But that simplified version only makes sense if you overlook some important facts about how the plague (which still exists) operates today. “The Black Death killed between 30 and 50 percent of the affected population,” says Sharon DeWitte, assistant professor of anthropology and biology at The University of South Carolina. “Modern plague, at most, kills between 2 and 3 percent, and that’s even in areas without access to modern medicine.”

What’s more, DeWitte says, recorded symptoms from the Black Death don’t entirely match up with those of modern plague. And the Black Death seems to have spread through populations faster and killed much faster than its modern cousin. The differences are striking enough that some scientists, including DeWitte at one point, have suspected that the Black Death might not have been caused by plague at all. But genomic reconstructions of ancient DNA suggest the two are one. So what changed? Ultimately, that’s the question that makes last month’s discovery of a new Black Death cemetery in London so important.

Given the vast numbers of people who died in the Black Death, there are relatively few burials that can be absolutely confirmed as containing Black Death victims, and only Black Death victims. DeWitte could only think of three when I spoke to her. But it makes sense. To put it simply, in the midst of a horrific catastrophe nobody was really thinking about how to makes sure the data would be nice and tidy for scientists to find hundreds of years later. Medieval writers didn't necessarily record information that would have helped archaeologists identify a Black Death cemetery. What's more, it wasn't even totally normal to bury nothing but Black Death victims together in one place. "A lot of them were just incorporated into existing cemeteries," DeWitte said.

That's made it difficult to know whether Yersinia pestis — the bacteria that causes the plague — really is present in Black Death victims. This work is already hampered by the degradation of DNA over the centuries. Finding tiny Y. pestis is hard enough, even in people who were killed by it. Mixed burials add the extra complexity of not knowing whether the body you're working on actually died from Black Death, to begin with.

Because of that, the best work in this field comes from England, where we have good documentation of a few places that were set aside specifically for victims of the Black Death. The newly uncovered cemetery might be one of those places — at any rate, there was definitely a recorded Black Death cemetery that would have been in about the same location.

If that turns out to be the case, then the bones of the people buried there could help scientists fill in the gaps on the Black Death.

In 2011, a team led by McMaster University paleogeneticist Hendrik Poinar became the first to reconstruct a full genome for Black Death era Yersinia pestis.

This was not a full and complete genome drawn from a single bacterium inhabiting the body of a single victim. Instead, the genome was patched together from bits and pieces of DNA in remains taken from London's East Smithfield cemetery. The small chunks were lined up to create a whole, similar to the way you make a panoramic photo by combining a series of different shots. Hendrik Poinar calls it a "draft" of the genome, rather than a smooth, polished work of biology.

The draft tells us a couple of things. First, the Y. pestis of the Black Death era is related to modern Y. pestis. In fact, it's probably the ancestor of all the strains of Y. pestis that exist today. Second — and this is the weird part — there is really not much difference between the old Y. pestis and the new. It boils down to about 100 genetic changes, few of which seem to have given the bacteria enough of an evolutionary advantage that they spread widely through the population.

Genetically, Y. pestis has barely changed. Its infection profile in the real world, though, has changed massively. That suggests that at least some of those small alterations in the genome must have been extremely important. But which ones? And why? To answer those questions, you could reverse-engineer the evolution of Y. pestis in the lab. "We'd have an opportunity to test those changes, one at a time, and find out," Poinar said. "... If we could do it in a form or fashion that wouldn't terrify people."

But, you know, good luck with that.

Instead, what would be really helpful is some burials from later outbreaks of the Black Death. Poinar's draft genome comes from bodies that date to the 14th and early 15th centuries. And his draft of the Y. pestis genome suggests that this bacterium might have a relatively slow rate of evolutionary change. During outbreaks, though, when there are more bacteria multiplying and they have more hosts to multiply in, change can happen faster.

"Now, if the new burial dates to the Great Plague of London, around 1665, I'd really like to see that," Poinar said. That outbreak was less deadly than earlier ones, killing "only" about 20 to 30 percent of the people who contracted it. If you could compare the DNA of Y. pestis of the 14th century with that of Y. pestis of the 17th, you might begin to see which changes ultimately made the bacteria less of a killer.

That, however, remains to be seen. So far, 13 bodies have been found at the new cemetery site. Those, unfortunately, are of the same vintage as the ones in East Smithfield. But, if the new cemetery is the recorded Black Death cemetery that experts think it is, then we know it was in use all the way up through the 1500s. Find the right bodies, and you might be able to get a peek at how Y. pestis was tamed.

Behold, a truly fantastic gift for the cat in your life — catnip-filled soft toys shaped like amoebas, cyanobacteria, and (pictured above) giardia.

