Monday, 19 December 2011

Body Hair as Parasite Protection

Does your body hair help you notice when something is crawling around looking for a place to bite? Does it discourage that ectoparasite from biting? Authors Isabelle Dean and Michael T. Siva-Jothy think the answer to both questions is ‘yes.’ A report in Biology Letters reveals the findings of a study that was designed to reveal whether our fine body hairs protect us from ectoparasites such as bedbugs.

Body hair appears to slow bedbugs down; the hairier
you are, the better! Image by Jiří Humpolíček
CC BY-SA 2.5

Bedbugs Are Slower on Hairy Skin

In a study of twenty-nine student volunteers, the researchers noted that bedbugs took longer to select a feeding site on hairy, as opposed to shaven, skin, (and the hairier the better) and that the volunteers were better able to detect the insects on unshaven skin. Thus, having all those fine hairs apparently helps us, in two different ways, to notice the bug before it bites.

Dean and Siva-Jothy point out that it’s already been shown that some insects that bite animals, including bedbug relatives, prefer to bite on relatively hairless parts of the body. It’s easy to see that such behavior would tend to favor bug survival if the bug goes unnoticed. In some circumstances, we can also see that hairier humans might have a survival advantage.

Does Body Hair Slow All Ectoparasites Down?

This study only looked at bedbugs; it would be interesting to see if the same thing happens with ticks (I can attest from personal experience that ticks have an amazing ability to traverse large areas of skin without ever being felt), kissing bugs, mosquitoes, black flies and other biting insects and arachnids.

So we know one possible reason why we have all those fine hairs all over us – and why we perhaps shouldn’t be shaving them off in a time of bedbug resurgence and increased tick-transmitted disease.

Dean, Isabelle, and Michael T. Siva-Jothy. “Human fine body hair enhances ectoparasite detection.” Biology Letters: Published online December 14, 2011, doi: 10.1098/rsbl.2011.0987

Monday, 12 December 2011

Malaria, Cryptosporidium, and Plants

It’s more than a decade now since scientists discovered that Plasmodium spp., agents of malaria, have plastids in their cytoplasm reminiscent of chloroplasts in plants. Chloroplasts are believed to be the descendants of free living cyanobacteria that were ingested by early cells, or invaded those cells, and then became part of cell structure and function. Chloroplasts in green plants provide energy when exposed sunlight.

[caption id="attachment_365" align="alignleft" width="185" caption="Cyanobacteria, NOAA"]Cyanobacteria, NOAA[/caption]

The plastid in malarial parasites – called an apicoplast – has the same origin as chloroplasts in plants and functions in similar ways. This suggests that Plasmodium spp. and their relatives: Toxoplasma gondii, Cryptosporidium spp., Cyclospora cayetanensis, Isospora belli, and Babesia spp., to name the main ones parasitic in humans, are more like plants than we typically think.

The plastid in Plasmodium spp. and other apicomplexans has lost the ability to produce energy from light, but it remains a vital part of the cell, synthesizing fatty acids, heme and other molecules. The organisms can’t live without their apicoplasts.

Aside from identifying an intriguing connection between some of our worst parasites and the plant kingdom, the discovery of the apicoplast has suggested new ways of treating infections with these parasites. Plasmodium spp. are notorious for developing resistance to antimalarial drugs, while Toxoplasma, Cryptosporidium, and Babesia have proven very challenging to treat and eradicate in the body. It could be that the agents to treat these infections are already in our possession – in the form of herbicides.

Lim, L., et al. The carbon and energy sources of the non-photosynthetic plastid in the malaria parasite. FEBS Lett. (2009),

Monday, 5 December 2011

Life Cycle of Malaria Parasites – A New Twist

The life cycle of Plasmodium spp., agents of malaria, is one of the harder ones for a parasitology student to grasp. It’s full of difficult words such as gametocyte and shizogony, and involves multiplication in both humans and mosquitoes - two hosts about as different from each other as one could imagine. Likewise, the immune system is so complex that most people can only achieve a basic understanding.

Recently, both of these things got more complicated as researchers discovered how malaria may evade the immune system and thereby survive for long periods and cause new bouts of illness later. Aha! Some old mysteries have been solved, but parasitology students will likely groan.

Two species of Plasmodium, P. vivax and P. ovale, have long been known to remain hidden away in the human liver after an initial episode of malaria, returning to the blood weeks, months, or even years later to start the infection all over again. Two other species, P. falciparum and P. malariae, do not stay within liver cells (hepatocytes) but can still mysteriously reappear after all parasites have disappeared from the blood. Where do these parasites, thought to multiply in humans only in red blood cells and hepatocytes, go? At last, we think we know.

A paper by Michelle N. Wykes et al reports that plasmodia can hide within dendritic cells—white cells that are an important part of the immune response intended to eliminate these parasites - in the spleen, multiply inside the cell and return to the bloodstream later to reinitiate malaria (“Rodent blood-stage Plasmodium survive in dendritic cells that infect naive mice.PNAS 2011).

