Smart Mites

Parasitologists commonly observe species in which one sex is more heavily parasitized than the other. For example, territorial male impalas carry a much higher tick load than bachelor or female impalas (paper by Mooring and colleagues found here).  Territorial males spend less time grooming to remove ticks and instead spend their time watching for intruding males and wandering females.

Most of the explanations I’ve read for why one sex is more heavily burdened by parasites have focused on how host behavior, physiology and immune status influences their infection status. Few studies have examined if males or females have higher parasite loads because parasites are actively choosing one sex over another.

I was excited yesterday to come across this paper which examined whether or not parasitic mites are capable of preferentially infesting one sex. These researchers had previously observed that female bats from the genus Myotis are often infested with more mites than are males and so they decided to examine whether part of this pattern could be explained by the parasites “preferring” females.

Mouse-eared_BatsMites can not survive very long on their own and require a host for food and energy. It’s in the mite’s best interest to try to stay in areas of high bat density. This way they have plenty of other hosts when they reproduce and their offspring need to find a host of their own. It’s also a good idea to have other alternatives nearby in case the bat that the mite is currently living on falls ill and the mite needs to abandon ship.

If you’re like me, then when you imagine what bats you envision a cave wall with bats crammed in there nose to nose. The bats that roost in these large groups are females with their young. The males on the other hand, are loners. Instead of roosting with the group, they find a place to hunker down on their own. This means that, given a choice, mites should prefer to infest females who will surround themselves with other tasty bats over males encounter other bats far less frequently.

MyotisResearchers decided to test whether or not mites were capable of preferentially infecting females given a choice between both sexes. They placed a male and a female bat into an enclosed arena where their movements were limited and released a set number of mites into the enclosure. After keeping track of the mites’ choices, the researchers released the bats into an outdoor arena. Ten days later, the bats were recaptured and mite survival was quantified.

I know lots of people who don’t seem to know what’s good for them, but the mites seem to have it all figured out. The mites choose adult females significantly more often than they choose adult males AND their survival on female bats was much higher than on males.

The exact mechanism by which the mites differentiate between the sexes is unknown, but it’s likely that they’re using hormonal cues.

The more I learn about parasites the more amazed I am at how good they are at keeping themselves alive. This study showed that they’re capable of making good decisions when picking a host and I’ve discussed in a previous post how parasites are able to alter the behavior of hosts that they’ve successfully infected. I wouldn’t be surprised to find that the decisions made by parasites are driving differences in parasite loads between the sexes in lots of other species as well.

Parasites: a weighty topic

Hey there, blogosphere!  I’m finally back in town and have caught up on the work that I missed while visiting the Kuris Lab at the University of California-Santa Barbara. This group of parasitologists addresses numerous interesting parasite-related questions, including those related to the importance of parasites in food web dynamics and the potential applications of trematodes as bioindicators.  


Carpinteria Salt Marsh in Santa Barbara

Carpinteria Salt Marsh in Santa Barbara

Recently, this group intensely studied 3 estuaries and calculated the biomass of the species found at each site.  The prevailing opinion at the time of this study was that parasites are probably not found in high enough abundances to play an important role in ecosystem energetics.  You can imagine how surprised everyone was then when the Kuris Lab showed that parasite biomass was often greater than the biomass of much larger groups of animals.  For example, if you stuck all of the trematode parasites found in an estuary on one scale and all of the estuarine birds on another, you’d find that the parasites weight 3 to 9 times (depending on the estuary) MORE than the birds!  These findings were published in Nature.


I think that studies like this are of immense importance because they change the way that we think about parasites.  Parasites capture our imagination by doing things to their hosts that are more gruesome and amazing than just about anything science fictions writers have come up with thus far.  Because of this, I think we tend to think of them as interesting anomalies and forget that parasites make up more than half of the species found on the planet.  Future work will surely continue to enforce that parasites are important in numerous ecological processes and in human culture.  

