The most boring, yet captivating, experiment in the world.

An experiment has been running in the School of Physics at the University of Queensland since 1927. Set up by Prof Thomas Parnell, it was to demonstrate the strange properties of pitch – a substance that seems solid at room temperature, but is actually an outrageously viscous liquid.

University of Qld pitch drop experiment, via Wikipedia via UQ

It’s very simple: Parnell heated some pitch, poured it into a funnel, let it set for three years, then cut the bottom off the funnel to let the room-temperature pitch drip. The first drop fell in 1938, and, fast-forward to 2012, we are now waiting for the ninth drop to fall. No-one has actually witnessed the drops falling – it seems that the pitch likes to work under cover of darkness, or perhaps during lunch breaks. Considering we now live in the digital age, UQ has set up a live stream of the experiment, which lives in a case in the foyer of the physics building, so you can watch for yourself. Hopefully this will mean that someone will catch the moment when the drop falls.

View the stream on the UQ’s pitch drop experiment page.

Monday Awesome: in awe of the Cav.


Bradley Wiggins won the Tour de France overnight, after dominating the race for weeks 2 and 3. While that is an awesome feat (especially as he’s the first Brit to do so), I would like to draw your attention to Mark Cavendish instead. Have a look at the video below, and admire the acceleration of the Cav in his final sprint to the finish line. (go to the link – I’m not having luck with the embed). At 5:50 Wiggins is at the head of the lead out train. At 6:30, Boasson Hagen leads Cavendish out and then he blasts out of the corner. Brilliant.

Raging against abominable science writing.

*This was edited on 27 July.

I love science. I love parasites and parasitology. I sometimes love cycling (I have a love/hate relationship with the bike) and I do love watching the Tour de France coverage, but I hate bad science writing. Journalists who do not check their facts about sciency-related things really grind my gears (ooh, a bad cycling pun!).

I found an article on the cycling website Velonews, regarding Chris Froome, of Team Sky. If I’d been drinking a coffee when reading this article, I’d have ended up spitting it all over my computer. Froome reportedly has schistosomiasis, also called bilharzia in the UK and some other places. That’s not the shocking bit though. There were some glaring errors in biology and epidemiology that I will explain:

Let’s get one thing clear. The pathogen that causes schistosomiasis is a trematode (several species of genus Schistosoma), and not a virus as mentioned three(!) times in the article. A trematode may also be called a fluke, and it is, most definitely, a metazoan parasite. While it does have a complicated life cycle (see below), including very small, possibly microscopic, larval stages in snails, the snails themselves are not microscopic. While we’re on the topic – the larvae do not “transform” into worms. There are no Optimus Prime schistosomes.

Life cycle of Schistosoma spp. (from CDC)

Also, the disease is not “obscure”, as mentioned in the piece. I think that the roughly 290 million people infected globally with schistosomiasis might have something to say about the disease being referred to as ‘obscure’ (ref: Mathers et al. 2007 PLoS NTD doi:10.1371/journal.pntd.0000114). Schistosomiasis is a serious disease. While it doesn’t kill as many people as malaria, as a chronic infection, it causes long-term health effects in sufferers including anaemia, malnutrition, and can affect organs such as the spleen, liver and bladder (depending on the species infecting). It is a neglected tropical disease, exacerbated by poverty in many cases, and should not be trivialised. Chris Froome can afford treatment for the disease, but millions of others are not so lucky to be in the same financial position.

It’s probable that only parasitologists have gotten upset about this (there are several incredulous tweets about it on my twitter feed). Parasitologists tend to be quite sensitive to these kinds of errors and levels of ignorance. It’s par for the course a lot of the time, when you work on something as disgusting as a parasite (yes, someone once said that to me). But discussing parasites is no excuse for sloppy writing. This is yet another example of journalists not checking their facts before writing. It’s not difficult. Even a quick look at Wikipedia would have been helpful in this instance.

Post-script: After writing this, I went back to the article to check it again. All references to ‘virus’ have been edited out. Hooray!

Tuesday weirdness: mattress dominoes.

I forgot what day it was yesterday. I’m sorry. However, on the few occasions where I’ve forgotten the Monday Awesome, I’ve provided you with something on Tuesday. Today’s is a bit weird, but let’s face it, Tuesdays are a bit strange anyway so it’s probably a good fit.

The world record for mattress dominoes has been broken in Shanghai, with 1001 people holding onto mattresses participating. I can’t embed the video, so you’ll have to go to the link (here) to watch it at the ABC News site. Here’s a screenshot of it:

screenshot of video of mattress dominoes

Several questions arise:

  • why does there have to be a person on each mattress?
  • was the previous record just beaten (at 1000 people/mattresses), or did they go all-out and smash it?
  • why mattresses…..?

It does look like fun though.

Devil facial tumour disease (or: Sometimes not everything comes back to parasites)

Last week, I had the pleasure of meeting some Tasmanian devils (Sarcophilus harrisii). They are the largest (extant) carnivorous marsupial, and are quite lovely, with broad, almost dog-like faces, and an odd loping gait that was rather endearing. The devils I met were housed at a wildlife park near Launceston and they are part of a carefully managed breeding program, as an insurance population, for the species. Devils in the wild are currently under siege from a nasty disease, devil facial tumour disease (DFTD), which emerged in northeastern Tasmania in the mid 1990s. The disease was determined to be a kind of cancer, transmitted via biting (McCallum et al. 2007, Lachish et al. 2011). DFTD causes large tumours on the faces and necks of devils, and are very nasty to look at so I’m not going to post any pictures. Devils usually die within six months or so of the development of a cancerous lesion, either by starvation or by secondary infections or metastasis (Deakin et al. 2012). The emergence of DFTD has altered population age structures and caused rapid declines in populations of devils across most of Tasmania (Lachish et al. 2011).

