Friday, 13 September 2013

Richard III of England and the Worms That Died With Him

King Richard III was buried under
what is now a parking lot, worms
and all. Image by Chris Tweed;
CC BY-SA 2.0

“The worm of conscience still begnaw thy soul!

So Queen Margaret curses the future Richard III in Shakespeare’s play Richard III. Though it’s not clear just how many worms of conscience the real Richard took with him to the grave, it seems some impressive intestinal worms did die with him.

King Richard III Had Worms

Remains identified as those of Richard III were recently discovered in Leicester, England. This in itself is an impressive piece of archaeology, but it gets more interesting for the parasite enthusiast: soil samples collected from beneath the pelvis of the remains contain eggs characteristic of the large intestinal roundworm: Ascaris lumbricoides, a worm that looks superficially like a large earthworm, and can grow to over a foot long. According to Roberts and Janovy, a female A. lumbricoides can produce 200,000 eggs a day.

Because soil samples taken from near the skeleton’s head, and samples taken more distantly from the remains don’t provide the same picture, it’s a fair conclusion that the eggs came from the decaying remains of the slain king and his worms. Realistically, given the period in which he lived, it isn’t surprising that those distant soil samples did contain a rare egg, and it would have been surprising if poor Richard didn’t have the parasites.

Eggs of Ascaris lumbricoides have been recovered from other archaeological sites in England dating back to at least 2600 years ago, so we know the worms were well established long before the Plantagenet dynasty came on the political scene there. The eggs are tough and resistant to harsh environmental conditions, and the toilet habits in medieval England were not exactly fastidious. The urban environment would have been widely contaminated with human feces.

The garderobe at Peveril Castle, Derbyshire, England was
typical of the concept: everything simply fell out of the
chute, sometimes into a pit, sometimes just onto the ground
outside. It was better than nothing. Image by Dave Dunford.

Between Gardyloo and the Honey Pot Men

Early medieval communities had household cleaning rituals we find less than charming today, such as tossing the contents of chamber pots out through the window onto the street. The cry of “gardyloo!” an English adaptation of the French gare l’eau, or “beware the water,” warned passersby to step out of the way (especially in Scotland).

By Richard’s time, many people did have garderobes (closets where they went to relieve themselves) and cess pits where the waste collected. There was less rank sewage lying around in the street, but hand washing wasn’t stressed, cess pits overflowed, and surface water was contaminated.

By the 19th century, honey pot men, or night soil men collected the sewage of cities and towns and sold it to farmers as fertilizer. This practice, too, would tend to spread intestinal worm eggs around on vegetables, but according to Alan Macfarlane, it was not common in the 15th century.

Worm Eggs, Dirty Water, and Dirty Hands

Richard III did not catch his worms directly from other people: the eggs require a couple of weeks in the right conditions to be infective. And he didn’t catch them as a child and simply keep them till the age of 33: A. lumbricoides worms only live about two years. No, he probably continually reinfected himself throughout his life by swallowing the infective eggs courtesy of contaminated food, water, and fingers.

"If thou hadst fear'd to break an oath by (God),” Queen Elizabeth says to Richard in Shakespeare’s play, "both the princes had been breathing here, which now, two tender playfellows to dust, thy broken faith hath made a prey for worms."

Today, children are the group best known for putting dirty fingers in their mouths, and for having worms, but given the poor hygiene of Richard III’s day, everyone probably had A. lumbricoides then. Though they weren’t quite the worms Elizabeth was thinking of, she might have been pleased to learn that Richard was prey for worms as well, and that he’d be remembered for them hundreds of years later.




Cheng, Maria. 2013. “Richard III's Worms of Discontent: Experts Say Hunchback English King Infected With Parasite.” The Associated Press. Accessed Sept 9, 2013.

Goble, Peter. “Honey Pot Men of South Stockton.” Delta Tech Systems Inc. Accessed Sept 9, 2013.  

Macfarlane, Alan. 2002. "The Non-use of Night Soil in England." Accessed Sept 9, 2013

Roberts, Larry S., and Janovy, John Jr. 2009. Foundations of Parasitology. Boston: McGraw Hill.

Wednesday, 28 August 2013

The Decline of the Screwworm Fly – Edward Knipling vs Cochliomyia hominivorax

Hundreds of screwworm larvae can infest
a single wound, doing unspeakable damage
and often causing death. Image courtesy
of the US Agricultural Research Service.
In July 2013 a British woman came to the attention of both the medical community and the media when she returned from Peru with maggots in her ear. The fly larvae had created a cavity connected to the ear canal and were feeding on healthy tissue in Rochelle Harris's head.

According to a Medical Daily story by John Ericson, Harris endured “unbearable pains emanating from one side of her face, pains that were eventually accompanied by menacing scratching sounds from inside her head” ("British Woman Discovers Flesh-Eating Maggots Inside Her Ear," July 16, 2013).

This is a horrific story, and many people reading it will have heard of the dreaded New World screwworm fly – Cochliomyia hominivorax - for the first time. In North America, too, we're unfamiliar with the fly - we've forgotten that it once infested the southern United States, spreading northward each summer as far as Canada. If not for entomologist Edward Knipling, it might still plague us, as it does parts of South America.

Edward Knipling Meets the Screwworm Fly

As a boy in the early 20th century, Edward Knipling worked long hours on his parents' Texas farm. There he encountered all manner of insect pests, including the maggots of the screwworm fly, which infested healing umbilical cords of newborn animals and any other open wound that the female fly could find.

Left alone, screwworm maggots feed on healthy flesh, quickly turning a small wound into a large, spreading one, and the odor generated by their activities attracts more female flies to lay their eggs. Infested animals often die. Humans aren't immune, with infested wounds and nasal sinuses most often reported.

According to biographers Adkisson and Tumlinson, Knipling “decided at an early age that he wanted to make a bigger contribution to agriculture than treating screwworm infested calves or pulling a sack down a cotton row” ("Edward F. Knipling, 1909 – 2000; Biographical Memoirs"). But Knipling likely had no inkling that his contribution would be to discover a way to eradicate C. hominivorax from the United States, Central America, and even Libya, in Africa, where it was accidentally introduced in the 1980s.

Knipling and the Idea of Screwworm Eradication

Edward Knipling combined scientific
knowledge and innovative thinking
to pioneer the sterile insect
technique. As a result, the screwworm
fly has been eradicated from much of
its range. Image courtesy of the US
Agricultural Research Service.
Edward Knipling sought a science career in entomology, ultimately earning a PhD in entomology from Iowa State University. During his studies, the United States recorded thousands of cases of screwworm infestation in livestock annually; some years saw hundreds of thousands of cases. The occasional human infestation occurred as well. Screwworm caused serious agricultural losses and horrible human illness.