Next post: The Kuris Lab’s work on brain altering parasites in killifish!


The enemy of my enemy is my friend


An acanthocephalan parasite

Acanthocephalan parasites are infamous for their ability to dramatically alter the behavior of their hosts.  These parasites often have multi-stage life cycles, meaning that they die unless the host that they’re currently residing in gets eaten by the next host in the cycle. Acanthocephalans are remarkably efficient at manipulating their intermediate hosts into ending up on the dinner plate of the next host in the cycle. 

One well-known example of this manipulation involves the acanthocephalan parasite Polymorphus minutus and its crustacean intermediate host Gammarus roeseli.  The definitive host of P. minutus is a waterbird which scoops G. roeseli out of the water.  The usually defense by G. roeseli to avoid being consumed by the waterbird is to hunker down at the bottom of a streambed and hide in the rubble. The parasite is capable of counteracting this defensive mechanism, presumably by altering the concentration of serotonin in the crustacean’s nervous system. This manipulation causes the the host to swim to the water surface and clamp down on the surrounding vegetation.  In a closely related system (a different species of Gammarus and a different Polymorphus parasite), this behavior has been found to significantly increase consumption of infected gammarids by waterbirds.  In essence, the parasite causes its tiny host to swim up to where the predators are feasting and hang out until it becomes dinner. 


Gammarus roeseli

Gammarus roeseli

The interests of G. roeseli and the parasite P. minutus are clearly not aligned when it comes to waterbird predation. There is, however, one thing that they can agree on.  Neither of them want to end up in the stomach of other predators (fishes, crustaceans, etc.). Non-waterbird predators represent a dead end for both members of the party.  The old addage “the enemy of my enemy is my friend” goes a long way here, and recent studies suggest that the parasite enhances the host’s ability to stay out of harm’s way when their interests converge. 

Three-spined sticklebacks
Three-spined sticklebacks

Medoc et al. 2009 have shown that gammarids infected with P. minutus have a leg up on their uninfected counterparts when it comes to avoiding predation by three-spined sticklebacks.   Infected gammarids spent more time hiding in vegetation near the water surface and suffered much lower predation rates.  Additionally, another recent study found that infected gammarids are up to 35% faster when escaping a predatory crustacean.  

This phenomenon has received little attention in the literature.  The few studies that have looked at whether or not parasites “help” their hosts escape from mutually unfavorable predators have reported mixed results.  Some studies have found that infection increased the host’s susceptibility to all predators, whether or not they’re included in the parasite’s life cycle.  

The two studies decribed above showed that the gammarids could escape from predators if escape involved moving fast or hiding near the water surface. But, although the parasites have evolved an excellent host manipulation, it’s probably not perfect.

For example, in the above system where parasites make gammarids cling to water surface vegetation in order to be eaten by birds, it is likely that by doing so the gammarids become vulnerable to other predators. At that water level, there should be a number of other predators that can take advantage of the defenseless gammarids. How fine-tuned the parasite’s control of the gammarid can be is an interesting question deserving future study.

On another note, I’m heading to Santa Barbara tomorrow to meet Armand Kuris and Kevin Lafferty, two immensely awesome parasitologists who I hope to collaborate with for my dissertation work.  When I return on Thursday, I’ll surely have fun stories about the stuff I learned.  Wish me luck!

Should scientists be better public servants?

In an earlier blog I chastised parents for taking advice from celebrities like Jim Carrey and Jenny McCarthy on important health topics.  In the days since I wrote that blog I’ve been wondering about the scientist’s role as a public servant.  Could the scientific community have done more to counter this misinformation, perhaps preventing the decrease in vaccine use that we’re currently witnessing?

I believe that the answer is yes, we could have done more.  Vaccines aren’t the only area where greater scientist involvement could make a difference.  I’m confident that just about every scientific subdiscipline has something important to offer the public.

