…as you can see by looking at the cool video of science bloggers at the American Society of Microbiology meeting. You do get to meet fellow PT blogger Tara Smith there, as well as our buddy Larry Moran.

The latest edition of Animalcules, a monthly carnival of microbiology blogging, is up over at Aetiology.

The early word is that PT contributor Reed Cartwright (real webpage) (alter ego) has, despite being a PT poster, helping to construct the PT blog, and spending his time annoying creationists, managed to PASS his dissertation defense. Watch out world, here comes Dr. Cartwright.

I believe Prof. Steve Steve is planning the all-night bash in Athens as we speak. I wonder how spatially explicit population genetics sounds after a few pints of bamboo beer?

by Kevin Padian, Professor, Department of Integrative Biology; Curator, Museum of Paleontology; University of California at Berkeley.

Last Tuesday William Dembski began posting diatribes on his weblog accusing me of racism. He based them on a second- or third-hand report that he received from one of his acolytes who got the basic facts wrong. Dembski didn’t bother to check them before jumping to his accusation.

But worse things have happened in the world. I could have responded to Dembski immediately, because I was sure of my facts, and I’m happy to stand on my record. But I wanted to wait until I could get a tape of the talk, and to be sure that no one could reasonably interpret my comments as Dembski and his acolytes did.

That took until Friday afternoon, at which point I immediately sent an e-mail to Dembski’s Discovery Institute address. On Monday morning I received an apology from him, which he posted on his website. I consider the matter closed.

However, I would like to clarify the record on several additional points that have come up:

Good news, we have been nominated for the Best Blog Community. Voting will open at the end of the week.

One thing I love about this place is how random interesting tangents will spring up in the comments. I wrote a brief post awhile back about some funny/sad AiG cartoons, which morphed into a discussion of snake evolution in the comments section. Dr. Fry’s comments in that discussion led to 2 follow-up posts on his work on the evolution of snake venom, and in the second thread, here, Steviepinhead has mentioned a new Archaeopteryx finding with better-preserved feet:

Steviepinhead wrote:

…A new Archaeopteryx fossil with exquisitely-preserved feet has been found. In previous finds, the feet were fairly scrunched up. Because there were enough other bird-like features, the less faithfully-preserved feet were assumed to be bird-like as well, with a rear-pointing toe.

It turns out that that toe actually points forward, and is set off to one side, strongly resembling the arrangement of toes of Velociraptor and similar dinosaurs.

Thus, Archaeopteryx turns out to be even more of a mosaic of bird and dino features than previously thought. You might even call it a transitional fossil.

Early-bird fossil features dinosaur feet

Have you ever wondered how Kevin Bacon and the lights of fireflies related to malaria and power grids? I know it’s something that’s kept me up many a sleepless night. One word: interconnections.

Many of you have probably heard of the “Six degrees of Kevin Bacon” game. This is based on the work of Stanley Milgram beginning in the 1960s, and brought up again more recently in a 1998 Nature paper, “Collective Dynamics of ‘Small-World’ Networks,” by mathematicians Watts and Strogatz. Milgram conducted a number of studies using his “lost letter technique,” in which letters were sent out and then needed to be forwarded onto reach their destination. In one instance, Milgram sent out 160 letters to individuals in the midwest, with instructions to pass them along to acquaintances who would be most likely to reach his stockbroker friend back east. Almost all of the letters that reached the stockbroker did so via one of 3 friends—and most did it within 6 steps–hence the “six degrees of separation” idea. Similarly, Duncan Watts first became interested in the “small world problem”—the idea that all of us are more closely connected than we realize—after watching fireflies flash in synchrony, and wondering how they accomplished that. What Watts, Strogatz, Milgram, and others were investigating boiled down to a series of links in a network—hubs and connectors. As Watts and Strogatz showed in their 1998 paper, all it took to make a “small world” from a regular network was the addition of a few “short cuts” (see figure from their paper, right). This elegant and seemingly simple structure of networks explains not only connections between movie stars and scientists but also cellular metabolism, ecology webs and the World Wide Web itself.

