By: Stavana Strutz, PhD Candidate, Parmesan Lab, University of Texas at Austin

Science Friday has a short article and video about how making egg nog far in advance of consumption using raw eggs and booze actually does kill salmonella. Just remember that added brandy or dark rum to egg nog you've made that day won't save you.

I've also wondered whether SteriPENs can kill the bacteria in more viscous and not quite clear liquids as well. So could you just swirl your egg with a steriPEN? Maybe these Rockefeller fellows could try that out as well.
 
 
By: Stavana Strutz, PhD Candidate, Parmesan Lab, University of Texas at Austin 

So back in February I wrote a Parasaturdays post about dengue in the United States. You should have a gander at that page if you're totally unfamiliar with the pathogen. The most recent news besides the new FDA approved test, is evidence of dengue in Houston during the last decade.
Picture
Image via WHO, Engorged Aedes aegypti
Why would anyone even think to test for dengue in Houston when the nearest other United States dengue occurrence is more than 400km away along the Texas/Mexico border? At a recent Diseases in Nature conference in San Antonio and Neglected Tropical Diseases conference in Houston I heard Dr. Kristy Murray from the Baylor College of Medicine speak about how the perfect ecological scenario is brewing in Houston for dengue transmission. Houston has mild winters contributing to the year-round survival of dengue vector mosquito species such as Aedes aegypti and A. albopictus. Additionally, many of Houston's residents travel to dengue endemic areas. 

If a handful of those individuals came back with dengue virus in their blood, they could pass it on to the mosquitoes in Houston. Most dengue infected individuals will never even experience symptoms while an unlucky 5% of the infected will experience a severe manifestation that can lead to death. The gross symptoms of dengue are high fever, muscle and joint pain, measles-like rash, mucous membrane bleeding, fatigue and sometimes shock or internal hemorrhaging. This is why I always say if you have flu-like symptoms, a rash, and a recent arthropod bite, you should head to your doctor ASAP.

So back to the point: Murray conducted a retrospective serology study of Houston patients between 2003-05 who had symptoms consistent with arboviral disease. Out of 3768 CSF and serum specimens, 47 had anti-DENV IgM antibody! Eighteen of those patients met the case definition for dengue fever. The other interesting but also sad piece of information from her talk was that two of the positive individuals died. One was a 92 year old woman who had been bedridden for 2 years with no recent travel outside of Houston who I think if I remember correctly did not have air conditioning and would leave her windows open. The other woman, 49 years old, had traveled to Mexico somewhat recently. 84% of the cases who had tested positive via Ab or direct RT-PCR had no travel history to dengue endemic areas!

Basically, Murray and her team found autochthonous transmission to occur in Houston [at least a lot of evidence for it]! Physicians in the Houston area should at least be aware that this is a possibility in the area. It seems as though there has been more education about other tropical/novel pathogens in the United States like Chagas disease and West Nile virus. Here is yet another one to add to the list.
 
 
By: Stavana Strutz, PhD Candidate, Parmesan Lab, University of Texas at Austin  

Oh wait, it never really left. It was a novel pathogen to the United States until it was introduced to New York in 1999. Then it spread across the entire country in 4 years and is now an established pathogen. The main reservoirs are birds although it has even been found in alligators. Culex Mosquitoes are the primary vector. If you notice lots of dead crows in your city, make sure you are using insect repellent. When it first spread through New York, birds, especially corvids, were dying in droves. 
Picture
Map source: http://www.southwestclimatechange.org
Several media outlets have been broadcasting a recent case of West Nile in a north Texas man and a new case has now been confirmed in Houston. The map below shows counties where West Nile virus has been detected in mosquitoes. This is definitely a conservative measure, many more counties probably have infected mosquitoes but have not discovered them yet or have no detection program set up. 