[caption id="attachment_360" align="alignleft" width="300" caption="Dendritic cell, image by Judith Behnsen et al, Creative Commons 2.5"]Dendritic cell[/caption]

Plasmodium spp. are not the first parasites known to use the host’s immune system against it in this way: Leishmania sp. parasites invade macrophages, an immune cell intended to kill them, and multiply within the cell before bursting out and spreading to other cells in the body. Other parasites, such as the schistosomes and trypanosomes, trick the immune system in other ways.

This discovery will have implications for the treatment of malaria. Not only will it offer new possible targets for drug therapy or vaccine, it will oblige us to take these infected white cells in the spleen into account in treating infections. The authors suggest that parasites within the dentritic cells may be in a state of “arrested” development and thus able to live a long time before reappearing. I’m wondering what role these arrested parasites might have in the development of drug resistance in Plasmodium spp. parasites.

Tuesday, 29 November 2011

Interview on

Adam Dunn, author of Rivers of Gold and The Big Dogs, has posted an interview with me on his website, Dunn's latest book deals with a different kind of "parasite:" the less than saintly financial gurus of Wall Street. My favourite review of The Big Dogs (for obvious reasons) is "Dunn's writing is like the candiru fish. It squirms its way into one's cerebral cortex & is quite difficult to dislodge." (Col. Lee T. Guzofski, Chief Executive Officer, G2G Enterprises, Inc.)

It was a pleasure corresponding with Adam Dunn.

Tuesday, 15 November 2011

Drinking Surface Water

While discussing a relatively low coliform and E. coli count in well water recently, a water treatment professional told me that he didn’t think drinking this water would be any worse than drinking from a stream.

[caption id="attachment_331" align="alignleft" width="300" caption="Don't drink surface water"]Migrating geese[/caption]


My initial response to this is that one must understand it’s not the E. coli and coliforms that we need to worry about. These organisms are markers for fecal contamination of water. Your guts and my guts are already full of them. It’s the other things that come with feces that make it imperative we take a low count seriously—viruses such as Hepatitis A, and parasites, such as Giardia, Cryptosporidium, and Toxoplasma. If E. coli and coliforms are in your water, these other things might be there too. Boil.

And furthermore, the days when we could safely drink from streams or other surface water are long gone. Yes, it may look crystal clear. It may be flowing through “pristine” woodland (is there such a thing any more?), but beavers and other mammals living near water carry Giardia; migrating birds carry Cryptosporidium, and wild cats can contaminate water with Toxoplasma. A lot of other things could be there too. Maybe you’ll get away with drinking from a stream, and maybe you won’t—all surface waters are contaminated.

There are seven billion people on Earth now, all defecating daily (and millions don’t have toilets). There are still municipalities that discharge untreated sewage into surface water—rivers, lakes, and coastal marine water. There are millions of cows living in feedlots, and millions of feral cats – their wastes often wash off land into surface water. There are millions of migrating Canada geese in North America, visiting surface water all along their migration route.

It has been said that if feces were fluorescent, the tropics would glow at night. Let’s face it, if we include animal feces, the entire temperate region and much of the arctic/antarctic would glow as well. Boil.

Monday, 22 August 2011

Naegleria fowleri, Terror of Swimmers

It’s two thirds of the way through a long hot summer (in some places) and numerous swimming holes have had lots of time to warm up to temperatures well above average. Tragically, this sometimes results in deaths due to infection with Naegleria fowleri, especially in warmer regions such as the southern United States. Naegleria, sometimes referred to as the “brain-eating parasite,” is an environmental amoeba that can, given the opportunity, gain access to the human brain through the back of the nose.

Naegleria Thrives Where Water is Warm

Naegleria does not habitually parasitize humans, but it does multiply in warm waters, and if swimmers draw water up the nose, infection can follow. (This year, one victim reportedly infected himself using a neti pot – a device used to rinse the sinuses.) Once infected, very few people survive the dreadful illness that Naegleria causes. Victims, of course, are typically those who enjoy water sports and games – the young, fit, and healthy.

Deaths due to N. fowleri are often widely reported, especially now that we have the internet. After such a death, people call for disclosure of the bodies of water involved, more public education, and surveillance. This is entirely understandable, but these demands really do miss the point. Naegleria is an environmental organism, widely distributed in nature, and well known for multiplying in warm bodies of water. It could be in any warm water, even the stuff in your hot water tank (as in the neti pot story). We can’t eradicate it, or even pinpoint where it will turn up next except in the most general terms.

If you really want to avoid this risk (and it is a small small risk) don’t swim in water warmer than 80F (26.7C). Never draw warm water up your nose unless it has been sterilized. If there is a risk of drawing water up the nose, use nose plugs or a nose clip.

Naegleria Deaths in Perspective

The reality is that any activity carries a certain risk, even sitting at home. For comparison, the number of fatalities from N. fowleri in the United States in the decade from 2001 to 2010 is thought to be about 30, an average of three per year:

  • In that same time period, National Geographic reports that more than 400 people were killed by lightening.

