Tuesday, December 27, 2005 

Last grand rounds of '05

...is up a The Health Care blog. Still mostly out of internet contact for a few more days, so check out the best of 2005 over there!

Saturday, December 24, 2005 

Population-based surveillance for MRSA

NHANES is an abbreviation that's quite familiar to epidemiologists of all stripes: the National Health and Nutrition Examination Survey. This survey dates back to 1956 with the passage of the National Health Survey Act, providing legislative authorization for "a continuing survey to provide current statistical data on the amount, distribution, and effects of illness and disability in the United States." Generally, information from these surveys has been used to look at the effect of nutrition, particularly micronutrients, on the health status of the population, or subgroups within the population. However, survey data and biological samples obtained from those enrolled in these studies can be used for other purposes as well—-and one recent study took advantage of this. A new publication by Kuehnert et al. uses NHANES samples to examine colonization with Staphylococcus aureus. As with many pathogens, a significantly greater number of us are asymptomatic carriers of this bacterium than are sickened by the pathogen. Additionally, strains of S. aureus that is resistant to the antibiotic methicillin (methicillin-resistant S. aureus, MRSA) appear to be increasing in prevalence in the community. I say, “appear to be,” because no good, population-based study had been carried out to date. This new study begins to fill that void.

Samples from 9,622 people enrolled in the NHANES study in 2001-2 were examined for S. aureus colonization; almost a third (32.4%) were found to be positive. Extrapolating to the U.S. population, that means that almost 90 million people are colonized with this pathogen. Prevalence was found to be highest in the 6-11 year age group, and males were slightly more likely to be colonized than females.

75 of the S. aureus-colonized individuals were carrying MRSA--.8% of the population, or about 2.3 million Americans. In this analysis, MRSA was found more frequently in older age groups, and in females. However, when community-acquired MRSA (in contrast to nosocomially—or hospital-acquired—isolates) were analyzed separately, the groups most at risk again were young children and African-Americans. As previous studies have shown that those who are colonized are at a higher risk of subsequent MRSA disease, this puts a significant amount of our population--and particularly, our children--at risk of developing serious disease due to this bacterium, which is extremely difficult to treat.

Additionally, MRSA disease in individuals who have no nosocomial exposure has increased in the past several years. Since the data from this study comes from samples taken in 2001-2, these results can be compared to more recent data. For example, other studies conducted at various sites in 2001 found MRSA prevalence rates of .6-2.8%. However, by 2004, a study of 500 healthy children using identical methods found colonization rates of 9.2%, an increase of greater than 10-fold in that community. Likewise, a 2004 study of youths in San Francisco found a MRSA colonization rate of 6.2%, and a Texas study earlier this year reported a 22% MRSA colonization rate. Certainly with these numbers, the increasing find of community-acquired MRSA becomes much less surprising. The bad news is, we don't currently have a way to keep this from increasing even further, and there are few options in the pipeline as far as treating MRSA. A vaccine is in the works, but clinical trials--for both vaccines and new drugs--take time and money. Meanwhile, thousands of people worldwide are dying from this pathogen each year. As usual, the best prevention is simply to wash your hands and generally practice good hygiene--something to keep in mind while you gather with your loved ones during this holiday season.

Cheers, and have a good one--I'll be out for a few days with the kiddos and extended family myself.

Friday, December 23, 2005 

Those who do not learn from history...

My favorite essay arguing against intelligent design isn’t one of Gould’s, or Dawkins’, or Sagan’s. Rather, it’s one that has portions I disagree with, but the eloquent prose simply can’t be beat:
"The analogy which you attempt to establish between the contrivances of human art, and the various existences of the Universe, is inadmissible. We attribute these effects to human intelligence, because we know beforehand that human intelligence is capable of producing them. Take away this knowledge, and the grounds of our reasoning will be destroyed. Our entire ignorance, therefore, of the Divine Nature leaves this analogy defective in its most essential point of comparison.

You assert that the construction of the animal machine, the fitness of certain animals to certain situations, the connexion between the organs of perception and that which is perceived; the relation between every thing which exists, and that which tends to preserve it in its existence, imply design. It is manifest that if the eye could not see, nor the stomach digest, the human frame could not preserve its present mode of existence. It is equally certain, however, that the elements of its composition, if they did not exist in one form, must exist in another; and that the combinations which they would form, must so long as they endured, derive support for their peculiar mode of being from their fitness to the circumstances of their situation."
These come from an 1814 essay by Percy Bysse Shelley, analyzing the claims in William Paley's Natural Theology, a text which explores arguments very similar to those used by modern-day ID advocates. So similar, in fact, that although some of the minor details have changed, Shelley's refutation of it can be easily used today.

As this essay demonstrates, and as recently highlighted in this post, it behooves us to know our history—and none know this better than those who teach the subject. University of Iowa history professor Douglas Baynton wrote an interesting letter to the Washington Post this past Saturday, offering a unique perspective on the “controversy” regarding Intelligent Design by using 19th century geography texts to speculate about how a course using intelligent design might look. He cites three precendents: “Physical and Intermediate Geography” (1866), the 1873 “Physical Geography,” and “Elements of Physical Geography” from 1868. Baynton writes,
These textbooks seem also to have been intended to provide solace for the existentially anxious. All of them offered in one form or another the reassurance that “Geography eaches us about the earth which was made to be our home.” Earth by itself “could not be the abode of man,” advised one. “Therefore, two indispensable agents are provided—the sun and the atmosphere.” The entire vast history of the planet was summed up as the “gradual formation by which it was made ready for the reception of mankind.” The lay of the land had been thoughtfully arranged for our benefit: “As the torrid regions of the earth require the greatest amount of rain, there are the loftiest mountains, which act as huge condensers of the clouds.” Because the breezes that blew down mountainsides cooled the inhabitants below, the highest were located in the hottest pars of the world “for the same reason that you put a piece of ice into a pitcher of water in summer, rather than in winter.”
Of course, these are very similar to the arguments put forth in Natural Theology and a number of other texts over the centuries, reviewed briefly here.

Baynton continues,
Another book explained that all the plants and animals that lived and died for eons did so precisely because humans, during their industrial era, would need the coal. The author observed that “the wisdom of this Plan is further recognized in the fact that the coal is found, mainly, in those parts of the earth that are best fitted for human habitation—in the United States, Great Britain, Western Europe, British America, and China.”
I wonder what these same authors would say today if they were aware of our efforts to extract oil in the Gulf of Mexico, Siberia, Alaska, etc.-—not exactly the best fit areas for human habitation. This is the problem with correlating religious ideas to natural phenomena, and assigning purpose in a scientific setting. One may be able to make a theological argument outlining what God’s Plan is, but it’s not a scientific endeavor. Baynton notes this:
Design arguments…reverse such practical explanations, replacing natural causality with supernatural predestination. In doing so, useful answers that open up further questions are replaced by answers that are emotionally satisfying but intellectual and practical dead ends. After all, once you know that mountains exist because they were meant to exist, what is left to do but sit in your armchair and mediation on the wisdom of their design?
And this is a big reason why scientists are so frustrated with intelligent design—it doesn’t provide us with anything useful. When ID advocate Guillermo Gonzalez was asked at his talk at the University of Northern Iowa what the practical applications of ID were; how it could be used in a practical sense to explore avenues not possible with current scientific methodology? He answered (paraphrasing) that it was "a truth that can be known, leading us to ask more questions and examine the evidence more carefully"--but that's something scientists do, anyway. And sure, who can disagree that the pursuit of truth is a noble thing? But ID is not a scientific truth. It is a religious conjecture, identical to those pointed out by Baynton. Consider, for example, Gonzalez’s thesis in “The Privileged Planet:” that habitability and observability must correlate, because God (oops, The Designer) meant for us to be able to see the magnificence of the Universe. Isn’t this just as silly, and just as arbitrary, as the idea that coal was placed in the specific spots on this earth that “were most fit for human habitation?” Additionally, how does one ascertain the motivations of this mysterious Designer—-the central tenet of The Privileged Planet and other ID writings-- without first knowing their identity; a question which Discovery Institute Senior Fellow Johnathan Witt notes here, is religion.

I suppose, however, that my suggestion that the premise of Gonzalez’s book is silly will be construed as a personal attack. A recent EvolutionNews article regarding a seminar led by Iowa State University professors Hector Avalos, Jim Colbert, and Michael Clough titled “Why the Overwhelming Consensus of Science is that Intelligent Design is not Good Science” contains another Gonzalez assertion that “Avalos and the other critics of ID on campus have to date resorted to misrepresentations of ID and personal attacks on me.” Rather ironic, considering Gonzalez's own attacks and accusations of lying, and the fact that ID is, in essence, little more than a giant misrepresentation of evolutionary theory.

Additionally, Witt complains that the authors of the Iowa State Daily article gave Gonzalez only one sentence: as they mention, “one sentence for the man at the center of the Iowa State controversy,” and call it “fishy.” My, my, what egos—and a bit of misrepresentation of their own. Though they’ve spun all of the activity in Iowa as an attack on Gonzalez, not once in the petitions that over 400 Iowa faculty signed is there a mention of “the man at the center of the Iowa State controversy.” It’s not an attack on Gonzalez, or Fred Skiff, or any other Iowa faculty who may support intelligent design. The Discovery Institute tries to play this as an “academic freedom” issue: that by criticizing ID, we’re scientific “McCarthyites”. So, where is *our* academic freedom to say that we feel ID is a load of garbage? No one has said Gonzalez shouldn’t be able to research ID, should he actually manage to find some way to do so. No one has said he can’t believe in it. No one has questioned his credentials as an astronomer. What has been said is that we don’t believe that ID is suitable for teaching in science classes, and that ID “theory” is intellectually vacuous. It’s a dead end. ID proponents have repeatedly said it’s not a theory of mechanism, so even once it has been established that something has “been designed,” there’s no way to determine *how* it was designed; and it’s a question of theology, not science, to ask “why” The Designer created it that way.

Baynton ends his essay with the thought:
The details have changed, but the fundamental habits of thought at issue have not. Do we want children to learn what is currently known and, more important, what remains to be discovered, about the physics of planetary motion? Or rather should they learn that “As the earth is round, only half of it can be lighted at once. In order that both sides may be lighted, the Creator has caused the earth to rotate”?
It may be, as Baynton notes, a solace to think that this is the explanation for the Earth’s rotation. It may even be a correct explanation; I’m not in a position to say. But either way, it’s a theological stance, not a scientific one.

A quote from Patrick Hazard states, "History in our kind of society is not a luxury but a necessity." Perhaps if more people were aware of the history of intelligent design "theory," less time would be wasted working to keep it out of science classes.

[Note: I'd planned to post this Tuesday, but didn't want it to get lost in all the Dover issues. I think, given the decision and the role the history of the ID movement played in that, it's even more relevant today that this history is considered.--T]


(Geography image from http://users.erols.com/ziring/povray.htm)

Thursday, December 22, 2005 

Iowa Academy of Science supports Dover decision

IAS president Paul Bartelt has a piece in today's Des Moines Register.
Respect religious beliefs, but don't teach them as science
Proponents of intelligent design are working in many states to legally incorporate ID into the science curricula of public schools. On Tuesday, however, U.S. District Judge John Jones ruled that ID is not science and cannot be taught in Dover, Pa., public-school science classes. The Iowa Academy of Science agrees with this decision.

The Dover trial made it very clear that the arguments of ID are not scientific, and the basic message of ID is the same as young-earth creationism: Evolution is wrong, and a literal interpretation of Genesis explains everything we see in our world. The argument of ID that there is an "intelligent designer" behind the universe may be a good theological topic, but it has no place in science classrooms.

***

The Iowa Academy of Science and the science community, in general, respects religious belief and has no intention of diminishing religion in society. Central to the academy's mission, however, is to educate Iowa's citizenry about science. Science hasn't all the answers to questions about life on earth, but evoking a supernatural explanation, as ID advocates, will not advance our understanding of our physical world.

