Monday, January 28, 2013

Clearing the Bad Air: Let's Talk About Malaria!

It occurred to me today that I have yet to post about one of the most famous and infamous parasitic diseases: Malaria.  The name of this disease literally translates to "Bad Air" because early conquistadors believed you could get it from breathing in...well...bad air.  This misconception came along as the Spanish pushed into the tropical regions of the New World and lost many lives to this strange new (to them) tropical disease.  It's interesting to note that although the Spanish believed  the disease originated in the New World, it has been established in recent times that the disease was actually brought to the New World by the Spanish...who brought with them slaves from Africa that were likely already infected.  Today we understand far more about this devastating disease.  Because of its prevalence in tropical regions and its socio-economic impact, this disease has probably been THE most studied parasitic disease.  Billions of dollars have been spent battling the disease and the impacts that it has on countries around the world.  But let's not get too far ahead of ourselves....

Plasmodium (in yellow) bursting RBCs
Malaria is caused by protozoan parasites belonging in the genus Plasmodium.  Like all protozoa, these parasites once belonged in kingdom protista, but some texts now break that kingdom into several others.  In such texts, these belong to kingdom Chromalveolata under the subgroup Alveolata, or in some cases kingdom Alveolata may be listed.  While phylogeneticists debate the true kingdom-level classification, we will move on to more solid taxonomic statuses.  There are no debates at all as to which phylum Plasmodium belongs.  Because of the collection of organelles that function in host-penetration processes known as the "apical complex", these parasites and their brethren are placed within phylum Apicomplexa.  Because they lack a conoid, they are placed in class Aconoidasida ("a" meaning "without").  They are within order Haemosporida along with other malaria-like organisms and piroplasms.  And, naturally, they belong to guessed it...Plasmodiidae.  There are four species of Plasmodium that infect humans: P. falciparum, P. ovale, P. malariae, and P. vivax.

Life Cycle
Ask any undergraduate biology student with a few years of classes under their belt to draw you the life cycle of Plasmodium.  Go on...I'll wait....Did they do it?...Correctly?...Awesome!  The life cycle for this parasite is often one of the first life cycles encountered by students of biology.  Let's start with the vector.  This parasite is spread via bites from female mosquitoes belonging to the genus Anopheles.  
Anopheles Up Close and Personal
As the mosquito bites you, tiny sporozoites wiggle their way out of the salivary glands of this vector and into your blood stream.  It rides the tide of your briskly moving currents of blood until it reaches the liver, where it invades liver cells (a.k.a. hepatocytes).  Here, the sporozoites undergo a rapid form of multiple asexual divisions known as schizogony to produce merozoites.  The merozoites break out of the hepatocytes and seek out red blood cells (a.k.a. erythrocytes) to infect.  Once inside, the host erythrocytes become transformed into factories producing additional merozoites and bursting (a.k.a. "lysing") to release 8-24 new merozoites that seek out more erythrocytes.  While some merozoites are content to continue to reproduce in this manner, others will develop into gametocytes.  When an uninfected Anopheles female comes around to take a blood meal from a person housing Plasmodium, many of the gametocytes are ingested with the blood.  These cells mature in the gut of the mosquito. Eventually, male and female gametocytes will fuse to create  zygotes (a.k.a. "ookinetes" in this case), which will eventually become sporozoites.  After developing into this motile, infective form, the sporozoites move into the mosquito's salivary glands and the cycle is complete.

Outsmarting Our Immune Systems
Plasmodium is a devious little dude.  These parasites are largely protected from the treat of a host's immune system because they live within cells rather than outside of them.  This hides them from circulating immune police, such as macrophages.  However, erythrocytes are prone to aging because they work so hard for our bodies.  When these cells pass through the spleen, they are checked for signs of damage or aging, and are subsequently filtered out of regular circulation.  The parasites becomes the cutting edge of anti-aging technology for these little cells by using proteins to prop up the cells, making them seem young to the busy spleen, and saving the parasites' homes for another road trip through the circulatory system.  Some species, such as P. falciparum, will even go so far as to produce adhesive proteins that force cells to stick to walls of small vessels in order to save themselves from being processed via the spleen.

