Immunoblogging

I exist and new website!

2008-01-10T15:19:00.002+13:00

It's been an extremely long time now, but here it is my new website:

Animacules.

I decided to make a shift to new software and a new way of doing things, because I found the interface here (requiring two seperate sites for full management) was becoming far too clunky. Wordpress offers a few more options and such as well, but ultimately I enjoyed my time on this site and it was good times had by all. But now it is time to move on and such forth.

Anyway, update links as you will good ladies and gents and head on over to Animacules.

Insert ominous music here

2007-07-12T07:37:00.001+12:00

Oh Verizon

2006-12-09T23:24:00.000+13:00

Since when did .002 cents become the same as .002 dollars? I wish I could multiply cents and get the same figure in dollars (somehow).

I'd be a lot richer :/

Oh Hwang

2006-11-01T14:31:00.000+13:00

First he gets done for fraud, then we find out he tried to get eggs from his research assistants and now it turns out he was even going to associate himself with the Russian Mafia:

The defense also said the embezzlement charges, involving funds provided by corporate sponsors, should be dropped, as most of the funds in question are accounted for or still in the bank. Hwang stood by his previous claims that suspicious personal items--such as a car for himself and his wife--were bought with money earned from lectures and publications. Hwang said that some of the allegedly misappropriated money was used for expenses in pursuing unsuccessful projects, which included an effort to clone a mammoth that involved the Russian mafia, and another project to clone a Siberian tiger native to North Korea. In official documents, he claimed to have used the money to buy cows for research.

That's sure a long way to fall from the top of the mountain to...well... this. The only thing I want to know is, what on earth were the Russian mafia wanting with a Wooly Mammoth?

What a mouthful!

2006-10-26T18:58:00.000+13:00

There is something almost disturbing about watching this video of a pelican eating a pidgeon (I kid you not). I didn't know that pelicans were even prone to attacking pidgeons, but I tell you what, that pidgeon seems to have put up one hell of a fight before going down (literally). The amazing things that animals do.

Treadmills and Shrimps!

2006-10-13T00:14:00.000+13:00

For some reason, this really amuses me.

I have no idea why.

Nutrigenetics sting

2006-10-11T15:20:00.000+13:00

While perusing the American Journal of Bioethics, I noticed this really quite amusing piece by Ricky Lewis on nutrigenetics. Some companies are apparently taking samples of peoples DNA and then using the resulting data to try to customise diets to them based on their genes. Sounds like a fairly neat idea in theory, but the Government Accountability Office (GAO) decided to put one such company to the test:

Here’s how the GAO targeted four nutrigenetics company websites. They took DNA from a 9-month-old girl and from a 48-year-old man. Then they concocted diet/lifestyle profiles for 14 “fictitious consumers,” 12 from the baby’s DNA, and 2 from the man’s. For example, the baby girl was transmogrified into a 6-foot-tall, 210-pound 45-year-old man who smokes and doesn’t exercise, drinks a lot of coffee, and eats a lot of fat. The baby also became a 72-year-old woman who weighs 100 pounds and stands 4’9”, regularly exercises, never smoked, doesn’t drink coffee, and eats fried foods. To make it interesting, the researchers also submitted cat and dog DNA but did not disclose whether the cat preferred Friskies to Fancy Feast or the dog Alpo to Purina so as not to tip their hand.

You'll have to read the whole thing, because spoiling the result would really ruin all the fun.

Tired of the same ole whack a mole game

2006-10-03T18:16:00.000+13:00

In a post entitled "I grow weary of ID", Jason Rosenhouse points out some more hillarious ID contradictions. The stupidity of Bruce Chapmans comments where Bruce claims that there is ID research, but nobody will tell you who is doing it and where it is being done because of some darwinist 'conspiracy', is not really being sold very easily. Quite frankly, to rip off a common New Zealand advertising meme:

ID has a prosperous and highly successful research program. Yeah right.

As it still appears that the ID movement doesn't even have a theory to begin with you can imagine my skepticism at anyone claiming there is ID 'research' being done using a DOA "theory". This really isn't the point I want to talk about though from Jasons post, but rather this from a little later in:

Which brings me to the title of this entry. When I got started in this biz, I felt like I learned something by taking the ID folks seriously. The No Free Lunch theorems are beautiful and fascinating, but I would know nothing about them if the sordid little mind of William Dembski hadn't figured how to use them to bamboozle people into thinking their were mathematical flaws with evolution. The research I did while investigating the claims of Jonathan Wells and Icons of Evolution taught me a great deal about the real state of biological research. Fighting these ignorant charlatans was an act of grim necessity, but at least they provided some food for thought.

But look where they are now. They had their day in court and came off looking like fools. The only books they talk about now are the hysterical political screeds by Ann Coulter and Jonathan Wells, neither of which presents anything remotely new. And when you ask them to tell you about the state of ID research, not even actual results mind you but just a description of the work itself, they get belligerent and nasty.

You know, I have to agree entirely with this but with a slightly different tangent. Once upon a time I used to learn a lot out of arguing with creationists and the ID crowd on the various issues about biological evolution. Having to look through the scientific literature on a wide range of subjects from geology, mathematics, biology and more to whack the various pseudo-babble put forth used to be an entertaining and perhaps dare I say, even educational, enterprise. I would always come away having found something new in my searches for counter arguments.

Now, tying in things about why I've been so absent from blogging as well, is the fact I've been reflecting somewhat on the whole issue and my attitude has changed heavily. You see, while once I was like Jason always learning something from these debates, I now fail to get anything out of them at all anymore. After a while, it's always the same arguments, it's always the same counter-arguments that can effectively deal with that nonsense and just as soon as you do it, the same crap comes up again. It ends up after a while getting to a never-ending game of whack-a-mole and to be perfectly honest I find that extremely boring and just not worth my time anymore.

Sure, the political arguments of creationists (like the ID movement) have advanced continually in trying to strawman some thing or another, but these usually have little or no relevance to anything scientific at all. In fact, there is a complete lack of any new science in terms of the latest creationist nonsense. It's always the same flagella, darwinist conspiracy, second law of thermodynamics (dressed up with new rubbish to make it seem more intelligent than it really is) and such forth arguments that have been put up for years. The terms change, but ultimately it's just the same nonsense, it's been refuted by many others (usually more specialised than me) and usually really well at that.

So linking things back to my disappearance from blogging, I've had a good think about what I really want to say online and how I want to present myself. To put it simply, the same idiotic creationist arguments just make me highly antagonistic these days. I'm not sure how to describe the feeling I get from arguing with creationists, other than saying it's equivalent to the feeling you would get from telling someone not to put a fork in the electrical socket and watching them do it anyway. It's just got to the point where playing whack-a-mole just gets highly derisive or sarcastic replies from me. I can't even be bothered really arguing much with creationists now like I used to.

For example, I would once have spend most of an afternoon or evening researching the topics in question, interpreting things (or asking someone who did know) and then posting my counter arguments. This of course is very time expensive as you can imagine, unless of course the argument moved into my areas of interest in microbiology or immunology (where I already knew the required information). But over time, I've found that I can literally, search back posts I've written elsewhere and just copy and paste it. The arguments put forth in a post from 3 years ago (if it still exists) can often suffice completely for answering a creationist argument today. Again, this is because creationist arguments have merely adapted depending on political circumstances and putting new lingo on old redundant arguments. It's still the same broken arguments despite the changes in how it's presented.

This has just led to me getting more sarcastic in my posting style with creationists and I no longer bother putting in the time or effort. To neutral observers, I'm sure at times this has seemed that I've either not had an answer to the argument or that I've given up in frustration. In reality, it's just getting bored of whack-a-mole and wondering why I'm wasting my time. Even after taking a huge break from blogging and even generally arguing about the subject on internet forums, I just haven't been able to lose that feeling of "Yay, whack-a-mole again, what could I be doing with my time?".

Inevitably, there comes a point where you just have to say to yourself "Why bother anymore?". I don't get anything out of arguing with creationists anymore, I don't learn anything, I've heard all the defunct arguments they can put forward before and so I really wonder "What's the point?". It's not like I've got some complacency about creationists, just because they continually make themselves to be idiots in the most public of ways possible like at the disasterous Kitzmiller vs. Dover trial doesn't mean they aren't a very powerful political (but note, not scientific) movement. There are places on the internet however that cater to smacking creationists around very efficiently, like the Pandasthumb, Pharyngula and of course Talk Origins.

With my time however, I feel I can get a lot more about talking about issues in science that actually interest me. How biological systems like the immune system evolved, issues in science like the ethics surrounding gene therapy, public and animal health issues like the Escherchia coli H7:O157 outbreak in spinach (or Tb in badgers ;)) for example. Playing whack-a-mole with creationists is just not worth the time or effort anymore, especially considering how many other fascinating things in science there are to discuss (plus I still have a looooong list of stuff to write about ;)).

Finally, to end this rather large rant I'd like to comment that I don't care what ID researchers think of their own research. Until they publish some of this much vaunted 'research' that is always just around the corner (Always...) I couldn't care less. Talking about doing research is entirely irrelevant to the point of actually doing it. When the ID/creationist movement produces actual science I think it will be worth discussing. Somehow I doubt the ID/creationist lot are bothering with the "science" part and will stick to the "baffling people with bullshit" part.

Oh and I am in an especially good mood because I just began my PhD <3 Yes, that does mean new website soon, because I've been meaning to move to a new site once I got all of this sorted out.

Diet Coke + Mentos = Awesome

2006-09-17T05:51:00.000+12:00

HA!

What is going on?

2006-09-16T19:05:00.000+12:00

Well, it's probably as good a time as any to explain what on earth has been happening with this blog and such forth over the numerous dark months of inactivity. As always with many things in life, things that occur in the "real world" often interfere with other plans that one has for things online. Unfortunately for me, I was intending to have a new website up and running with many of my previous posts updated and revised. This very obviously never happened, primarily due to a wide array of things getting in the way of my plans. The main reason that nothing has happened just yet is that I've been running around sorting out my PhD for the past couple of months (an unbelievable amount of paperwork is involved!).

Now that everything appears to be in order and that I'm starting to get re-interested in blogging again, means that with some luck I should be moving to my new website at some point soon. This of course is all conditional on other things, such as my initial workload in the lab and other things that could potentially interfere.

I do apologise for the long stretch of absence and general lack of blogging on my part.

43rd Skeptics Circle

2006-09-16T19:03:00.000+12:00

The 43rd Skeptics Circle has been posted over at Adventures in Ethics and Science. I hear there are puppies involved.

42nd Skeptics Circle

2006-08-31T21:16:00.000+12:00

Welcome to the 42nd meeting of the skeptics circle. Many of you have wondered where I have been over the past months and what has exactly been going on down in the lowest part of the world. Well my excuse is that, uhhhh, hmmmm...Ah yes, we've been invaded by the undead [of course, why didn't I think of this before]. Oh yes, they are everywhere down here I assure you and we're knee deep in them. Billions of them. Here is an example picture:

See what I mean? Absolutely crawling with the undead [they are there I assure you, they are just camera shy]. Can't cross the street without having to dodge numerous zombies all after your brains. What's worse is they are all into various forms of pseudoscience, woo and quackery. Perhaps it might all be the result of dumping too much nuclear waste into the rivers and I assure you, we'll be returning to the subject of nuclear waste later in the circle. Everything ultimately is blamed on nuclear waste eventually anyway. First it's poisoning the water, then ruining the air quality, then making people sick and eventually raising the living dead. You know how it goes.

So it's a good thing you've all turned up so we can try and set them straight with some good old fashioned skepticism to the head. I've personally always liked the sledgehammer of science myself, but the lawn mower of anti-woo has its own appeal [even if it's very messy] and there is always the shotgun of reason. Whatever your weapon of choice, there are many ways of dispatching crazy pseudoscientific zombies, but the problem with the living dead and I'm sure you can appreciate the many problems we are facing, is that they keep coming back regardless. Reminds me of arguing with creationists, no matter how many times you dispatch their arguments there are always more of them and the old ones come back anyway [tis quite the problem with the unliving dead, you can't kill them you see, because they are already dead. Haha, see the dilemma?].

Currently the creationists have been shacking up with a really good friend of theirs: the dreaded Hitler zombie. While not hanging out in my pool (making it all mucky) and shouting incomprehensible things at people he doesn't like, the Hitler zombie often enjoys eating the brains of people making ridiculous comparisons between evolution, himself, NAZIdom and various other aspects of the third Reich. Thankfully, Scientia natura tackles some of the ridiculous arguments creationists make on this topic in evolution, Darwin and Hitler. When they aren't trying to compare evolution with Hitler, creationists resort to other ridiculous arguments instead as Tara Smith from Aetiology covers in Influenza viruses = evidence for design. Those whacky ID creationists, what won't they claim? Finally, the Pandas Thumb has a lovely series covering the latest collection of ridiculous claims in Johnathan Wells' new book. I don't recommend buying the book and instead just reading the rebuttal. Your sanity will thank me for it later. If you ask me, I'd rather face the zombies than deal with creationists nonsense.

Staying on the science front in this circle, Jonswift has another piece of wonderful satire covering how science is undead-errr how science is dead. Haha. *Ahem*. Sorry about that, couldn't resist a little zombie themed humour there. Carrying on, Divided we Stand, United we Fall takes on some of the bizarre claims that Anne Coulter has made about global warming researchers (among other thing). Personally, I keep a copy of her book around with me at all times as zombies won't attack you when they see it. Seems to fool them into thinking you're one of them, which is very handy for popping down to the dairy for a few moments without harassment.

Speaking of taking creationists to task, the Pooflinger writes about the stupidity inherent in having to consider 'both sides' in back of the book. Rockstars' ramblings also comments on the fallacy of using 'both sides' to justify anti-evolution nonsense. Finally, speaking of math, the Bad Astronomer also has a public service announcement, reminding us in the skeptical community that it's always healthy to correct your own mistakes. Especially when they are mathematical.

Moving along from the creationists, remember earlier on how I mentioned that Nuclear Waste? Well, it turns out there is a great solution for that and it's even sponsored by a celebrity! Yes, I'm talking about using Kabbalah Water to clean up nuclear waste and Madonna apparently really likes the idea. Thankfully, some of our contributors have decided to wham some sense into this undead beast, with Skeptico commenting that Madonna solves nuclear waste problem. If that wasn't enough, Humbugonline also tackles the issue in Mad Madonna the Comedian. I wonder if that water works on zombies- or was it holy water that was supposed to be effective against the undead?

The subject of this circle now turns onto the ever fun topic area of medical woo, pseudoscience and just plain crazy. Firstly, we'll begin with the Beaver examiner noting that South Africa donates $100-million towards garlic research. This should show those normal 'HIV priests' that clovology should be taken seriously as garlic research is seriously important for numerous reasons. Take it from me, when you're knee deep in zombies then come the vampires. What's good on vampires? That's right, Vampires. South Africa will be making a good investment in anti-vampire technology for the future. Speaking of Garlic, scientia natura also recognise how powerful it can be in a quack healers deception.

Orac from Respectful Insolence brings us some more skeptical blogging to do with medical woo in two cases, firstly the pause that refreshes and heals. I always wondered why people told me yellow snow was bad for you. He also brings us a look at Abraham Cherrix, a child whose parents are attempting to avoid conventional treatments so they can use nutty altie ones in starchild Abraham Cherrix: It's over. Unfortunately, when it comes to mistakes that occur with normal conventional treatments and alties, things never work out as Bronze Dog explains.

Carrying onto our final skeptical topics for tonight, a guest post by Mum to Laura on Autism Street wonders what people would think of a "blindness spectrum". EoR, over at the second sight wonders at the tactics some crazies will go to try and sell their books to the gullible in Jesus is real - Oh, and buy my book! PS: You should buy my upcoming book as well: How to defend yourself from a zombie attack with nothing but a spoon, a wire and some table salt. Speaking of somewhat strange things people propose, Socratic Gadfly covers the use of regaining your 'inner child' to treat abuse cases in some thoughts on child abuse recovery counseling, AA, PTSD and related matters. Finally, the Saga of Runolf wonders just what happened to animal planet in the great animal planet disappointment.

Also, before we all leave satisfied in a skeptical driven zombie genocide well done, let us all bear tribute to Douglas Adams who has long since ceased to be with us. Nothing with the number '42' in it can go without at least mentioning him. He was a really great writer and he will always be missed. So that's all for the circle this week and most importantly, thanks to all those who submitted articles. I do hope you've enjoyed this entertaining romp around skeptical thinking and be prepared for the next circle, which will be hosted by Janet D. Stemwedel at Adventures in Ethics and Science. Anyway, it's time for me to go and- wait, what's that sound at the door? Moaning? Hungry moaning? Scratching? Cracking... Oh no...they've breached the defences! There are hundreds of them, they're in the room and oh dear Go[.sd.assd.zhjai

[Disclaimer: Yes, somewhere along the line I have gone completely and utterly mad. MUAHAHHAHAHAHAHA]

A very confused skeptics circle

2006-05-26T08:23:00.000+12:00

Oh Skeptico, how much fun it must be to have someone first smurf you and then make a blog with a similar name as well! Confused? Well so was I, but all the answers are in this weeks skeptics circle hosted by our good pal Skeptico and his...uhhh pet smurf.

As for me, things will be starting to change shortly although it will be after the weekend or so. I'm going away for a weekend to help move stuff around in a relatives house so I probably won't be available. After that, it's about time to move things along with my new blog I think :D

Carnival of the wee animacules

2006-05-19T05:09:00.000+12:00

The latest edition of all things small and microbial has been posted at Aetiology. The carnival seems to be going into a monthly format now from it's previous bi-weekly one, which indicates that we need a few more regular hosts and those willing to submit entries. Make sure you let Tara (from Aetiology of course ;)) know if you want to submit something to the carnival or host a future edition.

Where am I?

2006-05-18T17:37:00.000+12:00

As a couple of commenters have wondered where I've gone I'll give everyone a quick update as to what has happened. Basically, I'm making a new site and I've basically busy doing that at the moment. Stimulated by Ocellated who suggested going to a .com and going to word-press (which I've concluded I rather like), I've started to design and move most of the stuff on this blog to a new one. It's not done yet, partly because I suck at web-design and am more of less doing things by a random 'trial and error' process and I've had a bit of drama. For example having one of my teeth removed recently (long story) and been busy organising various other real life dramas (real life drama is the best kind I've found). So that's been a bit of distraction from my goal of making a much improved site that is a little 'my own' as opposed to 'generic template' style here.

Until then, I've been a little active on another blog I'm a co-contributor on, namely Limed for the Truth, which is a blog set up by members of the Penny Arcade community and has a wide array of different posts and topics. I recently re-wrote and updated an earlier piece I did on this blog discussing antibiotics over there if you're into that sort of thing. As for the exact future of this blog, it's probably going to be inactive shortly and this will probably be one of the last updates here. Once I've got my new blog up and functional I'll obviously be posting a link. Until then there won't be a lot of activity here except for the odd random post. I'll be posting more frequently (on similar topics) over on Limed for the Truth though. Including the importance of keeping your dental microbes in check, especially when you crack a tooth and don't go to your dentist until it's too late....

For reading in the mean-time, I would suggest having a look at the stony skeptics circle over at The Second Sight, which was posted a wee while ago (I've been on the net a bit sporadically as of late ;)). Additionally, tommorow there will be the carnival of the wee animacules at Aetiology if you're wanting some microbial goodness.

So the short and skinny of it all is that I'm making a new site and organising stuff in "real life" (whatever that is ;)). As I'm rather keen and interested in my new site, I've kind of relegated this one a wee bit while I work on there. If you want to know what I'm doing in the mean-time, I will be posting every so often over at Limed for the Truth. Oh and yes indeed Mr. Swift, I did take a bit of time to play some videogames ;) Gotta get them before I start my PhD and subsequently won't have the time to play them :D

Still alive

2006-05-03T20:07:00.000+12:00

Just a post to let you guys know that I'm still alive and trying to figure out what I'm wanting to do with the site. Unfortunately, with my graduation ceremony coming up in only a couple of days I've been a little busy handling that at the moment. I should probably have decided to attend the graduation ceremony back in december last year, but that would require the prompt return of the various paperwork involved. Unfortunately, while relocating to another part of the country it turns out that's not something that was particularly possible to do.

Normal blogging will resume eventually, but I've given up trying to make predictions on when exactly that is going to happen. :)

Oh blog memes

2006-04-30T22:27:00.000+12:00

This one I noticed from Orac, PZ Myers and Grrlscientist was fairly amusing:

Your Theme Song is Born to Be Wild by Steppenwolf

"I like smoke and lightning
Heavy metal thunder
Racin' with the wind
And the feelin' that I'm under"

A total independent spirit, you can't be held down or fenced in.
You crave the feeling of wind on your face... and totally freedom.

What's Your Theme Song?

At least it isn't Hit Me Baby One More time or something. That would be just sneaky.

iNoodle

2006-04-30T03:31:00.000+12:00

May our music be touched and protected by his Noodly Appendage.

One judge with a sense of humour

2006-04-28T22:12:00.000+12:00

The British Judge that threw out the plagiarism case against Dan Brown and the Da Vinci Code has had a bit of fun with his decision. As it turns out, he's inserted various italicised letters into the overall text and codebreakers are trying to figure out what message he left. Which it seems some clever chap managed to do (see the linked article). I was hoping for something on how silly the whole case was to begin with, but the judge was just having a bit of fun it would appear.

At least he has a sense of humour.

The 33rd skeptics circle

2006-04-28T00:33:00.000+12:00

The next edition of the skeptics circle has been posted at Science and Politics and contains the usual skeptical goodness for digestion. I recall that Orac is still looking for future hosts and so it might be worth paying him a visit if you'd be interested in doing that.

Site redesign

2006-04-27T19:10:00.000+12:00

I finished Dragon Quest VIII and so that means things will be getting back to normal around here pretty shortly. First up I'm hoping to get some ideas for redesigning the site. As you can see, this blog isn't overly different in look to pretty much every other blog on blogger. It looks a little bland as a result to me and it always somewhat miffs me that it looks like every other blog. I've done a bit of 'personalisation' on the site every so often, like adding the little antibody under the title (that's what the Y shaped globular thing is if you've ever wondered). Overall however, it's still pretty much the same as it was when I first started it.

Now I'm not saying there is anything wrong with the good old blogger.com template. It's perfectly functional and my numerous experiments with it have allowed me to figure out quite a bit of HTML. The guy who made the thing originally certainly did a very good job, but it's just not mine if you can appreciate what I'm getting at. So I intend to 'personalise' the site over the next couple of weeks. What this means is all sorts of random errors and general chaos. I don't expect most of the things I try and do to work the first time (if at all), so if the blog explodes or something then just assume I've done something horrible to it.

The other thing I'm trying to figure out is my RSS feed. Apparently it's not working, or working some of the time or it just doesn't behave in any sensible manner. To be honest I'm still rather clueless as to what I've done to it and am working to correct the problem. With luck the site redesign will allow me to figure out what exactly I did to it.

Finally, if you're looking for some reading to do and haven't seen the latest carnival of the wee animacules, then that was posted recently at the Biotech Weblog. It was fairly small last week though so we need a few more people making submissions. Or alternatively, a couple of regular submitters not playing computer games :p

Oh dear

2006-04-23T20:58:00.000+12:00

I had absolutely no idea that Dragon Quest VIII would be able to capture my attention so thoroughly since I bought it a week ago. I'm nearly finished with the game now, it's probably one of the longest games of its type I've ever played and so things will hopefully return to normal by monday. Well hopefully anyway, depends on how quickly I get through the last couple of dungeons :D

In future I think I shall remind myself to never buy a new RPG when I intend to do a large amount of blogging. It's usually not a very good idea for my overall productivity :p In any event, while I was effectively taken out by the charming nature of Dragon Quest VIII, I did get time to read an excellent paper in Nature Immunology by several Pandas Thumb posters. Essentially Andrea Bottaro, Matt Inlay and Nicholas Matzke clearly describe the devastating role that immunology played in the defeat of 'Intelligent design' in the Kitzmiller vs. Dover trial in december last year. Effectively the Nature Immunology paper gives a clear message of thanks to the many hundreds of scientists who actually do research into the evolutionary origins of the immune system (one of my key interests these days). Additionally, to give ID adovcates even more of a headache is this annotated bibliography of the 68 articles presented to Behe at the trial.

Finally, apologies to anyone looking forward to the posts outlined previously, but rest assured I haven't forgotten to do them and I'm certainly not forgetting about the blog. Just a tad distracted tis all ;)

Dragon Quest: Journey of the Cursed King

2006-04-15T16:57:00.000+12:00

I've been playing this game for much of today and am absolutely loving it. It simply opitimizes exactly what I like about the Japanese role-playing games and feels very much like old Super Nintendo Entertainment System (SNES) games I used to play. It's a lot harder than most other JapRPGs I've played though, especially as the monsters in regular encounters are much more of a challenge. The art style of the game is also pretty good as well, probably as it was done by the same artist who did Dragonball Z and some of the animations are quite amusing. Overall it's a fun game experience and I think there will be many hours wiled away levelling up my little computerised avatars and smacking around monsters.