ID proponents press school districts to provide "equal time" and to "teach the controversy." Even on the campuses of Iowa's universities, discussions are being held on whether or how to teach ID.

Americans place a high value on fairness, and providing equal time for ID seems only fair, right? The Iowa Academy of Science has high regard and respect for the value placed on fairness; however, it is not that simple. ID proponents would have science teachers recognize a deity "behind the universe." If so, to be fair (and constitutional), teachers would have to include discussions about the many different deities revered by human societies. Our government cannot give preference to any one religion, including Christianity.

What many people do not understand is that within the science community, there is no controversy about evolution. The controversy is among the general public.

Entire text available at the link.

 

Mike Argento weighs in

One of the best commentators on the Dover trial (IMO, of course) was local reporter Mike Argento, of the York Daiily Record. (Previous posts on his stories here and here.) He has a new story on the final "smackdown" here.
Just wait until Pat Robertson gets a load of this.

If you thought the election and the removal of that inflamed boil on democracy that was the Dover school board had doomed Dover to an eternity of perdition, filled with pain and suffering and the lamentations of the damned echoing over a Muzak-like soundtrack of Britney, Clay and other soulless pap, you ain't seen nothing yet.

You should take a few minutes - well, an hour or so - to read federal Judge John E. Jones III's ruling in the case of Kitzmiller v. Dover.

If the election convinced Robertson that Dover will fall into the hands of Satan, he will most certainly interpret the judge's ruling as a sign that Armageddon is truly upon us.

It was telling that, moments after Jones' ruling landed, Dover was beset upon by a plague of locusts, poisonous toads rained from the sky and some obsequious jerk from Fox News arrived in town to interview residents about their role in the coming apocalypse.

OK, none of that happened, except for the Fox News thing.

Dover is once again driving the national SUV down the highway to hell by, as Robertson has famously said, turning its back on God. And now the judge is providing the map.

If only national reporters covered science with his combination of humor and a no-holds-barred bullshit detector...I can dream, I guess.

Wednesday, December 21, 2005 

So, is it over?

One question I received from a reporter yesterday asked, essentially, if the fight against intelligent design is over with yesterday's decision. MSNBC has an article along a similar theme today, and those interviewed in the article say the same thing I did: it ain't over by a long shot. (PZ has some similar sobering thoughts on the topic). While I do think the decision handed down yesterday will make it more difficult for anyone contemplating introducing ID into the classroom, as suggested in the MSNBC article, all that means is that the focus will have to shift a bit. I suspect we'll see more of "teach the controversy" and less push to teach intelligent design--something the Discovery Institute has already moved to, anyway.

Additionally, while ID has been the major thorn in the side of pro-science groups, it's obviously not the only bad science out there: just the best-funded. As discussed a few days ago, we still have huge challenges to deal with regarding science education in this country--and ID is but one facet of that. We still have groups that regularly spew misinformation about HIV/AIDS, vaccination, global warming, etc.--and certainly, the evolution deniers won't be going away. Answers in Genesis is working on their "creation museum", the Discovery Institute is still crying about the decision, and certainly ID proponents around the country are going to regroup and work on a revised strategy. This isn't something that's going to go away, and it's not time to rest on our laurels.

My central passion has always been working to teach good science, and get both students and the general public interested in and educated about scientific topics--and that won't change just because we've achieved a major victory against one faction of the anti-science movement. Thus, while I whole-heartedly salute and appreciate the efforts of all of those involved with this trial, the fact remains that we still have much more work to do. I hope many of you who've become interested in these issues during the Dover trial will stick with us as we deal with future challenges as well.

 

Kitzmiller decision--required reading

Okay, after going through the whole Kitzmiller decision last night, and damn, it's good. Really, incredibly good. This should be required reading. Jones' disgust at the whole thing comes through loud and clear. On page 29:
Although proponents of the IDM (Intelligent Design movement) occasionally suggest that the designer could be a space alien or a time-traveling cell biologist, no serious alternative to God as the designer has been proposed by members of the IDM, including Defendant's expert witnesses.
He discussed this at length, clearly connecting the dots between the Discovery Institute, the Wedge Document, Pandas and People, right up to the Thomas More law center and the Dover school board. On page 31,
A "hypothetical reasonable observer," adult or child, who is "aware of the history and context of the community and forum" is also presumed to know that ID is a form of creationism...The evidence at trial demonstrates that ID is nothing less than the progeny of creationism. What is likely the strongest evidence supporting the finding of ID's creationist nature is the history and historical pedigree of the book to which students in Dover's ninth grade biology class are referred, Pandas. Pandas is published by an organization called FTE, as noted, whose articles of incorporation and filings with the Internal Revenue Service describe it as a religious, Christian organization. Pandas was written by Dean Kenyon and Percival Davis, both acknowledged creationists, and Nancy Pearcey, a Young Earth Creationist, contributed to the work.

As Plaintiffs meticulously and effectively presented to the Court, Pandas went through many drafts, several of which were completed prior to and some after the Supreme Court's decision in Edwards, which held that the Constitution forbids teaching creationism as science. By comparing the pre and post Edwards drafts of Pandas, three astonishing points emerge: (1) the definition for creation science in early drafts is identical to the definition of ID; (2) cognates of the word creation, which appeared approximately 150 times were deliberately and systematically replaced with the phrase ID; (3) the changes occurred shortly after the Supreme Court held that creation science is religious and cannot be taught in public school science classes in Edwards.
The Pandas book was definitely a slam-dunk, though many other factors clearly contributed as well: the history of the decision by the Dover board to have their teachers announce the disclaimer, and the adoption of the Pandas book as an "alternative" text (and the lies that were told about it during the trial); the Wedge document; Behe's arrogant testimony (dissected further at Pharyngula); and the overwhelming view from the community that ID was indeed religious, as measured by opinion letters in the local newspapers. The latter is something that could be very important in any future trials of this nature: even if the proponents are careful to say that the designer in ID can be "a time-travelling cell bioloist" or whatever, the community is going to be more vocal in their belief that ID is a religious idea, and the designer is God.

This, truly, has given those of us who've been fighting ID a "merry Kitzmas."

Edited to add: Ed and Burt's Skeptic article about the trial has been released here with some more "behind the scenes" material. Check it out. Additionally, for a one-stop-shop of links to discussion of the trial and the decision, check out The Questionable Authority.

Tuesday, December 20, 2005 

New Grand Rounds

This week's Grand Rounds is up over at Medpundit. Lots of good stuff. If that doesn't keep you busy, check out DarkSyde's inteview with Chris Mooney over on DailyKos. Busy today, but I'll have more up tomorrow.

 

Victory!

Plaintiffs Prevail
The much-awaited decision in the Kitzmiller et al. v. Dover Area School District is now available.

The 139 page document finds for the plaintiffs.

Judge Jones finds that “intelligent design” is not science. The DASD ID policy violates both purpose and effect prongs of the Lemon test, and also violates the Pennsylvania constitution.

Much more here, here, and here, and I'm sure more will follow. (Update: Ed has a "thank you" list here, and Mike mentions others here. As someone who got to watch a bit behind the scenes, there was definitely an amazing amount of work that went into this case--and what I saw was only the tip of the iceberg. Kudos to everyone involved.)

Haven't read the (139 page!) decision yet--perhaps my reading for tonight.

Update: Discovery Institute pans the ruling, calls Jones an "activist judge:" link. Funny that Jones was appointed by GW...

Monday, December 19, 2005 

Bill Maher and his anti-vaccination claims. Again.

Bill Maher has again discussed his anti-vaccination views, this time on Larry King. Among other claims, Maher says that polio was wiped out due to better sanitation, and that getting the flu shot increases your chances of developing Alzheimer's. Orac has more detail on the claims and the dubious source of the "Alzheimer's/flu shot" link. I wonder how Maher would explain the decrease in African measles that's followed an increase in measles vaccination there?

Funny how so many of these people who label themselves "skeptical of Western medicine" (including Maggiore and her brand of HIV-deniers) don't apply that same skepticism to their "alternative health" claims. Maher decries vaccination, a cornerstone of modern public health, by apparently spouting the unlikely claims of an seemingly disgraced MD. Maggiore et al/ say HIV doesn't cause AIDS, and instead of treatments shown by medical science to be effective, she advocates homeopathy and nebulous "toxin elimination" as a healthy alternative. No wonder it's so hard to get young people in the U.S. interested in science; it's all just a big conspiracy and we're always wrong anyway, so why bother?

 

Breakthroughs in progeria research

Progeria, (officially, "Hutchinson-Gilford Progeria Syndrome"), is a rare fatal disease that makes the victim appear, as the name suggests, prematurely old. Although these children are born looking healthy, onset of the disease occurs around 12-24 months, affecting about 1 out of 4 million children. Symptoms include growth failure, hair loss, and other diseases of aging: atherosclerosis and stroke, arthritis, hip dislocation, aged-looking skin. Most children die of heart disease by the age of 13; life expectancy averages between 8-21 years. (A marked contrast to the story of Brooke Greenberg, a 12-year-old who still looks like an infant).

First described over a hundred years ago, progeria is caused by a mutation in the LMNA gene. This gene produces the Lamin A protein, which is the structural scaffolding that holds the nucleus of a cell together. It's thought that this mutation makes the nucleus unstable, leading to premature aging seen clinically. It was reported earlier this year that a class of anti-cancer drugs called farnesyltranferase inhibitors may help children with this condition. In tissue culture, these drugs finish a job that is blocked in progeria patients--snipping off a farnesyl group thought to somehow "gum up the works" in the cell and lead to progeria. Now, new research suggests possible reasons for this "gumming."
One study found that some of the lamins turn up in the wrong place—too tightly linked to the membranes of the nuclear envelope to participate properly in key stages of cell replication.

The researchers said this would disrupt DNA replication, and be a likely factor in the rapid march of cells toward premature “senescence,” a cellular version of aging. Whether similar missteps and miscues by nuclear lamins are part of normal human aging is the question that draws researchers onward, said Goldman. But the findings are consistent with a widespread belief among biologists that a key cause of ordinary aging is damage to DNA and mistakes in gene replication, two interrelated problems.

Another study found that the most common type of mutant lamin re-organizes regions of chromosomes that are key in controlling gene expression. These portions of chromosomes, known as heterochromatic regions, are kept inactive for various reasons; for example, one of the two female X chromosomes is deactivated in this fashion in order to avoid having them duplicate their work.

One of the hallmarks of the X chromosome heterochromatic region is that it is linked to molecules known as methylated histones. But the researchers found that in a girl with the progeria syndrome, the quantities of these molecules and of an enzyme required to form them were abnormally low.
It's often said that funding for research is unbalanced. Why do we spend so much money on a disease that only affects a relatively few people? Why isn't more money spent on heart disease and stroke, leading killers in the U.S., for example? If heart disease causes, say, a third of all deaths, shouldn't it get a third of the research dollars? This case shows why it shouldn't be quite that simple. Progeria is a rare disease, affecting only a handful of children in this country--but research in this area may lead not only to treatment and/or prevention of progeria, but also to a better understanding of the molecular mechanisms that cause us all to age. You simply don't know where the next brilliant insight is going to come from, whether it be specific disease-related research, or your morning breakfast cereal.

 

Persons of the year

Time names Bono, Bill and Melinda Gates Persons of Year
Bono is a co-founder of the DATA (Debt, AIDS, Trade, Africa) organization, which fights poverty and HIV in the developing world. From that organization was spawned the ONE Campaign to Make Poverty History.

"It has been a great year for global health to get more visibility," Bill Gates said Friday. "The more people know about it, the more they want to act."

The magazine said that while sudden disasters grab the headlines, other tragedies unfold daily.

"And who is proving most effective in figuring out how to eradicate those calamities? In different ways, it is Bill and Melinda Gates, co-founders of the world's wealthiest charitable foundation, and Bono, the Irish rocker who has made debt reduction sexy," Time's managing editor Jim Kelly writes.