Symptoms of Malaria
The symptoms of malaria may not appear until 8-30 days post-infection.  As the parasites enter into the phase of their life cycle in which they invade erythrocytes and force them to burst, people tend to spike fevers.  In some instances, people infected by P. viviax won't display symptoms for several months or even years post-infection.  This is because this species produces hypnozoites, which allow for long incubation periods and late relapses of infections.

The most common symptoms are flu-like in nature: headache, fever, shivering, joint and muscle pain, vomiting...but some are more severe such as anemia, jaundice, and retinal damage.  The most defining symptom is paroxysm.  Paroxysm is a period of coldness followed by chills and then by high fevers and sweating.  The time frame of paroxysm states is dependent upon the type of malarial parasite with which one is infected.

The World Health Organization (WHO) splits malaria cases into two categories: "Severe" and "Uncomplicated".  To be classified as "severe", one must demonstrate any of the following: decreased consciousness, significant weakness (e.g. inability to walk), loss of ability to eat, convulsions, low blood pressure, breathing difficulties, circulatory shock, kidney failure, red (hemoglobin-rich) urine, uncontrollable bleeding, enlarged liver, enlarged spleen, pulmonary edema, low blood glucose, acidosis, high levels of lactate, or an extremely high parasite level present in the blood.  The disease can progress to an even more severe form (if infected with P. falciparum) known as cerebral malaria.  This form presents with neurological problems such as seizures and comas.
Diagnosis, Treatment, and Prevention
Malaria is diagnosed by finding the parasites in a blood sample.  This can be through microscopic examinations of blood smears, or through antigen-based diagnostics tests.  The later is more accurate, but also more costly, and these tests are not yet sophisticated enough to tell how many parasites are present within a sample.  Polymerase Chain Reaction (PCR) has been shown to diagnose malaria efficiently, but is not widely used due to its complexity.

People diagnosed with malaria are usually treated using chloroquine in areas where Plasmodium isn't already resistant. Because resistance is so prevalent, most patients are also given mefloquine, doxycycline, or Malarone.  To prevent resistance, many places are now instituting the use of artemisinin-combination therapys (ACTs), which involves treating with traditional anti-malarial medications in conjunction with artemisinin compounds.  ACT is about 90% effective if used to treat "uncomplicated" forms of malaria.  When treated correctly, patients can experience a complete recovery. 
Various Anti-Malarial Medications
"Severe" forms of malaria were once treated with quinine, but now artesunate is more widely used because of its efficiency.  Treatment also includes supporting patients by helping them manage high fevers and seizures as they come and go as well as monitoring respiratory rates, blood pressure, and blood glucose levels.  This form of malaria can progress so fast that it can cause death within days or in some cases hours.

To prevent malaria, most tropical regions take on a three-pronged approach:
1) They give out prophylactic medications (if they can afford to do so).
2) They work to eliminate Anopheles mosquitoes.
3) They devise ways to prevent people from getting bitten by mosquitoes.

Prophylactic medicines are often the same medicines used for treatment (mefloquine, chloroquine, Malarone, etc.).  Travelers heading to malaria-endemic regions begin taking prophylactics a few weeks before leaving and continue taking them for about a month after coming back home.  (I personally took Malarone when I traveled to Panama for two weeks, and I didn't have any problems, but many people have side effects of this and other such drugs.)  This form of prophylaxis is not typically practical for residents of malaria-endemic areas because drug resistance and partial immunity can come from prolonged use.  This is also a costly endeavor, and has had many historical roadblocks.

To prevent mosquito bites, people can use DEET-based repellents and insecticide-treated mosquito nets.  Treating the nets with insecticides reduces the chances of mosquitoes living long enough to find a way to breech the nets themselves.
A woman tucks a mosquito net into her child's mattress.
 Some places have instituted spraying for mosquitoes (both indoors and outdoors).  Indoor spraying is highly effective as the mosquitoes tend to land on wall surfaces after taking in blood meals.  The WHO advises the use of 12 insecticides for such purposes.  Like anti-malarial drugs, these insecticides should be used in combination to prevent resistance.

Community-aimed educational programs are also helpful in preventing the spread of malaria.  After all, knowledge is power!  Seriously!  Teaching people to cover areas with stagnant water that could become mosquito-breeding grounds, as well as helping people to recognize the signs and symptoms of malaria can greatly reduce the number of malaria cases reported in an area.
An old poster encouraging people to spray for mosquitoes.