So how do we get this information to the public?  It won’t be easy, but I think we need to be proactive.  We could contact newspapers, TV stations and radio stations, for starters.  We could contact local high schools and offer to give special lectures to students during their scheduled science classes. 

But the question remains, “Are we obligated to do anything?”  It likely depends on which scientific position you hold, but the contracts that most of us have signed in no way state that we’re obligated to educate the public.  That being said, I think it’s important to remember that taxpayers pay our bills.  Whether you’re funded by NSF, NIH, the university or college that you work for or some other government agency, it’s likely that state and federal tax monies are going towards funding your projects and paying your bills. 

Despite this, it is the case that what we’re actually being paid to do is to either teach courses or conduct research.  Our bills are also being paid by the students sitting in the courses that we teach.  In fact, in academia at least, too much public service could be detrimental to your career.

Why don’t scientists spend more time engaging the public?

The answer, in my mind, is because it’s often detrimental to our careers.  It’ll probably take a lot of time and effort to really get the public’s attention (especially when we’re going up against celebrities) and many of us are in a system where we can’t afford to offer that kind of a time commitment.

If you’re a professor going up for tenure, then you’re going to be judged on a set of predetermined criteria.  I have yet to go through the tenure process myself (I’m still a graduate student), but I believe I have a pretty good understanding of what the criteria are for achieving tenure.  The tenure committee focuses on how many papers you’ve published and where you published them, how many courses you taught and how well you taught them, how capable you were at establishing your lab, and how much service you provided to the department and the institution as a whole. 


Carl Sagan

Carl Sagan

If you’re going to excel in all of these areas in the space of 7 years, then just about any activity you engage in that isn’t focused on achieving these ends is going to set you back.  I know people who have even put off having the children that they eventually want until after they’ve received tenure because they don’t even feel like they have time any spare time at all.  During the years when you’re really getting into the groove of what kind of a scientist you’re going to be, you’re keenly aware that you don’t have time to spend communicating with the public.  This is critical because, as far as I can tell, not making tenure is devastating to one’s career.


Once tenure has been reached, there is still no incentive to spend one’s time with the public.  Professional scientific societies and the scientific community as a whole primarily praise and award achievements in research, not public education.  So again, time spent communicating with the public is time that you’re taking away from advancing your career. 

So what is the solution?

I don’t think that change is going to come without a push from research institutions and professional societies.  For example, I think it would be absolutely fantastic if universities hired scientists who were paid to spend all of their time finding ways to communicate with the public.  They should be required to stay on top of important public issues (swine flu, vaccines, etc.) and should then disseminate this information through public media as well as more direct avenues (public lectures, etc.).

Alternatively, universities could offer professors limited teaching loads for a semester every couple years in return for time spent educating more publicly.  They would be charged with discussing whatever topics are pertinent in their field and would be required in some way to show that they had made a strong effort to get this information out.

The problem with both of these solutions is that they require even MORE taxpayer money to get them accomplished.  Hiring a scientist whose sole job it is to educate the public wouldn’t be cheap, nor would paying a professor who wasn’t teaching (as college students sitting in a classroom are paying tuition which keeps the university running).


E.O. Wilson

Until we figure out another solution, our hopes rest on the few scientists who really do try to reach out to the public.  There are and have been a few greats.  My personal favorites are Carl Sagan and E.O. Wilson

Many others have good intentions, but end up preaching to the choir.  Some choose channels that have a tendency to reach people who are already science minded.  Others close out those that they need to educate by insulting them for holding different beliefs or for not understanding the concepts that we’re trying to get across.  I guess my point here is that, if you’re a scientist interested in public education, please please please stay patient and don’t fuel the growing stereotype that scientists are assholes.  This makes it difficult for us to get the public to listen when it’s really important.

In conclusion….