In January, the Bill and Melinda Gates Foundation committed $750 million to improving access to child immunizations, accelerating introduction of new vaccines and strengthening vaccine delivery systems.

The foundation focuses on education, global health, improving public libraries and supporting at-risk families, according to its Web site.

2004's Man of the Year: George W. Bush. I think Time made a better choice this year; kudos to them for emphasizing global health and poverty.

Sunday, December 18, 2005 

Doonesbury does ID

Link



This illustrates nicely what *should* happen, but alas, all that antibiotic resistance stuff is only "microevolution," which even most die-hard young earth creationists (YECs) can accept:
so, no second-thoughts about using modern medicines or vaccines that were developed using evolutionary principles. They just say that the evolution of antibiotic resistance is "evolution within the kind," which is peachy-keen. Of course, no one can say exactly what a "kind" is, and whether it's along the same lines as a "species," "genus," "family," etc. They obviously can't base it just on DNA similarity, either. Though what they will affirm, of course, is that "my grandpa wasn't no monkey!"--but chimps and humans are about 98% similar on the DNA level, while even within a species of bacteria, 2 different isolates can share as little as 70% of their DNA sequences. So, while these 2 isolates of E. coli would certainly be the same "kind" (heck, often you hear of one single "bacterial kind"), the 98% similar humans and chimps are different "kinds."

You may think the IDists are better--but not really. At least the YECs are fairly consistent in their position, while some IDists won't even go on record as accepting an old earth; some have said they don't believe in common ancestry, while some, like Behe, have said they do--but, y'know, God (oops, The Designer) just tinkered with certain parts along the way. Even the examples IDists use--bacterial flagella, blood clotting--would be examples of "microevolution," which even YECs accept in theory, yet the IDists feel those scenarios couldn't have happened without some kind of external intelligent guidance.

*scientist head go boom*


Edited to add: PZ weighs in, touching on similar points. Sadly, I think he manages to attribute a silver lining to the situation. (Okay, maybe a bronze one). I *must* be sleep-deprived when PZ is more optimistic than I am, yikes!

 

Secret of surviving sepsis, say scientists

Infection is a complicated process. Every day, we're all carrying organisms that have the potential to kill someone. A recent article in the Journal of Infectious Diseases, for example, found that just under a third of us are colonized with Staphylococcus aureus, a leading cause of skin and soft tissue infections. From our noses, to our mouth, to our gut and elsewhere, we are literally teeming with organisms--so much so that, by the numbers, the cells in our body are more bacterial than human. But generally, we don't get sick. When epidemiologists investigate infectious disease, we consider a number of factors: the genetics of the pathogenic organism; the genetics of the host; environmental and cultural factors; host nutritional status; host immune status; and a plethora of other specifics which may affect development of disease. Still, when we discuss host genetics, we've mostly been looking at nuclear genes: those on our 23 pairs of chromosomes. An interesting study out in The Lancet today suggests that view is too narrow.

Recall that within our cells are organelles, each with a specialized function. One such organelle is the mitochondria, the "power plant" of the cell. Much evidence has been put forth that suggests these organelles evolved from bacteria, engulfed by primitive eukaryotic cells. As such, these organelles have their own DNA, separate from that in our nucleus. Differences in this mitochondrial DNA (mtDNA) has been previously shown to affect sperm motility, and to affect the risk of individuals for development of some late-onset neurodegenerative diseases. However, the current study looks at how differences in mtDNA can affect survival after sepsis (bacterial infection of the bloodstream).

Variations in the mtDNA were previously studied by the authors of the current study. By investigating single nucleotide polymorphisms (SNPs) in the mtDNA, they grouped people by mtDNA haplogroup (10 different ones were identified). Don't get confused with the terminology--basically, they just looked at changes, and grouped people together using the differences they found. One of these groups--haplogroup H--was found to be most common in their study population (41.3% of the population). They wanted to see if this had any bearing on survival after sepsis--if haplogroup H people survived more often than their non-haplogroup-H neighbors.

And, yep, indeed they did. Haplogroup H folks showed higher survival over 180 days than those without the haplogroup, and were a bit over 2 times more likely to survive to that point than those in other mtDNA haplogroups. They were also found to generate "a significantly higher core temperature" than those in other haplogroups--in other words, on average, they spiked higher fevers. This might sound like a bad thing, but a fever is actually one of the body's elegant defenses against infection: the increase in body temperature can slow the growth of , or even kill, some bacterial pathogens. Additionally, the increase in temperature also increases the rate of enzymatic reactions, increasing metabolism and speeding tissue repair. (The fever response is also one that's incredibly conserved, from an evolutionary standpoint. Even ectotherms--"cold-blooded" animals--create a "fever" by basking in the sun during an infection). It's not known if this higher fever temperature is the key to the differential survival in the groups, but it's an intriguing finding. It's also interesting to note that, though haplogroup H is the most common in the population, it's the most recently evolved. Could it have been selected for due to this, and potentially other, effect on infection mortality? Infectious disease has certainly played a role in shaping our genomes--for example, sickle cell carriers who are more resistant to malaria; or cystic fibrosis carriers who are more resistant to typhoid. This may be yet another example.

It should be noted that this was a fairly small pilot study--150 people were enrolled, so larger studies will be needed to see if this finding is repeated, and if so, just what the mechanism is that renders them more likely to survive. Definitely food for thought, and a reminder of yet another level of complexity to consider for those of us who seek to sort these kinds of things out.

Friday, December 16, 2005 

Avian flu in Malawi?

Avian influenza suspected in Malawi

Malawi dispatched blood and tissue samples to neighboring South Africa on Friday to be tested for avian influenza after thousands of migratory birds were found dead on a hill in the central Ntchisi district.

Agriculture officials expressed alarm after local villagers started scooping up the dead fork-tailed drongos -- known locally as namzenze -- to eat earlier this week in the district about 200km east of the capital, Lilongwe.

"Someone alerted police that people are feasting on mysterious manna from heaven," said Wilfred Lipita, director of livestock and animal health in the Ministr of Agriculture and Food Security. "We sent officials to caution the people not to eat them, since they may have the avian flu which has proved deadly to humans in other countries."

Note that it's not even certain yet that they died of influenza, much less the high-pathogenicity H5N1 strain. Still, H5N1 was said to be expected in northern and central Africa "within months"--and that was only at the beginning of December. I doubt anyone asked for avian flu in their stocking this year--hopefully Africa didn't get an unpleasant early Christmas present.

 

2005 Koufax nominations are open

Here. (ETA: OK, they went and closed that thread on me. Read the first one to see who's already been nominated, then post yours here.)

What are they? From the FAQ:
The Koufax Awards are held annually to honor the best of left-leaning bloggers. A "Sandy" will be awarded based on reader votes in each of a number of categories. It is like the Oscars for lefty bloggers, except that we do not allow overly long, overly sentimental speeches by the winners.

***

What is the purpose of the Awards?

There are three purposes of the Koufax Awards. First, as I wrote last year:

At its core, the Koufax Awards are meant to be an opportunity to say nice things about your favorite bloggers and to provide a bit of recognition for the folks who provide us with information, insight, and entertainment usually for little or no renumeration. The awards are supposed to be fun for us and fun for you.

The second purpose of the awards is to provide some exposure for blogs that you may have overlooked for some reason or another. There are lots of good blogs out there (more everyday) and no one can keep track of them all. We hope to call your attention to new blogs or blogs that deserve a chance to capture your attention. That is the reason for our policy of providing a link to every blog mentioned in the nomination process (despite the fact that assembling such links is an incredible amount of work). Please use those links to visit the blogs you have not previously read. You will not often regret it.

The most important purpose of the awards is to help build a sense of community between and among lefty bloggers and readers of lefty blogs. The awards provide an opportunity to say something nice about bloggers you like and to have something nice said about you. Please try not to take the idea of winning and losing too seriously. The primary rules of the contest are be nice and have fun.

There are 15 different categories, so check them out and nominate your favorite blogs. Last year, Panda's Thumb was up for best group blog, and Pharyngula was up for best expert blog--but neither took home (um, figuratively) an award. I'm compiling my list of faves to submit and spread around some love...

 

Napoleon lice 'n' mites

I've been meaning to blog this paper discussing evidence of louse-transmitted disease in corpses unearthed from Napoleon's army for a few days now, but haven't had the time to sit down with it. Now afarensis has saved me the work.

afarensis notes, however, that they extracted DNA from tooth pulp to amplify B. quintana (a louse-transmitted agent of trench fever), and says,

I will also be the first to admit that I have no idea how the DNA got into the pulp cavity in the first place...

Simple: via the bloodstream. Dental pulp is a living tissue, receiving a blood supply like any other tissue in the body—and any pathogens that are carried in the blood supply can end up there as well. Dental pulp is good for these ancient investigations because since it's surrounded by the tooth material, it's unlikely to be contaminated with other pathogen DNA, and it's more protected from decay and therefore a usable sample is more likely to be extracted. To my knowledge, this was pioneered by Michael Drancourt and Dider Raoult, both of whom are authors on the louse paper; the first publication on the technique was this one on Yersinia pestis DNA, which I'd not a half-hour ago mentioned in the comments to this thread. It's fascinating stuff--Drancourt and Raoult have also used it to examine B. quintana in a 4000 year old tooth, among other projects, which have significantly pushed forward the field of paleomicrobiology.

 

Did Macbeth have mad cow?

I love these historical analyses of disease--real, or fictional. One historical event that has been the subject of much speculation over the decades has been the Plague of Athens, a mysterious outbreak that is thought to have changed the direction of the Peloponnesian War, and for which the cause still remains uncertain:
[2] As a rule, however, there was no ostensible cause; but people in good health were all of a sudden attacked by violent heats in the head, and redness and inflammation in the eyes, the inward parts, such as the throat or tongue, becoming bloody and emitting an unnatural and fetid breath.

[3] These symptoms were followed by sneezing and hoarseness, after which the pain soon reached the chest, and produced a hard cough. When it fixed in the stomach, it upset it; and discharges of bile of every kind named by physicians ensued, accompanied by very great distress.

[4] In most cases also an ineffectual retching followed, producing violent spasms, which in some cases ceased soon after, in others much later.

[5] Externally the body was not very hot to the touch, nor pale in its appearance, but reddish, livid, and breaking out into small pustules and ulcers. But internally it burned so that the patient could not bear to have on him clothing or linen even of the very lightest description; or indeed to be otherwise than stark naked. What they would have liked best would have been to throw themselves into cold water; as indeed was done by some of the neglected sick, who plunged into the rain-tanks in their agonies of unquenchable thirst; though it made no difference whether they drank little or much.

[6] Besides this, the miserable feeling of not being able to rest or sleep never ceased to torment them. The body meanwhile did not waste away so long as the distemper was at its height, but held out to a marvel against its ravages; so that when they succumbed, as in most cases, on the seventh or eighth day to the internal inflammation, they had still some strength in them. But if they passed this stage, and the disease descended further into the bowels, inducing a violent ulceration there accompanied by severe diarrhea, this brought on a weakness which was generally fatal.

[7] For the disorder first settled in the head, ran its course from thence through the whole of the body, and even where it did not prove mortal, it still left its mark on the extremities;

[8] for it settled in the privy parts, the fingers and the toes, and many escaped with the loss of these, some too with that of their eyes. Others again were seized with an entire loss of memory on their first recovery, and did not know either themselves or their friends.
This plague has been attributed to bubonic plague, toxic shock syndrome and/or necrotizing fasciitis due to Streptococcus pyogenes or Staphylococcus aureus, Salmonella, yellow fever, malaria, Ebola, influenza, and smallpox, to name just a few. Typhus seems to fit the description best, but it's likely that a cause will never be known with certainty.

Another much-wondered-about historical disease is the English sweating sickness. The New England Journal of Medicine has an article on the sickness here for those of you with access:
In the summer of 1485, a rapidly fatal infectious fever struck England: "A newe Kynde of sickness came through the whole region, which was so sore, so peynfull, and sharp, that the lyke was never harde of to any mannes rememberance before that tyme."