Ultimately, the best approach would be to prevent malaria rather than to treat it. (More cost effective and less costly in terms of human life.)  However, the monetary costs of instituting a program for prevention are beyond the means of the countries where malaria posses the biggest threat to public health.  Luckily, there are some amazing researchers (namely Jay Keasling...go on...Google him!) working to produce an anti-malarial drug that can be mass-produced cheaply.  Thanks to this kind of research, and humanitarian efforts directed at distribution, the next few decades are sure to reduce the number of annual cases of malaria.  It will be interesting to see how things change from a socio-economical perspective in response to a decline in a disease with such wide-reaching impacts on global health and economies.

Moral of the Story 
Though I could go on and on and on about malaria, this post has already gotten rather lengthy, so we will call it quits for today.  Maybe a future post will discuss the amazing way some populations have developed genes that prevent them from contracting malaria...or we could delve deeper into the work of Jay Keasling.  Perhaps a future post could discuss the history of malaria, an exciting tale of man's ups and downs as he fights to erradicate a disease that just won't seem to die.  For now, at least you can proudly say that you know the basics about malaria.  So if you ever travel to malaria-endemic areas, be sure to take your antimalarials (before, during, and after), sleep with a special insecticide-drenched, netted canopy surrounding your bed, and be sure to invest in plenty of DEET!

P. falciparum...because I can't resist a rainbow-colored image!
(Even if it is artificially done! :p)

Saturday, January 19, 2013

Leucochloridium paradoxum

Brood Sacs of L. paradoxum
 Sometimes (in fact, more often than not) parasites aren't satisfied with living inside a host, they feel the need to actually manipulate that host.  This is often the case with intermediate hosts like ants and snails that only serve the parasite for a part of the parasite's life cycle.  Parasites need to make it to their final host in order to reproduce and live out their adult lives.  In many instances, this means that the intermediate host needs to be manipulated in some way that attracts the parasite's definitive host so that the parasite doesn't have to wait around and hope that the intermediate host gets eaten by the right host quickly. This parasite is one such manipulator, and how it manipulates its snail host is a thing of both beauty and amazement.

Leucochloridium paradoxum is also called the "green-banded broodsac" and is a type of flatworm belonging to phylum platyhelminthes.  It is a type of fluke, further classifying it as a member of class trematoda. It is a digeneid worm that falls into order strigeidida alongside the human parasite Schistosoma.  It belongs to family leucochloridiidae. It belongs in the genus leucochloridium, which houses many parasites of snails and other invertebrates.

Life Cycle
This parasite begins its life as an egg falling from the sky surrounded by a safety net of bird feces.  After landing in a splatter on the ground, a tree branch, or other area frequented by snails it waits for someone to come along that likes to eat bird droppings.  Enter an amber snail of the Succinea genus that shows up for a nice bird poop meal. The snail feasts upon the bird's feces and ingests our little parasite egg. 

The parasite makes its way out of the egg and takes the form of a miracidium. After living in the gut a short while, the miracidium begins to wander around the body.  Some of the miracidia will wind up near the head as the others overtake the snail's internal organs. The ones that reach the head change into their next developmental stage known as a sporocyst stage. In this stationary stage, the parasite begins to replicate itself until it produces a large "brood sac" that grows in size and begins to invade the snail's eye stalks. Here the sac begins to take on specific color patterns of yellow and green bands as it continues to grow. Within the sac, sporocysts are being produced, but so are the next life stage known as the cercaria stage.  Some cercariae stay in the sac as they are while others change into a metacercaria stage to await a bird gut paradise. The invasion renders the poor snail's vision in the infected eye stalk useless. (Most of the time only the left eye stalk is infected, but there plenty of instances were both eye stalks fall victim to these parasites.) 

Now the parasites override the snail's natural instincts to stay in dark areas safe from bird predators and forces the snail our into the light.  The light instigates a twitching movement of the brood sac.  This twitching becomes more rapid as the worms are exposed to more light.  The convulsing action of the eye stalk coupled with the coloring of the underlying brood sac looks like caterpillars to birds.

Along comes a bird looking for a tasty snack, and there goes the snail. In some cases, the birds only snag the eye stalk rather than eating the whole snail. When this happens, the snail is able to regrow its eye stalk, but the stalk is likely to be reinfected by some of the parasites already living in the snail's guts.

