Author Topic: MRSA: What Health Care Providers Should Know  (Read 835 times)

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MRSA: What Health Care Providers Should Know
« on: January 07, 2008, 08:59:29 AM »
In the battle of humans vs. bacteria, a new enemy has emerged as the most feared “superbug” of 2007. Forget West Nile and bird flu – Methicillin Resistant Staphylococcus Aureus (MRSA) is suddenly all over the media. It is an overdue and well-deserved spot in the limelight.

MRSA rose to prominence last month when a CDC report published in JAMA estimated that nearly 19,000 people had died of MRSA infections in 2005. Compare that with AIDS, which killed about 17,000 in the same year, and it becomes readily apparent that most of the country is unaware of the degree of threat posed by MRSA. In fact, many people still do not know what MRSA is.

Here is a quick primer on MRSA to help answer any questions your patients, friends, and family may have.

What is MRSA?

Most healthcare professionals know that culture results which return as “Gram positive cocci in clusters” are an ominous code for Staph aureus. Its name means ‘golden clusters of seeds,’ which describes not only its microscopic appearance, but also its golden sheen when grown on a blood agar plate.

Staphylococcus aureus is a bacterium that was discovered in 1880 in surgical abscesses. Staph has a talent for antibiotic resistance, and it became resistant to penicillin nearly immediately after penicillin was introduced in the 1940s. Methicillin is an antibiotic that was used to treat this penicillin-resistant staph, but as the bug continued to collect resistances, MRSA was born.

MRSA is a strain of staph that was identified in 1961. MRSA is by no means a new bacteria, it is only new to the public consciousness. Due to the mathematics of infectious disease, MRSA has exploded along an exponential curve and now represents the majority of all staph infections seen in ICUs and in the ED.

Is MRSA really a “superbug”?

MRSA is potentially lethal, as is its parent, the pan-sensitive Staph aureus, often via bloodstream infections or bacteremia that leads to sepsis and ultimately to septic shock. However, MRSA is not deemed a superbug simply due to its resistance. It also has increased morbidity due to the accumulation of toxin genes via bacteriophages, such as Panton-Valentine leukocidin (PVL). A bacteriophage is basically a virus containing a snippet of DNA that can spread through a population of bacteria, similarly to the way a bacterial infection spreads through a human population. PVL is called a ‘leukocidin’ because it has the ability to burst white blood cells (leukocytes).

MRSA may be fearsome in its rapidity and pure purulence, but it is not invincible by any means. Most medical students know that MRSA can be treated empirically with vancomycin, a “big gun” antibiotic. However, many may not be aware that MRSA is also often susceptible to such “small guns” as doxycycline or trimethoprim/sulfamethoxazole. As with any infectious disease, the best strategy is to start broad coverage antibiotics immediately with any suspicion of MRSA infection, and then to narrow coverage based on culture and sensitivity results. A CA-MRSA abscess, the most common manifestation that a normal, immunocompetent member of the community might face, can still be treated with a simple incision and drainage (I&D) of the wound. CDC recommendations suggest not adding antibiotic coverage unless the patient is immunocompromised, has severe local symptoms or signs of systemic infection, or does not respond to I&D. Antibiotic choices for outpatient treatment of MRSA skin infection include clindamycin and doxycycline.

Friends, family, and patients who are concerned about the danger of MRSA should be congratulated on their awareness of public health issues, then reassured with the following facts:

    * Colonization with MRSA does not equal infection. Many people (an estimated 2 million in the U.S.) carry MRSA with no symptoms at all.

    * MRSA infection is treatable with proper antibiotics, and does not always require antibiotics.

    * Simple prevention strategies can greatly reduce the likelihood of a MRSA infection, particularly a severe one.

Who’s at fault for the spread of MRSA?

One of the controversial aspects of the rise in MRSA infections is whether doctors or patients are to blame. Doctors point their fingers at patients who demand antibiotics regardless of whether they are indicated, and patients likewise are concerned that doctors have been reckless with their prescriptions.