Remember to spray on the DEET and deter those little winged syringes from making a blood meal out of you! You may not be a demographic of high risk (young, old, or immunocompromised) but who wants to get a fever and nasty headache or take the risk of coma, paralysis, and death? For more information about the WNV, follow this link: http://www.cdc.gov/ncidod/dvbid/westnile/wnv_factsheet.htm
Picture
Infected mosquitoes (2012), USGS Disease Maps
I apologize for the meager post, I'm in Maryland for a wedding right now. Next week it'll be good, I'll be talking about dengue in Houston or any parasites I come across on the road trip back.
 
 
By: Stavana Strutz, PhD Candidate, Parmesan Lab, University of Texas at Austin 

Dr. Peter Hotez generated dramatic headlines with the publication of his most recent article in PLoS Neglected Tropical Diseases when he compared Chagas disease to HIV/AIDS in terms of the many burdens of the disease.  The article noted the similarities and differences between Chagas disease and HIV/AIDS but many news outlets seemed to only hone in on the similarities and somewhat sensational title of the article itself. Read the article yourselves and decide! It’s freely available at the link below:
http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0001498
So why am I writing this post today? Because some of the responses to the existence and the severity of the disease in Texas are extremely dismissive. The facts need to be weighed realistically, both sides shouldn’t be sensationalizing the subject…but what else can we expect in a bipolar media world? In fact, it’s a shame that the topic has degenerated to this point where individuals in the health community are taking sides and potentially misinforming the public. Dr. Besser, a former director at the CDC Agency for Toxic Substances and Disease Registry and the current ABC news Health and Medical Editor responded, “The disease detectives need to keep their eye on it. But this particular bug and the way it spreads infection is only found in Latin America, not here in America.” The program also declared very strongly that “You cannot get Chagas disease in America, period. And the kissing bugs in Latin America are a different kind of bug.”

I’m writing because I disagree and I’ve talked to the disease detectives Besser called upon. They are keeping their eyes on it and they are concerned! After doing research on the geographic distribution of Chagas disease vectors in North America myself and attending the Dr. James Steele Diseases in Nature conference in San Antonio this past week and the Research! America forum on Neglected Tropical Diseases two weeks ago in Houston, I heard the evidence  firsthand! The pathogen is causing autochthonous infections in Texas. 

Even my sister’s late dog, Jake, tested borderline positive for Chagas disease exposure with an antibody titer of 1:80 as did the kissing bugs on her property in south central Texas. She had two different species of the vectors Triatoma gerstaeckeri and Triatoma sanguisuga present. Sadly, she has gone on to lose 3 more of her dogs in the past year to strange and hard to diagnose illnesses. Three of the four dogs had heart problems: arrythmias, enlarged heart, and valve problems. One passed away in 2 weeks with acute Chagas symptoms, however, this dog was never tested for the disease. Only one dog was tested for the disease and tested positive. She asked multiple times along the way to get them tested and was dismissed repeatedly. This is why it is so important to increase education and research of this pathogen. My sister lost four of her pets, her friends, in a year in what proved to be an extremely expensive and heartbreaking mystery.
Picture
Tammy's dog, Jake, in a Holter Monitor Vest to test his heart beat. He had arrythmias and congestive heart failure.
Dr. Roger Sanchez sees the human side of the disease and discussed recent patients testing positive for the disease that had no travel history outside of the United States. Additionally, RIPA maps show that Chagas disease is being detected at blood and tissue collecting facilities all over the United States, these can’t all be immigrants. 8% of military training dogs and more than 100 monkeys at the San Antonio primate colony are infected with highly pathological Chagas disease. It may be easy to dismiss dog infections but when our close relatives and other humans start to get sick, it’s hard to say that the strain of Chagas present here is not very pathogenic. Now you start to understand why Dr. Hotez felt the need to make such a striking comparison in the first place! Nobody is listening!
Picture
http://www.aabb.org/programs/biovigilance/Pages/chagas.aspx
Fortunately, the disease may be finally made reportable in Texas this coming January. To learn more about the pathology of the disease, I suggest checking out the CDC's website where there is an excellent training module for physicians: http://www.cdc.gov/parasites/chagas/