I look forward to reading your comments in regard to this post.  I’m sure that there’ll be controversy over whether or not we should feel obligated to spend our time communicating with the public.  I’m not suggesting that all scientists should be obligated to do this, but simply that we could probably make a big difference if we did find ways to spend at least some of our time correcting misunderstandings and spreading new information.  What do you think?

Bacteria communicate more efficiently than I do

Some things are just better done in groups.  For example, it’s better to wait until you have a large group of allies before going to war.  People know this, and apparently bacteria do as well.

If a lone bacterium where to “decide” that it was time to launch an attack on its host, then the host’s immune system would probably be able to hone in on this individual and remove it rather quickly.  The bacterium’s chance of success increases dramatically when it’s acting in conjunction with lots of other bacteria at the same time.  Bacteria figure out how many of their allies are present through a system known as quorum sensing.

When a bacterium’s receptors detect a sufficient number of allies close by, a series of important genes related to accomplishing specific tasks are switched on or off.  By this mechanism, everyone goes into attack mode together. 

Bacteria use quorum sensing in other ways too.  My favorite example involves a bioluminescent bacteria called Vibrio fischeri.  Bioluminescent bacteria produce a glowing light, similar to the lights emitted by firefliesVibrio fischeri have an unusual symbiotic relationship bobtail squids

bobtail_squidDuring the day, these bacteria reside in a portion of the squid’s mantle, where they’re provided with ample resources for growth and reproduction.  By night, when the squid is ready to hunt, the bacteria have sufficiently multiplied to the point where they reach quorum.  At this point, they begin bioluminescing as a group.

So why would the squid want to be carrying around a bunch of brightly lit bacteria? Well, on moonlit nights the squid casts a distinctive shadow on the sea floor as it hunts, attracting the attention of predators. 

The light produced by the bacteria cancels out the squid’s shadow.  The squid’s bacteria pouch contains a filter, which the squid uses to dim the light to the point that the amount of light emitted from the pouch matches the amount of light shining on the side of the squid facing the sky.  In return for a good meal and a safe place to call home, the bacteria help the squid hide from its predators.

At the end of the night, the squid squeezes most of the bacteria out of the pouch, leaving enough so that quorum will be reached again the following night.

Current quorum sensing studies are attempting to better understand mechanisms bacteria use to coordinate attacks on the human body.  By figuring out how bacteria communicate with one another, it may be possible to disrupt their communication efforts and less the efficiency with which they attack.

If you’re interested in learning more, the Bassler Lab  does a lot of awesome work on quorum sensing.

You are what you eat

toxoplasma_gondii_tachyOne of the most interesting parasites is the protozoan Toxoplasma gondii. This sucker is everywhere and capable of some pretty amazing behavioral host manipulations.

 Nearly all warm-blooded organisms can be an intermediate host for this parasite. The parasite reproduces asexually in this host and forms cysts in its muscles and brain tissues. The parasite “wants” (in an evolutionary sense) its intermediate host to be consumed by its definitive host (wild and domestic cats) and has evolved elaborate mechanisms for altering its host’s behavior to make this happen. For example, infected mice become more active and more willing to spend time in open areas.

 Studies in rats have produced even more surprising results. Rats have an innate aversion to cat urine because it is usually a very good indicator that a predator is in the area. A study comparing rats infected with Toxoplasma gondii to uninfected controls discovered that not only do infected individuals lack the characteristic aversion response, but they actually seem to be drawn TO cat urine, a behavior which is certainly risky for a rodent.

 So parasites seem pretty capable of modifying the behaviors of rodents. But what about people?

 For many years, infection by Toxoplasma gondii in people wasn’t thought to be serious. Infected individuals would exhibit flu-like systems for a few days to a month or so, but after that would no longer feel “sick.” However, we now know that individuals remain infected because the parasite forms antibiotic resistant cysts that continue to reside in muscle and brain tissues.

 Recently, some labs have begun looking at whether or not Toxoplasma gondii has subtle behavioral effects that may have been overlooked in the past. Research is accumulating to suggest that this is indeed the case.