According to Jessica Snyder Sachs, the author of “Good Germs, Bad Germs,” one of the big misconceptions that physicians have had about MRSA is “that it’s just a hospital bug. We have for years had patients dying of MRSA from the community.” Snyder Sachs points out that up until recently, physicians simply did not consider the diagnosis of MRSA unless patients had some exposure to a healthcare scenario such as a nursing home or a hospital. Invasive infections that are most dangerous are certainly far more likely in those who have these exposures, but in order to select appropriate antibiotics to prevent non-invasive infections from becoming invasive, MRSA must be considered in those with no risk factors at all.

Of course, the other side of the coin is that patients must be educated as to why antibiotics should not be used unless necessary. Patient ‘ordering’ of antibiotics in the manner of ordering a meal at a fast food joint has been lampooned by physicians, but as any drug-seeker knows, it takes more than one person to obtain a prescription medication. Consider whether antibiotics are necessary before prescribing, and consider discontinuing antibiotic therapy if cultures are negative or if coverage can be narrowed.

What is the difference between CA-MRSA and HA- MRSA?

Community Acquired (CA)-MRSA and Hospital Acquired (HA)-MRSA have historically been significantly different bacteria. HA-MRSA strains tend to have accumulated resistance to more antibiotics, but CA-MRSA is actually more toxic. CA-MRSA can replicate more rapidly and is more often associated with PVL toxin, presumed to be a key factor in how CA-MRSA infections notoriously produce necrotic lesions such as abscesses or hemorrhagic pneumonia. New studies have shown that CA-MRSA can basically pulverize white cells, with or without PVL toxin, and that makes CA-MRSA hard for our bodies to defend against despite the fact that it is not resistant to as many antibiotics as its hospital-acquired cousin. There are several of these highly virulent strains of CA-MRSA that are now wreaking havoc in the community, the most famous of which is the USA300 strain.

What are the best ways to prevent MRSA infections?

MRSA is spread mainly by direct and indirect contact with human hands - transmission by droplet/airborne routes is uncommon. Simple things like handwashing and use of gloves and gowns are still the best ways to prevent the spread of infections. For your patients, the most important things are not only to wash hands, but also to keep cuts and abrasions clean, dry, and covered. As many have noted, regular maintenance of hygiene in high-risk areas, such as locker rooms, is key. “What we don’t want is a one-time massive cleaning after a student has a case of MRSA.” Jessica Snyder Sachs points out, referring to the recent media blitz regarding MRSA infections in schoolchildren. “I also think that this is an opportunity to educate people about MRSA pneumonia that is community-acquired and tends to come on the heels of the flu” — another great reason to be sure that you and your patients get the flu shot annually.

What are some system-related ways to combat the spread of MRSA?

“We desperately, definitely need more antibiotics in the short term, because we are running out of them,” states Jessica Snyder Sachs. “In the long term, we need other solutions. The bacteria can evolve around antibiotics too quickly.” As examples of these future solutions, she notes that not only is there a MRSA vaccine in development, but also scientists are considering how we can detoxify MRSA. After all, many people are colonized with MRSA and do not have any manifestation of infection. What if we could leave the MRSA in place, but turn off the toxins? Or what if we could use our body’s ability to host friendly bacteria to create a hostile environment for MRSA?

In the past, mild forms of staph have been used in an attempt to displace virulent staph, or to prevent the virulent staph from colonizing in the first place. These are some of the exciting antibiotic-free ideas that we may see in the future. For now, making a habit of regular handwashing and good hygiene, particularly in the hospital, is the best way to fight MRSA. Any systematic change that helps to facilitate or ingrain a “culture of handwashing” (not to mention stethoscope-washing) will help. Reassure your patients that using regular soap, alcohol-based foams or hand sanitizers are all good ways to prevent MRSA that do not encourage further resistance. The use of cleansers that contain antibiotic ingredients like triclosan is unnecessary and should be discouraged.

This is not the first time that resistant strains of staph aureus have emerged and caused deadly infection. A prior pandemic of resistant staph called ‘phage type 80/81? caused the deaths of many mothers and babies from sepsis in the 1950s and 1960s. Studies have shown that CA-MRSA causing infections now is directly related to this killer staph from the past. In infectious disease, the adage that “history repeats itself” is as true as ever. Will the cycle continue? Unless we start fighting staph infections with smarter plans instead of with ever-bigger “guns”, the answer is most certainly yes.

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