I also had the opportunity to interview Ed Wozniak who is leading some of the most important epidemiological, ecological, and behavioral research into the vectors and their behavior.  Ed also works on rabies and handles venomous snakes. He says he doesn't have a death wish, I think he is just an adrenaline junky. Ed works in region 8 of Texas with the Zoonoses Control division of the Texas Department of State Health Services. He strongly disagrees with those who say Chagas isn't a problem in Texas, but don' take my word for it, read the interview below!
Interview with Ed Wozniak, June 21, 2012:

Dr. Bessner has recently said that the triatomine kissing bugs found in Texas do not transmit Chagas disease to humans, what is your response?
That’s not right at all. Really we have a lot of the species here that are also present in Mexico and well known to be vectors of Chagas disease, including Triatoma gerstaeckeri and [Triatoma] lecticularia for instance.

A paper was published in the last few years that stated the reason why Chagas disease is so low here is because we have better housing and the insects don’t defecate while feeding. But you’ve found something different, right?
The housing does probably impede exposure to some extent but it does not prevent it. I’ve gotten hundreds of bugs found in or on houses, mostly Triatoma gerstaeckeri but occasional [Triatoma] lecticularia and [Triatoma] sanguisuga, and Triatoma protracta woodi. Those bugs do find their way into the house. They find their way into the people’s bedrooms and are oftentimes recovered after they’ve fed on the inhabitants. They wake up with a bite wound and they tear into the bedding and they find the bug.

Picture
Photograph from Ed Wozniak. T. gerstaeckeri feeding and defecating.
So what about the timeframe of defecation?
I find the time frame of defecation to be really quite variable. I’ve had Triatoma gerstaeckeri defecate while feeding, right in front of me. And I’ve had other ones that feed and you know, it’s a while after before they defecate. Once they’re full of blood though they tend to be heavy and do not wander far from where they took their blood meal.  That’s why people oftentimes find them in their bedding. I’ve got it photographically documented, of them feeding and defecating at the same time.

So what would you say is the prevalence rate of the disease in the triatomines you’ve sampled?
In the bugs it varies between what we’ve tested so far, between 35-75%.

How does that compare to other countries where Chagas disease is endemic and a problem?
It’s actually higher than some of those areas and comparable to some of the others. 50% is pretty high and that’s a good average.

So where in Texas have you sampled, actually?
I’ve sampled mostly across south central Texas, from Edwards county, Val Verde county, Uvalde county, Medina, Bexar, and a couple other counties east of San Antonio.

Picture
Image from Ed Wozniak. Five species of triatomine found in central Texas.

Would you say the triatomines are ubiquitous in the landscape, spread kind of evenly everywhere?
Nah, different species seem to have somewhat of a difference in preference of habitat. [Triatoma] gerstaeckeri seems to prefer the more arid region although I have seen them east of San Antonio as well. [Triatoma] sanguisuga is definitely further east.

I also know that you have sampled them in other interesting areas, like your house. Where did you find them around your house, so people reading this know where to look for them?
Mostly around where there ‘s lights but I’ve also found them on the dark sides of the house as well. I’ve watched the bugs out in the field, around the house and I’ve seen them come and go out of crevices, really thin crevices, in many cases where you look at it and you really don’t even see an opening and yet they squinch down and squeeze right on in there.

Here’s a question and I get this a lot because I’m looking at how climate change may be affecting the spread of leishmaniasis and I heard even some professors at UT say that Chagas disease didn’t use to be here and it’s here now because of climate change. I feel like I haven’t actually seen any evidence in the literature but is there some truth to that statement that transmission is actually increasing and Chagas disease didn’t used to be here in the past or has it sort of always been here and just…
I think it’s been around for a while. Somebody sent me a really old article dated back to the 1950s of finding Trypanosoma cruzi in bugs in Texas but there may be increased awareness and there may be increased numbers of bugs now. There seems to be a lot more of them, a lot more of them get turned in, that may be an increase in knowledge of the general public.  But it also could be that some of these species are adapting to these modern houses.