 Personality surveys have yielded mixed results, but the majority of surveys reveal that Toxoplasma gondii infected individuals exhibit significantly different behaviors than uninfected controls. For example, personality inventory results suggested that infected males are more vigilant, frugal, suspicious, jealous and less rule-following than male uninfected controls (any other women finding themselves wondering if particular ex-boyfriends were carrying heavy parasite loads??). Infected women, on the other hand, show a higher “superego strength,” meaning that they’re more moral, warm, persistent, rule-conscious and outgoing. These behavioral differences are more noticeable as time goes on.

 But that’s not all! Both infected men and women show higher apprehension, greater insecurity, and a decrease in novelty-seeking behaviors. Importantly, infected individuals appear to have slower reaction times than uninfected individuals. If you’re wondering whether or not the difference in reaction times is enough to matter, then consider the finding that infected individuals are 2.65 times more likely to be in a traffic accident than an uninfected individual.

 Finally, and perhaps most perplexing, is the finding that infected females are pregnant for a longer and are more likely to give birth to a son than a daughter.

 An important disclaimer should be made here. Because purposefully infecting people would be unethical, we can’t scientifically compare human behaviors before and after infection with Toxoplasma gondii. This means that it’s currently impossible to figure out whether this parasite induces the behavioral changes or whether individuals with a certain personality type are simply more likely to become infected.

 The jury is still out on the mechanism the parasite uses to induce these manipulations. Promising research suggests that manipulation of the dopaminergic system is to blame, but I’m not yet aware of anything conclusive.

 So how do people become infected in the first place? One common way tsteak1o come in contact with the parasite is through the consumption of uncooked meats. Lots of warm-blooded animals contain infective Toxoplasma gondii cysts in their muscles, so countries in which people often enjoy undercooked meats have a higher occurrence of infection.

 Additionally, having cats around can increase infection risks. Toxoplasma gondii offspring are passed into the environment with a cat’s feces, where they become infective a few days later. Consuming the parasite and becoming infected can occur after changing a litter box or gardening (if cats have been defecating in the garden), for example.

 Infection rates in a population depend on diet and feline exposure, and infection rates have been reported to be as high as 80% in some areas. In the United Kingdom, for example, a report revealed that up to 38% of stored meat samples contained Toxoplasma gondii.

 These results have interesting implications! First of all, it’s almost scary to ponder whether or not some of the behavioral attributes that you consider to be quintessentially “you” are subtly modified by parasites. Second, how much of the differences between cultures can be explained by differences in infection rates? Might it be more dangerous to drive in countries where people eat a lot of uncooked meat, for example? Also, can information about how parasite behavioral manipulations tell us about how our brain works? Hopefully, the future holds more answers!

 Read more(!):

 Lots of work on this topic have been done by the Flegr lab and a review of their work on how Toxoplasma gondii effects human behavior can be found here.

 A review of the rodent literature by Joanne Webster can be found here.

 A paper on how Toxoplasma gondii may affect human culture by Kevin Lafferty can be found here.   

Stress and your brain


I just returned from a lecture by Dr. Sapolsky on the campus of UC Davis. This guy does some awesome research!  And has some awesome hair!  Here is a synopsis of his talk:

When an individual (human or otherwise) encounters a particularly stressful situation, their body releases glucocorticoid hormones in response (e.g., cortisol release in people). These hormones divert energy away from numerous bodily functions and send that energy to important muscles that your body may need to help you escape. For example, your body will put off ovulating for awhile so that the energy can instead go to your thighs, which need to quickly carry you away from the predator at your heels.

When stressors are acute and stress responses infrequent, then this system works wonderfully. Unfortunately, organisms in highly social societies (e.g., primates like ourselves) often experience frequent, chronic stress. This means that our stress hormone levels are frequently high and are continuing to divert energy away from particular bodily functions in order to prepare it for use elsewhere. One area where this is especially a problem is in the part of the brain known as the hippocampus (important in long term memory and spatial navigation).


