The microbiology of zombies, part III: “We’re all infected”

Warning: here be spoilers

In many latter-day zombie movies, books, and TV shows, zombie-ism has a biological cause. In 28 Days Later, the infection is caused by the “Rage” virus, which escaped from a lab when animal rights activists break in and release a group of infected chimpanzees. Of course, one of the animals promptly bites one of its “liberators,” and the infection spreads rapidly throughout Great Britain. In Zombieland, it’s a mutated form of “mad cow” disease. The Crazies, it’s the Trixie virus; World War Z, the Solanum virus; Resident Evil, the T virus. I could go on and on. Zombie causation has clearly evolved from the early days of radiation or curses, and has become a biological phenomenon in most modern zombie tales.

The Walking Dead is no exception. Though the claim is made in season 1, episode 6 (“TS-19”) that the outbreak could be caused by just about anything–bacteria, virus, parasite, act of God–I call shenanigans. In the previous episode (“Wildfire”), Jenner, the CDC scientist, is processing tissue taken from Test Subject 19, and the visualization under his microscope looks very viral. Of course, take this with a few pounds of salt, since he’s using a light microscope and can also see the nice alpha-helical DNA strains within the pathogen (in real life, things just don’t look like this) and unless you’re one of the giant viruses, you can’t see viruses, much less DNA, under the microscope Jenner uses anyway. But still, it looks pretty viral-y to me, which is why I typically refer to it that way:

screenshot wildfire virus

Microbial zombification makes sense in today’s culture. My colleague Brooks Landon notes: “…zombies represent a better monster for the modern, post-9/11 world. They provide a release for feelings of being overwhelmed by abstract and intractable events like global economic crises, terrorism, and pandemics.” In the past decade or so, we’ve seen the emergence of SARS, multiple outbreaks of influenza including a new pandemic strain, the continuing HIV crisis, Nipah, Hendra, more Ebola, just to name a handful. Infectious diseases are commonly in the news, and many times are unfortunately over-hyped, leading to a collective nervousness of all things microbial.

The infected zombie is further boosted by a number of recent studies, largely in insects, that demonstrate a type of pathogen-directed “mind control:” zombie ants, zombie grasshoppers, and zombie cockroaches, just to name a few. A recent video game has exploited the ant fungus idea, mutating it into a form that infects humans. Even rodents (and possibly humans) can have their behavior apparently influenced by a parasite called Toxoplasma gondii, which makes rodents lose their fear of cat scents and may influence the development of schizophrenia in humans, or more controversially, even affect sexual inhibitions. If germs are already controlling our minds–why couldn’t they turn us into zombies?

And certainly, there are some candidate microbes which could, in theory, cause at least the “living” form of zombie-ism, even if they couldn’t necessarily raise you from the dead. The Trixie virus, for example, is supposed to be a weaponized rhabdovirus–the family of viruses that includes rabies. Rabies virus infection certainly causes aggression and biting. The virus is spread via saliva, so biting is the main way it is transmitted between animals. In a recent book, Rabid, the authors trace rabies through history, and note that it may be at the root of many zombie (and vampire) tales. Rabies can also hide out in the body for awhile before showing symptoms, as the virus travels up the nerves toward the brain. This is why a bite near the head progresses to symptoms much faster than, say, one to the foot. Typical time from bite to symptoms is in the neighborhood of 6 weeks, depending on the location of the bite and dose of virus one receives, but extreme cases have been documented, with symptoms not showing up for as long as 8 years. And, like has been done on The Walking Dead, one of the ways that bitten victims would try to avoid symptoms would be to cut off the affected limb before the infection spread. (Ouch).

Could something like the “we’re all infected” scenario used in the Walking Dead occur in real life? Maybe. With rabies, victims could appear physically fine for months to years. Even more extreme, there are a number of germs which can remain with people throughout their entire life. The virus that causes chicken pox, for example, doesn’t ever really go away. Your body fights it off enough to keep it in check after the initial rash, but it hides out  in your nerves and can come back in later years as shingles. Other herpes family viruses have a similar lifestyle: symptoms can come and go, but the virus never really leaves. The human papilloma virus (HPV) can also persist for years in some people (most infected people appear to clear this one, though). A bacterium called Helicobacter pylori can live very happily in a person’s stomach–sometimes causing ulcers, but going completely undetected and causing no symptoms in most people. And of course, HIV, which does not go away except in a few notable and high-profile cases. So the concept is, as they say, biologically plausible.

The problem isn’t necessarily with the microbiology, then, but with the epidemiology. How did everyone get infected so quickly? We know that the plague took an incredibly short time to spread (Jenner says less than 200 days in the first season, and “less than 63 days” since it went pandemic)–but how? That’s a missing link in this scenario. We know the pathogen can certainly be spread by bites and then cause zombification that way, but other forms of inoculation (such as getting sprayed in the eyes or nose with zombie blood) don’t seem to have that effect. Is it in the water? If so, that would be some damn rapid spread, since early on Jenner noted that this appeared to be a true pandemic–present around the world. How would that happen?

In the air? Possibly, but even most airborne microbes don’t hang out indefinitely; they’re dispersed by wind to levels below those able to cause infection, or killed by sunlight or other environmental conditions. So even if you had a herpes- or HIV-like virus that could hide out in the body for an extended period of time without causing symptoms, how did *everyone* get it in such a short timeframe? Some scenarios in other books and movies put the blame on bioterrorism. The above-mentioned Trixie virus, for example, was a bioweapon which was only accidentally released when the plane carrying it crashed. Spread of Trixie in the movie ended up being only local, but transmission beyond that is hinted at the end. A true bioterrorist attack could, theoretically, account for simultaneous outbreaks all over the world.

Finally, though the “infected zombie” is now the most common type, it should be noted that this isn’t really new. George Romero, widely recognized as the grandfather of the modern zombie, acknowledges that he “ripped off” his idea for Night of the Living Dead from Richard Matheson’s I am Legend–a vampire story from 1954. The cause of that vampirism?

Bacillus vampiris–a bacterium.

 

See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part IV: hidden infections

Student guest post: Are parasites causing a rise in the global HIV epidemic?