Giardia are microscopic parasites that can invade the guts of vertebrate animals, including cats and humans. Generally, you get it by ingesting giardia-infested feces. For humans, this mostly means contaminated drinking water, because giardia are harder to kill than you might think. They can survive quite happily outside of a host and are resistant to chlorine.

Blue giardia cat toy

Read more on giardia (and see pictures) at the CDC website

Although scientists think that coronaviruses are actually responsible for a significant percentage of the illnesses that we call the "common cold", the most famous coronavirus is SARS, which killed almost 1000 people in 2003. That doesn't sound like many, but comparing deaths to diagnosed cases reveals a fatality rate of 10%. (There's a good chance this number doesn't give you the full picture. It's likely more people contracted SARS than ended up diagnosed with it, simply because, if your illness isn't severe, you don't usually bother to get diagnosed. To provide some context, the 1918 flu pandemic had an estimated fatality rate of 2.5%.)

All of this explains why a newly identified coronavirus — which may be the cause of two deaths and a couple of outbreaks of respiratory illness in the Middle East — is getting so much attention and causing people to freak out a little. The virus (which doesn't actually have a name yet) is part of the same family as SARS. SARS was a scary virus. So this new virus has everyone a little on edge, too.

The key thing to remember, though, is that this new virus is not SARS. And there's a lot we don't yet know about it.

I want to point you toward a couple of sources you should be following as this story plays itself out.

First off, Vincent Racaniello's Virology Blog has some good background on the discovery of the new virus and will help you understand how scientists identify a virus, to begin with.

The novel coronavirus was first reported by Ali Mohamed Zaki on ProMED-mail on 15 September 2012, from a 60 year old male patient in Saudi Arabia with pneumonia and acute renal failure who died in July. The virus was isolated by culturing sputum on Vero and LLC-MK2 cells, and identified as a coronavirus by polymerase chain reaction. Dr. Zaki sent the virus to Ron Fouchier in the Netherlands who sequenced its genome and confirmed that it is a beta-coronavirus closely related to bat coronaviruses.

Ron Fouchier doesn’t believe that we should become overly worried about these cases: "There are now six known human coronaviruses; one of them is SARS, but four cause the common cold and are quite innocuous. So let’s keep both feet on the ground and not blow this out of proportion."

The fact that the virus has been isolated from individuals with severe respiratory disease does not mean that it is the causative agent. To prove this requires additional work, as Fouchier notes: "For starters, we’ll find out whether animals get sick from this virus. You can isolate a virus from a patient, but that does not mean they died from it; to show that it causes disease you need to fulfill Koch’s postulates. That’s what we did for SARS, and it’s what we hope to do here; we’ve applied for emergency ethical approval. The most obvious animal species to put this virus in are mice, ferrets, and perhaps monkeys." Proof that the new coronavirus is an agent of respiratory disease would come from its isolation from additional patients with the disease.

Next, head over to the Superbug blog, where journalist Maryn McKenna has some good information about the social context of this virus.

The concern underlying these developments is that exposure to the new virus seems to have occurred only or primarily in Saudi Arabia, which houses Mecca, the physical heart of Islam — and which, next month, will be the center of the worldwide annual pilgrimage known as the Hajj. The Hajj brings more than 2 million people to the country, in extraordinarily crowded conditions, and when those pilgrims leave, they disperse all over the world.

The spread of disease during the Hajj has always been a concern (discussed, for instance, in this UK document from 2005, when avian flu H5N1 was a cross-border threat), and the Saudi authorities have always taken it seriously, including requiring that pilgrims be vaccinated in order to be granted a visa. According to news reports today, they are ramping up scrutiny of visitors, who have already begun arriving: The first official day of the pilgrimage season this year is tomorrow, Sept. 27, though the central observances in Mecca do not begin until Oct. 24.

Finally, Helen Branswell is a health reporter for The Canadian Press. She covered the SARS outbreak in 2003 and is reporting on this new virus, as well. She's very good. Keep an eye out for her byline. That's news you can trust.

Professor John Watson, head of the respiratory diseases department at the Health Protection Agency, said to date there is no sign of spread to health-care workers.

That is important because health-care workers often serve as inadvertent sentinels of the spread of infectious diseases. During SARS, for instance, health-care workers were disproportionately affected, catching the new virus from patients they were struggling to save.

"Preliminary enquiries have revealed no evidence of illness in contacts of these two cases, including health-care workers," the British agency's release stated. "Based on what we know about other coronaviruses, many of these contacts will already have passed the period when they could have caught the virus from the infected person."

Researchers at MIT used network theory to put together a model of how an infectious disease might spread around the world with the help of American airports. The model shows which features—geography, connectivity, levels of use—most impact the spread of disease and use that to predict which airports would be at the heart of an outbreak.