Continued at Aetiology

I discussed here new research on venom evolution that topples some old conventional wisdom. It seems this and another study are already making waves in that field. Genealogy of Scaly Reptiles Rewritten by New Research

The most comprehensive analysis ever performed of the genetic relationships among all the major groups of snakes, lizards, and other scaly reptiles has resulted in a radical reorganization of the family tree of these animals, requiring new names for many of the tree’s new branches. The research, reported in the current issue of the journal C. R. Biologies, was performed by two biologists working at Penn State University: S. Blair Hedges, professor of biology, and Nicolas Vidal, a postdoctoral fellow in Hedges’ research group at the time of the research who now is a curator at the National Museum in Paris.

Vidal and Hedges collected and analyzed the largest genetic data set ever assembled for the scaly reptiles known as squamates. The resulting family tree has revealed a number of surprising relationships. For example, “The overwhelming molecular-genetic evidence shows that the primitive-looking iguanian lizards are close relatives of two of the most advanced lineages, the snakes on the one hand and the monitor lizards and their relatives on the other,” Vidal says.

Carl Zimmer has a post today about the work of Dr. Bryan Grieg Fry on the evolution of snake venom. If that name sounds familiar to those of you who aren’t reptile specialists, you may have run across Dr. Fry’s homepage, or you may have seen his research profiled previously on Panda’s Thumb here, or you may have read comments by the good doc in this thread. Zimmer, as always, has an excellent overview of Fry et al‘s new paper in Nature (link ), but he didn’t emphasize the one sneak peek I received from Bryan. So, I thought I’d add a bit to Carl’s overview.

(Continued at Aetiology…)

I first ran across the thylacine (aka “Tasmanian tiger” or “Tasmanian wolf”) when I was preparing to teach a summer course on vertebrate zoology for a local Catholic college during grad school. While I’d had a decent amount of organismal biology and zoology as a college undergrad, I was a bit rusty from a few years of only studying organisms lacking nuclei, so I was looking for a quick refresher as well as some interesting topics for final paper assignments for the course. Just announced around that time was a “breakthrough” in the attempt to clone the thylacine, so I introduced that to the class in a discussion of the effects of geographic isolation, and had a nice discussion of both the molecular techniques and the ethics of a Jurassic Park-type scenario.

(Continue reading at Aetiology)

Ebola is one of my favorite pathogens. With the reputation it has, many people assume it’s killed many more worldwide than it actually has. People hear of Ebola and all kinds of grotesque images come to mind: organs “liquefying” (doesn’t really happen quite like that); bleeding from every orifice (okay, that one can be on-target); the victims dying a horrible death from a virus with an incredibly high mortality rate. There are four known subtypes of Ebola, named for their place of isolation: Ebola Reston, Ivory Coast, Sudan, and Zaire. Together with their cousin, the Marburg virus, they make up the family of viruses known as filoviruses.

Marburg was the first of these to be recognized, causing an outbreak in Germany (caused by infected African research monkeys) in 1967. The Ebola Zaire strain (EBO-Z) and the Ebola Sudan strain (EBO-S) surfaced at almost the same time in 1976. The outbreak in Zaire resulted in 319 cases (90% mortality), while in Sudan, 284 cases were identified (53% mortality rate). EBO-Z then wasn’t seen for almost 20 years, re-surfacing in Gabon in 1994, and once again in Zaire (Democratic Republic of Congo) in 1995. Another EBO-Z outbreak occurred in 2001-2 in Gabon and The Republic of Congo, causing about 120 cases, 79% of them fatal. Overall, less than 2000 known human infections and 1100 deaths have resulted from Ebola since its discovery in 1976. That’s an average of 38 deaths worldwide per year over the last 29 years. Compare that to a virus such as influenza, which kills 36,000 every year in the United States alone. Or even a fairly common microbe like E. coli, which causes thousands of deaths each year due to bacterial sepsis. Worse, none of these even come close to malaria, which causes over 200 deaths worldwide every hour. The numbers make it clear that, as far as mortality goes, Ebola is small potatoes—we have more to fear from our hamburger than from this exotic African virus. Yet, the Ebola mystique lingers.