Student guest post by Carrie Ellsworth

During the summer of 2010 I spent two months in Ghana studying a parasite called schistosomiasis. We worked in a small town called Adasawase to determine prevalence and treat the schoolchildren who were infected. We were told that schistosomiasis was not a major health concern for the people in the town because they were often faced with other diseases that had more immediate and severe health consequences than a parasitic infection. It became apparent that if we wanted the people of this small town to take this health threat seriously, we needed to stress the long term health sequelae that could arise due to schistosome infections.

Carrie picture 1

(Personal photo taken in Ghana in 2010)

Our research group decided to implement an educational portion to our schistosomiasis control program. Through a Knowledge Attitudes and Practices survey, we found that most schoolchildren in the town reported learning about health from their teachers in school. We held a meeting with all teachers and administrators from Adasawase to educate them on the transmission, symptoms, and long term implications of schistosomiasis infections. When the possibility of greater transmission of HIV to individuals with schistosomal infections came up in discussion, we suddenly had everyone’s complete attention. You could have heard a pin drop on the cement floor of the school room.

Recently, the BBC reported that over 25% of schoolgirls between the ages of 10 and 14 in South Africa are infected with HIV. The World Health Organization has shown that HIV prevalence is much higher in females living in urban areas than in any other demographic group. More than 2/3 of the world’s population living with HIV/AIDS lives in Sub-Saharan Africa. Many efforts have been made to decrease the prevalence of HIV in Africa but few people have looked at the possibility of a parasitic infection possibly contributing to the transmission of HIV.

Carrie picture 2

(http://www.who.int/gho/urban_health/outcomes/hiv_prevalence/en/index.html)

Schistosomiasis haematobium is a species of waterborne parasite that specifically affects the urogenital system of infected individuals. When people with S. haematobium urinate in stagnant water, they deposit schistosome eggs. The eggs develop into larvae which then enter a freshwater snail to continue its life cycle and mature. It leaves the snail and matures into its infective stage while in the water. The mature larval form of the parasite burrows through the skin of an individual who has contact with contaminated water. Once inside the body, the mature larva develops into an adult worm and then travels to the blood vessels surrounding the bladder. The male and female will mate to produce eggs which penetrate through the bladder wall and are passed in the urine to continue the cycle.

The treatment for a schistosomiasis infection is an inexpensive anti-helminthic medication called Praziquantel. Common signs of a S. haematobium infection are bloody and cloudy urine. Damage to the bladder wall is inevitable and if the infection becomes chronic, damage to the kidneys can also ensue. Chronic genital sores can develop in females with S. haematobium infections when the schistosome eggs are deposited in the uterus, vulva, cervix, and vagina. These lesions are believed to put the females with S. haematobium infections at a greater risk of contracting HIV. A study conducted in Zimbabwe showed that women ages 20-49, who had genital lesions due to a urogenital schistosomiasis infection, had a 3-fold higher risk of having HIV than women without a schistosomal infection.

There are 207 million cases of Schistosomiasis worldwide, and 112 million of those cases are urogenital Schistosomiasis found in Sub-Saharan Africa. This creates a significant overlap between areas of Africa that are endemic to HIV/AIDS and Schistosomiasis. This has caused many scientists to question whether a greater effort to control S. haematobium infections would be an effective method of decreasing the prevalence and transmission of HIV/AIDS in Africa.

Carrie picture 3

(http://blogs.plos.org/speakingofmedicine/2013/05/06/female-genital-schistosomiasis-fgs-sub-saharan-africas-secret-scourge-of-girls-and-women/)

There is a Schistosomiasis Control Initiative (SCI) based out of London which is attempting to implement schistosome control methods in areas that are endemic. A study done in Burkina Faso showed that a single mass treatment with Praziquantel was shown to decrease the prevalence of S. haematobium by 84% in girls and 78% overall for up to 2 years. The WHO has a strategy of mass drug administration (MDA) in which school aged children in areas that have a greater than 10% prevalence of schistosomiasis would receive Praziquantel on a biannual basis, and areas that have greater than 50% prevalence would receive treatment on an annual basis. Treatment with Praziquantel results in a parasitological cure but will not heal genital lesions that have already developed from a S. haematobium infection. For this reason, prophylactic treatment starting at a young age is crucial in using this method as a means to decrease HIV prevalence.
It only costs about 32 cents to treat one child with Praziquantel. In most developing countries Praziquantel is distributed through bulk sales to the government. From there, the government dispenses its allotted Praziquantel out to different programs. The organizations that supply developing countries with Praziquantel include UNICEF and the World Health Organization among many other international organizations. Data has shown that a schistosomiasis infections increase susceptibility to HIV, elevate viral replication, exacerbate immunosuppression and increase transmission of HIV. Due to these findings, greater emphasis on schistosomiasis control is being pursued as a means of decreasing the ever growing HIV/AIDS prevalence in Africa. Widespread distribution of Praziquantel to schoolchildren in countries endemic to both schistosomiasis and HIV/AIDS could potentially prevent 120,000 new cases of HIV/AIDS in the next decade.

If treatment with Praziquantel for one child costs $0.32, then treating 70 million children would cost $22 million for one year. If a 10 year plan was implemented that treated every one of those 70 million children biannually, that would cost approximately $112 million. Compare that with the $18.8 billion that has been proposed to be spent over the next 5 years by the U.S. President’s Emergency Plan for AIDS Relief (PEPFAR). The cost of treating 70 million children for schistosomiasis over a 10 year span is dwarfed by the projected costs of the PEPFAR and could potentially make a significant change in the rising trend of HIV infections in Africa.
All of the research points towards mass treatment with Praziquantel as being the most cost effective and successful method of decreasing the number of schistosomiasis infections and HIV/AIDS transmission. The cooperation between HIV and schistosomiasis control programs is critical in ensuring the success of such a program. Combatting two of Africa’s top health concerns with one simple low cost medication would do wonders for lowering the morbidity and mortality rates of many African countries.