Are there any other public health statements you’d like to make for the readership of the blog?
It is also quite possible for people to become sensitized and have an allergic reaction to the bite of the bugs, which indicates 2 things. Both that there is repeated exposure and the fact that they’re pumping in salivary fluid that has allergenic proteins in it.

Can you describe what a bite of one of these triatomines looks like again?
It’s been described to me like as a mosquito bite. Oftentimes, in a lot of cases, there is a visible perforation or hole in the center. In some cases you may not see that if it swells. It’s just kind of a red raised lesion on the skin.

Picture
Photo from Ed Wozniak. Triatoma gerstaeckeri is the largest of the kissing bugs here, about the size of a quarter.
What kind of research do you think needs to be done here in Texas and what are you planning on doing in the next 2 years or year?
I think more work needs to be done on Trypanosoma cruzi strains that are present because that’s another argument the people have made: that the strains we have are not pathogenic. But the pathology that’s been seen in nonhuman primates and dogs certainly suggests against that. I’d like to see more reservoir host surveillance. If Mexican Free Tail Bats, for instance, are really good hosts and can carry that parasite around? They can easily bring different strains, strains from areas known to have major problems with it right here into Texas. They migrate all the way from all Central America up here and bat caves are great ways to look for triatomines, especially the immature stages.

So if someone finds a triatomine in their home, what should they do with it?
If it they think they’ve been exposed to it, probably the best thing to do is get it tested and if it tests positive then I would recommend that they go to their physician and describe what happened and ask that they draw a blood specimen for testing.

Should they send their triatomines to you?
They can send them to me if they like and I will gladly speciate them and send them on to a testing facility.

Follow-up questions, June 22, 2012:
What is your other hypothesis concerning another invasive species impacting Chagas disease in Texas?
I don’t know if it would necessarily impact Chagas disease or be susceptible to T. cruzi per say but the Mediterranean gecko has colonized houses and it lives in the same cracks and crevices as the bugs. During the day the geckos are in their asleep and easy prey for the bugs, especially the immature stages [of the bugs]. I tested to see if the bugs would feed on such a host and found that they went for them with vigor beyond what I expected. Within minutes they were attached to ‘em and feeding and fed to completion and molted off of those blood meals and they’re just fine. I raised up several batches of [Triatoma] gerstaeckeri nymphs that I hatched from eggs all the way to up to third stage nymphs. I shipped those all off to CDC for their colony. To the best of my knowledge they still have those insects. Now they’re up to the last nymphal stage and I think some of them have maybe molted to adults.

So basically, this could be helping the triatomines, especially tg, maybe adapt to modern houses because there is now a continuous food source and might be leading to increases in population size?
Unlike the situation in south America where they live in thatched roofs and they have ready access to peridomestic wildlife or the people or the people’s domestic animals that live inside the huts, our houses are a lot tighter so they don’t have as much access to us but they could very well live within the space between the exterior and interior walls where those lizards are at and those lizards are a readily available blood source.

And if you see the lizards in your house that means that if the lizards can get in then the triatomines can get in?
Yeah, they can slip in when you open the door or whatever just like a lot of other things. There may be other ways they get in too, we find them in our house occasionally and we do find triatomines as well.


Here is Ed's contact info:
Edward Wozniak
2201 east main st room 151
Uvalde, tx, 78801

Edward.Wozniak@dshs.state.tx.us

If you find a triatomine and want to send it in, download the submission form from the TDSHS found here:
http://www.dshs.state.tx.us/idcu/health/zoonosis/Triatominae/


 
 