Hopefully it won't affect blogging too much ;)

Blog direction

2006-04-14T17:45:00.000+12:00

When I first started this blog last year the intent was to argue against certain claims made against the MeNZB vaccination scheme in New Zealand (hence the title and the little quip under it). As it turns out, that particular thing has become rather moot these days and the media, public and everyone else has pretty much moved along. This is probably the result of the fact the vaccination regime has actually worked, which always does a lot to end all various people fussing around.

So the result really is now to establish a more solid direction to what I want to do with the blog. I've become less and less interested in nuts as time has gone on. For example, there are many blogs that are dedicated to the debunking of claims from creationists like the Discovery Institute, general nutters and all sorts of others. While I will definitely continue to add my 2cents on discussions on claims from said groups in my relevant subject areas (Microbiology and immunology), it's unlikely that I'll have a lot to add in other subjects as many other blogs cover the area (quakery debunking) quite well. For example, see this post by Ian Musgrave from the Pandas thumb on the hillariously ineffective response of the DI to the recent hormone evolution paper in Science, as a good example of what I'm meaning. Many more examples abound on many other blogs I visit regularly like Pharyngula, Respectful Insolence and Dispatches from the Culture Wars.

Where to go on this blog? Well, I'll probably continue to write on subject areas that interest me (or manage to rile me up) more so than plain 'debunking' of various claims, which are usually the same ones as made last month/week/year that never seem to die. As a result, I'll probably blog a lot more about microorganisms, their relationships with us and how we can benefit from microbes. For examples of what I mean, my series on bovine tuberculosis in britain (Part I, Part II, Part III and Part IV), farm animal cannibalism, probiotics (here and here), microbes I find interesting like the plague (Here and here*) and mare reproductive loss syndrome. Additionally, I also hope to write a lot more about the vertebrate immune system and why immunity to microbes has been such a critical factor in our evolution. This will be along the lines of my current posts on MHC (Part I, Part II and Part III, with some updates to come as I've read a lot more since) and I intend to elaborate more on the evolution of Toll-like receptors in future (a very soon future) as well.

Most importantly, I intend to keep more to things that I say I will do. For example, I have not forgot that I was supposed to write more about TLRs, the alternative theories about the black death* and such, it's just I unfortunately haven't managed to get around to doing the reading. In future, I hope to keep more to what I say I will write, so that if you see "post tommorow" that post will turn up 9/10 tommorow. Not uhhh, next week or maybe even a couple of months as the current blogging schedule seems to work with me :p

So what is to come? Well there will be the continuation of the Bovine tb series next week and future posts on the ethics of talking openly about bioterrorism, which is why this series hasn't been continued yet if you've wondered. In fact, I was going to delete the post until it was included in a carnival of the wee animacules, so I decided to keep it up but not continue it. There will be many toll-like receptor posts next week and how zany those scientists who work with Drosophila melanogaster are. For a change, I also intend to write a post about how bacteria help us in our daily lives as opposed to their typical PR of being evil pathogens (among other things). Finally, I hope to go over how plausible a 'doomsday' virus could be and how we could combat it.

So the new direction is really more about writing about and explaining interesting science on evolution and microbiology, which would otherwise go unnoticed to most non-scientists. I'll leave the debunking of creationists (for example) in areas out of my field of expertise to the professionals.

*There is quite a lot of debate on the issue, so I'm taking my time to read everyones opinion andvarious back and forth exchanges in certain journals.

Sobering up Intelligent Design

2006-04-14T16:38:00.000+12:00

I'll put a link into this great Pandas Thumb post analysing an essay written by Elliott Sober*, Intelligent Design theory and the supernatural - the "God or Extra-Terrestrials" reply, which takes on the ID argument and establishes how ID inherently can't escape from a supernatural designer.

Abstract: When proponents of Intelligent Design (ID) theory deny that their theory is religious, the minimalistic theory they have in mind (the mini-ID theory) is the claim that the irreducibly complex adaptations found in nature were made by one or more intelligent designers. The denial that this theory is religious rests on the fact that it does not specify the identity of the designer — a supernatural God or a team of extra-terrestrials could have done the work. The present paper attempts to show that this reply underestimates the commitments of the mini-ID Theory. The mini-ID theory, when supplemented with four independently plausible further assumptions, entails the existence of a supernatural intelligent designer. It is further argued that scientific theories, such as the Darwinian theory of evolution, are neutral on the question of whether supernatural designers exist.

I certainly think that Sobers essay is interesting and he makes some new points that I hadn't considered much before. Personally however, I've never thought that the way "ID" is set up now would ever include aliens period. Natural aliens would have methods that we could potentially establish and look for in making life as we knew it. The fact ID research don't try to establish anything about the potential methodology the designer(s) 'used', indicates heavily that their 'designer' is supernatural and as a result doesn't have a detectable methodology.

*You see what I did there? I took the guys name and made a witty pun with it in the title of the post. I'm so awesome!

A poo-filled skeptics circle 32

2006-04-14T01:13:00.000+12:00

The next edition of the ever exciting collection of skeptical knowledge has been posted at the Pooflingers anonymous. Lots of entries and a large side story to keep you entertained this week.

Britains Boy Soldiers

2006-04-12T00:25:00.000+12:00

I intend to write a little more on this later, but I just watched a documentary on the history channel about underage boys who signed up and served in the British army in World War 1. I highly recommend seeing it as it's an amazing documentary and the subject matter (I found) is really moving.

It's hard to imagine that so many of these underage boys, some as young as a mere 14 years old, would want to sign up and join a brutal pointless war of attrition where nobody really actually won. Out of what, you would have to imagine, would possess someone of that age to want to join into the military? Some sense of patriotism that they would serve their country in a glorious war (that turned into nothing more than a meat grinder)? Worst of all, was that with the high attrition rate on British forces in France, many of them were simply 'coerced' into joining the army and often without their parents knowledge. Possibly the most inhuman aspect of it (to me) was that the British army knew that many of their supposed 'soldiers' were underage and just pretended to ignore the problem.

I knew before that in both World Wars underage boys had served in the military by lying about their age, but I had no idea that so many underage boys served in World War 1 and just how young some of them could get. Well worth viewing this documentary if you can catch it on the history channel or similar in future.

Seguin Gazette-Enterprise articles have been updated!

2006-04-11T09:19:00.000+12:00

Remember those articles from the Seguin Gazette-Enterprise that lambasted Dr. Pianka that disappeared? Well guess what, do a search on Dr. Pianka now and have a look at what the results are: they're back!

Update: Actually it appears the articles may not have been altered but instead have just been replaced. The April 2nd article from the Seguin Gazette-Daily does not appear to have survived and these are just other articles. I'm not sure if these have been updated as it appears that the reason for their disappearance has been explained thanks to the investigation undertaken by the Questionable Authority.

He was actually quite surprised to hear that the articles were not available online. Apparently, the company had directed that the transcript and the audio recording from the speech be removed because both were at least partially incomplete. That was apparently misunderstood, with the result being that all of the materials were removed. He has since gotten back in touch with the Gazette-Enterprise, and the articles are now back online.

Now everything makes sense. They were removed originally as the transcripts posted were incomplete at the companies request and now two of the articles (From april 4 and april 5) are back. The april 2nd article is still missing.

Further Update: Now the April 2nd article is back as well. Looks like it was just a mistake.

Jonathan Witt goes to the Quote Mine

2006-04-11T08:19:00.000+12:00

I noticed this link to an analysis of the Discovery Institutes (DI) response to the new fossil fish Tiktaalik, which has creationists everywhere running around with chickens with their heads cut off in 'damage control', from the Dispatches from the Culture wars. The DI 'response' is so inane it doesn't deserve linkage, but you can find it at the link to Steve Reulands take-down if you really want to bother reading more DI garbage. I only suggest reading so many DI 'responses' and press releases because the general abuses of logic contained generally inflict cummulative damage if too many are read at once.

Anyway, Steve notices that Jonathan Witt quotes a paleontologist called Henry Gee in responding to the fossil finding. Somewhat unsurprisingly, like most creationist quotations of actual scientists, it seems that Jonathan Witt has hopelessly mangled the meaning of the quote. Additionally, it seems that Henry Gee is a fairly popular target of quote mining, so much so he even has made a public statement on the matter.

More analysis of the DIs farcical posts on Tiktaalik can be found on the Pandas Thumb (here and another post here) and on Ed Braytons blog, Dispatches from the Culture Wars. Also, just so nobody can claim that I've forgot that Answers in Genesis still writes stupid things as well, Lancelet has given a suitable paddling to AiG nonsense on the fossil here and a second post here.

It's link love to takedowns of creationist nonsense tuesday!

Two responses to ID propaganda

2006-04-11T06:24:00.000+12:00

Last week, Science published an article by Bridgham et al., (2006) Evolution of hormone-receptor complexity by molecular exploitation. The paper shows how an irreducibly complex interaction between a receptor and its hormone that it binds to can evolve. Naturally, the DI got visibly upset over actual research, published in actual journals, performed in actual labs demolishing their claims they have put out in popular books made for the public. One of their responses, if you can call it that, can be found here and is about as incredulous as you would expect from the DI.

Since that, there have been two very good responses to the nonsense thrown out by the DI response. Firstly, I would point you to this excellent post by Carl Zimmer at the Loom. His commentary is particularly cutting but he makes one particularly brilliant point (emphasis mine):

Is it me, or is it strange that intelligent design advocates are telling biologists that they aren't working hard enough, that they are not getting enough results from their lab work? Remember, this is the same Michael Behe whose sole peer-reviewed paper in the past eight years was a computer model (and a pretty poor one, it turned out). Compare that to the work of Joe Thornton, the principal investigator on the new paper. In the past eight years he's published twenty papers on hormones and their evolution: he's been sequencing hormone receptor genes, working out how they respond to different hormones, determining how they're related to one another, and even resurrecting them after 450 million years of oblivion.

Ouch. I felt that one from all the way over here in New Zealand! Further, another response that is worth noting is from the Pandas Thumb (of course), where Ian Musgrave notes how slippery the definition of IC is. Additionally he also shows how the definition of IC isn't really that well defined to avoid any form of significant falsification.

Yet this “system” is precisely the thing that Behe uses in his exemplar for the Behe and Snoke paper, the binding of DPG to haemoglobin. And Behe has said in testimony to the Dover trial (3) that the Behe and Snoke paper on evolution of binding sites is about irreducible complexity. So if the evolution of the DPG binding site (where you only need two mutations to make a functioning DPG binding site) is an example of IC, then the evolution of the aldosterone binding site is also (note 2). As the BCT paper specifically cites the Behe and Snoke paper, you would expect they would look at the ideas contained in the paper, not “Darwins Black Box”. Behe has had a long history of citing examples of molecular IC. He has even called disulfide bond “irreducibly complex” (2). So his disavowal of an example that directly addresses the Behe and Snoke paper (3) is particularly disingenuous.

Not that Behe has ever thought much of actual scientific research anyway.

Ren and Stimpy creators blog

2006-04-10T07:42:00.000+12:00

I noticed from Penny Arcade a link to the blog of one of the guys who did Ren and Stimpy. I thought it was worth a read as I've always been a great fan of the original Ren and Stimpy series. The post I found interesting was the one discussing 'organic' drawing styles. Basically, the post compares the drawing styles of cartoons that use more 'soft' style shapes against the new trend of using geometric shapes to form characters. For example, think of the older cartoons like the looney tunes and Ren and Stimpy, against the way Genndy Tartakovsky uses hard geometric shapes to make characters in Dexters Lab/Samurai Jack and such forth.

Personally, I like both styles but I do admit that the organic style of animation does seem to be going out of fashion a bit.

The role of cattle movements in the bovine TB epidemic

2006-04-08T05:27:00.000+12:00

Part IV: Mycobacterium bovis, the English bovine tuberculosis outbreak, badgers and the culling debate.

Although bovine tuberculosis (BTB) is known to spread through wild-animal populations and is readily transmissible between cattle, the role of large scale cattle movements could be an important indicator for the spread of BTB. The current epidemic is concentrated in a large central area in the south west of England and Wales, with a large number of outlying foci of infection outside of this core area. Essentially, within the core region it’s predicted that internal factors such as animal reservoirs (badgers), environmental conditions and relaxation of adequate control measures maintain BTB rates. The question is if the movements of infected cattle or material can explain the distribution of BTB. Conveniently, a study published in Nature sought to answer precisely this question and will be the subject of this post.

Gilbert et al., 2005. Cattle movements and bovine tuberculosis in Great Britain.

In their study Gilbert et al., (2005) made a computer model designed to predict the spread of BTB to new areas from the ‘core’ region by using movement data obtained from the British Cattle Movement Service (BCMS). The BCMS was set up in 1996 after the BSE outbreak in Britain and is essentially a large scale monitoring system to trace the births, deaths and movements of cattle across the UK. Part of this system is the Cattle Transfer System (CTS), which keeps the record of cattle movements and was what the authors based their study on.

Importantly they avoid a problem with the way that the CTS records the cattle movement data, which may have compromised the papers results considerably (See supplemental material). You see, every cattle ‘movement’ recorded by the CTS is in reality recorded twice. Once for the “on” movement and another for the “off” movement meaning that all cattle movements have to be paired to make sense of it. When this procedure is actually done, a large amount of the data from before 2000 is shown to be rather inaccurate (there aren’t two movements recorded correctly for example), but is very accurate data for the period from 2000-2003.

Another limitation of the study that the authors put forward (again, supplemental material) is the reliability and time disparity between tuberculin testing. Depending on when an animal is tuberculin tested, it may show to be positive for BTB before or after it has moved, giving an inaccurate impression of where the animal actually was infected and if it was pre or post movement. This would particularly affect the results from regions with less BTB than other areas of the UK, as these areas tend to perform tuberculin tests less frequently. The authors of the paper discount this as a problem reasonably, as the disparity in time between testing is not going to be a uniform problem affecting all of the cattle herds uniformly. Basically, some herds will be tested very regularly and a few will not, which while this adds some further random variation doesn’t affect the overall strength of the association.

Bearing these two factors in mind the question really is: Does their predictive model correlate with the observed BTB spread? The answer in short terms is that it does and it does so with quite a high degree of accuracy. For example, take one of the figures showing the models BTB prediction against the actual observed rates of BTB:

Figure adapted from Gilbert et al., 2005. Cattle movements and bovine tuberculosis in Great Britain. This is one of four comparative maps generated from their model in the paper, in this case showing the result obtained from "2002" against the observed BTB incidence from the same year. This is also performed again for 2003, 2004 and for 2005. 2004 and 2005 do not show the smaller map because BTB incidence data wasn't currently available when the authors did the study.

Here you can see that their modeled BTB distributions and the projections from their model on the larger map of the UK for 2002. The darker the colour on the map, the higher the predicted probability that there will be a presence of BTB in that area. The smaller inset map is the observed frequency of BTB. The figure above and others from the paper demonstrate there is a high correlation between cattle movements and the presence of BTB in a region. Generally speaking, where cattle are being moved around from ‘core’ areas particularly it is associated with spreading BTB to ‘remote’ areas.

What the model doesn’t show and how to experimentally confirm the study

One place where the model shows abnormalities is that there are regions that have numerous cattle imports, yet the disease fails to persist for any meaningful period of time. It’s important to bear in mind that this could have several explanations, the first of which being that the cattle are only temporarily held in the region. For example, they could arrive and be immediately slaughtered on arrival, such as to an abattoir, which wouldn’t give any time to spread the disease. Another possibility is the lack of wildlife reservoirs, namely badgers in any meaningful capacity in the region, which is also the explanation I would favor, in particular given the association between badgers and BTB (see part III). A final explanation may be that these regions are not prone to many movements from ‘core’ areas, which reduces their risk considerably.

This study could also be interesting to contrast with the known spread of BTB in general regions. As it predicts BTB spread based on cattle movements, it does immediately present a means to experimentally verify it on the ground (so to speak). Given their model, it should be expected that movements from areas with BTB should be associated with the detection of certain Mycobacterium bovis spooligotypes (basically strains). This is because the imported infected cattle should bring with them their M. bovis types and therefore spread that to the uninfected herd. Over time, based on what cattle movements went into a region and what spooligotypes infected cattle bought with them, you would expect to see those spooligotypes in subsequent herd breakdowns.

Here is where I become somewhat skeptical. It’s known from previous experiments which have analysed the spooligotypes of M. bovis from badgers and cattle that these tend to be shared between the two species (see part III). This also tends to be isolated by geographical regions, with a mixture of spooligotypes but only a few ‘oddball’ ones that aren’t shared between badgers and cattle. In the model predicted by Gilbert et al., 2004, where cattle movement is the primary motivator for BTB spread it also implies cattle to cattle spread. The lack of spooligotype mixing between regions from studies conducted in Ireland (for example) have shown spooligotypes of M. bovis tend to be similar in a region but not between them, raises concerns over cattle movement as a predictor of M. bovis. It may be likely that cattle movement helps to spread the infection to a new region, but is not sufficient to determine if the disease will be able to establish in the new region.

Conclusion

It’s clear from the Gilbert paper that cattle movements are playing some role in the spread and establishment of BTB in the UK. The question is still open as to what that exact role is and how the movement of cattle would spread BTB to other regions. For example, how well does such a model deal with the rates of BTB spread among ‘closed’ herds in the UK that do not actively import cattle from elsewhere? It would be interesting to compare the incidence in BTB among “closed herds” with the regions predicted by this study as being at risk for BTB from “on” cattle movements. In any event, if cattle movement is an important indicator, it immediately opens up simple ways of reducing the spread of BTB such as by implementing pre-herd tuberculin testing before movements (which I think is being implemented now).

In any event, this does not resolve the problem with badgers as a large reservoir for M. bovis. Ultimately, this debate has become rather invective and polarized over one key issue: If the control of M. bovis requires the culling of badgers in order to be accomplished. In the next part of this series, this immensely important aspect of the control program will be discussed in Part V: Will culling badgers have any effect on the control of bovine tuberculosis?

References

Gilbert M., A. Mitchell, D. Bourn, J. Mawdsley, R. Clifton-Hadley and W. Wint (2005). Cattle movements and bovine tuberculosis in Great Britain. Nature, 435:491-496. Also see the supplementary materials published with the papers as well.

Mare reproductive loss syndrome and caterpillars

2006-04-07T21:00:00.000+12:00

This is a story of two organisms and the identification of a really unusual way for bacteria to end up in a place they really should be. One of the organisms involved in this story happens to be a horse:

The other organism involved is the Eastern tent caterpillar (Malacosoma americanum):

You might be thinking at the moment as to how that tiny caterpillar interferes with a horse. After all, the caterpillars in question are a communal bunch that spin little “tents” and horses shouldn’t really have any particular interest in caterpillars. Most remarkably however, these caterpillars are known to be associated with a disorder in pregnant horses called Mare Reproductive Loss Syndrome (MRLS). Most interestingly in this story is the proposed mechanism by which, this tiny (6cm long) caterpillar is responsible for causing a bacteriological infection of the developing fetus and ultimately killing it. But first, it’s time for a bit of background.

What is MRLS?

(Information is from Webb et al. 2004, unless otherwise referenced)

In central Kentucky USA from late-April to May of 2001 an unusually high number of spontaneous equine abortions suddenly started to occur. The rapid rise in abortions among early mare fetuses (a gestation time of around 40-150 days) was particularly prominent, with some farms having up to 60% higher early fetal losses compared with the ‘normal’ rate of 3-5%. As Kentucky prides itself on its horses and they are important in the economy of the area, the news was naturally incredibly disturbing. To illustrate the impact of this disease on the Kentucky economy, it resulted in thousands of mares aborting their fowls and with an estimated loss of over $425 million (!) dollars (Potter et al. 2005). The unknown disease was designated mare reproductive loss syndrome and was rapidly investigated.

Investigation of pregnant mares by ultrasound revealed that the fluids around the fetus were often extremely cloudy. Examination of the dead fetus revealed the presence of numerous bacterial species, but most interestingly no specific pathogens known to be associated with fetal abortions in horses. Instead, the isolated bacteria tended to be associated with commensals such as non-β haemolytic streptococci, actinobacilli, Serratia marcescens and many other bacteria. The majority of these identified with either oral commensals (like the streptococci) or bacteria commonly associated with the gut microbiota such as Enterobacter and Serratia spp.

More curious was the lack of pathology observed in the mother horse itself. Although some horses had some symptoms, such as pericarditis, the majority did not present with a fever or other indication of a systemic bacterial infection (despite this being present in the fetus). This unusual pathology raised the question that the bacteria were a secondary infection and something else, such as an ingested toxin was causing the spontaneous abortions. During the investigation of the outbreak of MRLS, it was found that a caterpillar, the Eastern tent caterpillar (ETS) had a large population explosion at around the same time that the outbreak of MRLS occurred. Could the caterpillar population explosion explain the sudden appearance of MRLS?

Demonstrating a link between caterpillars and MRLS.

The most conclusive paper on the link between MRLS and the ETC was performed by Webb et al., 2004 (See the full reference below). This study performed three experiments that demonstrate ingestion of ETC is associated with MRLS after the results of a pilot study (also performed by these authors) showed promising evidence of a link between MRLS and caterpillars. The three experiments were:

Experiment 1: This compared three groups of pregnant mares in the pasture to replicate what would be ‘natural’ transmission of caterpillars into the horse. One group was on a caterpillar diet, which involved adding a certain density of caterpillars onto a sealed off section of pasture and allowing the horses to basically eat them with their usual feed. Another group was exposed in the same manner to caterpillar frass (see the picture of the caterpillars above, frass is, as far as I understand, what the stuff they spin is called). Lastly, there was the control group that lacked any caterpillars or frass.

Experiment 2: This is very similar to experiment 1 except that this time they fed pregnant mares directly either frozen or autoclaved M. americanum caterpillars or alternatively, another species of caterpillar called Lymantria dispar.

Experiment 3: Finally, they wanted to investigate which part of the caterpillar was specifically involved in causing MRLS. They used saline, whole M. americanum larvae and several different dissections (Such as cuticle, hind-gut and haemolymph*) of the caterpillars and fed these again to pregnant mares.

To put a long story short, their results demonstrated a clear link between the caterpillars and MRLS. Experiment one demonstrated that horses in pasture would ingest the caterpillars and would go on to develop MRLS, while horses fed on caterpillar frass and not fed on anything caterpillar associated did not.

The second experiment demonstrated something very interesting the autoclaved caterpillars did not produce MRLS in any of the 5 horses, while the frozen caterpillars did induce MRLS (in 3 of 5 mares). We’ll come back to this later so bear this in mind for now. The control L. dispar caterpillars did have one abortion in the group but it was not associated with MRLS.

Finally, the last experiment demonstrated that whole caterpillars were able to induce MRLS (as expected) and that MRLS abortions were associated with the outer cuticle (exoskeleton) of the caterpillars most strongly.

Now, the results of this research are incredibly interesting as it hasn’t really been seen before that an insect like a caterpillar could cause such an unusual disease. It’s especially surprising that this disease has only been discovered recently, especially because it’s caused by a common insect that covers a wide area of the United States. The question now remains as to what mechanism could cause MRLS? It’s known that lepidopteran** insects have numerous chemical defense mechanisms and are capable of producing poisons among other toxins. Another potential candidate is the build up of compounds such as cyanide in the cuticle of the insect.

However, perhaps the most intriguing answer to this puzzle isn’t a toxin, poison or similar, but instead a quirk from the caterpillars physical defenses.

Caterpillars with built in bacterial syringes

(The reference for this section comes entirely from Tobin et al., 2004, which is a fascinating paper).

An interesting hypothesis for the potential pathogenesis of MRLS is the “Septic penetrating setae”. Now setae are fairly common structures on a lot of different insects and are basically pointy tubes on the surface of the animals’ exoskeleton. These pointy tubes have numerous functions, but the most obvious is for defense by basically making the insect unpleasant to eat. This is because setae are basically pointy sticks*** and they penetrate into tissues causing considerable irritation. The hairs of the red rump tarantula are basically hollow spikes that are flung into the skin and eyes of an attacker. This causes severe irritation and allows the spider time to flee the scene of the crime.

Image of setae showing their general structure, with the size of these being around 20μm in diameter and demonstrating the pointy ‘barbs’ that cover the structure. The image was acquired from Tobin et al., 2004, and the photos were originally from Henry H. Southgate, University of Kentucky.