References:
“HIV and AIDS Statistics: Worldwide.” Statistics: Worldwide. AmfAR, Nov. 2012. Web. 10 June 2013. <http://www.amfar.org/about_hiv_and_aids/facts_and_stats/statistics__worldwide/>.
Hotez PJ, Fenwick A (2009) Schistosomiasis in Africa: An Emerging Tragedy in Our New Global Health Decade. PLoS Negl Trop Dis 3(9): e485. doi:10.1371/journal.pntd.0000485
Hotez, Peter J., Alan Fenwick, and Eyrun F. Kjetland. “Africa’s 32 Cents Solution for HIV/AIDS.” PLoS Neglected Tropical Diseases 3.5 (2009): E430. Print.
“International Strategies for Tropical Disease Treatments – Experiences with Praziquantel – EDM Research Series No. 026: Chapter 5: The International Supply of Praziquantel*: Global Distribution of Praziquantel.”

International Strategies for Tropical Disease Treatments – Experiences with Praziquantel – EDM Research Series No. 026: Chapter 5: The International Supply of Praziquantel*: Global Distribution of Praziquantel. World Health Organization, 2013. Web. 10 June 2013.
Kosinski, Karen C., Kwabena M. Bosompem, Miguel J. Stadecker, Anjuli D. Wagner, Jeanine Plummer, John L. Durant, and David M. Gute. “Diagnostic Accuracy of Urine Filtration and Dipstick Tests for Schistosoma Haematobium Infection in a Lightly Infected Population of Ghanaian Schoolchildren.” Acta Tropica 118.2 (2011): 123-27. Print.
“Schistosomiasis.” World Health Organization. Web. 10 June 2013. <http://www.who.int/mediacentre/factsheets/fs115/en/>.
“Schistosomiasis: Epidemiological Situation.” World Health Organization. N.p., n.d. Web. 10 June 2013. <http://www.who.int/schistosomiasis/epidemiology/en/>.
Secor, Evan W. “The Effects of Schistosomiasis on HIV/AIDS Infection, Progression, and Transmission.” Current Opinions on HIV and AIDS 7.3 (2012): 254-59. Print.
Simon, Gregory. “Combined Schistosomiasis and HIV Control Programs: Saving Lives AND Money”. End the Neglect. N.p., 7 May 2013. Web. 11 June 2013. <http://endtheneglect.org/2013/05/combined-schistosomiasis-and-hiv-control-programs-saving-lives-and-money/>.
“South Africa: ‘Over 25% of Schoolgirls HIV Positive'” BBC News. BBC, 14 Mar. 2013. Web. 10 June 2013. <http://www.bbc.co.uk/news/world-africa-21783076>.
Temple, Bliss. Schistosoma Haematobium (blood Flukes). Schistosomiasis Haematobium (blood Flukes). Stanford University, May 2004. Web. 10 June 2013. <http://www.stanford.edu/class/humbio103/ParaSites2004/Schisto/website.html>.

Student guest post: Unintended Consequences

Student guest post by Naomi Kirschenbaum

Although we can never know, there are estimates in the range of 15,000 displaced pets in the wake of 2005 Hurricane Katrina.  Many of the dogs found their way to shelters and homes in our community around the Monterey Bay in California.  As a local veterinarian the most notable observation I saw was how it “seemed” that so many were heartworm positive.  Six years later we have a published study finding a 48.8% prevalence of heartworm in these dogs.

This story is an example of a few important lessons.  First, how things seemed to me, in my clinical practice turned out to be 48.8% of the dogs, not all.  (Of course in our area we may have had a different subset of positive dogs, but I thought, in general, they were nearly all heartworm positive). Secondly, how long it takes for a study to be done and published.  In this case the study I referenced has a six year interval between the event and publication of data examining an aspect of concern.

Now, let’s step into the present.  I’m currently taking courses for a Masters in Public Health at the University of Iowa to branch out from my basic training in veterinary medicine.

Yesterday, in a course I’m taking we had a lecture on a group of zoonotic diseases, Trypanosomes.  This group of little single celled organisms, protozoans, causes problems all over the world.   In Africa it causes, Sleeping Sickness, in Latin America, Chagas’ disease.  We don’t hear a lot about it here in North America.

What came to my attention was a disease described in dogs, here, in the U.S. caused by one in this group called Leishmania.  Dogs are a known reservoir in areas where these diseases are endemic but these U.S. reports starting in the late 1990’s were in two breeds with whopping over representation, specifically Foxhounds1 and Neapolitan Mastiffs.

That’s weird, I thought.  I’ve been a small animal veterinarian for a long time and those are not two very common breeds.  What’s up?

The first two things you need to know have to do with our basic understanding of where this parasite lives and how it infects mammals.  It has been traditionally thought a mammal becomes infected from the bite of an insect vector (tsetse fly in Africa or sand fly in South America), which is carrying the protozoa.  Also, although this occurs more rarely, you can become infected by direct contact with the blood of an infected animal into your tissue, read blood-to-blood transmission.  This second bit of information will be important later.

As well from studying these outbreaks in Foxhounds, one research group received a donated pregnant bitch they new was infected which allowed them to examine the puppies and look to see if they were also infected.  They found Leishmania in the puppies.  This lends evidence of transmission of the organism from mother to puppies in utero. Their thought is the Leishmania protozoan circulates in the mother’s blood and crosses over the placenta to infect the developing fetuses.

An important point here is the novel idea that transmission of the infection can be vertical and DOES NOT REQUIRE A VECTOR.  This would mean you could sustain the parasite in a mammal population where it has never lived before and would not normally be expected to be able to live.

This disease is endemic in parts of Europe and these two breeds, although fairly rare here in the U.S., often are imported from Leishmania endemic areas to be incorporated into U.S. breeding stock lines.   These imported dogs are very valuable and key to their breeding programs.

The work done showing vertical transmission from mother to pup suggests we can establish the infectious agent in a host indefinitely.  So far we are lucky and the areas where these dogs live don’t have vector insects readily available.  I wouldn’t count on that lasting too long.  Between global travel and climate change alone, and if historical record of disease spread with so many other zoonotic infectious agents is any guide, it’s really, likely, just a matter of time.

So a final concern, more immediate, goes back to that second route of traditional transmission I described above, the direct contact, blood-to-blood infection.   Here’s the thing.  These dogs, the Foxhounds and Neapolitan Mastiff’s that are infected are breeding dogs.  Breeding dogs, by definition, are sexually intact.  Dogs that have their “parts” can more often get into scrapes (read: fights).  When dogs fight they really can tear each other up.  The fighting often occurs around the head, neck and ears.  All fight wounds bleed, a lot.  Ears especially bleed like stuck pigs.