By: Stavana Strutz 
Picture
Ectomacroparasitic pubic lice: http://www.cdc.gov/parasites/lice/pubic/index.html
So I'm going to talk about some parasites today that even Xzibit would be proud of: parasites carrying parasites. There are macroparasites and microparasites. Macroparasites are basically parasites you can see: ticks, helminths, lice, etc. They can be endoparasitic (within the host) or ectoparasitic (outside the host). Microparasites, such as  viruses, bacteria, fungi, and protozoa, require a microscope and are generally endoparasitic. 
Picture
Sandfly and endomicroparasitic leishmaniasis protozoan parasites: http://www.cdc.gov/parasites/leishmaniasis/index.html
There are also epiphytic plant parasites like mistletoe. I bring up this example to remind readers that plants also have to fight off ectoparasites and endoparasites. And then there are brood parasites like the cuckoo bird who lay eggs in other bird species' nests and parasitoid ichneumonid  wasps that lay eggs inside of caterpillars Alien-style. Both these organisms have portions of their life cycle that are not reliant on a host. I wanted to share the last three examples because they are not generally what people think of when initially imagining parasites. There is a huge amount of diversity when it comes to the free-loaders of the world.
Picture
Ichneumon parasitoid wasp injecting eggs into a cabbage moth caterpillar: http://resource.wur.nl/en/wetenschap/detail/best_friends
Now that we've gone over some terminology, let's get to the theme of today's post. Two months ago at Nerd Nite near the very end of my talk I brought up the topic of recent outbreaks of murine typhus in central Texas. Murine typhus is a bacterial disease (Rickettsia typhi) carried by fleas and spread by their feces, not to be confused with typhoid fever that is caused by a different bacteria, Salmonella typhi. This is yet another reason you should not scratch bites or touch gross looking wounds on your body...you never know what you might be further spreading into them. The symptoms of murine typhus include headache, fever, rash, vomiting, chills, and muscle pain. It can be fatal but is nowhere near as deadly as epidemic typhus transmitted by lice. There were 33 cases reported in 2008 from Travis county and cases have been increasing over the last decade.
Picture
2008 Cases of murine typhus: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5845a4.htm
So murine typhus is a bacterial endomicroparasite living within a macroparasitic flea! Even our parasites get parasites! Now, you're probably more concerned with what this means for humans. During my Nerd Nite talk I warned that this year would be especially good for flea survival because of increased spring time precipitation and thus could increase flea-borne diseases. Fleas need a humid environment for their larvae to survive; this is why it is so important to clear brush that might create a hospitable microclimate. Sadly, a month after that talk a north Travis county resident died from murine typhus. So far there have only been 2 reported cases from Travis county, which is far lower than the previous year's total of 54...but we still have months to go. So now is the time to get the word out.
Picture
Data from: http://www.statesman.com/news/local/travis-county-resident-dies-of-typhus-in-first-2374627.html
I made the above graph just to illustrate visually how much the disease is increasing. Last year there was more than a 100%  increase of the disease from the year before and more than 3 times the cases in 2010 within Travis county. This is a new record within Texas and Travis county for cases! 

Now if you've been paying attention you may have found an inconsistency with my logic from the previous paragraph. Earlier I stated that increased precipitation leads to more fleas and thus more flea-borne diseases...but according to this graph, last year during the worst drought in Texas history, murine typhus cases sky rocketed! My hypothesis is that the normal animal hosts of the fleas probably suffered huge population losses forcing fleas to bite pets instead of their normal diet of raccoon, possum, hare, and rodent. Additionally, wildlife is attracted to urban center water sources and if the wildlife are more stressed due to drought, their immune systems may not be fighting off the infection as well leading to higher parasitemias in the blood. While droughts can be good for killing disease vectors, they can also cause them to look for other blood meal sources such as pets and humans. So again, what does this mean? This means that now that we're entering summer after a wet spring...those increased wildlife populations may move into urban centers again looking for water. I would guess we are entering the higher risk months RIGHT NOW.

So what can you do? Here are some tips taken from the Statesman article referenced in the above graph:

■ Keep homes, yards and pets flea-free.

■ Eliminate outdoor pet food that can attract animals with infected ticks or fleas.
■ Avoid places that may be infested with ticks or fleas.
■ Wear long sleeves, slacks, socks and shoes and use insect repellent containing DEET.
Report typhus cases to the health department at 972-5555.
Contact Mary Ann Roser
at 445-3619


Personally, I've found fleas to be bad both this year and last year. Also, ticks can transmit another closely related rickettsial species causing sylvatic typhus so avoid ticks too! Ticks spread a lot of nasty and poorly understood parasites.