So what is the relation between Eastern tent caterpillar setae, mare reproductive loss syndrome and the bacterial infection that induces the abortion? It turns out that the setae are structures that happen to be hollow and they are also liable to fragmenting once they are ingested. Their small size, which is small enough to fit inside a large enough blood capillary (especially when fragmented) and is sharp enough to penetrate tissue, may be able to cause MRLS. The mechanism that is proposed works something like this:

1) The pregnant horse starts to snack down on a nice lunch of caterpillar.

2) A) Setae are broken off the caterpillar, penetrating gum tissue and other areas of the mouth to enter into the bloodstream. This is aided by the ‘spikes’ on the setae that allow the structure to progress more efficiently in moving tissue.

B) Alternatively, the setae make it through to the gut where they penetrate the thin epithelial lining. Again, movement of the intestine and the sharp spikes on the setae enable the fragments to enter into the bloodstream and move around the body.

3) Along with the penetrated setae, bacteria are carried along as passengers inside or alternatively on the surface of the setae until they hit a suitable ‘target’. In this case, certain ‘immunoprivileged’ organs such as the eye, reproductive organs and yes, even the amniotic fluid/uterus where the fetus is developing.

4) Once the setae ‘hits’ one of these organs with its bacterial passengers, or alternatively a critical number of setae have hit, it establishes an infection. This infection then progresses rapidly (less than 38 hours) and leads to the development of MRLS.

This hypothesis for the mode of action that ETCs cause MRLS is actually quite compelling as an explanation. Firstly, it demonstrates the link between the typical commensal bacteria often found in aborted fetuses, recalling they are primarily from the mouth and also some from the gut. It’s unlikely that the setae are punching a hole in the mouth or gut, followed by general septicemia as recall that the mare itself rarely has any associated symptoms. This provides weight to the explanation that the setae (or fragments) carry the bacteria to their target without exposing its passengers to the immune system. Basically a ‘direct delivery’ style system and finds the uterus often (compared to other regions, which is much less frequent) due to its general size, significant movement and shape.

Further, remember how I earlier said to keep in mind the autoclaving experiment from the Webb et al., 2004, study? Autoclaving basically works by heating up stuff to a large temperature, usually about 121-124 degrees. As well as intense heat, there is also a considerable amount of pressure in the chamber during a cycle as well. If you recall, the autoclaved caterpillars were not able to cause MRLS and this could have been the result of the disruption of the internal structure of the setae. Although this concept hasn’t been proven and doesn’t rule out a toxin (which could be deformed as well), it provides a compelling piece of evidence that could corroborate this hypothesis.

What to take from this

This entire line of enquiry shows that diseases and other disorders are not always the simple interaction of X pathogen causing Y disease in a specific host. Sometimes there are some very complicated external factors that may cause a disease but not be directly responsible for it. The association of these caterpillars and an abortive disorder in horses is one such example. Additionally, the implication that setae cause the entire disorder by a simple quirk of their structure is a fascinating finding. It is worth noting, before I get too enthusiastic, that the “Septic penetrating setae” hypothesis has yet to be experimentally confirmed. For my money though, I hope it’s the correct answer because it would provide a fascinating and highly novel mechanism. Microbes gaining entry into vulnerable tissues by using a ‘built-in’ syringe from another organism is just too interesting a concept to be wrong.

*Haemolymph=Insect blood. It’s a combination of interstitial fluid and their oxygen transporting blood vessels. In us, as an example, our interstitial fluid is separated from our blood and not mixed together.

**EG: Butterflies.

***Yeah, this is a simplification.

References

Potter D.A., L. Foss, R.E. Baumler and D.W. Held (2005). Managing Eastern tent caterpillars Malacosoma americanum (F) on horse farms to reduce risk of mare reproductive loss syndrome. Pest Management Science, 61:3-15.

Tobin T., J.D. Harkins, J.F. Roberts, P.W. Vanmeter and T.A. Fuller (2004). The mare reproductive loss syndrome and the Eastern tent caterpillar II: A toxicokinetic/clinical evaluation and a proposed pathogenesis: Septic Penetrating Setae. The International Journal of Applied Research in Veterinary Medicine, 2:142-158.

Webb B.A., W.E. Barney, D.L. Dahlman, S.N. DeBorde, C. Weer, N.M. Williams, J.M. Donahue and K.J. McDowell (2004). Eastern tent caterpillars (Malacosoma americanum) cause mare reproductive loss syndrome. Journal of Insect Physiology, 50:185-193.

Dr. Pianka speech transcript available

2006-04-07T16:21:00.000+12:00

Update IV: All the transcripts and newspaper reports from the Seguin Gazette-Enterprise have gone! Unfortunately I did not save the whole transcript (I took large chunks of it however) but the information below is still correct. I believe that someone will have saved it somewhere on the great interweb so I'm certain the determined could find a copy. The retraction of this story gives considerable weight to the concept that Mims has got things horrifically wrong.

Update V 10/4/06: The Telic Thoughts bloggers have decided to retract their articles on the subject. Kudos to them.

With the whole hoop-la over the Dr. Pianka speech it turns out that a full transcript of a speech he gave at St. Edwards has been released and is available here. I'm going to quote two parts of this speech that disregard and annihilate the account of the disgruntled creationist Forrest Mims, who evidentally lives in a very different reality than we do.

This is an AIDS infected piece of a human. Each of those little round things is an HIV virulent that can infect a new human. Basically, they use their T-cells to they make copies of themselves.

HIV is a pandemic spread worldwide. It's increasing in frequency in a lot of places and it's a big concern to everybody. But, it's not gonna be the one that gets us cause HIV is too slow, it lets us live several years so it can pass itself on to new hosts.

Uh, it's no good, it's too slow.

Now when you get to these viruses — Ebola Zaire has potential. It kills nine out of ten humans. It's never gotten out of Africa cause its so virulent it kills everybody before they can move. I mean it kills you within a day or two.

Uh, you can only catch Ebola Zaire by contact with a human that's infected. It causes you to bleed. It breaks capillaries and you bleed out your orifices and if you go out and touch somebody who's sick with it you get it and you die, too — or nine times out of ten.

Ebola-Reston did get out of Africa and to the U.S. in the form of green monkeys that were imported for medical research and it's named after Reston, West Virginia where they have quarantine facility for these monkeys. And, uh, they had this epidemic and all the monkeys died but they didn't have contact with each other. But they were sharing a common, uh, ventilation system. So, this is in this room, air was circulating being pumped back, and so on. Uh, monkeys in a room that breathe the same air caught it.

Now it is only a matter of time until Ebola got here evolves and mutates a little and it will be airborne, and then I think we might finally get a take. And when it sweeps across the world — we're gonna have a lot of dead people. Every one of you that is lucky enough to survive gets to bury nine. Think about that. I doubt Ebola is gonna be the one that gets us. I think it will be, uh, something else.

But did you ever wonder why things like SARS and now what the Avian Flu are continually cropping up? They're cropping up because we were dumb enough to make a perfect epidemiological substrate for an epidemic. We bred our brains out, and now we're being pegged. The microbes are gonna take over. They're gonna control us as they have in the past. Think about that.

Here's a breath of fresh air: Aldo Leopold. This is the start of the tiny little up. You've got to the lowest of the low where the microbes are gonna get you. Now, were gonna try to come up a little bit. Aldo Leopold was a conservation biologist before anybody else was. He was in wildlife management at the University of Wisconsin back in the ‘50s. And Leopold died young, but his children have put together a collection of his essays and made this book, "A Sand County Almanac." I encourage all of you to read it. It brings tears to my eyes at some of the things in it. I mean I literally break down and weep.

But one of the things Leopold said was each generation doesn't know what it lost — the last generation remembers.

No advocacy for the annihilation of the human race and the full transcript even demolishes my previous essay on the topic. Going by what I originally understood, which was admittingly very limited, it turns out that I responded to things that Dr. Pianka doesn't actually think himself either. I do intend to readdress the "Killer virus" scenario in a future post, but Dr. Pianka answers a lot of the 'criticisms' I bought up in my post anyway in the full speech. I find it hard to disagree with what he says, although I still think the death toll is absurdly high and there are numerous problems with the 'viral doomsday' scenario I'll cover in a new post. In any event, I don't see him advocating the genocide of the entire human race at all there. However, let's contrast what Dr. Pianka has actually said with what Forrest Mims, disgruntled creationist, had to say:

"This guy is a loose cannon to believe that worldwide genocide is the only answer," said Mims, who filed two formal petitions with the academy following the meeting.

“He recommended airborne Ebola as an ideal killing virus,” Mims said. “He showed slides of the Four Horsemen of the apocalypse and human skulls. He joked about requiring universal sterilization. It reminded me of a futuristic science fiction movie with a crazed scientist planning the death of humanity.”

And

But there was a gravely disturbing side to that otherwise scientifically significant meeting, for I watched in amazement as a few hundred members of the Texas Academy of Science rose to their feet and gave a standing ovation to a speech that enthusiastically advocated the elimination of 90 percent of Earth’s population by airborne Ebola.

And finally, let's contrast what Mims claims above with the final part of the St. Edwards speech:

So he says in a stationary world as opposed to one that's grow, grow, grow where everybody has to elbow the other guy and compete to get to the front and be concerned about who's going to win and who's going to lose everyday in the stock market. And in a stationary world we can focus in on things that really matter. And he used a phrase that I really love — the art of living. We can work on the art of living. Think about that.

The art of living? From Dr. Doom? Dr. Death? Dr. Wipe out all humanity with a virus? But this man hates humanity, hates life and thinks that genocide is the only option to humanities over-population. With the clear honesty and integrity of Mims, how could this possibly be true! Clearly the transcript at the Gazette-Enterprise is a fake!

/Sarcasm off for now, I believe that anyone who reads the transcript kindly provided by the Gazette-Enterprise, reads the accounts from Mims and puts 2+2 together can clearly see Mims has really got it horrifically wrong. It's also clear that someone, namely Forrest Mims owes an apology to Dr. Pianka and I feel should even resign from his position. He's made Dr. Pianka out to be a terrorist, he's humiliated the University of Texas and he's made a mockery of himself. Even with the fact this is a different speech, the content is so similar to what we understand of the Texas Academy speech that I've no real reason to think they are significantly dissimilar.

Update: Now I think of it, also make sure you check out the Pandas thumb account and the numerous quotes from media and others who took Mims seriously. There are going to be a lot of people feeling silly tommorow.

Update II: An interesting analysis of the Edwards transcript compared with quotes from the newspaper that started it all, the Sequin Gazette Daily, has been posted at the Questionable Authority. It's a very interesting post and raises some real doubts about some of the media frenzy over Dr. Pianka.

Update III: I also noticed this post on Ocellated, where Jay has actually been speaking with several students who attended the talk and gives a good impression of what Dr. Pianka is like. I recommend reading his entire post, but if you want what I think is the part that really cuts through many of the core issues it's this part:

While I may be disappointed and certainly find things to disagree with Pianka about, his accusers sink to new depths. Wanting to follow my own advice and not show angst myself, I simply cannot articulate my frustration that people are so convinced of their position, that lying then becomes a justified means to defeat their “enemy.” Indeed, viewed in this light, we can understand that hate has become their prime motivation.

And they do all this in the name of Jesus. What a crazy world we live in.

Immensely well said.

I have to link this guy

2006-04-07T03:17:00.000+12:00

Jon Swift is fast becoming one of my favourite bloggers and he's just sealed the deal with me when I read this post:

When I became a convert from Judaism to born-again Christianity after watching The Chronicles of Narnia, I thought things were going to get a lot easier for me. After all, Jews have historically been the most hated people on Earth. And while Jews are a minority in this country, 85% of Americans call themselves Christian. I thought I would be sort of like a black person who suddenly turns white or a gay person who suddenly turns straight (which apparently happens all the time according to my new Christian brothers).

Oh dear and that's just the introduction! What I like most about his blog is how he is plain enough about the satire he writes to be obvious, without sounding completely unlike what he is trying to make fun of.

Ohhhh

2006-04-06T22:31:00.000+12:00

I was perusing PLoS just now and I saw this interesting looking paper on the analysis of MHC molecules from possums. The paper also provides interesting insights into the evolutionary origins between the complex MHC gene regions of higher mammals (us!) and the rather minimal MHC gene regions of birds. Although I haven't read the paper fully just yet, it's yet another paper that provides yet more answers, questions and insights into how the immune system evolved.

So much interesting research to write about, so little time.

Reconstructing an Ancestral Mammalian Immune Supercomplex from a Marsupial Major Histocompatibility Complex. Belov K. et al 2006. PLoS, 4:317-328.

Animacules volume V posted

2006-04-06T20:45:00.000+12:00

The fifth edition of the Carnival of the wee Animacules has been posted at Complex Medium. So whip your flagellum around over there and metabolise some great posts into smaller ....words or something.

Tommorow will be the next in my series on the UK Mycobacterium bovis outbreak and the badger culling debate. It's been a little delayed while I read a couple of extra papers on the topic.

New Zealand bird flu laws

2006-04-06T18:19:00.000+12:00

The government here has decided what it will do if the current H5N1 bird flu pandemic reaches New Zealand.

Legislation giving the government the power to close New Zealand's borders in the event of an influenza pandemic has been introduced in parliament.

The bill adds influenza to the list of diseases that can be quarantined - along with cholera and yellow fever - and allows the Prime Minister to activate temporary powers to manage a pandemic.

Those temporary powers mentioned there include forcing people not to gather in public places (I would assume this would include churches as well), the creation of mass graves (if required I guess) and the ability to quarantine infected individuals and (probably) enforce treatment on them. At the moment I'm not sure on the probability that H5N1 will reach New Zealand, but it has been detected in Scotland recently, which appears to have provided the impetus for our government to propose these law changes.

It comes into effect in august but may be fast-tracked depending on how the situation develops.

Fast-Food Ice has some nasty stuff in it!

2006-04-05T23:12:00.000+12:00

This was a neat science project and some really good thinking for a 12 year old girl. What she did was test the ice from fast-food restaurants and compared it against water taken from toilets. The results speak for themselves I think:

Jasmine Roberts never expected her award-winning middle school science project to get so much attention. But the project produced some disturbing results: 70 percent of the time, ice from fast food restaurants was dirtier than toilet water[!].
The 12-year-old collected ice samples from five restaurants in South Florida — from both self-serve machines inside the restaurant and from drive-thru windows. She then collected toilet water samples from the same restaurants and tested all of them for bacteria at the University of South Florida.

That's an impressive thing to find and the result is not only interesting but it's actually had a relevant effect! A couple of the restaurants in question are changing their sanitation practices with regards to their ice machines and have even asked her back for more testing. In explaining why the toilet water was so clean, which wasn't expected they conclude that it's because the water comes from sanitised reservoirs. I would probably propose that it's the amount of degergents (among other things) used to clean the toilet, which would definitely clean the clock of most fecal coliforms like Escherichia coli.

None the less, that's a remarkably well thought out experiment for a 12 year old and if she keeps that up she'll have a good future in science.

Hooray for science!

2006-04-05T17:57:00.000+12:00

This is far too awesome:

A team of scientists has grown human bladder sacs in the laboratory and successfully transplanted them into people.

They are hoping that they can grow other organs as well like kidneys, livers and hearts. This will heavily reduce the requirements for donors and with some luck may even make organ transplants much cheaper. What's best about this is unlike a transplant, where you're never really going to have an identical tissue match and so the chance of rejection is always there, these are made from the patients own cells. This is really great technology and I hope it starts to see wide use.

Dr. Pianka and Ebola

2006-04-05T10:42:00.000+12:00

Well it certainly seems like Dr. Pianka has managed to stick his foot firmly in the cow patties and now it's raining cow pats all over him! Everyone and their dog seems to have jumped on this issue and there is quite a large amount of drama going on among blogs, the news media and all sorts of other places.

Firstly, I'll link to this post on the Pandas Thumb that talks about the issue and this one on Pharyngula gives links to various people on the situation. Personally, I recommend reading various accounts for your-self and determining who is merely acting idiotically to blow this whole thing out of proportion. A lot has been said on the issue about what was and wasn't said by Dr. Pianka, with most combatants on the issue never actually hearing Pianka speak at the event. Now as some may realise if you've read my blog for a while, I tend to ignore these examples of spinning brown toilet paper in a bowl drama, as I don't know the full facts and would rather not comment on something I don’t know the full details on. Me being in New Zealand, it's somewhat predictable that I didn’t hear Dr. Pianka speak and I'm not about to pretend I did like some are. I will state that from the general comments I've read, it does seem the whole thing is being blown out of proportion by creationists like Forrest Mims and ID blogs (like Telic thoughts and Uncommon Descent) for propaganda purposes.

In any event, what quite frankly interests me more is the science behind what Dr. Pianka is claiming. Dr. Pianka makes the point that our burgeoning human population is just getting far too high and that eventually, if we don't manage our population numbers, nature (as in, the trees and stuff, not the journal Nature) will do it for us with an incredibly lethal virus. The virus that Pianka seems to think would be a suitable candidate is the Zaire strain of Ebola. Now it's important to bear in mind that Ebloa strains are named after the geographical location they were found in, which should explain the "Zaire" part of the name and have various different lethality rates. Ebola Sudan, for example has a lethality rate of around 60%, while Ebola Zaire has an amazing lethality rate of 90%, which is undoubtably the reason that Dr. Pianka picked it as his prime example killer virus.

This is because Dr. Pianka in his talks claims that the larger the human population becomes, the more susceptible it would be to having it's numbers devastated by such a virus leaving a mere 10% left. A full 90% lethality rate for a virus is a horrific thing to think about for anyone and Ebola itself enjoys a high "fear mythology" among the general public. The problem I see with all this coverage of what Dr. Pianka said/didn't say/what people hope he said is the lack of any critical analysis of this potential super virus plausibly wiping out 90% of humanity. It's almost like nobody wants to discuss the actual science behind the claim and instead focus on trying to make Dr. Pianka say whatever the listener wants people to believe he said.

So is it actually possible? The first thing that’s important to realize is that Ebola isn’t all it’s cracked up to be in the mind of the public. As far as being an infectious disease goes it’s pretty poor. Although the method of transmission of Ebola is still a relative mystery, one idea is that it’s spread from bat guano or some other animal to human transmission vector (infected meat?) to bush workers. It then spreads further when the workers die from traditional funeral practices in Africa where the bowels are ‘cleared’ of material before being the person is buried. From there the Zaire epidemic virus was spread through the reused needles of health care workers to new victims. Once the CDC moved in and put a stop to the traditional funeral practices, cleaned up the use of infected needles and isolated infected individuals the epidemic was halted relatively quickly.

Now, Ebola (a member of the filovirus family) is a horrible virus to actually get and belongs to a little private club of viruses that cause “haemorrhagic fevers”. Essentially these viruses kill by basically ripping apart the blood vessels of the unfortunate host causing huge amounts of internalized bleeding. This internal bleeding is devastating on the patient as it reduced blood pressure (and hence will lead to organ failure eventually), dyspnea and gives victims the classic ‘zombified’ look with the sunken eyes, clinging skin and lack of pallor. Death typically occurs very rapidly, often preceded by a violent amount of spastic convulsing that causes the infected individual to splatter blood all around them. Usually after around one to two weeks after infection as the unfortunate individual finally dies from septic shock or sheer blood loss, although if they are lucky they may simply drown in their own blood first. An even luckier few manage survive, although it doesn’t seem that serum antibodies are involved in this defence*.

Undoubtedly the first reaction to this from our point of view is “how horrible!” but from a viral point of view you should see such a process as “how stupid”. Why stupid you ask? Well, the first thing to do is imagine you are a little Ebola particle and you want to make more little Ebola particles, which is pretty much the only thing that viruses do. You have several very important considerations when you’re a virus:

1) You must be able to get into the host in some manner.

2) You must be sufficiently virulent to overcome the innate immune system. Being destroyed before you’ve done anything isn’t much fun.

3) Then need to be able to find the right cell or cells you replicate in and then be able to actually get inside of them.

4) Even when inside a cell you still need to be able to find where you replicate, such as the cells nucleus or just in the cytoplasm.

5) After all that and you’re happily replicating away you still need to get back out of the cell. Not always as easy as it sounds!

6) Once you’ve finished there you have the additional problem of the host adaptive immune response catching up and you’ve got to deal with that too.

7) You might now think “Surely no more” but nope, you’ve got more to do because what comes in must come out…somehow. You’ve got to have a mechanism for getting to another person or all your little progeny are going nowhere fast.

So you can see that the life of a virus is actually pretty complicated and it’s not as easy as some might think for a virus to do its thing. There is a wealth of problems facing a virus that wants to spread among people and Ebola, like many viruses solves some problems really well but is really bad at other things. What Ebola is bad at despite its gruesome reputation actually make it an amazingly ineffective pathogen for the doomsday world scenario.

To figure out why it’s best to ask the following question: What kind of host are we for Ebola anyway? Well, the answer is fairly simple, we’re a dead end host and for Ebola we’re not something it wants to infect. What I mean by this is when Ebola infects a human being the virus finds that it replicates like mad but it can’t escape. All of the subsequent viral progeny are doomed, the host is usually doomed as well and neither the virus or host wins, much like an audience watching Alien vs. Predator. If this is the case of course, it’s natural to wonder why Ebola is so virulent to the point of being self-destructive in a human. The simple answer is that we’re not the host that Ebola is interested in infecting and it’s evolved to infect another organism.

This is because pathogenic interactions are an example of co-evolutionary warfare between the host and the pathogen. A change in virulence of the pathogen may adversely affect the ability of the virus to spread from one individual to another and on the other hand, a change in the host immune system may force the virus to get around the problem. Ebola is adapted to infect whatever it normally infects in nature (I’ll propose bats for now, but there are other candidates as well) and it’s mechanisms of avoiding immunity and virulence have evolved to combat those of its natural host. As it turns out, when that virus gets into us there are three possibilities that may occur: 1) The virus is immediately annihilated by immune defences or simply can’t replicate. 2) The virus destroys the host or 3) the virus evolves in some way so that it can survive in the new host population.

Ebola is stupid because it does number “2” on the list and because of the sheer rapid destruction of the host that it infects it hasn’t got any time for number “3”. Going back to the seven things a virus needs to do to succeed in a host population, let’s contrast Ebola with another very successful human viral STD, namely Herpes Simplex Viruses (I and II). Recalling those seven points were:

1) You must be able to get into the host in some manner.

2) You must be sufficiently virulent to overcome the innate immune system. Being destroyed before you’ve done anything isn’t much fun.

3) Then need to be able to find the right cell or cells you replicate in and then be able to actually get inside of them.

4) Even when inside a cell you still need to be able to find where you replicate, such as the cells nucleus or just in the cytoplasm.

5) After all that and you’re happily replicating away you still need to get back out of the cell. Not always as easy as it sounds.

6) Once you’ve finished there you have the additional problem of the host adaptive immune response catching up and you’ve got to deal with that too.

7) You might now think “Surely no more” but nope, you’ve got more to do because what comes in must come out…somehow. You’ve got to have a mechanism for getting to another person or all your little progeny are going nowhere fast.

Let’s examine how the two viruses fair on these points against one another:

1) A poorly understood mechanism of transferring between people, but isn’t very efficient as Ebola cannot spread by aerosol transmission and seems to require direct blood or tissue contact.

1) Herpes can spread through direct contact from simply rubbing infected skin on either the lips or genitals.

2) Ebola overwhelms the host innate immune system and rapidly causes infection. I’m not sure on the molecular details of this, but the high infection rate obviously means that Ebola gets past these mechanisms fairly easily.

2) Herpes simplex viruses can interfere with host innate immune defences, such as interfering with the intracellular production of interferon and preventing the cell from going into apoptosis (cellular suicide).

3) Ebola targets receptors that are found on a wide array of cells on the body and can infect nearly any kind of tissue it encounters. To accomplish this trick it tends to degrade the integrity of the epithelia surrounding blood vessels and can escape virtually anywhere in the body.

3) Herpes simplex virus typically targets skin epithelial cells and also cells of the nervous system. It generally only replicates in the skin cells, which is what makes those horrible warts and in the nervous system it tends to hide out.

4) Again, Ebola manages to succeed in this department and can replicate in a wide array of cells.

4) Herpes is somewhat smarter than Ebola here. In its target cells the virus tends to replicate like crazy but in non-target cells the virus integrates itself into the cells nucleus and hides away dormant.

5) Ebola gets out of cells by blasting them apart by producing huge hordes of viruses.

5) Herpes simply sneaks out of nervous cells by tagging along actin filaments and ‘roaming’ down them as if it’s being pulled along a rope. To get between cells it likes to infect it can simply spread using specialized proteins and jump between cellular tight junctions without destroying the original cells.

