Toxoplasma gondii - Andrew Alexander’s Terrifying Parasite

“I felt like Frankenstein,” Alice Smellie quotes Andrew Alexander in the MailOnline. The Downton Abbey star apparently picked up a “terrifying” parasite more than a year ago and waited months for a diagnosis. When that diagnosis came, it was disturbing, no doubt, but “terrifying” is a bit over the top. (Admittedly, the prevailing dramatic and negative response to anything parasitic could account for the terror.)

 

The series Downton Abbey is set in the early 1900s.
No one was worried about toxoplasmosis then, but
other parasites were much more common in England
  than they are today.
      Image by JB + UK_Planet; CC BY 2.0

Toxoplasma gondii, a Terrifying Parasite

Alexander had Toxoplasma gondii – often simply called toxoplasma. Smellie writes that the not-so-terrifying toxoplasmosis is actually “an incredibly common bacterial infection.” She’s right that it’s common; in fact, as many as a third of people living in the UK are infected with the parasite. But T. gondii is not a bacterium, it’s a protozoan.

What qualifies T gondii as a disturbing, and concerning, parasite? A handful of things:

• It lives in your tissues, including the brain, and once you have it, you have it forever. 
• A first exposure during pregnancy can have truly terrifying implications for the fetus. 
• If you have it and your immune system falters (with AIDS for instance), reactivation of the infection can be fatal. 
• There is evidence that T. gondii can change behavior, and it is implicated in some forms of mental illness. 
• Acute infection can make you look like Frankenstein. (Well, it can cause swollen lymph nodes but it usually doesn’t).

Andrew Alexander’s Forever Parasite

Most people who walk around with T. gondii in their tissues never know they have it. The acute infection is typically mild and goes undiagnosed. Perhaps one or two in ten infected people have more severe symptoms like Alexander: flu-like symptoms with fever, headache, sore throat, achy muscles, swollen lymph nodes. Within a few weeks, even these people usually feel better, though it can take much longer.

When good health returns, it means that the immune system has won the battle – at least for now. The parasite is no longer multiplying rapidly and spreading; it has formed tiny cysts and basically gone dormant. In the parasite’s perfect world, a carnivore eventually eats the host and the parasite gets to infect that carnivore next. I suspect, however, that Andrew Alexander’s bradyzoites have reached a dead end.

How Did Andrew Alexander Catch Toxoplasma gondii?

Most people catch T. gondii in one of two ways:

• By eating meat that is not fully cooked. Lots of people eat rare, or raw, meat; domestic and wild animals are often infected with T. gondii. The meat you buy from the butcher might well contain bradyzoites. 
• By swallowing infective oocysts that have been passed in cat feces. Cats are the only host in which T. gondii multiplies sexually, and during acute infection, a cat passes millions of oocysts.

Smellie’s article relates that Alexander became ill after returning from Africa. Did he catch T. gondii there? Possibly. But he could have picked it up just about anywhere. This parasite is ubiquitous. Where was he one to three weeks before becoming ill? That’s where he got it.

Further reading:

Drisdelle, Rosemary. Parasites: Tales of Humanity's Most Unwelcome Guests. University of California Press. 2010

Smellie, Alice. "I looked like Frankenstein... the cast gathered round as if I was about to expire: Downton's Andrew Alexander reveals his battle with a terrifying parasitic infection." MailOnline; Oct 12, 2013.

"Toxoplasmosis: Toxoplasma Infection." The Center for Food Security and Public Health, Institute for International Cooperation in Animal Biologics. May 2005

Elephantiasis and Wolbachia: The Bacteria Behind the Worms

Horrific parasites sometimes turn out to be mere vessels.

Filarial worms, nematodes that are transmitted by insects and live in the tissues, cause horrible disfigurement, disability, blindness. The common names for the diseases they cause are descriptive and apt: elephantiasis, and river blindness.

Wucheria bancrofti, and Brugia malayi nematode worms live in human lymph vessels. Prolonged presence of the worms there often results in the affected part – often a limb or the scrotum - becoming grossly enlarged and deformed. Microfilaria, the worm’s young, circulate in the blood.

Elephantiasis results in almost
unbelievable disfigurement of
various parts of the body.
Imagine living with this.
Tropenmuseum of the Royal
Tropical Institute (KIT)
CC BY-SA 3.0

Onchocerca volvulus adults live together in nodules in the skin. Their young migrate through the skin and, over the long term, can cause discoloration, aging, and sagging of the skin. Worse, microfilariae in the eyes cause blindness.

