. S. aureus infections are often fatal in nature and are associated resistance to several beta-lactam antibiotics used in hospitals.[1] These strains are known as MRSA (methicillin resistant S. aureus).[2] Historically, it had drawn special attention since 1970 due to its association with several nosocomial outbreaks and cross infections. [3] The epidemiology of this organism has changed over years. Life-threatening infections which were limited only in hospitals are now becoming widespread in community.[4] High usage of antibiotics in hospitals and selection pressure of these antibiotics has been implicated in development of multidrug resistance (MDR) in hospital acquired MRSA (HA-MRSA) strains. Likewise, increased use of antibiotics in animal feed has resulted in emergence of a new MRSA strain (livestock associated MRSA or LA-MRSA) with multiple non-beta lactam drug resistance.

Pertaining to the difference in virulence, pathogenicity, risk factors and drug resistance, MRSA strains are highly variable in different geographical areas. Even within a country, there may be local variation in MRSA strains.[5,6] MRSA prevalence varies from 20% to 54.8% in different parts of India,[7,8,9] while a recent study shows 29.1% prevalence in South India.[10] Antibiotic susceptibility pattern indirectly correlate with pathogenicity and therefore may be helpful in tracing the dissemination of the predominant MRSA strain or emergence of new MRSA strain. The transmission of Staphylococcal infection can be effectively reduced by stringent infection control measures and judicious use of antibiotics.[11] Conventional anti-MRSA antibiotics like Vancomycin, Teicoplanin, Linezolid and Daptomycin are currently in clinical use. However, development of resistance to many of these drugs has been identified worldwide. Vancomycin resistant and intermediate MRSA strains (VRSA and VISA) have been reported sporadically. Furthermore, it has also shown increase in the minimum inhibitory concentration (MIC) to Glycopeptides over years indicating reduced susceptibility. With the emergence of resistance to these drugs along with scarcity of newer anti-MRSA in the pipeline, the therapeutic options are likely to be further narrowed in future. Conversely, novel bioactive natural products have been identified to display anti-MRSA activity. Current research suggests these natural products have the prospect of being considered for treatment of MRSA infections. This review critically appraises conventional antibiotics and bioactive natural products with anti-MRSA activity.

Anti-MRSA antibiotics and their resistance

mechanisms

Methicillin

Methicillin (originally called Celbenin) was the first beta lactamase resistant semisynthetic penicillin developed in 1960 to treat infections with penicillin resistant S. aureus. However, methicillin resistant strains of S. aureus emerged within one year of its clinical use.[12] The early reports of MRSA among European countries were from UK and Denmark.[13] MRSA has also been reported from India as early as 1964.[14] Methicillin exerts its antimicrobial activity by inhibiting transpeptidase mediated peptidoglycan cross-links by after binding with cell wall PBPs.

Methicillin resistance is mediated by an additional PBP (PBP2a) with low affinity for beta-lactam agents and it confers resistance to methicillin as well as other beta-lactam antibiotics. The mecA gene coding PBP2a along with two regulator genes (mecI and mecR1) is carried by SCCmec. Expression of mecA gene is usually inducible and regulated by mecI, mecR1 and additional genes like blaI, blaR1, femB, aux. [15] Apart from mecA mediated resistance, other resistance mechanisms which are not associated with treatment failure are also described.[16] Alteration of existing PBP by mutation in the beta lactam drug binding domain may give rise to resistance in S. aureus which are termed as MODSA (moderately oxacillin resistant S. aureus). Similarly few penicillinase hyper-producer S. aureus strains described as BORSA (borderline oxacillin resistant S. aureus) can slowly hydrolyse methicillin/oxacillin by type-A staphylococcal beta-lactamase resulting in borderline MIC and low level resistance.

Vancomycin

Vancomycin is currently the antibiotic of choice for treating MRSA infections. It is a branched glycosylated tricyclic peptide belonging to the glycopeptide antibiotic class. It binds to the growing ends of peptide chains and prevents their interaction with transpeptidase enzyme. Although reports of MRSA strains with diminished susceptibility to this antibiotic are not infrequent,[17] only few reports of vancomycin resistant S. aureus (VRSA) showing MIC ≥ 32 μg/ml have been documented. Four VRSA carrying vanA gene were reported from USA between 2002 and 2006.[18] Later Tiwari et al. reported vanA negative VRSA in 2006[19] and recently Saha et al. recovered one isolate of VRSA from Kolkata.[20] Vancomycin intermediate S. aureus (VISA) is characterized by MIC between 8-16 μg/ml. It was first reported in Japan in 1997.[21] Subsequently it was reported from United States and Europe. Intermediate sensitivity among MRSA has also been reported from South India.[22]

Linezolid

It is a new drug class, the Oxazolidinones. It binds to domain V of 23s RNA and prevents correct protein synthesis. Linezolid resistance occurs when at least 2 copies of 23s RNA genes are mutated specially with increased clinical use and the control measure is aggressive antibiotic stewardship (reducing its clinical use).[23] First case of linezolid resistance in MRSA was reported in 2001[24] and subsequently 8 cases in the US, 2 in Germany and 1 each in Brazil, Colombia and the UK. Spanish outbreak of linezolid resistant S. aureus had a different cause, the importation of the cfr gene carrying plasmid, which also mediates resistance to the older drugs clindamycin and chloramphenicol.[25]

Daptomycin

It is a calcium-dependent cyclic lipopeptide anti MRSA drug which act by depolarization of the bacterial cell membrane. However, due to its lipophilic nature it gets incorporated in alveolar surfactant and deposited in alveoli instead of bacterial cell membrane and results in eosinophilic pneumonia limiting its therapeutic use.[26] There is no defined resistance breakpoints for S. aureus, isolates are either categorized as susceptible or nonsusceptible.[27] Since vancomycin prolonged exposure is related to decreased daptomycin susceptibility, it should be ruled out by rechecking daptomycin MIC when a patient is unresponsive to this combination.[28]

Streptogramin antibiotics

These are derivative of Streptomyces pristinaespiralis. They are categorized into – group A (e.g. dalfopristin) and group B (e.g. quinupristin).[29] It is available for therapeutic use as combination of quinupristin and dalfopristin (30:70 ratio) which is more potent than single agent and may be active even when there is resistance to one component. Both quinupristin and dalfopristin bind to 50S ribosome at different sites to form a stable tertiary complex, and inhibit protein synthesis of bacteria. Genes coding Streptogramin inactivating enzymes (erm, msr, vat) can occur on transmissible elements. Drug elimination by efflux has also been described.[30] The first report of resistance to this antibiotic in MRSA was from France in 1975.[31] Diverse range of the resistance ranging from 0% to 31% has been detected in different studies globally.[32] Different groups in India have reported variable rate of resistance with the maximum of 64% as observed by Deep et al.[29,33]

Clindamycin and inducible clindamycin resistance

Clindamycin is a lincosamide antibiotic classically used for infections by aerobic Gram-positive cocci and anaerobes. Clindamycin resistance in S. aureus may be classified in one of the three phenotypes, designated as MLSBi, MLSBc and MS respectively.[34] Inducible resistance to Streptogramin B, macrolide and lincosamide in S. aureus is attributed to erm gene encoding an enzyme which methylate adenine residue of 23s rRNA.[34] This inducible clindamycin resistance has been found more frequently among MRSA strains and it often leads to treatment failure as it is not detected in routine antibiotic susceptibility tests.[35] It requires detection by a simple test, frequently described as D-test.

Bioactive natural products anti-MRSA activity

Indian medicinal plants

Indian continent is blessed with 120 families and 130000 species of plants. Many of these are known to have medicinal properties. From historical time, various parts of these plants have been used in treatment of communicable as well as non-communicable diseases. However, the bioactive phytoconstituents contributing to antimicrobial properties are yet to be discovered.

Recent research has identified Acorus calamus, Lawsonia inermis, Hemidesmus indicus, Holarrhena antidysenterica, Punica granatum, Plumbago zeylanica, Camellia sinensis, Delonix regia, Terminalia chebula, Emblica officinalis and Terminalia belerica have in vitro antimicrobial action against MRSA. A. calamus also known as sweet flag, calamus and bach, grows throughout India, especially in hills of Manipur and Nagaland. Its rhizome has effect on nervous system and has been used as antihypertensive, sedative, antianxiety, antispasmodic, anticonvulsant as well as for bronchial infection, chronic diarrhoea and dysentery. Several studies reported bactericidal activity of its rhizome and leaf extracts.[36,37,38]

Emblica officinalis, Terminalia chebula and Terminalia bellirica fruits are constituents of a polyherbal Ayurvedic medicinal formulation known as Triphala. Its antioxidant, antimicrobial, anticancer, anti-allergic, cardiotonic, hypocholesterolemic and hepatoprotective properties are well recognized and it has been used in treatment of malabsorption, constipation, dyspepsia and hyperglycemia for its multiple health benefits.[39] Although human clinical trials have not been conducted to support its use in infections, evidence from in vitro studies and animal models suggests each component of Triphala have anti-MRSA property.[39,40,41]

Likewise, leaves of Camellia sinensis (tea),[40,41] Lawsonia inermis (mehndi)[41] and Azadirachta indica (neem),[40,42,43] Holarrhena antidysenterica (Kurachi) bark,[36] Delonix regia (Gulmohar) flowers,[41] Punica granatum (Pomegranate) rind,[41,44] Hemidesmus indicus (Anantamul) stem[36] and Plumbago zeylanica (Chitra) root[36] has shown in vitro activity against MRSA [].

Table 1

Medicinal plants in Indian traditional medicine with anti-MRSA properties

Miscellaneous medicinal plants

With the increase in awareness of medicinal value of plants and herbal component, several studies have investigated the antibacterial properties of herbal plants against MDR pathogens in current years. This trend is seen worldwide and developed countries are no exception. Significant activity against MRSA have been documented in studies which used extract of plants mentioned in traditional medicine of Thailand (Garcinia mangostana, Quercus infectoria),[44] Nigeria (Terminalia avicennioides, Phyllantus discoideus, Ocimum gratissimum, Acalypha wilkesiana)[45] and Australia (Eremophila alternifolia, Amyema quandong, Eremophila duttonii, Lepidosper maviscidum).[46] Voravuthikunchai et al. found that Quercus infectoria, Garcinia mangostana and Punica granatum had highest antibacterial activity and MICs for MRSA were 0.2-0.4 mg/mL, 0.05-0.4 mg/mL and 0.2-0.4 mg/mL respectively.[44] In another study, the MICs of ethanol extracts of four Nigerian plants i.e. A. wilkesiana, P. discoideus, T. avicennioides and O. gratissimum ranged from 18.2 to 24.0 mcg/ml.[45] While the leaf extract from Eremophila duttonii was most bactericidal among five Australian medicinal plants in reducing the number of viable cells of MRSA,[46] ten Italian plants exhibited MRSA biofilm inhibition with minuscule bacteriostatic activity.[47]

Active phytoconstituents with anti MRSA activity

Despite ample research evidence of anti-MRSA activity of various plant products, there is lack of adequate information about precise phytoconstituents possessing anti MRSA activity. Most studies have investigated anti-MRSA activity of different plant parts (leaf, bark, flower, rind, fruit etc.) extracted in various solvents (aqueous, methanol, ethanol, ethyl acetate etc.) and expressed the result of phytochemical analysis of these extracts in terms of presence of alkaloids, terpenoids, flavonoids, phenols, steroids and glycosides. Since in most instances isolation of each phytochemical in pure form and re-testing their anti-MRSA activity not attempted and these phytochemicals are often unnamed or named generically (as alkaloids, terpenoids, flavonoids, etc.), it is difficult to assign the anti-MRSA activity to a particular component.

Among the compounds with reported anti-MRSA activity, β-asarone from Acorus calamus rhizome, mansonone F from Ulmus davidiana var. japonica, galloylated flavonol rhamnosides from Calliandra tergemina leaves, Prenylated flavonoids from Desmodium caudatum root, eupomatenoid-5 from Piper regnellii leaves are important.

Beta-asarone is cis-isomer of 2, 4, 5-trimethoxy-l-propenylbenzene, and the active constituent of A. calamus. Sujina et al. found that beta-asarone was the major constituent (92.4%) in A. calamus essential oil and showed 12 mm zone of inhibition and 2.5 mg/ml MIC value against MRSA.[48] In contrast, Devi et al. reported minimal antibacterial activity of its extracts and β-asarone.[49]

Mansonone F is an anti-MRSA sesquiterpenoid quinone compound of U. davidiana var. japonica present in the fourth fraction of root extract of U. davidiana obtained by silica gel column chromatography.[50] It has been found to have potent antimicrobial activity against gram positive bacteria including MRSA. However, its activity against gram negative bacteria is insignificant.

Kaempferol-3-O-(2″,3″,4″-tri-O-galloyl)-α-L-rhamnopyranoside, quercetin-3-O-(3″,4″-di-O-galloyl)-α-L-rhamnopyranoside, and quercetin-3-O-(2″,3″,4″-tri-O-galloyl)-α-L-rhamnopyranoside are three novel galloylated flavonol rhamnosidesides from C. tergemina leaves. Chan et al. found these phytocompounds exert lytic effect on MRSA.[51] Moreover, acylation of these rhamnosidesides is critical for their anti-MRSA activity. Likewise, seven prenylated flavonoids and one prenylated chromanochroman isolated from Desmodium caudatum also showed in vitro anti-MRSA activity.[52] Prenyl or a 2,2-dimethylpyran group in these compounds are essential for their antimicrobial action.

Marcal et al. spectroscopically identified eupomatenoid-6, eupomatenoid-5, eupomatenoid-3 and conocarpan as the major constituents of P. regnellii leaf extract.[53] Among these components, eupomatenoid-5 only had antibacterial properties and was responsible for anti-MRSA activity of P. regnellii.

Future prospects

The lack of newer antibiotics under development, emergence of drug resistance among several pathogenic bacterial species and their world wide spread along with limited therapeutic options with antibiotics attributed to their higher toxicity and comorbidities in patients have heralded the futility of antibiotics in near future. Although natural herbal products are in use for centuries for treatment of infective ailments, not much is known about their active principles, scientific basis of use, pharmacological and safety profiles. A vast area of traditional medicine has remained undiscovered. Hence, phytochemistry became more relevant in treatment of MDR pathogens like MRSA. However, some aspect needs to be addressed. Difference in extraction method, instruments and raw materials (plants grown on different regions) may lead to wide variation in results and needs standardization.[43] Most studies utilize diffusion methods for determining antibacterial activity and interpret the results in terms of size of zone of inhibition (ZOI). Unlike antibiotics phytochemicals do not have universally accepted guidelines on ZOI cut offs for diffusion method and also ZOI cannot reflect the concentration of phytochemicals in infected tissues required to inhibit bacterial growth. Hence, it may be more appropriate to determine the MIC and MBC. Since plant extract may contain numerous substances and one or more components may contribute to antibacterial activity, the identification of the active phytoconstituent from a plethora of alkaloids or glycosides of the extract often become challenging. Finally, the in vitro antibacterial action needs further support by animal studies and human clinical trials to determine the safety profile, therapeutic window and optimum dosage schedule in addition to its therapeutic efficacy before considering for routine use.

Staph Infections-An Herbalist’s Perspective | Northeast School of Botanical Medicine

Warning-this article contains graphic photos of staph infections

First Aid Station-Herbal medicine and other supplies

Definitions
  1. Commensal-when one organism obtains food or other benefits from another organism without harming or benefiting the other organism.
  2. Exotoxin-toxins released from bacteria that can cause damage and harm.
  3. Folliculitis-an infection of a hair follicle.
  4. Microbiota-the group organisms that form ecological communities that live within us and on our skin. They include bacteria, viruses, fungi, and other microorganisms. They can be beneficial, neutral, or pathogenic.
  5. MRSA (Methicillin-resistant staphylococcus aureus)-an antibiotic-resistant form of staph.
  6. Opportunistic pathogen-a pathogen that takes advantage of an altered environment, such as a disturbance in the immune system.
  7. Pathogen-a disease-causing organism. These include bacteria, viruses, fungi, protozoa, and worms.
  8. Sepsis-an infection that enters the bloodstream where the body’s response causes potential damage to organs and tissues. This is an emergency medical condition.
  9. Slough (‘sluff’)-a mass of dead cells and tissue seen during the inflammatory phase of wound healing.
  10. Toxic shock syndrome-a life-threatening disorder caused by the release of toxins from bacteria. In the 1970s, it caused a number of cases through the use of super-absorbent tampons.
Background

Staphylococcus aureus (‘staph’) is a gram-positive bacteria commonly found on human skin and in the upper respiratory tract. While it is generally a commensal component of the skin microbiota, it can also become an opportunistic pathogen leading to skin infections, sinusitis, and food poisoning. It can also lead to lethal conditions such as toxic shock syndrome and bacterial sepsis. In this article, I will be focusing on treating its place in skin infections.

Some of the common skin infections I see in first aid are open infections, abscesses, folliculitis, and boils.

Staph exhibits extensive genetic variation, though only a limited number of these variants pose a risk for human health. While there are multiple strains of staph, they are often clinically divided by those that are resistant to antibiotics and those that are not. The most common pathogenic strain is Methicillin-resistant staphylococcus aureus (MRSA), which can be hospital-acquired or community-acquired (meaning that it is spread in a non-healthcare setting). It is one of the most common hospital-acquired infections in the US, with up to 500,000 cases a year.

There is currently no vaccine for Staphylococcus aureus.

Contagiousness and Patient Education

Staph is contagious through multiple pathways, including skin-to-skin contact, pus, and fomites such as towels and clothing. This means health care workers must be cautious to avoid spreading this infection while administering treatment as well as disposing of infected materials.

It is important to discuss possible contiguousness with patients. This is especially true for some of the events where hugging is commonplace, as well as people volunteering in kitchens and other places where there is potential for spreading the infection.