6) Ebola succeeds better than many pathogens here because it’s so incredibly fast. The adaptive immune system typically takes a week or so to get going, but with the speed of infection and the sheer numbers it just overwhelms the adaptive immunity. This is so prominent a factor that it’s not even thought that adaptive immunity has much of an effect on the success or failure of Ebola to kill its victim.

6) Herpes is very clever in this regard. It rapidly replicates and is very infectious for the periods that it is replicating. In addition to this, herpes can hide in the nervous system, which is ‘immuno-privileged’ where it can’t be touched easily by the immune system. When the individual becomes stressed or otherwise immuno-compromised, it comes back out wanders down the nerves actin filaments and causes a new infection. In this manner it’s no surprise that a flower you give your girlfriend will last for a week, but Herpes will last for life.

7) Ebola fails miserably right on the finish line. It does everything else rather well, but when it comes to getting out of the host it gets a big fat ZERO. Firstly, it kills its host way too quickly to have maximum contact with other individuals to spread more viral particles too. Additionally, signs of an infected individual are fairly obvious due to its distinctive symptoms and infected individuals are effectively bed-ridden (can’t move around). This means they are easily quarantined or spotted by health-authorities. Additionally, its requirement to be spread by direct contact with blood makes it difficult to spread to new individuals as say, skin contact or by aerosol transmission.

7) Now this is how you do things. Herpes can secrete itself onto the surface of epithelial cells and can be spread simply by rubbing ones genitals against the infected genitals of another person. This means Herpes gets around problems like condoms (although condoms do help a bit as well too some degree) and removes any requirement for fluids. It’s also able to make its own open sores if required and once established in a new host is there for life. This is also another massive advantage, as herpes lasts so long it has a persons entire lifetime to spread to another individual. It maximizes the amount of total hosts it can get to and sure enough, Herpes manages to infect millions and probably billions of people world-wide.

Best of all and is the other key to Herpes success is that it causes no overtly obvious symptoms of disease until late into an infectious cycle. The host that doesn’t know about the virus hasn’t got the chance to change their behavior to avoid being infected or spreading the disease further.

So in terms of these two viruses I would rather be Herpes than Ebola. Ebola has the reputation sure, but Herpes at least has a chance of spreading itself to other humans and surviving. There is little point to being a virus if you can’t spread to another human being! So let’s reanalyze the claim that Dr. Pianka makes that Ebola may be a candidate for wiping out 90% of the human population in this world.

Firstly, as I’ve described above, Ebola isn’t going to have hosts that are infected but display sub-clinical infection. Now what I mean by a sub-clinical infection is an individual who has disease, they are directly producing virulent virus, but does not have any outward signs of a fever or any harmful symptoms (see an earlier post I wrote here for more details). This allows the virus to slip under the radar of health authorities and basically avoid detection to infect as many people as it can. As you can imagine, Ebola isn’t anywhere near as subtle as this and infected individuals could be spotted, quarantined and monitored very quickly.

Secondly and working against Ebola again is the fatality rate. It simply kills too many of the people it infects. Ebola would likely run out of hosts well before it managed to infect a wide amount of the human population. For example, if you are a virus as lethal and generally quick off the gun in causing infection as Ebola, you may wipe out the entire population of a village and never get the chance to be taken to the next village, say 20km away. You may think that “well, we’ve got planes and stuff” but bear in mind the claim is that we’re looking at a virus that wipes out 90% of humanity and it has to get to that 90% first. Not everyone lives in cities or areas with easy access by planes or even other forms of transportation!

Thirdly and most definitely what will put a nail in the Ebola as humanities destroyer coffin is the problem with person to person transmission. As I mentioned earlier, the main chance I see of Ebola transferring between people is the large amount of blood, sputum and other fluids discharged around by dying patients as they convulse near death. This mechanism, while horrific is probably not going to be sufficient to transfer from quarantine facilities, hospital staff and even other patients. The reason for this is that containment mechanisms, such as positive pressure sealed rooms, hazard suits and other protective mechanisms can be taken to avoid contact with infected blood. Additionally, even without all of these protective measures, many of the health-care workers and CDC researchers that had contact with Ebola infected patients didn’t manage to acquire an infection.

Lastly and again relating to transmission is this concept of Ebola ‘developing’ the ability to transmit by an aerosol route. With the way Dr. Pianka seems to put across this concept it would seem only a matter of time that Ebola could develop this trick. Nothing could be further from the truth. The first significant development for Ebola to be able to do this would have to be for some form of selective pressure on its natural host. For example, there would have to be selection for either the virus to move from its current means of transmission in its natural host, which could be through an insect vector or by a fecal oral route, to the lungs or mucosal surfaces (like inside your nose). Next, the virus would have to develop a means where it could survive in the outer environment such as dealing with desiccation (drying out) or high amounts of UV light. Finally, even past that point it would have to develop mechanisms of recognizing where it is and binding onto lung tissue.

I’m not one to do the creationist/ID tactic of making up huge numbers purely on whatever I feel will suit the answer I want best, but I would be hesitant to think that Ebola would have a solid selection pressure to alter its natural mode of transmission (it obviously works) to an aerosol method. It could happen, but the mechanism isn’t very likely and as a candidate for the extermination of 90% of the human race it’s not a very good one. There are many other viruses that would be much more capable of such a ‘super-pandemic’ as required by the scenario given by Dr. Pianka, but even then there are considerable problems with a virus killing that many people.

Dr. Pianka may be a fan of Ebola for whatever reason and may genuinely think it’s a good candidate for the downfall of humanity. Unfortunately, this is probably based a lot more on the fearsome reputation of Ebola and less on the actual science of a virus capable of creating such a large scale pandemic.

April Fools Day

2006-04-01T23:46:00.000+12:00

As is my custom from year to year, I'm not going to bother reading virtually anything on the internet both today and also tommorow (because it's not the first in some crazy places on the planet yet). It's just better for general sanity.

If I wanted to read nonsense that gets repeated every year, like the almost guaranteed DNF carnards that appear on gaming sites:

Duke Nukem Forever has been cancelled/is coming out soon/George Broussard has covered himself with chocolate etc

Followed by back slapping by said visitors with those sites with:

DUKE NUKEM FOREVER? MORE LIKE DUKE NUKEM TAKING FOREVER. M I WITTY RITE?

U R!

O RLY!

Which inevitably follows, I would just read the Discovery Institute Intelligent Design blogs. It's April Fools over there with every post all year round and the best part is, the joke is always the same because they haven't come up with new material in over 10 years.

31st meeting of the skeptics circle

2006-03-31T16:17:00.000+12:00

Abel Pharmboy at Terra Sigillata has hosted one of the biggest skeptics circles I've seen in a while. There is a plethora of skeptical entries this week on a wide range of topics so it's well worth the visit. The next circle is being hosted by our very own pooflinger at Pooflingers Anonymous so presumably check over there for contact details.

What evidence suggests badgers infect cattle with M. bovis?

2006-03-30T20:52:00.000+12:00

Part III: Mycobacterium bovis, the English bovine tuberculosis outbreak, badgers and the culling debate.

Critical to the entire culling controversy as a control measure for M. bovis is what the exact role of the Eurasian badger (Meles meles) in the spread of bovine tuberculosis. If badgers are the principal source of bovine tuberculosis, then a cull would make sense and would have the maximum effect on reducing breakdowns (a case of bovine tuberculosis in a cattle herd). If badgers are not the principal source of bovine tuberculosis, or alternatively they are but cannot spread bovine tuberculosis to cattle, then a cull is just going to be a needless waste of time with ultimately no effect as several conservationists have argued. So what does the scientific literature actually say?

Are badgers actually infected with bovine tuberculosis and if so, can they secrete Mycobacterium bovis?

One of the most recent studies relevant to this question is from Chambers et al., (2002) and investigated the current serological tests for identifying badgers that shed Mycobacterium bovis. This study compared two methods, notably ELISA (Enzyme Linked ImmunoSorbent Assay) and Western blotting against direct culture of M. bovis for accurately identifying infected badgers. Importantly, this study was set up to determine if these techniques could accurately determine if a badger was secreting M. bovis. Essentially, the scientists picked an area that had endemic infection with M. bovis among cattle herds and captured 128 badgers. Of these sampled badgers, 44 were confirmed to have secreted M. bovis at some point in their life as confirmed by the ELISA, Western blot and culture detection methods.

With the use of all three methods concordantly it makes it virtually impossible that the result is incorrect or outside factors such as other environmental mycobacteria (Primm et al., 2004) are responsible and as such, the study clearly implicates badgers as a host for M. bovis. Of course, science does not stand simply by itself but rather through the work that others have done in the past and what studies have followed afterwards. Here the consensus is overwhelming. For instance, a previous study from Gallagher and Clifton Hadley (2000) shows that badgers had M. bovis infection in both lung tissue and in their urine from post-mortem examination. Other studies from Costello et al., (1999) and Olea-Popelka et al., (2005) have found that badgers are infected with M. bovis and most importantly, the same strains of M. bovis tend to be shared between cattle and badgers in the same area (this is an important point, more on this later however).

Further, the two key ‘trials’ conducted on the effects of badger culling by Donnelly et al., (2002, 2006) in England and the “Four counties” trial in Ireland by Griffin et al., (2005). Both of these studies have found that bovine tuberculosis is present among badgers around farming areas. Typical prevalence of infected badgers tends to fluctuate widely, with some researchers finding infection rates around 20% and others up to 50% (Corner L.A.L., 2006). In short, numerous studies have all universally been able to find badgers that have been infected with M. bovis. The question remains as to if infected badgers secrete M. bovis that can infect cattle?

In order to spread efficiently from badgers to cattle it’s important to realize that several factors need to occur for any chance of transmission:

1) Badgers need to come into contact with cattle or alternatively, cattle come into contact with feces and other excretions of badgers.

2) Infected badgers must be able to secrete M. bovis to cattle through excretions such as sputum and urine.

3) M. bovis in badger excretions must have some mechanism to survive the passage from a badger to cattle.

We should also expect if these three things are found and that if badgers are transmitting M. bovis to cattle (somehow), then we’d also expect to see the same spoligotypes in cattle and local badgers. So once again, what does the literature say on these three issues?

Possible means of transmission of cattle to badgers.

Several studies have identified that badgers are not afraid to come into contact with cattle, although the circumstances in which badgers come into contact differ. Phillips et al., (2003) and Corner L.A.L. (2006), both report that cattle will typically avoid badgers if at all possible. Interestingly, both papers note that heavily infected badgers tend to behave aberrantly and that cattle will frequently investigate by licking, sniffing and biting. This matches similar observations of cattle in New Zealand investigating brushtail possums that are dying of TB.

Additionally cattle are also highly likely to come into contact with the excretions of badgers such as urine, feces and sputum. As badgers excrete copious amounts of infectious bacteria in their sputum (coughed up fluid), urine and from infected bite wounds this does pose a possible risk for cattle grazing in fields visited by badgers (Krebs et al., 1998; Phillips et al., 2003; Scantlebury et al., 2004 and Young et al., 2005). Additionally, badgers are also capable of surviving with tuberculosis for months or even years and may be infectious for long periods of time, until they eventually succumb to infection (Phillips et al., 2003; Scantlebury et al., 2004 and Corner L.A.L., 2006).

Finally, it is also the case that cattle will graze areas that have been used as latrines or ‘crossing points’, essentially places badgers tend to go over often when moving from field to field, which poses a potential risk of ingesting M. bovis. Interestingly the main means of infection in cattle is from aerosolized particles and not from ingestion. This is supported by the fact infected lesions and bacteria from infected cattle are typically isolated from around the head region more so than GALT* (Phillips et al., 2003).

Scantlebury et al., (2004) noted that intensively farmed cattle tended to graze badger latrines and crossing points immediately due to sward (grass) competition. Conversely, cattle farmed in less dense numbers tended to scratch and sniff latrines or badger urine (crossing points) but ultimately avoid these areas. Rates and reasons for cattle investigation or consummation of swards infected with badger excretions should deserve further analysis.

Finally M. bovis is more than capable of surviving outside of the host once it has been excreted. As mentioned in part II, mycobacteria are particularly hardy organisms and have a wide metabolism. M. bovis in soil samples has been demonstrated to be viable for months by culture and may even be viable for years (Young et al., 2005). This is because although previous studies that have failed to culture M. bovis after long periods of time, molecular methods for the detection of RNA have indicated the organism could still be present but non-culturable (Young et al., 2005). In a similar manner to other microbes, it is possible for a viable organism to exist in the environment that cannot be cultured for whatever reason (Colwell and Grimes, 2000).

The final link in the chain.

Generally infected badgers tend to be found in clusters, with the surrounding cattle farms also infected with the same strains of M. bovis (Costello et al., 1999; Smith et al., 2003; Griffin et al., 2005 and Olea-Popelka et al., 2005, 2006). Additionally, many studies have indicated that badgers may roam relatively widely and have varying levels of contact with cattle, see for examples Griffin et al., 2005 and Olea-Popelka et al., 2006. As mentioned earlier, this concordance between the general spoligotypes in an area being the same between those found in infected cattle and nearby infected badger setts resolves the issue. It’s almost certain that badgers are to some degree responsible for spreading M. bovis to cattle, even if the exact mechanism is unknown and has yet to be illucidated (Olea-Popelka et al., 2006).

It’s very clear that badgers can be infected by M. bovis, excrete the organism in their sputum and urine due to chronic infection of the lungs and kidneys and that the same strains of M. bovis that infect badgers are found in cattle. Also importantly, the proactive culling portions of the Donnelly et al., (2003, 2006) study and the Griffin et al., (2005) “four counties” trial have shown considerable drops in the prevalence of herd breakdowns**. Finally however, if you’re the sort of person who requires a more ‘visual’ aid, then I would propose having a look at this poor badger (Horrific image! Do NOT click it unless you like copious amounts of pus!), which has died of tuberculosis and believe me, it’s not a pretty sight.

However, despite the strength of the evidence presented from the literature supporting a link between badgers and bovine tuberculosis, it’s insufficient to resolve the issue mentioned in the opening paragraph. Even if badgers are responsible for spreading tuberculosis, the role of cattle will also need to be determined as it may be possible that badgers are only a symptom, and not the cause of the high prevalence of BTB in the UK. Keep checking back soon for this question to be addressed in Part IV: The role of cattle movements in the bovine TB epidemic.

*GALT=Gastrointestinal Associated Lymphoid Tissue.

**I will point out before someone else does, that I’m aware the reactive culling part of the Donnelly studies have shown an increase in herd breakdowns. I’m not deliberately ignoring this point as I intend to cover this later in the series.

References

Chambers M.A., W.A. Pressling, C.L. Cheeseman, R.S. Clifton-Hadley and R.G. Hewinson (2002). Value of existing serological tests for identifying badgers that shed Mycobacterium bovis. Veterinary Microbiology, 86:183-189.

Colwell R.R. and Grimes D.J. (2000). Nonculturable microorganisms in the environment. ASM press Washington D.C.

Corner L.A.L. (2006). The role of wild animal populations in the epidemiology of tuberculosis in domestic animals: How to assess the risk. Veterinary microbiology, 112:303-312.

Costello E., D. O’Grady, O. Flynn, R. O’Brien, M. Rogers, F. Quigly, J. Egan and J. Griffin (1999). Study of restriction fragment length polymorphism analysis and spoliogotyping for epidemiological investigation of Mycobacterium bovis infection. The Journal of Clinical Microbiology, 37:3217-3222.

Donnelly C.A., R. Woodroffe, D.R. Cox, J. Bourne, G. Gettinby, A.M. Le Fevre, J.P. McInerney and W.I. Morrison (2003). Impact of localized badger culling on tuberculosis incidence in British cattle. Nature, 426:834-837.

Donnelly C.A., R. Woodroffe, D.R. Cox, F.J. Bourne, C.L. Cheeseman, R.S. Clifton-Hadley, G. Wei, G. Gettinby, P. Gilks, H. Jenkins, W.T. Johnston, A.M. Le Fevre, J.P. McInerney and W.I. Morrison (2006). Positive and negative effects of widespread badger culling on tuberculosis in cattle. Nature, 439:843-846.

Gallagher J. and R.S. Clifton Hadley (2000). Tuberculosis in badgers: a review of the disease and its significance for other animals. Research in Veterinary Science, 69:203-207.

Griffin J.M., D.H. Williams, G.E. Kelly, T.A. Clegg, I. O’Boyle, J.D. Collins and S.J. More (2005). The impact of badger removal on the control of tuberculosis in cattle herds in Ireland. Preventative Veterinary Medicine, 67:237-266.

Krebs J.R., R.M. Anderson, T. Clutton-Brock, C.A. Donnelly, S. Frost, W.I. Morrison, R. Woodroffe and D. Young (1998). Badgers and bovine TB: Conflicts between conservation and health. Science, 279:817-818.

Olea-Popelka F.J., O. Flynn, E. Costello, G. McGrath, J.D. Collings, J. O’Keeffe, D.F. Kelton, O. Berke and S.W. Marin (2005). Spatial relationship between Mycobacterium bovis strains in cattle and badgers in four areas in Ireland. Preventative Veterinary Medicine, 71:57-70.

Olea-Popelka F.J., J. Phelan, P.W. White, G. McGrath, J.D. Collins, J. O’Keeffe, M. Duggan, D.M. Collins, D.F. Kelton, O. Berke, S.J. More and S.W. Martin (2006). Quantifying badger exposure and the risk of bovine tuberculosis for cattle herds in county Kilkenny, Ireland. Preventative Veterinary Medicine, epub ahead of print.

Phillips C.J.C., C.R.W. Foster, P.A. Morris and R. Teverson (2003).The transmission of Mycobacterium bovis infection to cattle. Research in Veterinary Science, 74:1-15.

Primm P., C.A. Lucero and J.O. Falkinham III (2004). Health Impacts of Environmental Mycobacteria. Clinical Microbiology Reviews, 17:1,98–106.

Scantlebury M., M.R. Hutchings, D.J. Allcroft and S. Harris (2004). Risk of disease from wildlife reservoirs: Badgers, cattle and bovine tuberculosis. Journal of Dairy Science, 87:330-339.

Smith N.H., J. Dale, J. Inwald, S. Palmer, S.V. Gordon, R.G. Hewinson and J.M. Smith (2003). The population structure of Mycobacterium bovis in Great Britain: Clonal expansion. PNAS, 100:15271-15275.

Young J.S., E. Gormley and E.M.H. Wellington (2005). Molecular detection of Mycobacterium bovis and Mycobacterium bovis BCG in soil. Applied and Environmental Microbiology, 1946-1952.

V for Vendetta

2006-03-30T19:59:00.000+12:00

I just came back from this movie and all I can say is that it's politically heavy handed but overall it's a very good film. There are some things that don't make much sense and sometimes the movie is all over the place, but is overall far from the boredom that the Matrix sequels ended up being. It's definitely worth seeing.

PNAS cover this week

2006-03-29T21:53:00.000+12:00

This weeks cover photo for the Proceedings of the National Academy of Sciences (PNAS) is really nice. The photo is of some rat alveolar macrophages taken from the lungs of rats taking up some polystyrene disk particles. I think it's a very pretty looking photo and demonstrates the wonderful function macrophages have in being the 'clean up' crew of the body. The photos accreditation is to Julie A. Champion who is the author of an interesting paper published in that issue of PNAS, which is looking at how particle size and shape affects the uptake of particles by macrophages.

Wonderful photo. As a side note, I would suspect the sample was prepared for a scanning electron microscope and then the subsequent captured image above has been 'colourised' (just like Ted Turner!) by a computer. Normally images that you see through electron microscopes aren't very pretty and are pretty much just all grey.

How evil am I?

2006-03-29T18:57:00.000+12:00

You Are 24% Evil

A bit of evil lurks in your heart, but you hide it well.
In some ways, you are the most dangerous kind of evil.

How Evil Are You?

A bit disappointing really. It seems that I've fallen well behind in being corrupted by anime, blaming my flatulence on others and evilution. I need to try harder it seems.

Chick tract on chemicals

2006-03-29T16:37:00.000+12:00

Jack Chick likes to write comics that tend to generally convey his anger about certain issues or things he finds offensive: just about anything in other words. One of his older comics was on a group of people playing DnD and was basically a huge strawman. I won't directly link it, because Jack Chick deserves no extra bandwidth in general and out of consideration for the mental health and stability of my readers. It is good then that Bronze Dog from Rockstars' Ramblings has come up with a highly amusing 'edit' of the original Jack Chicks comic. It certainly has inspired me to try an "argument ad baculum" on anyone who disagrees with me.

Awesome giant centipede video

2006-03-28T16:59:00.000+12:00

I saw this video over at pharyngula and concluded it was too awesome not to provide yet another link to. Essentially this is a video of a >1 foot long giant centipede (Scolopendra) attacking, killing and then devouring a mouse. There is only a few seconds of squeaking after the first strike and then the copious amounts of poison that the animal secretes through its maxillipeds (the part that bites the mouse). It's worth noting for those watching the video (probably with some horror) that the maxillipeds aren't what the centipede uses to eat the mouse. These structures are adapted to secrete venom and additionally kill by impalation (a favoured tactic of other large arthropods like tarantulas as well), but they do have mandibles and if you watch the head closely, you can observe the centipede chewing away on the mouse with its mandibles (under the head).

Centipedes are very underrated killers of the arthropod world. This is obviously the start of an effective (and equally horrible) PR campaign.

Update: I missed it the first time, but also note the spots of liquid that suddenly appear between the joints of the centipedes body as it wrestles with the mouse. I would guess that's actually even more venom, although I've normally only heard of centipedes releasing venom from between their leg joints and not their main segments. That's a pretty awesome adaptation if they can secrete venom that way as well though. It's not entirely without precedent though, the centipedes close relatives milipedes are known to secrete cyanide and other toxic compounds from their joints when harassed.

Plush Kiwa Hirsuta

2006-03-27T16:46:00.000+12:00

Remember that furry crustacean that everyone was oogling over from a while back? Well it looks like the obvious thing to do, which would be to make a plush toy of it has now officially occured. I think the toy version looks great and I would most definitely buy one if I ever got the opportunity.

How much does my blog own me?

2006-03-27T15:35:00.000+12:00

I noticed that several sciencebloggers did this amusing little test to determine how much their blogs own them. Apparently, this site owns 31.25% of me or something like that. At least it's not a majority share, which I would like to think my passion of science or my obsession with spiders would own the rest of me easily. They can battle it out.

Oh the Onion

2006-03-27T15:02:00.000+12:00

I love the Onion, which is so good at satire that sometimes people mistake articles from it for the real thing. Usually they manage to hit home on various points or just make a particularly funny joke. The latest edition has the following 'brief' about a chicken interviewed about having Bird Flu:

DILLON, SC—A chicken at Perdue Farms' Dillon plant downplayed reports of illness Tuesday, saying she was feeling much better. "I might have had a touch of some sort of flu, but I'm over my fever and keeping the ol' corn down. B'cawk!"

I suspect that the chicken wouldn't have even got past the first few sniffles with the current climate about bird flu. Speaking of bird flu now I think of it, if you haven't been to Effect Measure lately and read their excellent summary of two papers about bird flu and where it potentially binds onto human lung tissue, I would very much recommend doing so. It's very well written and much better reasoned than the mainstream news reports, which seem to always miss the key points.

What makes Mycobacterium bovis such a problem?

2006-03-26T20:32:00.000+12:00

Part II: Mycobacterium bovis, the English bovine tuberculosis outbreak, badgers and the culling debate.

Mycobacteria represent a large group of incredibly tough environmental bacteria that have in many cases adapted to be successful pathogens, which are classically very slow in killing their victims. One such mycobacterial disease is tuberculosis, caused by Mycobacterium tuberculosis, which is probably one of the oldest described diseases known to man. The hardy organisms have been found to be responsible for the deaths of Egyptian Pharaohs and the disease was often described as “White plague” in the middle ages. This was because heavily infected victims cough up an off white frothy substance, packed with M. tuberculosis and blood, called sputum. M. tuberculosis is remarkable in another way; as one of the most significant diseases humans passed to animals (rather than vice versa), in this case to cattle some 6 to 10 thousand years ago. The product of that jump over the species barrier was Mycobacterium bovis, which is today one of the most prevalent and significant pathogens of domestic and wild animals.

Why mycobacteria are such good pathogens

Mycobacteria represent an ultimate trade off between factors that make them highly difficult to kill for the host immune system and yet heavily restrict their own growth. This means that mycobacterial diseases are classically slow taking months or years to cause disease, are usually very debilitating and go completely undetected until it’s too late. Arguably the most important factor for the success of mycobacteria such as M. bovis as a pathogen is their amazingly tough cell wall.