The hippocampus has lots and lots of glucocorticoid receptors. When an individual is frequently stressed, then energy is frequently being diverted AWAY from hungry neurons in this region. Neurons in chronically stress individuals are therefore experience a state of near constant low energy. Most of the time, this low energy state does not result in neuron death.

Unfortunately, extremely high stress situations (such as strokes, gran mal seizures, etc.) can push the neurons past their tipping point, resulting in cell death and a loss of brain mass in the hippocampus. After an event such as a stroke, the body maladaptively (but understandably!), responds by releasing more stress hormones. This causes further energy deprivation to the neurons, knocking many of them out.

So what can we do to preserve neurons after events such as strokes? You can inhibit the body from producing glucocorticoids, you can bind up glucocorticoid receptors in the hippocampus so they can’t respond to the glucocorticoids, or you can supply the hippocampus with additional nutrients to make up for the energy loss. The problem with these three solutions is that they’re mainly effective if you implement them very soon after the event and they can only dampen negative effects.

The Sapolsky lab has recently been working on an awesome new solution to this problem. While cortisol is associated with neuron death, estrogen seems to have a regenerative effect. So how do you get the hippocampus to release estrogen in response to increasing cortisol levels? The answer: surprisingly, gene therapy through the use of VIRUSES.

Viruses inject themselves into cells and direct the cells to produce particular proteins that the virus requires in order to replicate. Scientists now use viruses to direct cells to create proteins that code for particular proteins that scientists would like the cell to produce.

Here is the genius of the Sapolsky Lab. The lab has manufactured a virus that gets cells to produce a protein that is BOTH a glucocorticoid receptor and a molecule that binds to estrogen receptors. In anthropomorphic terms, this protein knows when stress levels are up and goes to estrogen receptors to tell cells to start producing estrogen. The result is neuron regeneration INSTEAD of neuron death after super stressful events.

Although this solution is brilliant, it comes with some serious drawbacks. First, it requires purposefully introducing a virus into a patient. Even worse, lots of the viruses that are the most suited for this technique are related to pretty nasty viruses. There are fears that a virus may sometimes recover its ability to become infective once it is in the patient and the possibility also exists that the patient’s body will recognize the disease as foreign and mount an immune attack against it. Unfortunately, the problems don’t end there.

The viral vector also needs to be introduced directly into the hippocampus. It would be a bad thing for the entire human body to begin upregulating estrogen in response to stress, so it’s important that the virus injection be targeted. One of the only methods for getting the viral vector into the hippocampus is to use a needle to inject it directly. Clearly, you will not be able to drill a hole and inject a needle into the head of a patient experiencing a gran mal seizure. You don’t really want to be removing the skull cap of stroke victims either. At the moment, there is no clear solution. Dr. Sapolsky even postulates that, if this problem isn’t solved in the next decade or so, then you can expect funding for this area of research to dry up real fast.

Kind of makes you wish research on nanobots (robots that work at super microscopic scales) were moving along faster, huh? If we could manufacture nanorobots to deposit these viral vectors in the hippocampus, the problem would be solved. Unfortunately, these tiny biological works are more theoretical than anything at the moment.

While no biological nanobots have been created at this time, work on nanomachines has been progressing. The Tour Lab at Rice University was able to create a “nanocar”, the movement of which could be controlled through the use of a scanning tunneling microscope.  It seems promising to me that we’ve at least figured out how to manufacture molecular robots and have figured out how to direct their movements!

Hopefully science comes up with a way to safely utilize the Sapolsky Lab’s viral invention. In the meantime, you should check out some of Sapolsky’s books!


Monkeyluv: and Other Essays on Our Lives as Animals

Junk Food Monkeys

Why Zebras Don’t Get Ulcers 


EditTravels with Darwin posted a summary of the last part of Sapolsky’s talk focusing on his primate work