University Times

The first two cases of infection caused by vancomycin-resistant Staphylococcus aureus (VRSA) in the United States were detected this year — in Pennsylvania and Michigan — according to the federal Centers for Disease Control (CDC) and Prevention.

“VRSA is regarded as the ultimate in antibiotic resistance, a really nasty germ that can kill in its own right and is resistant to the most potent antibiotics we have” including the powerful drug vancomycin, said David L. Paterson, director of UPMC Health System’s new Antibiotic Management Program.

Healthy people with unimpaired immune systems generally are not at risk for S. aureus infections (which makes even super-virulent VRSA a poor choice as a bioterrorism weapon, Paterson pointed out).

But sick and infirm individuals — including, by definition, most hospital patients — are vulnerable to infections by VRSA and less resistant strains called vancomycin-intermediate S. aureus (VISA). The first known U.S. case of infection caused by VISA was detected in a Michigan man in 1997.

Like infections by other S. aureus bacteria, VRSA and VISA infections tend to cause nothing more serious than skin boils in healthy victims. But in people with weakened immune systems, the bacteria can cause pneumonia, heart infections, meningitis and fatal blood infections.

S. aureus in its various forms affects as many as 9 million Americans each year and is the No. 1 cause of hospital infections in the world, according to the CDC.

To date, VRSA and VISA isolates in the United States have been found to be treatable by other FDA -approved drugs. But at the rate that S. aureus bacteria have been developing resistance, some scientists question how long medicine can keep ahead of the killer bugs.

VRSA and VISA represent the latest developments in a bacterial saga that began millions of years ago. Staphylococcus aureus bacteria are commonly found on the skin and in the noses of healthy people. The bugs are believed to have evolved from rodlike bacilli that preyed on the first vertebrates to live on land.

Over millennia, S. aureus evolved tough cell walls and other defenses, extreme toxicity and the ability to mimic a wide variety of disease symptoms. Unlike most bacteria, S. aureus can survive for years without moisture or a food source.

Prior to the 1940s, when penicillin became widely available and the development of other antibiotics soon followed, S. aureus killed more people worldwide than pneumonia and tuberculosis, some epidemiologists believe.

At first, penicillin tamed S. aureus. But within a few years, mutant strains of the bacteria were producing enzymes that undercut penicillin’s effectiveness. By the late 1940s, nearly 60 percent of S. aureus strains found in American hospitals were penicillin-resistant.

S. aureus proceeded to outmaneuver a procession of other drugs until, by the mid 1950s, researchers were reporting that half of S. aureus infections in hospitals were resistant to most available antibiotics.

Scientists countered during the early 1960s by engineering semi-synthetic drugs that included methicillin, which nullified the enzymes that had protected S. aureus against penicillin.

But strains of methicillin-resistant S. aureus (MRSA) soon began appearing. To the shock of the medical world, the bacteria had developed resistance to a human-engineered drug.

In 1958, the FDA approved a new, synthetic antibiotic called vancomycin. It was expensive and toxic enough to cause serious side effects, but vancomycin proved to be the only drug that worked consistently against MRSA.

Developing resistance to vancomycin would require bacteria to execute such a complex series of genetic mutations that scientists doubted it was even possible. And yet, by the late 1990s, strains of vancomycin-resistant S. aureus began appearing.

— Bruce Steele