Be vigilant against staph

WITH ABOUT 19,000 people dying nationwide each year from antibiotic-resistant staph infections, it's important to be vigilant in personal hygiene, public health surveillance and aggressive countermeasures at a level consistent with the fight against AIDS infections.

Indeed, more people die in the United States each year from staph infections than from AIDS.

Local officials confronted the deadly bacteria recently in Spanish Fort, when a high school football player developed an infection. To their credit, school officials called in a professional cleaning crew to disinfect school buildings.

Fortunately, the Spanish Fort student recovered, but others who have contracted staph weren't so lucky. A Valley, Ala., woman died in October of complications from MRSA (methicillin-resistant Staphylococcus aureus) infection, becoming the first MRSA victim in Alabama.

It's estimated that 90,000 people have MRSA in the United States at any one time, though most of the cases occur in hospitals where health care professionals take aggressive measures against any infection.

Staph bacteria, though, are often present on the skin and in nasal passages. The "super bug" drug-resistant bacteria live among easily treatable bacteria and can enter a person's bloodstream through a minor scrape or cut, or through the skin pores.

Moreover, the dangerous bacteria can live on towels and other items that have come in contact with skin, jumping onto new hosts who come in contact with them, spreading and leading to an outbreak (defined as three or more cases).

Ironically, these super bugs occur because of the medical community's aggressive use of antibiotics against normal bacteria. Because of this widespread use, some bacteria become resistant to drugs.

But staph infections can be prevented, which is where personal hygiene comes in. Health officials suggest frequent washing of hands, showering after exercise, avoiding using someone else's towel, razor or other personal items that come in contact with skin, and cleansing of exercise equipment in public gyms.

Public health officials, too, can do more by requiring more aggressive reporting of individual cases, especially those that develop outside hospitals. With public awareness, personal hygiene and public health watchfulness, outbreaks of MRSA from community sources can become a health problem of the past.



© 2007 Press-Register. All rights reserved.

Study of staph shows how bacteria evolve resistance

Antibacterial resistance doesn’t happen overnight. But until recently nobody knew exactly how long it took — or how it happened at all. Now, by studying blood taken from a single patient over a period of months, Rockefeller University researchers have been able to trace how a common strain of bacteria adapted its genes to counteract the antibiotics used to try to kill it, until it finally emerged into the kind of fully resistant microbe that is wreaking havoc in hospitals worldwide. Total elapsed time: 90 days.

This is the first time that such a process has been observed “within” a patient, and the results, published in the May 21 issue of the Proceedings of the National Academy of Sciences sheds light on how such resistance occurs through selective pressure, says the study’s lead investigator, Alexander Tomasz, head of the Laboratory of Microbiology at Rockefeller University.

“What is thrilling is that we got as close as one can to the birthplace of antibiotic resistance in a patient, and now we can study which of the genetic mutations we found are really essential for resistance,” Tomasz says. If the genetic alterations they discovered are common to all known mutated strains of the bacteria — which Tomasz suspects is true — then knowing these genes may help clinicians design ways to block multidrug resistance, he says.

The microbe they isolated is Staphylococcus aureus, which is one of the most frequent causes of a wide range of hospital- and community-acquired infections, and is best known as the cause of toxic shock syndrome. The pathogen has acquired resistance to the majority of available antibiotics, including, recently, vancomycin, which was believed to be the only major agent that could treat it. “It has fantastic adaptive capabilities which have led to the worldwide spread of resistant lineages that are posing serious limits to clinical treatment,” Tomasz says.

But no one has known how such resistance occurs — whether it happens within individual patients, or whether patients with wounds pick up resistant microbes that have somehow infiltrated hospitals.

In this study, Tomasz, along with first author Michael Mwangi, a postdoc in the Tomasz lab, Eric Siggia, head of the Laboratory of Theoretical Condensed Matter Physics, and collaborators from Rockefeller, the Howard Hughes Medical Institute, the U.S. Department of Energy and Cornell University, obtained access to the blood of a patient with congenital heart disease who was treated extensively, but unsuccessfully, with several antibiotics including vancomycin. The team isolated the bacteria from the blood, and then used the whole-genome “shotgun” sequencing method to work out the entire genetic structure of S. aureus as it changed. They sequenced both the initial isolate and the later drug-resistant bacterium. The comparison of the two sequences showed that the resistant bacterium carried 35 mutations in 33 places on its genome and also showed that the mutations showed up in the intermediate isolates in a sequential order in parallel with the gradually increasing resistance to vancomycin. Although initially sensitive to vancomycin, some of the bacteria were probably able to “hide” from the antibiotic in the tissue of the patient’s heart valve, Tomasz says. “The bacteria can bury themselves there and form a wall made of fibrin and platelets, and in that way, microbes in this abscess can selectively adapt to antibiotics in the bloodstream.”

The researchers discovered that as the bacteria acquired resistance to vancomycin, they also became resistant to a new antibiotic, daptomycin, which was thought to be able to treat multidrug-resistant S. aureus. “This is more than we bargained for,” Tomasz says. “The patient wasn’t even exposed to daptomycin, yet the bacteria acquired a resistance to it.” Further testing revealed that one of the mutated loci associated with decreasing vancomycin susceptibility resembled that found from isolates recovered in different regions of the world, raising hopes that these findings will indeed offer a representative model of resistant S. aureus, and may someday lead to new mechanisms for fighting drug-resistant staph.

Proceedings of the National Academy of Sciences 104(22): 9451-9456 (May 29, 2007)