People try to break up the fighting dogs.  People get bitten all the time doing this.  (Read: Do not try to break up fighting dogs yourself, but that’s another essay of it’s own).  The dog blood that is all over the dogs is now all over you.  You have an open bite wound.  The dog’s blood now is mingling with your tissue and blood.  You now have Leishmania.  This is the problem.

The good news is if you are immune-competent you should mount a good response to this insult and have a very good likelihood of clearing the infection.  It will require a significant effort calling upon both arms of your immune systems, the cellular and the humoral.  Unfortunately you will not be immune to reinfection should another exposure event occur.  The bad news is if you are in anyway immune compromised, not so good.  You are likely to get clinical illness.

I guess our best hope at this point in time is to help breeders see the need and importance of choosing disease free dogs.  Encourage them to buy and bring only dogs that they have tested and know are free of Leishmania into the U.S.  I know breeding for phenotype and working characteristics and abilities is the holy grail of breeders, but can’t we do it looking at the bigger picture, the greater good?

1Monti, Dean (June 2000). “Hunters hounded as leishmaniasis is diagnosed in Foxhounds”. J Am Vet Med Assoc 216 (12): 1887, 1890.

“Spillover” by David Quammen

Regular readers don’t need to be told that I’m a bit obsessed with zoonotic disease. It’s what I study, and it’s a big part of what I teach. I run a Center devoted to the investigation of emerging diseases, and the vast majority of all emerging diseases are zoonotic. I have an ongoing series of posts collecting my writings on emerging diseases, and far too many papers in electronic or paper format in my office to count. Why the fascination? Zoonotic diseases have been responsible for many of mankind’s great plagues–the Black Death, the 1918 “Spanish” flu pandemic, or more recently, HIV/AIDS. So you can imagine my delight when I read about Spillover, a new book by David Quammen on zoonotic diseases.

I’ve previously highlighted some of Quammen’s work on this site. That link goes to a 2007 story he wrote for National Geographic on “infectious animals,” which really serves as a preview to “Spillover,” introducing some of the concepts and stories that Quammen elaborates on in the book.

“Spillover” is wide-ranging, tackling a number of different infectious agents, including viruses like Nipah, Hendra, and Ebola; bacteria including Coxiella burnetii and Chlamydia psittaci; and parasites such as Plasmodium knowlesi, a zoonotic cause of malaria. HIV is a big part of the story; Quammen devotes the last quarter or so of the book to tracing the discovery and transmission of HIV from primates to humans, and from 1900 to present-day. He even takes the time to explain the basic reproductive number–something that’s not always a page-turner, but Quammen manages to do it well and without being too tangential to the rest of the story; much more of a Kate-Winslet-in-Contagion than Ben-Stein-in-Ferris Bueller delivery.

Indeed, “Spillover” is somewhat unique in that it doesn’t read quite like your typical pop science book. It’s really part basic infectious disease, part history, part travelogue. Quammen has spent a number of years as a correspondent for National Geographic, and it shows. The book is filled with not only well-documented research findings and interviews with scientists, but also with Quammen’s own experience in the field, which gives the book a bit of an Indiana Jones quality. In one chapter, he details his adventure tagging along with a research team to capture bats in China, entering a cave that “felt a little like being swallowed through the multiple stomachs of a cow.” This was after an earlier dinner in which he describes his encounters with the an appetizer of the “world’s stinkiest fruit” (I’ll keep the description of the smell to myself) with congealed pig’s blood for a main dish (bringing to mind the scooping out of monkey’s brains in “Temple of Doom”–and the various zoonotic diseases that could be associated with those, come to think of it).

Quammen’s book is an excellent, and entertaining, overview of the issues of zoonotic disease–why do they emerge? Where have they come from? How do they spread? The only thing that’s missing is more of a cohesive discussion about what to do about them. However, that’s rather understandable, as we certainly have less of a grasp of this question than we do about the others (and even with some of those, our knowledge is spotty at best). I hope “Spillover” will inspire another generation of future germ-chasers, as “The Coming Plague” did almost 20 years ago.

Concerned about Crypto?

This is the fourteenth of 16 student posts, guest-authored by Caroline Rauschendorfer. 

Cryptosporidiosis, known more commonly as crypto, is a gastrointestinal (GI) disease caused by parasites of the Cryptosporidium genus. If infected with crypto you may experience diarrhea, nausea, vomiting, fever, and abdominal cramps that can last up to two weeks. Definitely something you want to avoid, if possible, but at least it usually resolves on its own without medical intervention and is rarely fatal in otherwise healthy individuals. [3]

The most common disease causing organisms for crypto are C. hominis and C. parvum. C. hominis is a version of the parasite that sticks mainly to humans. Historically, large outbreaks of crypto tend to be caused by drinking water that has been contaminated with wastewater. In 1993 a large outbreak of crypto occurred in Milwalkee, Wisconsin, making 403,000 people ill. It was thought to be caused by a failure of drinking water purification. It is also possible to get crypto from a variety of other places as well: swimming in contaminated water, eating contaminated food, or from infected livestock. [3]

It is this last possibility for transmission that I am most concerned with. As I said earlier, C. hominis sticks primarily to people; but C. parvum, another type of Cryptosporidium, has the ability to infect most major domestic livestock. [2] As a second year veterinary student, this is a health concern for me. C. parvum is particularly common in cattle, and frequently causes infection in young calves. Crypto infected calves either come into a large animal clinic or are seen by a veterinarian on farm for being a “poor-doer” and having watery diarrhea. Veterinarians and veterinary students often come in close contact with these sick calves during treatment and can become infected themselves. As a matter of fact, contracting crypto as a veterinary student during your large animal rotation is practically a right of passage.

Many studies have been done looking at the prevalence of crypto in cattle, with a variety of results. One similarity between most studies, however, is that the prevalence of crypto is generally higher in calves than in adult cattle. Results from different studies ranged from 7.5 to 49% of U.S. dairy calves infected with crypto. [2] This means that working with calves puts you at an even greater risk of becoming infected with crypto.