  • In 2004, an average of nine people accidentally drowned per day in the United States (Poseidon).

  • In 2004, almost 4000 people died in fires, mostly residential.

  • Each year, more than 33,000 people are killed in automobile accidents in the United States (NHTSA).

Deaths due to N. fowleri are quick, horrifying, and tragic, but this disease shouldn’t be blown out of proportion. It’s rare. Exercise reasonable caution while swimming (submerged hazards, drowning, pathogens, dangerous aquatic animals etc.) and enjoy the summer.

Tuesday, 16 August 2011

Is Babesia Spreading or Not?

Babesia microti was first recognized as a potential cause of human infection in New England in 1969. Before this, human cases of babesiosis involving other Babesia species were recognized in other places, chiefly Europe. The appearance and persistence of Babesia microti have been associated with high deer populations, increased human contact with the deer tick, Ixodes scapularis, and the presence of Lyme disease.

[caption id="attachment_316" align="alignleft" width="300" caption="Ixodes scapularis, image by Stuart Meek"][/caption]

In 2003, a paper published in the American Journal of Tropical Medicine and Hygiene noted “Human babesiosis generally is detected in sites where Ixodes ticks are endemic only after Lyme disease has become well established” (Krause et al, “Increasing Health Burden of Human Babesiosis in Endemic Sites," 68(4)). Why?

It’s tempting to explain away the late appearance of babesiosis by saying, well, physicians aren’t familiar with it, no one is looking for it, and most cases are mild anyway, so it’s simply being missed. As well, no one’s collecting data on diagnosed cases, so the incidence is unknown.

A current article published on discusses the work of Stephen Rich at the University of Massachusetts Amherst's Laboratory of Medical Zoology (Clark, “Much to Learn About Babesia’s Spread”). Rich’s research on Ixodes scapularis suggests that Babesia microti is spreading inland at a much slower rate than Borrelia burgdorferi, the organism that causes Lyme disease.

Rich’s work tells us that the organism truly is not well established in new locales – there’s not as much of it there. This likely explains why cases of babesiosis lag behind cases of Lyme disease, but it still raises a big question mark. If ticks and Lyme are spreading, why is Babesia not spreading just as quickly? The answer isn’t clear, but it appears that something is slowing down transmission of Babesia from host to host.

Rich doesn’t say that Babesia is absent in places where ticks and Lyme have appeared, he says there is a “much lower incidence” (qtd. in Clark). I suspect that incidence will rise over time – it may take years – and eventually make babesiosis a significant health concern over a much larger geographical area. I hope surveillance and medical knowledge stay ahead of it. If nothing else, the risk of contamination of the blood supply should fuel increased interest in this organism.

Wednesday, 20 July 2011

Where Did Toxoplasma gondii Come From?

Toxoplasma gondii, one assumes, evolved as a parasite of cats. Is this a safe assumption? All the texts tell us that the cat is the only animal in which T. gondii completes the sexual phase of its life cycle, which is strong evidence for the cat being the original host. It is possible that there are other hosts in which T. gondii can produce gametocytes and reproduce sexually – maybe we just haven’t found them yet. Maybe we haven’t looked exhaustively either. Nonetheless, in the absence of evidence to the contrary, I’ll stick with the assumption that T. gondii evolved in cats.

T. gondii was first discovered in Tunisia in 1908. By coincidence, Northern Africa is also one of the places where the cat is thought to have been domesticated (there or present day Iraq) and this explains my somewhat illogical but long held assumption that T. gondii probably evolved in Africa. There is actually no reason why the parasite couldn’t have evolved in some other feline species and spread to domestic cats later.

One theory has it that T. gondii evolved in South America.

[caption id="attachment_309" align="alignleft" width="162" caption="Did prehistoric jaguars have T. gondii?"]Prehistoric cat statue from Guatemala, Simon Burchell[/caption]

The paper “Globalization and the Population Structure of Toxoplasma gondii,” reports an odd distribution of genotypes: one is found worldwide, one is found everywhere but South America, and several more are found only in South America. The authors' (Lehmann et al, PNAS July 25, 2006) interpretation is that there was an early split, originating in South America and leaving two populations to evolve in isolation from each other. One evolved in the “old world” and today is found everywhere but South America. The other is found everywhere, but apparently only spread very recently from its origins. Several more never left South America.

So maybe Toxoplasma gondii came from a prehistoric cat species in South America. It's a place to start.

(Image by Simon Burchell. Creative Commons)

Friday, 15 July 2011

Must We Hate Worms?

Is the revulsion we feel toward intestinal worms (in fact, anything called a parasite) innate or learned? If we hadn’t been surrounded by the “yuck factor” all our lives, grossed out by anything that wriggles or crawls, would we view them with disgust or curiosity? I think it would be more in the realm of curiosity.