Unlike other bacteria, the cell walls of mycobacteria are heavily composed of lipids that make them extremely tough. This tough wall makes it very difficult for cells of the immune system, like macrophages to break down the organism and M. bovis will survive quite well in microphages. Despite the advantage of higher protection such an unusual cell wall does come with some key trade offs. Their cell wall is not very permeable to many substances, giving the microbe a tougher time acquiring nutrients and the organism spends large amounts of energy synthesizing fatty acids.

Another unusual characteristic of mycobacteria is that they have only one or two 16S ribosomal RNA cistrons (compared to 7 in Escherichia coli). This contributes to the immensely slow growth of mycobacteria as ribosomes are essential in the rapid production of new proteins, so the inability to rapidly produce more ribosomes means the microbes maximum growth speed is pretty much capped. Comparing E. coli to M. bovis is rather like comparing a Ferrari with a broken down jalopy with one wheel missing.

It can take (for example) up to two weeks to grow mycobacteria to useful numbers for an experiment in a lab, compared to one day for E. coli. Although seemingly a stupid idea for the organisms survival initially, it does have two key advantages. It’s very useful against antibiotics that target the ribosome, as only one mutation can instantly make the organism resistant and prevent any real damage. Additionally a slow growth rate makes it very easy to assess a changing situation and adapt to the new situation without committing to an ‘all or nothing’ style scenario.

Finally, mycobacteria are easily aerosolized (so they spread between individuals easily), are taken up by macrophages rapidly and are fairly drug resistant (largely due to their cell wall and their slow metabolism). Worst of all, the large presence of environmental reservoirs of mycobacteria makes an effective vaccination difficult. The current BCG vaccine (Bacillus of Calmette-Geurin) has often been found to be ineffective in providing immunological protection and part of the suspected reason for this is ‘confusion’ of the immune system by environmental mycobacteria.

M. bovis provides a particular threat to farm economies

Perhaps the most prominent reason for the problem with eliminating M. bovis from cattle is the large host range that M. bovis exhibits. As well as cattle and to a lesser extent humans the organism is known to infect badgers, possums, deer, sheep, ferrets, oxen, buffalo, lions and wildebeest. This immensely large host range makes control of the disease almost impossible in areas where there is a wild animal reservoir that can prevent elimination of M. bovis. The large host range of M. bovis is almost certainly a result of its wide metabolism and the fact most mammalian immune systems are pretty similar.

Elimination of this disease in some places of the world, such as New Zealand and the United Kingdom that has animal reservoirs is hence very difficult. Making things worse, the suspected animal reservoirs are also found in close association with cattle that are susceptible to infection. The important question that needs to be answered is what role do these vectors play in the transfer of M. bovis to cattle? Join us back this week for part III: What evidence suggests badgers infect cattle with M. bovis?

References

Primm P., C.A. Lucero and J.O. Falkinham III (2004). Health Impacts of Environmental Mycobacteria. Clinical Microbiology Reviews, 17:1,98–106.

Salyers A.A. and D.D. Whitt (2002). Bacterial Pathogenesis: A molecular approach 2nd edition. ASM press, Chapter 19:291-310.

Previous post by me about the origins of M. bovis. The quoted paper in particular.

Britannica upset with Nature

2006-03-26T15:44:00.000+12:00

A while back, Nature posted a comparison of the free encyclopaedia wikipedia with that of the formal published Britannica. It appears that the general conclusion Nature reached, which was that wikipedia was sometimes as accurate or even better than Britannica on scientific articles has struck a nerve. Nature begin their response pointing out what they were accused of:

In our issue of 15 December 2005 we published a news article that compared the Internet offerings of Encyclopaedia Britannica and Wikipedia on scientific topics (“Internet encyclopaedias go head to head”, Nature 438 (7070) p900-901; http://dx.doi.org/10.1038/438900a). Encyclopaedia Britannica has now posted a lengthy response to this article on its website, accusing Nature of misrepresentation, sloppiness and indifference to scholarly standards, and calling on us to retract our article. We reject those accusations, and are confident our comparison was fair.

The original analysis didn't seem to have been flawed in any particular manner and seemed to have been perfectly fair, though I feel Britannica does have a few legitimate complaints in places. Firstly, Nature did only take smaller segments from articles to show their reviewers and often some of the complaints were addressed in the larger body of text. Additionally, Nature seems to have taken material that is from other editions of the encyclopaedia, which are intended for younger audiences or not included in the main edition of Britannica. I do see that as a valid complaint because that would skew the analysis. After-all Nature are implying the wiki gets as accurate as the encyclopaedia Britannica, which is a somewhat different thing than their other publications.

Otherwise, through reading both the responses from Nature and Britannica, it does seem that Britannica were trying to save face and their reputation primarily as many of their complaints, such as shortening articles, were equally applied to wiki articles by Nature. Of course this defensive response from Britannica does make sense, who would want to be beaten out by a free online encyclopaedia that's not even written by experts? This point in particular seems to have got Britannicas goat, as you can see here from the opening of Britannicas response:

In its December 15, 2005, issue, the science journal Nature published an article that claimed to compare the accuracy of the online Encyclopædia Britannica with Wikipedia, the Internet database that allows anyone, regardless of knowledge or qualifications, to write and edit articles on any subject.

Which then moves onto a typical attack that the wiki often hears from its detractors:

Wikipedia had recently received attention for its alleged inaccuracies, but Nature’s article claimed to have found that “such high-profile examples [of major errors in Wikipedia] are the exception rather than the rule” and that “the difference in accuracy [between Britannica and Wikipedia] was not particularly great.”

Arriving amid the revelations of vandalism and errors in Wikipedia, such a finding was, not surprisingly, big news. Within hours of the article’s appearance on Nature’s Web site, media organizations worldwide proclaimed that Wikipedia was almost as accurate as the oldest continuously published reference work in the English language.

This is often a problem with the wiki, particularly on controversial issues like evolution, the holocaust and other contentious articles that are prone to vandalism. Many of the articles on wikipedia are of a very high quality however and are well maintained by individuals with expertise in their fields. Unfortunately, the wiki seems better for "fan cruft" and other similar information like details about popular computer games or anime series than as a scholarly resource at the moment.

In any particular event, I think that Nature probably weren't as careful with their analysis as they could have been originally. Some of the mistakes that Nature claim to have identify in the Britannica articles do not appear to be overly relevant at times (see Britannicas response for some details). Without seeing what the same reviewers thought about the relevant wikipedia articles, it would be impossible to determine if there was any real reviewer bias either way. Hopefully Nature will produce a more detailed response that clarifies how their reviewers went about determining errors and the like. Importantly, I would like to know how Nature decided what parts of the articles to take as that could heavily impact on the end result.

When public health, farm economics and conservation collide

2006-03-25T20:23:00.000+12:00

Part I: Mycobacterium bovis, the English bovine tuberculosis outbreak, badgers and the culling debate.

One of the most prominent problems for public health authorities and a countries economy comes from infectious diseases that target farmed animals. There are a wide number of pathogens that affect the animals that we grow as food that present a real public health risk, such as Campylobacter jejuni in chickens, Escherichia coli O7H157 in cattle and mycobacteria like Mycobacterium avium subspecies paratuberculosis in sheep. Control of these organisms often involves improvements in animal husbandry, such as simple measures like keeping animals separated and the use of improved diagnostics or vaccinations. Where these control measures become insufficient is when the disease has other vectors, which are also in high numbers and present unique difficulties in controlling or eliminating. Such is the problem that several countries face in controlling bovine tuberculosis, caused by Mycobacterium bovis a relative of one of man-kinds earliest known pathogens, Mycobacterium tuberculosis.

M. bovis historically was a considerable risk to human health, as the organism is viable in milk and of course in the meat of infected cattle. An inquiry in 1934 determined that M. bovis was responsible for some 2,000 tuberculosis deaths (around 6% of the total, the rest being caused by the human specific M. tuberculosis). Today, M. bovis is not much of a problem in humans, as the introduction of milk pasteurization and particularly tuberculin testing has entirely eliminated bovine tuberculosis as a human and animal health threat. This is because tuberculin testing allows for the identification of animals potentially infected with M. bovis and their rapid slaughter and removal from the herd. This policy has completely eliminated M.bovis from cattle herds world wide, except in certain countries such as the United Kingdom (notably Wales, Ireland and England), New Zealand and the state of Michigan in the United States of America.

The question then has to be asked in what makes these regions so different from the rest of the world? The simple answer (but in reality not so simple answer) is the presence of other animals that serve as a vector for M. bovis. In New Zealand, the principal reservoir is the brushtail possum (Trichosurus vulpecula), in Michigan (USA) it’s white tailed deer (Odocoileus virginianus) and in the UK the Eurasian badger (Meles meles). In each country the test and slaughter method has managed to almost entirely wipe out M. bovis from cattle, drastically reducing rates particularly in the 1950s and 1960s, until around the 1980s where M. bovis makes a massive comeback. In the UK particularly, rates of bovine tuberculosis in cattle have increased rapidly and equally as quickly spread to other farms.

As a result of these vectors, which provide a large reservoir for M. bovis, it makes the typical control methods insufficient to completely eliminate the disease. This means that the continued re-infection of herds previously cleared of bovine tuberculosis becomes a considerable problem, as like its human cousin M. tuberculosis, M. bovis takes its time in causing any visible disease. This means an infected animal can fly under the radar for months exhibiting no particularly visible signs of infection and be excreting dangerous numbers of infectious bacteria in its sputum, feces and other excretions. As a result where M. bovis infection is rampant, there is a considerable economic burden on farmers in terms of more regular tuberculin testing, herd movements being locked down (put on restriction) until they pass two clear tuberculin tests and the overall loss of animals.

As many of you are probably thinking, the best way theoretically to control a vector borne disease is surely to directly control the vector and vectors that prevent the elimination of M. bovis. A particularly attractive option on the surface is to engage in a mass elimination of the potential vector from around farmland, to attempt to prevent contact between the infected vector and uninfected cattle. Unfortunately the way things work in reality is often much more difficult than theory. Compared to the large numbers and difficult terrain that the possums have on their side in New Zealand, in the UK badgers are implicated as the vector and are not particularly difficult to find as they leave obvious marks of their habitation. A large scale cull should be the obvious solution except for one key problem: The British love their badgers.

There is a considerable conservation and animal rights movement in Britain that heavily opposes any potential cull of badgers. As a result the control of M. bovis has become a considerable political football with two sides, farmers who want to cull badgers and animal rights organizations that claim badgers are being used as a ‘scapegoat’. With neither side giving an inch and the decision about the next potential badger cull to come soon; the UK debate about the best means to control M. bovis raises an important question as to how scientists, government officials and the public should interact in the control of infectious diseases.

In solving this, numerous lines of inquiry will have to be explored to determine what the best solution that all sides could agree on would be. Firstly, it is worth looking at the biology and history of Mycobacterium bovis that make it such a successful pathogen. Then in terms of resolving this debate, it’s essential to determine the role that the Eurasian badger plays in the spread and persistence of M. bovis in the UK against other potential factors.

Once the link between M. bovis and the badger as a vector has been established, an analysis to see what benefit (if any) that culling would present on reducing herd breakdowns (confirmed cases of bovine tuberculosis in a cattle herd). Finally an analysis of other potential solutions other than culling such as ‘wildlife friendly farming’ and particularly vaccinating badgers. Finally, after these factors have been considered, we’ll revisit the original question and discuss what sort of compromise between health officials, farmers and conservationists could work.

Join back tomorrow for part II of this series: What makes Mycobacterium bovis such a problem?

Recommended reading

Although I haven’t cited anything in particular for this introduction, there are a lot of papers on this topic and there are a few that are particularly useful in understanding what will be discussed over this week here. If you have access to pubmed or other search engines, a read of some of the following papers would be recommended although not strictly required as they will be discussed in detail as the series goes on:

Gilbert M., A. Mitchell, D. Bourn, J. Mawdsley, R. Clifton-Hadley and W. Wint (2005). Cattle movements and bovine tuberculosis in Great Britain. Nature, 435:491-496.

Phillips C.J.C., C.R.W. Foster, P.A. Morris and R. Teverson (2003).The transmission of Mycobacterium bovis infection to cattle. Research in Veterinary Science, 74:1-15.

Carnival of the wee animacules

2006-03-25T12:31:00.000+12:00

Although I'm a little late on this one, the carnival of the wee animacules has been posted at Science and Politics.

Canwest apologises

2006-03-23T16:06:00.000+12:00

Canwest who own the TV station C4, which boldly decided to show the South Park episode "Bloody Mary" that offended just about every Catholic in New Zealand, has decided to apologise.

Broadcaster C4 says it is very sorry for any offence it caused by showing the controversial South Park Bloody Mary episode.

In a statement the broadcaster says the Standards Committee did not uphold any of the formal complaints it received about the show, which showed a statue of the Virgin Mary menstruating.

But C4 chief operating officer, Rick Freisen, sincerely apologised for any offence taken and said the broadcaster would not repeat the episode even though it is allowed to do so.

I'm so very convinced that they are being very sincere and that it isn't due to other factors like potential boycotts or similar. In any event I must pass my congradulations to C4, seeing as they've happily decided to donate whatever spine they may have had and I can assure you, spines are something that is hard to come by in the media these days. Maybe someone else can find a use for it.

[Note: No offence to our invertebrate masters is intended by this post]

Bloody trackback spam...

2006-03-21T22:47:00.000+12:00

I've had to delete over 30 assorted trackbacks from various sites spamming online poker to irritable bowels anonymous or something. I'll take it as a sign that I must be getting popular.

Bioessays journal editorial and reflections

2006-03-20T16:23:00.000+12:00

Thanks to PZ Myers, I was introduced to a journal I had not encountered before called Bioessays that I've become a dedicated reader of ever since. They often publish some interesting evolutionary hypotheses, particularly on subjects of my interest such as the immune system and origins of vertebrates. Recently, the editor Adam S. Wilkins has decided to write a piece about Intelligent Design and how scientists should approach the subject. I particularly like his concluding paragraphs, which I'll quote here as the paper probably isn't free and I think he's made a very pertinent point:

Furthermore, those scientists with passionate anti-religious convictions should accept that Science can no more disprove the existence of a Deity or immortal souls than religious people can prove the existence of either. More tolerance of private religious belief, coupled with insistence on what scientific evidence does actually tell us about the history of the world and living things, would be appropriate.

If, in contrast, scientists insist on atheism as the only ‘‘logical’’ belief system or demand that people choose between ‘‘evolutionism’’—the quasi-philosophic belief in evolution as a guide to what should be—and belief in God, the outcome is not in doubt. More than half the people in the U.S. would choose religion and reject the science. The consequences of this would be far wider than simply the confusion of school children about the history of life on this planet. Once one has rejected scientific evidence for an ancient Earth and a long evolutionary history of living things, it becomes correspondingly easy to start denying other scientific evidence, for instance evidence on climate change, resource depletion, the nature of pandemics, the causes of species extinction and much more.

I fully agree with this with the caveats that we shouldn't be afraid to admit that many prominent atheists do think that evolution strengthens their position. For example, Richard Dawkins (who always seems to come up) has stated that "Darwin made it possible to be an intellectually fulfilled atheist" and Paul Myers from Pharyngula has written several pieces on how he feels, which I recommend reading incidentally. This is usually used as some sort of launching point that all evolutionists are atheists and that evolution degrades religious beliefs blah blah blah froth at the mouth blah blah whatever. I think some introspection here might be of some use.

Here's a little story for those who are interested in reading a bit of (probably somewhat incoherent in places) rambling about my reasons for my faith. About 6-7 years ago after probably one of the worst years of my entire life, I lost my faith in God and rejected Christianity completely. I really was a very bitter and angry fellow at the time, having felt that God had deliberately tried to do me in, my family, my friends and virtually everyone else I knew. Because of these rather bad experiences and my already considerable dislike of religion that had been building for a while, I became what most would identify as a "strong atheist". My atheism at the time was directly the result of what I saw around me, such as problems with family members and friends, the world in general and my general angst as an angry young man (And I mean angry).

Science never really came into the picture for my rejection of Christianity and God at the time. You could attribute that to more to general angst and general disillusionment with religion. In fact, I probably wouldn't have cared less about what science had to say on the nature of God because having gone to a Catholic school, nobody ever introduced me to the concept that religious concepts would be directly contrary to science anyway. This of course never became overly relevant, because even with my initial introductions to creationism of the full YEC variety on university bulletin boards and with someone handing me Behes Black Box in my first year of university. Although I only had a relatively poor grasp of science at the time, there was something that never quite made sense with the arguments of the YEC creationists/stealth creationists that I debated with.

I have to concede that creationism merely reinforced my atheism at the time. In fact, I thought Christianity was more ridiculous after encountering creationism than I ever had before. Yet, although this might sound somewhat odd after what I have written just now, I did inevitably regain my faith in God and am unashamed to admit that I'm Christian. Bearing in mind that I was formerly Christian, then became an atheist and now went back, this would seem to make me a 'flip-flopper' I guess one could say. The main thing that made me rethink about things was the Christians I met at University during my second year (and beyond).

I've always been one for actions rather than anything else and I was very impressed with the Christians I met. I found they weren't the general hate mongers that I had frequently come to associate with Christianity like Fred Phelps and Pat Robertson. Many of them are among my best friends still and people who I probably get along best with. I also lost my impression of general Christian bloody minded fundamentalism from my association with these people. I found that many Christians hold a wide range of views on various topics, including scientific ones like evolution, social issues and about the bible itself. Most importantly, I liked the attitudes of many Christians I met, the way they treated others and the fact they still retained a genuinely held belief in God that I once had.

After a lot of reconsideration, I came back to God after careful introspection and decided that many of the core beliefs of Christianity still made sense to me. I should point out that I've never regarded the bible as literal and in particular I've always regarded many stories in the bible as being allegorical or poetic in nature to demonstrate a point, but not be literal history (where they simply fail to make sense, despite what creationists may protest about). In many regards however, I never allow my faith in God, based entirely on reasons from my own introspection to hinder how I view or observe the world around myself. I keep my science as science and God as faith, which I soon found after asking various Christians I met was not an uncommon view.

And so in the end I came back to God and I can even say that I have a more strongly held faith than I did before I lost it originally. This is probably because of the fact I've had a longer time to think about things, but also because my knowledge and general opinions have matured a lot more than what they were. Plus, I'm not as angry anymore, well except when debating where I still can dish out a bit of sass.

I suppose after such a lengthy rant, which was entirely unplanned so it has no real particular point, I should get to whatever it is I'm trying to say. Quite frankly, I don't care if Dawkins (or any atheist) says that evolution allows them to be certain about their atheism. It doesn't particularly bother me, because science isn't something I regard as being in conflict with my belief in God. If I held my belief in God as something that is in conflict with science, maybe I would regard the statements from the likes of Dawkins as threatening and proof of evolution destroying Christianity or some similar nonsense. We shouldn't hide the fact that knowing what is good science is something that a lot of groups, such as atheists, will claim as something that supports their view. Personally, I think evolution and the way nature works is a testament to the power and creative ability of God. Like Adam points out in his editorial that I agree with so much, I can't prove to Dawkins what I believe and Dawkins would have a [probably] impossible time using science to convince me God doesn't exist.

Of course, atheists are almost the 'boogeyman' for Christianity and have been promoted to that spot far too prematurely. I find that it's Christians that are degrading Christianity more than anything else. Those who want to hold concepts like creationism/ID being opposed to decent actual science are doing more harm than they are good, but probably only minimal damage in the end. It's individuals who proclaim that Christians should follow their general bilge and rhetoric like Pat Robertson, Fred Phelps, Kent Hovind and Anne Coulter that do more damage to Christianity than any science ever could. If you ask atheists or those who reject Christians beliefs about the sorts of 'Christians' they have in their minds, they'll tell you about the loud mouthed dribbling of the likes of the above as what their impression of general Christianity is.

The response of numerous Christians demonstrates that not even 'we' like them overly much. There are not many Christians who would like to concede that Fred Phelps, who protests at the funerals of soldiers with his band of escaped lobotomy patients, is a Christian himself. We just shove aside the fact he publicly claims he is Christian, because we know that he isn't following the tenants of Christ in spitting out his virulent spiels about homosexuals or whatever. Unfortunately, he's loud, he's very much in the media spotlight with his antics and these actions speak almost as loudly as the failure of the general majority of Christians to oppose and publicly criticize their ridiculous assertations.

If you ask me what is driving people from churches, making people question their faith and generally degrading the position of Christianity as being relevant in today’s world, it's the lack of moderate Christian voices against fundamentalism.

Blogging this week

2006-03-20T15:44:00.000+12:00

I'm a little behind on my reading due to watching the Black Caps give the West Indies what-for in the test matches, so most of the stuff I wanted to write about will be a little delayed. I'm currently looking into the plans to cull badgers in England, which will be the subject of discussion this week and I'm still planning on writing more about the evolution of the immune system (TLRs part II). Other stuff to follow will be more about one of my favourite topics (antibiotic resistance) and I'm looking into alternative theories about what caused the black death as a follow up to this post.

In any event, well done to the Black Caps for a well deserved test series win and without the distractions of the cricket there should be more blogging (hopefully).

Excellent new blog

2006-03-17T10:07:00.000+13:00

Good Math, Bad Math by Mark Chu-Carroll is a new interesting blog that covers pseudosciences love of abusing mathematics. I first noticed this blog when Mark did a take-down of the horrific statistical analysis used in the latest paper produced by the Griers at Respectful Insolence. He's since moved onto different subjects now including analysing the mathematics of William Dembski. I highly recommend a read.

Skeptics cirlce posted

2006-03-17T09:39:00.000+13:00

The 30th Skeptics Circle is now up and ready for skeptical minds at Paige's Page. This one is quite big with quite a few particularly interesting articles, with possibly a submission from Kelly Jolkowski being one of the best. Essentially, her son Jason has been missing and in her families desperation they turned to 'psychic' help. Unfortunately, she has found that the psychics aren't quite able to live up to their claims and she has a blog dedicated to discussing the numerous frauds and psychic conartists she has encountered. There are numerous other great articles too as always, so head on over and get to some reading!

Amazing quote

2006-03-16T12:09:00.000+13:00

There are few quotes that are said today that come off as being both very pertinent and insightful, but this one from Jamie Raskin a professor of law from AU is right up there. Speaking in opposition to a bill that would propose a blanket ban on homosexual marriage, the republican senator presumably thought they were being witty when they began the following exchange:

At the end of his testimony, Republican Senator Nancy Jacobs said: "Mr. Raskin, my Bible says marriage is only between a man and a woman. What do you have to say about that?"

Raskin replied: "Senator, when you took your oath of office, you placed your hand on the Bible and swore to uphold the Constitution. You did not place your hand on the Constitution and swear to uphold the Bible."

The room erupted into applause.

I don’t think that poor Jacobs would have had any response to that.

Gay genes and sperm donors

2006-03-15T10:44:00.000+13:00

Scientists really should avoid putting their foot in things sometimes:

A Christchurch scientist [Dr. Frank Sin] has drawn the ire of the gay community and fellow scientists by saying infertile couples should be told if their potential sperm donor is gay because of evidence that homosexuality is genetic

I think this is frankly ridiculous. Yes, homosexuality probably does have some degree of genetic basis that is probably further conditioned by the environment an individual grows up in. The problem here, that I can see, is that it puts a gay donor into some sort of category like they have a disease. Further, this is only one step away from starting to specify what sort of characteristics children should have. Perhaps we should start having parents who are dark haired give 'informed consent', because maybe I don't want a kid with dark hair. Maybe we should extend it to donors who are of specific ethnicities as well, perhaps using the justification of higher rates of diabetes, certain cancers or heart disease as the reason.

This is just ridiculous and I certainly hope nobody takes this recommendation seriously.

New Zealand HIV rates rise 17%

2006-03-14T14:39:00.000+13:00

This report I saw over at scoop magazine is somewhat concerning, indicating that there has been a fairly substantial increase in the rates of HIV transmission across the board.

Of the 183 new diagnoses, 89 were men-who-have-sex-with-men (up 19% on 2004), 73 (35 men and 38 women) were infected heterosexually (no increase on 2004) and six were children diagnosed with HIV through mother-to-child transmission, four of whom were born in New Zealand to mothers who had not beed diagnosed with HIV. There are now more people living with HIV in New Zealand than ever before.

“What this tells us,” said New Zealand AIDS Foundation Board Chairman Hoani Jeremy Lambert, “is that no-one in New Zealand can afford to be complacent about HIV. Treatments might have improved but this is still a deadly serious virus. It has a major impact on health and wellbeing and people still die prematurely, especially infected children.”