Now the cercariae in the bird's gut can make their way to the intestine and become adult worms. The metacercariae and sporocysts will change into cercariae and follow suit.  This bird's last meal has now created a new, large, vibrant parasite population with the bird's body.  The adult worms are monecious (having both sexes' reproductive parts within one individual) and will begin to cross-fertilize with other individuals or will self-fertilize to create eggs.  The eggs will be passed in the bird's feces, thus completing the parasite's circle of life.

That's for the Birds!
Despite the way that these parasites disfigure their snail hosts, they don't really cause any harm to their bird hosts. They live in the bird's intestines eating waste material and pumping out a LOT of eggs to ensure their species' survival.  After all, not all bird droppings get eaten right away...many dry out, which kills our little parasite eggs before they can be eaten by a snail.  Some sources say that shore birds are the preferred host for this parasite, and others say that birds like crows, sparrows, and finches are more likely to play host.  The only real criteria for a definitive host seems to be that the host be a bird living in temperate North American or European forests that house amber snails and like to eat green and yellow-banded caterpillars. The types of birds that do play host to the parasite are rarely eaten by humans, therefore human infection with this parasite is unlikely.

Peckhamian Mimicry and Extended Phenotypes
One of the coolest things about this parasite is how it can be used to teach people a variety of biological concepts.  First and foremost it displays an incredible ability to manipulate host behavior, a fundamental concept in studying parasites. It also brings up an important point about fecundity in organisms that have high egg mortality rates. If you know that many of your offspring are going to die, you can ensure your species' survival by producing an overabundance of eggs to compensate. These worms developed the ability to pump out lots of eggs in response to having a low egg survival rate.  That topic leads us into a discussion of evolution, which blows my mind with regard to how this species ever evolved such a complex and unique life cycle.

Continuing with the concept of evolution, one can bring up the idea of extended phenotypes.  An extended phenotype is the idea that a phenotype (outward expression of an internal combination of genes) does not have to be limited to internal biological processes like the creation of proteins that give rise to physical features. The idea is that one's phenotype can be extended to include the effects of a gene on the environment outside of an individual organism's body. This parasite is a good example of such effects.

It is a good example of a form of mimicry called aggressive mimicry or Peckhamian mimicry.  In this type of mimicry, an organism pretends to be a prey item or a member of the opposite sex to take advantage of a predator or potential mate.  We see this with Australian katydids that mimic the sounds of cicadas to attract and eat cicadas of the opposite sex.  We see this with many other animals that will mimic sounds, behaviors, pheromones, and even the way that a prey item/mate looks to be able to get what they want.  In this case, the worm pretends to be a caterpillar and gets eaten, but this is all part of an intricate plan to take over the bird's gut and convert it into a trematode egg factory and distribution center.

Moral of the Story
Although Leucochloridium paradoxum has no ecological impact on humans, is certainly interesting and important for teaching budding biologists about the wonders of nature.  Like most parasites, its life cycle is utterly fascinating. Yet despite all of the nasty things it does to the snail, it doesn't really hurt the bird at all.  And the snail doesn't necessarily die from all the abuse, but I'm sure there are some emotional issues one might develop from having an eye plucked out by a bird after being invaded by green-banded eye bandits if snails do in fact have emotions. Below is a link to a video of a pulsating infected eye stalk. You should definitely check it out! Gotta love some nature footage! ;)

Sunday, January 13, 2013

Trichinella spiralis

Today I'm here to talk about one of the most interesting and insidious little parasites out there.  It's the smallest nematode that invades humans and is one of the world's most clinically important and widespread parasites. Imagine, for a moment, a parasite that not only invades your body to feed off of your yummy insides, but one that also manages to force your own body into being a slave to its decadence. This is the modus operandi of Trichinella spiralis.  But before we get into that, let's check out its taxonomic specs.

Larval form coiled in a spiral.
T. spiralis is a nematode (a.k.a. "roundworm") and thus belongs in phylum nematoda under kingdom anamalia. It belongs to class enoplea, which is largely comprised of non-parasitic species.  However, two orders withing this class contain parasites: Dioctophymatida and Trichurida. Take a guess which one this little guy belongs to! That's right, order trichurida (you're smart as a whip!...though we aren't talking about whipworms...oh wait! We are talking about whipworms!) This order is home to many worms of veterinary importance as well as to human whipworms like Trichuris trichuria. (*Side Note* Anytime that you see the prefix Trich- it means something in relation to hair. It comes from a Greek word which means "hair". Whipworms took on this prefix because they appeared hair-like morphologically to early biologists.) Like human whip worms, T. spiralis belongs in the family Trichinellidae.

