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emergence of hospital-acquired and Community-acquired antibiotic resistant bacteria
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Staphylococcus aureus (SA)—Antibiotic Resistance (General)

Throughout history, Staphylococcus aureus (SA) has been a dangerous pathogen once it has successfully breached the normal defense system. The first effective antibiotic against SA, penicillin, became available in the 1940s. Soon after, SA evolved resistance to penicillin, and by the late 1950s, 50 percent of all SA were resistant. Today, fewer than 10 percent of SA infections can be cured with penicillin.

The next weapons against SA, methicillin and cephalosporins, became available in the 1960s and 1970s. By the late 1970s, some strains of SA had evolved resistance to these drugs. Today, as many as 50 percent of SA isolated from U.S. hospitals are resistant to methicillin.

The last effective defense against methicillin-resistant SA (called MRSA) is vancomycin. However, the increasing use of vancomycin has set the stage for the evolution of vancomycin-resistant SA (called VRSA). Antibiotic use and resistance represent a vicious cycle: The more doctors use vancomycin, the more they create an environment that encourages the evolution of VRSA.

Staphylococcus aureus (SA)—Antibiotic Resistance (MRSA)

MRSA, or methicillin-resistant Staphylococcus aureus, are strains of the bacterial pathogen Staphylococcus aureus (SA) that have evolved resistance to the antibiotic methicillin. These strains are also likely to be resistant to other antibiotics used to treat SA infections. MRSA strains first appeared in the late 1970s and currently 40-50 percent of SA isolated from U.S. hospitals are resistant to methicillin. These infections are treated with the powerful antibiotic vancomycin. Scientists hypothesize that the strains of SA most likely to evolve resistance to vancomycin are the MRSA.

Staphylococcus aureus (SA)—Antibiotic Resistance (VRSA)

Scientists expect strains of the bacterium Staphylococcus aureus (SA) that are fully resistant to the antibiotic vancomycin to evolve soon. Vancomycin-resistant Staphylococcus aureus (VRSA) is the term used to describe these strains. The expected emergence of VRSA is alarming because vancomycin is the only antibiotic that is effective against MRSA, strains of SA that are resistant to the antibiotic methicillin (MRSA).

Although VRSA—strains of SA that are fully resistant to vancomycin—do not currently exist, medical workers have recently isolated strains of SA that are four times more resistant to vancomycin than SA strains found previously. Because infections due to these strains do not respond to the usual doses of vancomycin, many physicians and other experts incorrectly refer to them as VRSA. They should be described as SA strains with intermediate resistance to vancomycin. Infections due to these strains can be cured using higher doses of vancomycin.

Microscopic view of bacteriaStaphylococcus aureus (SA)—Definition

Staphylococcus aureus (SA) is a bacterium that is commonly found on the skin and in the eyes, nose, and throat of animals and humans. SA is one of the most common causes of infections worldwide. Though not a problem for healthy adults, SA is potentially virulent and can cause serious infections of the skin, eyes, brain, blood, and respiratory and digestive tracts, as well as bone and connective tissue. Some SA infections, such as bacteremia, have death rates of 40 percent.

surgeons operating on a patientStaphylococcus aureus (SA)—Risk Factors

Although the body's defenses must be weakened or breached before Staphylococcus aureus (SA) bacteria cause disease, many people are potential victims of SA infections. SA enters the body through wounds such as burns, deep cuts, or surgical incisions. People whose immune systems are weakened from bouts with other diseases—hospital patients with influenza, leukemia, skin disorders, or diabetes, or patients recovering from kidney transplants—are vulnerable. Patients receiving radiation or chemotherapy also are more susceptible to SA infection. In 1992, nearly 1 million of the 23 million U.S. citizens who had surgery developed infections, most of them due to SA. Likewise, SA poses a threat to newborns, whose immune systems are not yet fully functioning.

Staphylococcus aureus (SA)—Transmission

Because Staphylococcus aureus (SA) bacteria can survive dry conditions, they remain alive for long periods of time on dust particles, clothing, furniture, or hospital equipment. SA is able to grow with or without oxygen. This allows the bacteria to survive the aerobic conditions of the skin or nasal passages, waiting for an opportunity to invade deeper tissues. Once inside, SA can produce powerful toxins that further destroy and disrupt the body's tissues. SA can also resist immune system cells that engulf and destroy invading bacteria, making it a formidable adversary for the immune system.

A high percentage of hospital workers are passive carriers for SA, harboring the bacteria on their skin and in their upper respiratory tracts without showing any symptoms. For this reason, SA often spreads from patient to patient via the hands of hospital workers. SA also spreads via dust, clothing, furniture, or medical equipment that has been in contact with infected patients.

Antibiotic Resistance—Cost

As more and more strains of disease-causing bacteria become resistant to commonly used antibiotics, physicians must switch to other, often more expensive drugs. For example, switching from the penicillins to methicillin in the treatment of Staphylococcus aureus (SA) infections increased treatment costs about 10-fold.

It is difficult to assess the overall cost of antibiotic resistance. A report from the Government Accounting Office indicates that no federal agency adequately monitors antibiotic resistance or evaluates its social and financial costs. One estimate, however, places the annual cost of antibiotic resistance as high as $5 billion per year.

Antibiotic Resistance—Definition

Antibiotic resistance describes the condition of bacteria whose growth and reproduction is unaffected by particular antibiotics. Bacteria have a variety of mechanisms for evading the toxic effects of antibiotics. In some cases, the bacterial cell membranes are altered so that an antibiotic cannot enter the cell. In other cases, resistant bacteria actively pump the antibiotic out of the cell as soon as it enters. Still other resistant bacteria make an enzyme that degrades an antibiotic as soon as it enters the cell. There are also other mechanisms for antibiotic resistance.

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