Over the past few months, West Africa has been experiencing the biggest and most deadly Ebola outbreak on record and deforestation is a key part of why.
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More than 100 people reportedly fell ill with food poisoning while attending a high-profile Food Safety Summit in Baltimore, Maryland. The 1,300 attendees included representatives from the Food and Drug Administation, Centers for Disease Control and Prevention, Tyson, McDonald's, and many more agencies and food companies. (NBC News)
I'm 38 weeks pregnant now. Two weeks ago, my husband and I both got Tdap vaccines — tetanus, diphtheria, and pertussis. This despite the fact that we've both gotten Tdaps relatively recently, within the last six years, thanks to a home renovation lifestyle that involves regular exposure to rusty nails.
So why re-up on the Tdap before the birth of our baby? It's all about the pertussis. Also called whooping cough, pertussis is particularly hard on infants. Pre-vaccine, it killed 4000 Americans every year, and most of them were new babies — and infections are on the rise in this country, so there's actually a reasonable risk of a newborn coming into contact with the bacteria that causes pertussis. But the larger problem is with the pertussis vaccine, itself. It doesn't have the staying power it once did. A little over 20 years ago, we switched the formulation for pertussis vaccines. There were good reasons for doing that — the "new" formula has fewer side effects. But it also doesn't seem to protect people as well for as long. In fact, the protection starts to wear off within a year of vaccination.
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In July, millions of people will travel to Saudi Arabia to celebrate the Muslim holy month of Ramadan. When they do that, they might be at risk of contracting MERS — Middle Eastern respiratory syndrome — a coronavirus, similar to SARS. They could also be at risk of carrying MERS back to their home countries. Unfortunately, Saudi Arabian authorities have released so little information about MERS that global public health experts don't know how to advise these pilgrims as they prepare for travel. We don't know where MERS came from, we don't know what its infection patterns are or how the disease has changed since it was first identified. It's not even certain that we know the true extent of infections and deaths, given that the Saudi Arabian government has been releasing that information in batches, sometimes months after those infections and deaths actually happened.
Helen Branswell is one of my favorite sources on global public health and pandemic disease. She's got a guest post at Scientific American blogs that explains what we do know about MERS, and why the lack of information is such a big problem.
The new virus was first isolated in June 2012. But its existence came to the world’s attention only weeks before last October’s hajj, when an Egyptian infectious diseases specialist who had been working in Saudi Arabia’s second largest city, Jeddah, reported that he had treated a man who died from an infection caused by a new coronavirus. Whether MERS has or can gain the capacity for sustained person-to-person spread is unknown.
... Infectious disease experts are aghast that this late into MERS’s spread the world still has no idea what puts people at risk of infection, how long the incubation period is, when people are contagious or whether there are mild cases that are being missed because surveillance is focused on finding sick people in hospitals. They put the problem squarely at the feet of the Kingdom of Saudi Arabia (KSA), which accounts for 41 of the 55 infections to date.
Seven hundred years ago, millions of Europeans were wiped out by a disease we still don’t entirely understand. The Black Death might seem like a pretty open-and-shut case at this point: It was caused by plague-bearing fleas that hitched rides on the rats that infested a grim and grimy medieval world.Read the rest
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.
Read more on giardia (and see pictures) at the CDC website
Coronaviruses are a family of relatively large viruses. The name comes from the fact that, under a microscope, coronaviruses all look like they are surrounded by little halos. Those "coronas" are actually little proteins that cover the surface of the viruses and help them gain access to the cells they invade.
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.
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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
Xenophobia is neither the fear of Xeni, nor of Xena. Rather, it's more about knee-jerk mistrust, dislike, and hatred for people who aren't part of your group. We've come to associate it with not liking people from other countries, but it applies to smaller-scale, less formal tribalism, as well.
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.