Sudor Anglicus, later known as the English sweating sickness, was characterized by sudden headaches, myalgia, fever, profuse sweating, and dyspnea. Four additional epidemics were reported in the summers of 1508, 1517, 1528, and 1551, after which the disease abruptly disappeared. Contemporary observers distinguished the condition from plague, malaria, and typhus. Later suggestions included influenza, food poisoning, an arbovirus, and an enterovirus as possible causes.
(For the record, the authors suggest a rodent-borne virus, such as a hantavirus, as a potential causal agent.)

Historical diagnoses aren't limited to epidemics; historical figures are also fair game. Those of you familiar with the story of how Jeffrey Taubenberger eventually came to sequence the 1918 influenza virus probably know that it all began with an investigation of chemist John Dalton's eyeballs. Dalton was color-blind, and left instructions that, upon his death, his eyes be preserved and examined to figure out why he saw the world differently than everyone else. A 1995 Science paper found that Dalton was a deuteranope; that is, he had trouble discriminating small differences in hues in the red, orange, yellow, green region of the spectrum. And while Dalton may have wanted to know what ailed him, it's likely that Shakespeare never expected the suggestion made in this paper published almost 400 years after his death that the Bard had syphilis.

And don't think fictional characters and epidemics are off the hook just because, y'know, they're not real or somethin'. A 1989 Journal of the American Medical Association paper concluded that porphyria was the disease that caused the fall of Edgar Allan Poe's house of Usher. And a few years ago, a paper in Emerging Infectious Diseases explored the idea that Poe may have been inspired by Ebola or another hemorrhagic fever for his short story, "The Masque of Red Death."

Now, in the current issue of Clinical Infectious Diseases, Norton et al. suggest that Macbeth may be an account of an early prion disease.
Macbeth's descent into madness often elicits psychological interpretations, but he experienced neurologic and cognitive deterioration as well. This brings into question whether a psychiatric disorder alone could fully account for his condition. Any patient today, particularly one from Scotland, presenting with a similar rapid decline in neurologic, psychiatric, and cognitive function, accompanied (as in Macbeth's case) by involuntary movements, hallucinations, and insomnia, would require an evaluation for variant Creutzfeldt-Jakob disease.
They even have a whole table dissecting the passage, sign or symptom described, and prion diseases that share these symptoms. Does it get any better than this?

They continue,
Although we contend that Macbeth's presentation is compatible with a spongiform encephalopathy, no evidence corroborates that this is what Shakespeare intended. Nevertheless, Shakespeare showed an uncannily prescient understanding of prion disease transmission via exposure to neural tissues: "[Once], when the brains were out, the man would die / And there an end; but now they rise again / With twenty mortal murders on their crowns" (3.4.78–80). Conceivably, Macbeth was exposed to infectious prions during an early encounter with the weird sisters, whose necromantic brews contained a variety of human and animal organs. Proclaiming, "Round about the cauldron go / In the poison'd entrails throw," (4.1. 4–5), they added, for example, a human nose and liver tissues that are capable of carrying infectious prions. It is not clear that anyone consumed the witches' brews, but if Macbeth had, that could explain the exposure. Furthermore, Shakespeare foreshadowed current culinary controversies in prion disease epidemiology by warning his audiences to "eat our meal in fear" (3.2.17) until the time when "we may again / Give to our tables meat" (3.6.33–34). (A character in Twelfth Night declares "I am a great eater of beef, and I believe that does harm to my wit" [1.3.85–86]).

Just another reason to study those classics...you never know what you might glean from them.

Thursday, December 15, 2005 

New Ebola outbreak in African primates?

From ProMed:

Early reports of great ape mortalities from local people in the Cuvette-Ouest region of the Congo Republic are currently being investigated by a wildlife health team including Dr Alain Ondzie of WCS in coordination with government authorities and researchers in the area. If carcasses can be found, samples will be sent for diagnostic work to CIRMF/IRD network partners. The RoC Ministry of Health is mobilizing community outreach efforts while the wildlife investigation is underway.

This is in the same area where there was an Ebola outbreak earlier in 2005.
Ebola in African primates has been a real problem since about 2001. While, as I mentioned previously, human cases of the disease have been fairly minimal, primate researchers estimate that thousands of gorillas have died in the past decade from Ebola during outbreaks in Gabon and Côte d'Ivoire. In Gabon, gorilla sightings (or other evidence of their presence, such as dung and trails) decreased by 50% in a few short years; chimpanzee sightings decreased by 88%. Eight groups of gorillas that had been monitored by primatologists for 10 years disappeared completely between October 2002 and January 2003. Several gorilla carcasses that were found were positive for Ebola, suggesting this played a role in the population decrease.

I mentioned here that fruit bats may be a reservoir for Ebola, and that a hypothesis has been put forth that Ebola may be a plant virus. Gorillas are, of course, vegetarians; some species eat up to 200 different plant species. Chimpanzees are omnivores, but fruit and leaves still make up a large percentage of their diet. Again, this idea is still unconfirmed, but it's intriguing.

Refs and further reading:

Formentry et al., 1999. J Infect Dis. "Ebola virus outbreak among wild chimpanzees living in a rain forest of Côte d'Ivoire." 179S1:S120-126.

Leroy et al., 2004. Science. "Multiple Ebola virus transmission events and rapid decline of central African wildlife." 303:387-90.

Vogel, G., 2003. Science. "Can great apes be saved from Ebola?" 300:1645.

 

More than just a pretty face

Staphylococcus aureus. The name means, literally, "golden grape clusters." Upon staining, these round bacteria are visualized in clumps that resemble bunches of grapes. Every microbiology student is familiar with the most notorious member of the Staphylococcus species, S. aureus, which often produces a distinct yellow pigment when grown on agar plates containing blood. This bacterium itself causes a wide range of illnesses, ranging from food poisoning to deadly skin infections. Of great concern is the fact that strains that resist a number of antibiotics--including methicillin--have been increasingly isolated no only in hospital settings, but also in the community. Vancomycin-resistant strains have also been isolated, but are not yet widespread.

It was recognized almost 25 years ago that the S. aureus yellow pigment consists of a number of carotenoids, similar to those produced in carrots and other fruits and vegetables. Studies of these carotenoid pigments have revealed their free-radical scavenging properties, protecting cells and tissues from the damaging effects of free radicals and singlet oxygen. (In other words, they’re antioxidants). Interestingly, one mechanism by which phagocytic cells of the host immune system destroy pathogenic invaders is via release of reactive oxygen species. Do these bacterial carotenoids protect S. aureus against damage initiated by the host immune system?

This question was investigated in a paper published this summer in the Journal of Experimental Medicine. Here, they investigated a mutant in the crtM gene, a critical gene in the carotenoid biosynthesis process. crtM mutants lack pigment and do not produce carotenoid, but other than that, were similar to the wild-type bacterium. In vitro, the mutants were more easily killed by oxygen and hydrogen peroxide—but when the crtM gene was added back in on a plasmid, the bacterium could again resist oxidative killing at a level similar to the wild type.

Looking at this mutant in a mouse model of infection, they also saw that the mutant did not cause skin lesions as the wild-type isolate did, suggesting the carotenoid is important in vivo. Finally, they also transformed an isolate of group A streptococcus (Streptococcus pyogenes) not known to produce carotenoids with the plasmid carrying the crtM gene—causing the isolate to produce a faint yellow pigment. When they examined the lesion pathogenesis in mice injected with the wild-type and the crtM-positive isolates of S. pyogenes, they found that lesions formed were larger with the crtM-positive isolates. So, while the wild-type was already invasive, addition of the carotenoid gene made them even nastier.

I wrote previously about pili being discovered in gram-positive bacteria: once it’s found in one species, it begins a search in other, related, species—and indeed, pili have now been found in groups A and B streptococci, and will probably be found in other gram-positives. Likewise, carotenoid pigments were first investigated as an antioxidant virulence factor last year in the group B streptococcus (GBS, Streptococcus agalactiae). This is another gram-positive bacterium; clinically, it is an important cause of neonatal meningitis and other invasive infections. This bacterium also produces a carotenoid pigment that can give the colonies a slightly orange tinge. Interestingly, it was found that knocking out the gene that produces the GBS hemolysin cylE (a protein that breaks open blood cells, producing a characteristic clearing around a colony on a blood agar plate) renders the colonies both non-hemolytic and non-pigmented, though it’s not yet known whether this is a direct or indirect effect. Additionally, these cylE knockouts were reduced in virulence in a mouse model of infection and more easily cleared by the host. They were also more susceptible to oxidative damage in a macrophage killing assay—so, similar to S. aureus, presence of the carotenoid increases the virulence of the bacterium.

Previous studies examining the role that the GBS hemolysin plays in disease pathogenesis has focused on damage the hemolysin is able to inflict upon host cells. Investigating it from the angle of protection of the bacterium, rather than damage to the host, represents a shift in thinking about bacterial virulence. It also opens up a new avenue for antimicrobial targets—creating drugs to render the bacteria’s defenses inadequate, thereby allowing the host’s own immune clearance mechanisms to operate more effectively. Finally, it suggests that other microbes that produce antioxidant carotenoids or melanin, such as cystic fibrosis pathogen Burkholderia cepacia--an organism that is often notoriously difficult to kill once patients are colonized—and fungus Aspergillus fumigatus, the leading cause of fungal infections worldwide. The challenge here, of course, will be to design drugs that target these microbial carotenoids but are safe to humans. With this research, an observation that has been more of a curiosity and diagnostic determinant has become a possible way to get a handle on these important pathogens.

Tuesday, December 13, 2005 

Six years ago today

...I was suffering the worst pain I'd ever experienced. I arrived at the hospital a bit before 1AM, and spent the next four hours or so walking around in agony. By 5AM, I decided I was ready for some of the good drugs, but the nurse informed me it was too late--time for the real fun to start. My daughter was born at 5:23AM, December 13, 1999--five long grumpy days after her due date. I was supposed to have a final exam that day.

My daughter wasn't exactly, erm, scheduled--but no contraceptive is 100% effective. I'd just been accepted to grad school, married less than 6 months, and hello, baby on the way. Kids had always been in the long-term plan, and since where my husband and I grew up, 23 was practically ancient to have your first baby, we bought a crib, set up a nursery, and hunkered down to become parents. It occurred to me for all of a minute to postpone grad school, but I've always been up for a challenge, so never gave that option serious consideration. I admit, though, that it was unnerving to say the least to be sitting in class during the last trimester of my pregnancy, discussing every possible chromosomal and developmental abnormality that can happen during development, with outcomes ranging from mildly bad to, of course, fatal. *Not* recommended for the faint of heart.

Luckily, she had pretty good timing. A mid-December birth meant that I already had Christmas and New Year's off, so I didn't have to miss too much time in the lab. I took off exactly 4 weeks (though I made up the missed exam a week after she was born), then headed back to the lab. Since daycare was a huge financial burden on a grad student's stipend, we got creative. My husband had a 7-to-4 job, so I worked around that, going in a lot of weekends and generally staying home one or two days during the "normal" work week to cut daycare costs. Again, I was fortunate: I'd already worked in the lab for almost a year prior as a technician, so even though I'd officially been a grad student for only a few months, I was already independent in the lab and didn't need someone to watch over my shoulder--allowing me to be in there on a Sunday at 7AM or a Wednesday at 1AM and get my work done.

Being a parent and a graduate student ain't easy. Obviously, the money sucks--at that time, my stipend was just over $13,000/year, and then they took out more every month for parking and health insurance. At my school, the health care also was pretty terrible: incredibly, though well-baby checkups were paid for, infant vaccinations weren't even covered. To top things off, I had (make that *have*) pretty hefty student loan payments from undergrad. Nothing like using the ol' charge card for diapers and groceries.