In his book Parasites and Parasitic Infections in Early Medicine and Science, R. Hoeppli describes early attitudes toward parasites. Even within the last few hundred years, many people believed they arose spontaneously from intestinal contents, blood, even dust and ashes. And “in China,” he writes, “there existed from ancient times the widespread belief that one should have at least three worms in order to remain in good health” (p. 164).

Robin M. Overstreet has investigated the deliberate ingestion of parasites for various reasons by humans and found that parasites are often deliberately eaten and sometimes even regarded as delicacies (“Flavor Bugs and other Delights,” Journal of Parasitology: 89(6)). Overstreet describes a boy “open[ing] the intestine (of a possum) where a lump existed to allow the tapewoms to squirt out, remov[ing] the feces from the worms, and drop[ping] each writhing organism straight into his mouth.”

A former co-worker described an encounter with a small boy who was playing with a rather large roundworm, whirling it around while holding on to one end. When asked where he got it, he calmly indicated that it had come out of his nose.

These things suggest that a horror of worms is not a natural characteristic of humans. Similarly, Hans Zinsser writes that “as wise a man as Linnaeus suggested that children were protected by their lice from a number of diseases” (Rats, Lice and History, p. 139).

[caption id="attachment_301" align="alignleft" width="249" caption="Portrait of Carolus Linnaeus by Alexander Roslin, 1775"]Linnaeus, by Alexander Roslin[/caption]

I’ve often suggested that if it were possible to keep mosquitoes out of your back yard, it would be socially unacceptable to have any there. I believe that’s what’s happened to parasites. If they were unavoidable, we’d accept them as part of life, like mosquitoes and mud puddles. In the handful of decades since we’ve been able to avoid having parasites in developed countries, we’ve also learned to abhor them.

Wednesday, 13 July 2011

Getting Parasites from Animals

An article by Peter Michael on (“Dingo Poo Spreading Deadly Parasites to Humans,” July 13) interests me for several reasons. First, the “deadly parasite” involved is Ecinococcus granulosus, which is by no means a new parasite for people in many parts of the world. It was once a big problem anywhere sheep were raised because sheep dogs could pass the worm’s eggs to people. Today, mostly because sheep dogs typically get better preventative care, the parasite is slowly losing ground.

It’s a bitter twist, then, that wild canines that have lost their fear of humans and come into human communities are now a source of infection. Therein lies the other thing that interests me. A few of the people who commented on that article have it right: it’s not that these wild animals are “encroaching” on us; it’s that we have encroached on them, and we’ve been doing that ever since the first human settlements with the beginning of agriculture and domestic animals.

[caption id="attachment_296" align="alignleft" width="200" caption="Dingos by Joshposh, Creative Commons 3.0"]Dingos by Joshposh, Creative Commons 3.0[/caption]

Before we grew our own food and raised animals, how often would we have come in close enough contact with an animal to catch a disease? Sporadically: when an animal was killed for food, when we shared the same cave perhaps, and by accident. Now we breed them and invite them in by carelessly providing food: cattle, pigs, birds, dogs, cats, fish, raccoons, dingos, rats, mice, and lots more. Meanwhile, we destroy their habitat and oblige them to adjust. Civilization is bad for our health: so many devastating diseases would be rare if we had not settled down and brought animals, and their parasites, into our space, one way or another.

Of course, without civilization, people would be rare as well. Most of us wouldn’t be here, I wouldn’t be writing this, and there wouldn’t be an internet. So one wonders, was it all worth it, and where does it stop?

Monday, 11 July 2011

Babesia in the Blood Supply

Blood transfusions have saved a lot of lives, my own included, but gone are the days when we thought that the chief concern with blood transfusions was transfusion reactions. Units of blood today are subjected to a growing battery of tests to detect infectious agents, because many pathogens are found in the blood stream and can easily be passed from donor to recipient, setting up a new infection. Blood transfusion can pass along HIV, hepatitis, malaria, trypanosomiasis, and a host of other things. Now, Babesia is recognized as being common enough to be of concern for the blood supply.

Babesia is a tiny blood parasite usually transmitted by a tick bite. The tick responsible is the same species that transmits Lyme disease, and babesiosis appears to be following in the footsteps of Lyme, appearing in places where Lyme has emerged, notably the northeastern United States.

[caption id="attachment_290" align="alignleft" width="300" caption="Babesia in ticks, mice, and humans"]Babesia Life Cycle Diagram[/caption]

In some places, studies show, about one in ten people have antibodies to Babesia,  indicating that they have been infected. Because the diagnosis is often missed, and because, while fatal in some cases, the infection goes unnoticed in many people, the infection is likely considerably more common that we think.

It looks as though we’ll need to add a screen for Babesia to the processing of blood units for transfusion, at least in places where Lyme disease is common. Though babesiosis is mild in many cases, anyone receiving a blood transfusion is likely more vulnerable to serious illness. Reliable, cost effective, large scale screening methods, however, take time to develop and implement.