Author
Stavana Strutz is a doctoral candidate in the Parmesan lab who studies disease ecology and evolution. 
 
 
This coming Wednesday, April 11, I'll be speaking at Nerd Nite about so-called "tropical" diseases in the United States. Nerd Nite basically is a forum for individuals to share their nerdy interests with the rest of the community in a laid back setting. It started nine years ago in Boston and eventually spread around the world. Now there are Nerd Nites all over the globe!

I'm excited to have a platform where I can share disease ecology and my own research with non-scientists. I think diseases are fascinating (obviously), and I figure if others were exposed to them in a fun non-infectious intellectual way...they might think so too! A lot of people are just really turned off (or perhaps scared is a better word) by biology. The study of diseases, especially local ones, is a good way to pique interest because it gives them a reason to care, it might actually affect their health one day. Of course, I don't want to be an alarmist scientist in any way. 

I have to thank Dan Warren, another writer on the blog,  for the name of this talk: "Hot, Wet, and Infectious: Tropical Diseases in the United States."  The theme  for this month is Hidden Structures. The organizers must have thought that there are patterns in disease occurrence, which there clearly are! The other speakers will be discussing Austin traffic and the origin and creation of words. For more information about this week's Nerd Nite check out the website: http://austin.nerdnite.com/

I hope to see you there!

Author
Stavana Strutz is a doctoral candidate in the Parmesan Lab who studies disease ecology and evolution.

 
 
Tuberculosis isn't a disease you often hear about in the United States, however, if you live in Texas you might be familiar with it. Texas is one of four states (California, Florida, New York) that accounts for half of all TB cases diagnosed in the US.  Recently north Texas experienced a string of 5 outbreaks in high schools and colleges. The latest campus is Tarrant County College, which is only about 6 miles away from the house I grew up in and where I took calculus during my first summer off from UT as an undergrad.   The Centers for Disease Control reports that cases in the US are at the lowest they've ever been since TB was first nationally tracked in 1953 although some areas like Bexar county continue to see TB cases on the rise.
According to the World Health Organization:
"World TB Day raises awareness about the global epidemic of tuberculosis (TB) and efforts to eliminate the disease. One-third of the world's population is currently infected with TB. The Stop TB Partnership, a network of organizations and countries fighting TB, organizes the Day to highlight the scope of the disease and how to prevent and cure it.

The annual event on 24 March marks the day in 1882 when Dr Robert Koch detected the cause of tuberculosis, the TB bacillus. This was a first step towards diagnosing and curing tuberculosis. WHO is working to cut TB prevalence rates and deaths by half by 2015."


For more information on TB, check out the CDC page:  http://www.cdc.gov/tb/default.htm 
Author
Stavana Strutz is a doctoral candidate in the Parmesan lab at the University of Texas at Austin studying disease ecology and evolution.
 
 
As part of various research projects, I have occasionally developed methods for testing hypotheses about ecological and evolutionary phenomena.  A point of confusion occasionally arises for some people using these tests when they come to the point of having to compare their empirical observations to a null distribution: it’s not something they’ve done so explicitly before, and they’re not quite sure how to do it.  In this post I’m going to try to explain in the simplest possible terms how hypothesis testing, and in particular nonparametric tests based on Monte Carlo methods, work.

Let’s say we’ve got some observation based on real data.  In our case, we’ll say it’s a measurement of niche overlap between ENMs built from real occurrence points for a pair of species (figure partially  adapted (okay, stolen) from a figure by Rich Glor).  We have ENMs for two species, and going grid cell by grid cell, we sum up the differences between those ENMs to calculate a summary statistic measuring overlap, in this case D.
Due to some evolutionary or ecological question we’re trying to answer, we’d like to know whether this overlap is what we’d expect under some null hypothesis.  For the sake of example, we’ll talk about the “niche identity” test of Warren et al. 2008.  In this case, we are asking whether the occurrence points from two species are effectively drawn from the same distribution of environmental variables.  If that is the case, then whatever overlap we see between our real species should be statistically indistinguishable from the overlap we would see under that null hypothesis.  But how do we test that idea quantitatively?