Some are not a shock. ("Oh, you say JFK and LAX could serve as worldwide hubs for disease?") But the model also reveals some surprising spark points. Like, say, Anchorage. It's also interesting to see the order that the model ranks airports in. Would you believe that Honolulu has more disease-spreading power than Atlanta?

Read the full journal article at PLOS One, an open-access scientific journal.

Read a short summary at the Nature Medicine blog

Over at the Scientific American blogs, science writer and biologist Rob Dunn talks about some of the theories for why something as seemingly antisocial as xenophobia could have been beneficial to our ancestors—at least under certain circumstances. The key, he says, might be disease. Not cooperating between groups, refusing to share resources, and generally going out of your way to avoid strangers makes sense if those strangers are infected with something that could kill you.

If I'm understanding Dunn correctly, the research and theorizing on this topic isn't saying xenophobia is good. Nor is it saying that all xenophobia grows out of a conscious, reasonable fear of disease. It's more like, the times when xenophobia did turn out to be coincidentally beneficial happened to reward people who were more likely to pass on xenophobic tendencies to their offspring (whether those tendencies were genetic or cultural is hard to say). Thus, the tendency continues, even in situations where it's actively detrimental. And Dunn points to an interesting recent study that showed deadly white-nose syndrome is causing xenophobic-esque changes in the behavior of bat populations.

Although it looked as though the little brown bats and several other species might soon face extinction, at least in some regions and perhaps even in North America, the little brown bats have begun to rebound in some places, albeit modestly. A new paper out this week takes notice of one of the reasons they appear to be rebounding, the bats are avoiding each other. Little brown bats (at least historically) tend to roost in large, groups, one next to the other, bumping fuzzies as it were. But not anymore. More and more, this new study, led by Kate Langwig, a graduate student at Boston University, suggests, the bats are spreading themselves out in their roosting caves, their hibernacula. Once, they clumped, warming themselves around the tiny fires of their bodies. Now, they go it alone.

Langwig’s results are preliminary, as she and her colleagues are the first to admit. She has measured the change in the bat roosting (and abundance) before and after the arrival of the disease, but she has not really studied the behavior of the bats and how it is they come to be spaced apart. Yet, the bats the are important from the perspective of the basic biology and conservation of the bats and so there remains much to do and much that can be done. For example, it would be good to know if the probability of transmission of the disease really goes down when the bats are further apart. It would also be interesting to figure out if the same individuals that were once nuzzling up next to each other, are now hanging out on their own.

Read the rest of Rob Dunn's post on xenophobia and disease

The good news is that, since the 1940s, getting people to get themselves tested has been the hard part. Once you know the gonorrhea is there, antibiotics have made it both easy and cheap to treat. The (more) bad news: That's changing.

At her Superbug blog, Maryn McKenna talks about the threat of antibiotic-resistant gonorrhea—it's not just an issue of health, it's also an issue of how much health costs. So far, there's not been gonorrhea reported that's immune to all the drugs we can throw at it. Just the inexpensive drugs. Anticipating big problems when treating gonorrhea becomes a pricy proposition, the World Health Organization has put together a plan for improving treatment today.

The plan specifically calls out an aspect of the growing resistance problem that we highlighted at SciAm: Community control now depends on rapid molecular tests that identify the gonorrhea organism (Neisseria gonorrhaea) but cannot distinguish between drug-susceptible and antibiotic-resistant organisms. Hence, patients who were treated, and then went back to their doctors with the same symptoms, were assumed to have been cured and then reinfected. Physicians have not had the tools to identify ongoing infections that never responded to treatment — and patients who had those resistant, not-responding infections then went on to unknowingly infect others.

In order to address that problem, the plan calls specifically for improvements in lab capacity, diagnosis and surveillance, as well as asking for things that apply to the greater problem of antibiotic resistance: improved awareness, bigger efforts at prescribing antibiotics appropriately and better drugs. One thing that it particularly calls for — as the CDC did in the New England Journal last February — is for physicians to start applying a “test of cure,” actually checking microbiologically to see whether a patient who was prescribed an antibiotic for gonorrhea is clear of infection, or harboring a resistant strain.

Of course, that's expensive, too. The cheapest option is still to not get gonorrhea at all. Get tested. Make sure your partners are tested. And use protection. In the future, we're not going to be able to afford treating some STDs as "no big deal".