By 1937 Knipling was studying the life cycle of C. hominivorax with colleague R. C. Bushland, and  the two made an important observation: female screwworm flies mate only once. Knipling knew that  he might be able to turn this against the pest, but the puzzle of just how one might use it to advantage had to wait until the end of WWII, when he had time to return to it.

Adkisson and Tumlinson write that Knipling thought “that if male flies could be produced in large numbers, sterilized, and released into the environment they might out-compete... the wild fertile males in breeding with females... If a sufficient number of sterile males could be released into the wild population," Knipling thought, the sterile males might “breed the screwworm population into extinction.”

How to Sterilize a Screwworm Fly

Knipling's idea raised two questions: how do you sterilize a male screwworm fly without damaging it in other ways, and how do you rear large numbers of screwworm flies in the laboratory? He knew that radiation could render insects sterile because of work done on fruit flies.

Now working in Washington DC, Knipling couldn't do the experiments himself, but Bushland, still in Texas, took it on. With scarce resources himself, Bushland had to innovate: he used X-ray equipment at the Brooke Army Hospital in San Antonio, Texas, to investigate sterilization, by trial and error. Meanwhile, Knipling worked on determining just how many sterile male flies were needed.

Bushland had already devised a laboratory diet for raising screwworms; now he, and others, worked to modify it to make it cheaper and better suited to mass production. The final test would be trials to see if  the sterile male approach actually worked.

The screwworm fly, Cochliomyia hominivorax is
aptly named: hominivorax means man eater.Image
courtesy of The Mexican-American Commission
for the Eradication of the Screwworm.
Screwworm Eradication in the United States

The first screwworm eradication trial took place on Sanibel Island, off the coast of Florida. Researchers released 39 sterile males per square kilometer each week for eight weeks, and saw the screwworm population drop off to virtually zero; however, screwworm flies continued to migrate from the mainland, so the island wasn't rendered screwworm free.

A second trial on the island of Curaçao in 1954 used four times as many sterile flies, and eradicated C. hominivorax in just three and a half months. The method worked.

The years that followed saw the construction of large facilities devoted to producing millions of sterile screwworm flies, and eradication programs, beginning in Florida. Cochliomyia hominivorax was eradicated in Florida in 1959; the process took longer in southwestern states because of continual reintroduction from Mexico, but the US was free of screwworm by 1982.

Screwworm Eradication in Central America

By 1984, there were no screwworm flies north of the Isthmus of Tehuantepec in southern Mexico, and today Central America is screwworm free all the way to the Panama - Columbia border.

Affected countries in South America are now using integrated pest management, including active surveillance, insecticides, chemical attractants and traps, and the sterile male technique to control and, one day, eliminate C. hominivorax from the last of its range.

If Rochelle Harris returns to Peru when she's older, she might not have to worry about another encounter with the screwworm fly, but if she does meet it again, she'll be ready. John Ericson quotes her, after her ordeal: "I'm no longer as squeamish as I was about bugs," she [says] "How can you be when they've been inside your head?"

Additional Reading

Adkisson, P., Tumlinson, J. 2003. "Edward F. Knipling, 1909 – 2000." Biographical Memoirs. 83.

Ericson, John. Jul 16, 2013. "British Woman Discovers Flesh-Eating Maggots Inside Her Ear." Medical Daily.

Mastrangelo, T., Welch, J. B. 2012. "An Overview of the Components of AW-IPM Campaigns Against the New World Screwworm." Insects. 3.

Novy, J. E. 1991. "Screwworm Control and Eradication in the Southern United States of America." In: New World Screwworm Response to an Emergency. World Animal Review. Special issue.

Tuesday, 27 August 2013

Cryptosporidium: A Parasite That Gets Into Drinking Water and Swimming Pools

Swimming pools become contaminated with infective
oocysts of Cryptosporidium when ill people have
accidents in the water.
Image courtesy of the US Dept of State.
Cryptosporidium spp. are tiny parasites that cause outbreaks of diarrhea. Contaminated drinking water is a common source of cryptosporidiosis, but there are others, including swimming pools and food.

At least two species of Cryptosporidium infect humans, and they are increasingly familiar causes of outbreaks. In recent years, online searches have constantly turned up swimming pool closures and boil water orders attributed to Cryptosporidium. Such outbreaks may indeed be more common; we may be getting better at identifying the parasites in outbreaks; and it may be that Internet reports mean that more people hear of it – all three factors likely play a part in the raised profile of these parasites.

When Cryptosporidium contaminates a municipal water supply, it can make many people sick at once, and this happens relatively easily because of the parasite’s small size and its ability to survive chlorination.

An oocyst (pronounced oo-oo-cyst) of  Cryptosporidium sp., the infective stage of the organism, is spherical and only about three to five one-thousandths of a millimetre wide. Environmentally resistant, it survives cold, chlorination, and salt water. It’s found in surface waters all over the globe - municipalities that use surface water supplies must do more than chlorinate water to avoid an outbreak. Most rely on filtration.

In the summer of 2013, an outbreak of cryprosporidiosis in Baker City, Oregon highlighted the risks of unfiltered water supplies, even when the watershed appears pristine. Even municipal water filtration systems can famously fail - more than 300,000 people got cryptosporidiosis in Milwaukee in 1993 due to inadequate treatment and filtration. In terms of numbers, a contaminated water supply is the most common source of human infections, but how does Cryptosporidium get into the water, and how else can we catch it?

Cryptosporidium in Livestock

Dairy and beef cattle suffer from and spread Cryptosporidium parvum. Young calves catch it and suffer severe diarrhea, while older cattle continue to carry the parasite and spread it. Runoff from pastures into rivers and wells after heavy rain is an important source of Cryptosporidium in surface waters. Ranched elk and bison also spread the parasite.

Cryptosporidium in Human Sewage

Untreated sewage from human communities often contains oocysts of Cryptosporidium. When sewage effluent is discharged into bodies of water without proper treatment, as it frequently is, especially after rainfall when treatment plants are overwhelmed, oocysts are discharged with it.

Canada Geese and other water birds could potentially
spread Cryptosporidium from cattle pastures to
distant surface waters.
Image by Robert Lawton; CC BY-SA 2.5.