I have this disturbing feeling that so much of this could be related to the presence of anti-retrovirals making individuals too complacent. In the minds of many, these drugs have 'cured' HIV so it's no longer as dangerous to go and have unsafe sex. This is far from the truth however as the article mentions:

“The medicines delay the progression from HIV to AIDS but they are not a cure and they do not prevent transmission of the virus to others,” she said. “Prevention is still our best option. A properly used condom is close to 100% effective against the virus and HIV screening of all pregnant women would practically eliminate mother-to-child transmission.”

I think the ABC strategy that worked so well in the past is worth repeating. It's essentially Abstinence, Be faithful (Monogamy ftw) and finally Condom use. Another good idea I think would be to make sure that highschoolers are given better sexual education, which would hopefully leave them better informed about how STDs behave and spread.

Insanity of War.

2006-03-14T06:24:00.000+13:00

World War 2 has been an interest of mine since I was still in high school and over time I’ve read pretty much anything about it I could get my hands on. Of all the authors and various books written about WW2 two of the best are arguably Stalingrad and Berlin, which were both written by Antony Beevor. These two books changed my opinion on World War 2 more than anything else because both accurately and clearly detailed the depth of insanity men fall towards in war.

One of the most poignant examples of this was when a group of German soldiers (If I recall correctly, they may have be Russian) were burying one of their comrades. They covered the man with branches collected from nearby trees, when one of the other soldiers cried out that they were “Enemy branches!!” causing the soldiers to fanatically recollect the foliage and burn it. Another example was a German solider facing the huge soviet offenses to charge to Berlin in 1945, comparing the attacking Russian waves to animals that were simply out to be killed or kill him. The Russians of course weren’t terribly better with many Russian soldiers, still incredibly bitter from the siege at Stalingrad, going on a murdering and raping spree against German civilians in order to get revenge.

The violence, inhumanity and sheer disregard for human life demonstrated on the Eastern front of WW2 demonstrates war at its very worst. Russian commanders in their attempts to race to Berlin to beat the Americans, not to mention each other, wasted huge amounts of human life. This is because the Russians frequently chose to attack using large bludgeoning waves of troops against well entrenched positions. Casualties, even considering the small numbers of German defenders, were often extremely high and better firing support, reconnaissance and preparation before attacks Russian commanders could have avoided such high losses.

Adolf Hitler also played his part in exacerbating both the war and the loss of human life. Hitler held to an untenable position where he would not concede even an inch of land that his forces had previously gained. This resulted in long, bloody and most importantly pointless sieges such as Budapest, which I get the impression Hitler thought he could turn into a German equivalent of Stalingrad. Hitler too was also completely deluded, at one point ordering phantom divisions that never existed and engaging in wasteful assaults such as the Ardennes campaign of 1944. Panzer divisions lost in that attack would have been better served on the eastern front, which would have been more useful than simply being easy targets for American and British planes.

Unfortunately, the western Allies are not entirely guilt free from (needlessly) adding to the already horrific death toll of WW2. The fire-bombing of a small German city called Dresden in February 1945 demonstrates a similar mindset in many ways to the revenge rapes/murders on civilians carried out by the Russians. Dresden had no important industry, was not in any area that would be essential for allies to cross and had a small population. The town was almost entirely annihilated by the combined American/British air raid and over 300,000 people were killed. The air-raid was nothing more than a revenge attack for the bombings on British cities (1941) and the V-2 rocket attacks (~1944-1945).

Although I’ll concede that world war 2 was a war that needed to be fought as the evils of NAZI German and Imperial Japan needed to be combated, what never needed to happen were so many incidents where peoples lives (regardless of what side they were on) were destroyed for no purpose. Such are the depths that wars frequently sink towards, where human lives become nothing more than little plastic figurines on a table to be cashed in for more territory, materials and prestige.

Sources: Berlin: The Downfall 1945, and Stalingrad both written by Antony Beevor and more than worth reading even if WW2 isn't your area of interest.

Awesome menu!

2006-03-13T12:04:00.000+13:00

This is the best restaraunt menu I have ever seen before. From the "Carbon burns fresh particularly must" to the "Carbon burns fatty cow New Zealand", which I will leave to you to figure out what they are implying there, this is probably one of the most interesting menus I have ever seen. There is more hillarity as well and I'm still trying to figure out if this is just an elaborate hoax or not.

(Spotted at Pharyngula who spotted it originally at Helminthlog. If I was psychic I would predict this going around the blogosphere fairly quickly)

Amazing game of cricket

2006-03-13T11:19:00.000+13:00

It's not every day when you see a game of cricket have over 400 runs hit in one innings, but when it does happen it's an incredibly amazing event. Of course, I have to concede that when it's Australia vs. pretty much anyone and you see Australia get 434, you don't really expect the other team to beat that. This naturally led to several Australian fans posting messages such as this one on the tonk blog (a part of the Sydney Morning Herald).

"Could there possibly be a hole deep enough for Smith by the end of that innings- We'll see now who chokes under the pressure of having to get 435 to win.

I predict the record for the greatest winning margin will also go tonight."

Unfortunately for this particular Australian cricket fan (Quin), he's going to look mighty silly because South Africa pulled off an absolute blinder to win the game. I could watch cricket like that any day, especially when Australia lose ;) I can tell you what though, I would not want to be a Mr. Lewis on his way back to Australia any time soon. The Australian media, which is in shell shock at the moment, is going to recover they are going to eat Lewis alive and Ricky Ponting (the Australian captain) is going to be dessert.

Now this is televangelism

2006-03-12T20:19:00.000+13:00

Jay from Ocellated posted a link to this devious little idea to spice up a televangelists show. Robert Tildon while getting into his televangelism, stops inexplicably every so often, grimacing and screwing up his face in odd ways, apparently claiming the "Holy Spirit" is writing around in him (I'll put my money on hot mexican beans!). In any event, such pauses only call for one thing: the addition of the wonderful sound of flatulence! Farting Preacher accomplishes this goal, with several edited videos that add these most delightful of bodily noises on cue to his show.

Now that's my kind of televangelism. As smelly as it is a dirty and underhanded way of taking advantage of peoples beliefs.

Awesome rant

2006-03-12T02:06:00.000+13:00

This is very easily one of the best rants I've ever read:

I'm not satisfied with quick non-answers to hard questions. I possess both righteous indignation and humility in the face of ignorance. I reject the idea that religiosity automatically makes someone an expert on anything, especially matters of science. And I just might know what the hell I'm talking about. Who the hell do I think I am, spouting such arrogant, highbrow bullshit?

Well said indeed by Evil Monkey (of closet fame) and the rest of the rant pretty much hits the nail on the head on a wide variety of issues, including how science is popularised in the media, ID and the life of most young prospective scientists.

Zardoz!

2006-03-11T20:51:00.000+13:00

While reading pharyngula earlier, I encountered a link to a review of a movie called Zardoz. I have to admit, that review convinced me that movie is comedy gold in the making and I'm not going to have to see it. There truly is such a thing as a movie so bad, it's actually good! Besides it has Sean Connery in it, he couldn't possibly do anything wrong right?

Revisting probiotics

2006-03-10T21:52:00.000+13:00

Although the last time I wrote on the subject of probiotics was somewhat pessimistic in tone, it should be emphasized that I think the entire concept is a really good idea. For one thing, bacteria as a general rule have a bad reputation among the general public that is worse than any other group of organisms. After all, microbes are linked to terrorism, disease, cooties and generally thought of as being associated with unhygienic practices. The number of people who cringe at the idea that milk is consistent mostly of bacteria is quite substantial. Very clearly, microbes have a major public relations problem and probiotics are a way of conveying to the public that there are ‘good guys’.

In fact, before I continue with the remaining substance of this post, I should point out the majority of normal bacteria aren’t out to get you. Microbes do numerous important things for every person on the planet and all completely without thanks or even a simple acknowledgement. For example, one of the most important functions bacteria that live on your body is to inhibit the growth of pathogenic microorganisms that try to establish themselves. As a further bonus, the gut microflora may communicate with the immune system, helping to appropriately target hostile microorganisms (see references of the previous post and below for some more information).

Obviously, these facts are essentially the basis for probiotics and what makes them such attractive options for treating certain illnesses. How exactly probiotics are supposed to do so and if they are even effective is somewhat under contention. To discuss this, some questions that arose from a comment left by impatientpatient are worth addressing below.

To begin:

1.VSL-3 is a fairly new product on the market and has specifically been tested on colitis, I believe, at the University of Alberta. It was a tiny study with what looks to be promising results. Pain and dysfunction was relieved a a fair majority of patients using this. Is this a place to start in seeing if probiotics or blends work?

Almost certainly, although small study sizes can only give indications that something is working or not. A much larger study that follows people for a longer period of time is required to definitively establish a protective effect, but many initial results do look good. The science is there to suggest probiotics can be an effective treatment for certain inflammatory bowel disorders, which are predominantly thought to be caused by abberant immune reactions between the native microbiota and the host immune system.

2.I was fortunate to have a doctor that recognized C Diff when she saw it. But I continue to have flare-ups of excuciatingly painful magnitude (drop to the floor clutching my stomach) on occasion a year after this infection.

I did use Lactobacillus Acidophilus, as Flagyl and Vancomycin pretty much have a fair bit of a failure rate. It was an education, trying to find something that would benefit me in any way. Yeast- used like pool shock once, and lactobacillus and time seemed to resolve the acute infection. I do not know why I continue on occasion to be in pain and all, but a dose of lactobacillus seems to help.

Herein lies the problem. As a patient, I decry pseudoscience. I would like to know if somthing has efficacy and why- I am not about to take anyone's word for something these days without researching it extensively. I think that is not a terrible attitude to have. I did research probiotics and I did find what seemed to me a plausible cause and effect- over the short term only. But until someone does a giant study-- and a proper double blind placebo trial- I rely on a fairly sketchy body of evidence. Was it LB, time or placebo effect that caused my condition to lessen? I don't know. I hope it wasn't the placebo effect. I hope it was a combination of time and LB.

Without any direct familiarity with the particular disorder and what may be going on, I would possibly guess that the Lactobacillus acidophilus may be helping. At the same time, it’s possible that the probiotic isn’t doing anything other than aiding the reestablishment of the microflora. The original infection of the Clostridium difficile may have thrown things out of whack and the antibiotics compounded the problem. All that may have been required was some time to reestablish the microflora and put things back to semi-normal. I could imagine that flare ups may reoccur after a subsequent encounter with another pathogen (not always another bacterium at that), with the resulting immune response re-activating ‘confused’ immune cells that attack the normal microflora again.

3. The other problem is that many doctors have really no idea of how horrid C Diff can be. And many do not recognize it. That can cause C DIff to morph into colitis, Crohns and even death. How can this be addressed?

There really isn’t a lot that can be done here except to educate and retrain doctors. In many respects the worst aspects of disease is that the early symptoms are all very similar. For example, most cases of meningitis start as something that just looks identical to the flu and can be very easily misdiagnosed. As

New Zealand

is currently experiencing an epidemic of bacterial meningitis, caused by Neisseria meningitidis, this issue is a considerable problem. With many diseases the line between a painful long lasting disorder or even death, can often be the time between onset of symptoms and recognition and treatment of the disease at early stages. The response from health authorities here was to provide more information to the general public to spot symptoms, promote greater awareness of the disease among health authorities and analyse potential cases more closely.

4.How can you measure gut flora in people? And could you do an experiment that did this before, during and after treatment with probiotics? NEOPHYTE but curious. Can stool cultures be helpful in this regard? Could you measure levels of C Diff and probiotics in a stool culture?

There are several ways of analyzing the gut flora of people and the majority of methods all involve pooh in some way. The first method is to simply take a nice slice of waste material, set it up on a microscope slide and eyeball what is there. Generally, you can find a lot more microorganisms by such cursory examinations than you can manage to actually culture. Obviously, looking at a bunch of rods, cocci and various squiggly things isn’t actually going to tell you overly much.

As a result, molecular methods are a much better way of finding out what the microbiota actually consists of. The way this is done is by exploiting wide amounts of natural variation among different bacterial strains in their 16S ribosomal RNA (rRNA) sequences. This little gene is useful because it has some regions that are constant (not changing) and other parts that are hyper-variable and change a whole lot. This allows scientists to easily amplify a range of 16S rRNA fragments by a technique called PCR (Polymerase chain reaction). These sequences can be separated out by gel electrophoresis and sequenced to identify what organisms are present. During an experiment, an investigator can determine if known bacteria are present before, during and after an experiment, so the answer to the second part of your question is also yes.

Of course this “poo print” has its problems, which a paper in Science by Eckburg P. et al illuminated quite clearly. The first problem is fairly simple, what bacterial species we have identified conclusively through sequencing is a tiny part of what is really there. We may be able to identify general groups of bacteria, but for families we don’t really have a lot of information on it makes identification hard. The other problem comes from the fact stool cultures are used as a model for the entire gut microbiota. This may not actually reflect reality very well, as some species may not be present in high numbers or may be hard to detect for other reasons.

Lastly of course, because this is a molecular technique that can work off even a single strand of 16S rRNA (theoretically at least), it’s difficult to verify the exact numbers that an organism is actually present in. This is one of the other problems with probiotics as a whole, you may be able to show they are present and possibly even persist, but the probiotic organism may end up an oppressed minority and not be able to affect anything.

On the whole however, I see a considerable amount of benefit to the use of probiotics, especially to recover from using antibiotics and serious infections of the gastrointestinal tract like Clostridium difficile. Obviously, more basic work needs to be done on the gastrointestinal tract microflora, particularly on how they interact with the immune system and which members are prominent in this interaction. This research would have obvious benefits to the understanding of probiotics as well.

References

Eckburg P.B., E.M. Bik,C.N. Bernstein, E. Purdom, L. Dethlefsen, M. Sargent, S.R. Gill, K.E. Nelson and D.A. Relman (2005). Diversity of the Human Intestinal Microbial Flora. Science, 308:1635-1638.

Patel J.B. (2001). 16S rRNA Gene Sequencing for Bacterial Pathogen Identification in the Clinical Laboratory. Molecular Diagnosis, 6:313-323.

Carnival of the wee animacules is up

2006-03-10T06:28:00.000+13:00

The third meeting of the wee animacules carnival is now up over at Aetiology. It's a special one at that, because it commemorates a once a year special occasion, the birthday of the much loved Paul Myers from Pharyngula. Presumably punch and birthday cake can be found at his blog.

Snuppy the puppy is..... drumroll

2006-03-10T02:53:00.000+13:00

A clone! As it turns out, although Hwang managed to basically humiliate the entire field of stem cell research by fraudulently falsifying data, at least the dog Snuppy is 100% genuine clone. Two studies published this week in Nature, by two independent groups one led by the Seoul National University Investigation Committee and the other by Heidi G. Parker et al show conclusively Snuppy is a clone. Interestingly though, the paper by Heidi G. Parker et al indicates the group is still somewhat skeptical of the overall result, citing several problems with a totally conclusive assessment of their results.

Firstly, they note they did not personally draw the blood samples used by them in the experiment but a third party did. They don't anticipate this to be a problem however, but probably mentioned it for completeness in case the result was disputed (which looks unlikely). Additionally, they were not provided samples from the original oocyte (egg) donor, which was tested by the SNUIC, so they cannot make a definite assessment of if the results from the mitochrondrial analysis they attained were expected.

Overall however, I think we can now bury the hatchet over the whole question if Snuppy is a clone or not.

Farm animal cannibalism strikes again?

2006-03-09T21:06:00.000+13:00

Cannibalism is one of those practices that, at least as far as humans go isn't very high on the list of things that are socially acceptable. One of the numerous problems with cannibalistic practices is the transmission of diseases, after all what infects dinner is just as easily going to infect the cannibal. It should be reasonable common sense as a result not to feed a farmed animal the remains of their fellow animals. This would greatly aid the spread of an infectious microorganism through a herd and possibly even rapidly increase virulence (which is often directly correlated to the ease of transmission).

The case example of why this practice shouldn't be performed, with any animal, is the dramatic outbreak of bovine spongiform encephalopathy (BSE) in Britain. BSE was found to be spread by an infectious protein called a prion, which is predominantly found in the brain and spinal matter of the remains of cattle. Worse, these parts were frequently fed back to other cattle as a supplement to their feed, providing an easy method of transmission for the infectious prions. The worst part of the entire discovery was not just that other cattle could be infected in this manner, but the potential spread of the disease between beef from infected cattle and humans. This led to the culling and suffering of a large number of animals and an overall ban on British beef that lasted a considerable time.

The entire result was a heavy economic and consumer confidence toll on British farmers and on the entire beef industry that cost millions (billions?) of pounds. Predictably, the practice of feeding dead cattle back to other cattle was immediately halted. With such a brilliant example of why allowing cannibalism with farm animals is a silly, you would probably imagine that most places would ban the practice regardless of species. Unfortunately, an outbreak of a disease among pigs on South Island farms recently in New Zealand, may be linked to feeding pigs the remains of other pigs imported from overseas (emphasis in the quote below is mine and I shortened the length, indicated by the ….)

An animal health expert says a pig disease that has struck the heart of New Zealand's pork industry is almost certainly Post-weaning Multi-systemic Wasting Syndrome (PMWS).

PMWS is a highly contagious viral disease that kills young pigs up to 12 weeks old. It has forced the closure of about six pig farms in the North Island.

Vets have been investigating a disease outbreak that has so far killed about 1,000 piglets on eight to 10 farms near Christchurch in Canterbury.

……………

He says it is possible that the Canterbury PMWS outbreak has been caused by infected imported pig meat being fed to pigs in foods scraps.

Feeding waste material to pigs has recently been banned again.

Obviously this is a severe disease and has resulted in a heavy economic loss for several farmers. The disappointing part is that lessons of the past from the emergence of BSE clearly weren’t heeded, especially if the outbreak is conclusively found to be linked to cannibalistic practices. Although the disease, called Post-weaning Multi-systemic Wasting Syndrome or PMWS is not suspected to be dangerous to humans, the outbreak still demonstrates important principals about how diseases may result from farming practices.

PMWS is caused by a virus called porcine circovirus 2 (PCV2), which was first identified in 1997 and is probably one of the most puzzling diseases around. PMWS is diagnosed not by using molecular techniques such as antibodies, but instead through the manifestation of certain symptoms that occur over the course of an infection. This is because antibodies to PCV2 can be detected amongst herds that do not show any overt signs of disease, indicating the organism is present but inexplicably not causing an infection. As a result, the following clinical symptoms are used to describe the disease: wasting (rapid loss of body weight), dyspnea, enlarged lymph nodes, diarrhea, pallor (loss of skin colour) and jaundice. Additionally, in some cases animals may exhibit coughing, pyrexia (a fancy term for fever), gastric ulceration (often leading to anemia), meningitis (an infection of the meninges surrounding the brain) and dropping dead (which is terminal).

How PCV2 causes such a wide array of symptoms and even how it initiates disease is the puzzling aspect about it. Experimental animal models have largely failed to reproduce the disease by using PCV2 by itself except in certain cases. Interestingly, more success has been attained when PCV2 was injected with other viruses, such as Porcine parvovirus. Regardless of the mechanisms that determine if the virus becomes infectious, when PCV2 does it targets some of the most vulnerable members of the herd, namely piglets aged between 7-15 weeks old. Possibly the most striking characteristic of PMWS is the overall mortality rates in infected animals, potentially getting as high as 40% and can even induce pregnant sows to abort their fetuses.

Dealing with the virus is equally difficult, because it tends to be widespread throughout the herd and circoviruses are notoriously difficult to kill with antiseptics and detergents. Containment and control requires more practical, such as reducing herd sizes, keeping animals separated by age and reducing animal density. As can be seen, the biology PVC2 and the linking of the outbreak to imported pig meat being used on the farms, raises an intriguing hypothesis as to the potential aetiology of the disease. Let us imagine a potential scenario from a land far, far away….

On a farm in an unknown land, a sick piggie called Mr. Pork wakes up to a pretty bad headache among other things…

Mr. Pork: Owww my head, I feel under the weather here. I know, I’ll go to farmer Brown for help! He’ll know what to do!

Farmer Brown: Why hi there porkie, how’s your day going?

Mr. Pork: I’m feeling a bit under the weather here and I may be getting ill!

Farmer Brown thinks to himself: I’d better do something about this before it spreads!

Farmer Brown: Well I have just the solution there Mr. Pork, we should go and visit Dr. Mallet. He’ll fix you all up!

Mr. Pork: Oh that sounds great, let’s go and –

*CLUNK*

Farmer Brown: Off to the sausage factory for you!

Later at the pork to sausage factory….

Worker 1: What are we going to do with all the left-over pig bits?

Worker 2: Let’s package them up as supplemental feed and send them to New Zealand.

Worker 3: Genius!

Anyway, returning from the realm of imagination, there may be solid indications that this is a possible origin of the PMWS outbreak in New Zealand. The suspected causative agent PCV2 has already been widely identified in New Zealand pig herds, and has caused outbreaks in the North Island previously. It is theoretically possible that a disease transmitted from infected pigs overseas, such as a different serotype of Porcine parvovirus that is not immunologically present here in New Zealand was in the imported meat. Once fed to the pigs on the farms in question, it encountered the ‘native’ PCV2 and potentially triggered the silently waiting virus to a full blown infectious disease.

Of course, this is not the only explanation but given the biology of the disease it’s a fairly compelling place to at least make a start. This is of course where one would expect the government to step, but unfortunately, it doesn’t actually appear such assistance is going to be quite what some farmers may expect:

Canterbury pig farmers at the centre of a disease alert have been given a clear message from the government that it will not step in with an eradication plan.

The Ministry of Agriculture and Forestry's Biosecurity Authority has advised the government that eradication of the suspected disease, PMWS or Post-weaning Multi-systemic Wasting Syndrome, is not viable.

Well, that almost sounds to me as if they are throwing in the towel before they even try to do anything. At the very least, by identifying why the outbreak occurred and potentially trying to contain or eliminate the cause authorities could do a fair amount of good. While I do suspect that elimination of PVC2 may be unfeasible although containment and other measures should at least be attempted. If there is a positive to be taken from the recent outbreaks, it’s that feeding pig remains back to other pigs has been re-banned. I guess you take your victories where you can get them.

References

Chae C. (2005). A review of porcine circovirus 2-associated syndromes and diseases. The Veterinary Journal, 169:326-336.

Darwich L., J. Segal and E. Mateu (2004). Pathogenesis of postweaning multisystemic wasting syndrome caused by Porcine circovirus 2: an immune riddle. Archives of Virology, 149:857-874.

Harding J.C.S. (2004). The clinical expression and emergence of porcine circovirus 2. Veterinary microbiology, 98:131-135.

Can't argue with them? Burn them!

2006-03-09T19:04:00.000+13:00

An incident where someone attempted to physically burn down the Holocaust History Projects building. The incident has been widely noted among other bloggers, particularly Orac at Respectful Insolence who has more details. I think the whole attempt is entirely reprehensible and I sincerely hope the idiots behind the attempted arson are caught.

Theistic evolution and creationism

2006-03-08T20:42:00.000+13:00

Over at "He Lives" the blog of the ever indominable David Heddle, he complains that the Pandas Thumb denisens don't like to give specific definitions of what makes a 'creationist'. Apparently, Dr. Heddle comes up with some conspiracy theory that they are just avoiding alienating 'good guys' such as theistic evolutions (like myself) and many Roman Catholics such as Ken Miller. I think David seems to believe that the PT crew would think I may get highly insulted and have a hissy fit or something.

To quoteth from Davids post, noting that reading the whole thing is best for establishing proper context:

Creationist: someone who believes, to some nonzero but unspecified extent, that invoking supernatural intervention is necessary to explain the natural world.

I accept that as nice, concise description. No muss, no fuss. There are, however, problems for the PT faithful with that definition—I’ll get back to that point.

Later in his definition, Russell performs a little sleight of hand. After arguing that theistic evolutionists might be shoe-horned into this definition, he adds: “But as long as they recognize that their understanding of divine intervention can never fall under the purview of science, they’re not ‘creationists’.”

I happen to agree with the original definition as well, I am also a creationist in a sense because I view God as creating the world via natural laws (physics, evolution, chemistry etc), usually called "theistic evolution". Calling it "theistic evolution" is IMO, simply a bait and switch to simply avoid the rather distastful association with creationists like AiG and Hovind. The key difference between theistic evolution compared to standard creationism is that I do not view signs of that creation are directly and empirically visible in nature. Ergo, I don't buy fine tuning for example and most importantly, I do not want my metaphysical beliefs taught in schools. In fact, I would be opposed to people teaching that God directly used evolution to create man as *fact* in a science classroom, simply because there is no empiracle justification for such a claim. What I believe is different from what science tells us about the natural world and how it works, with one of the things it can't tell you about is what role God played in it.