Life Cycle
This parasite has an interesting life cycle. It begins with an uninfected animal eating an infected animal.  This can happen amongst domestic animals such as pigs or amongst wild animals living in various environments. Epidemiologist W. C. Campbell constructed four life cycles based on the involved hosts of this parasite. The first was the domestic cycle, which involved pigs and is the most important cycle that involved accidental human infection. The other three may be due to other species of Trichinella and may also involve accidental human infection, but is far less common than the first cycle. These three cycles are known as sylvatic cycles and involve different animals for different climatic regions. To keep things simple, we will only talk about the domestic cycle today.

Cross section of muscle tissue containing nurse cells.
For the domestic cycle to complete itself, a human has to eat some infected pork that has not been cooked well enough to kill off the parasite. Once inside the human body, the parasite larvae are released from their cysts that were formed in the pig's muscle tissue. The larvae mature into adults in the small intestines and search for mates. When a male and a female find one another, they mate and produce offspring that are deposited in the mucosa. The larvae migrate out of the mucosa and follow bloodstreams until they find a nice, quite piece of skeletal muscle to call home.  The larvae encyst in the muscle tissue and form what are called "nurse cells".  These "nurse cells" actually manipulated the surrounding tissues into bringing it nutrients rather than sounding the alarms and bringing in a brigade of immune cells to fight off the invading parasite.  Inside its cozy little nurse cell, the parasite lives awaiting the day that the human will die and be eaten by another suitable host in order to complete its own life cycle.  Little does it know that humans are more often dead-end hosts for these little guys.

Nurse cells that formed in a pig's diaphragm.
The nurse cells begin by instigating new blood vessel formation. The environment inside muscles is hypoxic, meaning that it lacks an adequate amount of oxygen. This environment stimulates other muscle cells to start secreting angiogenic cytokines, which form the new blood vessels that surround the single muscle cell into which the larva will penetrate. The cell continues to pump out the cytokines at the parasite's demand and the cell maintains a constant state of hypoxia. Some research has shown that these cytokines may also lead to an increase in collagen production, further protecting the cell.

Within pigs, this parasite is transmitted by pigs eating infected meat scraps from other animals or from their common practice of cannibalism. (Trust me, I grew up on a pig farm...YES Wilbur will eat his babies if their mother accidentally lays on them, suffocating one while nursing three. They are stupid, dirty creatures, and they deserve to be eaten. Plus, bacon is delicious!)

 After becoming infected, a person may start having symptoms in as little as 12 hours or as much as 2 days. As the worms move through the body, they damage parts of the intestine and cause immune responses that result in inflammation.  Such responses can manifest as nausea, vomiting, sweating, and diarrhea. 5-7 days later, some people experience fevers or facial swelling (a.k.a. "facial edema"). After 10 days, people will experience intense muscular pain, difficulty breathing, low blood pressure, and possible nervous disorders.  The disease can cause severe damage to the heart, respiratory issues, or kidney malfunction that can eventually lead to death.

An artist's depiction of a
larva in a nurse cell.

In pigs, the symptoms are often undetectable unless the parasite load is so much that it can cause fatality (uncommon).

Diagnosis, Prevention, and Treatment

For a muscle biopsy, you have to make
an incision in the skin to reveal the
underlying muscle, then a hollow
needle is used to extract a small
amount of muscle tissue for
laboratory analysis.
For humans, Trichinosis is often misdiagnosed as flu due to the similarity of symptoms. To confirm a suspected case of trichonosis, a  doctor may order a muscle biopsy (which is invasive and rather painful from what I hear) or a seriological test.

Pigs are diagnosed following ELISA testing.

To prevent the transmission of this disease, the US has a national surveillance system that tracks reported cases and inspects sources of possible contamination. The pork industry has also made changes in order to reduce pig exposure to this disease and to recognize warning signs of infection in order to treat pigs before being slaughtered for their meat. Laws have also reduced risk of human infection by regulating pork processing procedures, such as providing guidelines for specific cooking and freezing temperatures and times as well as for curing procedures.