Cryptosporidium in Wild Animals

Many species of wild animals can be infected with Cryptosporidium parvum, one of the species that infects humans. Dogs, cats, goats and mice are among them. Although this does not appear to be a significant source of water contamination, migratory birds may be a different story.

Cryptosporidium parvum is known to pass unharmed through the gut of a Canada goose without making the bird sick. Thus a goose can ingest millions of oocysts while pecking corn kernels from cow dung in Maryland, and discharge them into a watershed in Pennsylvania. It’s not clear how much geese and other migratory birds contribute to the spread of Cryptosporidium.

Direct Person to Person Spread of Cryptosporidium

Oocysts of Cryptosporidium are infective as soon as they are passed in stool. Thus, an infected person can pass on the parasite with dirty hands or objects contaminated with feces. Likewise, infected animals can pass the infection directly to other animals or to humans.

Cryptosporidium in Swimming Pools

It’s fairly common for swimming pools to become contaminated with Cryptosporidium - sometimes people go swimming and have minor “accidents” in the water, or feces work their way out of leaky diapers. Chemical treatment of swimming pools must reach high concentrations in order to kill the oocysts and pool filtration systems cannot remove them —or at least not fast enough to prevent some swimmers from swallowing some with a mouthful of water.

Food and Cryptosporidium


Food items can potentially be contaminated with oocysts of Cryptosporidium, particularly produce that has been irrigated with contaminated water. Because of this, and other disease-causing organisms that may be present, produce that will be eaten raw should be thoroughly washed.

Oocysts of Cryptosporidium have been found in oysters along the eastern seaboard of North America where human sewage effluent and runoff from agricultural lands flows into the ocean, probably because . oysters feed by filtering nutrients from the water around them. Eating raw oysters or other raw shellfish is, therefore, a potential source of cryptosporidiosis.

Though it is more common in warm climates,  Cryptosporidium is found in surface water everywhere - never drink untreated water and heed any boil water advisory issued by your local water utility.


Alberta Government. “Relationship Between Beef Production and Waterborne Parasites (Cryptosporidium spp. and Giardia spp.) in the North Saskatchewan River Basin.” Agriculture, Food and Rural Development. Apr 2006.

Graczyk, T. K. et al. “Giardia sp. Cysts and Infectious Cryptosporidium parvum Oocysts in the Feces of Migratory Canada Geese (Branta canadensis).” Applied and Environmental Microbiology 1998 Jul; 64(7), pp. 2736-8.

Roberts, Larry S. and John Janovy Jr. Foundations of Parasitology 8th Ed. Boston: McGraw Hill, 2009.

Terrey. Lynn. “Goats Not Behind Baker City Parasite Suspected of Sickening Thousands, Officials Say.” Oregon Live: The Oregonian; Aug 21, 2013 Accessed Aug 21, 2013.

Friday, 23 August 2013

Angiostrongylus vasorum - Canine Lungworm Larvae in Snails, Slugs, and Slime

Is this the face of a killer? This slug, Arion rufus, has
been shown to carry Angiostrongylus vasorum larvae.
Image by Guillaume Brocker; CC BY-SA 3.0.

The roundworm Angiostrongylus vasorum goes by many common names: canine lungworm, canine heartworm, French heartworm – all descriptive labels acknowledging the fact that the adult worms reside in the heart and pulmonary artery (the blood vessel that carries blood from the heart to the lungs) of domestic dogs and wild canine species.

Life Cycle of Angiostrongylus vasorum

The life cycle of A. vasorum is complex:
  • Adult worms produce eggs that are carried to the lungs by the blood circulation.
  • The eggs hatch in the lungs, releasing larvae, which break through into the air space of the lungs, travel up the airways to the throat and are swallowed.
  • Passing through the intestine, larvae are deposited in the environment with feces.
  • Slugs and snails feeding on dog feces either ingest the larvae or the larvae penetrate the mollusk’s foot and undergo further development in the mollusk’s tissues.
  • Infective larvae are released in the slime secretions left behind by snails and slugs, or are ingested with the mollusk when it is eaten by something (frogs, dogs, etc.)
  • It is thought that dogs swallow the larvae and become infected when they eat snails and slugs, when they eat frogs or other animals that have eaten infected snails and slugs, or when they eat or lick things that are contaminated by slug or snail slime.
  • Larvae migrate to lymph nodes, where they develop further, and then move to the heart and pulmonary artery.

Dogs Eat Snails and Slugs

Dogs eat slugs and snails, and frogs. While many dog owners will readily agree with this statement, it leaves others, like me, scratching our heads.

Would my dog eat a slug or snail? She has never shown the slightest interest in doing so (and there are lots where we live).

Would she eat a frog? Sniff it maybe. Play with it maybe. Step on it by accident; yes, I’ve seen this. Eat it? No.

Would she eat a food item left lying on the ground and possibly crawled over by slugs and snails (or with slugs and snails still on its surface)? Definitely.

And that is one of the reasons why I was particularly interested in this video of the movements of snails in a British garden at night.

I had no idea they traveled so far and so fast.

Risk of Angiostrongylus vasorum Infection

A lot is still unclear about A. vasorum.  We don’t know what the most common route of infection is: snails, slugs, slime, frogs etc. We don’t know how many dogs have the parasite but exhibit no symptoms. We don’t know how many larvae a dog would need to ingest to become ill.

And of course, different species of slugs and snails are likely to differ in the distance they travel and the number of larvae they leave in their wake. Clearly, however, wherever A. vasorum occurs, all dog owners should take the threat seriously. As Eric Morgan et al write, the infection “is associated with coughing, dyspnoea [shortness of breath], exercise intolerance, weight loss, vomiting, abdominal pain, lumbar pain, neurological signs, heart failure, bleeding diathesis [tendency to bleed], and sudden death.”



Barcante, Thales Augusto, et al. "Angiostrongylus vasorum (Baillet, 1866) Kamensky, 1905: emergence of third-stage larvae from infected Biomphalaria glabrata snails." Parasitology Research 91.6 (2003): 471-475.

Fletcher, Damien. "Snails Can Travel at One Metre an Hour and Piggy-back on Others' Slime to Save Energy." Mirror News. Aug 23, 2013.

Morgan, Eric R., et al. "Angiostrongylus vasorum: a real heartbreaker." Trends in Parasitology 21.2 (2005): 49-51.

Thursday, 22 August 2013

Bed Bugs in New Products, Retail Stores, Imported Goods

In his Aug 22, 2013 blog post for the Huffington Post, Andrew Rennie describes a bed bug encounter. “Plainly visible on our brand-new sheet set, purchased at a big-box retail chain,” he writes, “was a bed bug. Dead, thank God, but its tiny, contorted legs twisting skyward still filled me with… dread” ("Parasites and Profiteering," Huffpost Living). 