In terms of what David discusses, the 'creationists' that the likes of the Pandas Thumb crew basically dislike are those pushing 'creation science' or those of the Discovery institute led ID movement. For the record, I have never been personally attacked by any atheist on the pandas thumb for my religious beliefs (engaged voiciferously however) or even on internet infidels. I have had my faith in God attacked numerous times by creationists, highly visciously as well, and usually at every opportunity to do so. This is partly why I am so immensely aggravated (or frustrated) in discussions with creationists and my accompanying lack of patience at times.

As to Russel attempting to make a 'loophole' for me or something, I find it rather commendable but unnecessary. I'm not embarassed that I believe in God and I'm equally not embarassed to admit I believe God used natural principals like evolution to make what we see today. I don't require a disclaimer on my beliefs that reads:

But so long as you agree to think you can't test for Gods interactions with the natural world we won't call you a creationist, *nudge* *nudge* *wink* *wink* eh eh

For all intents and purposes a theistic evolutionist is a creationist. The difference is the political and ideological motivations are entirely different from the stealth creationists and the typical YEC/OEC groups that want to 'dismantle' evolution.

In terms of definitions, I want to stress again I have little problem with someone thinking I'm a 'creationist' because technically that's what a theistic evolutionist is to begin with. Trying to define 'creationist' without the "God* created the world part" is impossible. I believe God created the world and I don't see the point in hiding that fact behind a layer of bollocks. It doesn't mean that I give any credence to ID creationism (as the discovery institute tries to hide it) or to biblical creation science. Reading what I have wrote on evolution at this blog or elsewhere should make that immensely clear.

If the fact I happen to have my beliefs about God lowers an atheists respect for me (or anyone else for that matter), rather than the quality of what I actually write here, that is their decision and I couldn't care less.

Update: David Heddle has made a reply to my response to him. Looks like I could be on two fronts soon once Krauze posts his reply to my reply to his reply. Oh my!

*Or Allah, or a collection of deities or a flying spaghetti monster. Whatever.

That "court stunt" again

2006-03-08T05:26:00.000+13:00

Reading yet another report on the now infamous "Dover Trial" where ID was categorically handed a massive defeat in the Pennsylvania Gazzette, I can do nothing more than crack a little smile upon seeing my favourite court stunt mentioned again:

Behe claimed that mainstream scientists had produced “no detailed, rigorous explanations for how complex biomedical systems could arise by random mutation and natural selection.” The biochemical intricacy of the immune system is one such purposeful arrangement of parts. “I see no Darwinian explanation for such things,” he stated.

During cross examination, Rothschild stacked up on the witness stand 58 articles from prestigious journals like Science, Nature, Molecular Cell, and Proceedings of the National Academy of Sciences. All of them described research on the evolution of the immune system. “Is your position today that these articles aren’t good enough?” Rothschild challenged. He then piled on 10 textbooks with titles like Origin and Evolution of the Vertebrate Immune System.

“What I strongly doubt is that any of these address the question in a rigorous fashion,” the star witness replied, adding later that “I haven’t read them [all].”

“It was the high point of the trial,” Harvey recalls. “Anyone who studies that cross examination would realize that Professor Behe’s work is bankrupt. Eric just took it to pieces and did it brilliantly.”

Once again it's very evident just how devastating an effect and simply memorable that part of the trial has ended up. It was just so poignant a moment to have Professor Behe, surrounded by numerous articles from the very scientists he just derided as having no satisfactory answer admitting he hadn't even read the relevant literature. Bear in mind that after the trial Behe claimed that he had shown the other side was "full of rhetoric and bluster". Unfortunately for Behe, his testimony was completely essential in the massive defeat suffered by the school board at Dover. That moments such as the one above are continually mentioned in the media as essential in the defeat, you have to wonder if Behe is really wishing that he'd done a Dembski and avoided getting on the stand to begin with.

The McPassion

2006-03-08T02:58:00.000+13:00

There is something distinctly wrong about this. Who could have possibly thought of commercialising christian concepts in a shameless attempt to sell stuff. Not to mention doing it in a manner that isn't really that funny either.

*cough*

A history of plague

2006-03-07T21:00:00.000+13:00

Human history is largely characterised by two major forces, warfare and infectious diseases. In many cases these have been directly linked to one another, with new pandemics closely following after a war has subsided such as the 1918 influenza pandemic. In other cases the outbreak of a disease has directly affected the outcome of a war, such as the decimation of Napoleons army by typhoid fever halting his march on Russia. Among these ranks is a disease that does not really enter the publics mind often today, the black death. Caused by Yersinia pestis, the black death (plague) was responsible for depopulating much of Europe, breaking down the feudal system and facilitating the rise of a middle class redistributing power. With the rise of antibiotics, plague ceased to be much of the threat that it once was and has mostly been eliminated from the developed world. Today, plague is a considerable threat only in developing countries and from emerging uses as a biological weap

What is the black death?

The black death is caused by a gram-negative coccobacillus called Yersinia pestis, which actually has a few family members that can be fairly nasty also, such as Yersinia enterocolitica and Yersinia pseudotuberculosis. Like a large number of highly infectious diseases plague is an example of a zoonosis or a disease that is spread from animals to humans, in this case originating from fleas that live on rats. When the rat population becomes low, or the animals are predated on by the likes of cats, the fleas are forced to vacate home and find a new host. Very often, this host happens to be a nearby human and the bacteria are transmitted into the unfortunate person through the fleas bite.

Once inside the body, the Y. pestis is capable of very rapidly disseminating throughout the bloodstream and has a particular affinity for the lymphatic system, with the lymph nodes being the primary target. Lymph nodes are important, because the organism homes in on them and begins to disrupt normal immune function. Essentially, the organism uses a battery of virulence mechanisms to set up a catastropic immune reaction that causes large amounts of uncontrolled inflammation.

This inflammation has two primary effects. The first is to cause the large swelling that forms buboes, which is where the disease gets the name 'bubonic plague', although at the moment it's unable to spread from person to person. Secondly, the inflammation causes blood vessels to become 'leaky', normally a response to let lymphocytes pass to a site of infection but in this case causes widespread internal bleeding. Coincidentally, this is also why plague is called the "black death", because the blood pools in the extremities of the body such as fingers and around the mouth. This accumulated blood then dries under the skin and turns black, giving a solid indication of the terminal stages of the disease. Once this internal bleeding begins, Y. pestis seizes the opportunity to rapidly disseminate through the bloodstream and spread everywhere.

At this point there are generally only two possible outcomes. The first is that the victim simply dies from sceptic shock, where the loss of fluids from the internal bleeding causes a drastic drop in blood pressure and subsequent drop in circulating oxygen causing organ failure. In a cruel irony however, the second potential effect is the infected individual survives only for the organism to establish itself in the lungs. Here the bacillus cause further damage and become even more dangerous becoming penumonic plague. This form of plague is spread through exhaled aerosol droplets and can kill within hours due to being 'pre-conditioned' to the human body.

Reactions to the plague

In the modern world, when we get sick or are having a hard time with an organism you can very often get antibiotics or other treatments to solve it. After all, today we have a great appreciation of the fact diseases aren't caused by demons or sinister spirits, but rather by the interactions of infectious microorganisms and their hosts. Unfortunately, when the plague was at its worst such understanding was not available and the fearful reaction of most Europeans to infected individuals was sometimes worse than dying of plague. Many plague victims were simply buried in large mass graves and worse still, infected individuals and their entire families in London were often simply sealed into their own homes and left to die. There are towns and cities in England that have expanded over and simply built on top of these testimonials to human ignorance.

Even if you survived this wasn't a guarantee that you would make it through, as it was sometimes suspected that those not struck down by the disease were protected by the devil. The resulting fearful mob that formed simply stoned the individual to death or occasionally burnt them at the stake. Possibly the most poignant example of this ignorance leading to immensely violent reactions was the observation that Jews suffered less from the plague than others. Numerous massacres of Jews occured as a result, not just from fear of the plague but also as a reaction against the religious and political institutions the peasantry saw as having failed them. Additionally, lepers (infected with an entirely different organism, Mycobacterium leprae) and anyone else with a skin condition were also massacred as they were thought to aid the spread of the disease.

As well as violent reactions there were also those of confusion and despair that gripped your average European. Confidence in practitioners of a 'science' called alchemy waned as numerous alchemic concoctions failed to do anything or just made symptoms worse. Additionally, skepticism surrounding the claims of the Catholic Church increased with the ever rising death toll as priests failed to cure plague victims and were struck down themselves regardless of belief in God. This led to many Europeans going to other relgious sects, like the crazy flagellants which rapidly rose in popularity or alternatively seeking more secular solutions.

The effects of the plague were considerable as a result on the future leadership and direction that Europe would take. With an estimated two thirds of Europes population wiped out by the pandemic, plague had numerous key effects on the European population. The power of the Church was greatly weakened by the plagues effects, leading to the replacement of several practices with more secular ideals. Secondly, the recession caused by the plague crashed land prices and the decimation of the population increased the amount of food per individual. This resulted in a redistribution of wealth among the average peasant, which inevitably led to the rise of the middle class and the redistribution of political power as a result.

Even with this effect, it's still important to bear in mind that some 25 million people died and some completely needlessly. The devastating effects of the plague were further amplified by numerous human factors as well. The culling of cats, seen as servants of witches, in several towns in England led to the plague spreading more rapidly due to the lack of predation on rats. In many cases the plague exposed how, when faced with such immense death, people reverted to nothing more than animals full of ignorance, bigotry and fear when everything they previously relied upon (Religion, their leaders, alchemy etc) failed to provide answers.

Plague in the modern world

Today plague is largely considered a 'dead' disease in the developed world. Although still dangerous to get, it tends to be rare and most people would not encounter it on a day to day basis. Even if you did manage to contract plague, there are numerous antibiotics that are effective against the organism such as tetracycline and streptomycin. The treatment certainly isn't pleasant, intravenous injections of an antibiotic never are, but it's highly effective and the patient has an excellent chance of survival. Unfortunately, the same situation cannot be said for the developing world. There, plague continues to be a killer due to insufficient stocks of key antibiotics required to adequately treat the disease and poorer standards of hygeine, such as living in close association with rats.

Worse still, Y. pestis is one of the best potential biological weapons currently around. It's firstly very well armed already, with a battery of virulence mechanisms including several type III secretion systems, which are used to inject toxins into cells and Y. pestis can directly destroy cells of the immune system (particularly neutrophils). Additionally, antibiotic resistant forms of Y. pestis have also been found, although thankfully only in isolated cases and do not appear to be widespread. Finally, unlike numerous biological weapon candidates, like ebola or anthrax, Y. pestis has the potential to spread between people allowing it to more rapidly disseminate through a population.

So although plague may be far from its original glory days, the potential of this organism for future outbreaks and particularly from drug resistant forms, cannot simply be ignored as a mere vestige of the past.

References

Anisimov A.P., L.E. Lindler and G.B. Pier (2004). Intraspecific diversity of Yersinia pestis. Clinical microbiology reviews, 434-464

Galimand M., A. Guiyoule, G. Gerbaud, B. Rasoamanana, S. Chanteau, E. Carniel and P. Courvalin (1997). Multidrug resistance in Yersinia pestis mediated by a transferable plasmid. The New England Journal of Medicine, 337:677-680.

Salyers A.A. and D.D. Whitt (2002). Bacterial Pathogenesis: A molecular approach 2nd edition. ASM press, Chapter 13:203-215.

Quack quack quack

2006-03-07T18:08:00.000+13:00

I noted with some interest a trackback link to the blog "telicthoughts", run by Mike Gene, Krauze and friends who have an intense interest in ID. I wondered what it could be about, considering that my post was really going back to discussing things more pertinant to good old YEC type creationism. I should have anticipated that Krauze would be out there twisting words like a professional spinster and this time I was the target. For some reason, Krauze seems to believe that by addressing the tenants of a young earth creationist article, by pointing out specific contradictions between that kind of creationism and what they are saying, I'm somehow admitting that ID isn't creationism.

Wait. Man what? Krauze makes an amazing leap of logic, which is almost as amazing as his placement of New Zealand in Australia (he claims I'm Australian, which would be like someone calling an Australian a New Zealander, or calling a Canadian an American for example). Krauze then criticises me for not adhering to some definition that John Lynch from Stranger Fruit gave for creationism, which I've decided to reproduce below:

Firstly, that a very restrivtive definition of creationism as it only encompasses young-earth creationism and ignores a number of viewpoints that are proudly creationist (day age, gap, etc). Secondly, what's the definition of intelligent design? We're not told, but are lead to believe that it is different from evolution (it is) or creationism sensu lato (it is not).

Which in fact I do happen to agree with. Reading Krauzes post over at Telic thoughts however, you would think that I've somehow contradicted myself, despite never stating anywhere in that post what definition of 'creationism' I was using. I didn't think this was required actually, because it should be fairly evident that the Baraminology Study Group is a YEC organisation. I naturally constructed my arguments around what the particular YEC groups happen to claim. If I had been arguing against ID, as motivated by the discovery institute among other organisations, I would have framed my arguments differently. I still regard ID as nothing more than creationism, but just dishonest creationism and I'm not sure what point that Krauze thinks he has made.

At the end of his post he comes out with this little tidbit:

What makes this even more ironic is the fact that when we were discussing my poll, Donnell left a comment (although under the name “Aegeri”) , accusing me of using “stacked definitions”. Apparently, the accuracy of a definition depends on who is using it.

This conclusion is evidentally what Krauze thought was being a particularly witty 'zing' moment. Unfortunately for Krauze, much like his claim New Zealand is in Australia, his point has gone south and been flung into the ocean. His "poll" to many other science bloggers, which included PZ Myers, Tara Smith, John Lynch among others, used a highly stacked definition of creationism that was entirely too narrow to be of any use. Krauze attempted to basically manipulate the poll to get the answers he wanted, so that he could probably make a post with a vacant non-existant point (much like this one about my post yesterday) but didn't quite get his way. Instead, they didn't react terribly well prompting Krauze to make a silly accusation of some "group think" to not answer the poll fairly, essentially claiming the bloggers he emailed couldn't think for themselves.

Of course, I didn’t say anything about a “conspiracy” or about “marching orders from Elsberry.” I’m simply pointing out the likelihood that respondents were being influenced by the public pronouncements from ID critics that the poll was flawed because it lacked ‘the only answer an ID critic would give’.

In other words from Krauze, I'm not accusing you of a 'conspiracy' I'm accusing you of being unable to think for yourselves and following the leader. For the record, I couldn't care less what other people respond in a poll regardless of who they are and would answer on my own volition. I would like to think that other science bloggers, many with degrees in their relevant fields would also happen to like thinking for themselves also.

At the very least, it should be self evident from a cursory look over my blog where I'm from.

Update: He corrected where I am from in the original post.

Creationists love the immune system

2006-03-06T20:50:00.000+13:00

If there is one thing I like most about life, it's watching the mental gymnastics that creationists try to go through in explaining the immune system of vertebrates. The problem such a system poses is two fold for the average creationist, the first being that supposedly before the 'fall' there isn't any death. Secondly, they then run into the problem of how such an incredibly complicated system like the immune system all of a sudden arises to combat disease causing organisms, which also appear all of a sudden for some reason immediately after making an immune system important. Especially viruses like the pox virus, which has an extremely large DNA genome, numerous individual proteins and comes complete with a large amount of anti-immune system factors. In particular, functions of receptors that seem almost exclusively used in the immune response in vertebrates, but not shared among other "lower" animals weaken the creation argument especially.

The Toll-like receptor (TLR), which has a detailed and well established function in immune function in vertebrates is a good example of this problem. As I've wrote previously (and hope to go into more detail in the future), the Toll receptor (what TLRs in vertebrates is named after) has different functions in invertebrates such as worms and the fruit fly Drosophila melanogaster (see update). Rather than being a direct part of the immune system of these organisms, Toll functions primarily as factors that aid development of the organism, essentially telling cells which way is 'up' and which way is 'down' so they develop properly. This signalling function in vertebrates is used for a different function, where the TLR has been hijacked for its signalling ability for recognising different 'bits' of pathogens, like lipopolysaccharide, DNA (CpG motifs) and other things to activate adaptive immunity. This is a classic example of co-option of a receptor with one function that has been adapted entirely for another (see the previous post for a good reference).

Of course, creationists obviously disagree and then have to come up with any contrived excuse to explain away this prediction. Interestingly, in a group of abstracts published by the Baraminology study group for a conference they held, which David Rintoul was kind enough to alert me to, one of the abstracts was talking about the invertebrate Toll. The abstract, Investigating the Presence of Toll-like Receptors on the Cell Surface of Earthworm Coelomocytes focuses in particular on those of invertebrates, which the authors seem to think somehow justified this rather spurious claim:

Non-disease fighting functions of Toll may be of interest to creationists since this may represent a remnant of Toll’s function in the pre-Fall environment.

Now as I've said above, the problem with this statement isn't so much the fact that invertebrate Toll has non-disease fighting functions, which they very obviously do but the whole 'pre-fall' nonsense at the end. Firstly, it's important to consider what a TLR is actually doing in the human immune system at the moment. TLRs in humans are found on specific cells and usually specific TLRs to boot (we have around 14 of them, with probably more to be discovered). For example, macrophages and dendritic cells have the job of playing 'clean up crew' in the body and have batteries of TLRs to sense a wide array of pathogens. On the other hand, epithelial cells of the gut have TLRs as well but only a limited subset (usually involving detecting viruses) because they see less types of different pathogens.

This in itself deals a considerable amount of damage to the above hypothesis. In vertebrates, TLRs are almost exclusively linked to the adaptive immune system, which they are critical in the function of, and are usually found directly linked with cells of the immune system. They are not produced in every single cell in the body, noting that gut epithelial cells of the gut are an exception because those cells are directly on "the front lines" when it comes to seeing new pathogens. If TLRs before the 'fall' are used in non-immune functions in vertebrates as they are in invertebrates, why are they only found in such close association with cells involved in immunity and virtually nowhere else? There is somewhat of a logical disconnect between noting what is ultimately the evolutionary relationship of developmental TLRs to the present day immune TLR, to suddenly claiming that this non-immune function is what they were doing before disease 'existed'.

Of course, this obvious localisation of TLRs makes full sense unless you're a creationist. If these have a non-immune function, I wonder what the authors actually proposed they were doing in antigen-presenting cells and the like before there was disease. Taking up space? They aren't playing a role in overall development, as you can knock out TLRs to compromise immunity without hindering growth of normal every day cells. This does stuff numerous cells of the immune system however, but that should be fairly obvious considering the entire point of TLRs are to detect pathogens and stimulate immune cell maturation and differentiation.

This problem of the localisation of these TLRs is not the only one of course. For example, why is it that TLR 11 in humans is a useless pseudogene yet in other animals is completely functional? Why is there such an incredible variation among TLRs between different animals, some having among 30-40 while others such as us Humans having a much lower amount. Are other animals after the fall just more diseased than we are? Without engaging in majorly wierd mental gymnastics, it's just incredibly difficult to support the immune system being 'created' when there is no disease then suddenly 'poofing' into existence (mind, Professor Behe thinks 'poof' is a legitimate explanation for things). This poofing occuring in the correct cells with the correct receptor patterns to spot diseases that never existed, which coincidentally have themselves just popped into existence with factors that allow them to destroy/subvert the immune system that never existed before either.

Is it just me, or is that utterly non-sensical? Many creationists tell me evolution is full of impossible 'just-so' stories and then come out with things like the above quote.... Hmmm, I think I'll take the 'orthodox' co-evolutionary warfare of pathogens and host immune systems thanks, as at least it makes sense.

Reference

Roach J.C., G. Glusman, L. Rowen, A. Kaur, M.K. Purcell, K.D. Smith, L.E. Hood and A. Aderem (2005). The evolution of vertebrate Toll-like receptors. Proceedings of the National Academy of Sciences, 102,27;9577-9582.

Update: I should point out that the TLR in Drosophila melanogaster should really be identifed as a Toll receptor as that organism is where these molecules were originally named and discovered. The TLR is named as it is because of the similarities between the D. melanogaster Toll receptor and a family of immune modulating receptors found in vertebrates. It's rather silly to call the original Toll receptor a "TLR" considering it's the receptor everything is supposed to look like. I apologise for any confusion and I've also cleaned up the definitions in this post so that the distinction is clearer.

29th Skeptics Circle

2006-03-03T22:33:00.000+13:00

The 29th meeting of the Skeptics circle has been posted at The Huge Entity. This time there is a poetry theme. Unfortunately, I spent all my poetic juice quite some time ago in my teen angst days.

Those were good times.

Penny Arcade scores some free donuts

2006-03-02T17:33:00.000+13:00

Over at Penny Arcade, they did this comic (Harsh language warning) lambasting the current state of affairs surrounding Sony Online Entertainments current online role-playing games. In the comic they compared Jim Lee teaming up with Sony with a man putting feces into Krispy Kreme donuts. As it turns out, Sony have a sense of humor and decided to send Gabe 1,200 Krispy Kreme donuts.

If only I could get some donuts after some of the internet arguments I've been in. I'd be rolling in millions of them.

MRSA using amoebae as a 'trojan horse'

2006-03-02T16:51:00.000+13:00

MRSA or Methicillin Resistant Staphylococcus Aureus is a grave concern in hospitals all over the world and not just for its lethality in patients. One of the biggest problems surrounding superbugs is getting rid of them once they are established in a hospital or other setting. As it turns out, one of the reasons that they might not be so easy to remove is due to the organisms surviving in other single celled organisms such as the humble amoebae. Amoebae are basically everywhere there is water and are little single celled animals that happen to like eating bacteria. In some cases however, the amoebae gets a meal that doesn't exactly want to die and instead uses the animal as a comfy home.

As it turns out MRSA is capable of this trick of living inside amoebae, which is of grave concern because this means water sources such as vases, sinks and even exposed drinking water with amoebae become potential MRSA reservoirs. To make a bad situation worse, living in amoeba may actually act as a means for improving the virulence and overall numbers of the bacterium, beyond those normally living on a bench surface. Studies with another pathogen, Legionella pneumophila have indicated that after growth in amoebae the organisms are both more pathogenic and more resistant to drugs than normal.

This is probably a consequence of being pre-adapted to the sort of environment they encounter in a human body, which tries to destroy them via a wide variety of defence peptides among other chemical mechanims. Additionally, living in an amoebae is in some respects very similar to living in human antigen presenting cells like macrophages, which is somewhat like getting used to the real thing. As they are also in higher numbers as well, it could be potentially even more disasterous for a patient that ends up infected with amoebae prepped MRSA.

In any event, after considering this finding, if I ever need to go to hospital I think I'll pass on having live flowers next to my bed.

The Da Vinci Code author sued

2006-03-01T19:39:00.000+13:00

One of the lawsuits that I'm following with keen interest is one surrounding a suit over the Da Vinci Code by Dan Brown. The premise of the book is that Jesus didn't die on the cross and he was in fact married to Mary Magdelene. Not only that they had children that carried on the divine bloodline and the Catholic church has been hiding this for centuries or something or another.

The merits or lack-thereof concerning this particular plot are not the subject of this post. The lawsuit surrounding it instead is.

You see, it turns out that the book written by Dan Brown is heavily based on work from other authors, particularly a book called "The Holy Blood and the Holy Grail". Two of the authors of that book, Michael Baigent and Richard Leigh are now arguing in court that Dan Brown basically plagiarised their research (but put it in a fictional setting). The case as a result asks very interesting questions as to if it's acceptable for an author to use academic research to write a fictional story around. Central to the claim of the case is if the original work (The Holy Blood and the Holy Grail) is protected by copyright and if this is the case, if Dan Brown unfairly copied their ideas without permission.

Now, I'm not very up with the particular law surrounding this case and I wouldn't know a lot about how the Judge may rule. What I do know, is that I don't like the implications that a result in favor of the plantiffs (Michael Baigent and Richard Leigh) could mean. For a start, a large number of the authors and books you've probably read found their inspiration from other authors or the real world. There is a fine line between directly copying someones ideas without permission entirely and merely using it as inspiration for your own novel. Consider as well that say someone writes a book on a potential biological terror attack based on literature published from the likes of PNAS. One paper (that is somewhat controversial) from that journal modelled the effects of a botulism attack on the United States through milk supplies. What if an author took that basic research as the inspiration for their own work of fiction? Could the original authors of the paper sue them?

What about just in general from other authors, who frequently borrow or take on new twists from other authors work. Dungeons and Dragons, for example was in large part inspired by the fantasy writings of the likes of J.R.R. Tolkien. Similarly, a lot of fantasy and horror borrow of great former authors, such as the Cthulhu mythos that has lived on in the minds of other writers well after the death of H.P. Lovecraft who came up with it. Even modern authors borrow extensively from one another, so if this lawsuit succeeds who is going to be able to tell what is a 'public' idea they can use and what isn't? There are numerous sticky situations that will arise should the court set a precedent (that I know of) in favour of the plantiffs.