In the case of good old parametric statistics, we would do that by comparing our empirical measurement to a parametric estimate of the overlap expected between two species (i.e., we would say "if the null hypothesis is true, we would expect an overlap of 0.5 with a standard deviation of .05", or something like that).  That would be fine if we could accurately make a parametric estimate of the expected distribution of overlaps under that null hypothesis, i.e., we need to be able to specify a mean and variance for expected overlap under that null hypothesis.  How do we do that?  Well, unfortunately, in our case we can’t.  For one thing we simply can’t state that null in a manner that makes it possible for us to put numbers on those expectations.  For another, standard parametric statistics mostly require the assumption that the distribution of expected measurements under the null hypothesis meets some criteria, the most frequent being that the distribution is normal.  In many cases we don’t know whether or not that’s true, but in the case of ENM overlaps we know it’s probably not true most of the time.  Overlap metrics are bound between 0 and 1, and if the null hypothesis generates expectations that are near one of those extremes, the distribution of expected overlaps is highly unlikely to be even approximately normal.  There can also be (and this is based on experience), multiple peaks in those null distributions, and a whole lot of skew and kurtosis as well.  So a specification of our null based on a normal distribution would be a poor description of our actual expectations under the null hypothesis, and as a result any statistical test based on parametric stats would be untrustworthy.  I have occasionally been asked whether it’s okay to do t-tests or other parametric tests on niche overlap statistics, and, for the reasons I’ve just listed, I feel that the answer has to be a resounding “no”.

So what’s the alternative?  Luckily, it’s actually quite easy.  It’s just a little less familiar to most people than parametric stats are, and requires us to think very precisely about the ideas we’re trying to test.  In our case, what we need to do is to find some way to estimate the distribution of overlaps expected between a pair of species using this landscape and these sample sizes if they were effectively drawn from the same distribution of environments.  What would that imply?  Well, if each of these sets of points were drawn from the same distribution, we should be able to generate overlap values similar to our empirical measurement by repeating that process.  So that’s exactly what we do!

We take all of the points for these two species and we throw them in a big pool.  Then we randomly pull out points for two species from that pool, keeping the sample sizes consistent with our empirical data.  Then we build ENMs for those sets of points and measure overlaps between them.  That gives us a single estimate of expected overlaps under the null hypothesis.  So now we’ve got our empirical estimate (red) and one realization of the null hypothesis (blue)

All right, so it looks like based on that one draw from the null distribution, our empirical overlap is a lot lower than you’d expect.  But how much confidence can we have in this conclusion can we have based on one single draw from the null distribution?  Not very much.  Let’s do it a bunch more times and make a histogram:
All right, now we see that, in 100 draws from that null distribution, we never once drew an overlap value that was as low as the actual value that we get from our empirical data.  This is pretty strong evidence that, whatever process generated our empirical data, it doesn’t look much like the process that generated that null distribution, and based on this evidence we can statistically reject that null hypothesis.  But how do we put a number on that?  Easy!  All we need to do is figure out what the percentile in that distribution is that corresponds to our empirical measurement.  In this case our empirical value is lower than the lowest number in our null distribution.  That being the case, we can’t specify exactly what the probability of getting our empirical result is, only that it’s lower than the lowest value we obtained, so it’s p < (whatever that number is).  Since we did 100 iterations of that null hypothesis, the resolution of our null distribution is 1/100 = .01.  Given our resolution, that means p is between 0 and .01 or, as we normally phrase it, p < .01.  If we’d done 500 simulation runs and our empirical value was still lower than our lowest value, it would be p < 1/500, or p < .0002.  If we’d done 500 runs and found that our empirical value was between the lowest value and the second lowest value, we would know that .0002 < p < .0004, although typically we just report these things as p < .0004.  Basically the placement of our empirical value in the distribution of expected values from our null hypothesis is an estimate of the probability of getting that value if that hypothesis were true.  This is exactly how hypothesis testing works in parametric statistics, the only difference being that in our case we generated the null distribution from simulations rather than specifying it mathematically.