Monday, 27 June 2011

Maps of Dog and Cat Parasites in the US

The Companion Animal Parasite Council (CAPC) website,, has posted maps of the United States showing the prevalence of dog and cat parasites based on lab results at two commercial laboratories. If you’ve ever wondered how common the common dog and cat parasites actually are, and you live in the US, these maps are enlightening. There are maps for tick borne diseases, hookworm, whipworm, Toxocara (roundworm), and heartworm.

One should take care drawing conclusions from the results. This data is not based on a survey of all dogs and cats, or even a survey of a representative sample of all dogs and cats. It is data based on lab results of dogs and cats (presumably dogs and cats with owners and homes) whose samples were submitted to two specific commercial laboratories. We can assume that submission of these samples was done for a reason, even if it was just a routine health check; we don’t know whether parasites were suspected in some or most of these animals, or what the average age of the animal was.

You can look at two presentations of the data: traditional and three-dimensional. The traditional is best if you are only interested in looking at data from one state. If you want to compare, however, I’d suggest the three-dimensional. It gives you an immediate visual comparison between neighbouring states and various regions based on percentage positive. The map for Lyme disease clearly – and unsurprisingly – shows a concentration in the northeast, while hookworm's stronghold in the southeast is equally obvious.

I wish this data included Canada, although I understand why it doesn’t. Looking at the results for the northern states may provide clues to prevalence in southern Canada (and what the heck is going on with Toxocara in North and South Dakota?), but there may be differences in veterinary care and other variables that can’t be taken into account.  I still think these maps are very interesting, even with all the unanswered questions.

Wednesday, 22 June 2011

Do Bedbugs Spread Diseases?

Bedbugs are in the news a lot these days. Bedbugs are on the rise; there’s an epidemic. Bedbugs have become resistant to the chemicals we’ve been using for years to kill them. The bugs are in used furniture, on airplanes, and they’re adept at spreading from one apartment to another by traveling along plumbing pipes. Some envision a world where we lose control altogether and everyone has bedbugs, like we all have the occasional spider now.

There’s a difference of course. Bedbugs don’t just live in our houses and they can’t be swept away. They live in our beds. They feed on our blood. The one saving grace has always been that they don’t transmit disease. They ingest blood pathogens when they feed, but no one has ever been able to demonstrate that they are capable of passing any of them on. Until now.

Apparently researchers in Vancouver investigated whether bedbugs could be responsible for the spread of antibiotic resistant bacteria, and found evidence that they could. They found bedbugs carrying antibiotic resistant bacteria, and suggested that because bedbug bites cause a break in the skin, not to mention subsequent scratching, they might provide an opportunity for these bacteria to colonize and cause infections.

As far as I can tell, it’s not proven yet, but the possibility that bedbugs might be spreading these agents looks stronger than ever before.

Lowe, Christopher F., and Marc G. Romney. "Bedbugs as Vectors for Drug Resistant Bacteria." Letter. Emerging Infectious Diseases, 2011 17:6.

Monday, 25 April 2011

Diseases We Share With Animals

What is a zoonosis? My dictionary says a zoonosis is “any infection or infestation that can be transmitted to humans from lower vertebrates under natural conditions” (Gage Canadian Dictionary). The MedlinePlus Medical Dictionary agrees: “a disease communicable from animals to humans under natural conditions."

This definition has always seemed so vague to me as to be virtually useless. Though there are some pathogens that only infect humans and can only be transmitted from human to human, they must be in the distinct minority. I’ve tended to think of a zoonosis as a disease of animals that can incidentally be transmitted to humans, thus excluding diseases that are common in humans. That others have made this distinction also is illustrated by statements such as this: “it is not a true zoonosis… it is endemic in humans, rather than periodically penetrating human populations from an animal reservoir…” (Mark Wheelis, Principles of Modern Microbiology, 2008).

Consider the beef tapeworm, Taenia saginata. The adult, sexually reproducing stage of this parasite – the tapeworm we are familiar with – lives in the intestines of humans, but we acquire it by eating the larval form in rare beef. We cannot get a beef tapeworm directly from another infected person, but is this a disease of animals? Since we have the adult worm, isn’t this more a parasite of humans passed to animals? (This would be an anthroponosis.)

[caption id="attachment_268" align="alignleft" width="300" caption="Cows get Taenia saginata from people"][/caption]

Giardia lamblia, agent of ‘beaver fever’ is another example. Sure, beavers carry it and pass it to people, but who had Giardia first, people or beavers?

If we go with Wheelis’ implied definition - a disease not endemic in humans, but which is transmitted to humans from animals periodically - we are left with many fewer pathogens. This would include parasites like Baylisascaris procyonis, an intestinal roundworm of raccoons that can be fatal in humans. These are things we only come in contact with rarely, by virtue of our lifestyles and cultural separation from nature. Presumably if we still lived the hunter-gatherer life, and ate more of our food raw, we’d be naturally exposed to these things sporadically just as other animals are.