No need to freak out yet, though. One thing that should be noted is: it is possible to come in contact with cryptosporidium and not become sick. Crypto is not difficult to kill, and will be removed from water by boiling it for at least 1 minute; however, routine chemical disinfection alone may not kill it. According to one study, crypto contaminates 65% to 95% of surface water and 45% to 65% of ground water in the U.S. This probably doesn’t sound like a good thing, but it actually might be.  According to another study, 35% of the U.S. population has antibodies to crypto. Repeated exposure to small doses of crypto may help build immunity against it. [4]

The body’s immune system fights disease in two ways: adaptive and innate immunity. Innate immunity is the part of your immune system that you are born with and involves the cells that patrol and recognize any type of foreign cell or molecule that might be inside your body, such as bacteria, viruses and parasites. Adaptive immunity is something that the immune system builds over time as your body is invaded by various infectious agents (viruses, bacteria, parasites, etc.). The cells that are part of the adaptive system produce a memory when they are exposed to these infectious agents so that if they encounter them again, they can mark them to be killed by other cells. In other words, innate immunity works very generally and very quickly, whereas adaptive immunity adapts to the specific infectious agent, but it takes longer to kick in. This works for crypto in that if your body is exposed to the parasite for the first time as a small amount in your drinking water, it may not be enough to make you sick, but if your adaptive immune system finds it and makes a memory it can fight off the parasite much better if you are ever exposed to it again. This would also be true if you were infected with crypto and had all the gross symptoms that go with it, it would just be more unfortunate. [5]

Immunity is also the reason why crypto, although not serious for health individuals, can be very harmful for the immunocompromised such as those on chemo drugs for cancer treatment, or people with HIV/AIDS. The number of immune cells in an immunocompromised person can be so low that they do not have enough to fight off an infection. If someone with HIV/AIDS becomes infected with crypto, it is much more likely to be lethal. [3]

Treatment of crypto for someone who is immunocompromised would be to administer blood serum, which contains immune cells, from a healthy person. This has been shown to help in some cases. Unfortunately there is no treatment for otherwise healthy individuals who become infected with crypto. Your only option is to wait out the two miserable weeks until your body fights off the parasite. In some cases, IV fluids may be helpful for people who become dehydrated from severe diarrhea. [3]

Thankfully, there are many ways to help protect yourself from crypto. The CDC recommends, as always, washing your hands, especially before eating or preparing food, after gardening, after using the bathroom, after changing children’s diapers, after tending to someone who is ill with diarrhea, or after handling animals and animal waste. The also recommend keeping your child out of daycare if they have diarrhea. At pools, lakes, and any other recreational water source, they recommend: not swimming if you have diarrhea, especially children with diapers; showering before entering the water; washing children thoroughly after changing their diaper or after they use the toilet before allowing them in the water; and not changing diapers at the poolside. The CDC recognizes livestock handling as a potential risk for crypto infection and have special recommendations for these people: minimize contact with animal feces, particularly young animals; always wear disposable gloves when cleaning up animal waste and wash hands when finished; and wash hands after contact with animals or their living areas. As a veterinary student these are all things I will have to keep in mind while treating animals to help prevent two weeks of misery for myself. [1]

References

1. Centers for Disease Control. http://www.cdc.gov/parasites/crypto/gen_info/index.html. Updated 2010.

2. Dixon B, Parrington L, Cook A, et al. The potential for zoonotic transmission of giardia duodenalis and cryptosporidium spp. from beef and dairy cattle in ontario, canada. Vet Parasitol. 2011;175(1-2):20-26.

3. Leitch GJ, He Q. Cryptosporidiosis-an overview. J Biomed Res. 2012;25(1):1-16.

4. Preiser G, Preiser L, Madeo L. An outbreak of cryptosporidiosis among veterinary science students who work with calves. J Am Coll Health. 2003;51(5):213-215.

5. Tizard IR. Veterinary immunology. 8th ed. Philadelphia, PA: Saunders; 2008.

Coexisting with Coyotes

This is the twelfth of 16 student posts, guest-authored by Stanley Corbin.

Disease in wildlife is an important concern to the health and safety of humans and domestic animals. The expanding growth of our nation and resultant land use changes with urbanization has resulted in a shrinking habitat and fragmentation for all animals, including humans. The effects of ecological disruption are universally recognized and adversely effects wildlife through multiple mechanisms.

Hand it to the coyote (Canis latrans) for its ability to exist with humans. The resilience of this animal can be attributed to its natural instincts, remarkable intelligence and survivability. Opportunistic is another word that can be used to define them. Once an animal roaming the mid-west prairies, their territory has expanded throughout the North American continent and beyond. Coyotes demonstrate their wily nature by meeting the challenges of the American landscape.  

Progression of coyote range expansion throughout North America and Mexico. (7) Click to enlarge. 

Precise population estimates of coyotes in the United States are not available and unclear at best. However, to put it in perspective, the California Department of Fish and Game estimates a population range of  250,000  to 750,000 animals.(1)  The greater metropolitan area of Chicago estimates home to between 200-2000 coyotes. (3) The coyote population in New York during the summer is approximately 20,000-30,000. (2)  In March 2010, a lone coyote led a police chase through lower Manhattan, deep in New York City.

Coyotes can thrive in suburban settings and even some urban ones creating a concern for public health. A study by wildlife ecologists at Ohio State University yielded some surprising findings in this regard. Researchers studied coyote populations in Chicago over a seven-year period (2000–2007), proposing that coyotes have adapted well to living in densely populated urban environments while avoiding contact with humans. They found, among other things, that urban coyotes tend to live longer than their rural counterparts. (3)

As with most all wild animals, the coyote population represents a reservoir for diseases. Zoonotic (animal to human) diseases in particular are on the rise, comprising 75% of emerging infectious diseases. Viruses, bacteria, fungi, internal and external parasites, and other pestilence are only the headings for what’s out there.