So there you go!  We now have a nonparametric test of our hypothesis.  All we had to do was (1) figure out precisely what our null hypothesis was, (2) devise a way to generate the expected statistics if that hypothesis were true, (3) generate a bunch of replicate realizations of that null hypothesis to get an expected distribution under that null, and (4) compare our empirical observations to that distribution.  Although this approach is certainly less easy than simply plugging your data into Excel and doing a t-test or whatnot, there are many strengths to the Monte Carlo approach. For instance, we can use this approach to test pretty much any hypothesis that we can simulate – as long as we can produce summary statistics from a simulation that are comparable to our empirical data, we can test the probability of observing our empirical data under the set of assumptions that went into that simulated data.  It also means we don’t have to make assumptions about the distributions that we’re trying to test – by generating those distributions directly and comparing our empirical results to those distributions, we manage to step around many of the assumptions that can be problematic for parametric statistics.

The chief difficulty in applying this method is in steps 2 and 3 above – we have to be able to explicitly state our null hypothesis, and we have to be able to generate the distribution of expected measurements under that null.  Honestly, though, I think this is actually one of the greatest strengths of Monte Carlo methods: while this process may be more intensive than sticking our data into some plug-and-chug stats package, it requires us to think very carefully about what precisely our null hypothesis means, and what it means to reject it.  It requires more work, but more importantly it requires a more thorough understanding of our own data and hypotheses.

Author

Dan Warren is a postdoctoral researcher in the Parmesan lab at UT Austin.

 
 
Picture
1870 Census Map of Malaria Mortality
I'm posting a more optimistic post this week, rejoicing in the fact that malaria has still not returned to the United States!  Malaria used to be endemic throughout portions of what is now the US in the 19th and first half of the 20th century. Occasionally,  mysterious infections are contracted here but are extremely rare. The CDC MMWR Surveillance Summary for 2010 just came out and only 2 out of 1,691 cases were "cryptic" in origin within the United States. Autochthonous cases still pop up, at least 76 cases from 1957-1994, so it isn't necessarily gone but has yet to reestablish itself.
Picture
http://www.cdc.gov/malaria/about/history/elimination_us.html
Malaria is thought to have entered North America via European colonists and African slaves in the 16th and 17th centuries. From 1946 to 1951 the Centers for Disease Control sprayed DDT and eliminated the parasite. Since then, cases of locally acquired malaria have been documented in legal immigrants, the homeless [in Houston, Texas], and migrant workers from endemic areas living in substandard housing. Anopheline mosquitoes, the primary vectors, prefer to feed in the evening and night when the host is most likely sleeping and not slapping them. Good housing in the US is thought to greatly decrease all sorts of vector-borne diseases that otherwise would be much more rampant.
Picture
http://www.cdc.gov/malaria/images/graphs/malaria_US_curves.gif
And no Parasaturdays post would be complete without a little background on the biology of the organism:
Monsters Inside Me was an Animal Planet series that ran from 2009-2010. It's a little dramatic but there are some cool computer generated animations of parasite life cycles. More videos can be found on the Animal Planet website if you feel like being very disturbed:  
http://animal.discovery.com/videos/monsters-inside-me/
More information on malaria can be found at the CDC website:  http://www.cdc.gov/malaria/about/history/ 

Zucker, J. (1996). Changing patterns of autochthonous malaria transmission in the United States: a review of recent outbreaks. Emerg Infect Dis, 2, 37–43.

Author
Stavana Strutz is a doctoral candidate in the Parmesan lab studying disease ecology and evolution.
 
 
I'm overdue for a Fish Fridays post, but I've just been way too busy with other stuff for the past few weeks.  Instead, have my apologies and a really cool video.  Francois Vautier installed an ant colony inside his flatbed scanner, and scanned the colony each week for the next five years.  The results are creepy, cool, and kind of beautiful.  You can see the results at  http://vimeo.com/13703448

Author

Dan Warren is a postdoctoral researcher in the Parmesan lab at UT Austin.