Anyway, since Baby #1 was the model of cherubic perfection (as of course, everyone thinks their own children are), and since my husband and I both have siblings who are close to us in age and we wanted that for our own children, we decided to confirm the fact that we were, indeed, insane. Baby #2 came along toward the other end of my PhD. (He was right on time, and no test that day--I was scheduled to give a journal club presentation. I'd already passed the file along to someone else, "just in case.")

Postdoc ensues, then I get to move up in the world as an assistant professor. Though family issues have always been a worry, now is when it really starts to kick in. (See, for example, this discussion, or this horror story). Again, I'm lucky on one level--I'm not planning on having any more children, so I don't have to worry about pregnancy, or maternity leave, or any of that jazz. I don't need to stress and tear my hair out trying to find the "right time" to start a family, since I already finished mine during probably the least-recommended stage of my career. My daughter is in kindergarten and my son goes to preschool, so our childcare expenses aren't quite as horrible as they once were. My husband now has his own business, so if I need him to watch the kids for some reason, he's flexible. But like many women in all different kinds of careers, I still feel pulled in a million different directions, and still worry about how taking time out for my kids will impact my career, and how spending so much time at my job will affect my children.

I'm all too familiar with the arguments on both sides of the "academics and children" fence. "Overall, academics have it good." We're "spoiled, whiny complainers;" we "want it all and don't want to sacrifice job or family;" our "ambitions are too high, we should lower them" (especially true for women who want a satisfying family life); "hey, the system as it works now gave us quantum mechanics and the Internet, so why fix what ain't broken?" On the other side, "academia loses a lot of good teachers and researchers when it comes down to a choice between family and career"--and besides, "how would we con those naive, innocent grad students into aspiring to stay in academia without some kind of move forward on family issues?"

In the discussion referenced above, physicist Ann Nelson left this comment (which sums up my feelings pretty well, and having an authority say it is even better):
The problem is that most people ASSUME that a woman cannot be a good mother and a good scientist. So at work we always feel we have to prove ourselves and do extra so people don’t say “see, she can’t be serious about science because she is a mother”. Then women who do need to take some leave or some time to breastfeed or need to leave work to pick up a sick kid worry that this is going to lead their colleagues to assume they have lost their committment to science. The other side of the pressure and stress is caused by the very large number of people who assume that only a SAHM [stay-at-home mom] can be a good mother, and a career oriented woman must be some kind of neglectful mother who is having her kids raised by strangers.
So, yeah, there's this too--guilt from all sides. You're never good enough as a scientist because you have a life away from the lab. You're never good enough as a mother because you have a life away from the kids. Is this just our paranoia, or does it really represent what people think? Do people really *say* this to us? Rarely--but it does happen. More often, I'll read it somewhere: a comment from a scientist about other scientists with families, and how their priorities aren't in line (or, one of the more overtly insulting lines I mentioned above). Or I'll see or hear a similar comment from a SAHM who is sure I'm screwing up my kids' psyches by having a demanding career.

Anyway, I worry, and I stress, and at the same time, I make the most of it. By all reports, my kids are doing great in school, both academically (well, as academic as kindergarten and preschool get) and socially. I've been here for almost a year now, am currently working on getting some more manuscripts submitted, and think I've had a pretty productive year. Things aren't going quite as swimingly in the lab, but I'll be starting at least 2 new projects after the new year, which will (hopefully) mean more papers and more grants, potentially by this coming summer. Next fall will bring more teaching duties, but it's a course I've taught before, so at least I'm not quite starting from scratch. In between, there will be birthday parties, and trips to the park and the lake, and Disney movies, and ice skating. And lots of creature-catching: we currently have about 5 wolf spiders in various jars around the house, and a small frog she caught in the creek out back in late fall as "pets." And yes, it will probably mean a few weekend mornings spent coloring in Mom's office while I finish up some work. If they need therapy as adults because of this horrible treatment, maybe I'll chip in for half.

Happy birthday, baby girl. I hope that 20 years down the line, the idea that you have to make a choice between your dreams and your family will seem a backwards and archaic notion, and that you go as far as you want along whatever path you choose. I may have to come with a journal article and highlighter in hand, but I'll be there, cheering you on.

 

Everything old is new again

...as Nick Matzke reveals.

I'm sure some of you paid attention to the goings-on in Cobb county, Georgia, earlier this year. To sum up, evolution-deniers had placed the infamous "evolution is a theory, not a fact" disclaimer sticker on biology textbooks in the district. Other parents sued to have them removed. In January, U.S. District Judge Clarence Cooper said that the sticker violated the Establishment Clause of the First Amendment--bye-bye stickers. The ruling was appealed, and the hearing for that appeal is scheduled to be held later this week.

So, now what you're up to speed, check out Nick's finding: a 1925 quote from the LA Times discussing evolution as a "theory, not a fact." Man, can't *anyone* on their side come up with some new material?

Monday, December 12, 2005 

Whole hog analysis of emerging diseases

As I've mentioned a bunch of times now, I work with the Center for Emerging Infectious Diseases here at the U of Iowa. Our primary focus is zoonotic diseases (diseases which are transmitted between species), and being in an agricultural state, we have a special interest in pathogens of agriculture. A new analysis by Mark Woolhouse and Sonya Gowtage-Sequeria in the journal Emerging Infectious Diseases has taken a closer look at the origin of zoonotic diseases. By the numbers:
  • Of the 1407 human pathogen species, 816 (58%) are known to be zoonotic.
  • Of the 177 emerging or reemerging pathogens, 130 (77%) are known to be zoonotic.
    • Therefore, zoonotic pathogens are disproportionately likely to be associated with emerging and reemerging infectious diseases.
First, they looked to see *what* is driving the emergence of these pathogens--what factors are causing them to "emerge?" They came up with a number of variables, and ranked them by the number of pathogen species associated with them:
  1. Changes in land use/agricultural practices
  2. Changes in human demographics and society
  3. Poor population health
  4. Hospitals and medical procedures
  5. Pathogen evolution (e.g., antimicrobial resistance, increased virulence)
  6. Contamination of food or water supplies
  7. International travel
  8. Failure of public health programs
  9. International trade
  10. Climate change
There's both good and bad in the ranking. The top two factors both give us many areas in which to intervene and prevent the emergence of additional pathogens. Agricultural practices can be analyzed to see exactly what it is that leads to disease emergence (crowding, new animals brought in and out, etc.), and this can be somewhat controlled. I'd guess demographics of humans are similar--more people in big cities and living in crowded conditions are great breeding grounds for new diseases. It's a challenge, but not as tough to deal with as climate change or poor population health. A real criticism is that, of course, the drivers of emergence to look at in the first place were chosen based on things the authors already assumed played a role in disease emergence, and we may be either missing something or falsely inflating one factor, but it's a start.

Breaking it down by groups of organisms, this association (between emerging disease and zoonotic pathogens) is strongest for bacteria and fungi, less so for viruses and protozoa. (The other category, helminths--parasitic worms--are already almost all zoonotic anyway, and very few are considered emerging or reemerging). Ungulates (hoofed mammals--deer, horses, swine, etc.) were found to be the most important species overall, see figure below. So, thus far, we have 1) importance of agricultural practices, and 2) hoofed mammals (including many you'd find on a farm). I have a feeling this paper is going to be oft-cited in our future grant proposals.

They next grouped the pathogens according to host range, and found that greater than 40% of the pathogens with the broadest host range (3 or more types of nonhuman host) were emerging or reemerging:



Finally, they looked at transmissibility. Most zoonotic pathogens aren't easily transmitted between humans--humans are either a "dead-end" host, or minimal human-to-human transmission occurs. To look at this graphically, they plotted the R0 (the "basic reproductive number" for each pathogen; the number of secondary cases due to each case) on the X axis, and the relative size of each outbreak an organism caused on the Y:


So, the good news is that most zoonotic pathogens don't cause major epidemics. But, as they note in the discussion, we don't have a good way right now to predict whether a new pathogen will behave more like rabies (frequently introduced into the population, but doesn't cause major epidemics) or HIV (likely rarely introduced, but capable of causing a global pandemic). This is why we take things like H5N1 so seriously--especially because that's a virus family which, historically, is out in the upper right corner of that graph above. Right now H5N1 is in the opposite corner--introduced fairly frequently in the last year (~130 odd times thus far), but without significant transmission between humans. Hopefully it will stay that way, as many zoontic pathogens do. But as the authors also point out, good surveillance is, once again, the key--and to be thorough, we should go even beyond humans and ducks in an effort to better understand our microbial neighbors.

 

Synopsis of Maggiore's Primetime Live Appearance

I didn't have a chance to blog this, but Christine Maggiore appeared on ABC's Primetime Live last week. For those of you who may be new to the story, she's the HIV denier whose 3-year-old daughter, Eliza Jane, died of AIDS-associated pneumonia. Maggiore dismissed the coroner's report, and had her own, erm, "expert" do a second autopsy; Orac discussed those findings here.

Orac has a good summary of the Primetime Live appearance; I was busy making snacks for my daughter to take to school the next day while Maggiore was on, so I wasn't able to take good notes. The whole incident was so sad; they played parts of the 911 call, and as Orac notes, it seemed clear from the story that EJ was much sicker for a longer period of time than Maggiore had previously suggested. Additionally, as Orac mentioned, she wasn't even convinced when the reporter gave her the exact evidence she asked for: pathology slides that showed that Eliza Jane had pneumonia. It was heartbreaking to watch her talk about her daughter, and the love she had for her was clear. But the bottom line remains: she went against consensus medical advice, and took risks with the lives of her children. And the worst part is that she continues to encourage others to do the same. Maybe their children won't get the national attention that Eliza Jane did; maybe some have already died due to advice from Maggiore and others like her. I don't know, and to my knowledge, no good studies have been done investigating how HIV denial groups like hers affect the opinion of others on the issue of AIDS causation. I hope EJ's legacy will make some of those deniers at least think twice about what they may be doing, not only to themselves, but to those close to them.

Friday, December 09, 2005 

ID rumblings in Muscatine, Iowa

From The Muscatine Journal:
Although they don’t all agree on the merits of intelligent design, most members of the Muscatine School District Board of Education believe that students should know about it, and they agree that it will likely be discussed by the Board within the next two years.

Ann Hart, vice president of the Muscatine School Board, said she would not remove evolution from the school district’s curriculum, because of its scientific basis, but that students should also know about intelligent design.

“I think somewhere along the line, intelligent design should be brought up because a lot of people believe in it; and, otherwise, kids aren’t going to understand it as well as they should,” Hart said. “I don’t think we should go in-depth with it, just let kids know what it’s about and that it’s what some people believe and then go on to evolution. I believe in evolution, for sure, but we do need to let kids know this is something that people believe.”
I wonder if she's contemplated that there are thousands of things "that people believe" that are not taught in schools, and by opening the door to one of them, you're leaving a crack for all the other nutty ideas that are out there.
Muscatine School Board member Clyde Evans said he would not be opposed to the teaching of intelligent design in Muscatine’s schools, and agreed that it would probably be discussed when the science curriculum was being reviewed.

Evans compared the workings of the human body, universe and nature to a fine watch in their design and operation. “I think if you look at how very complicated and very sophisticated it is, there’s probably as much credit for (intelligent design) as for (evolution), and probably more,” he said.
Ah, yes, Paley's Natural Theology...which, of course, ID isn't, according to Gonzalez et al. What's not noted is that many people believe in evolution *and* give credit to God at the same time. Earlier in the article (that I snipped out for brevity), the reporter describes evolution as an "unguided" force, but theistic evolutionists have no problem believing God played some role in how things turned out. Maybe someone should ship the school board a copy of "Finding Darwin's God" as a Christmas gift.
Board member Tom Welk was also supportive of intelligent design in school curriculum, although he said he had not studied the subject to the extent that he had an exact definition of intelligent design.

“Personally, I’m a believer,” he said. “We have not discussed it as a Board, but I would probably be supportive of it being taught. Of course, I’d still need an exact definition of it.”
*Snicker* Good luck with that--even the ID supporters don't agree on an "exact definition" of it.
Welk said that should intelligent design be discussed, he expected Iowan’s reactions and thoughts to be similar to the residents of Kansas.
A comparison to Kansas is not a good thing, as they just received a big fat F on their science standards.
Board member Paul Brooks said he was still deciding his position on intelligent design.