In these situations, It is useful to discuss what staph is and what it is not, and that it is a common infection. This helps people not feel bad or guilty about having this condition, which limits their capacity to touch others or work in places where it could spread. If they felt guilty, they may want to hide that they have staph and are more likely to spread it.

Personal Interest and Experience

I have been working at wilderness first aid clinics for over 25 years. Staph infections are common in these settings and range from mild to severe (though not toxic) forms. The infections are due primarily to the lack of available hygiene and sanitation. Also, since cuts and scratches are common in these rougher environments, there is more opportunity for infection to occur. Lowered immune resistance may be another factor.

The medical professionals on staff have taught me a lot, increasing my skill level in both diagnosis and treatment. I’ve learned how to lance abscesses and have gained more knowledge on which antibiotics may be the most appropriate and when hospitalization may be necessary.

Staph infection with (yellowish) slough

Assessment and Diagnosis

Assessment and diagnosis is based on visual and physical examination. Since Staphylococcus aureus is the most common bacteria to cause skin infections, it is usually assumed to be the causative agent when seeing a skin infection. We cannot culture the infection at these events, so we have no definitive way of knowing whether it is MRSA or not. And as MRSA and non-MRSA infections present similarly, we tend to treat them similarly, with the severity of the infection determining the course of action.

Spider bite or Staph Infection

It is common for people to think they have a spider bite when they have a staph infection. There are a couple of reasons for this, including that both often show up with no warning and can have a similar appearance. Since the bite of a spider is usually not felt, this can seem like a reasonable conclusion. Still, the reality of my experience is that the majority of people who think they have spider bites have staph infections. This is echoed by other medical sources. It seems people would rather have a spider bite, which is somehow ‘cooler’ (and non-contagious) than a staph infection.

Spider bites range from non-harmful (the majority) to venomous, and those can cause a lot of tissue damage. They can also become infected, so that adds another layer of complexity with diagnosis and treatment.  

Venomous spider bite in a later stage of healing

Importance of Sanitation

Due to the contagiousness of Staphylococcus aureus, it is pertinent to make sure all infectious waste is kept in a safe place where a human, dog, or other animals will not get into it. It does not need to go into hazardous waste, just to be kept safe. The waste products include dirty gauze pads and similar equipment as well as the wastewater. And since the bacteria can last for up to 24 hours and longer on surfaces and fabric, people should know that their clothes and bedding might harbor staph bacteria. Health care workers should wear gloves and dispose of them properly and wash well afterward, including sterilizing any tools involved.

Multiple staph infections

Treatment Protocols

Treatment Protocols

There are a few main strategies that I use for staph infections, which have changed over time. Internally I use a variety of herbs to help bolster immunity and fight infection. Externally I use both herbs and activated charcoal topically as well as medicinal soaks.

Treatment

Step 1-Options

Once a diagnosis is established, the first question for treatment is whether to use herbs, antibiotics, or both. This is primarily up to the patient. The options and considerations are discussed for both antibiotics and herbal medicines with each individual. Our goal is to provide agency for the patient, so they have the information to make informed personal choices.

If the patient wants antibiotics, a new set of choices emerges. Sometimes we have the antibiotics and the staff to administer them, but oftentimes we do not. If we don’t, they will have to go to a clinic or hospital, which will take time and money. So this partially depends on the individual’s resources. Also, many folks have had bad medical experiences making them resistant to seek medical help even if we think it is a good idea.

When discussing the options, we let the person know that taking herbal remedies will likely take longer and can be more complicated than pharmaceuticals. By ‘difficult’, I mean that they will generally have to come in at least once a day to have their bandages changed, wounds washed, and to have the remedies re-applied. They may also need to take the herbal preparations orally 2-3 times daily. The advantage is that we have the medicine at the first aid station, so they are available and free. And some people would rather use plant-based medicines than pharmaceuticals.

If the staph appears to be spreading, or if there is lymphangitis (red lines caused by the bacteria entering the lymphatic vessels), we set up a timeline, and if we don’t see improvement within a specific time frame, we suggest getting antibiotics. The timeframe is based on two main factors. The first is the virulence of the infection and how fast it is spreading. The other consideration is the patients’ own decision of how long they feel comfortable waiting until seeking further help. Again, we talk each person through these choices and try to give applicable and transparent information.

There are definitely times we suggest they seek immediate medical help. This is often due to the severity of the infection, especially if it is spreading rapidly or it is on their face where it might leave a scar. The other time we suggest medical assistance is when the person seems resistant to our helping them, and may spread the infection. If someone chooses the pharmaceutical route, we will give them whatever information we have about the closest clinics around. Depending on where the even it held, they could be a few hours away.

Opening and Draining Abscesses

Abscesses are a type of infection where the pus accumulates beneath the skin. They are often caused by staph bacteria and generally need to be opened and drained. Afterward, herbal remedies can be applied externally. Hot/warm compresses can be applied to an abscess close to opening to help it open fully and drain. Sometimes it is necessary to lance the abscess to allow it to drain. Anyone doing this should know the proper technique as well as have the proper tools. Sterilized scalpels or needles are used to open the abscess. For learning how to drain an abscess, I suggest working with an experienced professional. It is helpful to give pain-relieving and sedative herbal preparations beforehand, such as Hops and Valerian. If there is a medical person on staff, they can administer lidocaine before lancing to help relieve pain.

After it is opened, it can be useful to pack the open abscess with iodoform-packing strips. This is a thin roll of gauze permeated with a form of iodine to help it drain and prevent infection. These strips are packed into the now opened abscess with the wooden end of a cotton tip applicator or other tools. A short wick is left outside the hole. Each day some of the strip is pulled out and cut off. This helps the abscess drain and heal properly.

Abscesses can also be soaked in a strong herbal tea to help soften them as well as for their disinfectant properties. Herbs that are useful for this include Chaparral, Yarrow, and plants in the genus Berberis such as Oregongrape root and Barberry. Make sure the basin is clean before and after each use by either using a plastic liner or disinfecting it with bleach or another antiseptic cleanser.  

A staph abscess

External Applications

I generally alternate between herbal preparations (liniments and tinctures) and activated charcoal. I usually begin with the former, as they are easier to prepare and clean up. If after applying the herbal preparations and the infection seems to be clearing up quickly, I may stick to this treatment protocol. If the infection continues to worsen or does not appear to get better, I alternate between the two. The main way of knowing that an infection is worsening is that instead of engaging the healing process, the wound festers, potentially getting deeper, and is often filled with pus.

These treatments are usually applied daily for each staph infection on a person’s body. This can take a long time depending on how many staph infections they have, as there can be many per individual. After the initial examination, it is helpful to let them know approximately how long it may take to do this daily. This can help them make a decision. They may choose to seek conventional medical care, as the process is more straightforward and potentially less time-consuming, at least on a daily basis, though likely more expensive and initially more time-consuming as they will have to go to a hospital or clinic.

Opening and draining a staph abscess

External Applications-Activated Charcoal

Activated charcoal can be used externally to adsorb bacteria and exotoxins from the skin surface. There are two ways to apply the activated charcoal poultice. It can be placed on a piece of gauze and the activated charcoal side can be applied directly on the infection, or the activated can be made into a ‘sandwich’ in which is held between two pieces of gauze, and the gauze is placed over the wound.

It is important to use absorbent gauze with the activated charcoal sandwich so that it can wick up bacteria and exotoxins. Note the differences between absorb and adsorb. An absorbent assimilates the material throughout its body as with a sponge or gauze pad. In adsorption, the substance binds to the surface of the adsorbent material, such as the silica packets packaged with foods to adsorb moisture. Adsorption is an essential property of activated charcoal as it creates a tighter bond with the substance (bacteria or toxin), more effectively eliminating it from the infection site.

When the infection is not as deep or severe, the activated charcoal can be applied directly to the surface of the infection. When the infection cavity is deep, the activated charcoal sandwich is useful as it avoids depositing the charcoal directly into the wound, making it more difficult to clean up and heal.

To prepare the poultice, first moisten the activated charcoal in a container until it is slightly muddy in texture. Then spread it about 1 mm or so thick on a gauze pad. When making an activated charcoal sandwich, another gauze pad is placed on top of the activated charcoal, so it is held between two absorbent gauze pads. In both cases the poultice must be in direct contact with the infection. It should be held snugly but not too tightly against the infection.

Activated charcoal can be messy, and occasionally, after the gauze is removed, the patient feels a moment of distress as they see that the wound area is now black. They should be informed that this is just the activated charcoal and will eventually wear off. Gently wash off the charcoal between applications.

An activated charcoal poultice on gauze

External Applications-Herbal Preparations

There are a number of herbal tinctures and liniments that can be applied on gauze pads and applied topically to help with staph infections. While both tinctures (based in ethanol) and liniments (based in isopropyl alcohol) are effective, I prefer liniments as they are less expensive to prepare, and most first aid work is done for free. The advantage of tinctures is that they can also be taken internally.

Apply the below plant extracts directly onto a gauze pad until it is moist but not overly saturated.

The individual plants used in the tinctures and liniments come from several categories. I tend to use two antibacterial, one antiinflammatory, and one astringent herb. I keep these as individual medicines and mix them up as needed as well as having a few pre-made formulas on-hand. The vulnerary herbs are used after the infection has passed to help the skin regenerate.

Combinations for Staph Infections

Example 1

  • Japanese barberry root 3 pt
  • Myrrh reson 3 pt
  • Witch hazel inner bark 2 pt
  • Licorice root 1

Example 2

  • Chaparral leaf 3 pt
  • Propolis resin 2 pt
  • White oak inner bark 2 pt
  • Willow inner bark 1 pt

Herbs that can be applied topically.

Antibacterial

  1. Chaparral leaf-Larrea tridentata
  2. Echinacea root-Echinacea purpurea
  3. Japanese barberry root- Berberis thunbergii
  4. Myrrh resin-Commiphora species
  5. Oregon graperoot root-Berberis species
  6. Pine resin-Pinus species
  7. Propolis resin-Bee resin
  8. Yarrow leaf and flower-Achillea millefolium

Antiinflammatory

  1. Black birch inner bark-Betula lenta
  2. Licorice root-Glycyrrhiza glabra/G. uralensis
  3. Willow inner bark-Salix species
  4. Yarrow leaf and flower-Achillea millefolium

Astringent

  1. Blackberry root-Rubus species
  2. White oak inner bark-Quercus alba
  3. Witch hazel inner bark-Hamamelis virginiana

Vulnerary

  1. Calendula inflorescence-Calendula officinalis
  2. Chickweed herb-Stellaria media
  3. Comfrey root-Symphytum species

Chaparral (Larrea tridentata)

Internal Herbal Medicines

Along with external preparation, it is helpful to administer internal herbal medicines for their antibacterial and immune-stimulating properties. These are generally given in tincture form, though it is valuable to have a few available as a glycerite. Along with antibacterial and immune properties, herbal medicines for pain and/or sleep are useful if the infection is causing discomfort. These are given separately from the above categories.

If the infection is healing slowly, it may be beneficial to change the dosage, the combination of herbs, or both.

Before administering a tincture, remember to ask every individual if alcohol is acceptable to them. If it is not, switch to a non-alcohol preparation.

The initial loading dose is often about 4 ml, which is diluted in a 3 oz cup of water (usually followed by a water chaser due to the flavor). The patient can be given a labeled to-go bottle to take the preparation throughout the day without coming back to the first aid station.

The plastic bottles I use have caps rather than droppers (cost savings), and their dosage instructions are by the capful rather than the dropperful. The current bottle caps are 3 ml when filled. The dosage is usually about 1 capful 3 times daily. This comes out to about 2 ml per dosage as we dilute the medicine by about 1/3 so that it is easier to take. This will empty the thirty ml bottle in 3 1/3 days (3 ml x 3 times daily), and it may be refilled once or twice during the course of an event.

Each hand-written label should at least have the dosage. It can be helpful to have the practitioner’s name on the label so the patient can ask for them if they come back. It could also have the herbs and approximate parts so the formula can be replicated.

The pain and sleep remedies are taken as needed.

Combinations-Internal Preparations

Example 1

  • Oregon graperoot root 3 pt
  • Echinacea root 3 pt
  • Black birch inner bark 1 pt

Example 2

  • Echinacea root 3 pt
  • Myrrh resin 3 pt
  • Yarrow leaf and flower 2 pt
  • Licorice root 1 pt

Valerian (Valeriana officinalis)

Herbs for internal use

Herbs for internal use

Antibacterial

  1. Chaparral leaf-Larrea tridentata
  2. Echinacea root-Echinacea purpurea
  3. Japanese barberry root-Berberis thunbergii
  4. Myrrh root-Commiphora species
  5. Oregon graperoot root-Berberis species
  6. Pine resin-Pinus species
  7. Propolis resin-Bee resin
  8. Yarrow leaf and flower-Achillea millefolium

Antiinflammatory

  1. Black birch inner bark-Betula lenta
  2. Licorice root-Glycyrrhiza glabra/G. uralensis
  3. Willow inner bark-Salix species
  4. Yarrow-leaf and flower-Achillea millefolium

Pain and Sleep Herbs

  1. California poppy whole plant-Eschscholtzia californica
  2. Hops strobile-Humulus lupulus
  3. Jamaican dogwood inner bark-Piscidia piscupula
  4. Skullcap whole herb-Scutellaria lateriflora
  5. Valerian root-Valeriana officinalis
  6. Wild lettuce processed-Lactuca species

White willow (Salix alba)

Wrapping the Wound

Avoid using sticky tapes to hold dressings in place for staph infections. This is important as the staph bacteria can infiltrate cuts and small openings. When the tape is removed, it will also detach hairs leaving an area for the staph to colonize.

The activated charcoal poultice or herbal gauze pads can be held in place with a cohesive conforming bandage (Coban, Vetrap, and other trade names). These bandages adhere to themselves but not to skin or hair, making them easy to apply and remove. They are not reused but discarded after each use. Tape can be used to hold these bandages in place, but apply the tape to the outside of the cohesive bandage, not to the skin.

If the infection is in a place where you cannot wrap a bandage around it, such as the buttocks, use conformable cloth tape (such as Medipore) to hold the gauze in place.

These bandages should be snug enough to keep the gauze in place but not too tight to impair movement or circulation.

Tape holding a cohesive bandage in place

End Notes

While herbal medicine has an important place in first aid, including treating staphylococcus aureus infections, it is crucial for the herbalist to understand the depth of their clinical and assessment skills and when they need to seek further assistance. This might be for diagnosis, treatment, or both.  It is also important to know which modality of medicine or treatment will work best for an individual patient and their condition, whether it is herbal, conventional, or other.

For herbalists looking to gain these skills, they may inquire at health care teams at events and ask how they might fit in. If they are new to treating in these situations, they will be in an observational role. They can offer to help out by maintaining the premises or other jobs that need to be done.

As you can see from this article, treating staphylococcus aureus infections requires more than just knowledge about what herbs might be effective. It is essential to understand how to evaluate the infection, maintain sanitary conditions, to educate and give the patient agency to make their own informed decisions, and knowing what treatments might be most applicable and available. With this knowledge, herbalists can lend a helpful hand in treating these prevalent infections.

Herbal medicines for treatment of bacterial infections: a review of controlled clinical trials | Journal of Antimicrobial Chemotherapy

Abstract

Objectives: Many hundreds of plant extracts have been tested for in vitro antibacterial activity. This review is a critical evaluation of controlled clinical trials of herbal medicines with antibacterial activity.

Methods: Four electronic databases were searched for controlled clinical trials of antibacterial herbal medicines. Data were extracted and validated in a standardized fashion, according to predefined criteria, by two independent reviewers.

Results: Seven clinical trials met our inclusion criteria. Four of these studies were randomized. Three trials of garlic and cinnamon treatments for Helicobacter pylori infections reported no significant effect. Bacterial infections of skin were treated in four trials. Positive results were reported for an ointment containing tea leaf extract in impetigo contagiosa infections. Two trials of tea tree oil preparations used for acne and methicillin-resistant Staphylococcus aureus, and one trial of Ocimum gratissimum oil for acne, reported results equivalent to conventional treatments.

Conclusions: Few controlled clinical trials have been published and most are methodologically weak. The clinical efficacy of none of the herbal medicines has so far been demonstrated beyond doubt. This area seems to merit further study through rigorous clinical trials.

Introduction

Many hundreds of plants worldwide are used in traditional medicine as treatments for bacterial infections. Some of these have also been subjected to in vitro screening but the efficacy of such herbal medicines has seldom been rigorously tested in controlled clinical trials. Conventional drugs usually provide effective antibiotic therapy for bacterial infections but there is an increasing problem of antibiotic resistance and a continuing need for new solutions. Although natural products are not necessarily safer than synthetic antibiotics, some patients prefer to use herbal medicines. Thus healthcare professionals should be aware of the available evidence for herbal antibiotics. This review was undertaken to assess critically those antibacterial herbal medicines that been have subjected to controlled clinical trials.

Materials and methods

Computerized literature searches were performed on MEDLINE (via PubMed), EMBASE, CISCOM and Cochrane Library from their inception until October 2002. Primary search terms used were ‘herb’ or ‘plant’ and ‘antibacterial’ and ‘clinical trials’. Further searches were undertaken using the names of individual plants with antimicrobial effects as documented in vitro and also individual bacteria reported in clinical trials. Departmental files were searched and the bibliographies of articles located from all sources were searched for relevant clinical trials. No restriction on the language of publication was applied. Controlled clinical trials were included in the analysis if they reported experimental use of a single, whole plant extract for reduction or elimination of disease-producing bacterial populations colonizing humans. Trials of herbal rinses used for oral hygiene were considered to form a subject in their own right and were not included. Herbal mixtures were excluded as well as treatments solely for the prevention of bacterial infections or for stimulation of immunity. Single constituents derived from plant extracts are by definition not herbal medicines and were therefore excluded. All data were extracted by the first author according to predefined criteria (Table 1) and validated by the second author. The methodological quality of randomized trials was evaluated according to a score designed by Jadad et al.1 (maximum score 5).