Read more about the WHO plan and antibiotic-resistant gonorrhea at the Superbug blog ]]> http://boingboing.net/2012/06/08/the-end-of-cheap-std-control.html/feed 14 http://boingboing.net/2012/04/23/is-this-the-banana-your-grandc.html http://boingboing.net/2012/04/23/is-this-the-banana-your-grandc.html#comments Mon, 23 Apr 2012 20:33:01 +0000 Maggie Koerth-Baker http://boingboing.net/?p=156263

Over the weekend, I stumbled over a great Damn Interesting post about the history and future of the banana. Some of you already know the basic story here: Bananas, as we know them, cannot reproduce. The ones we eat are sterile hybrids. Like mules. The only way that there are more bananas is that humans take offshoots from the stems of existing banana trees, transplant them, and allow them to grow into a tree of their own. It's basically a cheap, low-tech version of cloning, and it has a long history in agriculture. (Note: This would be why Christian evangelist Ray Comfort's video on bananas has become a classic Internet LOL. In the video, Comfort presents the banana—particularly its seedless flesh, handy shape, and easy-access peel&mash;as a testament to the perfection of supernatural design ... completely ignoring the fact that all those things are the result of human-directed agricultural selection.)

The downside to this is that clones are, shall we say, not terribly genetically diverse. Turns out, a lack of genetic diversity is a great way to make yourself vulnerable to disease. Back in the 1950s, a fungus all but wiped out a variety of banana called the Gros Michael. Up until then, the Gros Michel had been the top-selling banana in the world. It was the banana your grandparents ate. You eat the Cavendish, a different variety that replaced Gros Michael largely on the strength of its resistance to the killer fungus.

Gros Michel and Cavendish bananas both look and taste different from one another. Born in 1981, I've probably never eaten a Gros Michel banana. And chances are, my grandchildren won't know the flavor of a Cavendish. That's because the Cavendish still suffers from the same, basic weakness as its forebear. Just like Gros Michel, all Cavendishes are exactly alike. So a plantation full of Cavendishes is highly susceptible being wiped out by disease.

The disease banana plantations now fear: Black Sigatoka, a different fungus that can kill trees and reduce yields in the survivors. The solution: Goldfinger, a new banana clone bred to resist Black Sigatoka. It's surprisingly difficult to track down a verifiable photo of the Goldfinger online. The one used here comes from the website of a Vietnamese fruit company. Based on this, and other photos I found, it looks our grandchildren will know a banana that is decidedly squatter than the bananas we know today.

If you've got photos of Goldfinger bananas, or if you've tasted them, post in the comments! My understanding is that these bananas are already semi-popular in Australia, Singapore, and other places in that general vicinity. It'd be great if Happy Mutants from that part of the world could tell the rest of us what we have to look forward to.

Read the post at Damn Interesting that inspired my hunt for a picture of the Goldfinger.

Read a Popular Science article from 2005 about banana breeding, banana monoculture, and the threat of disease.

When I was little, I read a Reader's Digest book of great disasters, which included a segment on the Black Death. One of the things the book tried to do was explain, on a child's level, why it wasn't easy to figure out that rats and fleas were the source of the plague. You couldn't just look for patterns, because there seemed to be no pattern. Half a household might drop dead while the other half only got a little sick, or remained entirely healthy. Plague doctors who handled the sick every day lived another 20 years. The real spread of disease wasn't like the movies, where one person coughing means everyone in close proximity is doomed.

One reason for the emergence of strange non-patterns like this is something called "super spreaders"—basically, some people spread disease more effectively than others. The infamous Typhoid Mary is the poster child for super spreaders, but the effect has been well-documented in a range of infectious diseases and it goes beyond the simple story of one woman who infected thousands. In fact, what makes the super spreader phenomenon so fascinating is that it isn't an anomaly at all. Super spreaders are the primary way some diseases spread. The Contagions blog—which is all about the history of infectious disease—has a great post up about this.

Eventually new models arose like the “20/80″ rule that says that 20% of cases are responsible for 80% of the transmission and formed a core ‘high risk’ group. This model works well for some diseases but not all.

For pathogens that do rely on super-spreaders, the majority of cases will not transmit the infection to anyone. This can lead to a sense of false security because it seems poorly communicated. As Galvani and May assert, “heterogeneously infectious emerging disease will be less likely to generate an epidemic, but if sustained, the resulting epidemic is more likely to be explosive”. Super-spreaders tend to beget more super-spreaders, although most of the cases they generate will still not transmit the infection to anyone. For example, a super-spreader begets 30 cases, 3 (10%) of which become new super spreaders. The rest may transmit to 0-1 people.

Super-spreading has been documented for HIV, SARS (Sudden Acute Respiratory Syndrome), measles, malaria, smallpox and monkeypox, pneumonic plague, tuberculosis, Staphylococcus aureus, typhoid fever, and a variety bacterial sexually transmitted diseases.

And that brings us back to medical mysteries because, the Contagion blog explains, we don't know exactly why some people are super spreaders and others aren't—or why some people are more vulnerable to infection than others. So far, what we have to go on is a list of well-established correlations.

Read about what makes a super-spreader at the Contagions blog.

Image: Thomas Bartholini's illustration of beak doctor from 1661. Via Wikipedia.