I like this picture of the medicine because
it looks like a worm was drawn on one
side of this pill! :p
The best way for you to ensure your own safety is to cook pork using hot enough temperatures for long enough to kill off any potential parasites. Or if you are really paranoid, you could freeze the meat for awhile first, and then cook the hell out of it. (No one likes a rare pork chop anyway, right?!

To treat trichinosis, humans and pigs are both prescribed antihelminthic drugs such as mebendazole or albendazole. In humans, this is not always affective. Humans also receive corticosteroids and painkillers to cope with the pain of the infection as it is being treated.

Moral of the Story
Mmmm...Teriyaki pork loin!
Is it cooked all the way through?...
The moral of the story today is to follow good food safety guidelines when preparing pork. (Or bear, or rats if you are into that sort of thing.) It is less important in this country than it would be in countries with less regulation in the pork industry, but it's still always a good idea to make sure you cook your pork all the way through. Trichinella spiralis is only one of many parasites that you can contract from eating undercooked pork. Just do yourself a favor and make sure there's not any pink left by the time you are ready to chow down on some teriyaki pork loin or mojito lime pork chops. (Don't judge, both of those are delicious!)

Because I can't NOT post a picture of a parasite colored in rainbow...

Sunday, January 6, 2013

Why Can't We Be Friends?: A Brief Discussion of the Lost Friends Theory

A long while back, I briefly mentioned something known as "The Lost Friends Theory".  It is also known more scientifically as "The Depleted Biome Theory", but Lost Friends just sounds more fun! The idea behind this theory, no matter what you decide to call it, is that as new medical technologies emerge and rid us of all the bad things that live within us, such as our favorite little hookworms, our bodies actually lose some of their immunological capabilities.

Sounds a little bogus, right? It actually makes perfect sense! Consider for a moment the fact that human parasites, such as parasitic worms, have evolved alongside us throughout most of human history.  Such enduring symbiotic relationships would have to have affected the way each organisms' bodies functions on at least some minor level.  If a population has been carrying a particular intestinal parasite for generations, it would only make sense for that population to eventually develop bodies that either (A) find a way to rid themselves of their parasites or (B) find a way to coexist with their parasites. 

It seems that as far as our hookworm friends are concerned, (B) was the body’s choice for many human populations.  Hookworm infections were once notoriously bad in the southern part of the United States.  Thanks to John D. Rockefeller, hookworms were essentially eradicated in the south, leading to healthier, more productive citizens who could now enjoy a much better quality of life.  While this monumental public health achievement was vital to re-energizing the southern economy, it didn’t go completely without consequence.  Generations later, people whose bodies had adapted to deal with the commonly occurring hookworm infections began to develop health issues that ranged from mild allergies to severe intestinal diseases. 

The causes of such issues were not linked to a loss of hookworms in the body until much, much later.  Research has now shown that having hookworms within your body causes the body to launch an immune response that increases the amount of mucus put out by your intestines. This response is vital to suppressing chronic diseases such as ulcerative colitis, celiac disease, and Crohn’s disease.

For a more technical description of how the immune system works with (or without depending on your perspective) parasites, see one of my older posts titled: Helminthic Therapy. That post does a great job dealing with the creation of regulatory T cells and the interplay of interleukin genes with helminths and autoimmune diseases. Here’s the link if you are interested:

Anyway, back to the discussion at hand.  So by losing friends, like our hookworms, we have caused our immune systems to freak out on our bodies. This immunological temper-tantrum has put us at greater risk of developing autoimmune issues such as the intestinal issues mentioned previous, but also for diseases such as asthma, hayfever, multiple sclerosis, and various food allergies.

Not to fear, however, for as they say, knowledge is power. By knowing that these diseases may be brought on by a lack of something, or someone (which I suppose is more correct), it is easier to treat patients that deal with such issues.  Helminthic therapy is one of the more exciting mechanisms we have developed to restore our lost friends and their benefits. The long description of this can, again, be found on a previous post. (See above link.) The short definition is that the patient is treated for such diseases by purposefully reintroducing a small, easily controlled, number of “parasites” into their bodies to elicit the proper immune response that will inadvertently treat their disease.  Scary as this sounds, it is a virtually harmless, painless treatment that has astoundingly positive results for people who suffer from some of the most brutally painful autoimmune diseases.