Results

Helicobacter pylori infections

Three trials were found that tested the efficacy of herbal products for the eradication of H. pylori; two tested different preparations of garlic (Allium sativum). A group of 20 H. pylori-infected patients suffering from dyspeptic complaints for >2 months were recruited by Aydin et al.2 A 2 week treatment with capsules containing an oil macerate of garlic (275 mg, three times a day) was compared with the combination of garlic with omeprazole (20 mg, twice a day) for the eradication of H. pylori. All subjects underwent endoscopy before and 1 month after the end of treatment, and the presence of H. pylori in biopsy specimens was confirmed by the urease test and by microscopy. Symptom scores and degree of gastritis, as judged by histological examination, were recorded pre- and post-treatment. Neither intervention resulted in the elimination of the organism, change in the severity of gastritis or a significant change in symptom scores (9.2 ± 1.55 versus 8.7 ± 1.70 in the garlic oil group, 9.0 ± 1.49 versus 8.5 ± 1.51 in the garlic oil plus omeprazole group). The authors considered that low levels of the antibacterial component allicin in the garlic capsules might account for the lack of effect. This trial has obvious weaknesses: it was not randomized, probably not patient-blind and its sample size was small.

Extracts of fresh garlic and capsaicin-containing peppers can inhibit H. pyloriin vitro and were tested for their ability to inhibit the bacterium in vivo in a crossover trial involving 12 individuals infected with H. pylori.3 Test substances were included in morning, noon and evening, Mexican-style meals. Subjects participated in a minimum of 3 trial days (negative and positive controls and one experimental ingredient). At least 2 days elapsed between test substances, with bismuth always being the last intervention tested to preclude lasting anti-H. pylori effects. During each test meal participants received one intervention: garlic (10 freshly sliced cloves), capsaicin (six freshly sliced jalapeno peppers), two tablets of bismuth subsalicylate (Pepto-Bismol, positive control) or no additions (negative control). The urea breath test was performed before the first meal of the day, before the evening meal and the morning after each test day. The results were used to evaluate the effectiveness of the therapies. Ten subjects received garlic, six received jalapenos and 11 received bismuth. Neither garlic nor jalapenos had any effect on urease levels (median urease activity pre- and post-garlic 28.5 versus 39.8 and jalapenos 43.7 versus 46.6; P > 0.8) but there was a marked reduction after ingestion of bismuth (55.8 versus 14.3; P < 0.001). Two patients experienced nausea and diarrhoea graded as severe after eating the jalapenos and 70% of those eating garlic complained of taste disturbance and body odour. This study suffered from lack of randomization and small sample size.

Nir et al.4 investigated the effects of treatment with an extract of cinnamon (Cinnamonum cassia) in 23 patients who were undergoing gastroscopy and had a positive urea breath test. Thirty-two patients were randomly allocated in a 2:1 ratio to the study and control groups but only 23 could be included in the final analysis. Fifteen received 80 mg/day cinnamon and eight received placebo for 4 weeks. Breath tests were repeated at the end of the trial period. There were some increased and some decreased urea breath test values in both groups, but overall mean values (pre- and post-cinnamon treatment 22.1 versus 24.4, placebo 23.9 versus 25.9) showed no significant changes. This trial was well designed but its sample size was small and therefore the possibility of a type II error cannot be excluded.

Staphylococcus aureus and Streptococcus pyogenes infections

One clinical trial compared the use of a combination of 4% tea tree oil (TTO) nasal ointment and 5% TTO body wash (intervention) with a standard 2% mupirocin nasal ointment and triclosan body wash (routine) for eradication of methicillin-resistantStaphylococcus aureus (MRSA).5 A total of 30 in-patients, either infected or colonized with MRSA, were recruited and randomly assigned to be treated with TTO or standard routine care for a minimum of 3 days. Infected patients also received intravenous vancomycin and all participants were screened for MRSA carriage 48 and 96 h after the cessation of topical treatment. Only 18 patients completed the trial. More patients in the intervention than in the control group cleared infection (5/8 versus 2/10). Two patients in the intervention group received 34 days treatment and one cleared the infection while the other remained chronically colonized. The inter-group differences were not statistically significant. This trial was too small to generate a conclusive result.

Strains of S. aureus and Streptococcus pyogenes are the causative agents of the painful and unsightly skin condition impetigo contagiosa. Sharquie et al.6 tested in vitro antibacterial properties of crude preparations of black tea (Thea assamica) and proceeded to a clinical trial in 104 patients with impetigo contagiosa. Tea extracts were incorporated in an aqueous lotion at a concentration of 1% (Group 1) and a vaseline base at a concentration of 5% (Group 2), and these preparations were applied at least three or four times a day. Cure rates in these groups were compared with cure rates in groups given framycetin and gramicidin ointment (Group 3) or oral cefalixin (Group 4). The 5% tea extract was as effective as antibiotic treatments (Groups 2–4 cure rates 81.3%, 72.2% and 78.6%, respectively). The cure rate in Group1 was 37.5%. Even though the total sample size of this trial seems large, the patient numbers in each treatment arm were low. Moreover, this study suffered from the fact that it was not randomized.

Acne

A single-blind randomized clinical trial (RCT) compared the use of 5% TTO gel with 5% benzoyl peroxide lotion for the treatment of mild to moderate acne in a group of 124 patients.7 Numbers of inflamed and non-inflamed lesions were counted at baseline and at monthly intervals for 3 months and both treatments were effective, although improvements were slower in the TTO group. There was a significantly greater reduction in inflamed lesions in the benzoyl peroxide group at all three follow-up visits. Skin discomfort during treatment was reported less frequently in the TTO group than in those using benzoyl peroxide (44% versus 79%). Without a placebo group it is difficult to decide whether this study demonstrates the presence or absence of a treatment effect and it may also have lacked statistical power to test equivalence between the two therapies.

A recent study tested a range of concentrations of Ocimum gratissimum oil in comparison with 10% benzoyl peroxide and a placebo, over a period of 4 weeks, for the reduction of acne lesions in a population consisting mainly of students.8O. gratissimum oil was incorporated at concentrations of 0.5%, 1%, 2% and 5% v/v in four different bases (polysorbate 80, cetomacrogol, petrolatum and alcohol) resulting in 16 parallel experimental groups. The number of lesions were counted daily by investigators throughout the test period and the time taken to achieve a 50% reduction relative to pre-treatment was noted for each subject. Preparations containing 2% and 5% Ocimum oil in alcohol and 5% in cetomacrogol were significantly more active than benzoyl peroxide (P < 0.05), while 2% oil in cetomacrogol had similar activity to the reference product. The most active 5% preparations produced skin irritation but the authors considered a 2% preparation in cetomacrogol to be suitable for the management of acne. The sample size of the individual treatment groups was too small to exclude a type II error.

Discussion

Perhaps the most striking result of this review is the extreme paucity of controlled clinical trials testing herbal antibiotics. In light of the long history and present popularity of their use, it is surprising that so few trials have tested the efficacy of herbal antibiotics. One obvious reason is the lack of patent rights on herbal medicines. Another reason could be that traditionally, herbal medicine has been hesitant to embrace modern methods for efficacy testing.

Although our search strategy was comprehensive, we cannot be sure that all clinical trials were located. Herbal medicine research is sometimes published in journals not readily accessible through electronic databases and negative trials may not be published at all. It might have been anticipated that trials of cranberry extracts would have been located since it has been used for decades in the management of urinary tract infection. Although a number of studies have examined the use of cranberry for prevention of recurrences of urinary tract infections,9 there are no published clinical trials of its use for treatment of infections10 and it therefore did not meet the inclusion criteria of this review.

Most of the clinical trials located had few participants. Herbal therapies were reported as being as effective as conventional treatments in two trials5,7 and one of the two herbal preparations used in a third trial was as efficacious as two conventional antibiotic regimens.6 The results imply that an O. gratissimum oil preparation is a promising treatment for acne.8 It was as effective as benzoyl peroxide but described as having an unpleasant odour that may, of course, render it less acceptable to patients.

H. pylori infection is common even in asymptomatic individuals and has been shown to be a risk factor for gastric cancer.11 Eradication of the organism can be difficult to achieve with conventional antibiotic therapies, requiring combinations of antibiotics, proton pump inhibitors and bismuth preparations.12 Moreover, adverse effects are regularly associated with these conventional treatments.11

Garlic is one of the most extensively researched medicinal plants.13 Its antibacterial action depends on allicin and is thought to be due to multiple inhibitory effects on various thiol-dependent enzymatic systems.14 Allicin is formed catalytically by crushing raw garlic or adding water to dried garlic, when the enzyme allicinase comes into contact with allicin. Steam distillation of mashed garlic produces garlic oil containing methyl and allyl sulphides of allicin, having the practical advantage of being more stable than allicin itself.

Two controlled trials of garlic preparations used to eradicate H. pylori infection recorded failure.2,3 A further two small trials15,16 without control groups (thus not meeting inclusion criteria of this review) similarly reported no significant results although the garlic preparations used were different in all four trials. Individual constituents of garlic oil and garlic powder have shown a range of potencies when tested in vitro against human enteric bacteria including H. pylori.17,18 Analysis of the herbal preparations used in clinical trials was reported and discussed by McNulty et al.,16 who suggested that active ingredients were at low levels or absent in the preparations used in trials published by Ernst15 and Aydin et al.2 Although the steam-distilled garlic oil preparation used in her own pilot trial had high levels of allicin sulphides, it also proved ineffective. It is possible that an effective treatment might be produced by optimizing the active antibacterial content of preparations and/or judicious use of a combination of conventional and herbal therapies. Garlic and omeprazole have demonstrated synergic properties when tested in vitro against some strains of H. pylori19,20 and the fact that their concurrent use was not effective in the trial reported by Aydin et al.2 may be due to low levels of active garlic components.

Cinnamon extracts in vitro exerted an inhibitory effect on the growth and urease activity of a number of strains of H. pylori21 and encouraged Nir et al.4 to conduct a clinical trial. At the concentration chosen the extract was ineffective in vivo and the authors suggested the possibility that eradication of the organism might be achieved using higher cinnamon concentrations or a regimen combining antibiotic and herbal therapy.

TTO products are widely used as topical treatments by the general public and have proved as effective as conventional treatments for the control of skin bacteria involved in acne7 and of MRSA in a hospital setting.5 Recent research suggests that TTO and its components compromise cytoplasmic membranes of S. aureus,22 weakening the cells’ ability to withstand the effects of other cytocidal agents. The public perception and potentially devastating results of uncontrolled MRSA spread in hospitals make it a prime target for a new strategy for eradication, and TTO could have a contribution to make in that context. RCTs of TTO have recently been reviewed and the authors concluded that, while it may prove useful as a topical antimicrobial, evidence from well-designed RCTs was lacking.23

A black tea leaf extract, presumed to derive its antibacterial effect from tannins and catechins, demonstrated results equivalent to antibiotic treatments for curing impetigo contagiosa.6 This simple and inexpensive alternative to conventional treatment may be worthy of further rigorous investigation.

In conclusion, the evidence summarized above tentatively suggests possible benefits from some herbal preparations with antibacterial activity. Further large-scale, well-designed clinical trials are required to provide more conclusive proof of their efficacy.

Acknowledgements

K.W.M. was supported by a research fellowship provided by the Boots Company, Nottingham, UK.

Table 1.

 Clinical trials of herbal antibacterial preparations

Reference Study design (Jadad score) Study sample Condition/bacterium treated Experimental intervention Control interventions Main outcome measure Main results 
Aydin et al.2 blinding not stated,  non-randomized,  comparative trial  with two parallel  groups 20 dyspeptic patients H. pylori 275 mg garlic oil,  3 times a day for  14 days 275 mg garlic oil,  3 times a day with  20 mg omeprazole  twice a day for 14 days negative histology  and urease test  1 month after end  of treatment neither therapy had  significant effect on  outcome measures  
Graham et al.3 open, non-randomized,  crossover trial 12 healthy adults with  H. pylori H. pylori (1) 10 cloves fresh  garlic with 3 meals  per test day (2) 6 jalapeno peppers  with 3 meals per  test day (3) bismuth subsalicylate  with 3 meals per  test day (4) no intervention with  3 meals per test day reduction of urea  breath test value no significant changes  with experimental  interventions,  significant reduction  after bismuth 
Nir et al.blinding not stated,  placebo-controlled  RCT with two  parallel groups (2) 32 patients undergoing  gastroscopy  (23 completed  treatment) H. pylori 40 mg cinnamon  extract twice a day  for 4 weeks placebo reduction of urea  breath test value no significant changes   in breath test values 
Caelli et al.5 blinding not stated,  RCT with two parallel  groups (2) 30 inpatients  (18 completed  treatment) methicillin-resistant  S. aureus tea tree oil 4% nasal  ointment and 5%  body wash for  1–34 days 2% mupirocin nasal  ointment and triclosan  body wash 2–14 days eradication of MRSA  colonization no significant difference  between groups 
Sharquie et al.blinding not stated,  non-randomized,  controlled trial with  four parallel arms 104 patients with  impetigo contagiosa  (88 completed  treatment) impetigo contagiosa (1) 1% aqueous tea  extract, several times  a day for 7–10 days (3) 15 mg/g framycetin  and 0.05 mg/g  gramicidin ointment  for 7–10 days cure rate (1) 37.5% cure (2)81.3% cure (3) 72.2% cure (4)78.6% cure 
    (2) 5% tea extract in  vaseline, 3–4 times  a day for 7–10 days (4) 40–50 mg/kg/day  oral cefalexin for  7–10 days   
Bassett et al.7 investigator blind,  comparative RCT with  two parallel groups (2) 124 patients with mild to  moderate acne (119  completed treatment) acne tea tree oil 5% water-  based gel for  3 months benzoyl peroxide 5%  water-based lotion  for 3 months changes in total  numbers of inflamed  and non-inflamed   lesions both treatments effective  in reducing lesions,  TTO has slower onset  of action 
Orafidiya et al.8 blinding not stated,  placebo-controlled  RCT with 18 parallel  groups (2) 126 subjects acne O. gratissimum  oil preparations, 0.5–5%  in four different bases,  twice a day for 4 weeks (1) benzoyl peroxide  10% lotion (2) placebo product activity =  reciprocal value of  number of days to  50% reduction in  lesion count (1) 2–5% oil in alcohol and  5% oil in cetomacrogol  base significantly more  effective than benzoyl  peroxide 
       (2) no 50% lesion reduction  in placebo group in test  period 
Reference Study design (Jadad score) Study sample Condition/bacterium treated Experimental intervention Control interventions Main outcome measure Main results 
Aydin et al.2 blinding not stated,  non-randomized,  comparative trial  with two parallel  groups 20 dyspeptic patients H. pylori 275 mg garlic oil,  3 times a day for  14 days 275 mg garlic oil,  3 times a day with  20 mg omeprazole  twice a day for 14 days negative histology  and urease test  1 month after end  of treatment neither therapy had  significant effect on  outcome measures  
Graham et al.3 open, non-randomized,  crossover trial 12 healthy adults with  H. pylori H. pylori (1) 10 cloves fresh  garlic with 3 meals  per test day (2) 6 jalapeno peppers  with 3 meals per  test day (3) bismuth subsalicylate  with 3 meals per  test day (4) no intervention with  3 meals per test day reduction of urea  breath test value no significant changes  with experimental  interventions,  significant reduction  after bismuth 
Nir et al.blinding not stated,  placebo-controlled  RCT with two  parallel groups (2) 32 patients undergoing  gastroscopy  (23 completed  treatment) H. pylori 40 mg cinnamon  extract twice a day  for 4 weeks placebo reduction of urea  breath test value no significant changes   in breath test values 
Caelli et al.5 blinding not stated,  RCT with two parallel  groups (2) 30 inpatients  (18 completed  treatment) methicillin-resistant  S. aureus tea tree oil 4% nasal  ointment and 5%  body wash for  1–34 days 2% mupirocin nasal  ointment and triclosan  body wash 2–14 days eradication of MRSA  colonization no significant difference  between groups 
Sharquie et al.blinding not stated,  non-randomized,  controlled trial with  four parallel arms 104 patients with  impetigo contagiosa  (88 completed  treatment) impetigo contagiosa (1) 1% aqueous tea  extract, several times  a day for 7–10 days (3) 15 mg/g framycetin  and 0.05 mg/g  gramicidin ointment  for 7–10 days cure rate (1) 37.5% cure (2)81.3% cure (3) 72.2% cure (4)78.6% cure 
    (2) 5% tea extract in  vaseline, 3–4 times  a day for 7–10 days (4) 40–50 mg/kg/day  oral cefalexin for  7–10 days   
Bassett et al.7 investigator blind,  comparative RCT with  two parallel groups (2) 124 patients with mild to  moderate acne (119  completed treatment) acne tea tree oil 5% water-  based gel for  3 months benzoyl peroxide 5%  water-based lotion  for 3 months changes in total  numbers of inflamed  and non-inflamed   lesions both treatments effective  in reducing lesions,  TTO has slower onset  of action 
Orafidiya et al.8 blinding not stated,  placebo-controlled  RCT with 18 parallel  groups (2) 126 subjects acne O. gratissimum  oil preparations, 0.5–5%  in four different bases,  twice a day for 4 weeks (1) benzoyl peroxide  10% lotion (2) placebo product activity =  reciprocal value of  number of days to  50% reduction in  lesion count (1) 2–5% oil in alcohol and  5% oil in cetomacrogol  base significantly more  effective than benzoyl  peroxide 
       (2) no 50% lesion reduction  in placebo group in test  period 

Table 1.