“I know what I believe, but I guess my feeling is I don’t know if I want atheist people in teaching positions trying to talk about intelligent design,” he said. “If I could determine who the instructors were, that’d be different. Right now, I’m confident our teachers give students a fair assessment of the creation.”
Hmmm, what "assessment of the creation" are your teachers now giving?? Sounds like Mr. Brooks is saying that if his teachers agree to indoctrinate kids in the specific way he agrees with, he'd be OK with it--but none o' them atheist teachers telling the young-ins that ID's hokey, now, y'hear??
But at least one Board member, president Jerry Lange, said he would feel uncomfortable with intelligent design in school curriculum. Lange did agree that it was likely to be an issue in the next two years.

Lange believed intelligent design was an attempt to put religious doctrine into schools, and while he did think it would be acceptable to introduce the idea to students as far as explaining its purpose, he would not support any significant teaching of intelligent design.
Thank you, Mr. Lange, for being the voice of reason.

As mentioned yesterday, Iowa doesn't have state science standards, so each district sets their own curriculum. This is good and bad for us: good, because the national ID groups can't simply target a state school board to push for inclusion of ID, but bad, because instead of potentially fighting one battle, we could potentially have to deal with this in every district individually. For Iowans interested in these issues, I'll again mention that we now have a Iowa Citizens for Science organization in our state, so keep an eye on that website and email me at iowascienceATgmailDOTcom for more information.

 

Thai 5-year-old becomes 70th known H5N1 death

Death toll from bird flu hits 70
A Thai boy has become the 70th Asian to die of bird flu, authorities said on Friday, as reports warned a flu pandemic could cost the U.S. economy hundreds of billions of dollars as well as millions of lives.

The death of the 5-year-old boy from the central province of Nakhon Nayok, 110 km (70 miles) from Bangkok, took Thailand’s bird flu death toll to 14 out of 22 known cases since the virus swept through large parts of Asia in late 2003.

It was not certain how the boy caught the virus, which usually strikes those in close contact with infected fowl or their droppings, senior health officials said. The boy, who died in hospital on Wednesday, was not known to have had direct contact with chickens, health officials said.

“We believe that the boy contracted the virus from his surroundings because, although his family does not raise chickens, there are chickens raised in his neighbourhood,” said Thawat Suntrajarn, head of the Health Ministry’s Disease Control Department.

China also reported a new case of H5N1, the fifth person in the country known to have been infected with the deadly virus. The 31-year-old woman, who lived in Heishan county of Liaoning province, has since recovered.
The news that the boy didn't have any known direct contact with birds is worrying. Hopefully this is an anomaly, or there's some unrecognized contact with birds that his family may not know about. If more of these "no known fowl contact" cases start showing up, it's really time to start battening down the hatches and preparing for the worst.

 

Science year in review

MSNBC has an article on the year in science. High on the list is the intersection of science and politics: cloning, climate,
The developments of the past year show that the "accepted wisdom" on science isn't as quickly or as widely accepted as perhaps it once was — partly because of a skeptical political climate, and partly because the Internet provides wider access for dissenting views. Those societal challenges are sparking the rise of a new breed of scientists: media-savvy folk who aren't afraid to join the fray themselves.
And this is both good and bad. They mention Gavin Schmidt of the RealClimate blog:
Schmidt and his co-bloggers get into the nitty-gritty of climate research, interacting earnestly with fans as well as foes in long strings of reference-rich commentary. It's not an approach meant to attract a mass audience or stir a political movement — and Schmidt doesn't mean it to be.
But while RealClimate, as they mention, is "reference-rich" and run by experts in the field, there are also, of course, sites like that by the Discovery Institute and other creationist groups, which, to many lay people, seem to be scientific and convincing, while the experts in the field scoff. It's great that we scientists are becoming better able to take new findings and explain them directly to the public, but it's unfortunate sometimes that there's so much "background noise" with the conspiracy theorists and anti-science brigade that it becomes difficult for many people to separate the wheat from the chaff.

Anyway, other hot topics of the year will come as little surprise to regular science readers: bird flu, hurricanes, evolution, and end-of-life issues, including Terri Schiavo and advances in neurology. I'd love to have a time machine and see how this year is reviewed 20 or 50 years from now. So many of the issues that we've gone through in the past year seem to be a tug-of-war between those of us who want to move forward, and those who want to send the country back to the "dark ages," where creationism is taught and the environment is ours to mutilate.

Thursday, December 08, 2005 

Is Indonesia even dumber than the United States?

Over on SciAm Observations, they report that Indonesia has threatened to close down NAMRU-2. For those of you unfamiliar, NAMRU-2 is an acronym for "U. S. Naval Medical Research Unit No.2", and they work over in Indonesia (and extend to other countries in the region) to do infectious disease surveillance, outbreak investigation, and a number of other public health activities. Most recently, they've also been vital in working on the diagnosis of avian flu cases in that country, as it's the only facility with a BL-3 laboratory in the country. From the sounds of things, the country is valuing playing the game of politics rather than securing the health of its people (I know, a familiar ring):
The official justification for shutting down the lab is that the memorandum of understanding between the governments of Indonesia and the United States, which set up NAMRU-2 in 1970, expired in 2000 and has yet to be renewed. Since 2000, however, the lab has continued its activities--which in addition to large diagnostic and surveillance programs includes training medical workers to recognize and treat H5N1-infected patients--without interruption. "From 1 January 2006," the letter dictates, "all NAMRU-2 activities will be terminated until a new M.O.U. between the Government of Indonesia and the United States Government has been signed."

The letter does not mention what concessions Indonesia aims to obtain from the U.S. But it closes by reminding health officials that every scientific article they produce in collaboration with a foreign researcher must be cleared by the ministry of health before it can be published.

This hits close to home for me, as a technician in my lab is supposed to head over to Jakarta next semester, after finishing her MPH degree this month. This is the first time I've heard of these threats...I'll have to check with her to see if they've been more forthcoming in her communications.

Edited to add: Effect Measure's take on the situation

 

State science standards are in

How did your state do? More info in this post on Panda's Thumb, with a table broken down by state rank here. Note: Iowa isn't on there. We don't have a set of state standards; it's left up to each district to decide what to teach.

Wednesday, December 07, 2005 

Institute of Medicine lays the smackdown on SpongeBob

The Institute of Medicine, an arm of the National Academy of Sciences, has gone on record saying that Food Marketing Aimed at Kids Influences Poor Nutritional Choices:

Food and beverage marketing targeted to children ages 12 and under leads them to request and consume high-calorie, low-nutrient products, says a new report from the Institute of Medicine of the National Academies. The report offers the most comprehensive review to date of the scientific evidence on the influence of food marketing on diets of children and youth.

Concern has focused on food and beverage marketing practices because of the increase in new products targeted specifically to children and youth over the past decade and the media's increasing role in socializing young people. Companies spent an estimated $10 billion to market foods, beverages, and meals to U.S. children and youth in 2004, and four of the top 10 items that children ages 8 to 12 say they can buy without parental permission are either foods or beverages.

The committee assessed hundreds of relevant studies and rigorously reviewed evidence from more than 120 of the best designed to determine what effects marketing may have on children's diets and health. Most of these studies focused only on television advertising, a shortcoming that should be addressed in future research, given that marketing strategies are rapidly evolving and now employ many tactics beyond television advertising, including Internet marketing, mobile phone ads, and product placements in video games and other media. For the most part, the committee did not have access to the substantial body of proprietary market research data held by marketing firms and food, beverage, and restaurant companies.

The committee found strong evidence that television advertising influences the food and beverage preferences and purchase requests of children ages 2 through 11 years old and affects their consumption habits, at least over the short term. Most advertising geared toward children promotes high-calorie, low-nutrient foods, beverages, and meals, which, the committee concluded, influences children to request and choose these products. There is not enough evidence to determine the extent to which marketing influences the preferences and consumption habits of 12- to 18-year-olds; too few studies have focused on teens.

The evidence on whether television advertising directly affects children's long-term dietary patterns is limited and less conclusive. However, nutrition studies show that America's children and youth are consuming too many calories and too much added sugar, fat, and salt. Moreover, they are consuming less-than-recommended amounts of many key nutrients, including calcium, vitamin E, and fiber.
You can find the report at this link to read all of the findings (note: it ain't free).

As a parent, I'm of a mixed opinion on this. I was still home for the Today show this morning, and the report was discussed, saying that pressure would be put on companies first to stop this kind of marketing, and if that failed, the legislature may very well take up the issue. Even as a public health professional, though, I think the bulk of the responsibility lies with the parents, not the government, to help our kids make smart choices. My kids are age (almost) 6 and 3 1/2, and of course they'd rather eat SpongeBob cereal than, say, Raisin Bran, or have a Barbie pop tart as a snack instead of a banana. But how much blame lies with the parents for buying the junk food in the first place (even if we're cajoled into it by our kids)?

There are lots of parents out there who absolutely ban "junk food" from their homes. I can understand that--it's not healthy, it's mainly empty calories, whole grains are better. But I don't know that's the way to go either--you're not teaching your children about temptation and smart choices, you're simply shielding them from it.

I don't know what the right answers are. My kids generally eat healthy. My husband or I cook something homemade almost every night. We try to limit the processed foods as much as possible, and my kids generally drink milk or water, with the occasional juice. But we do have "junk" around the house, and our kids definitely love cookies and potato chips and ice cream. I don't think that's necessarily a bad thing--even if it's junk food being marketed by Dora the Explorer and Shrek. I respect the IoM's work and trust their conclusions, but I wonder that the wrong things are going to come out of this--more regulation by the government, without a coincident increase in concern by parents.

 

What's causing the "Grisis Signis?"

This came over the ProMed email last week:

A new outbreak of widespread "madness", known as "Grisis Signis" among native Central American tribes, is affecting native Miskito communities on the northern Caribbean Nicaraguan coast, and health authorities have not offered any scientific explanation for this phenomenon.

The information, published today by "El Nuevo Diario" newspaper, indicates that this region of the country is also suffering famine caused by a plague of rats that devoured crops. It adds that at least 31 native persons in the northern Caribbean coast had been affected by "Grisis Signis", which provokes attacks of violence and hysteria.

Saul Miranda, head of the health center in Waspam, the main municipality on the Coco River at the Honduras border, told the newspaper that 21 cases were detected in the Raiti community, 729 km northeast of Managua. He added that 4 additional cases were detected in the community of Santa Fe, while in Krin Krin village, indigenous leaders reported 6 ill persons.

The illness causes seizures and hallucinations, affecting only Miskito natives, who interpret the affliction as the result of a curse or sorcery. Those affected become quite strong, attacking households and becoming violent when somebody tries to disarm them. Some walk around the villages armed with sticks and machetes, sometimes returning to their homes after having been absent for some days. The only way in which affected persons return to normal is by taking herbs given to them by a traditional healer ("curandero"), but after the episode they do not remember anything at all.

Duing other outbreaks [a similar outbreak was reported in October 2003], Health Ministry authorities have not offered any scientific explanation for this illness.

Meanwhile, Coco River communities have been suffering for many months from famine caused by a plague of rats, which devoured their crops, and they have also been affected by floods caused by the recent tropical storms and hurricanes. Government authorities, with support from the World Food Program (WFA), have brought food and support for these communities that have been historically affected by natural disasters.

Comments on the email mention that there are a number of infectious agents that have been previously noted to cause psychosis in sufferers, including brucellosis, leptospirosis, and even Lyme disease. Other possibilitites mentioned include mycotoxicosis, due to a fungal toxin that can cause hallucinations that has been implicated in the Salem witch trials. Non-infectious causes, such as vitamin deficiencies, may also play a role.

