Maps of Dog and Cat Parasites in the US

The Companion Animal Parasite Council (CAPC) website, www.capcvet.org, 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.

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.

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?

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.

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.

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.

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 (thelocal.se, 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, canids.org)

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)