 Clinical trials of herbal antibacterial preparations

Reference Study design (Jadad score) Study sample Condition/bacterium treated Experimental intervention Control interventions Main outcome measure Main results 
Aydin et al.2 blinding not stated,  non-randomized,  comparative trial  with two parallel  groups 20 dyspeptic patients H. pylori 275 mg garlic oil,  3 times a day for  14 days 275 mg garlic oil,  3 times a day with  20 mg omeprazole  twice a day for 14 days negative histology  and urease test  1 month after end  of treatment neither therapy had  significant effect on  outcome measures  
Graham et al.3 open, non-randomized,  crossover trial 12 healthy adults with  H. pylori H. pylori (1) 10 cloves fresh  garlic with 3 meals  per test day (2) 6 jalapeno peppers  with 3 meals per  test day (3) bismuth subsalicylate  with 3 meals per  test day (4) no intervention with  3 meals per test day reduction of urea  breath test value no significant changes  with experimental  interventions,  significant reduction  after bismuth 
Nir et al.blinding not stated,  placebo-controlled  RCT with two  parallel groups (2) 32 patients undergoing  gastroscopy  (23 completed  treatment) H. pylori 40 mg cinnamon  extract twice a day  for 4 weeks placebo reduction of urea  breath test value no significant changes   in breath test values 
Caelli et al.5 blinding not stated,  RCT with two parallel  groups (2) 30 inpatients  (18 completed  treatment) methicillin-resistant  S. aureus tea tree oil 4% nasal  ointment and 5%  body wash for  1–34 days 2% mupirocin nasal  ointment and triclosan  body wash 2–14 days eradication of MRSA  colonization no significant difference  between groups 
Sharquie et al.blinding not stated,  non-randomized,  controlled trial with  four parallel arms 104 patients with  impetigo contagiosa  (88 completed  treatment) impetigo contagiosa (1) 1% aqueous tea  extract, several times  a day for 7–10 days (3) 15 mg/g framycetin  and 0.05 mg/g  gramicidin ointment  for 7–10 days cure rate (1) 37.5% cure (2)81.3% cure (3) 72.2% cure (4)78.6% cure 
    (2) 5% tea extract in  vaseline, 3–4 times  a day for 7–10 days (4) 40–50 mg/kg/day  oral cefalexin for  7–10 days   
Bassett et al.7 investigator blind,  comparative RCT with  two parallel groups (2) 124 patients with mild to  moderate acne (119  completed treatment) acne tea tree oil 5% water-  based gel for  3 months benzoyl peroxide 5%  water-based lotion  for 3 months changes in total  numbers of inflamed  and non-inflamed   lesions both treatments effective  in reducing lesions,  TTO has slower onset  of action 
Orafidiya et al.8 blinding not stated,  placebo-controlled  RCT with 18 parallel  groups (2) 126 subjects acne O. gratissimum  oil preparations, 0.5–5%  in four different bases,  twice a day for 4 weeks (1) benzoyl peroxide  10% lotion (2) placebo product activity =  reciprocal value of  number of days to  50% reduction in  lesion count (1) 2–5% oil in alcohol and  5% oil in cetomacrogol  base significantly more  effective than benzoyl  peroxide 
       (2) no 50% lesion reduction  in placebo group in test  period 
Reference Study design (Jadad score) Study sample Condition/bacterium treated Experimental intervention Control interventions Main outcome measure Main results 
Aydin et al.2 blinding not stated,  non-randomized,  comparative trial  with two parallel  groups 20 dyspeptic patients H. pylori 275 mg garlic oil,  3 times a day for  14 days 275 mg garlic oil,  3 times a day with  20 mg omeprazole  twice a day for 14 days negative histology  and urease test  1 month after end  of treatment neither therapy had  significant effect on  outcome measures  
Graham et al.3 open, non-randomized,  crossover trial 12 healthy adults with  H. pylori H. pylori (1) 10 cloves fresh  garlic with 3 meals  per test day (2) 6 jalapeno peppers  with 3 meals per  test day (3) bismuth subsalicylate  with 3 meals per  test day (4) no intervention with  3 meals per test day reduction of urea  breath test value no significant changes  with experimental  interventions,  significant reduction  after bismuth 
Nir et al.blinding not stated,  placebo-controlled  RCT with two  parallel groups (2) 32 patients undergoing  gastroscopy  (23 completed  treatment) H. pylori 40 mg cinnamon  extract twice a day  for 4 weeks placebo reduction of urea  breath test value no significant changes   in breath test values 
Caelli et al.5 blinding not stated,  RCT with two parallel  groups (2) 30 inpatients  (18 completed  treatment) methicillin-resistant  S. aureus tea tree oil 4% nasal  ointment and 5%  body wash for  1–34 days 2% mupirocin nasal  ointment and triclosan  body wash 2–14 days eradication of MRSA  colonization no significant difference  between groups 
Sharquie et al.blinding not stated,  non-randomized,  controlled trial with  four parallel arms 104 patients with  impetigo contagiosa  (88 completed  treatment) impetigo contagiosa (1) 1% aqueous tea  extract, several times  a day for 7–10 days (3) 15 mg/g framycetin  and 0.05 mg/g  gramicidin ointment  for 7–10 days cure rate (1) 37.5% cure (2)81.3% cure (3) 72.2% cure (4)78.6% cure 
    (2) 5% tea extract in  vaseline, 3–4 times  a day for 7–10 days (4) 40–50 mg/kg/day  oral cefalexin for  7–10 days   
Bassett et al.7 investigator blind,  comparative RCT with  two parallel groups (2) 124 patients with mild to  moderate acne (119  completed treatment) acne tea tree oil 5% water-  based gel for  3 months benzoyl peroxide 5%  water-based lotion  for 3 months changes in total  numbers of inflamed  and non-inflamed   lesions both treatments effective  in reducing lesions,  TTO has slower onset  of action 
Orafidiya et al.8 blinding not stated,  placebo-controlled  RCT with 18 parallel  groups (2) 126 subjects acne O. gratissimum  oil preparations, 0.5–5%  in four different bases,  twice a day for 4 weeks (1) benzoyl peroxide  10% lotion (2) placebo product activity =  reciprocal value of  number of days to  50% reduction in  lesion count (1) 2–5% oil in alcohol and  5% oil in cetomacrogol  base significantly more  effective than benzoyl  peroxide 
       (2) no 50% lesion reduction  in placebo group in test  period 

References

1.

Jadad, J. R., Moore, A., Carroll, D., Jenkinson, C., Reynolds, D. J. M., Gavaghan, D. J. et al. (

1996

). Assessing the quality of reports of randomized clinical trials: is blinding necessary?

Controlled Clinical Trials

17

,

1

–12.2.

Aydin, A., Ersoz, G., Tekesin, O., Akcicek, E., Tuncyurek, M. & Batur, Y. (

1997

). Does garlic oil have a role in the treatment of Helicobacter pylori infection?

Turkish Journal of Gastroenterology

8

,

181

–4.3.

Graham, D. Y., Anderson, S.-Y. & Lang, T. (

1994

). Garlic or jalapeno peppers for the treatment of Helicobacter pylori infection.

American Journal of Gastroenterology

94

,

1200

–2.4.

Nir, Y., Potasman, I., Stermer, E., Tabak, M. & Neeman, I. (

2000

). Controlled trial of the effect of cinnamon extract on Helicobacter pylori.

Helicobacter

5

,

94

–7.5.

Caelli, M., Porteous, J., Carson, C. F., Heller, R. & Riley, T. V. (

2000

). Tea tree oil as an alternative topical decolonization agent for methicillin-resistant Staphylococcus aureus.

Journal of Hospital Infection

46

,

236

–7.6.

Sharquie, K. E., Al-Turfi, I. A. & Al-Salloum, S. M. (

2000

). The antibacterial activity of tea in vitro and in vivo (in patients with impetigo contagiosa).

Journal of Dermatology

27

,

706

–10.7.

Bassett, I. B., Pannowitz, D. L. & Barnetson, R. S. (

1990

). A comparative study of tea-tree oil versus benzoylperoxide in the treatment of acne.

Medical Journal of Australia

153

,

455

–8.8.

Orafidiya, L. O., Agbani, E. O., Oyedele, A. O., Babalola, O. O. & Onayemi, O. (

2002

). Preliminary clinical tests on topical preparations of Ocimum gratissimum Linn leaf essential oil for the treatment of acne vulgaris.

Clinical Drug Investigations

22

,

313

–9.9.

Jepson, R. G., Mihaljevic, L. & Craig, J. (

2002

). Cranberries for preventing urinary tract infections. (Cochrane Rewiew). In The Cochrane Library, Issue 4, 2002. Update Software, Oxford.10.

Jepson, R. G., Mihaljevic, L. & Craig, J. (

2002

). Cranberries for treating urinary tract infections. (Cochrane Rewiew). In The Cochrane Library, Issue 4, 2002. Update Software, Oxford.11.

Gaby, A. R. (

2001

). Helicobacter pylori eradication: are there alternatives to antibiotics?

Alternative Medicine Review

6

,

355

–66.12.

Harris, A. & Misiewicz, J. J. (

2001

). ABC of the upper gastrointestinal tract. Management of Helicobacter pylori infection.

British Medical Journal

323

,

1047

–50.13.

Boon, H. & Smith, M. (

1999

). The Botanical Pharmacy. Quarry Press Inc., Ontario, Canada.14.

Ankri, S. & Mirelman, D. (

1999

). Antimicrobial properties of allicin from garlic.

Microbes and Infection

1

,

125

–9.15.

Ernst, E. (

1999

). Is garlic an effective treatment for Helicobacter pylori infection?

Archives of Internal Medicine

159

,

2484

–5.16.

McNulty, C. A. M., Wilson, M. P., Havinga, W., Johnston, B., O’Gara, E. A. & Maslin, D. J. (

2001

). A pilot study to determine the effectiveness of garlic oil capsules in the treatment of dyspeptic patients with Helicobacter pylori.

Helicobacter

6

,

249

–53.17.

Ross, Z. M., O’Gara, E. A., Hill, D. J., Sleightholme, H. V. & Maslin, D. J. (

2001

). Antimicrobial properties of garlic oil against human enteric bacteria: evaluation of methodologies and comparisons with garlic oil sulfides and garlic powder.

Applied and Environmental Microbiology

67

,

475

–80.18.

O’Gara, E. A., Hill, D. J. & Maslin, D. J. (

2000

). Activities of garlic oil, garlic powder, and their diallyl constituents against Helicobacter pylori.

Applied and Environmental Microbiology

66

,

2269

–73.19.

Jonkers, D., van den Broek, E., van Dooren, I., Thijs, C., Dorant, E., Hageman, G. et al. (

1999

). Antibacterial effect of garlic and omeprazole on Helicobacter pylori.

Journal of Antimicrobial Chemotherapy

43

,

837

–9.20.

Cellini, L., Di Campli, E., Masulli, M., Di Bartolomec, S. & Allocati, N. (

1996

). Inhibition of Helicobacter pylori by garlic extract (Allium sativum).

FEMS Immunology and Medical Microbiology

13

,

273

–7.21.

Tabak, M., Armon, R. & Neeman, I. (

1996

). Cinnamon extracts’ inhibitory effect on Helicobacter pylori.

Journal of Ethnopharmacology

67

,

269

–77.22.

Carson, C. F., Mee, B. J. & Riley, T. V. (

2002

). Mechanism of action of Melaleuca alternifolia (Tea tree) oil on Staphylococcus aureus determined by time–kill, lysis, leakage, and salt tolerance assays and electron microscopy.

Antimicrobial Agents and Chemotherapy

46

,

1914

–20.23.

Ernst, E. & Huntley, A. (

2000

). Tea tree oil: a systematic review of randomized clinical trials.

Forschende Komplementärmedizin und Klassische Naturheilkunde

7

,

17

–20.

Herbal therapy associated with antibiotic therapy: potentiation of the antibiotic activity against methicillin – resistant Staphylococcus aureus by Turnera ulmifolia L | BMC Complementary Medicine and Therapies

  • 1.

    Nostro A, Blanco AR, Cannatelli MA, Enea V, Flamini G, Morelli I: Susceptibility of methicillin-resistant staphylococci to oregano essential oil, carvacrol and thymol. FEMS Microbiol Lett. 2004, 230: 191-195. 10.1016/S0378-1097(03)00890-5.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 2.

    Pereira MSV, Siqueira Júnior JP, Takaki GMC: Elimination of resistance to drugs by fluoroquinolones in bovine strains of Staphylococcus aureus. Pesquisa Vet Brasil. 2004, 24: 11-14.

    Google Scholar 

  • 3.

    Verhoeff J, Beaujean D, Vlok H, Baars A, Meyler A, Werkwn Van Der C: A dutch approach to methicillin-resistance Staphylococcus aureus. Eur J Clin Microbiol Infect Dis. 1999, 18: 461-466. 10.1007/s100960050324.

    Article 

    Google Scholar 

  • 4.

    Karras D: Antibiotic misuse in the emergency department. Acad Emerg Med. 2006, 13: 331-333. 10.1111/j.1553-2712.2006.tb01701.x.

    Article 
    PubMed 

    Google Scholar 

  • 5.

    Malhutra-Kumar S, Lammens C, Coenen S, Van Herk K, Goossens H: Effect of azithromycin and clarithromycin therapy on pharyngeal carriage of macrolide-resistant streptococci in health volunteers: A randomized, double-blind, placebo-controlled study. Lancet. 2007, 369: 482-490. 10.1016/S0140-6736(07)60235-9.

    Article 

    Google Scholar 

  • 6.

    Roe VA: Antibiotic resistance: A guide for effective prescribing in women’s health. J Midwif Womens Health. 2008, 53: 216-226. 10.1016/j.jmwh.2008.01.003.

    Article 

    Google Scholar 

  • 7.

    Purssel E: Evolutionary nursing: the case of infectious disease. J Adv Nurs. 2005, 49: 164-172. 10.1111/j.1365-2648.2004.03276.x.

    Article 

    Google Scholar 

  • 8.

    Lu Y, Zhao YP, Wang ZC, Chen SY, Fu CX: Composition and antimicrobial activity of the essential oil of Actinidia macrosperma from China. Nat Prod Res. 2007, 21: 227-233. 10.1080/14786410500463395.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 9.

    Mbwambo ZH, Moshi MJ, Masimba PJ, Kapingu MC, Nondo RS: Antimicrobial activity and brine shrimp toxicity of extracts of Terminalia brownii roots and stem. BMC Complement Altern Med. 2007, 7: 9-10.1186/1472-6882-7-9.

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 10.

    Benoit-Vical F, Grellier P, Abdoulaye A, Moussa I, Ousmane A, Berry A: In vitro and in vivo Antiplasmodial Activity of Momordica balsamina Alone or in a Traditional Mixture. Chemotherapy. 2006, 52: 288-292. 10.1159/000095960.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 11.

    Senatore F, Rigano D, Formisano C, Grassia A, Basile A, Sorbo S: Phytogrowth-inhibitory and antibacterial activity of Verbascum sinuatum. Fitoterapia. 2007, 78: 244-247. 10.1016/j.fitote.2006.11.010.

    Article 
    PubMed 

    Google Scholar 

  • 12.

    Singh G, Maurya S, Delampasona MP, Catalan CA: A comparison of chemical, antioxidant and antimicrobial studies of cinnamon leaf and bark volatile oils, oleoresins and their constituents. Food Chem Toxico. 2007, 45: 1650-1661. 10.1016/j.fct.2007.02.031.

    CAS 
    Article 

    Google Scholar 

  • 13.

    Gibbons S: Anti-staphylococcal plant natural products. Nat Prod Rep. 2004, 21: 263-277. 10.1039/b212695h.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 14.

    Gunics G, Farkas S, Motohashi N, Shah A, Harsukh G, Kawase M, Molnár J: Interaction between 3,5-diacetyl-1,4-dihydropyridines and ampicillin, and erythromycin on different E. coli strains. In Vivo. 2006, 20 (3): 367-372.

    Google Scholar 

  • 15.

    Molnar J, Molnar A, Spengler G, Mandi Y: Infectious plasmid resistance and efflux pump mediated resistance. Acta Microbiol Immunol Hung. 2004, 51 (3): 333-349. 10.1556/AMicr.51.2004.3.11.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 16.

    Braga R: Plantas do nordeste, especialmente do Ceará. 1976, ESAM (Coleção Mossoroense), Fortaleza, 3

    Google Scholar 

  • 17.

    Pio Corrêa M: Dicionário das plantas úteis do Brasil e das exóticas cultivadas. 1984, Imprensa Nacional, Rio de Janeiro, 3

    Google Scholar 

  • 18.

    Hosamani KM: Fatty acids in seed oil from Turnera ulmifolia. Phytochemistry. 1993, 34 (5): 1363-1365. 10.1016/0031-9422(91)80030-5.

    CAS 
    Article 

    Google Scholar 

  • 19.

    Antonio MA, Souza Brito AR: Oral anti-inflammatory and anti-ulcerogenic activities of a hydroalcoholic extract and partitioned fractions of Turnera ulmifolia (Turneraceae). J Ethnopharmacol. 1998, 6 (3): 215-228. 10.1016/S0378-8741(98)00049-X.

    Article 

    Google Scholar 

  • 20.

    Gracioso JS, Vilegas W, Hiruma-Lima CA, Souza Brito AR: Effects of tea from Turnera ulmifolia L. on mouse gastric mucosa support the Turneraceae as a new source of antiulcerogenic drugs. Biol Pharmac Bull. 2002, 25 (4): 487-491. 10.1248/bpb.25.487.

    CAS 
    Article 

    Google Scholar 

  • 21.

    Nascimento MA, Silva AK, Franca LC, Quignard EL, Lopez JA, Almeida MG: Turnera ulmifolia L. (Turneraceae): Preliminary study of its antioxidant activity. Biores Technol. 2006, 97 (12): 1387-1391. 10.1016/j.biortech.2005.07.009.