For a long time, we thought that the worms themselves, and the microfilariae, caused these terrible responses to infection – that the battle between the human body and the worms caused blindness and disfigurement. But now it’s becoming clear that the real culprit is not the worms, but a type of bacteria living inside the worms. The problem is Wolbachia pipientis.

Wolbachia and Filarial Worms

Wolbachia is best known for living in insects, where it is typically parasitic and sometimes causes fatal disease. In nematodes, the relationship is different. In nematodes, Wolbachia is a symbiont: the bacterium actually provides nutrients to the parasitic worm that the worm can’t otherwise get, and without the Wolbachia, the worm can’t survive.

Researchers now have compelling evidence that what the human immune system responds to is actually the Wolbachia, not the filariae or the microfilariae. It’s the Wolbachia that causes elephantiasis and river blindness.

Wolbachia, Filarial Nematodes’ Achilles Heel

Treatment of the diseases caused by filarial nematodes has proven difficult for many reasons, not the least of which is that few drugs kill the adult worms. The discovery of their reliance on Wolbachia reveals a weakness that may be the worm’s undoing: instead of finding a drug to kill the worms, we can use a drug to kill the Wolbachia.

Ironically, if it’s the Wolbachia that’s actually the culprit, the worms end up as collateral damage.

Schistosomes: The Snail, the Prawn, and the Dam

It’s a story that has played out in Africa all too often. A river is dammed to control flooding, or for hydroelectric power, or to create a water reservoir in case of drought (or all of the above at once). The dam, of course, creates a large lake and lots of good habitat along the shore for aquatic plants, which in turn support a large snail population.

Schistosome Life Cycle

People come to live near the water’s edge, to use the water and to fish. Generally, human contact with water is high, particularly for children and fishers. If schistosomes are present, along with the right snail species, escalating levels of schistosomiasis soon follow. This is how it works:

• People infected with schistosomes pass the eggs in urine or feces, and if those eggs find their way into fresh water, they hatch.

• The emerging larva seeks out an aquatic snail – only the right snail will do – and penetrates the snail, after which it multiplies asexually in the snail’s tissues.

• Larvae leave the snail host and, if a human enters the water, penetrate human skin, maturing to adult worms that reside in the tiny blood vessels around the bladder or intestine.

• Adult worms produce eggs which are passed in the urine or feces, and so on.

It makes perfect sense that water resource projects can result in rapidly increasing incidence of schistosomiasis because they bring together the two hosts of the parasites – the human and the snail – in circumstances ideal for transmission. We hardly need a more complicated explanation. It seems, however, that there’s at least one other factor that’s been left out: the African river prawn.

River Prawns and Schistosomes

River prawns are not small!
This is Macrobrachium carcinus (molt).
Clinton & Charles Robertson. CC BY 2.0

Fascinatingly, the adult river prawn lives in fresh water, but the young require brackish water – a mixture of river water and sea water – in order to survive. When we dam an African river, we cut off access to the river’s mouth where the water is brackish. Adult prawns cannot migrate downriver; young prawns cannot migrate upriver. The prawn population upstream of the dam is doomed. And what do prawns eat? Lots of things, but one of those things is snails.

So just as the dam provides beautiful habitat for the proliferation of snails, it also wipes out a key predator of those snails. Instead of tasty prawns, people living on the shores of the reservoir get schistosomiasis. That’s a bad deal.

At least one project – Project Crevette - is now rearing the prawns and releasing them into an affected river, effectively reducing the level of schistosomiasis and providing food and marketable prawns for the people in the area. That’s a good deal.

Michael B. New writes that postlarvae (the stage of prawn young that migrate upstream) of at least one species “can climb vertical surfaces and cross land, provided there is abundant moisture available” (Farming Freshwater Prawns: A Manual for the Culture of the Giant River Prawn Macrobrachium rosenbergeii. Food and Agriculture Organization of the United Nations, 2003, pg 10). One wonders how difficult it would be to re-establish the natural life cycle of the river prawn.

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 19^th 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 15^th 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.

 

 

Resources

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." alanmacfarlane.com. Accessed Sept 9, 2013. 

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

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.

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.

Sources

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.

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.”

Sources

 

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.