Updated Mon. Nov. 17 2008 8:15 AM ET

The Canadian Press

TORONTO — Alberta surgeons aren’t always following guidelines aimed at minimizing the risk patients will develop an infection as a result of their surgery, a new survey reveals.

By Mark Frauenfelder

I’ve read a lot of stories about antibiotic-resistant infections, but this New Yorker piece by Jerome Groopman called “Superbugs” stands out.

Frederick Ausubel, a bacterial geneticist at the Massachusetts General Hospital, in Boston, is searching for drugs to combat bacterial virulence, using tiny animals like worms, which have intestinal cells that are similar to those in humans, and which are susceptible to lethal microbial infection. The worm that Ausubel is studying, Caenorhabditis elegans, is one and a half millimetres in length. “You are probably going to have to screen millions of compounds and you can’t screen millions of infected mice,” Ausubel said. “So our approach was to find an alternative host that could be infected with human pathogens which was small enough and cheap enough to be used in drug screens. What’s remarkable is that many common human pathogens, including Staphylococcus and Pseudomonas, will cause intestinal infection and kill the worms. So now you can look for a compound that cures it, that prevents the pathogen from killing the host.”

The profligate prescription of antibiotics—for children and adults with upper respiratory infections, sinus infections, and even middle-ear infections—is a problem because most of these illnesses are caused by viruses, not bacteria, which are what conventional antibiotics attack. Of more concern is the direct connection between antibiotic use and the emergence of drug-resistant “superbugs”: As the medicine eliminates germs that are sensitive to it, drug-resistant mutant strains prosper. The result is a major public-health problem. Antibiotic-resistant infections such as methicillin-resistant Staphylococcus aureus may cause more deaths in the United States than AIDS does.

In the doctor’s office or the ER, it’s hard to tell the difference between bacterial and viral infections, and so doctors are tempted to prescribe antibiotics whenever they’re unsure. That’s especially true when doctors think that patients expect to take the medicine home, according to a recent study. Investigators interviewed patients with respiratory infections who went to the ER in 10 hospitals affiliated with medical schools, asking whether the patients expected to receive antibiotics and about whether they were satisfied with the care they received when they were discharged. The researchers also asked physicians why they prescribed antibiotics. The main conclusion was that doctors were significantly more likely to prescribe if they believed that patients expected them to—but did a lousy job predicting which patients those actually were. And the patients most satisfied with their care were the ones who left the ER with a better understanding of their condition, antibiotics or no antibiotics. The take-home message for doctors like me: Spend an extra five minutes talking to your patients about their medical problems, and you can send them away happy and without unnecessary medicine.

A system must be set up to monitor the global spread of a drug-resistant form of E.coli which can cause fatal blood poisoning, Canadian scientists urge.

Emerging and re-emerging infectious diseases, especially those caused by drug-resistant bacteria, are a major problem worldwide. Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) appeared rapidly and unexpectedly in the United States, resulting in an epidemic caused primarily by isolates classified as USA300. The evolutionary and molecular underpinnings of this epidemic are poorly understood. Specifically, it is unclear whether there has been clonal emergence of USA300 isolates or evolutionary convergence toward a hypervirulent phenotype resulting in the independent appearance of similar organisms. To definitively resolve this issue and understand the phylogeny of USA300 isolates, we used comparative whole-genome sequencing to analyze 10 USA300 patient isolates from eight states in diverse geographic regions of the United States and multiple types of human infection. Eight of 10 isolates analyzed had very few single nucleotide polymorphisms (SNPs) and thus were closely related, indicating recent diversification rather than convergence. Unexpectedly, 2 of the clonal isolates had significantly reduced mortality in a mouse sepsis model compared with the reference isolate (P = 0.0002), providing strong support to the idea that minimal genetic change in the bacterial genome can have profound effects on virulence. Taken together, our results demonstrate that there has been recent clonal expansion and diversification of a subset of isolates classified as USA300. The findings add an evolutionary dimension to the epidemiology and emergence of USA300 and suggest a similar mechanism for the pandemic occurrence and spread of penicillin-resistant S. aureus (known as phage-type 80/81 S. aureus) in the 1950s.

National Post Published: Monday, February 04, 2008

The World Health Organization announced mystifying news last week: The garden-variety influenza virus H1N1 that periodically besets the world, and is doing so this winter, seems to be developing a startling new resistance to Tamiflu (oseltamivir), the first and most important of antiviral drugs for influenza.

That such a thing should happen is curious. No one bothers much with Tamiflu as a primary weapon of attack against the regular flu– at least not outside Japan, where aggressive marketing by a subsidiary of the global patent-holder, Hoffman-La Roche, has convinced the populace to more or less pop the stuff like candy. For flu programs in nursing homes and hospitals elsewhere, other antivirals come a lot cheaper and work just as well.