I don't know how closely this outbreak is being examined, but I wonder if they're checking the rats for other parasites as well, in addition to the agents mentioned above. For those of you who haven't read Carl Zimmer's Parasite Rex yet, you're missing out on a fascinating exposition of all kinds of ways that parasites make their hosts do crazy things--"attacks of violence and hysteria" seem mild compared to causing animals to become sterile and raise parasite progeny as their own "young," for example; or causing a grasshopper to commit suicide.

This outbreak also allows me to mention another one of my pet interests, as I've noted before: infectious causes of chronic illness. It's long been known that infectious agents can mess with our minds: rabies was associated clinically with hydrophobia before the agent was ever isolated; similarly with the neurological effects of Treponema pallidum, the causative agent of syphillis. Are we seeing a new microbe here? A new clinical manifestation of an old one? Simple vitamin deficiency? I don't know, but I hope someone in the area is finding out.

Tuesday, December 06, 2005 

U.S. unprepared for health disaser

What. A. Surprise.
WASHINGTON - Hospitals are not prepared to handle the patients who would arrive after a disaster or a pandemic, most states have few plans in place for coping and the federal government has not taken charge of such preparation, according to a report released Tuesday.

Although President Bush released an influenza pandemic plan with great fanfare last month, and even though federal health experts have been issuing dire warnings for years, little has actually been done to get the nation ready, according to the Trust for America’s Health, or TFAH.

“While considerable progress has been achieved in improving America’s health emergency preparedness, the nation is still not adequately prepared for the range of serious threats we face,” the report from the non-profit health education group reads.
Well, knock me over with a feather. Who could have seen this coming?

 

On the more positive side

So, that NYT article discussed below about how difficult it is to receive funding for innovative research was a bit depressing, so as an antidote, check out this article, also from today's New York Times.
Addressing 275 of the world's most brilliant scientists, Bill Gates cracked a joke:

"I've been applying my imagination to the synergies of this," he said. "We could have sorghum that cures latent tuberculosis. We could have mosquitoes that spread vitamin A. And most important, we could have bananas that never need to be kept cold."

They laughed. Perhaps that was to be expected when the world's richest man, who had just promised them $450 million, was delivering a punchline. But it was also germane, because they were gathered to celebrate some of the oddest-sounding projects in the history of science.
Several of the grants awarded are described in the article; the entire list is here. Goes to show you that not everyone has to give up on innovative research to get ahead, or get funded.

 

...what if?...

I mentioned in October that ulcer researchers Barry Marshall and Robin Warren won this year's Nobel Prize in medicine for their research showing that Helicobacter was a cause of gastric ulcers. However, Marshall and Warren weren't the first to come up with that idea; indeed, there were earlier reports suggesting a connection. Antecdotal evidence from several hospitals suggested that ulcer sufferers improved when prescribed antibiotics, and a curved bacterium had even been seen in the stomachs of Boston ulcer patients back in the 1940s. Reports of this bacterium date back to even earlier in the century, but none were conclusively followed up. Indeed, the doctor who made the observation in Boston, A. Stone Freedberg, was discouraged from pursuing that line of research. Now, a half-century later, he will award the Nobel prize to the researchers who were able to do what he could not: grow Helicobacter pylori, and show that it was a cause of gastric ulcers. Today's New York Times discusses more of the story, a tale not only of "what ifs" but also of the role chance plays in science--even science good enough to win a Nobel.

 

New Grand Rounds!

This week's Grand Rounds is up at The Examining Room of Dr. Charles. These seem to be growing every week (maybe because now Medscape is publicizing it?). Lots of good posts this week. At the Biotech weblog, they discuss the use of fumarones to prevent biofilm formation, with the goal of making catheters and other implanted devices that are prone to infection safer. Red State Moron fleshes out the newest battle in the abortion debate: laws suggesting doctors "inform women seeking abortions that a fetus is developed enough after 20 weeks to feel pain." As RSM discusses, this is something that's not even been decided in the medical world, yet now they want to bypass that and write it into law. MedSleuth discusses the newest Clostridium difficile news--and s/he should know, having gone through a bout of C. difficile infection. Finally, over my med body! has a late submission on pattern recognition, and why it's not always a good thing.

Monday, December 05, 2005 

About your "poo print"

I admit it. I am not the most organized person. My office is one of those "don't touch anything--I know exactly where it is" kinds of places, in sharp contrast to the colleague I work with most frequently, who was in the Navy for 20 years and never has so much as a pencil out of place. I blame it on my business; I like to have everything within reach when I'm working on something, therefore it's more likely to be "filed" on the floor or on my desk than in an actual cabinet until the grant or manuscript is out the door. In the last month I've sent off 2 grant proposals, finished a new course submission, and sent off a journal manuscript (with another to follow shortly), so alas, the clutter is closing in on me, forcing me to spend today filing, reading journals that have been piling up on my desk, and just generally making my office space presentable to students once again. (Though after reading this post via Pharyngula, maybe it's better to keep it messy in here...)

Anyhoo, in the meantime, you might want to check out a discussion of probiotics over at Immunoblogging. The discussion of the introduction of new bacterial species into your native flora (your "poo print--" I'm totally going to steal that for a lecture on intestinal flora) goes nicely with my post on Clostridium, below.

 

Emergence of epidemic Clostridium difficile

Clostridium difficile has joined MRSA, SARS, avian influenza, and West Nile as a hot new emerging disease. This bacterium, a cousin to Clostridium tetani–the causative agent of tetanus--and Clostridium botulinum--the botulism bacterium—is a spore-forming anaerobe. Carried by about 3 percent of healthy adults, the bacterium is generally present as a metabolically inactive spore. The bacterium typically causes problems in the nosocomial (hospital) environment, where up to 40 percent of hospital patients may be colonized. Clinical disease generally presents as watery diarrhea and cramps, and is the most frequent infectious cause of nosocomial diarrhea, resulting in about 3 million cases per year. Mortality is generally low (less than 3 percent). Though not commonly fatal, these infections have a high monetary cost: each infection results in ~$3600 in excess health care costs, for a total of over $1 billion in the United States alone every year.

Ironically, it is antibiotic treatment that often precipitates manifestation of disease. In the 1974, a study by Tedesco et al showed that, in 200 patients given clindamycin, 41 developed diarrhea, and 20 had pseudomembranous colitis, a pathological finding characteristic of infection with C. difficile. Indeed, in the 1970s, the most common antibiotic associated with C. difficile disease was clindamycin; cephalosporins in the 1980s; and, in 2 new papers published in the New England Journal of Medicine, fluoroquinolones.

Like other disease-causing Clostridia, C. difficile produces a repertoire of toxins. Toxins A and B, released by the bacteria after colonization of the gut, are thought to be the main cause of disease pathogenesis. These toxins cause illness by disrupting the cytoskeleton of fibroblasts.

An increase in both the rate and severity of C. difficile infections has been noted since the 1980s—what underlay this increase? The emergence of a new, virulent strain was hypothesized, and that hypothesis was tested and confirmed in the reports by Loo et al. and McDonald et al., describing a new variant of this bacterium. This variant strain is resistant to fluoroquinolones, and contains an 18 base pair deletion in the tcdC gene. As this gene has been proposed to be a negative regulator of expression of the A and B toxins, it is likely that this mutation leads to the significantly higher toxin levels observed in these variants—reported to be16 to 23 times higher than strains without the deletion.

This isolate has been found not only in the US, but also in Canada, where it was responsible for 100 deaths over an 18-month period in a Quebec hospital. Additionally, analysis of the pulsed field gel electrophoresis (PFGE) patterns of 6000 historic isolates show that this variant has been present in hospitals dating back at least to the late 1980s. It is thought that the recent increase in incidence is due to increasing use of fluroquinolones. For instance, in one hospital studied in Pennsylvania, increase in disease incidence was correlated with a switch from levofloxacin to moxifloxacin; however, in another hospital, levofloxacin was found to be used in the largest percentage of patients who developed infection with C. difficile.

These outbreaks—again—underscore the need for active surveillance for infections. In a hospital situation, infections can be controlled by using careful procedures to avoid exposing non-colonized patients to C. difficile. Patient care equipment, including blood pressure cuffs and stethoscopes, should be used either only for the colonized patient, or thoroughly cleaned before using it on a second patient. Additionally, health care workers need to use actual soap and water to wash their hands between patients, as alcohol-based hand sanitizers aren’t effective in killing C. difficile spores. Finally, in the past, outbreaks of C. difficile disease have been controlled by restricting the use of antibiotics associated with disease outbreak—a difficult proposition for fluoroquinolone antibiotics. Therefore, we must be careful to use them in a more judicious manner--something microbiologists have long called for, anyway. Finally, as a greater percentage of our population is being housed in nursing homes and other long-term care operations, this is a problem we’re unlikely to see vanish anytime soon, unfortunately.

Further reading:

McDonald et al.. 2005. An Epidemic, Toxin Gene-Variant Strain of Clostridium difficile. NEJM, 353:2433. Link.

Loo et al.. 2005. A Predominantly Clonal Multi-Institutional Outbreak of Clostridium difficile-Associated Diarrhea with High Morbidity and Mortality. NEJM, 353:2442. Link.

Bartlett and Perl. 2005. The New Clostridium difficile -- What Does It Mean?. NEJM, 353:2503. Link.

Anonymous. 2005. Severe Clostridium difficile--Associated Disease in Populations Previously at Low Risk --- Four States, 2005. MMWR. 54:1201. Link.

Friday, December 02, 2005 

AMA Op-Ed: "loopy times," and what medical professionals can do

Though I'm not an MD myself, much of my research and my reading centers on medical issues, while another passion (as regular readers certainly must have noticed) is the "controversy" over evolution, and educating the public about the issues involved with that. So, in a nice convergence of these two topics, the American Medical Association has published an Op-Ed on the topic of evolution denial.

I’m afraid we live in loopy times. How else to account for the latest entries in America’s culture wars: science museum docents donning combat gloves against rival fundamentalist tour groups and evolution on trial in a Pennsylvania federal court. For those keeping score, so far this year it’s Monkeys: 0, Monkey Business: 82. That's 82 evolution versus creationism debates in school boards or towns nationwide—this year alone.
The most important part of his piece, IMO, addresses the role of the medical community in this "controversy:"
The medical community as a whole has been largely absent from today’s public debates on science. Neither the American Medical Association nor the American Psychiatric Association has taken a formal stand on the issue of evolution versus creationism. When physicians use their power of political persuasion in state legislatures and the US Congress, it’s generally on questions more pertinent to their daily survival—Medicare reimbursement, managed care reform, and funding for medical research. Northwestern’s Miller believes that the scientific community can’t fight the battle alone and that, as the attacks against science accelerate, the medical community will have to use its privileged perch in society to make the case for science. “You have to join your friends, so when someone attacks the Big Bang, when someone attacks evolution, when someone attacks stem cell research, all of us rally to the front. You can’t say it’s their problem because the scientific community is not so big that we can splinter 4 or more ways and ever still succeed doing anything”

So what does one do? How can a medical student, a resident, or a physician just beginning to build a career become active in these larger public battles? Burt Humburg, MD, a resident in internal medicine at Penn State’s Hershey Medical Center, is one role model. He’s been manning the evolutionary ramparts since his medical school days in Kansas in the late 1990s when he became active in Kansas Citizens for Science. On a brief vacation from his residency volunteering as a citizen advocate for the federal trial in Pennsylvania, he said education is the key role for the physician. While he realizes that medical students, residents and physicians might not view themselves as scientists, per se, he sees himself and his colleagues as part of the larger scientific collective that can’t afford to shirk its duty. “The town scientist is the town doctor, so whether we want it or not, we have the mantle—the trappings—of a scientist”.

There are many ways to get involved; from the most rudimentary—attending school board meetings, sending letters to the editor, and volunteering at the local science museum—to the more demanding—running for office, encouraging a spouse or partner to do so, or supporting candidates (especially financially) who are willing to speak out for science.