Yes, that would fill me with dread as well. Suddenly we’ve gone from “don’t buy (or otherwise salvage) used furniture” to “nothing is safe.” Even brand new products, apparently, straight from the store, can be infested with bed bugs. 

At its actual size – about 5 millimeters long – this female bed bug would resemble other insect species to the untrained eye. Image by Gilles San Martin from Namur, Belgium. CC BY-SA 2.0

Where Bed Bugs Come From

Rennie’s post was not about bed bugs: it was about lousy customer service, and on
that topic I agree with him one hundred percent. By the time I finished reading, however, I was more focused on the whole bed-bug-in-the-new-sheets thing. How ironic – that an adult bed bug would be found neatly packaged in sheets that had never seen a bed! Sort of like getting a free sample of dishwasher detergent with your new dishwasher... only, not.

I wonder, was that bug identified as a bed bug by someone who really knows their bugs? An awful lot of insects look superficially like a bed bug (and if those sheets were imported, we’re not just talking North American insects). If the bug had turned up in a box of cereal, would it have been a weevil? Or a grain beetle of some kind? If it had arrived in a flower pot from the local garden center, would Rennie have given it a second glance? What's the probability that new sheets are now coming complete with a bed bug infestation?

It’s not impossible that Rennie’s nemesis was a bed bug. Bed bugs certainly can travel in shipments from other countries. Bed bugs have been found in retail stores. They could be present in a sheet factory, sure, but unless the employees of that factory are sleeping there too, you wouldn’t expect that to be a very happy home for a bed bug – lots of places to hide when the lights are on, granted, but not much to feed on in the dark.

Bed Bugs in Retail Stores and Products

Bed bugs can’t recognize new sheets as pay dirt and plan ahead. They don’t know an unused sheet from a windsock, a pillow from a bag of marshmallows. It’s us they recognize, not items we have never used. A dead bug in a package of new sheets is no more likely to be a bed bug than one in a package of computer paper.

The University of Minnesota tells us where bed bugs are most likely to be found in a clothing store (unsurprisingly, they don’t specifically mention the linen department of a big-box store). High-risk locations include fitting rooms, returns areas, seating areas, cloth bags attached to shopping carts etc. These locations have something in common: they are exposed to the (used) clothing and belongings of numerous people who could potentially bring bed bugs into the store ("Let’s Beat the Bed Bug," 2012).

As David Emery points out in Urban Legends: “Email: Bedbug Infestations Due to Imported Clothing,” imported products have not been associated with bed bug infestations in retail stores (, 2010). Similarly, unused manufactured products are unlikely to introduce bed bugs into our homes. 

Is it a Bed Bug? Be Sure

Anyone who suspects they have found a bed bug should have it properly identified before spending time and money on a problem that may not exist. I suspect Rennie’s “bed bug” was an innocent look-alike, left with “its tiny, contorted legs twisting skyward” when it got caught up in whatever process folds new sheets and jams them into plastic packaging.

Wednesday, 21 August 2013

Manure and Latrines = Farming and Parasites

Pig sties are notoriously smelly places, but aged
pig manure makes excellent fertilizer.
 Image by MontagZen; CC BY-SA 3.0.

Almost twenty years ago, Jared Diamond wrote about the domestication of plants in Discover  ("How to Tame a Wild Plant," Sept 1994). "Human latrines," he wrote, "may have been a testing ground for the first crop breeders."

How so? Many plants get spread around when their seeds are eaten, passed through the digestive tract of the forager intact, and deposited in feces. Because humans tend to use latrines - designated outdoor toilets that they return to again and again - the seeds of the plants that early humans liked to eat got deposited in a concentrated area, and the wastes deposited with them provided fertilizer. Voila! Latrines would have effectively selected the choicest food items of early humans and aided their reproduction.

Because I'm interested in parasites, I couldn't help thinking that this very process also aided the transmission of intestinal parasites: choice food plants growing in areas used as latrines means people gathering food there, with resulting exposure to the eggs and larvae of intestinal worms (and probably protozoa as well).

"Our ancestors' garbage dumps," Diamond pointed out, "undoubtedly joined their latrines to form the first agricultural research laboratories." This, because larger seeds, roots and other plant parts that might reproduce would end up in the midden, or garbage dump, along with all the other food waste (think compost) and animal manure (if they had livestock), gaining a survival advantage in virtually the same way.

And now, in his article "Early Farmers and Manure: Stone Age Europeans Were More Advanced Than We Thought," (Decoded Past, July 3013) Frank Beswick reports on evidence that stone age people used animal manure as fertilizer as long ago as 6000BC. Beswick wonders "is it possible that the use of manure was a precondition of the development of agriculture?"

And I wonder how much it contributed to the parasites we share with domestic animals, particularly cattle and pigs.

Monday, 1 July 2013

The Candiru vs Peer Review

This is reportedly a candiru.
       It's a big one.
Image by em_j_bishop: CC BY 2.0

I think sometimes our faith in a system, and our love of a colourful story, deadens our common sense. Take the candiru, for example – Vandellia spp., the vampire catfish.

“This little charmer normally lives inside the gills of other fish to suck their blood, but is attracted to urine and reputedly able to wriggle up human's urinary tracts, where it lodges itself with sharp spines and can only be removed by surgery.”


The quote above came from the 2002 Lonely Planet guide to Brazil (pg. 75). First of all, these little catfish do not live in the gills of their fish hosts. They visit there to feed for all of about two minutes – more like a mosquito, really, than a parasite.

There is no scientific proof that they are attracted to urine. If one ever wriggled up a human urethra it wouldn't lodge itself so much as become stuck as a result of those spines, designed for a different situation entirely. Finally, there is only one published case – semi-documented and unconfirmed – and it was reportedly resolved by cystoscopy rather than surgery. (Samad, Anoar. "Candiru Inside Urethral." Urology Clinic.)

The Candiru in Academic Literature

While we'd like to expect better of Lonely Planet, it's only fair to excuse this case of bad information – the candiru has been reported widely and legitimized in publications that normally hold themselves to an even higher standard. For example:

  • From The New Encyclopedia Britannica 15th ed. Vol 2. (1990): “... parasitizes man and has been known to enter the urethras of bathers and swimming animals. Once inside the passage, it erects the short spines on its gill covers and may thereby cause inflammation, hemorrhage and even death...” (“Candiru”).
  • From a 1991 article by J. L. Breault in the Journal of Wilderness Medicine (2): “Forced extraction may cause lacerations of the urethral mucus membranes, which has caused death by exsanguination. Remedies have ranged from penile amputation and suprapubic cystostomy to application of a native herb that softens the spines” (“Candiru: Amazonian Parasitic Catfish”).