Continue reading at Aetiology

It’s always nice when there’s a groundbreaking article in the literature, and the subject just happens to be your baby. My current research focuses on Streptococcus agalactiae (group B streptococcus, GBS), a bacterium that is the leading cause of neonatal meningitis in the United States. It also is a leading cause of invasive infection in the elderly, and can cause sepsis and toxic shock-like syndrome in healthy adults. No vaccine is currently available.

But what’s garnered attention recently hasn’t been any clinical presentations or new case reports of GBS disease; it’s the bacterium’s DNA. Specifically, the whole genomic sequences of 8 different strains of GBS, and the conclusions the authors have come to regarding bacterial genetic diversity–that it may be “endless.”

Continue reading (at Aetiology).

Thus far this week, I’ve discussed the history of pandemic influenza in general, and avian flu in particular. I’ve discussed some issues that must be addressed to prepare us for a pandemic, and the groundbreaking resurrection of the Spanish influenza virus. Today I want to end the series with a look at how prepared we currently are as a nation, and highlight some personal preparedness steps you can take.

If you recall from Tuesday, the first outbreak of H5N1 was back in 1997. The anthrax attacks were in 2001. Surely by now we’re prepared for some kind of serious, large-scale, biological event, right? Well…

The Feds: “um, er, the dog ate my homework?”

The U.S. is still working on finalizing its Pandemic Influenza plan, which it keeps promising will be done “soon.” But scientists are a bit skeptical…

“We need more than just a plan; we need the resources to actually activate it,” said Jeffrey Levi, a pandemic specialist at the Trust. “The real test of the plan will be whether it comes with dollars attached.”

The current draft of the administration’s plan fills several hundred pages. It describes the role of the federal government in coordinating the response to a flu pandemic and outlines steps to be taken at all levels of government before and during an outbreak.

In addition to production and stockpiling of vaccines and antivirals, the plan seeks to conduct research, prepare public education campaigns and develop ways for hospitals to handle large numbers of patients.

Continue reading (at Aetiology)

The scientific community is all too familiar with the dangers an influenza pandemic could bring. The politicians and general public are starting to become aware of the issue as well; indeed, one can hardly open a newspaper or turn on the television without hearing about “bird flu.” So, what’s actually being done to prevent an influenza catastrophe? What are the issues? What can be done?

These are the questions that keep public health officials awake at night, because the answer is always that we’re not doing enough. While we may be resigned to the fact that a future pandemic can’t be completely prevented, the damage can be minimized. Today, I’ll discuss the problems we face, and the proposed solutions to counter them, when it comes to pandemic influenza preparedness.

Continue reading (at Aetiology)

Anyone working in the area of influenza virus epidemiology is familiar with the name Robert Webster. A virologist at St. Jude’s Children’s Hospital in Memphis, the native New Zealander has been leading the charge against influenza for well over 40 years. Barely out of graduate school, Webster hypothesized that something like genetic reassortment (which had not yet been discovered) occurred to cause the big changes that appeared among human influenza viruses, driving pandemics. He performed a simple experiment that cemented the course of his career: he found that serum from patients who had survived the 1957 influenza pandemic reacted with avian influenza viruses. Later genetic analyses showed that the “Asian flu” virus had indeed received 3 of its 8 gene segments from birds. It happened again in 1968: the pandemic virus was the result of a reassortment between human and avian influenza viruses. These observations led to more than 30 years of surveillance of waterfowl in many different countries, and the revelation that these waterfowl constitute a reservoir of all known subtypes of influenza virus.