I hope Costello's call is answered. Those of you who may feel that this topic isn't your concern--you're wrong. Many of the same people who deny evolution are the same ones who refuse vaccination, who deny that HIV causes AIDS (such as Phillip Johnson), who claim that abortion causes breast cancer (such as DI petition signer Joel Brind), who think that there's some big conspiracy by the "scientific elite" against the common man. Many have a fundamental mistrust and misunderstanding about science, and evolution denial is only one way it manifests itself.

I know, it's much easier to stay in your office and not deal with the issue, but please, we can use your help. Write a letter to the editor--people seem to respond better to those "M.D." initials after a name than the "Ph.D." (="ivory tower elitist") ones. Especially if you're a well- known and respected member of your community, showing that you support the teaching of evolution in your school district can really help. There are other ways you can help listed here, and every little bit helps.

 

New Archaeopteryx fossil provides further insight into bird, dinosaur evolution

Early-bird fossil features dinosaur feet

When it comes to feet, the earliest-known bird species had more in common with Velociraptors than cardinals.

Modern bird feet have a hind toe that points backward and helps the birds perch on branches, power lines, and pirates' shoulders. And until a recent discovery of an extremely well-preserved skeleton of the earliest-known bird species, Archaeopteryx, scientists believed it too had a "perching toe."

The new fossil, known as the "Thermopolis specimen," is incredibly well-preserved. It left clear impressions of its wing and tail feathers in the limestone it was encased in, and the skull is the best-preserved of all the 10 specimens ever discovered. But it may be the feet that prove to be the most important aspect of the find.


Other links:
Science summary
Science research article

Also posted on Panda's Thumb since I'm too far behind even in lay reading in this area to be able to make any insightful comments beyond, "this is so cool!" :) Hopefully some of the experts there will pick up my slack.

Thursday, December 01, 2005 

Are fruit bats a reservoir for Ebola?

As I've mentioned before, Ebola is a virus near and dear to my heart. (Figuratively, not literally. I'm not quite that enamored of it). In that previous post, I mentioned that we didn't know the reservoir of Ebola in nature. It certainly isn't for lack of trying that it wasn't determined previously. The first field studies took place shortly after the initial 1976 outbreaks in the Democratic Republic of Congo (DRC) and Sudan. In the former, 818 bedbugs, 1500 mosquitoes, 10 domestic pigs, one cow, seven bats, 123 rodents, eight squirrels, six Cercopithecus monkeys, and three small antelopes were sampled--all negative when viral isolation was attempted. In Sudan, almost 500 vertebrates were similarly tested--zilch. Similar results in 1977 and 1979 in the DRC. Following that outbreak, Ebola did not re-surface for a decade and a half, popping up again in a large 1995 outbreak in Kikwit, DRC. A total of 2814 vertebrates and a whopping 27,843 arthropods were captured during respective periods of 3 and 6 months after the end of the outbreak. Viral isolation was attempted from both categories of animals, and vertebrates were also tested for Ebola-Zaire specific IgG. No positive IgG reactions were obtained, and no viruses were isolated on Vero cells. The vertebrates included 1759 rodents, 539 bats, 114 insectivores, 184 birds, and 127 reptiles and amphibians. The arthropods included 15,118 mosquitoes, 124 blood-sucking flies, 6538 bedbugs, 144 fleas, 103 lice, and 5816 ticks.

Around the same time as the Kikwit outbreak, a case of Ebola was retrospectively identified in a primatologist who had been working on the Ivory Coast. So, scientists trudged back out there, collecting 1642 vertebrates (652 bats, 283 rodents, 398 insectivores, 27 monkeys and 282 birds) between 1996 and 1997. One red colobus monkey was seropositive, but virus was never cultured.

Finally, 242 vertebrates (24 bats, 163 rodents and 56 insectivores) were captured in the Central Africal Republic in 1998. Small Ebola-specific genetic sequences were amplified from organs of six mice and a shrew. However, although these results constitute the only biological evidence that Ebola may be present in healthy animals, no firm conclusions as to the reservoir status of these animals can be drawn, given the lack of specific serologic responses, the lack of nucleotide specificities in the amplified viral sequences, the failure of virus isolation, and the non-reproducible nature of the results. Still, it was heartening to finally have some positive results after so many dead ends. (All of this reviewed in Pourrut et al., "The natural history of Ebola virus in Africa." Microb Infect 7:1005-14).

Now, a new study in today's Nature has found similar results in fruit bats.

Like previous studies, the authors trapped a number of species while Ebola epidemics were occurring (this time, in Gabon). In total, 1,030 animals were captured, including 679 bats, 222 birds and 129 small terrestrial vertebrates. They found Ebola-specific IgG in 3 different bat species (a total of 16 positive individuals). Viral RNA was detected in the liver and spleen of a total of 13 of the individuals of these species as well, and found to be the Zaire subtype. (There are 4 known Ebola subtypes: Zaire, Sudan, Ivory Coast, and Reston, listed from highest to lowest virulence in humans). However, the bats that were antibody-positive weren't the same individuals that were PCR-positive. The authors suggest that the IgG+ individuals had likely already cleared the virus, and the PCR+ individuals had not yet mounted a significant immune response to the virus.

Is it biologically plausible that bats are a reservoir of Ebola? In a word, yep. Bats have long been suspected to play a role in Ebola transmission. Studies have shown that the virus can replicate in experimentally-infected bats, and index cases in outbreaks of not only Ebola, but also its filoviral cousin Marburg virus, have been traced to bat-infested locations: caves, warehouses. However, this is the first direct evidence of bat infection in the field. Finally, the authors note that each of the three bat species has a broad geographical range that includes regions of Africa where human Ebola outbreaks occur, and also suggest that changes in the bat's diet during the dry season (when Ebola mortality increases in the great apes) may make them more likely to spread the virus during that time.

Does this close the book on an Ebola reservoir? Hardly. This will, however, give scientists some targets to focus on.
The three species identified include Hypsignathus monstrosus (which has to win some kind of ugly animal award), Epomops franqueti, and Myonycteris torquata, pictured in that order. Future investigation can examine more closely the ecology of this species, and particularly its interaction both with humans and with the great apes in this region. The current study also cannot address how the bats themselves become infected. Is there another reservoir that they acquire the virus from? Is it transmitted between bats via secretions? Feces? Blood? Acquired from nursing on an infected mother, or during birth? Does it come from their diet? All the positive bats were fruit eaters, and it's been previously suggested that Ebola may be a plant virus (though the evidence for that is currently pretty sketchy). Nevertheless, all are potentially testable hypotheses in the field and/or in the lab.

Finally, an awareness campaign can be instituted, as they mention that villagers in the area may eat these bats. Some previous outbreaks seem to have correlated with the consumption of bush meat (in one case, a chimpanzee who had likely died from Ebola); therefore, this is one potential way the virus could enter the human population. Education may potentially ward off a future outbreak. It won't help the gorillas, but it's definitely a start, after a long and mostly fruitless (wink, wink) search.


(Images (c) N. Ebigbo for E. franqueti and (c) J. Fahr for M. torquata).

 

You go, (Professor) girl!

Meet Dr. Kristi S. Anseth. Dr. Anseth is a tissue engineer--reassembling life's basic building blocks into something that becomes living tissues within a body. At the age of only 37, she also has the distinction of becoming the first engineer to become a Howard Hughes medical investigator, "a prize usually reserved for Nobel-worthy researchers in the basic sciences," as noted in the article.

I've been lucky to have several good female mentors in biology and epidemiology; it's good to see an increase in female role models in other sciences as well, especially fields that are traditionally very male-heavy like engineering. Kudos.

 

Science blogs getting noticed by the big guns

PZ noted that Science magazine contained a blurb about Panda's Thumb in this post:
Darwin's contemporaries Thomas Huxley and Joseph Hooker championed his theory in print and in lectures. If they were alive today and had a little attitude, they might craft something like The Panda's Thumb, a Web log in which a cadre of Darwin's modern-day defenders pummels antievolution pseudoscience such as "intelligent design" (ID). The site gets its name from a Stephen Jay Gould essay about the giant panda's adaptation for stripping bamboo leaves--it's a jury-rigged feature a clever designer wouldn't engineer. Panda's Thumb regulars--who range from Ph.D.s and grad students to a businessman and a lawyer--comb the news media for follies to expose and errors to correct. The site provided blanket coverage of the recent trial on the Dover, Pennsylvania, school board's decision to require teaching of ID (Science, 18 November, p. 1105). Panda's Thumb also highlights evolution-related research, such as a study showing that the antibiotics produced by our immune systems may not be a panacea for drug-resistant bacteria.
Today, Nature gets into the game, featuring quotes from PZ as well as Revere from Effect Measure:
Scientists who blog see their activities as a useful adjunct to formal journals, not a replacement. "The standard scientific paper is irreplaceable as a fixed, archivable document that defines a checkpoint in a body of work, but it's static, it's very limited," says Paul Myers, a biologist at the University of Minnesota, who blogs at Pharyngula. "Put a description of your paper on a weblog, though, and something very different happens," says Myers. "People who are very far afield from your usual circle start thinking about the subject. They bring up interesting perspectives." By sharing ideas online, you get feedback and new research ideas, he says.

A senior US epidemiologist who blogs once or twice a day under the pseudonym 'Revere' on his public-health blog Effect Measure, has attracted a diverse readership. "About 1,500 people visit each day," he says. "If someone told me that I could show up at a lecture hall every day and deliver a short opinion, and that 1,500 people would show up to hear me, I'd be pretty satisfied — 1,500 is twice the subscription of many speciality journals."

But for most scientists and academics, blogs and wikis remain unattractive distractions from their real work. Many consider them an online version of coffee-room chatter, background noise that goes against the very ethos of heavily filtered scholarly information.
Sounds pretty rosy, so they do include a counter-point:
Yet even the most web-savvy scientists remain unconvinced that blogs have any useful role in science. "I have my doubts that blogging reduces information overload, but blogging will survive as it appeals to all the exhibitionists," quips Rolf Apweiler, a bioinformatician at the European Bioinformatics Institute in Hinxton, UK, and head of the UniProtKB/Swiss-Prot protein-sequence database.
Ouch. Rolf's certainly entitled to his opinion, but I wonder how much science weblog reading went into formulating it. Me, I write not to be an "exhibitionist," but because I am, quite simply, a complete science geek. I love reading about this stuff, and sharing what I read with others (and my friends and family are getting sick of it, heh). And even if no one reads it, just the act of writing about various topics forces *me* to give deeper thought to them, and improves my own understanding of the issue. I think (hope) this also makes me both a better scientist and a better teacher. And finally, one of my pet issues is making science available (and understandable) to the general public. Scientists often bemoan science journalists for not getting things quite right, so why not let them hear it straight from the horse's mouth, so to speak?

About me

  • I'm Tara C. Smith
  • From Iowa, United States
  • I'm a mom and a scientist, your basic stressed-out, wanna-have-it-all-and-do-it-all Gen Xer. Recently transplanted from Ohio to Iowa, I've spent most of my life in the midwest (with 4 years of college spent out east in "soda" territory). My main interest, and the subject of my research, is infectious disease: how does the microbe cause illness? What makes one strain nasty, and another "avirulent?" Are the latter really not causing any disease, or could some of those be possible for the development of chronic disease years down the road? Additionally, I've spent a lot of time discussing the value of teaching evolution, and educating others about "intelligent design" and other forms of creationism. My interest in history of science and medicine is also useful as a way to tie all of the above interests together. [Disclaimer: the views here are solely my own, and do not represent my employer, my spouse, that guy who's always sitting by the fountain when I come into work, or anyone else with whom I may be remotely affiliated.]
My profile

Links

Powered by Blogger
and Blogger Templates

Powered by Blogger

Creative Commons License
The Tangled Bank Locations of visitors to this page
Enter your email address below to subscribe to Aetiology!


powered by Bloglet


The Evolution Education Site Ring

This site ring is owned by John Stear

Previous Site

List Sites

Random Site

Join Ring

Next Site