MRSA(Methicillin-resistant Staphylococcus aureus) is a bacterium responsible for several difficult-to-treat infections in humans. It may also be called multidrug-resistant Staphylococcus aureus or oxacillin-resistant Staphylococcus aureus (ORSA).
MRSA is, by definition, any strain of Staphylococcus aureus that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.
Most MRSA infections occur in people who have been in hospitals or other health care settings, such as nursing homes and dialysis centers. When it occurs in these settings, it’s known as health care-associated MRSA (HA-MRSA). HA-MRSA infections typically are associated with invasive procedures or devices, such as surgeries, intravenous tubing or artificial joints.
Another type of MRSA infection has occurred in the wider community — among healthy people. This form, community-associated MRSA (CA-MRSA), often begins as a painful skin boil. It’s spread by skin-to-skin contact. At-risk populations include groups such as high school wrestlers, child care workers and people who live in crowded conditions.
MRSA is capable of resisting Beta-Lactamase resistant Antibiotics via the mecA gene. This is a gene that encodes Penicillin-binding-protein 2a (PBP2a). ?-lactam antibiotics have a low affinity for PBP2a, therefore cell wall synthesis is able to proceed in their presence.
S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, open wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years. Patients with compromised immune systems are at a significantly greater risk of symptomatic secondary infection.
In most patients, MRSA can be detected by swabbing the nostrils and isolating the bacteria found inside. Combined with extra sanitary measures for those in contact with infected patients, screening patients admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the United States, Denmark, Finland, and the Netherlands.
MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils that may be accompanied by fever and occasionally rashes. Within a few days the bumps become larger, more painful, and eventually open into deep, pus-filled boils. About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively. However, some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing (“flesh-eating”) pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM, though PVL was recently found to not be a factor in a study by the National Institute of Allergy and Infectious Diseases (NIAID) at the NIH. It is not known why some healthy people develop CA-MRSA skin infections that are treatable whereas others infected with the same strain develop severe infections or die. The bacteria attack parts of the immune system, and even engulf white blood cells, the opposite of the usual.
The most common manifestations of CA-MRSA are skin infections such as necrotizing fasciitis or pyomyositis (most commonly found in the tropics), necrotizing pneumonia, infective endocarditis (which affects the valves of the heart), or bone or joint infections. CA-MRSA often results in abscess formation that requires incision and drainage. Before the spread of MRSA into the community, abscesses were not considered contagious because it was assumed that infection required violation of skin integrity and the introduction of staphylococci from normal skin colonization. However, newly emerging CA-MRSA is transmissible (similar, but with very important differences) from Hospital-Associated MRSA. CA-MRSA is less likely than other forms of MRSA to cause cellulitis.
It’s all about survival of the fittest – the basic principle of evolution. Bacteria have been around a lot longer than us, so they’re pretty good at it.
There are countless different strains of a single type of bacteria, and each has subtle natural genetic mutations that make it different from another. In addition, bacterial genes are constantly mutating.
Some strains’ genetic makeup will give them a slight advantage when it comes to fighting off antibiotic attack. So when susceptible strains encounter antibiotics they die, while these naturally resistant strains may prove harder to kill. This means the next time you encounter S.aureus, it’s more likely to be one that has survived an antibiotic encounter, (i.e. a resistant one). Eventually, the strain becomes resistant to different antibiotics, even though they work in slightly different ways.
When you are prescribed antibiotics, you are advised to finish the entire course. If you don’t do this, there’s a chance that you’ll kill most of the bugs but not all of them – and the ones that survive are likely to be those that have adapted to be more resistant to antibiotics.
Over time, the bulk of the S.aureus strains will carry resistant genes and further mutations may only add to their survival ability. Strains that manage to carry two or three resistance genes will have extraordinary powers of resistance to a range of different antibiotics.
The reason hospitals seem to be hotbeds for resistant MRSA is because with many vulnerable patients, infections are common and easily spread. So many different strains are thrown together with so many doses of antibiotics, vastly accelerating this natural selection process.
At risk populations include:
*People with weak immune systems (people living with HIV/AIDS, cancer patients, transplant recipients, severe asthmatics, etc.)
*Intravenous drug users
*Use of quinolone antibiotics
*College students living in dormitories
*People staying or working in a health care facility for an extended period of time
*People who spend time in coastal waters where MRSA is present, such as some beaches in Florida and the west coast of the United States
*People who spend time in confined spaces with other people, including prison inmates, military recruits in basic training, and individuals who spend considerable time in changerooms or gyms.
*People in contact with live food-producing animals
A century or more ago people knew that an infection was bad news and could rapidly kill a patient. But these days, since the rapid development of antibiotics after World War Two, we often take the power of antibiotics for granted, and expect them to work without question. MRSA is dangerous because it takes us back to the days when little could be done to stop an infection.
MRSA is particularly dangerous in hospitals. It’s a fact of life in the NHS that hospital patients are at higher than normal risk of picking up a S.aureus infection on the wards.
This is for two reasons. Firstly, hospital populations tend to be older, sicker and weaker than the general population, and therefore more vulnerable to infection. Secondly, conditions in hospitals involve a great many people living cheek by jowl, examined by doctors and nurses who have just touched other patients – the perfect environment for the transmission of all manner of infections. This is why there are strict hand-washing and hygiene measures when entering and leaving wards, and between seeing different patients.
Once these patients develop an infection they’re less able than a healthy person to fight it and urgent treatment with antibiotics may be critical. But because MRSA is resistant to many antibiotics, it may quickly overwhelm a weak patient, or cause a festering infection (for example in a wound or a joint implant) that causes tissue destruction and chronic disability.
