Oh blog memes

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

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

One judge with a sense of humour

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

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

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

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

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

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

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

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

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!

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

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

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

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

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

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

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

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

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

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

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!

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!

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

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

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.