But wait. Doesn’t that create a contradiction? A zoonosis is supposed to be passed from animals to humans under natural conditions; but, doesn’t that mean a zoonosis is only a zoonosis because we live our lives in unnatural conditions?

Tuesday, 12 April 2011

Are Raccoons Cute? The Trouble With Raccoons

I have stood on my front deck on a late summer evening and watched a raccoon cross the street not 50 feet from my front door. I’ve seen young raccoons with their butts sticking out of my bird feeder, and I’ve seen their indented trails in the snow, where they venture out of their dens on warmer winter nights.

[caption id="attachment_263" align="alignleft" width="300" caption="Urban raccoon, Christopher Michaud, Creative Commons 3.0"][/caption]

Though no one who’s ever heard raccoons brawling at night would mistake them for cuddly friends, there’s something charming about their striped faces, their round furry physique, their dexterous paws.  I don’t let it fool me. These wild animals are becoming common in urban and suburban environments because we are feeding them. Where raccoons are living and eating, they are also leaving their droppings – in latrines. And where there are raccoon latrines, there will likely be Baylisascaris eggs (intestinal roundworm), and these can be deadly to people.

Raccoons, like people, don’t tend to spread their droppings at random all over the neighborhood: they establish latrines on horizontal surfaces such as fences tops, wood piles, roofs, branches. They return to the same place again and again, creating areas that are heavily contaminated with their feces, and which may contain millions of Baylisascaris eggs. Swallow those eggs by accident or chance, and you could be in serious trouble.

The eggs hatch after being swallowed, releasing larvae that migrate through the tissues and typically invade the head and brain, where they can do terrible damage. Children, and the mentally challenged are at highest risk because these people are more likely to put contaminated fingers in their mouths.

Raccoons are cute, but they should be cute in the wild, not in human communities. Don’t encourage raccoons – don’t feed them, keep them out of buildings, block access under decks, clean up latrines and remove contaminated soil or wood. Always consult a knowledgeable source about how to do this safely and effectively.

Wednesday, 9 March 2011

Malaria: Artemisinin and P. falciparum Dormancy

Relapse, recurrence, recrudescence, resistance, dormancy: these terms are all relevant when explaining why malaria sometimes makes a reappearance after it has been treated. Plasmodium sp. parasites have a whole arsenal of ways to foil our best attempts to get rid of them.

The terms above all mean something quite specific. Garcia and Bruckner explain that relapse and recurrence refer to a return of the infection that arises from merozoites remaining in the liver (Diagnostic Medical Parasitology, 1997). This is well documented with P. vivax and P. ovale, and is also responsible for the long period of time that can pass between infection and onset of symptoms.

[caption id="attachment_255" align="alignleft" width="300" caption="Plasmodium falciparum parasites in blood: CDC, Dr. Mae Melvin"][/caption]

Recrudescence, according to Garcia and Bruckner, results from parasites remaining in the red blood cells after treatment. Drug therapy has failed to kill them. This is not necessarily due to drug resistance – it may be because too little drug was administered or because the drug did not remain in the blood long enough - but resistance can play a part. When some individual parasites have a genetic ability to escape the effects of a drug, and are able to multiply and re-establish the infection after all the rest have been killed, drug resistance is the basis of recrudescence. Recrudescence is often seen with P. falciparum.

Now, Andrea Codd and others report on research that provides scientific evidence for dormancy (“Artemisinin-induced Parasite Dormancy: A Plausible Mechanism for Treatment Failure," Malaria Journal 10:56). It seems that treatment with artemisinin induces a dormant state in P. falciparum parasites in the blood, from which they can return and begin to multiply once again. The researchers describe it as “a drug-induced temporary pause in the development of some parasites.” This is a distinctly different situation from parasite survival due to the drug failing to kill all the parasites, or actual drug resistance, and it is yet another way that malaria can appear to be gone, and then return.

While the effect has only been observed in the laboratory so far, Codd et al propose that dormancy may account for many instances of recrudescence, and speculate that dormancy may occur with other antimalarial drugs as well.

The more we learn about Plasmodium spp., the better we see how versatile they are, how well equipped to survive, no matter what we throw at them.

Tuesday, 1 March 2011

Guinea Worm Eradication

The guinea worm, Dracunculus medinensis (dragon worm, serpent worm, medina worm) is the parasite of nightmares, the horrifying thin white worm that comes out through the skin causing terrible and enduring misery. It is real, but it may not be real for much longer.

Savelugu, Ghana; Feb. 8, 2007; Credit: The Carter Center
At Savelugu Hospital in Northern Region, Ghana,
former U.S. President Jimmy Carter and his wife,
Rosalynn, watch as a Guinea worm health worker dresses a
child's extremely painful Guinea worm wound.