Tassie devils (taken at Trowunna Wildlife Park).

Generally, cancers are not transmissible between hosts/victims, although a notable exception to this rule is canine transmissible venereal tumour (see Belov 2012 for example) which is a sexually-transmitted sarcoma in dogs, so the revelation that DFTD was transmitted between devils prompted a bit of a discussion about whether this new disease was perhaps parasitic. I don’t have a reference for that statement – I remember Hamish McCallum (Griffith University) presenting something about it at a conference a few years back, but could not find any references on this idea. It came up again at the conference I was at last week and was discussed by Greg Woods (immunologist, University of Tasmania). The discussion was subsequently reported in the Launceston Examiner newspaper (July 3) as Scientists have said strong evidence was emerging that the catastrophic Tasmanian devil facial tumour disease should be regarded as a parasite.”, which got me all riled up as it was not true at all. Perhaps they shouldn’t get the work experience kids to write articles for them, but bad journalism and poor communication of science is a whole other argument for another day. Let’s get back to the devils.

So what is it then?

DFTD, as mentioned above, is a transmissible cancer. It is thought that the cancer, which is highly metatstatic, originated from one female devil probably in the early 1990s (Deakin et al. 2012, Murchison et al. 2012). Devils are a fighty bunch. Many interactions, including feeding and reproducing, involve biting each other. Devils usually end up feeding communally on carcasses and biting is used as a communication mechanism in order for everyone to get in and have a snack. Here (below) is a photo I took of some captive devils feeding, and while I watched, a couple more came over for a snack and a bit of fighting was observed as the newcomers jostled for position. The cancer itself has its origins in mutant Schwann cells (which are associated with nerve fibres) and was passed from animal to animal, rather than being a cancer that spontaneously arose independently in animals (Belov 2012). We know this because many cancer samples have been examined, and they have been found to all be clones of each other and their genetic composition is remarkably stable (Deakin et al. 2012). Spontaneously arising cancers would display more genetic heterogeneity in the mutations observed, but this is not seen in DFTD cancer cell lines.

Devils feeding (taken at Trowunna Wildlife Park).

The mechanism by which the cancer arose is unknown, but is probably just a (really bad) random mutation. The reason why it is so dangerous to devils is that it metastasizes quickly (in about 65% of cases), and, somehow, evades the devil’s immune system (Belov 2012). Therefore, the devil does not fight the infection. Tasmanian devils have very low MHC diversity (Major HistoCompatability) (Belov 2012). This is a key aspect of mammalian immune system function, as MHC works towards recognizing ‘self’ from ‘non-self’ in the context of fighting infectious pathogens. Low genetic diversity of MHC would mean that devils may be increasingly susceptible to infection by some pathogens. The result of all this is that devils pass a new kind of cancer to each other, which is highly virulent, and in combination with the devils’ bitey behaviour and slightly wonky immune response that does not recognise the cells as pathogens, kills many devils. Rapid deaths cause population declines, and the threat of extinction (McCallum et al. 2007).

But does that make DFTD a parasite?

In a word, no. Just because this cancer behaves in a different way to which we are accustomed, does not make it parasitic. As we know, canine transmissible venereal cancer is also transmitted between hosts/victims, so DFTD is perhaps not as unusual as first thought. The virulence of DFTD is largely due to its ability to metastasise quickly (killing the host fast), aided by the devil immune system lacking the ability to recognise these cells as pathogens. Although parasites can occasionally cause nasty pathology and sometimes kill their host, it is not in their best interests to do so. DFTD, on the other hand, seems to have no such qualms and if left unchecked, would likely take down the entire species in the wild. While cancer tumours grow in such a way that they are able to acquire nutrients (through angiogenesis in cancerous cells, which is quite a nifty process in itself) from the host’s body, that is a feature of all cancer tumours – in humans and animals. Does that mean that all cancers are therefore parasitic? No. Parasites have a life cycle, for a start, and cancer cells divide by binary fission like other cells. These processes are not the same as each other. Further, parasites are separate, distinct, organisms to their hosts, whereas DFTD has more or less the same DNA as its devil hosts. DFTD cancer cells can be identified as devil DNA.

Final word

DFTD is a transmissible, highly virulent cancer affecting Tasmanian devils. The transmission method of the cancer means that young devils are affected and this causes populations to decline because many devils do not live long enough to reproduce. Thankfully, there is a real push for research into understanding the cancer in order to combat it. Whether that’s a vaccine or something different, I don’t know. It’s too soon to tell. But hopefully a solution will be found before the devils’ populations get to the point of no return.


Belov 2012 Bioessays 34: 285–292 DOI 10.1002/bies.201100161

Deakin 2012 PLoS Genetics 8(2): e1002483. doi:10.1371/journal.pgen.1002483

Lachish 2011 Heredity 106, 172–182 doi:10.1038/hdy.2010.17

McCallum 2007 EcoHealth 4, 318–325, DOI: 10.1007/s10393-007-0118-0

Murchison 2012 Cell 148, 780–791 DOI 10.1016/j.cell.2011.11.065

Blog to check out: Parasite of the Day

Screenshot of Parasite of the Day blog

I got to meet Tommy Leung (University of New England, Australia), author of the blog Parasite of the Day, while a-conferencin’ last week in Launceston. If you aren’t satisfied with the parasitological offerings here at IncreasingDisorder (and let’s face it, I do provide a fairly eclectic mix of subject matter), go check out Parasite of the Day. They even have some recent posts on Acanthocephala.