Although I don't care for Dan Brown in particular as a writer, I do no think that he is particularly guilty of doing anything wrong or worse, just outright plagiarism. If anything all he's guilty of doing is what pretty much every other author in history has done, provide a new take or twist on a story that someone else has told.

Eggs! Eggs! Eggs! The sequel

2006-03-01T17:07:00.000+13:00

Well looks like the things I was wanting to do didn't get done in a hurry, mostly due to a quick trip down south so that I could visit some of my friends I haven't seen in a while. Although I intended to do some blogging, my lack of a computer combined with no time to read around what I was going to write prevented any blogging. Upon my return in any event, I was informed of a new nursery web that had formed in the backyard made by a spider I had photographed previously, Dolomedes minor.

What I found was probably the biggest nursery spider I have ever encountered. She was gigantic and I immediately took the spider (and its equally oversided nursery) in for a quick photoshoot.

Click here for the full sized image.

As can be seen from this photo, the spider is quite a bit bigger than the last one and isn't clutching an egg sack. This is because she has already spun her nursery, which is a structure that looks something like this:

Click here for the full sized image.

So if you've ever wandered around the countryside in New Zealand and wondered what all those little white balls on plants were, they are most likely the spiderling nurseries these animals make.

Finally, another good photo that shows the spider in good detail.

Click here for the full sized image.

Easily the biggest nursery web spider I've ever found and as much of NZ fauna seems to be, was quite happy for a photoshoot so long as the nursery wasn't poked much.

In any event, I have done some stuff for blogging soon on plague and I also intend to write more about probiotics in response to some questions I recieved.

This is a fairly good summary

2006-02-23T22:07:00.000+13:00

I think Penny Arcade have a good summary of how a lot of Japanese RPG games plots dialogue tends to go: painfully. If you've never experienced the kind of dialogue you often get in these games, you should think of a really bad poet who thinks he's amazingly profound that repeats every concept every 2 lines. Because if you don't get it the first time, you might get it after they beat you over the head with it after the millionth time.

Meeting dares

2006-02-23T21:35:00.000+13:00

Looks like Tara has decided to take me up on my dare. It's actually not a bad picture, especially considering whoever took it managed to get a small girl to smile who was suffering from chicken pox.

Speaking of free speech

2006-02-22T18:24:00.000+13:00

In a similar vein to the recent row over the caricatures of the prophet Mohammed, there is an especially offensive episode of South Park called 'Bloody Mary' that is very offensive to Catholics. In the episode, to be shown in New Zealand three months early due to all the controversy surrounding it, there is a statue of the virgin Mary that bleeds from its vagina and then sprays blood all over the Pope. As you can imagine, Catholics all around the country are incredibly offended and some are even threatening to boycott channel 3 and TV4 (who are owned by Canwest).

Personally, it's once again plain ridiculous to get so upset over this sort of thing because it just makes people more curious. If nobody said anything about it, I doubt anyone would realise its existence except for the people that watch South Park, which is pretty much renowned for being offensive to just about everybody. Now, instead of a boycott they've just managed to stir up much more interest in the the cartoon. In fact, I have to concede that even I am more than a little curious as to what the show contains and may even watch it, when otherwise I wouldn't have bothered. With various calls to ban the cartoon as well, it once again raises the issue of where free speech should and should not be protected. In this case, although I'm 100% certain the cartoon is just a load of idiotic nonsense, I again support the TV company for sticking to their guns and displaying the cartoon anyway.

No matter how 'offended' something makes you, there is always a solution that actually works and that is even built in to every TV remote. It's called an "off" switch. Some people need to get more familiar with it.

David Irving is jailed for Holocaust Denial

2006-02-21T19:13:00.000+13:00

Well, David Irving played with fire when he went back to Austria due to his controversial views on the holocaust and now he's been made the martyr he has aiming to be. An Austrian court has decided to imprison him for a whopping 3 years, which does in fact seem to have given him a rather nasty surprise if his reaction is anything to go by. He initially pleaded guilty, but after the decision shocked him he is now apparently going to appeal the decision.

You know, I find the very ideals surrounding holocaust denial to be generally reprehensible, especially with how much historical fact is frequently abused to various degrees. In this case however, I think the Austrian court has done the wrong thing. Simply because D. Irving has a particularly controversial and somewhat misguided view of history, however much it concerns the suffering of some six million people, he should not have been jailed for his views. Jailing him will simply make him out to be a martyr and goes against the sort of principles that 'democracy' supposedly stands for.

I'm beginning to wonder more and more if people think that free speech should go only as far as those you agree with. If that is what free speech is supposed to be, then it sounds somewhat more like a dictatorship of the majority rather than a true democracy. Just because someones views are repugnant/inflammatory doesn't automatically mean they should be jailed for it.

Also, Ocellated has some further comments that I thought were dead on.

More blogging to come

2006-02-21T18:58:00.000+13:00

I've been a little AWOL as I've been catching up on a lot of reading and finishing some of the PS2 games that I've managed to accumulate. Hopefully be back to a normal schedule on thursday, where I have some things I've been working on to post.

Back from galavanting

2006-02-17T11:55:00.000+13:00

One of the best things about living in New Zealand is how close we are to a lot of forest and the ocean. Wandering a mere 5 minutes walk from where I lived, I was able to get up close and personal with quite a bit of nature. Although I failed to take a camera on this occasion, the trip was quite productive including finding some species of sheetweb spider that I had never seen before. Perhaps the most interesting encounter was climbing over a rock only to be two feet away from a very large seal, which gave one of us at least quite a considerable fright.

In any event, while I have been resting off this delightful trip, it turns out that the 28th skeptics circle has been posed over at Unused and Probably Unusable. So if you've been itching to read some skeptical writing, I would certainly head on over there and indulge.

Gone galavanting

2006-02-16T07:25:00.000+13:00

Gone hiking for today. More substantial blogging soon, in the meantime I've posted some of the more interesting posts I've made previously on the left.

Also, make sure you look at this comic currently doing the rounds at the moment. I have my Klingon costume ironed and ready for the coming reckoning, do you?

Aetiology and chicken pox parties

2006-02-15T20:05:00.000+13:00

Over at Aetiology, Dr. Smith takes us into the wierd and wonderful world of holding chicken pox parties.

Like I said, I should have known this was probably still going on. I remember when I had chicken pox in first grade, and my cousin brought her three kids (who were my age--tangled family tree and long story) over to our house with the purpose of infecting them. It worked, and within a few days there were 6 of us spotted kids. But--this was in 1982, long before the introduction of the varicella vaccine here in the United States. Chickenpox "parties" were deemed a better alternative to potentially encountering the disease as an adult--when the frequency of serious complications is higher.

I find it more than morbidly fascinating that anyone would deliberately hold 'parties' to spread an infectious disease. I can almost picture what the event must look like, with children performing the chicken dance while spitting in each-others mouths. Sadly, I got my various childhood diseases without much celebration let alone having my friends over to collect on my misery as well. That the practice apparently continues even today is a bit curious as well, although I suspect it might have something to do with parents misinterpreting the hygiene hypothesis. A vaccine is perfectly acceptable immune stimulation as a real 'virulent' organism is. This is because the same processes that make a vaccine work are the same that allow your immune system to destroy an invader to begin with.

This was quite the revelation as well:

So far, I've escaped with little more than a few scars on my forehead (I admit, I was a scratcher) and the ugliest childhood picture *ever*, since I decided to do some surgery on my bangs while I was pocked--resulting in about quarter-inch long, very crooked bangs. Did I mention I also had giant pink glasses and a few missing teeth at the time as well?

Indeed, quite the image and I double/triple/quadruple dare Dr. Smith to post said picture. :D

Justice department does it again

2006-02-15T18:58:00.000+13:00

I always thought the whole point of running rehabilitation programmes was so that offenders were less likely to reoffend. I guess that might not exactly be the case:

A parliamentary select committee hearing has been told that inmates are more likely to reoffend if they have been involved in one rehabilitation programme.

Looks like someone needs to re-think how these are run.

Ohio dumps 'critical analysis' plan

2006-02-15T15:57:00.000+13:00

One of the more recent 'battlegrounds' in the US concerning the teaching of good science has now been resolved with science carrying the day. The Ohio school board has voted 11-4 to drop the 'critical analysis' plan, which is essentially a bunch of refuted intelligent design arguments against evolution. With some luck that state can go back so some degree of sanity.

Evolution vs. Design: Man made biological weapons part I

2006-02-14T17:48:00.000+13:00

Biological agents that cause disease have a long and terrible history in human warfare. During the crusades, a common tactic to break a seige was to toss the rotten corpses of animals into the starving populace to spread disease. Much of the army that Napoleon marched into Russia was struck down by typhus, which ground his offensive to a halt and caused him to retreat. Even more recently in World War 2, the Japanese were very interested in the use of biological and chemical agents. Projects conducted by the Japanese included dropping plague infected fleas onto Chinese cities and experiments with anthrax. Anthrax was considered as a last resort biological weapon by the British military, with an island off the coast of Scotland being rendered completely uninhabitable by various tests.

Today, unlike in the previous examples the threat of biological weapons is much greater, because technology has advanced to the point where we can simply design our own pathogens to be more effective weapons. Indeed, there has been a lot of concern over the potentials of newly altered biological weapons as potential WMDs (Weapons of Mass Destruction). The candidate list for organisms is also pretty long including such former greasts as smallpox as well as anthrax, plague, bacterial toxins like botulism, ebola and even influenza. As a result, being able to determine the hallmarks that would give away a potentially human designed organism could be essential in stopping it.

For example, an engineered strain of a virus could have entirely different functions compared to the normal wild-type. An organism that typically doesn't spread very easily person to person, could be engineered so that it is able to be aerosolised and spread through the air. This would greatly increase its ability to cause general havok by more rapidly spreading throughout the target population. The question that arises is how to determine if an organism is designed by human techniques, or if the pathogen is just another example of a newly emerged pathogen that has arisen by evolutionary processes.

This distinction is in fact fairly difficult to make in reality. Virulent microorganisms are highly capable of switching their genetic material around between one another by a process called Horizontal Gene Transfer (HGT). HGT involved numerous different mechanisms, but microorganisms are capable of simply grabbing DNA that is in the environment (say from other dead cells releasing it), circularised stretches of DNA often containing unique genes called plasmids, viruses can transfer genes from one organism to another (including between entirely different kingdoms) and even mobile stretches of DNA called transposons. A number of pathogens today, like several of the dreaded 'superbugs' that are found in hospitals such as MRSA (Methicillin Resistant Staphylococcus aureus) are the direct result of past HGT events.

So what sort of features would give away a pathogen that was designed by humans? Well this determination can only be made not by some irrelevant 'probability' calculation but by understanding the methods, motives and limitations that humans have when engineering new organisms.

Painting a scenario of a potential biological attack:

In this hypothetical scenario, patients manifesting signs of a rapid respiratory disease have been found in New York city with a nasty cough, quickly followed by a rapid scepticemia after a few days and almost inevitable death. Doctors observe to their horror that patients fail to respond to all front line antibiotics and the CDC (Centers for Disease Control) are rapidly called in to investigate. Their investigations simply confirm what health authorities already suspect, the disease in question is pneumonic plague caused by one of mankinds oldest enemies, Yersinia pestis. However, investigators are particularly worried by the complete unresponsiveness to the key antibiotics used to typically treat plague streptomycin, chloramphenicol and tetracycline. Most clinical strains of Y. pestis are nearly universally susceptible to antibiotics it raises a disturbing prospect: Is this a newly emerged and potentially epidemic quality kind of plague?

Even more agitating to investigators is another possibility that this is not a natural organism, but is instead the product of tampering by individuals attempting to utilise it as a weapon. Investigators have good reason to think this is a possibility, as in 2001 letters containing anthrax spores were distributed to several senators. Although only 5 people were killed and 13 infected, it was a pertinent reminder of the willingness and ability for potential terrorist organisations to employ biological agents. The source of these attacks is still unknown even to the present day and the perpetrator could still be at large. That investigators could be looking at a biological weapon with more on the way becomes a very real prospect.

The first step in combating the new strain after appropriate quarantine measures are taken, is to sequence the genome of Y. pestis strains collected from infected patients, as well as any extrachromosomal elements such as plasmids. Once done, investigators begin their analysis and their attention is immediately drawn to a large plasmid not normally associated with strains of plague found in America. Sequencing reveals the presence of a region of the plasmid with almost 4 different antibiotic resistance genes. Resistance plasmids are not particularly new in terms of Y. pestis, as highly multidrug resistant strains have already been found existing naturally in nature. Investigators analysing the strain immediately recognise something unusual, each of the genes is linked together by sequences exactly matching those recognised by restriction enzymes.

Restriction enzymes are the workhorses of clinical microbiology, biotechnology and genetics. Restriction enzymes are produced by bacteria to defend themselves from attacks from viruses called bacteriophages. By recognising specific repetitive sequences in the attacking viruses DNA, they prevent an infection by essentially chopping the viral genome into bits. One of the unusual properties of some of these enzymes is that when they 'cut' the target DNA they leave overhanging stretches of DNA. These overhangs can then be used to string together different genes that have been cut by the same restriction enzyme. Potentially as well, these enzymes could be used to string together antibiotic resistance genes and virulence factors needed to make a new biological weapon.

The investigators soon discover that this region of the plasmid containing the antibiotic genes are indeed linked by restriction enzymes, specifically using two that are very commonly available, EcoRI and BamHI. While this leads weight to the conclusion that the organism could have been designed by humans, it does not immediately indicate that this is the case. Genes for resistance have been used in biotechnology for numerous years, including in applications on plants and other transgenics including modified bacteria. In many cases, the antibiotic resistance genes are used as markers to select for bacteria that support the plasmid for replication purposes. After insertion into a plant or similar, the gene is useless for the plant but is still kept as a passenger into the environment.

As a result, it is theoretically possible that the genes on this plasmid are possibly derived from antibiotic markers used in standard genetic engineering. This could potentially explain the structure of this antibiotic group as a simple leftover from their previous application. Ruling this hypothesis out will require a deeper investigation into what antibiotic markers are commonly used in genetic engineering and particularly the question "how could Y pestis have aquired these genes?". Further, numerous important clues to the origin of this organism await to be found on the chromosome of this new strain and the plasmid it carries.

References:

Anisimov A.P., L.E. Lindler and G.B. Pier (2004). Intraspecific diversity of Yersinia pestis. Clinical microbiology reviews, 434-464

Galimand M., A. Guiyoule, G. Gerbaud, B. Rasoamanana, S. Chanteau, E. Carniel and P. Courvalin (1997). Multidrug resistance in Yersinia pestis mediated by a transferable plasmid. The New England Journal of Medicine, 337:677-680.

Roberts R.J. (2005). How restriction enzymes became the workhorses of molecular biology. PNAS, 102:5905-5908.

Salyers A.A. and D.D. Whitt (2002). Bacterial Pathogenesis: A molecular approach 2nd edition. ASM press, Chapter 13:203-215.

Xtra broadband: Ever so slighly less backwards

2006-02-13T19:22:00.000+13:00

As many in New Zealand are already aware, we're frustratingly behind when it comes to the wonders of broadband internet. In general it is very expensive, very slow and has been capped quite harshly. Telecom has of late, decided to generously make us slightly less backwards by upgrading the speeds so we can feel slightly better for paying a hideous price for not much. As it turns out, the new telecom 'upgrade' may not actually be all that worth-while after all. Although probably not as positive a sign as some would believe, it is a start at the very least.

Evolution of the Immune system: MHC part III

2006-02-11T20:00:00.000+13:00

In the last of this three part series (part I and part II), I'm going to be moving away from the distant past of the origins of this molecule and instead focusing on the current evolutionary factors that influence the high diversity of the MHC among humans. As mentioned in the first part of this series, the MHC is best characterised by its extreme diversity. The most common HMC types in humans, HLA-A (Or Human Leukocyte Antigen), HLA-B and HLA-DRB1 have 243, 499 and 321 different alleles respectively with more probably to find. As more genes in the MHC region are sequenced and compared from human populations world-wide, it turns out this is a typical characteristic of MHC loci. Although it would at first seem to be a relatively intuitive answer as to why the MHC has such a wide array of expression.

In its role in immunity, the ability to bind different peptides and recognise a wide range of different immunological insults would encourage diversity. In reality, the answer is not so obvious and the actual mechanisms that maintain MHC diversity are not properly understood. For example, although MHC regions between vertebrates have a similar structure being clustered together in single gene complexes, as comparisons between the gene regions that comprise the class I and class II MHCs in mammals and chickens reveal key differences. Mammalian MHCs have a lot more diversification among their loci while in chickens the B-complex codes for only two class I and two class II genes, of which only one of these genes is actually polymorphic.

Even with the different structures in other vertebrates, there is emerging support that MHC diversity is encouraged by an arms race against infectious parasites. Malaria in particular seems to be driving the diversification of different HLA class I and II haplotypes. Going back to chickens, there is strong evidence to associate the presence of certain class II MHC alleles with susceptibility to Mareks disease induced by a herpes virus, which causes a potentially lethal T-cell lymphoma. Similarly, studies conducted on mice indicate that mouse MHC haplotypes (H2 in this case) play important roles in determination of susceptibility to infection with Mycobacterium tuberculosis.

With this link in mind it leaves the question as to the mechanisms that caused the divergence in the first place. As Piertney and Oliver detail (see Piertney S.B. and M.K. Oliver (2006). The evolutionary ecology of the major histocompatibility complex. Nature, 96:7-21 for more information on this topic) there are two main hypotheses that propose to explain this high diversification. The first is negative frequency-dependant selection, where new or rare alleles may be selected when organisms are exposed to a novel pathogen. Essentially, picture a group of animals that have just been exposed to a debilitating new organism such as ebola. Some isolated members of the population may have a MHC allele that makes them more resistant than others in the population. As the pathogen spreads, those with the resistant MHC allele are able to breed more successfully than those without it and the frequency of their respective MHC increases.

Over time however, the original epidemic starts to wane due to the increased amount of resistance the original pathogen begins to hit a brick wall. As it can no longer spread as easily, due to the build of immunity combined with resistance, selection would favour pathogens that are not recognised by this allele or alternatively the emergence of a new pathogen. Corresponding to the original situation, if other members had a slightly different MHC allele that rendered them resistant to this new pathogen the frequency of their MHC type will increase. After repeated rounds of assaults from new microbial challenges and this rise and fall of different alleles being favoured, inevitably leads to the distribution of multiple MHC types.

Alternatively, another explanation called the overdominance hypothesis proposes that MHC diversity arises from heterozygosity at the MHC loci. Essentially, because humans have two different copies at their MHC alleles that can produce a wider array of different peptide chains. This allows for the recognition of a larger number of potential microbial structures than an individual who was homozygous (two of the same MHC allele). As a result, individuals with the least overlap between the peptides they produce would be favoured and be able to respond to a wider array of different pathogens.

It is worth noting that these two processes of negative frequency-dependant selection and overdominance are unlikely to be mutually exclusive processes (teach the controversy!). Determining how these processes affected selection in the past is also very difficult, as natural populations tend to be of relatively small sizes and may be challenged by several pathogens at once. Of course, selection and maintenance of new MHC alleles may not simply be just from selection from parasitic relationships. Evidence also suggests that sexual selection may be equally as important in maintaining diversity in both humans and in animals.

Recalling that in part I, a proposed original function for a proto-MHC like molecule was as a mechanism to ensure that organisms maintained a more diverse gene pool. It turns out that MHC in current vertebrates may play a role in sexual selection. This was first observed in studies with mice, where females preferentially mated with males who were MHC-dissimilar to themselves and vice-versa. How mice (and possibly other animals including humans) determine how similar a potential mates MHC alleles are is probably complicated, but is theorised to be heavily dependant upon olfactory (smell) senses. This is because the makeup of MHC genes can affect the concentration of violatile acids that make produce odour in sweat and urine.

One clear example where MHC molecules were found to profoundly affect mate choice appeared in the Proceedings of the National Academy of Sciences (PNAS) last year. The paper by Milinsky et al (referenced below) investigated if the peptides produced by MHC of the three spined sticklebacks (Gasterosteus aculeatus) could interact with the animals olfactory senses. Their results give strong evidence that MHC molecules can influence sexual selection, as fish preferentially moved into water with peptides produced from different MHC and not into water demonstrating similar peptides that their own MHC would produce.

Conclusion

Over this three part series I have detailed only a very narrow range of the total research that has gone into the evolution of this critical system. From beginnings as a simple mechanism to prevent asexually producing organisms from reducing the diversity of their gene pools to a critical component in immunity, the modern MHC is an example of a complex system built from simpler precursors over evolutionary time. Clearly important in this system was the original whole genome duplications that gave rise to modern jawed vertebrates some 766 and 528 million years ago. These allowed for the duplicated genes to be co-opted and diversified to form the required systems for the modern MHC function. Additionally, selection pressures from parasites and even sexual selection continue to ensure that MHC genes remain highly diverse.

In all, there are still a great deal of unanswered questions surrounding both the origins of this system and how such large gene diversity was derived. Unfortunately, there may never be definitive answers to these questions, as many of the organisms that developed the first immunological novelties have long since gone extinct or modified their original systems. It is important however, to realise that scientists working on this field have provided numerous important insights into the mechanisms of evolution and how systems such as the immune system arose. Even more importantly, that researchers continue to publish giving us even greater insight and furthering our understanding, even if it may never be truly complete.

References:

Messaoudi I., J.A. Guevara Patino, R. Dyall, J. LeMaoult and J. Nikolich-Zugich (2002). Direct link between mhc polymorphism, T-cell avidity and diversity in immune defence. Science, 298:1797-1800.

Milinski M., Siân Griffiths, K.M. Wegner, T.B.H. Reusch, A. Haas-Assenbaum, and T. Boehm (2005). Mate choice decisions of stickleback females predictably modified by MHC peptide ligands. PNAS, 102:4414-4418.

Pichugin A.V., S.N. Petrovskaya and A.S. Apt (2006). H2 complex controls CD4/CD8 ratio, recurrent responsiveness to repeated stimulations, and resistance to activationinduced apoptosis during T cell response to mycobacterial antigens. The society for leukocyte biology, 79:1-8.

Piertney S.B. and M.K. Oliver (2006). The evolutionary ecology of the major histocompatibility complex. Nature, 96:7-21.

Hill A.V. (1999). The immunogenetics of resistance to malaria. Proceedings of the Association of American Physicians, 111:272-277.

Immunoblogging

I exist and new website!

Insert ominous music here

Oh Verizon

Oh Hwang

What a mouthful!

Treadmills and Shrimps!

Nutrigenetics sting

Tired of the same ole whack a mole game

Diet Coke + Mentos = Awesome

What is going on?

43rd Skeptics Circle

42nd Skeptics Circle

A very confused skeptics circle

Carnival of the wee animacules

Where am I?

Still alive

Oh blog memes

iNoodle

One judge with a sense of humour

The 33rd skeptics circle

Site redesign

Oh dear

Dragon Quest: Journey of the Cursed King

Blog direction

Sobering up Intelligent Design

A poo-filled skeptics circle 32

Britains Boy Soldiers

Seguin Gazette-Enterprise articles have been updated!

Jonathan Witt goes to the Quote Mine

Two responses to ID propaganda

Ren and Stimpy creators blog

The role of cattle movements in the bovine TB epidemic

Mare reproductive loss syndrome and caterpillars

Dr. Pianka speech transcript available

I have to link this guy

Ohhhh

Animacules volume V posted

New Zealand bird flu laws

Fast-Food Ice has some nasty stuff in it!

Hooray for science!

Dr. Pianka and Ebola

April Fools Day

31st meeting of the skeptics circle

What evidence suggests badgers infect cattle with M. bovis?

V for Vendetta

PNAS cover this week

How evil am I?

Chick tract on chemicals

Awesome giant centipede video

Plush Kiwa Hirsuta

How much does my blog own me?

Oh the Onion

What makes Mycobacterium bovis such a problem?

Britannica upset with Nature

When public health, farm economics and conservation collide

Carnival of the wee animacules

Canwest apologises

Bloody trackback spam...

Bioessays journal editorial and reflections

Blogging this week

Excellent new blog

Skeptics cirlce posted

Amazing quote

Gay genes and sperm donors

New Zealand HIV rates rise 17%

Insanity of War.

Awesome menu!

Amazing game of cricket

Now this is televangelism

Awesome rant

Zardoz!

Revisting probiotics

Carnival of the wee animacules is up

Snuppy the puppy is..... *drumroll*

Farm animal cannibalism strikes again?

Can't argue with them? Burn them!

Theistic evolution and creationism

That "court stunt" again

The McPassion

Snuppy the puppy is..... drumroll