Judging by these sources and others published by academic presses and peer reviewed journals, subject as they are to editorial scrutiny, peer review, and fact checking, one would think that the consequences of a personal encounter with the candiru were well documented medical knowledge.

The library website at the University of Victoria says “Peer review ensures that an article-and therefore the journal and the scholarship of the discipline as a whole-maintains a high standard of quality, accuracy, and academic integrity. When you consult peer-reviewed sources, you are tapping into a wealth of established, verified knowledge” (, accessed July 1, 2013).

A 2013 Review of the Evidence for Candiru Attacks

Nonetheless, Dr. Irmgard Bauer, in her 2013 investigation of two centuries of literature describing the candiru, found little in the way of verification. “...most reports are...repeated again and again,” she writes, “based on the same stories already described elsewhere... After careful distillation, very little [evidence] remains and of that little, even accounts sounding like first-hand descriptions become suspect.” (“Candiru – A Little Fish With Bad Habits: Need Travel Health Professionals Worry? A Review.” Journal of Travel Medicine; 20:2.)

What happened here? In 200 years, did no one go to the trouble to verify candiru reports until now? The candiru is like the Sasquatch's rich city cousin: in contrast to the Sasquatch, consistently disinherited by science because there is no evidence for it, the candiru has been repeatedly legitimized by science and reputable publishers despite the lack of evidence. All we really have for sure is a translucent little fish that takes a blood meal from a fish larger than itself, and a bunch of anecdotes. It really isn't even a parasite.

And we wonder why it's important to consult original sources?

I wrote about what we know about the Candiru for Decoded Science: "Candiru- A "Don't Pee in the Water" Horror Story Debunked."

Wednesday, 12 June 2013

Parasites and Networks - Food Webs, Epidemiology

When we think about how parasites fit into nature - their close interaction with their hosts, their reliance on specific hosts in a specific sequence, their ubiquitous presence in the environment - a network (or web) context makes sense. Recently, two articles  have come to my attention; they represent parasites in webs in similar ways but for different reasons.

Parasites Affect Food Webs

This food web for a mosquito would be much
more complex - and of much more relevance
to humans - if it included parasites.
Illustration by Tyler Rubley. CC BY-SA 3.0



The first is "Parasites Affect Food Web Structure Primarily Through Increased Diversity and Complexity." by J. Dunne and co-authors (PLoS Biol 11(6): e1001579), published on June 11, 2013. These researchers added parasites to aquatic food webs and asked whether the changes that resulted (a much more complex food web) could have been caused by the addition of any large group of organisms, or whether food web structure was altered by parasites in unique ways.

Beyond the central findings of that study, the article raised (or re-raised) a question for me: if we know that parasites are an important component of an ecosystem, if we know that they affect food webs in both generic and unique ways, why do they never appear on endangered species lists? For every endangered species, there should be a list of parasites that depend on that host species for survival. And why do conservationists routinely rid endangered animals in captivity of their parasites, knowing that if that species ever returns to the wild, it will do so without its specialist parasites, potentially to its detriment?

Parasites Predict Disease


The other paper is "Centrality in Primate–parasite Networks Reveals the Potential for the Transmission of Emerging Infectious Diseases to Humans" by José María Gómez and co-authors , published in PNAS (110:19 2013).  Like the paper by Dunne et al, this research builds a food web, but this web has parasites as the main consumers - a network of nonhuman primates that share parasites (or that are consumed by the same parasites, to look at it from the parasites' viewpoint).

The point is to examine whether this web can predict where diseases of primates are likely to jump to humans. The authors "found that primate species having higher values of centrality in the primate–parasite network harbored more parasites identified as EIDs [emerging infectious diseases] in humans and had parasite communities more similar to those found in humans." These species, then, are more likely to be the source of emerging infectious diseases in humans. Another good reason to include parasites in food webs.

Food webs tell us where parasites fit, and I think that is something we really need to understand, for our own sake and for theirs.

Friday, 22 March 2013

Disseminated Strongyloidiasis - Interesting Things to Note

A recent case of disseminated strongyloidiasis, reported by the New England Journal of Medicine highlighted a couple of intriguing features of this catastrophic disease: in the absence of an effective immune response, worms can mature in the lungs as well as the intestine, and, there's something special about corticosteroid drugs that makes an unfortunate success of the worm.

Adult Strongyloides stercoralis in the Lungs

The case report of disseminated strongyloidiasis by Schroeder and Banaei describes adult worms, both rhabditiform and filarifom larvae, and ova containing active larvae in a tracheal aspirate. A similar case is reported by Bava et al. Typically, you'd find only filariform larvae in the lungs, and adults are almost never seen, even in the stool, because the adult females spend their time migrating through the tissues of the intestinal lining (and there are no parasitic males).

A larva of Strongyloides stercoralis. At a later stage, this larva would
be capable of penetrating and migrating through tissues like skin, or the
lining of the intestine. Image: CDC

I assumed that the adults found in this case had actually matured in the lungs rather than migrating there from the intestine. A 2004 paper in Clinical Microbiology Reviews agrees. Keiser and Nutman write “...findings suggest that filariform larvae develop into adults in the lungs... This hypothesis is supported by... autopsy studies showing adult worms in lung tissue.” In this scenario, the parasite could be multiplying very rapidly with new worms originating not only in the intestine, but in the lungs as well. One can only imagine the numbers of parasites that could be present within a short period of time.

Corticosteroids and Strongyloides stercoralis

We know that corticosteroids can initiate disseminated strongyloidiasis. But do they just give the worms a green light by suppressing immune response, or do they actually favor the parasite? Corticosteroids prevent production of eosinophils and cause the rapid destruction of eosinophils that already exist; these cells are part of the body's immune response to parasites. But it's thought that corticosteroids actually contribute to the success of S. stercoralis in another way. Gary Simon writes in Medical Parasitology that “they may stimulate female worms to increase larval output and promote molting of rhabditiform larvae into the invasive filariform larvae.”