Fortunately, the rabies virus is rather uncommon in coyotes as reported. The only exception was the 1974-1998 rabies epizootic (epidemic in animals) in south Texas. The world’s largest wildlife oral rabies vaccine (ORV) drop, 11.6 million doses covering over 189.6 square miles, was performed beginning in 1995 and led to the total elimination of the domestic dog-coyote (DDC) variant by 2006. (4) A study performed by the USDA, APHIS, Wildlife Services, National Wildlife Research Center concluded; “In Texas, the use of the ORV stopped the northward spread and led to the progressive elimination of the DDC variant of rabies in coyotes”. (5) This campaign was a win for our tax dollars as well. The economic evaluation study yielded “total estimated benefits of the program approximately ranged from $89 million to $346 million, with total program costs of $26,358,221 for the study period”. This represents benefit-cost ratios that ranged from 3.38 to 13.12. (5)

Coyote rabies surveillance reported by the Center for Disease Control (CDC) for 2010 declared 10 confirmed cases. None of these cases were DDC variant, which remains non-detected from the populations. The raccoon variant and skunk variant represented 8 (AL, GA, NC, NJ, NY, NYC) and 2 (CA, CO) cases respectively. (6)These coyote rabies cases were diagnosed from New York City (1) on the east coast to California (1) in the west, confirming the widespread distribution of this terrestrial carnivore. An interesting fact that comes from this data is that the coyote is not a player in the zoonotic rabies front. From a public health concern, a human has a significantly greater chance of contracting the disease from the backyard domestic cat.

Canine Distemper Virus is an enzootic disease (prevalent in an animal population) in the coyote. The neurological form is rightfully confused with a rabies infection as the two appear similar clinically. Humans are not susceptible to the disease, however it is highly contagious to dogs. Greater Yellowstone Park has a dynamic management study to assist with the surveillance of the disease enzootic in the parks coyote population.

The parasitic disease Sarcoptic mange is what gives the animal the “mangy” look. Caused by the mite Sarcoptes scabei, the disease in humans is called Scabies. Severely affected coyotes are unsightly and are perceived as threatening by their appearance. The compromised condition may explain the increased frequency of nesting and scavenging in suburban areas, especially in daylight hours. Coyotes with extensive mange infections are not considered aggressive as concluded by The Cook County, Illinois, Coyote Project.(7) Human infections from animal sources are short-lived and self-limiting due the highly host species-specific nature of the bug.

A recent hot epidemiological study conducted in Santa Clara County, California, identified coyotes as a wildlife reservoir for a disease caused by Bartonella vinsonii subsp. Berkhoffii .(8) The disease in humans is characterized by endocarditis, an inflammation of the interior lining of the heart. The study was prompted by the coyote bite of a child who developed symptoms compatible with Bartonella infection. Among 109 coyotes sampled, 31 animals (28%) were found to be bacteremic and 83 animals (76%) had Bartonella vinsonii seropositve antibodies. The disease is thought to be transmitted by insect vectors (ticks, biting flies, fleas), however further studies are necessary to elucidate additional modes of transmission to humans.(8) Bartonellosis in domestic cats is commonly called “cat scratch fever”, caused by a different species variant of Bartonella. The role coyotes play in this emerging infectious zoonose and public health concern are yet to be resolved.

Additional diseases exist in the coyote populations warranting public health attention. Anyone concerned with coyote interaction and communicable diseases will need to seek information relative to their geographical location. The ubiquitous nature of this animal and the corresponding diseases posing risks to humans and domestic animals respectively are regionally specific.

Coyotes are here to stay. Most every state (excluding Hawaii) has a control program in effect to manage the public health risks and deprivation to human welfare. The Humane Society of the US has issued techniques to resolve coyote conflict and how to discourage coyotes.  Project Coyote champions innovative solutions to live in peace with the coyote despite differences, especially in terms of human policy. (9) A collaborated and integrated management approach is required to maintain a balance of needs for this specie of animal and humans. Wildlife specialist Jeffery Green summarizes; “regardless of the means used to stop damage, the focus should be on damage prevention and control rather than elimination of coyotes”. (10)

Pet owners need to adapt to coyote presence and take precautionary measures in securing their animal’s health and safety. Routine core vaccinations and other preventative health care are effective in stopping the transmission of nearly all the important diseases from the coyote to a pet animal.

Coyote attacks on humans are rare; the coyote human avoidance factor is responsible for the low incidence. In the cases of human attacks, approximately 30% were reported as humans feeding coyotes. (8) Additionally, greater than 50% of the human attack cases were in California, (8) where coyotes have a longer history of habituation with humans.

A person who sees a coyote should feel lucky since they avoid humans and are mostly invisible.

The most important advice to prevent human exposure is: do NOT feed coyotes and ensure your environment is NOT coyote friendly. Any attempt to domesticate or habituate the coyote will surely be a kiss of death for its existence. Survival of coyotes is dependent on living side by side but not together with humans.

The “tricksters still run wild and provoke all sorts of all-too-human difficulties, pitting the spirit of the wild against the sturdy values of our American farmers and their need to protect livestock. Somehow we need both”. (11)

Our Canadian neighbors at The Royal Canadian Geographical Society  conclude; “the more we cut down habitat and build, the happier the scavenging and opportunistic coyote”. (12)

As they say in Texas, “when the human population fails, cockroaches and coyotes will survive”. (13)

References:

  1. L.A. County Department of Animal Care and Control website. Accessed June 15, 2012. Available at: http://animalcare.lacounty.gov/coyote.asp
  2. New York State Department of Environmental Conservation website. Accesses June 15, 2012. Available at: http://www.dec.ny.gov/animals/9359.html
  3. World Science website: Thriving under our noses, stealthily: coyotes.  Accessed June 13, 2012. Available at:  http://www.world-science.net/othernews/060105_coyotefrm.htm
  4. Texas Department of State Health Service website. Accessed June 12, 2012. Available at: http://www.dshs.state.tx.us/idcu/disease/rabies/orvp/statistics/
  5. Stephanie A. Shwiff, PhD; Katy N. Kirkpatrick, BS; Ray T. Sterner, PhD. Economic evaluation of an oral rabies vaccination program for the control of a domestic dog-coyote rabies epizootic: 1995-2006. JAVMA, Vol.233, No.11, Dec.1, 2008. Available at http://www.avma.org/avmacollections/rabies/javma_233_11_1736.pdf
  6. Jesse D. Blanton, MPH; Dustyn Palmer, BA; Jessie Dyer, MSPH; Charles E. Rupprecht, VMD,PhD. Rabies surveillance in the United States during 2010. Vet Med Today: Public Veterinary Medicine. JAVMA, Vol. 239, No. 6, September 15, 2011. Available at: http://avmajournals.avma.org/doi/pdf/10.2460/javma.239.6.773
  7. The Cook County, Illinois, Coyote Project website. Accessed June 13, 2012. Available at: http://urbancoyoteresearch.com/Coyote_Project.htm
  8. Chang CC, Kasten RW, Chomel BB, Simpson DC, Hew CM, Kordick DL, Heller R, Piedmont Y, Breitschwerdt EB. Coyotes (Canis latrans) as the reservoir for a human pathogenic Bartonella sp.: molecular epidemiology of Bartonella vinsonii subsp. Berkhoffii infection in coyotes from central coastal California. J Clin Microbiol. 2000 Nov; 38 (11): 4193-200. Available at: http://www.ncbi.nlm.nih.gov/pubmed/11060089
  9. Project Coyote website. Accessed June 15. 2012. Available at: http://www.projectcoyote.org/programs.html
  10. Jefferey S. Green, Urban Coyotes: Some Summary Thoughts. Proceedings of the 12th Wildlife Damage Management Conference (D.L. Nolte, W.M. Arjo, D.H. Stalman, Eds. 2007
  11. Shake-Spear’s Bible.com website; Coyote: An Instant Classic. Post by Roger Strirtmatter, October 25, 2011. Accessed June 13, 2012. Available at: http://shake-speares-bible.com/2011/10/25/coyote-an-instant-classic/
  12. The Royal Canadian Geographical Society website. Accessed June 13, 2012. Available at: http://www.canadiangeographic.ca/wildlife-nature/?path=english/species/coyote/2
  13. Personal correspondence; James Wright; Tyler Texas. Retired Texas Department of State Health Service official.

Is Chagas Disease Really The New AIDS Of The Americas?

This is the seventh of 16 student posts, guest-authored by Joshua Pikora.

Recently an article published in PLoS Neglected Tropical Diseases titled Chagas Disease: “The New HIV/AIDS of the Americas” caused a stir in the media receiving coverage through Fox News and The New York Times among others.  This article, as the title indicates, claims that Chagas disease is the new AIDS of the Americas and likens the current situation of Chagas disease to that of the first two decades of the AIDS epidemic, but is that truly the case1?  The argument that I gained from the article is that the early decades of the AIDS epidemic and Chagas disease affected similar demographics of people, and that the current number of AIDS patients and Chagas disease patients with cardiomyopathy in the Americas are similar.  The argument that the populations are similar is that both diseases affected those living in poverty, that do not have access to medical care, and hidden populations homosexuals in the case of AIDS and immigrants in the case of Chagas1.  Also the numbers of those living with AIDS and Chagas disease with cardiomyopathy cited in the article are similar with 2-5 million people with cardiomyopathy and roughly 3 million people with AIDS1.  Additionally the article also argues that they are both chronic conditions, are expensive to treat and are stigmatizing1.  While this is a compelling argument I believe that the differences between the two diseases outweigh these similarities, and these similarities alone do not warrant declaring Chagas disease the “new” AIDS.  In my opinion the article is well written, and puts together a case to support their claim, but while I do not mean to discredit the article, or to imply that Chagas disease is not a serious disease and should not be addressed, I disagree that it is as big of a problem as AIDS is, and was in the early decades of the epidemic.

Beyond simple differences between the disease like that Chagas disease is caused by a protozoan and AIDS is cause by a virus I have several problems with the claim that Chagas disease is the “new” AIDS of the Americas.  My first problem with the claim is that, in my opinion, in order for something to be the “new” AIDS, AIDS itself must be dealt with first, and as the article makes clear, AIDS is still a problem in the Americas with 1.6 million people living with AIDS in Latin America and the Caribbean, and 1.2 million living with AIDS in the US1.   The second issue I have with the claim is that it includes North America.  The article states that 8-9 million people are living with Chagas disease in Latin America compared to 300,000 in the US, with most of them being immigrants and vector transmission being rare in the US1,2.  While I would agree that Chagas disease is a serious problem in Lating America that needs more resources, I still would not compare it to AIDS as the two have very different levels of burden, and need to be addressed in different ways based on transmission.

The article does point out that Chagas disease and AIDS do share some modes of transmission, but they also have some unique modes as well.  Both AIDS and Chagas disease can be transmitted from mother to child vertically, and through blood transfusions1.  However, according to the article the rate of vertical transmission of  Trypanosoma cruzi 5%-10% pales in comparison to that of untreated HIV which is 15%-40%, though the rates of vertical transmission of HIV when antiretrovirals are being used is only 1%-2%1.  In the case of blood transfusions the US has screened for T. cruzi since 2007 and HIV since 1985 and blood banks in Latin America also screen for T. cruzi2,3.  Though AIDS and Chagas disease do share these modes of transmission they also have vastly different modes.  Chagas disease is primarily a vector born disease, using triatomine bugs as vectors, with transmission occurring by the bug’s feces getting into the site where the bug bit the host2.  There is also evidence of Chagas disease being transmitted through food contaminated with the feces of infected triatomine bugs1.  On the other hand AIDS can be sexually transmitted, and can be transmitted by using needles that have been used by an infected person3.

The article does describe several ways in which AIDS and Chagas disease are different.  The first of these is based on the differences in morbidity and mortality between the two diseases.  The article cites that annual deaths and lose of DALYs in the Americas is five times greater for AIDS than it is for Chagas disease, which shows a clear gap between the two1.  Another difference the article points out is that while AIDS is almost always fatal, only 20%-30% of people with Chagas disease will develop cardiomyopathy, displaying another gap between the diseases1.  A third difference that the article states between Chagas disease and AIDS is the number of medications available for the diseases.  While there are no medications that cure AIDS there are a number of antiretrovirals available to use as treatment, whereas there are medications available that can cure Chagas disease if caught early these medications are few in number and are infective against the chronic form1.  The amount of time that the medications need to be taken also differs between the diseases, with antiretrovirals being needed for life for AIDS patients, and medication for Chagas disease needing to be taken for one to three months1.

While both AIDS and Chagas disease are serious disease and Chagas disease is a particularly important issue that needs to be addressed in Central and South America, I do not believe that it is appropriate to call Chagas disease the “new” Aids of the Americas or even of Latin America.  Whether the title of the article was a ploy for attention or an honest belief may never be known, but hopefully this media attention can increase the awareness of Chagas disease and efforts to contain it, without distracting from the still important issue of AIDS.