There are probably many more examples of how we have put ourselves at risk for various health issues by trying to make ourselves healthier. Paradoxical as it may seem, such is the beauty and mysterious nature of the ever-evolving field of medical science. The Lost Friends Theory is actually a subset of a broader hypothesis called “The Hygiene Hypothesis” which extends this concept to bacteria and viruses.

Moral of the Story
Things are rarely as they seem. It is important that we don’t allow our bodies to be ransacked by preventable diseases, but it is just as important that we don’t wipe out organisms that our body depends on to keep itself healthy. The idea of parasites living inside one’s body is a terrifying thought.  This perception is a result of decades of movies and books that attach a stigma of what Carl Zimmer calls, “A precise horror” to the concept of parasitism. As rational human beings, we sometimes need our perceptions to be challenged.  Such is how we better our chances of unlocking the mysteries of the biological universe. Perhaps it would be good for us to see the often unrealized potential of parasites by looking at these creatures in a less frightening light. Maybe if we start seeing them for what they really are, not agents bent on bodily domination, but rather just as organisms trying to complete their own small circle of life, then we would be able to more easily digest the idea of them being useful, and invited guests. After all, we are ourselves a great conglomerate of a multitude of organisms working together to form what we call our individual selves.  We are positively teeming with bacteria and invisible mites that all add up to the complexity of who we are. So why not make a little room in our bodies for organisms that may alleviate our autoimmune problems if we face them? Why not reconnect with our lost friends when needed? 

Tuesday, January 1, 2013


In light of my last post about Brazil releasing a vaccine for Schistosomiasis, I felt it would be a good idea to do a post on Schistosoma itself. Schitosomiasis has a long history with humans. In fact, some sources assert that it was a common cause of death amongst the ancient Egyptians during the Greco-Roman period. It continues to be a problem today that about 1/6 of our world’s population has to deal with. It is to blame for lowered productivity and social stigmas that drag down the economies of developing countries. Its population even exploded as man feebly attempted to divert the great waters of the Nile. (*Side note*: As cases mounted due to Nile irrigation projects from the 1950s-1980s, people were being treated with shots of tartar emetic, which later increased the spread of hepatitis C via unclean needles….good job, Egypt!)

Like all helminths, this worm belongs to kingdom Animalia.  It is a type of flatworm known as a “fluke” putting it in phylum Platyhelminthes and class Trematoda.  Other platyhelminths include tapeworms and some nifty non-parasites called turbellarians (google it…they are really neat!) The term “fluke” is synonymous with the term “trematode” and I might use them interchangeably, so beware! This particular parasite is in order Strigeidida under the suborder Strigeata.  It further belongs to the family Schistosomatidae.  Members of this family spend their larval stages within molluscs and their adult stages within vertebrates.  All members are dioecious (meaning they have separate male and female sexes) unlike many other flatworms that are hermaphroditic (having male and female organs within a single individual).  The family has14 genera, 9 of which infect birds. 

Unamused Hippo is Unamused
The only genus that infects humans is the genus Schistosoma. Seven species within Schistosoma infect humans, but there are other mammals that carry Schistosoma.  Most of these other animal are ruminants, but there are two species that infect hippos. (I’ll list one of them here because the name is intuitive, so you will never forget it: Schistosoma hippopotami.)

Life Cycle
These parasites are known as “blood flukes”…and I bet you can guess why! (Because you are a smart cookie!) The first person to ever describe the full life cycle was Dr. Piraj√° da Silva in 1908. 

S. haematobium egg
S. mansoni egg
Let’s start with the eggs.  The eggs of these little guys are pretty scary-looking. They have tiny spines that may be found in various places on the egg depending on the species of Schistosoma from which they came. Eggs are passed via urine or feces from an infected host into a fresh water system.  The eggs then hatch, releasing a miracidium that then proceeds to penetrate a snail host (which is often species specific). Inside the snail, the parasite undergoes a few different morphological changes before popping out as a tailed cercaria. These cercariae swim about in the water until they find a suitable host and then they burrow their way into that host through the host’s skin.  They then wiggle their way into the circulatory system and eventually make their way to a specific destination in the body where they mate and spend the rest of their lives eating and pumping out babies.  The destination depends on the species of Schistosoma that is infecting its host. Some like the liver, some like veins associated with the intestines, and some like the bladder.

