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 A key factor in the development of antibiotic resistance is the ability of infectious organisms to adapt quickly to new environmental conditions. Bacteria are single-celled organisms that, compared with higher life forms, have small numbers of genes.

 Therefore, even a single random genetic mutation can greatly affect their ability to cause disease. And because most microbes reproduce by dividing every few hours, bacteria can evolve rapidly. A mutation that helps a microbe survive exposure to an antibiotic will quickly become dominant throughout the microbial population. Microbes also often acquire genes from each other, including genes that confer resistance.


  The advantage microbes gain from their innate adaptability is augmented by the widespread and sometimes inappropriate use of antibiotics. A physician, wishing to placate an insistent patient who has a virus or an as-yet undiagnosed condition, sometimes inappropriately prescribes antibiotics. Also, when a patient does not finish taking a prescription for antibiotics, some bacteria may remain. These bacterial survivors are more likely to develop resistance and spread. Hospitals also provide a fertile environment for antibiotic-resistant germs as close contact among sick patients and extensive use of antibiotics select for resistant bacteria. Scientists also believe that the practice of adding antibiotics to agricultural feed promotes drug resistance.

 For all these reasons, antibiotic resistance has been a problem for nearly as long as we've been using antibiotics. Natural selection of penicillin-resistant strains in a bacterium known as Staphylococcus aureus began soon after penicillin was introduced in the 1940s. Today, antibiotic-resistant strains of S. aureus bacteria as well as various enterococci (bacteria that colonize the intestines) are common and pose a global health problem in hospitals. More and more hospital-acquired infections are resistant to the most powerful antibiotics available, such as vancomycin. These drugs are reserved to treat only the most stubborn infections to slow development of resistance to them.  There are multiple signs that the resistance problem is increasing.
   In 2003, epidemiologists reported in The New England Journal of Medicine that 5 to 10 percent of patients admitted to hospitals acquire an infection during their stay and that the risk for a hospital-acquired infection has risen steadily in recent decades.  Increasing reliance on vancomycin has led to the emergence of vancomycin-resistant enterococci infections. According to CDC, prior to 1989, no U.S. hospital had reported any vancomycin-resistant enterococci but subsequently, such microbes have become common in U.S. hospitals.  The first S. aureus infections resistant to vancomycin emerged in the United States in 2002, presenting physicians and patients with a serious problem. In July of that year, CDC reported that a Michigan patient with diabetes, vascular disease, and chronic kidney failure had developed the first S. aureus infection completely resistant to vancomycin. A similar case was reported in Pennsylvania in September 2002.

  In 2004, the third reported case of vancomycin-resistant S. aureus (VRSA) in the United States was reported in New York. This case highlighted the failure of several standard automated susceptibility tests to identify vancomycin resistance in that isolate and suggests that additional VRSA cases may have occurred nationwide but escaped detection. Since then, three additional cases of VRSA, all occurring in Michigan, have been reported to CDC.  Strains of S. aureus resistant to methicillin are endemic in hospitals and are increasing in non-hospital settings such as locker rooms and day care centers. Since September 2000, outbreaks of methicillin-resistant S. aureus (MRSA) infections have been reported among high school football players and wrestlers in California, Indiana, and Pennsylvania, according to CDC. During the 2003 football season, an outbreak of MRSA occurred among members of a professional football team.  A number of cases of community-associated MRSA have also been reported, including cases in patients without established risk factors.

   Ionic Silver is an excellent antimicrobial, with relatively low toxicity against non-target organisms. However, prolonged high intake of ionic silver may lead to health problems, such as argyria. In an inorganic matrix, silver ions are slowly released via an ion-exchange mechanism. The release of silver ions from the surface is slow, but just fast enough to maintain an effective concentration at and near the surface of the material. Once the silver ion leaves the surface of the matrix and reaches the surface of the microorganism, its mechanism of antimicrobial action begins. Uptake of silver ions by a microbial cell can occur by several mechanisms, including passive diffusion and active transport by systems that normally transport essential ions.

   While the silver ions may bind non-specifically to cell surfaces and cause disruptions in cellular membrane function, it is widely believed that the antimicrobial properties of silver depend upon silver binding within the cell. Once inside the cell, silver ions begin to interrupt critical functions of the microorganism. Silver ions are highly reactive and readily bind to electron donor groups containing sulphur, oxygen and nitrogen, as well as negatively charged groups such as phosphates and chlorides. A prime molecular target for the silver ion resides in cellular thiol (-SH) groups, commonly found in critical proteins called enzymes. Enzymes become denatured because of conformational changes in the molecule that result from silver ion binding. Many of the enzymes that silver ions denature are necessary in the cellular generation of energy. Society has become increasingly aware of the growth of bacteria, mold and fungi, especially in public facilities like schools and hospitals.
 Common topical antimicrobial treatments, such as ethyl alcohol, anti bacterial soaps and disinfectant sprays kill harmful germs, but provide no residual protection and do not prevent recontamination.   The best solution for long term protection and cleanliness, therefore, is to use antimicrobial substances on surfaces at risk for bacterial/fungal growth, or cross contamination through the touch transfer of these microbes.   Papules appear from 12 to 120 hours following exposure to contaminated water.

 This is a tale of a vicious disease that has a preference for human flesh, and an appetite that surpasses the worst of nightmares. However, this is not a Hollywood horror movie. This one is made by Mother Nature, and is very, very real. This is a story of one such real case. Learn how this near death experience changed there lives forever for the better. Warning! This book contains Graphic Pictures.

 Surviving MRSA: Learn How to Protect Yourself

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