Eosinophils in the blood are part of the
immune response to parasites. Image by
Iceclanl. (cropped)  CC BY-SA 3.0

So it looks like giving corticosteroids to a patient with S. stercoralis expands the “territory” in which the parasite can reproduce, hobbles the immune system's attempts to control it, and boosts the worms' fecundity and maturation. Given all of this, it's easy to see why it might be difficult to save a patient suffering from disseminated strongyloidiasis, unless the problem is discovered quickly. It also sheds some light on why other types of immunosuppression are relatively less catastrophic.



Bava  BAJ, Cecilia D et al. “Adult Female of Strongyloides stercoralis in Respiratory Secretions.”, Asian Pacific Journal of Tropical Biomedicine 3:4, April 2013, Pages 311–313

Keiser PB, and Nutman TB. Strongyloides stercoralis in the Immunocompromised Population.” Clinical Microbiology Reviews. 17:1, January 2004, 208–217.doi:10.1128/CMR.17.1.208-217.2004

Castelletto ML, Massey HC Jr et al. "Morphogenesis of Strongyloides stercoralis Infective Larvae Requires the DAF-16 Ortholog FKTF-1." , PLoS Pathogens 5(4): e1000370. doi:10.1371/journal.ppat.1000370

Schroeder L, and Banaei N. Strongyloides stercoralis Embryonated Ova in the Lung.” New England Journal of Medicine: March 21, 2013; 368:e15

Simon, G. “Strongyloidiasis.” In: Medical Parasitology. Satoskar AR et al eds. Austin: Landes Bioscience; 2009, pg 31

Tuesday, 19 March 2013

Beauveria bassiana - A Fungus That Kills Bed Bugs

Beauveria bassiana is a fungus that is well known for killing insects. Spores of B. bassiana adhere to the cuticle (the outer protective covering) of the insect, begin to grow, and work their way through to the inner tissues. There the fungal growth continues, taking nutrients from the host's body until the insect dies. Because B. bassiana is lethal to many insects, including their larvae, it has been grown and distributed commercially for use in agricultural control of insect pests. It makes sense to wonder whether it could be used to control bed bugs as well.
Beauveria bassiana is grown for control of agricultural
pest insects. Image courtesy of Keith Weller.

Beauveria bassiana Kills Bed Bugs

A study by Alexis Barbarin et al tested B. bassiana against bed bugs, and the results indicate that the fungus is lethal to the pests: not only does it kill virtually all bugs that come in contact with it, infected bugs can carry it back to daytime hiding places and pass it on to other bugs that have not been otherwise exposed. Barbarin el al propose that B. bassiana might rid a bed bug infested building of its bugs.

Bed Bug Traps Using Beauveria bassiana

In their study, Barbarin et al exposed bed bugs to a mixture of oil and fungal spores on various surfaces, and found that jersey knit cotton transmitted the infection most effectively. Though further research is required, they propose that a fabric bed skirt impregnated with B. bassiana spores might be an efficient means of infecting a resident bedbug population. Presumably any trap designed so that all bedbugs climbing onto or leaving the bed would have to pass through it could be used to infect them with the fungus.

Is Beauveria bassiana Safe for Humans?

Beauveria bassiana is generally regarded as safe for humans and it's already being used for insect control applications all over the world without dire consequences for human health. This fungus is already naturally occurring in the environment. However, there's reason to be cautious with this approach. A study that tested fungi isolated from poultry barns found that B. bassiana has several virulence factors that potentially “increase [its] survival, growth, and propagation... in animal tissue.” Authors Taira el al comment, quite correctly, that otherwise harmless fungi can cause serious infections in people whose immune systems are already compromised. Such people include AIDS patients and organ donor recipients among others.

These grasshoppers were killed by Beauveria bassiana.
Fungal growth is visible on the insects' remains.
Image courtesy of Stefan Jaronski.

Cases of both deep tissue infection and skin infection caused by B. bassiana have been reported in the medical literature (Figueira et al). The possibility of skin infection, in particular, prompts second thoughts. Beauvaria bassiana does not wipe out bed bugs on contact: it takes time for the infection to kill. Therefore, bugs that have contacted the fungus will still visit the sleeping host to feed. And while feeding, they will create a break in the skin, often with severe irritation resulting, and possibly introduce fungal spores. This does not seem like a good plan.

Beyond the possibility of skin infection arising from contact with the bugs, a spore impregnated bed skirt would presumably contaminate a living space with fungal spores pretty thoroughly, and fungal spores are as hardy and as hard to eliminate as bed bugs are. Under the right conditions, they could remain viable for a very long time, possibly protecting against reinfestation by bed bugs, but also a potential hazard for the immunocompromised occupant of, or visitor to, the space.


Barbarin AM, Jenkins NE et al. “A Preliminary Evaluation of the Potential of Beauveria bassiana for Bed Bug Control.” Journal of Invertebrate Pathology 111 (2012) 82–85

Figueira L, Pinheiro D et al. “Beauveria bassiana Keratitis in Bullous Keratopathy: Antifungal Sensitivity Testing and Management.” European Journal of Ophthalmology 22:5 (2012) 814-818

Taira CL, Marcondes NR et al. “Virulence Potential of Filamentous Fungi Isolated From Poultry Barns in Cascavel, Paraná, Brazil.” Brazilian Journal of Pharmaceutical Sciences 47:1 Jan./Mar. 2011

Tuesday, 12 February 2013

Every Living Thing: A Book Review

Every Living Thing: Man's Obsessive Quest to Catalog Life, from Nanobacteria to New Monkeys
by Rob Dunn
Harper 2010 ISBN 978-o-06-143031-2

“The biological world does not revolve around us... life is smaller than we imagined, ...we are a smaller part of life than we imagined,” and we occupy a “marginal position in the biological universe” (Every Living Thing p. 59 - 60). With Rob Dunn, you know where we stand. But from that marginal position, he's written a fascinating book about the life we share our planet with, and the key people who've helped us learn what we know about that life.

I found Every Living Thing to be a eye-opener in two ways. First, it reminded me forcefully that in spite of all that we know, we still don't know much. For someone who once believed (albeit a very long time ago) that all the answers were out there – you just had to go to the right library and ask the right question – it was both bewildering and liberating to realize that what we don't know is actually in the majority. To contemplate the vast quantity of scientific knowledge stored in academic libraries and realize that it is only the beginning is truly shocking.

'Animalcules' illustrated by
Anton van Leeuwenhoek; c1795.
Second, Dunn has illuminated the lives and accomplishments of some people who are frequently mentioned only briefly, even in the most interesting science books. I knew that Antonie van Leeuwenhoek discovered Giardia lamblia when he observed it in his own stool by looking through his own glass microscope lenses. I did not know that he was the first person known to observe microscopic life of any kind; that he discovered two entire kingdoms of life; that he was a family man with five children. I didn't know that two scientists who changed the world in very different ways – Lynn Margulis and Carl Sagan – were actually married to each other at one time. The book is full of surprises like that.