    CAS 
    Article 

    Google Scholar 

  • 22.

    Jana S, Deb JK: Molecular understanding of aminoglycoside action and resistance. Appl Microbiol Biotechnol. 2006, 70: 140-150. 10.1007/s00253-005-0279-0.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 23.

    Smith E, Williamson M, Wareham N, Kaatz G, Gibbons S: Antibacterial and modulators of bacterial resistance from the immature cones of Chamaecyparis lawsoniana. Phytochemistry. 2007, 68: 210-217. 10.1016/j.phytochem.2006.10.001.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 24.

    Freitas FI, Guedes-Stehling E, Siqueira Júnior JP: Resistance to gentamicin and related aminoglycosides in Staphylococcus aureus isolated in Brazil. Lett Appl Microbiol. 1999, 9 (3): 197-201. 10.1046/j.1365-2672.1999.00617.x.

    Article 

    Google Scholar 

  • 25.

    Brasileiro BG, Pizziolo VR, Raslan DS, Jamal CM, Silveira D: Antimicrobial and cytotoxic activities screening of some Brazilian medicinal plants used in Governador Valadares district. Rev Bras Cienc Farm. 2006, 42: 195-202. 10.1590/S1516-93322006000200004.

    Article 

    Google Scholar 

  • 26.

    Javadpour MM, Juban MM, Lo WC, Bishop SM, Alberty JB, Cowell SM: De novo antimicrobial peptides with low mammalian cell toxicity. J Med Chem. 1996, 39: 3107-3113. 10.1021/jm9509410.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 27.

    Coutinho HDM, Costa JGM, Falcão-Silva VS, Lima EO, Siqueira Júnior JP: Enhancement of the antibiotic activity against a multiresistant Escherichia coli by Mentha arvensis L. and chlorpromazine. Chemotherapy. 2008, 54: 328-330. 10.1159/000151267.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 28.

    Fryer FA: A chemical investigation of Damiana (Turnera diffusa). Specialites. 1965, 112: 21-25.

    Google Scholar 

  • 29.

    Perez RM, Ocegueda GA, Munoz JL, Ávila JG, Morrow WW: A study of the hypoglycemic effect of some Mexican plants. J Ethnopharmacol. 1984, 123: 253-262. 10.1016/0378-8741(84)90054-0.

    Article 

    Google Scholar 

  • 30.

    Cáceres A: Plantas de Uso Medicinal en Guatemala. 1996, Editorial Universitaria, San Carlos de Guatemala, 1

    Google Scholar 

  • 31.

    Kristiansen JE, Amaral L: The potential management of resistant infections with non-antibiotics. J Antimicrob Chemother. 1997, 40: 319-327. 10.1093/jac/40.3.319.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 32.

    Van Bambeke F, Glupczynski Y, Plesiat P, Pechère JC, Tulkens PM: Antibiotic efflux pumps in prokaryotic cells: occurrence, impact on resistance and strategies for the future of antimicrobial therapy. J Antimicrob Chemoth. 2003, 51: 1055-1065. 10.1093/jac/dkg224.

    CAS 
    Article 

    Google Scholar 

  • 33.

    Gunics G, Farkas S, Motohashi N, Shah A, Harsukh G, Kawase M, Molnár J: Interaction between 3,5-diacetyl-1,4-dihydropyridines and ampicillin, and erythromycin on different E. coli strains. Int J Antimicrob Agents. 2002, 20: 227-229. 10.1016/S0924-8579(02)00159-0.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 34.

    Hemaiswarya Sh, Kruthiventi AK, Doble M: Synergism between natural products and antibiotics against diseases. Phytomedicine. 2008, 15: 639-652. 10.1016/j.phymed.2008.06.008.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • 35.

    Wagner H, Ulrich-Merzenich G: Synergy research: approaching a new generation of phytopharmaceuticals. Phytomedicine. 2009, 16: 97-110. 10.1016/j.phymed.2008.12.018.

    CAS 
    Article 
    PubMed 

    Google Scholar 

  • Increasing the use of herbal treatment of staphylococcus aureus infections to prevent life-threatening illness

    By Rachel Ogis, Intermediate Student, 2011

    Staphylococcus aureus bacteria are Gram-positive facultative anaerobes that grow in grape-like clusters and contain a pigment called staphyloxanthin which causes the characteristic golden colour of their infections. They are highly virulent, partially due to the pigment that has an antioxidant action that helps the bacteria evade death.

    S. aureus occur on the skin and in the noses of healthy people without causing problems. However if the skin becomes punctured Staph bacteria can enter the wound causing a Staph infection.

    Staph infections can present in several different ways. Topical infections range from folliculitis and boils, impetigo, cellulitis, and Scalded Skin Syndrome to mere pimples. Internal infections include meningitis, endocarditis, osteomyelitis peuomonia, toxic shock syndrome (TSS), bacteraemia and sepsis. It is one of the five most common causes of nosocomial infections; along with methicillin-resistant Staphylococcus aureus MRSA, Pseudomonas aeruginosa, Acinetobacter baumannii, and Ventilator Associated Pneumonia (VAP).

    Folliculitis is an infection of the hair follicles where tiny white-headed pimples appear at the base of the hair shafts, sometimes with a red area around each pimple. The infection can flare up on an area where there has been some friction such as after shaving. Folliculitis can worsen into a boil where the Staph infection spreads deeper and wider under the subcutaneous layer of the skin. The head can break and pus, blood or an amber coloured liquid can drain out. Boils can be treaded with warm fomentaions but be sure to either discard or carefully wash the cloths used to prevent Staph from spreading.

    Impetigo can occur anywhere on the body. It is often seen in pre-schoolers and young kids especially during the summer months. Impetigo is most often seen arising in one spot where the skin was broken and it becomes an angry blister. The infection can progress to cover the whole area or other areas with small red dots that eventually form a small white head of pus. These little blisters will grow large in diameter unless treated. The blisters form a crust that is moist and yellow or amber coloured around the edges and bloodied on the top. If the crusts are removed they reform.

    Cellulitis is a Staph infection that is uncommon but more serious and occurs in the deeper layers of the skin. It starts with inflammation and redness around a cut or sore and 

    then slowly spreads into nearby tissues. Red lines may connect the infection to nearby lymph nodes, which can also become infected and swell up. This is known as lymphadenitis.

    Scaled Skin Syndrome most often affects newborns or pre-schoolers. The illness begins with a localized Staph infection but the Staph bacteria produce a toxin that causes a rash all over the body. It can be accompanied by a fever and the rash can blister. As the blisters burst, the top layer of skin peels off and the skin looks burned and red. Most children with this Syndrome are hospitalized because the infection affects the body the same way as a serious burn would, leaving them susceptible to secondary infections. Most children make a full recovery when treated properly.

    MRSA is a type of staphylococcus that is resistant to the beta-lactam antibiotics and cephalosporin’s. It can cause more serious problems such as bone infections or pneumonia. Certain kinds of antibiotics given to patients will have an increased chance of secondary infection with MRSA.

     

    These include glycopeptides, cephalosporin’s and quinolones especially flouroquinolones used to treat pneumonia.

    Pneumonia can be caused by viruses, bacteria, fungi and parasites. However in S. aureus or Streptococcus pneumoniae infections, the antibiotics used can lead to secondary infections from breathing tubes and MRSA colonized health care workers.

    Meningitis is usually caused by infection from viruses or micro-organisms. Trauma to the skull can allow Staphylococcus bacteria to enter and cause meningitis.

    Endocarditis is the inflammation of the inner layer of the heart or endocardium. A S.aureus infection of the endocardium and heart valves is hard to treat because natural defence mechanisms such as white blood cells or drugs cannot reach the tissue as the valves do not receive any dedicated blood supply. These are called acute endocarditis and have a poor prognosis for recovery.

    Toxic Shock Syndrome occurs when S. aureus releases a superantigen toxin. That allows the nonspecific binding of major histocompatibility complex (MHC) II with T cell receptors. Up to 20% of the bodies T cells can be activated at one time which can cause a cytokine storm and multisystem disease and multi organ failure.

    Bacteremia is the presence of bateria in the blood. This means that a localized infection can spread to other organs in the body through the bloodstream. This occurs in meningitis and endocarditis. Sepsis or blood poisoning is a whole-body inflammatory state combined with an infection. Septicemia with a pathogenic organism such as S. aureus can lead to sepsis and usually requires ICU treatment with intravenous fluids and antibiotics.

    Most Staph infections can be treated herbally, but they are very contagious and can be passed easily from family member to family member. The most important thing is to clean your hands carefully, not to share the bath and to wash all clothing and wash clothes carefully after use.

    Boils, Impetigo and Scaled Skin Syndrome are traditionally treated with a topical steroid ointment and oral antibiotics. However a decoction of alcohol-soaked Usnea taken orally for the duration of the infection can turn the infection around. Soak the Usnea overnight in any kind of alcohol and then decoct with water for 30 minutes. The kids don’t like the taste but you have to get it into them. The boils and impetigo can be halted with German Chamomile oil dabbed on and powdered goldenseal dusted over the scabs. Our infection took almost five weeks to clear up and the white scars or marks where the largest scabs were are still visible.

    This is a photo of Saraphina with her second infection. I didn’t take any photos of the first infection in September 2010. That infection lasted 3 weeks on her. This time around it lasted only 1 week.

    Around the world, different herbs have been used for treatment by indigenous peoples. In asia, Hochu-Ekki-To is a mixture that includes ginseng and is widely used for staph infections. In South America, Pau d’Arco has been used for thousands of years by healers.

     

    My great granny used a Oplopanax horridium decoction boiled for over 12 hours internally for boils. Another good antibiotic herb I used was a decoction of Echinacea angustifolia tincture mark used both internally and topically as a wash.

     

    This is what the bacteria look like under a microscope. They grow in clusters in contrast to the stings of spheres that Streptococcus grow in.

     

    MRSA is a life-threatening infection. In a study by Yamada et al., 2011 they quote a 39.9% mortality rate in the MRSA infected patients treated with an immunosuppressive drug. An antibiotic treatment can no longer be relied on to take care of these infections – a herbal ally can save your life in this case. In a study by Yang et al., 2010 they found that Illicium verum – a Chinese herb called Chinese star anise showed substantial antibacterial activity against Methicillin-resistant S.aureus. It can be further developed into antibiotic medicine due to their proven antibiotic activity. In an individual case in Japan, a man was given Hochuekkito when fighting a Streptococuss pneumoniae infection and recovered after 6 months of treatment where antibiotics had previously failed to improve his condition (Nakayama et al., 2011).

     

    MRSA are resistant to betal-lactam antibiotics and so they use a few other drugs now such as Vancomycin and some newer oxazolidonoes and daptomycin. They are administered intravenously. However these resistant strains are always adapting and there is now a Vancomycin intermediate-resistant S. aureus (VISA) strain. Psilocybe semilanceata has been shown to strongly inhibit the growth of S. aureus. Additionally, hospital staff are finding that by diffusing essential oils of lemongrass, holy basil, thyme and lavender into the hospital room, the rate of infection is drops.

    Natural Honey to Eradicate Nasal Methicillin resistant Staphylococcus aureus (MRSA) A Randomised Control Trial

    Methicillin-resistant Staphylococcus aureus (MRSA) is an endemic pathogen of public health concern in Ireland, as in many other health systems. For the nasal clearance of MRSA, the site that is often colonised in humans, the antibiotic mupirocin remains one of the most successful topical antibiotics to date. However, increasing bacterial resistance to mupirocin and limited effective alternate antibiotic options necessitate the need for unconventional approaches to eradicate nasal MRSA. Colonisation is a precursor for infection, and infections due to MRSA are associated with a greater risk of treatment failure, increased patient mortality and higher costs.

    Natural honey has been used by many traditional systems of medicine as a healing agent. In modern medicine, it is used as a wound healing agent. A recent Cochrane review reports that honey appears to heal partial thickness burns more quickly than conventional treatment, and infected post-operative wounds more quickly than antiseptics and gauze.

    Interest in an alternative agent for nasal decolonisation of MRSA led the researcher to the pilot study that employed medical grade honey (MGH). The results of the pilot study were encouraging which lead to the conduct of a clinical study ‘Natural Honey to Eradicate Nasal MRSA (NHNMRSA) a Randomised Control Trial (RCT)’. Patients were recruited from Beaumont Hospital to the single centre open label RCT, which investigated the comparative efficacy of nasal decolonisation of MRSA using MGH and mupirocin 2% nasal application.

    Patient characteristics, including age, gender, comorbidity, dependency of care, presence of invasive and indwelling devices, skin integrity, colonisation with multi-resistant drug resistant organisms, MRSA status on study enrolment, past decolonisation attempts and mupirocin use, as well as infection prevention and control practices during the study period were assessed, to determine the impact if any, on the outcome of intervention on nasal MRSA. The data were then analysed to establish the correlation, if any, between the outcomes of the and between the intervention and control groups. The relationship between nasal as well as non-nasal MRSA colonisation was assessed, in addition to other factors that are previously reported as factors associated with failed decolonisation.

    Five specific objectives formed the foundation of the RCT, the key findings of which are summarised. The first objective a literature review on mupirocin resistance (MR), presented a comprehensive picture on the prevalence of MR, which ranges from 1% – 81%, associated chlorhexidine resistance, which ranges from 0.6% – 91%, as well as multi drug resistance among MRSA isolates. The emergence of high-level MR amongst coagulase negative Staphylococci (CoNS) isolates indicates an expanding reservoir of plasmids encoding MR, which can be transferred to other CoNS strains as well as to S. aureus including MRSA. HLMR and resistance to other antibiotics amongst CoNS curtails the oral antibiotic options for prolonged treatment of prosthetic infections with CoNS. Resistance to mupirocin and chlorhexidine limits the options for patients who may benefit from MRSA suppression or decolonisation therapy. Alternative agents such as octenidine dihydrochloride, polyhexanide, ethanol (70%), sodium hypochlorite, lysostaphin, omiganon pentahydrochloride, natural honey, tea tree oil, silver and bacteriophages have been investigated with varying success for MRSA decolonisation. However, therapeutic trials of alternative agents that show some promise must be further evaluated in clinical trials before they can be recommended for use in clinical practice.

    In the RCT, robust comparability of the study participants in the intervention and control groups was confirmed on univariate analysis. The univariate analysis also confirmed that none of the patient variables analysed was of statistical significance on the patient outcome, i.e. eradication of nasal MRSA. On an intention to treat (ITT) analysis, 18 (36%) in the intervention group and 25 (50%) in the control group were decolonised of nasal MRSA. A c2 test was performed to assess the difference in the rate of decolonisation of MRSA between the intervention and control group. There was no statistically significant difference between the two groups (c2=1.999, p=0.157). On a per-protocol (PP) analysis,in the intervention group 18 (43%) participants and in the control group 25 (57%) participants were decolonised of nasal MRSA, however, a c2- test showed no significant difference (c2=1.675, p=0.196). Based on the ITT and PP analysis, as there was no statistical significance difference in the outcome of nasal MRSA decolonisation between the intervention and control groups, the null hypothesis was not rejected. On multivariate logistic regression, concomitant non-nasal MRSA colonisation was significantly associated, (c2=7.241, p=0.008) with persistent nasal MRSA. In addition, altered skin integrity and the application of more than two courses of mupirocin 2% nasal ointment prior to RCT enrolment were also associated with persistent nasal carriage of MRSA. However the less than anticipated number of patients enrolled in the study impacted on the power to detect significant differences between the intervention and control groups.

    The third objective was to determine and compare bacterial susceptibility to mupirocin and changes over time from first identification to completion of the RCT. Of the historic, baseline and final isolates, mupirocin susceptibility (MS) was 91%, 88% and 77% respectively. The prevalence of MR progressively increased from the time initially identified to the end of the study, 8% on first time identification, 12% at study enrolment, and 23% at the end of study. New acquisition of MR amongst RCT participants was 10% and of all the cases who newly acquired MR, 75% were HLMR. The acquisition of MR necessitates the monitoring of MS amongst MRSA isolates, risk assessment, the judicious use of mupirocin as well as the use of alternative agents for MRSA decolonisation.

    Laboratory investigations of MRSA isolates and assays to determine antimicrobial efficacy of MGH together formed the fourth study objective. The MRSA isolates were characterised using spa typing and compared where available, at three time points; historic, baseline and on study completion. Of the baseline and persistent MRSA isolates (143), 26 different spa types were identified. The common spa types were; t032, 59 (41%), t515, 19 (13%), t127, 17 (11.8%) and t4599, 10 (7%). Based on the spa types, a sequence-type (ST) could be inferred for 110 (77%) isolates. The common STs were ST22, 91 (63.6%), followed by ST1, 17 (11.8%), and one isolate each of the ST5 and ST8 type. In summary, the spa type of the carriage isolates did not appear to influence the outcome of the nasal decolonisation. Persistent colonisation with the same spa type was evident even over relatively long time-spans. However, replacement of the colonising spa type was also identified.

    The minimum inhibition concentration (MIC) and minimum bactericidal concentration (MBC) of MGH (test honey) was determined using laboratory assays. The MIC determined using the agar well diffusion method demonstrated antibacterial activity of test honey at 5% and higher concentrations for the clinical and reference MRSA isolates. Using the broth micro-dilution method to differentiate bactericidal or bacteriostatic action, it was established that the MIC and MBC of the test honey were both 12.5% to the MRSA isolates tested. The findings are in concordance with reports by other investigators who have reported MIC at concentrations of 4% and higher to antibacterial honey.