In the UK, where MRSA is commonly called “Golden Staph”, the most common strains of MRSA are EMRSA15 and EMRSA16. EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published. EMRSA16 has been found to be identical to the ST36:USA200 strain, which circulates in the United States, and to carry the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes. Under the new international typing system, this strain is now called MRSA252. It is not entirely certain why this strain has become so successful, whereas previous strains have failed to persist. One explanation is the characteristic pattern of antibiotic susceptibility. Both the EMRSA15 and EMRSA16 strains are resistant to erythromycin and ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly, for example in the nasal mucosa and in the tonsil tissue ,. Erythromycin and Ciprofloxacin are precisely the antibiotics that best penetrate intracellularly; it may be that these strains of S. aureus are therefore able to exploit an intracellular niche.
Community-acquired MRSA (CA-MRSA) is more easily treated, though more virulent, than hospital-acquired MRSA (HA-MRSA). CA-MRSA apparently did not evolve de novo in the community but represents a hybrid between MRSA that spread from the hospital environment and strains that were once easily treatable in the community. Most of the hybrid strains also acquired a factor that increases their virulence, resulting in the development of deep-tissue infections from minor scrapes and cuts, as well as many cases of fatal pneumonia.
In the United States, most cases of CA-MRSA are caused by a CC8 strain designated ST8:USA300, which carries SCCmec type IV, Panton-Valentine leukocidin, PSM-alpha and enterotoxins Q and K, and ST1:USA400. Other community-acquired strains of MRSA are ST8:USA500 and ST59:USA1000. In many nations of the world, MRSA strains with different predominant genetic background types have come to predominate among CA-MRSA strains; USA300 easily tops the list in the U. S. and is becoming more common in Canada after its first appearance there in 2004. For example, in Australia ST93 strains are common, while in continental Europe ST80 strains predominate (Tristan et al., Emerging Infectious Diseases, 2006). In Taiwan, ST59 strains, some of which are resistant to many non-beta-lactam antibiotics, have arisen as common causes of skin and soft tissue infections in the community. In a remote region of Alaska, unlike most of the continental U. S., USA300 was found rarely in a study of MRSA strains from outbreaks in 1996 and 2000 as well as in surveillance from 2004–06 (David et al., Emerg Infect Dis 2008).
In June of 2011, the discovery of a new strain of MRSA was announced by two separate teams of researchers in the UK. Its genetic make-up was reportedly more similar to strains found in animals, and testing kits designed to detect MRSA were unable to identify it.
Antibiotics are not completely powerless against MRSA, but patients may require a much higher dose over a much longer period, or the use of an alternative antibiotic, often needing intravenous administration or with less tolerable side-effects, to which the bug has less resistance.
MRSA is just one of a number of infections causing major challenges for health workers, and some are concerned that the situation can only get worse. There is no doubt that there is an urgent need to develop new and better antibiotics and, more importantly, to work harder to prevent infection spreading and use the antibiotics we already have more efficiently.
There is some evidence that MRSA in hospitals is already decreasing, as a result of better protocols to deal with the bacteria and prevent infection developing (with strategies such as regular screening of patients and use of eradication treatments).
To keep MRSA and other infections at bay, prevention is your best weapon. It is highly recommended that all individuals keep their immune system functioning to its best ability.
This can be done most efficiently by:
* taking a good daily multi-vitamin and mineral supplement
* drinking a minimum of 32 oz. of pure water every day
* practice good hygiene methods
* take a good immune system booster like astragalus or ashwagandha every day (be sure to check for allergic reactions)
* only take echinacea if you feel like you are fighting off some bacterial or viral infection AND…..do not take echinacea for longer than 3-4 weeks at a time (it will loose its effectiveness if taken regularly as a preventative).
* you can use a hand sanitizer, which is mostly alcohol, or an effective substitute is Aloe Gel. Aloe is an excellent anti-bacterial and is also a wonderful skin lotion, where as alcohol can be drying.
* the following herbs have proven beneficial in the treatment of MRSA:
For Pneumonia: usnea, garlic, goldenseal, cryptolepsis, eucalyptus, boneset, wormwood, juniper, grapefruit seed extract, oils of thyme or oregano and olive leaf extract.
For surgical/skin infections: any of the above plus honey or sage.
For Bacteremia: echinacea, garlic, usnea or boneset, all given in massive doses.
* A complementary treatment that should not be overlooked is LIGHT THERAPY. A blue light with a frequency of 470nm (nanometers) has been shown to kill MRSA in as little as 2 minutes when shown on the skin at the infection site. This is an extremely useful therapy for those exposed to this infection. Please contact a CAM practitioner for more information on light therapy and other therapies for the treatment of MRSA and other health conditions.
MRSA is a serious medical condition that, unfortunately, has become more prevalent in recent years as this bacteria becomes more resistant to antibiotics.
ClinicalIt has been reported that maggot therapy to clean out necrotic tissue of MRSA infection has been successful. Studies in diabetic patients reported significantly shorter treatment times than those achieved with standard treatments.
Many antibiotics against MRSA are in phase II and phase III clinical trials. e.g.:
Phase III : ceftobiprole, Ceftaroline, Dalbavancin, Telavancin, Aurograb, torezolid, iclaprim…
Phase II : nemonoxacin.
Pre-clinicalAn entirely different and promising approach is phage therapy (e.g., at the Eliava Institute in Georgia), which in mice had a reported efficacy against up to 95% of tested Staphylococcus isolates.
On May 18, 2006, a report in Nature identified a new antibiotic, called platensimycin, that had demonstrated successful use against MRSA.
Ocean-dwelling living sponges produce compounds that may make MRSA more susceptible to antibiotics.
Cannabinoids (components of Cannabis sativa), including cannabidiol (CBD), cannabinol (CBN), cannabichromene (CBC) and cannabigerol (CBG), show activity against a variety of MRSA strains.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose
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