If there is anything that makes Every Living Thing a challenge, it's frequent jumps through time and space, and from third to first person narrative. Far from being chronological, the narrative draws unexpected connections throughout. The reader who is fully engaged and paying close attention will be fine. Others may feel suddenly disoriented and have to retrace their steps to find out how they got from 1960s California to 1848 Brazil; from first person contemplation of becoming a father, to endosymbiogenesis. The connections are relevant; they clarify and enlarge the picture, but it is, at times, quite a ride.

Dunn has a talent for explaining complex science in a way that the general reader can understand and he combines this talent with great storytelling. This grounds the people he writes about in a context of everyday life we can all relate to, and results in a very interesting and relevant science book. It's easy to imagine that Every Living Thing will end up in the reference section of a lot of personal libraries, including mine.

At one time, I was a great fan of Stephen Jay Gould, but today I'd have to say that both in print and online, Rob Dunn is my favourite science writer. I hope this strong beginning is just the first of many fascinating science books.

Tuesday, 5 February 2013

Was Joshua the Hero Of Jericho? (Schistosoma and Jericho)

The Jordan Valley near Jericho.
From the OSU Special Collections
and Archives.
Reform Judaism Magazine has published an adapted excerpt from my book Parasites: Tales of Humanity's Most Unwelcome Guests. The excerpt is a shortened version of my retelling of the story of Rahab, Joshua, and the Battle of Jericho, with the blood fluke Schistosoma hematobium as a central character.
Reform Judaism Magazine is an interesting publication. The online version features a number of articles that would appeal to any reader: titles that caught my eye include "Were the Jews Slaves in Egypt?," "The Divinity of Dementia," and "A Paragraph that Changed History" ("Why Jesus' last supper could not have been a Passover meal..."). Fascinating.

It's my pleasure to be published in this magazine. You can read Was Joshua the Hero of Jericho? on the internet.

Thursday, 31 January 2013

Echinococcus multilocularis Liver Cysts in Dogs

Infected foxes spread Echinococcus
multilocularis to dogs.
Image by Andy Potter; CC BY-SA 2.0.
As any good parasitology text will tell you, liver cysts caused by Echinococcus multilocularis typically occur in rodents: animals like voles, lemmings, and mice. The disease is called alveolar echinococcosis, or alveolar hydatid disease, and it occasionally occurs in people too, if eggs of the tapeworm are accidentally swallowed.

Echinococcus multilocularis liver cysts in dogs

The liver cyst caused by E. multilocularis is a larval stage - a stage that multiplies asexually in the cyst. The adult stage of the parasite is found in canids, members of the dog family: arctic foxes, red foxes, jackals, coyotes, domestic dogs. Thus, the 2009 discovery of a liver cyst in a domestic dog in British Columbia, Canada (Jenkins et al.), is puzzling and alarming.

This scenario is not actually so bizarre. Taenia solium, or pork tapeworm, has a similar story: humans normally host the adult tapeworm in the intestine after consuming the larval cysticercus in undercooked pork. But if a human swallows the tapeworm egg instead, the eggs hatches and the larva moves into the tissues – sometimes the brain – and forms a cysticercus.

When humans have T. solium cysticerci in their tissues, the disease is called cysticercosis – or, in the brain, neurocysticercosis – and this can be much worse than having the tapeworm in the intestine. Clearly, in a dog, a liver cyst that can grow large enough to compromise liver function, and spread to other parts of the body, is worse than hosting a tapeworm in the intestine as well.

In cysticercosis in humans, and presumably alveolar echinococcosis in dogs, the tissue cysts often originate from the hosts own intestinal tapeworms. In humans, it’s poor hygiene and hand to mouth transmission. In dogs, it’s grooming – licking eggs off soiled fur. This raises the question: have dogs always frequently had the liver cysts when they had the worms or has something changed?

Echinococcus multilocularis spreading to new places

Jenkins et al. remark that “compared with native North American strains, European strains of Echinococcus multilocularis appear to have greater potential to cause alveolar hydatid disease (AHD) in humans.” The strain found in British Columbia was a European strain; perhaps they have greater potential to cause AHD in dogs as well. Do we know?

The British Columbia dog apparently did not have the adult tapeworm in its intestine and the authors speculate that the parasite may have been introduced by an imported infected dog. This, too, is alarming. It brings to mind my discussion of E. multilocularis in Parasites: Tales of Humanity’s Most Unwelcome Guests, in which I relate the identification of Echinococcus multilocularis in wild canids smuggled into the Eastern US for fox hunting.

If one imported dog can introduce the worm to British Columbia, what is the likelihood that many illegally translocated infected canids have not spread the worm as well? Is alveolar echinococcosis simmering in rodents, dogs, and people in the eastern United States?


Jenkins EJ, Peregrine AS, Hill JE, Somers C, Gesy K, Barnes B, et al. Detection of European strain of Echinococcus multilocularis in North America [letter]. Emerg Infect Dis [serial on the internet]. 2012 June.

Roberts, Larry S., and John Janovy Jr. Gerald D. Schmidt & Larry S. Roberts’ Foundations of Parasitology 8th ed. Boston: McGraw Hill, 2009. Pg 354-5.

Thursday, 24 January 2013

Echinococcus multilocularis and Alveolar Echinococcosis

The tapeworm Echinococcus multilocularis normally spends its adult life in the intestine of a fox, usually an arctic or red fox. The fox acquires the worm by eating an infected rodent. In turn, the fox passes eggs in its feces, which rodents accidentally eat. In the intermediate host (the rodent or, sometimes, a human) the parasite occupies the liver rather than the intestine.

Alveolar echinococcosis

The adult Echinococcus multilocularis tapeworm is very
small. The head (or scolex) of this one is to the right.
Image: CDC
In the liver, the larva forms an alveolar cyst, a cyst composed of thin-walled chambers that multiply until the parasitic growth looks a bit like a mass of bubbles. These bubbles may break away and be carried to other parts of the body where they continue to grow. This is one reason why the alveolar cyst of E. multilocularis is often likened to a malignant tumor.

This is a nasty parasite and published accounts of the course of the disease in humans are rather horrifying. It spreads and is difficult to treat. It’s often fatal. This one, you never want to get. The literature and the media, meanwhile, lend the distinct impression that E. multilocualris is spreading and cases of alveolar echinococcosis in humans are becoming more common.