Living Encopula
(Female's head is in orange
poking out of the canal .)
One of the more interesting aspects of the life cycle for S. mansoni is that these parasites are monogamous.  The males have a special canal that runs the length of their bodies which is referred to as the “gynecophoric canal”.  The smaller, more slender female finds a mate and slips into this canal to live out her life, literally, inside of the male. This life style is called living “encopula”. They only take one mate, and if the female dies, the male retains her dead body within his canal until he too dies. He eats a ton of glucose that he passes on to her as she pumps out eggs that invade the liver or are passed out of the host to start the life cycle over again. Homosexuality has also been observed in these animals even though the anatomical fit isn’t quite as perfect. When curious scientists tried to separate the homosexual couples mechanically, they always went right back to one another. How cool is that?!?

As previously stated, there are seven species that infect humans.  These infections are aptly named “schistosomiasis” despite which species causes the infection.  Most of the species are found in or near South East Asia or Africa, but there is a species that spans from Africa and the Middle East all the way to the Caribbean and into South America.  This disease infects a large portion of the human population.  In fact, it runs right behind malaria in terms of the devastating socioeconomic impacts. The CDC and the WHO both classify schistosomiasis as a NTD (Neglected Tropical Disease).  This is WHY it was such a BIG DEAL when Brazil announced that they had finally found a vaccine for this detrimental and disfiguring disease. That and the whole first-vaccine-against-a-worm thing…that was important too. :p Anyway, back to the disease.

Schistosomiasis is sometimes called “Bilharzia” (after the first physician to describe the cause of urinary schistosomiasis in 1851: Theodor Bilharz) or “Snail Fever”. S. mansoni and S. intercalatum cause intestinal schistosomiasis. S. haematobium causes urinary schistosomiasis. S. guineensis can cause liver disease. S. malayensis is rarely known to infect humans at its preferred host is von Muller’s rat. And finally, S. japonicum and S. mekongi cause Asian intestinal schistosomiasis.
The disease itself is often chronic and debilitating, but not necessarily fatal. 

Skin lesions left from Schistosoma penetration.
Symptoms include abdominal pain and diarrhea, coughing, anemia and malnutrition, elevated white blood cell counts, fevers, fatigue, enlargement of the liver or spleen, genital sores, and dermatitis caused by host skin penetration. The longer the infection, the more detrimental the parasites are to their hosts, often leading to calcifications and cancers if left unchecked for too long. (*Side Note*: Because young boys often pick up S. haematobium when they reach puberty and start working in rice fields, they will often experience bloody urine. Infection in these cultures is so pervasive, that this is not seen as abnormal, but as a form of “male menstration”. There are even instances of boys who didn’t go into working in rice fields, thus they didn’t get infected, and parents taking them to doctors to find out why their sons weren’t menstruating! Wild huh??)
Diagnosis, Treatment, and Prevention
To diagnose schistosomiasis, most hospitals test for antigens using ELISA and a patient’s blood sample.  This is the best method for diagnosis, but it can also be diagnosed via demonstration in a stool sample, or (rarely) a urine sample. Sometimes a tissue biopsy is performed, but is less commonly used because it is more invasive.

To treat patients diagnosed with schistosomiasis, most places recommend a single, yearly dose of a de-wormer known as praziquantel. Outside of the US, some places have developed species specific treatment such as oxaminiquine for S. mansoni and metrifonate for S. haematobium

To prevent the transmission of this disease, some areas treat fresh water sources with chemicals to kill off the snail intermediate hosts. However, these chemicals often kill more than just the snails. Even if they didn’t, the snails are still a vital part of the ecosystem, so every time this prevention method is used there are ecological effects that forever change the flora and fauna of the freshwater sources.
Now, because Brazil is awesome, we have…for the first time ever…an effective vaccine against schistosomiasis. Check out my last blog post for more details.

Moral of the Story
If your son didn’t get his period, it’s totally normal! :p If he did, see a doctor and get rid of it! (Reference from The Jerk, anyone?) Anyway, the vaccine for this is super awesome, and super important. It will be interesting to see the socioeconomic impacts that this vaccine has over the next few years! :D

Another thing we can take away from this is that there are great examples of monogamy among animals...there's even homosexual monogamy! Ahh true parasitophilia in the strictest  sense of the made-up word! It's enough to make you want to weep with joy!