    The participant’s perception on MRSA carriage and their experience following the use of MGH and mupirocin 2% was evaluated which formed the basis of the fifth objective. An adapted brief illness perception questionnaire (BIPQ) that composed of nine elements was utilised to collate patient perceptions of MRSA. In summary the participants perceived MRSA colonisation as a chronic condition and that it did not have serious consequences on their daily lives. They were in general emotionally detached from the condition and few had MRSA related symptoms. Although most participants felt they had limited or no control over carriage, decolonisation was considered beneficial, indicating the importance attached to treatment/control of MRSA. The survey result shows a sub-optimal understanding of MRSA among 40% of patients that necessitates measures to target improving knowledge about MRSA. Such an intervention should enable patients to understand MRSA acquisition and transmission as well as adherence to treatment/decolonisation, potentially leading to better outcomes.

    A Likert scale type rating was used in the product experience questionnaire (PEQ) to collate participants’ experiences of MGH cream and mupirocin nasal application. In the investigative group, most patients (95%) concurred that Medihoney™ Derma Cream was easy to apply, not sticky (90%), did not lead to a runny nose (85%) and they did not experience an unpleasant sensation (95%). Based on the participants’ response it could be inferred that Medihoney™ Derma Cream may be applied to the human nasal passages with minimal undesirable effects. In the control group, most respondents (87%) concurred that mupirocin 2% nasal ointment was easy to apply, but it was sticky (20%), and a runny nose was experienced by 33% of respondents. Almost all (95%) respondents agreed that they did not experience any unpleasant sensation following its application. Overall the patients’ preferred choice was a natural alternative to an antibiotic, if available, for MRSA decolonisation.

    The NHNMRSA RCT, I believe, is the first study that has used MGH for nasal MRSA decolonisation. The RCT results o

    Culture for Staphylococcus aureus (S. aureus) and determination of sensitivity to an extended spectrum of antimicrobial drugs (Staphylococcus aureus Culture. Bacteria Identification. Antibiotic Susceptibility, enlarged testing)

    Interpretation of results

    Interpretation of test results contains information for the attending physician and is not a diagnosis. The information in this section cannot be used for self-diagnosis and self-medication. An accurate diagnosis is made by a doctor, using both the results of this examination and the necessary information from other sources: anamnesis, results of other examinations, etc.d.

    Units of measurement: in the study of breast milk – massive / non-massive growth.

    For other types of biomaterial – CFU / swab.

    Form of issuance of results

    When Staphylococcus aureus is found, indicate its species name (Staphylococcus aureus) and the degree of contamination (semi-quantitative assessment). When this microorganism is detected, antibiotic sensitivity is determined regardless of the titer.The list of AMPs can be found
    here.

    Attention! It is not possible to order the determination of sensitivity to the extended spectrum of AMP and to determine the sensitivity to bacteriophages. To do this, you need to order tests no.
    459-P and No.
    459-F, respectively.

    In the absence of growth of Staphylococcus aureus, the result is “no growth of S. aureus”.

    Attention! Staphylococci of other species, when detected as a result, are not indicated.

    Interpretation of the results of the study “Culture for Staphylococcus aureus (S. aureus) and determination of sensitivity to an extended spectrum of antimicrobial drugs”

    Normal growth of Staphylococcus aureus is absent.

    Approximately 25-40% of the population are permanent carriers of this bacterium, which can persist on the skin and mucous membranes of the upper respiratory tract without causing clinical manifestations of infection. However, they can be sources of infection for others.

    Etiologically significant S. aureus is considered if it is isolated from breast milk, wound discharge, abscess contents, etc.

    Infections and heart

    Tyabut Tamara Dmitrievna, Professor of the Department of Cardiology and Rheumatology, Bel MAPO, Doctor of Medical Sciences

    Year of health. Read and pass on to another

    Among the various pathologies of the heart, diseases that arise as a result of the negative effects of infectious agents on the heart occupy a considerable share.
    Infectious agents are a huge number of microorganisms found in the world around humans. These include bacteria, spirochetes, rickettsia, protozoa, pathogenic fungi, viruses. If in the last century bacteria were the main culprits of heart damage, then in recent years the importance of viral infections has increased.
    Infectious agents can have a direct damaging effect on the heart muscle – the myocardium, or cause certain negative changes in the immune system, which leads to disruption of its functions.
    The immune system is a set of cells, organs and tissues that carry out immune reactions, the main meaning of which is to protect the human body from the negative effects of environmental factors. Protection is carried out by recognizing foreign cells or substances that have entered the human body, neutralizing them or removing them from the body.
    The functions of the immune system are regulated by the nervous and endocrine systems. The variety of powerful stressful influences that accompany the life of a modern person leads to a dysfunction of the immune system, and, therefore, weakens its defense against the effects of infectious agents.Therefore, quite often, infectious lesions of the heart occur against the background of excessive stress, mental trauma, negative events in a person’s life (conflict at work or in the family, illness of loved ones, loss of work, divorce, death of a loved one, etc.).
    Protection of the body from infections – bacterial, viral, fungal or parasitic – is carried out by two systems of immunity: congenital, determined by genetic factors transmitted from parents, and acquired, which is formed during a person’s life.
    Allocate natural and artificial immunity. Natural immunity is formed as a result of the transmission from mother to fetus through the placenta or with milk of ready-made protective factors, as well as as a result of contact with the pathogen (after an illness or after latent contact without the appearance of symptoms of the disease). Prevention of infectious lesions begins with the conception of a child and continues after his birth – a healthy mother and breastfeeding are the best methods of prevention at this stage of a person’s life.
    After the birth of a child, artificial immunity is also included in the protection, which is formed during preventive vaccinations. Compliance with the vaccination calendar is the basis of prevention in the subsequent stages of a person’s life. Currently, vaccinations are carried out against the most common and severe infections, but there are a huge number of other microorganisms that have a damaging effect on the human body in general and the heart in particular.
    Winter has come, and with its arrival the number of colds is increasing.The most common colds include acute tonsillitis (tonsillitis), exacerbations of chronic tonsillitis, pharyngitis.
    Tonsillitis is an inflammation of the pharyngeal tonsils, which are secondary organs of the immune system. The cause of both acute and chronic tonsillitis is pathogenic microorganisms ( bacteria, viruses and fungi ), which, penetrating into the tissue of the tonsils, cause an inflammatory process and can have a general negative effect on the body in the form of intoxication.
    Acute and chronic processes in the tonsils proceed differently. The manifestations of sore throat are severe sore throat when swallowing, enlargement of the submandibular and cervical lymph nodes, fever up to 39-40 degrees, headaches and muscle pains, general weakness associated with intoxication. These symptoms require mandatory, early medical attention. Chronic tonsillitis and its exacerbations can be manifested by a slight increase in temperature, especially in the evening, sore throat or slight sore throat, combined with increased fatigue, morning weakness, restless sleep, impaired appetite, which ultimately reduces a person’s ability to work.This condition is called tonsillogenic intoxication. Very often the patient, having visited many specialists, leaves them without answering the question: “Why does he have a fever?” And the whole point is only in chronic inflammation of the tonsils, in the treatment of which these symptoms disappear. Many people suffer exacerbations of tonsillitis “on their feet”, do not attach importance to its symptoms. And in the future they pay for this by the development of complications. There are several reasons for the occurrence of tonsillitis – structural features of the tonsils, impaired immunity, adverse environmental factors – hypothermia, viral colds.Among the factors causing exacerbation of tonsillitis, there are social – poor-quality nutrition, unfavorable environmental conditions, maximum employment at the workplace, stress, working conditions, everyday life, smoking, and medical – diseases ENT organs pathology of the paranasal sinuses, individual features of the structure of the ENT organs (curvature of the nasal septum, enlargement of the turbinates, diseases of the nasopharynx (adenoids, polyps), frequent respiratory diseases, as well as dental caries.Chronic inflammation in the tonsils can be promoted by immunodeficiency states, other diseases of internal organs, and concomitant endocrine pathology.
    In chronic tonsillitis, up to several dozen (usually about 30) types of microorganisms – fungi and bacteria can be found in the tonsils, but the main cause of the disease is streptococcus.

    Tonsillitis caused by beta-hemolytic streptococcus.

    In the presence of chronic tonsillitis, a large amount of pus accumulates in the lacunae, consisting of dead microbes, white blood cells – leukocytes, and other cells (purulent-caseous plugs). Pathogenic microbes multiply in the purulent contents of the lacunae. The waste products of microbes from the tonsils enter the bloodstream and lead to the development of tonsillogenic intoxication, manifested by fatigue, pain in muscles and joints, headaches, decreased mood, low-grade fever.The tonsils become a repository of infectious agents, from where they can spread throughout the body and cause inflammation. Frequent illnesses further weaken the immune system, which leads to the further development of tonsillitis. This is how a vicious circle of disease is formed.
    Chronic tonsillitis is dangerous complications associated with the spread of infection throughout the body. These include paratonsillar abscesses, · damage to the heart (tonsilogenic myocardial dystrophy, acute rheumatic fever), blood vessels, kidneys.
    Tonsillogenic myocardial dystrophy refers to often developing, but much less often diagnosed lesions of the heart muscle in chronic tonsillitis. It is caused by toxins from bacteria in the tonsils and products of local inflammation and tissue breakdown.
    Clinical signs tonsillogenic myocardial dystrophy are caused by impaired activity of the autonomic nervous system (autonomic dysfunction) and impaired metabolism in the heart muscle (electrolyte, protein), which results in impaired energy production in the heart muscle.In the early stages of development, tonsilogenic myocardial dystrophy is manifested by a high heart rate – tachycardia, interruptions in the work of the heart – extrasystole, shortness of breath with intense physical exertion, and a violation of the general well-being of patients. With late diagnosis, signs of heart failure appear, the volume of load causing shortness of breath decreases, and more severe rhythm and conduction disturbances appear. With timely diagnosis and treatment of an extracardiac factor – chronic tonsillitis, which caused the listed changes in the heart muscle, they are reversible and gradually the structure and functions of the heart muscle
    are restored.
    The greatest danger for the prognosis and quality of life of patients is represented by heart damage in acute rheumatic fever.
    Acute rheumatic fever (ARF) – post-infectious complication of tonsillitis (sore throat) or pharyngitis caused by group A beta-hemolytic streptococcus, in the form of a systemic inflammatory disease of the connective tissue with the predominant localization of the pathological process in the cardiovascular system (carditis), joints ( migratory polyarthritis), the brain (chorea) and skin (erythema annulus, rheumatic nodules), which develops in predisposed individuals, mainly young people (7-15 years old).In the Russian Federation and the Republic of Belarus, the incidence of rheumatic fever ranges from 0.2 to 0.6 cases per 1000 child population. The primary incidence of ARF in Russia at the beginning of the 21st century was 0.027 cases per 1000 population. The frequency of newly diagnosed chronic rheumatic heart disease (CRHD), which includes heart defects and specific changes in valves (marginal fibrosis), detected by ultrasound examination of the heart – 0.097 cases per 1000 population, including rheumatic heart disease – 0.076 cases per 1000 adult population.The available statistical differences between the incidence of primary morbidity of acute rheumatic fever and chronic rheumatic heart disease indicate the presence of a large number of undiagnosed acute forms of the disease.
    The time interval between the transferred acute streptococcal tonsillitis, pharyngitis, exacerbation of chronic tonsillitis and the onset of manifestations of acute rheumatic fever is 3-4 weeks. In acute rheumatic fever, all structures of the heart – endocardium, myocardium, pericardium, can be affected.Damage to the myocardium (heart muscle) is always found. Manifestations of heart damage can be palpitations, shortness of breath associated with physical activity or at rest, pain in the heart region of an aching nature, which, unlike angina pectoris, do not have a clear connection with physical activity and can persist for a long period of time, palpitations, interruptions in the work of the heart, paroxysmal rhythm disturbances – atrial fibrillation, atrial flutter. Usually, heart damage is combined with an articular syndrome of the type of arthralgia – pain in large joints (knee, shoulder, ankle, elbow) or arthritis (inflammation) of the same joints.Joint inflammation is characterized by pain, changes in the shape of the joint caused by edema, reddening of the skin in the area of ​​the affected joint, a local increase in temperature and dysfunction of the joint in the form of restriction of range of motion. Small joints are much less likely to be affected. The inflammatory process in the joints is of a migratory nature and quickly passes against the background of proper treatment. Damage to the heart and joints is usually accompanied by an increase in body temperature, weakness, sweating, and disability.In some patients, there are lesions of the nervous system, skin rashes of the type of erythema annulus and subcutaneous rheumatic nodules.
    For the diagnosis of acute rheumatic fever, there are diagnostic criteria that include clinical, laboratory and instrumental data, as well as information about the previous infection caused by group A beta-hemolytic streptococcus, its rheumatogenic strains. A timely diagnosis allows the patient to recover during therapy with antibiotics, glucocorticoid hormones, and non-steroidal anti-inflammatory drugs.However, with late treatment, non-compliance by patients with motor regimen, presence of genetic predisposition, non-sanitized focal infection (decompensated tonsillitis, caries), the outcome of acute rheumatic fever may be chronic rheumatic heart disease with or without heart disease. Heart disease occurs as an outcome of inflammatory lesions of the heart valves. The presence of a heart defect of rheumatic etiology requires the patient to be classified as a high-risk group for developing infective endocarditis, the most severe form of heart disease associated with infectious agents.
    Acute rheumatic fever refers to diseases in which prevention is essential to reduce both primary morbidity and recurrent episodes of illness (recurrent acute rheumatic fever).
    Primary prevention is aimed at reducing primary morbidity and includes a complex of medical and sanitary and hygienic measures, as well as adequate treatment of infections caused by beta-hemolytic streptococcus group A. , first of all – chronic tonsillitis and caries.The tonsils are thoroughly sanitized by repeated rinsing and rinsing with solutions of antibacterial agents, vacuum aspiration of the pathological contents of the lacunae. If this does not give the desired result, the issue of surgical treatment is discussed – removal of the tonsils. In each case, the choice of treatment tactics is determined by the otolaryngologist and therapist, cardiologist or rheumatologist.
    Adequate treatment of tonsillitis and pharyngitis is aimed at suppressing the growth and reproduction of streptococcus in the body with the development of streptococcal pharyngitis, tonsillitis, tonsillitis.The basis of treatment is antibiotic therapy in combination with anti-inflammatory drugs, which should be carried out for at least 10 days with mandatory control of a general blood test, urine, and according to the indications of a biochemical blood test, when signs of illness appear, at the end of treatment and a month after the first signs of illness appear. A laboratory study carried out within these terms allows you to correctly diagnose, determine the effectiveness of treatment, and, most importantly, not to miss the onset of the development of complications in the form of acute rheumatic fever.
    Secondary prevention is aimed at preventing the development of recurrent acute rheumatic fever and disease progression in persons with ARF. It is performed in patients who are not allergic to penicillin drugs. The drug used for prophylaxis in adults is benzathine benzylpenicillin (extencillin, retarpen) at a dose of 2,400,000 IU 1 time in 3 weeks intramuscularly. Prophylactic regimens depend on the age of the patient and the outcome of acute rheumatic fever.In accordance with the recommendations of the Association of Rheumatologists of Russia, secondary prevention includes the following regimens:

    • For patients with ARF without carditis (arthritis, chorea) – at least 5 years after the attack or up to 18 years (according to the principle “which is longer”).
    • For patients with healed carditis without heart defect – at least 10 years after the attack or up to 25 years (according to the principle “which is longer”).
    • For patients with a formed heart defect (including operated ones) – for life.

    The most severe and prognostically unfavorable heart disease associated with infection is infective endocarditis – a disease characterized by the development of an inflammatory process on the valve or parietal endocardium, including damage to large intrathoracic vessels extending from the heart, resulting from exposure to microbial infection. Most often these are various bacteria – streptococci, staphylococci, enterococci, Escherichia coli, Pseudomonas aeruginosa and many others.Described 119 different pathogens leading to the development of the disease.

    Aortic valve

    Mitral valve

    This is how the heart valves look during the development of infective endocarditis.
    Overlays of microbes, blood cells disrupt their function,
    destroy the valve and often require urgent surgical treatment.

    The prevalence of infective endocarditis at the beginning of the 21st century was 2-4 cases per 100,000 population per year.There is a widespread increase in the incidence rate, most pronounced in the older age groups and amounting to 14.5 cases per 100,000 of the population aged 70-80 years. Diagnosis of the disease is difficult. At the first visit to the doctor, the diagnosis is made only in 19 – 34.2% of patients. The average period from initial treatment to diagnosis is at least 1.5 – 2 months.

    A group of patients with a high risk of developing infective endocarditis is distinguished, which includes:

    • patients with previous infectious endocarditis,
    • patients with prosthetic heart valves,
    • patients with congenital blue defects,
    • patients after surgical operations on the aorta, pulmonary vessels
    • patients with acquired heart defects, primarily of rheumatic etiology (CRHD).

    In addition, a group of moderate (intermediate) risk was identified, which unites patients with the following diseases:

    • Mitral valve prolapse due to myxomatous degeneration or other causes with grade 2-3 regurgitation or multiple valve prolapse
    • Non-cyanotic congenital heart defects (excluding secondary ASD)
    • Bicuspid (bicuspid) aortic valve
    • Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis).

    It has been established that the pathogen must enter the bloodstream for the development of infective endocarditis. The most common cause of this can be dental manipulation, which is accompanied by damage to the gums and bleeding. In the presence of tooth decay or gum disease, bacteremia (the presence of the pathogen in the blood) can occur quite often.

