I don’t know if you’ve seen any of the posts here at Scienceblogs or Panda’s Thumb about the Discovery Institute’s newest protÃ©gÃ©, Dr. Michael Egnor. A professor of neurosurgery at SUNY-Stony Brook, Dr. Egnor has been pontificating on how “Darwinism” has nothing to offer to medicine; and indeed, that evolutionary biology has “hijacked” other fields of study. Mike has already aptly pointed out many of Egnor’s strawmen and intellectual dishonesties, so I won’t review them all. I’ve stayed out of the fray until now because I’ve had limited time and others have been handling it quite ably, but he keeps treading into (and butchering) my territory, so I just wanted to point out a few other things Egnor is waving away when he makes statements like this:
Preventing the emergence of resistant strains of bacteria is important work, but the insight that Darwinism brings to the problem — the unkilled ones eventually outnumber the killed ones — is of no help. We can figure that out ourselves. The tough work on preventing the emergence of resistant bacteria is done by microbiologists, epidemiologists, molecular geneticists, pharmacologists, and physicians who are infectious disease specialists. Darwinism, understood as the view that “chance and necessity” explains all biological complexity, plays no role.
Others have already addressed the blatant ignorance of this statement (spouted following a paragraph wherein he claims that the evolution of antibiotic resistance is just a tautology), so I’m actually going to leave the antibiotic resistance stuff alone for the time being. What I want to address instead are other areas where evolution is critical for insights into many of those fields Egnor mentions, especially since my own research is at the convergence of the first three he lists: microbiology, epidemiology, and molecular genetics.
Continue reading “Egnor just doesn’t know when to quit”
Influenza season is wrapping up here in the United States, and it seems so far that the 2006-7 season was pretty typical. The first cases of the disease were reported in late October, and cases were sporadic throughout November and early December. After increasing a bit in mid-late December of 2006, outbreaks declined slightly in January, and then picked up again later that month, increasing again in February before falling again, and continuing to do so in March. Early reports suggest that the vaccine matched the circulating strains pretty well, and that most of the isolates which were subtyped were serotype H1 influenza A viruses. Via the CDC, we can see the influenza outbreak and types of virus in the figure below:
What about H5N1? And pandemic influenza in general? More on that after the jump.
Continue reading “Influenza: the year in review, and looking forward”
Mycobacterium tuberculosis infection is as old as civilization. The bacterium infects approximately a third of the world’s population–roughly 2 billion individuals. It’s estimated that 8 million new cases are contracted each year–around a new infection every second. ~2 million individuals die as a result of TB every year. The bacterium also plays a prominent role in the history of microbiology: it was on March 24, 1882, that Robert Koch announced his discovery of the causative agent of the dread disease tuberculosis:
“If the importance of a disease for mankind is measured by the number of fatalities it causes, then tuberculosis must be considered much more important than those most feared infectious diseases, plague, cholera and the like. One in seven of all human beings dies from tuberculosis. If one only considers the productive middle-age groups, tuberculosis carries away one-third, and often more.”
Unlike many other feared infectious diseases of Koch’s time, TB still remains a significant killer worldwide, and its effect has only been exacerbated by the AIDS epidemic. However, a concentrated effort is being made to again attract attention to this bacterium.
Continue reading “World TB day 2007: “TB anywhere is TB everywhere””
I have a host of collected links and one-liner posts that I hoped I’d get to this week, but just didn’t have the time for. So, rather than let them collect dust any longer, I’ll put a number of “greatest hits” in microbiology and public health from the past week or so after the fold:
Continue reading “The week’s stories I missed”
Apologies for the blog silence again this week. Last week was a bit crazy and I’m still catching up for it. I have a write-up of last weekend’s evolution and intelligent design conference on the way, but before I attended that, I met up quickly for drinks and conversation with a few other Sciencebloggers. Left to right, The Intersection’s Chris Mooney, Evil Monkey of Neurotopia, me, and Orac of Respectful Insolence.
Check it out over at Scientia Natura.
When we think of the spread of antibiotic resistance between animals and humans, we tend to think of it going from Them to Us. For example, much of the research over the past 20 years on the sub-clinical use of antibiotics in animal feed has looked how this use of antibiotics as a growth promotant breeds resistant organisms in animals, which can then enter the human population via the food we eat. Along a similar line, I just mentioned Burt’s post post on cephalosporin use in cattle and the evolution of antibiotic resistance, where the worry is that use of these broad-spectrum antibiotics in animals will select for resistance that can then spread to humans. However, spread of resistant organisms is not a one-way street. For example, it has been suggested that transmission of methicillin-resistant Staphylococcus aureus (MRSA) has been transmitted both from horses to humans and vice-versa (see, for example, this Emerging Infectious Diseases paper). A new paper suggests that this phenomenon can happen even in animals that aren’t in such close contact with humans: chimpanzees.
Continue reading “Emerging Diseases and Zoonoses #26–Chimps at risk from antibiotic-resistant bacteria”
Just a reminder that there will be a symposium this weekend discussing evolution and intelligent design at Wartburg College in Waverly, Iowa. The event is geared toward those interested in matters of faith or science; teachers; principals; college students majoring in education, science and religion/philosophy; clergy; and parish educators. Scholarships are available for the first 200 K-12 educators, board of education members, school administrators, etc. who apply–still plenty of those left, so if you know anyone who’d be interested, point them in our direction. I’m including the text of one press release below the jump; all the information (including registration and hotel) can be found at the symposium website.
Continue reading “Nothing to do this weekend?”
I was out yesterday, and as such missed Lynn Margulis’ blog tour stop at Pharyngula. For those who may not be familiar with Margulis, she’s a professor at the University of Massachusetts, Amherst, and was the one who pushed the (now accepted) idea that chloroplasts and mitochondria in cells came about due to symbiosis. In the post announcing her impending arrival, there were lots of questions about her stance on HIV/AIDS. This is mostly due to a review she co-authored on Amazon of Harvey Bialy’s biography of HIV denier Peter Duesberg. The review ends: “As both Bialy and Duesberg emphasize, let us see the research results of those who show that cancer is ’caused by an oncogene’ and that ‘AIDS is caused by the rapidly mutating HIV virus’. Please point us to the published evidence.”
However, since this review was co-authored, it was uncertain how much of this was Margulis’ view alone. She answers that at Pharyngula; I’m going to quote it in its entirety here because it’s just so incredible:
Continue reading “Margulis on HIV/AIDS”