Guinea Worm History

 The guinea worm probably evolved in Africa – that continent is its stronghold – but in its heyday, it occurred in many parts of the Middle East and India, and as far north as parts of the USSR. As recently as the 1980s three and a half million people endured the nightmarish infection every year.  A Feb 28 New York Times article by Donald G. McNeil Jr. provides the number of cases recorded in 2010: less than 1800, all in Sudan, Mali, or Ethiopia (“Parasitic Disease: Guinea Worm Takes a Step Closer to Eradication, Jimmy Carter Says”).

McNeil writes that guinea worm “has proved notoriously hard to eradicate around the world.” When one considers, however, that of all the diseases afflicting humans, only smallpox has been eradicated to date, the fact that guinea worm is likely to be second is very impressive.

Guinea Worm's Weakness

What’s this dragon’s weak spot? Simply put, it’s the worm’s absolute reliance on people using the same pool of water as both drinking water and a place to sooth the unbearable lesion where the worm protrudes from the skin. Keep the parasite out of the water, or give people a means to avoid swallowing it (like drinking through a straw filter), and you prevent infection.

This is what’s been done. A multi-year 300 million dollar effort (relatively inexpensive as such efforts go) pushed forward by Jimmy Carter and the Carter Center, guinea worm has been beaten steadily back. I chronicle this dramatic effort in the book, Parasites: Tales of Humanity's Most Unwelcome Guests.  Odds are, this parasite will disappear forever in my lifetime.

Wednesday, 16 February 2011

Echinococcus multilocularis in Sweden

“Deadly Parasite Found in Sweden:” the internet headline caught my eye, and I had a strong suspicion right away. Scanning the article, I picked out the word fox, and I knew I was right. Apparently Echinococcus multilocularis has made its way to Sweden. I discuss this parasite in my book because of the way it has spread in North America from the north to the Midwest, and probably to the East Coast, primarily due to human activities.

[caption id="attachment_244" align="alignleft" width="300" caption="Foxes carry Echinococcus multilocularis, I, Malene: Creative Commons 3.0"][/caption]

The internet article, published by The Local (, Feb 14) doesn’t speculate about how the parasite got there; it just reports that it’s never been found in Sweden before, despite regular monitoring of foxes.  People will come up with lots of theories about the spread of this parasite, but the fact is, the prevalence of E. multilocularis has been increasing in Europe in both humans and foxes for decades. At the same time, it appears to be steadily spreading to new places. It’s appearance in Sweden was probably inevitable.

Researchers point out that the number of red foxes in Europe has increased dramatically in recent years due to environmental changes and human activities, and foxes are much more common in urban areas than in the past. These factors, as well as an increased awareness of the parasite, likely account for the higher numbers of human cases diagnosed. A study published in the June 2009 Issue of PLoS Neglected Tropical Diseases suggests that the original focus was in Switzerland or nearby, and that this focus has seeded expansion to new areas in Europe (Knapp, Jenny et al. “Genetic Diversity of the Cestode Echinococcus multilocularis in Red Foxes at a Continental Scale in Europe”)

Infected rodents could potentially be spreading it as well as foxes, and one wonders about this possibility with respect to Sweden, since an overland route for migrating foxes around the Baltic Sea and the Gulf of Bothnia would take a very long time. But, realistically, any number of animals could bring it in, and there is also the possibility that it has been present for decades at a low level, and is only being discovered now because people are actively looking for it. Interestingly, I found a report that said the population of red foxes in Sweden declined by more than 70% in the 1970s and 80s due to sarcoptic mange, so the fox population there may be on the rise due to recovery from that as well (“Red Fox: Vulpes vulpes.” D.W. MacDonald and J.C. Reynolds,

The spread of E. multilocularis to humans is certainly bad news: Roberts and Janovy say it chillingly and well: “this parasite… grows and infiltrates processes into the surrounding host tissues like a cancer.” (Foundations of Parasitology, 6 ed. McGraw Hill, 2000)

Monday, 31 January 2011

Pinworms and Human Immunity

Thoughts on pinworm infections...

I had a strongly worded email from someone who had apparently read, and taken exception to, one of my articles about pinworm (Enterobius vermicularis). I was a little surprised by the tone of the email - who knows why someone would become attached to this particular soapbox - but the vehement claim that the human immune system will eradicate a case of pinworm (enterobiasis) got me thinking.

One female pinworm can produce 10,000 sticky eggs.
Mentnafunangann; CC BY-SA 3.0

Will Pinworm Infection Resolve Without Treatment?

I’m of the understanding that a pinworm infection will resolve on its own eventually if left untreated – and I never said otherwise – but what role does the immune system play? Can the immune system kill the adult worms? We know that the immune system responds to parasites, but many parasites are good at evading immune attacks, and prompting moderation of the immune response. Enterobius vermicularis should be particularly good at this because it is one of our heirloom parasites: it’s been with us hundreds of thousands of years.

Add to this the frequently reported problem of reinfestation through swallowing eggs in the home/school environment and one begins to suspect that waiting for the immune system to do the job could be a long process. It’s clear that, for many people, the immune system is ineffective at eliminating the adults (they likely die of old age after a month or so), and unable to effectively kill larvae over the long term after initial exposure.