    Type of manipulation

    Frequency of bacteremia

    Extraction of teeth

    61-85%,

    Preventive dental treatment

    0-28%,

    Teeth cleaning

    0-26%,

    Depending on the initial state of the heart and endocardium, the disease can occur in two variants.Primary IE (30% of cases) occurs on the unaffected endocardium under the influence of severe infections (staphylococci, gram-negative microorganisms, fungi).
    Secondary IE (70% of cases) develops on valves or endocardium altered due to congenital or acquired heart defects.
    Diagnosis of infective endocarditis is difficult due to the fact that in the early stages there are no specific signs of the disease. Non-specific include fever, general malaise, weight loss, and decreased ability to work.Signs of heart damage are formed at 3-4 weeks of illness. Prior to this, the disease can be disguised as kidney disease, lung disease, strokes, thromboembolism in various internal organs, aggravation of chronic heart failure.
    Prevention of infective endrcarditis may reduce morbidity. According to researchers from France, 60 to 120 cases of infective endocarditis are prevented per 1500 patients who received antibiotic prophylaxis. The economic costs of preventing infective endocarditis are much less than their treatment

    For manipulations that can cause bacteremia and in which antibiotic prophylaxis should be carried out:

    • Bronchoscopy.
    • Cystoscopy during urinary tract infection.
    • Biopsy of urinary organs or prostate gland.
    • Dental procedures with risk of injury to the gums or mucous membranes.
    • Tonsilectomy, adenoidectomy.
    • Dilation of the esophagus or sclerotherapy of varicose veins of the esophagus.
    • Interventions for obstruction of the biliary tract.
    • Transurethral resection of the prostate.
    • Instrumental dilatation of the urethra.
    • Lithotripsy (stone crushing).
    • Gynecological interventions in the presence of infection.

    Not only doctors and patients themselves should be active participants in the organization and implementation of the prevention of infective endocarditis. Not a single most literate and knowledgeable doctor can implement a prevention program without the desire and understanding of the importance of prevention on the part of the patient himself.

    “If someone is looking for health, ask him first,
    is he ready to part with all the causes of his illness in the future, –
    only then can you help him.” Socrates


    This is the meaning of both non-drug prevention, which is based on the correction of many behavioral risk factors, and drug prevention.
    Knowing when to do prevention, you need to know and how to do it. The choice of prevention method is based on 3 principles. The first principle is to determine which group you belong to – high or intermediate risk. The second principle – to assess the tolerance of antibacterial drugs – have ever been recorded any allergic reactions to drugs of the penicillin series (penicillin, bicillin, ampicillin, amoxicillin, oxacillin, and others).Principle three – before which procedure is the prophylactic administration of an antibacterial drug carried out.

    When carrying out dental procedures or diagnostic and therapeutic procedures on the airways, esophagus, the following preventive regimens are recommended:

    For patients of all groups without allergy to penicillin drugs:

    • Amoxicillin 2.0 grams by mouth by mouth 1 hour before the procedure.
    • In case of problems with oral administration, ampicillin or amoxicillin 2 grams intravenously 30-60 minutes before the procedure.

    For patients allergic to penicillin drugs:

    • Clindamycin 600 mg or

    • Azithromycin 500 mg or

    • Clarithromycin 500 mg orally 1 hour before the procedure

    When performing manipulations on the organs of the urinary and genital and gastrointestinal tract, the following preventive regimens are used:

    • For persons who are not allergic to penicillin drugs: High-risk group – ampicillin or amoxicillin at a dose of 2 g intravenously and gentamicin at the rate of 1.5 mg / kg body weight intravenously 30-60 minutes before the procedure.After 6 hours, ampicillin or amoxicillin is taken orally at a dose of 1 gram.

    Intermediate risk group – Ampicillin (amoxicillin) 2.0 g intravenously 30-60 minutes before the procedure or amoxicillin 2.0 g by mouth 1 hour before the procedure

    High risk group – vancomycin 1.0 grams intravenously 1 hour before the procedure in combination with intravenous or intramuscular gentamicin at the rate of 1.5 mg / kg body weight.

    Intermediate risk group – vancomycin 1.0 gram IV 1 hour before the procedure

    The presented prophylactic programs for patients with acute rheumatic fever and infective endocarditis are not a prescription for purchase and a direction for administration of the drug. All preventive regimens should be discussed with the attending physician – therapist, cardiologist, rheumatologist. But without the knowledge of the patient himself, his awareness of the essence and significance of primary and secondary prevention of any disease, including infectious heart disease, to maintain a high quality of his life, it is impossible to carry out preventive measures.But it is precisely the prevention of both the disease itself and its complications that plays the most significant role. Any disease is easier to prevent than to cure.
    The importance of doctor-patient interaction was recognized by ancient healers. Hippocrates wrote: “Life is short, the path of art is long, opportunity is fleeting, experience is unreliable, judgment is difficult. Therefore, not only the doctor himself must be ready to do everything that is required of him, but also the patient, and those around him, and all external circumstances must contribute to the doctor in his activities.
    And the Chinese healer Lao-Jun writes about prevention:
    “If you want to save yourself from a catastrophe or solve a problem, then it is best to prevent their occurrence in your life in advance. And then there will be no difficulties.
    In order to cure a disease, get rid of a disease, it is best to be ready for them ahead of time. Then there will be a happy outcome. Currently, people do not pay attention to this and do not try to prevent, but direct their efforts to save themselves. They do not try to prepare ahead of time, but try to heal with drugs.Therefore, there are sovereigns who are not able to protect the sacrificial altar of state power. There are also such organisms that are not able to keep themselves intact for a long life.
    Thus, a man of wisdom achieves happiness when there are no omens yet. He gets rid of trouble when it has not yet appeared. After all, a catastrophe is born from small things, and disease arises from the subtlest deviations. People believe that little good is not useful, and therefore they do not want to do good.It seems to them that there will be no harm from a little evil, and therefore they do not strive to correct themselves. If you do not accumulate goodness little by little, then great Potency will not work. If you do not abstain from evil in small things, then a big crime will be committed. Therefore, we will choose the most important to show how it is born. “

    It is not easy to be a bacterium, or why antibiotics stop working

    Not every person in the modern world cares about their health, relying on pills, the development of medicine, youth or at random.However, even the most advanced medicine may not help if the disease is evolving at a tremendous rate. This happens with diseases caused by pathogenic bacteria, on which antibiotics cease to work. Because of the thoughtless use of such drugs, infectious diseases are becoming increasingly difficult to treat. How antibiotics work, why it is important to use them with caution, and why bacteria are increasingly becoming resistant to them – in our material.

    The story of a persistent bacterium

    Everyone knows how the British bacteriologist Alexander Fleming discovered penicillin in 1928 and how this antibiotic saved millions of people from infections during the Second World War.In 1938, penicillin was isolated in its pure form, but already in 1947, four years after the start of mass sales of the drug, the bacterium Staphylococcus aureus acquired resistance to it. The antibiotic was replaced by another, methicillin, but in 1961 Staphylococcus aureus mutated in relation to it. The bacterial strain was responsible for 37% of deaths from sepsis (general contamination of the body by microbes that enter the bloodstream) in the UK in 1999, up from 4% in 1991.

    Today, half of all Staphylococcus aureus infections in the United States are resistant to penicillin, methicillin, tetracycline and erythromycin. Therefore, vancomycin has become the only effective drug. However, strains of bacteria resistant to it began to appear already in the 90s. The first official case of vancomycin-resistant infection was documented in the United States in 2002. In 2011, a variant of vancomycin was introduced that can still kill Staphylococcus aureus.

    This is just one example of how bacteria have resisted drugs as a result of decades of evolution.Due to the fact that new and new strains of drug-resistant bacteria are constantly emerging, there is a huge variety of antibiotics in the world, a list of which can be found on Wikipedia.

    How do antibiotics work? They have “targets” to which their action is directed. For example, some antibiotics destroy the cell membrane, interfere with the synthesis of protein, RNA or DNA inside it. But bacteria divide very quickly, and as a result of mutations, the structure of any “target” of the antibiotic changes, so the drug ceases to work “, – explained a researcher at the Institute of Experimental Medicine Ekaterina Umnyakova during the extreme open lecture hall” Kurilka Gutenberg ”held at ITMO University.

    Source: depositphotos.com

    Why this happens: evolution of bacteria

    The ability of bacteria to acquire resistance to antibiotics is a stunning example of evolution in allowing bacteria to survive in an aggressive external environment. Resistance is acquired through random mutations, natural selection, and horizontal gene exchange.

    The latter largely contributes to the rapid spread of bacteria, as it allows them to exchange genes with each other.In this case, the transfer is also possible between cells (all bacteria are unicellular) of two different types. Cells transmit genes through a special “genetic bridge”. It is believed that in the early stages of life development, this process played a critical role. You can watch the transfer animation here.

    Scientists at Harvard Medical School have filmed the very process of the evolution of bacteria and their resistance to antibiotics. To do this, they built a huge Petri dish and divided the space in it into nine equal parts with special partitions with holes.They poured a special nutrient solution for the growth of the bacterium Escherichia coli into the cup and launched the bacteria into the side pens. Moreover, each subsequent compartment of the cup in the direction from the edges to the central section contained a dose of antibiotics ten times greater than in the previous one. The video shows how Escherichia coli , using random mutations and horizontal gene exchange, breaks down all barriers and reaches the section with a thousand-fold dose of the antibiotic in almost two weeks.

    This visual experiment clearly shows that only a small number of bacteria develop mutations. However, these organisms then reproduce rapidly and pass on their genes to the next generation. At the same time, less resistant bacteria become the “initiators” of further development and acquisition of resistance to antibiotics. In addition, mutations slow down reproduction. Thus, at some point, organisms simply do not have time to mutate and immediately multiply in a new aggressive environment before it destroys them.It is then that the “passage” of the bacteria through the barriers of antibiotics ends.

    A recent study by scientists from the University of Gothenburg showed that it is possible that genes for antibiotic-resistant bacteria can be transmitted even through polluted air in large cities. True, until bacteriologists understood whether these genes were “alive” or whether it was useless organic garbage in the air.

    So far, we have examined only a small number of air samples. In order to draw more accurate conclusions, we must continue to work.However, in the samples we examined, we found genes that are responsible for the resistance of bacteria to the drug, which is used as a last resort in the treatment of very serious and dangerous infections ” university.

    Why this happens: People use too many antibiotics

    Are people to blame for the fact that bacteria naturally evolve faster and harder to kill? And how! Anthropogenic causes are listed in the journal Pharmacy and Therapeutics.Basically, they all boil down to the fact that mankind uses too many antibiotics – this leads to an increase in their concentration in food, water, air, soil. As a result, bacteria quickly and easily adapt to antibiotics even outside the human body.

    Source: livejournal.com

    Approximately 30% to 50% of doctors prescribing antibiotics to patients are wrong, studies show. That is, patients are treated with the wrong drugs that can eliminate the pathogenic bacteria.Sometimes antibiotic treatment is not required at all, but patients continue to take it. In addition, in pharmacies, the sale of some antibiotics is not limited in any way, and a person who is not well versed in medicine tends to be treated with these drugs even for a mild cold or indigestion.

    Various antibacterial hygiene products are very popular today. Excessive use of them is not only unhealthy, but can also significantly harm the body. Not only do these remedies kill the beneficial bacteria on our skin, which protect against the same infections, but they also destroy the natural human immune system, because it no longer needs to fight bacteria on its own.Thus, a person becomes more defenseless against serious infectious diseases.

    In agriculture, antibiotics are used to accelerate the growth of animals and gain weight. In the United States, about 80% of antibiotics sold are used on farms. In addition, some of these drugs are sprayed on plants as pesticides. This leads to the fact that antibiotics get into the soil and groundwater. As a result, harm is done to the ecology as a whole.

    Ekaterina Umnyakova

    Is it really that dangerous? But what about modern medicine?

    About once every six months, there are reports in the media that another unkillable bacterium has been found somewhere.What do we do? Modern medicine offers several ways. You can create analogs based on existing antibiotics, that is, modify them for genetic changes in bacteria, or you can develop new drugs based on natural chemical compounds , ”comments Ekaterina Umnyakova.

    Antimicrobial peptides – protein structures inside various organisms, including the human one – are among such natural compounds, which Catherine studies.Peptides act in much the same way as antibiotics: they hit one of the “targets” in the bacteria, in particular, its membrane, as a result of which the cell “flows out” and dies. Bacteriophages are also widely studied around the world. These are viruses that selectively infect bacterial cells, most often multiplying inside them and, in some sense, dissolving them. More than 200 new bacteriophages can emerge from the resources of one cell. In some countries, the use of bacteriophages in medicine is prohibited, because it is not yet fully understood how these organisms can affect the work of bacteria and other cells beneficial to humans.

    Today, scientists use all available tools to model and synthesize new drugs for bacterial diseases. For example, scientists at the University of Oklahoma have used computer analysis of variations in antibiotic-bacterial interactions to speed up clinical trials. However, the natural evolution of bacteria, accelerated by the use of excessive amounts of antibiotics by humans, never stops and is difficult to keep up with.

    Who knows about Plague Inc? This is an application in which the player becomes a bacterium and he needs to infect and kill all of humanity.He receives different bonuses for each infected country, for which mutations useful for survival can be purchased. So that’s it. It seems that we are no longer playing games with bacteria, but they are playing with us , ”said Ekaterina Umnyakova at the Gutenberg Smoking Room.

    Plague Inc. Source: androidpluspc.com

    What to do?

    In October 2016, the World Health Organization published a list of guidelines that need to be followed by humankind to reduce the risks of drug resistance in bacteria.The authors emphasized that this is one of the most important problems of modern healthcare systems around the world, since dangerous infectious diseases such as pneumonia, tuberculosis and others are becoming much more difficult to treat. In addition, because of this, the duration of hospitalization of patients is increased, which leads, among other things, to economic losses. Therefore, humanity needs to change the way antibiotics are used, as well as to develop preventive measures against infectious diseases.

    Thus, a person should only take antibiotics as directed by a doctor.The workers of medical organizations themselves should inform patients as fully and accurately as possible about why they should not take these drugs thoughtlessly, and also prescribe them only in case of obvious need.

    Agricultural producers should abandon the use of antibiotics as a growth stimulant for animals and plants and use them only to treat the former. Authorities should legislate and promote such activities.

    In the second part, these recommendations may seem naive. Will the owner of the farm give up the benefits for the sake of the environment? Hardly, if it isn’t financially rewarded. However, each of us can make a difference and at least not harm ourselves by taking antibiotics with the regularity of coffee consumption. But for this you will have to start monitoring your health: sleep at least six hours a day, eat well and properly, play sports and warm up in the office. Can we?

    Skip to content

    v3_2011.p65

    % PDF-1.5
    %
    2 0 obj
    >
    endobj
    5 0 obj
    >
    stream

  • v3_2011.p65
  • Administrator
  • PageMaker 6.52012-01-31T11: 35: 52 + 03: 002012-03-22T12: 46: 04 + 03: 00Acrobat Distiller 6.0 (Windows)

    endstream
    endobj
    20 0 obj
    >
    stream
    HW [GfF ݽ mwf $ ZY3 [J] ‘qA! Zl? X
    6 + ~
    ?! – py RbƋyvV: sӧnqr2.XU \ 8u6eJTi. ׈ / 2 L) NxZ

    Feline bacteria treat antibiotic-resistant infections

    A research team led by Dr. Richard L. Gallo of the University of California, San Diego School of Medicine specializes in the use of bacteria and their derivatives to treat disease – a technique known as “bacteriotherapy”.

    As a reminder, our skin is inhabited by hundreds of types of bacteria that play an important role in skin health, immunity and the fight against infections.All animal species need to maintain a balance and diversity of healthy skin bacteria to combat potential pathogens.

    “Our health depends entirely on these ‘good’ bacteria,” explains Gallo. “They need our healthy skin to live, and in return, some of them protect us from the ‘bad’ bacteria. take advantage of our weakened defenses and cause infection. ”

    This is how methicillin-resistant staphylococcus Staphylococcus pseudintermedius (MRSP), which lives on the skin of domestic animals, becomes infectious when the animals are sick or injured.MRSP is a new pathogen that can spread from one species to another and cause severe atopic dermatitis or eczema.

    These infections are common in dogs and cats and can also occur in humans. As the name suggests, MRSP is resistant to common antibiotics and is difficult to cure in a clinical and veterinary setting.

    To solve this problem, the researchers studied a number of bacteria commonly found on dogs and cats. Scientists have grown these strains in the presence of MRSP.

    So they identified a strain of feline bacteria called Staphylococcus felis that was particularly good at inhibiting MRSP growth. They found that this particular S. felis strain naturally produces a variety of antibiotics that kill MRSP by destroying its cell wall.

    However, bacteria readily develop resistance to the antibiotics they encounter. To circumvent this obstacle, the four genes of S. felis encode four different antimicrobial peptides.Each of these antibiotics are capable of killing MRSP on their own, but working together they reduce the chances of these bacteria to survive to a minimum.

    Next, the scientists decided to find out if S. felis is suitable for treating a live animal.

    The most common form of the pathogen was applied to the skin of laboratory mice, resulting in redness and flaking. The researchers then treated the inflamed skin with S. felis bacteria or an extract of these bacteria.

    Peeling and redness of the skin of mice decreased after treatment with both drugs. This did not happen with animals that did not receive treatment. In addition, after treatment with S. felis , fewer viable MRSP bacteria remained on the skin of the mice.

    In the future, the researchers plan to initiate clinical trials to confirm whether S. felis can be used to treat MRSP infection in dogs.

    Bacteriotherapy such as this can be performed with topical sprays, creams or gels containing either live bacteria or purified antimicrobial peptide extract.

    Also, the authors of the work urge cat owners not to stop washing their pets, “so as not to inadvertently wash away the beneficial bacteria.” The skin has evolved to protect the “good” bacteria, so soap and detergents usually don’t wash them off.

    It is even possible that living with a healthy cat provides humans with some protection from MRSP. Another argument in favor of getting a mustachioed friend – however, it is important to monitor his health.

    The work of American researchers was published in eLife.

    Earlier we wrote that scientists have found out exactly how Staphylococcus aureus colonizes the skin of a healthy person, causing him atopic dermatitis. We have also reported on an antibiotic-resistant strain of Salmonella found in a domestic cat in Australia.

    We also talked about the fact that an antibiotic effective against a dangerous strain of staphylococcus was found … right in a person’s nose.