Webster’s worst fears seemed to be coming true in 1997. Hong Kong was experiencing an influenza outbreak in chickens so severe it had been nicknamed “chicken Ebola.” Humans were also affected. The first case was in a 3-year-old boy from Hong Kong. Though doctors knew he had died of the flu, they were uncertain of the strain, and sent samples off to several high-level laboratories for further testing. When it came back H5N1, the Centers for Disease Control and Prevention sent Keiji Fukuda to Hong Kong to investigate. After a month of searching, he and his team found no further evidence of infection with this avian virus in the human population—so they left, writing off the boy’s illness as a “freak occurrence.” They were premature. By the end of the year, 18 cases had been confirmed; 6 died. Clinical features often included a primary viral pneumonia and death quickly after onset of symptoms. The route of transmission in all cases appeared to be direct bird-to-human contact. Fearing a public health crisis, officials ordered the culling of Hong Kong’s entire poultry population. Analysis of the virus showed it to be a serotype H5N1 virus.

Continue reading (at Aetiology)

But I thought biologists were too “close-minded?”

Australians Barry J. Marshall and Robin Warren won the 2005 Nobel Prize in medicine Monday for showing that bacterial infection, not stress, was to blame for painful ulcers in the stomach and intestine.

The 1982 discovery transformed peptic ulcer disease from a chronic, frequently disabling condition to one that can be cured by a short regimen of antibiotics and other medicines, the Nobel Prize committee said.

Thanks to their work, it has now been established that the bacterium Helicobacter pylori, which the new Nobel winners discovered, is the most common cause of peptic ulcers.

It’s hard to avoid hearing about influenza virus these days. In all the noise, it’s tough to sort out the facts from the rumors and conspiracy theories. I’ve already discussed a bit about the basic biology in this post, so I’m not going to review that here (though a good overview can be found here for those of you who need to bone up on your influenza virus virology). So, this week, as a part of Pandemic influenza awareness week, I’ll be writing a 5-part series about various issues regarding influenza. Today, I’ll discuss the history of influenza, focusing on past pandemics. The rest of the week will address the following topics, with the goal of presenting a review of the facts without the scare-mongering:

1. “Avian flu” and H5N1, 1997-present
2. Where we are now—are we ready for a pandemic?
3. How do we prevent/control a pandemic? What models and surveillance can tell us
4. Other issues in influenza

So, without further ado, let’s dive into today’s topic:

A quick trip through the history of pandemic influenza (on Aetiology)

I’m sure many of you have been following the media circus related to the tracking of H5N1 influenza viruses (for example, this article, which contains the following quote):

“Right now in human beings, it kills 55 percent of the people it infects,” says Laurie Garrett, a senior fellow on global health policy at the Council on Foreign Relations. “That makes it the most lethal flu we know of that has ever been on planet Earth affecting human beings.”

Now, I’m a big fan of Laurie Garrett, and I obviously have no idea of knowing if this is all the said on the H5N1 mortality rate or if she elaborated further, but it’s quotes like this that lead people to stress more than they should about the H5N1 situation. A new paper just out in the Journal of Infectious Diseases (summary here) demonstrates one reason why the public shouldn’t start freaking out just yet.

Coming soon to Nebraska?

In the August 18^th issue of Nature (1), Donlan et al. suggest a novel way to save certain species of megafauna: bring them to the North American wilderness. (CNN summary/commentary here).

It’s not as outlandish as it may sound. As they point out, North America had many similar species until 13,000 years ago, including mammoths, camels, cheetahs, and lions. While they acknowledge there are differences between modern species and those which existed once upon a time in America, they suggest that the modern species are proxies for their long-extinct cousins, and could be used to “re-wild” North America. The authors suggest a mutually beneficial relationship: portions of the Great Plains benefit from tourism dollars, while the animals benefit from increased habitat and a decreased threat of extinction. Win-win, right?