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)

Pinworms and Human Immunity

Thoughts on pinworm infections...

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

One female pinworm can produce 10,000 sticky eggs.

Mentnafunangann; CC BY-SA 3.0

Will Pinworm Infection Resolve Without Treatment?

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

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

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

A Realistic Approach For Pinworm Infection

Further thoughts:

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


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


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


• When symptoms are severe and persistent, however, only the most stoic of patients would refuse treatment. I’ve never had the pleasure myself, but I’ve heard first hand accounts that were not pretty.

I suspect most people would choose to treat a pinworm infection but it's up to the individual.

Onchocerca volvulus and Wolbachia

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

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

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

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

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

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

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