    More news from the world of science can be found in the “Science” section of the “Watch” media platform.

    Staphylococcal infection

    STAPHYLOCOCCAL INFECTION. Currently, as a result of the widespread use of antibiotics, and sometimes their abuse, the problem of dysbiosis, the most important pathogenetic factor in the activation of staphylococcus, salmonella, E. coli and other opportunistic flora, has arisen.
    Staphylococcal diseases mainly affect young children or children weakened by other diseases.This feature is associated with the properties of the pathogen as a conditionally pathogenic microbe and forces us to focus on the reactivity of children. The main reason for the occurrence of staphylococcal infection is the violation of the mechanisms of natural resistance and the pathology of local immunity, since specific and local immunological reactions of the body play a leading role in the formation of autoflora.
    Up to 80% of pathogenic strains isolated from healthy individuals are resistant to one or more antibiotics.Staphylococci isolated from patients and staff, as a rule, are characterized by multiple resistance, often to 6-8 antibiotics. Therefore, the use of antibiotics for prophylactic purposes does not protect against purulent-septic diseases, and these drugs, being immunosuppressants and reducing the body’s defenses, contribute to the colonization of hospital strains of microbes, which are characterized not only by high virulence, but also by invasiveness. Limiting the use of antibiotics to strict indications can lead to a decrease in antibiotic resistance of staphylococci.
    Carriers of pathogenic staphylococcus play a significant role in the spread of staphylococcal infection. Carriage of staphylococci is characterized by wide distribution both among healthy and especially among sick people. The form of carriage can be different. There is a category of persons in whom staphylococci of the same serotype are constantly found. These seem to be true carriers. Carriers of different types of staphylococci are less dangerous, although the latter are also constantly found in them.Distinguish between temporary and non-permanent carriage.
    The clinical course of staphylococcal infection is characterized by a variety – from the most severe, generalized forms to lungs: sepsis, pneumonia, meningitis, abscesses of internal organs, enterocolitis, endocarditis, gynecological diseases, staphylococcal infection with scarlet-like syndrome, purulent-inflammatory diseases of the skin and soft tissues, etc. in such cases, the disease is of mixed etiology. In addition to staphylococcus, salmonella, intestinal, Pseudomonas aeruginosa or streptococcus, pneumococcus, etc. are sown.With microbial associations, the course of the disease is characterized by particular severity.
    A feature of the course of staphylococcal infection in children is the tendency to generalize the process. The highest incidence of sepsis among newborns (see).
    It has been established that staphylococci in 48-78% of cases are the cause of acute respiratory tract injuries. Staphylococcal pneumonia occurs either as an independent form of the disease (rarely), or as one of the syndromes of staphylococcal infection, or is combined with other infectious diseases, more often of viral etiology.In some cases of staphylococcal pneumonia, staphylococcus is sown in association with colibacillus, Pseudomonas aeruginosa, Proteus vulgaris, with fungi of the genus Candida, streptococcus.
    With staphylococcal pneumonia, as well as with other forms of staphylococcal infection, it is often possible to establish an epidemiological connection with pyoderma, other minor forms of staphylococcal infection; infection is often associated with family contact (mastitis, tonsillitis), nosocomial infection in maternity hospitals, children’s hospitals.The pulmonary form of staphylococcal infection is characterized primarily by the polysegmental nature of the lesion with the rapid, often lightning-fast development of destruction of the lung tissue, complicated by pneumothorax.
    Staphylococcal lung destruction. Currently, it is quite common due to the increasing importance of staphylococcus in the pathology of childhood. In the development of staphylococcal pneumonia, importance is attached to both the bronchogenic pathway of infection (during epidemics and sporadic cases of acute respiratory viral infections) and the hematogenous pathway of lung damage, when the infection comes from other foci, however, the bronchogenic pathway does not simultaneously exclude the hematogenous pathway.
    The biological specificity of staphylococcus is determined by the toxins it releases into the environment (lethal toxin, leukocidin, hemotoxin or staphylolysin, necrotoxin, entertoxin, etc.) and enzymes (coagulase, hyaluronidase, penicillinase, etc.). In the development of staphylococcal destruction, the leading role belongs to necrotoxin and hyaluronidase, under the influence of which in the lung tissue is very
    foci of necrosis quickly appear (in some areas of the lungs small atelectasis are formed), decay cavities – “staphylococcal bullae” (from 0.5 to 2-3 cm in diameter) are formed and conditions are created for the spread of infection to the pleura (fibrinous-purulent overlays).On the one hand, this brings to the fore the “pleural” symptoms (pyopneumothorax, total empyema), and on the other hand, it causes severe intoxication of the body, causes deep functional disorders of breathing and blood circulation, also associated with the acute development of “stress syndrome” in the chest cavity.
    For primary staphylococcal pneumonia, unilateral localization of the process with frequent and rather rapid (almost simultaneous) involvement of the pleura in the pathological process is more characteristic.The development of secondary staphylococcal pneumonia (these forms are less common than primary ones) occurs due to the generalization of purulent infection in the body (osteomyelitis, otitis media, pyoderma, etc.) more slowly and gradually.
    Primary staphylococcal pneumonia initially differs little from acute pneumonia of other etiology, but the development of the disease often becomes rapid. The lightning-fast course of the process sometimes gives reason to assume that patients have an acute abdomen (intussusception of the intestine, appendicitis, etc.)). Intoxication is rapidly growing, the manifestations of which can be hyperthermia (39-40 degrees C and above, a hectic-type curve), cardiovascular and respiratory failure (acrocyanosis even at rest, shortness of breath, cyanosis of the mucous membranes and skin). Children are restless, rushing about in bed, moaning periodically, sometimes screaming; sweating, chills, sclera injection, puffiness of the face, hyperemia of the cheeks (mainly on the side of the lesion), occasionally attacks of painful dry (less often wet) cough are noted.A breakthrough of the contents of one of the tense bullae into the pleural cavity is possible; As a result, the child’s already serious condition worsens dramatically, cyanosis develops acutely, cold sticky sweat appears, shortness of breath reaches 80 per minute, tachycardia – 170-180 per minute, the pulse becomes threadlike, a collaptoid state occurs. Less often, the symptoms of purulent pleurisy increase gradually. The affected half of the chest lags behind aspiration, with percussion, a shortening of the percussion tone is determined up to absolute dullness; during auscultation, in contrast to adults, ballroom breathing is determined, and with a bronchial shade, and the smaller the child, the more often such options are (thin chest, compressed lung).Above the bullae, breathing has an amphoric hue, various moist rales are heard. Displacement of the mediastinal organs to the healthy side is characteristic, especially in patients with valvular pneumo- or pyopneumothorax. A particular threat to life is the displacement and constriction of the main veins.
    Dynamic X-ray examination is of great, sometimes decisive importance in the diagnosis of staphylococcal destruction of the lungs. Initially, multiple dense shadows are found in the lungs within several segments, one or two lobes of the lung, on the 2-5th day, round enlightenments of various sizes with and without level (“dry bullae”) begin to appear, around which infiltration of the lung tissue is clearly defined …There are also signs of pleural damage with accumulation of pus or air in its cavity, or both. Therefore, one of the most important diagnostic studies along with X-ray is the puncture of the pleural cavity.
    When indicated, bronchography, tomography, pleurography, angiopneumography, radioisotope examination of the lungs, diagnostic (also therapeutic) bronchoscopy, thoracoscopy are performed.
    Staphylococcal enterocolitis accounts for 4 to 30% of all cases of acute intestinal infection.This is the most serious illness among all intestinal infections. Mortality reaches 13%.
    Mostly children of the first six months of life with an unfavorable premorbid background (prematurity, malnutrition, early artificial feeding, past illnesses, in particular acute respiratory and pseudofurunculosis, repeated prescription of antibiotics and other drugs, often mastitis in the mother) are affected. In this regard, gastrointestinal diseases of this profile are often considered not only as a result of infectious and toxic effects, but also as a consequence of a violation of the intestinal biocenosis as a result of a decrease in the body’s resistance or the action of antibiotics.
    Staphylococcal meningitis in children has the most severe course. Among all cases of purulent meningitis, meningitis of staphylococcal etiology accounts for 2-3%.
    Staphylococcus aureus in modern conditions is often the cause of septic endocarditis (in 67% of cases). It is detected in 95-100% of cases with purulent diseases of soft tissues and skin. Staphylococcus aureus aggravates the course of burns, various dermatoses, and in some of them is considered as an etiological factor.
    Treatment of staphylococcal diseases. The effectiveness of treatment depends on the timely diagnosis and early use of complex specific anti-staphylococcal drugs. Proper nursing of the child is of great importance.
    The most effective antibiotics are aminoglycosides (kanamycin, gentamicin) in therapeutic concentration in combination with semi-synthetic antibiotics of the penicillin series (methicillin, oxacillin, ampiox, which rationally combines the properties of ampicillin and oxacillin, etc.).), olemorphocyclin, seporin, erythromycin phosphate (intravenously), as well as fusidin, especially in combination with oleandomycin (indications for a combination of antibiotics are currently significantly narrowed, since there is also a negative effect; their combined use is advisable only in very severe cases ).
    Nitrofurans are widely used, in particular furagin K (intramuscularly, intravenously, and less often intraosseously).
    Antimicrobial drugs should be used with extreme caution and only in combination with drugs that stimulate defense mechanisms and restore ecological balance.
    In the acute period of the disease, means of passive immunization are shown – direct transfusions of donor blood, administration of antistaphylococcal plasma, antistaphylococcal (from donor blood) immunoglobulin intramuscularly, intravenous targeted immunoglobulin. Proteolysis inhibitors are used – contrycal (trasilol), synthetic agents – amben and the like. Correction of metabolic disorders, the use of symptomatic remedies are also necessary. According to indications (phlegmon, pneumothorax, etc.) produce immediate surgical intervention.
    When the patient’s condition improves, active immunization agents are used – staphylococcal toxoid, autovaccine, staphylococcal bacteriophage. To stimulate immunogenesis, prodigiosan, lysozyme, chlorophyllin are recommended. All this is used in combination with such biologically active substances as lactobacterin, bifikop, bifidobacterin, as well as metacil, vitamins.
    Prevention of staphylococcal diseases in children has not been sufficiently developed.In preventing the spread of infection, a strict
    must play a major role
    control over the sanitary and epidemic regime of medical institutions, control over pregnant women, postpartum women, newborns: timely detection of small forms of pyoinflammatory diseases in them and their immediate transfer if pathology is detected from physiological departments to wards and even departments with an infectious regimen. The centralization of sterilization units within medical institutions is of great importance.
    An important measure aimed at reducing the prevalence of staphylococcal infection is vaccination of pregnant women with purified adsorbed staphylococcal toxoid.
    Considering that the most often antibiotic-resistant cultures of staphylococcus are sown from feces, it is recommended to widely prescribe bifidobacterin to restore normal intestinal biocenosis: 1) to all premature and low-birth-weight babies in maternity hospitals, and subsequently in departments for pathology of newborns and premature babies within 1-2 1st month of life; 2) children who received antibiotics in the early neonatal period; newborns fed with donor breast milk, or children of mothers with lactostasis, cracked nipples, resumed breastfeeding after mastitis; 3) sick newborns and children 1 year of life (with sepsis, pneumonia, especially intestinal syndrome), especially seriously ill.Cancellation of bifidobacterin in sick children should be no earlier than 10-15 days after the end of treatment with antibacterial drugs.
    It is important to strengthen control over the use of antibiotics and immunosuppressive therapy.

    ATTENTION !!!
    The information obtained here is for reference only. Questions regarding the determination of the diagnosis and the use of drugs require consultation with your attending physician.

    90,000 Will bacteriophages solve the problem of drug resistance in infections?

    Bacteriophages can be an excellent substitute for antibiotics, which work worse for certain types of bacteria.

    Alexander Zharnikov, head of the project office “Development of bacteriophages” of NPO Microgen, holding “Natsimbio” of Rostec State Corporation Alexander Zharnikov, told Radio Komsomolskaya Pravda about this in an interview with Radio Komsomolskaya Pravda

    A. Chelyshev:

    – Hello, friends! You are listening to the Komsomolskaya Pravda radio station. We are all crazy about the coronavirus, while global health is facing an equally, perhaps more serious threat, which is caused by inappropriate antibiotic use and caused by the growing antibiotic resistance of microbes.To raise awareness of this issue, the World Health Organization hosted World Antimicrobial Awareness Week from 18 to 24 November. As part of this initiative, we will talk right now with the head of the project office “Development of bacteriophages” of NPO Microgen of the Natsimbio holding of Rostec State Corporation Alexander Zharnikov . Hello!

    A. Zharnikov:

    – Hello!

    A.Chelyshev:

    – NPO Microgen is developing the production of bacteriophage preparations in our country, preparations included in the strategy for preventing the spread of antimicrobial resistance in the Russian Federation for the period up to 2030.

    Let’s start with the fact that the therapeutic activity of antibiotics has been declining, they say, for a very long time. Today, doctors regularly speak out in the spirit that against the background of the coronavirus pandemic and uncontrolled intake of antibiotics, we, unfortunately, accelerate the process of the emergence of superbugs – bacteria with multiple antibiotic resistance.And we may subsequently face an almost less complex problem than the spread of COVID-19. How scary and dangerous is it all really?

    A. Zharnikov:

    – Yes. This is really serious. Antibiotic resistance, unfortunately, is not a hypothetical problem, today it kills more than 700 thousand people a year. And if nothing is done, according to WHO estimates, in 30 years it could overshadow the scale of deaths from oncology. If we compare people’s perception of the problem of antibiotic resistance, then I would turn to today’s experience – how our population, our compatriots perceived the problem of COVID-19.At first they laughed at her, then there were a lot of big and different conspiracy theories. Someone denied, but today it is obvious that everyone, either in the family or among friends, has sick people, there are even deaths, unfortunately. And when the problem gets very close, people begin to relate to it differently.

    The problem of antibiotic resistance is growing slowly and steadily. And, unfortunately, soon each of us, probably, can face it.

    A. Chelyshev:

    – And I must say that COVID-19 will even give an additional impetus to this process.Why? Because all people who are diagnosed with COVID-19 are prescribed one or even two antibiotics so that a bacterial infection does not join. And people are taking these antibiotics. And this will most likely affect, in the end, the acceleration of the process of the emergence of superbugs. And the spread of antibiotic resistance.

    A. Zharnikov:

    – Certainly. The more antibiotics we use, the faster this problem grows. This is why WHO is hosting this Antibiotic Awareness Week.

    Bacteriophages help fight those infections, the pathogens of which have developed resistance to existing antibiotics.

    A. Chelyshev:

    – What factors can ultimately slow down the process of loss of sensitivity to antibiotics?

    A. Zharnikov:

    – Reasonable and correct use of antibiotics in strict accordance with the doctor’s prescription.

    A. Chelyshev:

    – Let’s talk about what role bacteriophages can play in this? We know from school that there are such organisms – viral natures, bacteriophages, which are capable of destroying bacteria, even the most dangerous ones.

    A. Zharnikov:

    – Indeed, bacteriophages were discovered much earlier than antibiotics – this is 1915. This is an organism, which in terms of number, population of the planet is probably the most widespread on the planet. It is natural, it has no synthetic essence, there is a huge amount of them. And the bacteriophage is perhaps the very counterweight that has been continuously fighting bacteria on Earth for millions of years.

    A. Chelyshev:

    – How exactly can bacteriophages help with antibiotic resistance?

    A.Zharnikov:

    – If it is impossible to find an antibiotic for some bacterial infections, they turn to bacteriophages. Bacteriophages are often used in the treatment of nosocomial infections, where staphylococcus and streptococcus are common. These microorganisms have long developed resistance to antibiotics. And they have 100% resistance to some antibiotics.

    Phages are also indispensable in chronic forms of diseases with a recurrent course, that is, we are talking about people who have a reduced immune status.For example, diabetes mellitus or cancer patients on chemotherapy.

    Bacteriophages are absolutely harmless to humans.

    A. Chelyshev:

    – I wonder why bacteriophages can fight antibiotic-resistant superbugs if natural mutations of microbes are at the heart of the problem. It turns out that bacteriophages are somehow arranged differently?

    A. Zharnikov:

    – Yes, they are arranged in a completely different way. These are living microorganisms.And speaking of antibiotics, it’s a synthetic chemical. Naturally, the mechanism of bacterial mutations, the mechanism of developing antibiotic resistance to chemicals is completely different. And the mechanism of action of a bacteriophage on a bacterium is also completely different. A bacteriophage is a species microorganism and works exclusively with its own bacterium, that is, if we have a staphylococcal bacterium, then we must have a bacteriophage corresponding to this bacterium – staphylococcal. This bacteriophage finds the bacterium and through the receptors understands that this is exactly the one it needs.With the help of the legs, it attaches to it, pierces the bacterial membrane to the cell and injects its DNA inside. This is followed by the replication process. And from one bacterium, into which a bacteriophage of its DNA entered within 20 minutes, for example, we can obtain from 20 to 500 new bacteriophages, which enter the natural environment, destroying this bacterium. And then, exponentially, the “phages” find new bacteria and begin to lyse them.

    A. Chelyshev:

    – That is, to destroy.

    A. Zharnikov:

    – Dissolve.

    A. Chelyshev:

    – Well, how many actual strains of viruses are now that you use in the production of drugs based on bacteriophages?

    A. Zharnikov:

    – Today we manufacture 11 bacteriophage preparations. Among them are monovalent drugs, that is, those that work with one type of bacteria. There are polyvalent ones that target six or even eight different bacteria.

    A. Chelyshev:

    – Many will probably want to know now, but when the bacteriophage destroyed the population of bacteria that parasitized, for example, in the human body, what do they do then? Will they not start eating the person himself after that?

    A. Zharnikov:

    – Bacteriophages are absolutely harmless to humans.