Having said all that, it probably doesn’t matter all that much, except for those unfortunate individuals that experience bad symptoms.

A Realistic Approach For Pinworm Infection

Further thoughts:
  • Texts tell us that the majority of pinworm infections are asymptomatic, so lots of people have pinworms, don’t suffer any unpleasant symptoms, and eventually eliminate the worms on their own. (And if they have no symptoms, they’re less likely to spread it around.)

  • The ability to fight off enterobiasis likely varies from one person to the next, as it appears to with other parasitic worm infestations.

  • An overzealous approach to eradicating pinworms is probably unrealistic.  They’re so good at spreading themselves around, and we’re so poor at fighting them off, that actually getting rid of them is next to impossible.

  • When symptoms are severe and persistent, however, only the most stoic of patients would refuse treatment. I’ve never had the pleasure myself, but I’ve heard first hand accounts that were not pretty.
I suspect most people would choose to treat a pinworm infection but it's up to the individual.

Friday, 21 January 2011

Onchocerca volvulus and Wolbachia

In my book, Parasites: Tales of Humanity’s Most Unwelcome Guests, I discuss the efforts to treat people for river blindness - the difficulty of treating enough people for long enough to eradicate the disease. I also explore the fascinating relationship between the worm Onchocerca volvulus, and a genus of bacteria, Wolbachia. Wolbachia lives literally inside the cells of the worm, even within the embryos.

[caption id="attachment_231" align="alignleft" width="300" caption="Wolbachia inside a cell, Creative Commons Attribution 2.5 Generic"][/caption]

We know that O. volvulus can’t live without Wolbachia - that if you kill the bacteria with antibiotics, the worms die as well. Obviously Wolbachia does something for O. volvulus that it can’t do for itself. But what? This seems counterintuitive to our ideas of germs: a bacterial infection you can’t live without? But it is not so foreign really: even humans have bacteria living in their intestines that help to digest food and provide nutrients, and protect us from infection caused by less friendly species. Perhaps Wolbachia produces some vital nutrient for the worm that the worm can’t produce alone.

But here’s where the relationship gets more complex and more fascinating. Research indicates that the symptoms of river blindness are actually caused by the response of the human immune system to Wolbachia, not O. volvulus. While most of the bacteria are inside the worm, and therefore protected from the immune system’s attack, enough are exposed to keep the attack going, causing long term damage to host tissues but never wiping out the bacteria.

New evidence reveals that, meanwhile, our own immune cells targeted at Wolbachia shield the worm from the immune system like an invisibility cloak. The immune system doesn’t see the worm for the bacteria. So in essence, this is Wolbachia’s game: it uses Onchocerca to evade our immune defenses and causes river blindness. What we have here is not a horrible worm that uses human bodies and bacteria to provide its every need while unleashing dreadful disease on millions. What we have is a bacterium that uses a worm like a fortress to protect it while IT causes dreadful disease. It looks like the worm might be innocent.

University of Liverpool “Study sheds new light on river blindness parasite” January 12, 2011

Welsh, Jennifer. “River Blindness Parasite Relies on Bacteria to Fool Host” LiveScience Jan 19, 2010

Tuesday, 18 January 2011

Social Parasites: Trypanosomes Co-operate

We usually don’t think about the organisms that live on us, or in us, communicating or co-operating with each other. At least, I don’t. They use nutrients to grow, to reproduce, to spread. They may move around; they may mate, or simply divide by binary fission, but one hardly imagines them saying to each other “let’s go see what we can find over there,” or “we’ll work together to get past these host defenses.”

Of course they don’t literally have these conversations, but scientists are discovering that many organisms, even single celled ones, communicate with each other for the benefit of all. A recent article published by Medical News Today describes new research findings for Trypanosoma brucei, agent of African sleeping sickness.  Researchers have found that individuals of this species work together as a group to exploit their environment and likely do so to survive and invade tissues in the host.

That’s fascinating on several levels. First, it casts the enemy in a new light – it makes the invader somehow more easily understood from an anthropomorphic point of view (one should not attribute human qualities to protozoa, but it does feel comfortable - more comprehensible -  to think of them in these terms sometimes). It implies, too, that these life forms don’t get enough respect for their complexity and sophistication.

Second, it reminds us that there is still much we don’t know about many familiar species. African sleeping sickness has been a major health concern for well over a hundred years, and yet we’re only starting to understand the organisms that cause it. Finally, as the researchers have pointed out, knowledge like this may lead to better ways to prevent or treat the infection. Know the enemy.

Did I mention they’re beautiful? This is how they can look if they're co-operating on culture media.

[caption id="attachment_223" align="aligncenter" width="300" caption="Creative Commons Attribution 2.5, Oberholzer et al."][/caption]

Oberholzer M, Lopez MA, McLelland BT, Hill KL, 2010 “Social Motility in African Trypanosomes.” PLoS Pathog 6(1): e1000739. doi:10.1371/journal.ppat.1000739