Distribution of Echinococcus multilocularis


A map in a 1984 parasitology text showing the global geographic distribution of E. multilocularis suggests that the worm has not broadened its horizons much in the last thirty years. In 1984, its range included most of Asia north of 40º latitude, Central and Eastern Europe, northern Canada, coastal Alaska, and a patch right in the middle of North America bisected by the Canada – US border and by 100º longitude. Today the distribution is marginally wider: more of Central Europe, parts of Western Europe, and the patch in the middle of North America has grown as well. Sporadic cases appear in other far flung regions: northern Africa, British Columbia in Canada.

So E. multilocularis is perhaps creeping rather than sweeping around the northern hemisphere. In truth, human infections are still extremely rare. Alveolar echinococcosisis, however, is “emerging” in humans in European locations, and there’s concern that it might do the same in parts of North America (most North American cases in the past have been in Alaska). In a recent paper in PLOS Neglected Tropical Diseases, Nahorski  and others report that, in Poland, only two cases were known prior to 1980, compared with 121 cases diagnosed between 1990 and 2011.

Why is alveolar echinococcosis increasing?


Better diagnosis is certainly one reason for the increase, and Nahorski et al feel that many undiagnosed cases remain. They point to another possible cause however - a boom in the urban fox population. “In Poland,” they write, “the fox population increased from 67 000 in 1995 to 220 000 in 2006.” That’s a very significant increase, and many of the human cases came from provinces where the worm is especially common in foxes. The data led the authors to conclude that infected domestic dogs and cats are also important sources of the disease.

In order for a domestic animal to acquire the intestinal worm, the animal would have to eat an infected rodent. Cats, of course, are hunters, but according to the European Scientific Council Companion Animal Parasites (ESCCAP): “Cats, in contrast to dogs, are epidemiologically insignificant as sources of egg output as they are poor hosts for this worm.” Dogs are a different matter: they are good E. multilocularis hosts, and many domestic dogs do hunt. Many do not of course, especially urban dogs. One would have to know one’s dog to judge the relative likelihood that it would ever have E. multilocularis eggs in its feces, or on its fur.

Urban coyotes have little fear of people.
Image by Steve Jurvetson, Menlo Pk, USA;
 CC by 2.0
Do foxes live in North American cities like they do in Europe? It’s true we don’t often read or hear about this, but they do: the city of Mississauga is one municipality that has addressed the issue of foxes in the city. And if those urban foxes have E. multilocularis, that could contribute to the emergence of alveolar echinococcosis in humans. But in North America, we have another canid that likes to live in cities, and it, too, can harbour E. multilocularis: the coyote. A study of urban coyotes in Chicago concluded that there are hundreds, perhaps thousands of coyotes living in that city, and those researchers believe that “the results likely apply to most major metropolitan areas in North America.”

So, while there's no reason to be paranoid about this rare disease, awareness of it isn’t a bad thing. All the usual advice still applies: wash your hands often, keep your dog close, and provide your dog with good veterinary care including screening for intestinal parasites.


Beaver, Paul C., Jung, Rodney C., and Eddie W. Cupp. Clinical Parasitology 9th ed. Philadelphia: Lea & Febiger, 1984. Pg 534.

City of Mississauga. Animal Services: "Foxes." 1995-2013

ESCCAP. “Worm Control in Dogs and Cats: ESCCAP Guideline 01 Second Edition.” September 2010

Nahorski WL, Knap JP, Pawłowski ZS, Krawczyk M, Polański J, et al. "Human Alveolar Echinococcosis in Poland: 1990–2011." PLoS Negl Trop Dis 2013; 7(1): e1986. doi:10.1371/journal.pntd.0001986

Wagner, Holly. “On the Loose: Urban Coyotes Thrive in North American Cities.” Ohio State Research News. Last Updated 2005.

Wednesday, 9 January 2013

An Epidemic of Absence: A Book Review

An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.
By Moises Velasquez-Manoff.
Scribner; 2012 ISBN 978-1-4391-9938-1

“No matter who we are, we evolved with many more parasites and commensals, both large and small, than we generally encounter today. The implication—and let's face it, the hope—is that reestablishing contact with some of these organisms can rebalance the immune system.”

If Moises Velasquez-Manoff were to sum up his latest book, An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases, in under fifty words, the quote above would be a good choice (p. 61). In recent years, a growing number of researchers have explored the relationships between humans and the species that live with us—both those that cause disease and those that do not—and found evidence that we may be better of with many of them than without. Framing the information within his own experience of allergy and autoimmune disease, Velasquez-Manoff comes at this body of evidence from every conceivable angle, and by the last page one cannot help but be thoroughly convinced.

Studies show that regularly swallowing pig whipworm eggs
can alleviate symptoms of autoimmune diseases.
Image Bobjgalindo (enhanced) CC BY-SA 3.0

This topic, in the hands of someone suffering from allergies and autoimmune disease, could easily have come across as pseudoscience, but Velasquez-Manoff is meticulous about pointing out what is actually known through scientific research, and what is still theory or speculation. He deftly balances anecdotes with comments from reputable scientists and medical specialists, and his obvious grasp of the difficulties of proving causation lends the work great credibility. Similarly, his exploration of the “hookworm underground,” where individuals who are not medical professionals sell worm infestations to ill and desperate people, might have appeared sensational, but instead seems appropriate in the context of the narrative.

The examination of similar evidence from many different directions, however, occasionally makes one feel that the point has been made again. And again. By the time the author writes “Enough! What to do about it?” in the last chapter, the reader who has stayed the course is bound to breathe a grateful “yes!” This is not to say that the narrative is boring; it is not. But brevity is not its greatest charm.

One discussion in particular stands out from the rest of the book in both tone and relevance, and that is the author's detailed character assassination of Jasper Lawrence, one of the “hookworm underground” operators he meets. It's unclear why Velasquez-Manoff feels it's necessary to aim a stream of accusations – which may or may not be justified - at Lawrence. At best, Lawrence is anecdotal; he operates outside of mainstream medicine and doesn't contribute to the scientific literature. At worst, he's irrelevant. If the intent is to warn off anyone considering buying parasites from one of these companies, a clear explanation of the risks would have been a better choice.

An Epidemic of Absence is a good book about a subject that's likely to become more mainstream, and more important, as the science progresses. If you read nothing else, read the last chapter for the essence of the book. Then, if you want to understand it all thoroughly, start at the beginning and read the whole thing.