Works Cited

1. Hotez PJ, Dumonteil E, Woc-Colburn L, Serpa JA, Bezek S, et al. (2012) Chagas Disease: “The New HIV/AIDS of the Americas”. PLoS Negl Trop Dis 6(5): e1498.

2. Zieve, David. “Chagas Disease.” Pubmed Health. U.S. National Library of Medicine, 15 Sept. 2010. Web. 17 June 2012. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002348/.

3.  Dugdale, David. “AIDS.” Pubmed Health. U.S. National Library of Medicine, 9 June 2011. Web. 17 June 2012. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001620/.

Spotlight on Nasty Parasites: Echinococcus granulosus

This is the fifth of 16 student posts, guest-authored by E. Jane Kelley.

Did you know that some dogs might have a tapeworm in their small intestine that can cause the development of large cysts in people’s livers, lungs, and brains? This is not very common in the United States currently, though there are cases reported periodically (2), but in some areas of the world it is a huge problem. An infection that can spread from animals to humans or vice-versa is called a zoonotic infection.

The tapeworm is called Echinococcus granulosus and the cystic disease it causes is called hydatid disease (http://www.cdc.gov/parasites/echinococcosis/) .  Human beings are considered a “dead-end” host because they are not usually the host of the parasite. The most common life cycle of the tapeworm involves dogs as the definitive host (which means that the adult tapeworm lives in their intestine) and sheep as the intermediate host (which means that they have the immature stage of the parasite, called a metacestode, in their bodies). As you can imagine, this means that this infection is more common in areas of the world where there is extensive sheep-raising. There are other definitive hosts (such as foxes, wolves, coyotes, wolves and cats) and there are other intermediate hosts (cattle, goats, deer, rabbits, and rodents for instance), but the dog-sheep cycle is globally the most important as far as human disease.

Back to the life-cycle: the adult tapeworm is small and lives quite innocuously in the small intestine of the dog, not usually causing any problem for the dog. Tapeworm eggs are shed in the dog’s feces and, in the usual scheme of things, are ingested by sheep as they graze. The eggs develop into an immature stage of the parasite, which travels in the bloodstream from the small intestine to other organs such as liver and lung. After a while, the immature stage develops into a cyst in the liver and/or lung and the life cycle is complete when a dog eats organs from a dead sheep. In most cases, multiple small cysts (3-4 cm in diameter and they are fluid-filled) develop in the liver or lung of the sheep, but, remarkably, affected sheep do not usually show any clinical signs and the cysts are found at slaughter.

Sometimes humans ingest the eggs accidentally (this parasite is spread by what is called fecal-oral transmission from the dog to the human, use your imagination, enough said) and the cysts can form in the liver, lung, brain or other places in the human. In human beings, the infection tends to result in a single large cyst rather than multiple small cysts like the sheep. These can take years to develop and can become very large (20 cm in diameter or more). Some cysts in the liver do not cause problems, but cysts in the lung may cause respiratory problems such as coughing and shortness of breath and cysts in the brain are not good for obvious reasons. The treatment is surgical removal of the cyst.

Again, we don’t have much problem with hydatid disease in this country currently but there is potential for it to become more prevalent. It was believed to have been introduced in the early 1900s with infected livestock. Interestingly, the infection initially established itself in a domestic dog/domestic pig cycle (not sheep) in the east (8) and by the 1920s was in Mississippi, Louisiana, Tennessee, and Arkansas. By the 1970s, it was fairly prevalent in the sheep-raising areas of the west (Utah, Arizona, California, and New Mexico)(4) and there is a cervid (elk, moose, deer) cycle in wildlife in Canada, Alaska, and Minnesota (6). Recently in Montana and Idaho, approximately 60% of gray wolves sampled had adult tapeworms in their intestine and cysts were found in organs of elk, mule deer, and a mountain goat (5).

Let’s focus on Utah for a moment. Echinococcus granuosus was believed to have been introduced into the state in 1938 in sheep dogs from Australia (3). Sanpete County in central Utah is the area where most of the sheep-raising went on (and still does). In the 1970s Echinococcus granulosus was endemic in sheep and dogs in central Utah. Endemic means that the disease is constantly present in a certain area. About 25-30% of the dogs were infected and 13% of sheep carcasses examined had cysts (1,7). In addition, during this time period, there were several human cases. The close contact between sheep-herders and their families and the sheep dogs and sheep kept the cycle going. Also, the sheep were range sheep with common grazing allotments and contact with other dogs and sheep. Control measures such as proper disposal of dead sheep, hand-washing, regular deworming of the dogs and educating the families were implemented and greatly decreased the incidence of infection in dogs, sheep and people (1,3,7). However, there are occasional cases still in Utah so either control measures were not 100% effective and/or there is a wildlife reservoir of infection (such as coyotes). There have been 3 cases in humans reported to the Utah Department of Health since the 1970s and multiple liver and lung cysts were found in a slaughtered sheep in 2008.

In some areas of the world, such as China (11), Echinococcus granulosus is a serious and increasing public health concern. In China, it is considered an emerging or re-emerging disease (a disease that was at a low level but is recently causing many more infections). Eradication of hydatid disease has been achieved in some island countries such as Iceland, New Zealand and Tasmania (10). It is certainly an easier task to control infection on a relatively small island with a single government than in other areas. Control of infection involves measures previously mentioned such as  regular deworming of dogs, proper disposal of sheep and cattle carcasses, stray dog control, education about the importance of hand-washing, and elimination of wildlife reservoirs if present. This is not as easy as it sounds and requires long term commitment which may be a problem in countries with economic and political unrest. For example, in Kazakhstan (a country in central Asia), after independence from the Soviet Union in 1991, social and economic changes have brought about changes in animal husbandry (from large collective farms to smaller farms with closer contact between people, dogs, and livestock) such that incidence of Echinococcosis has been increasing in people, dogs, and livestock (9).

In the United States, hydatid disease is less likely to become a serious problem because we have a relatively stable government and the infrastructure for the handling of carcasses and stray dog control. However, there are parts of the country where this still exists and, I don’t know about you, but I don’t relish the thought of having a huge cyst in my liver or brain. For those of you who kiss your dogs, have you seen what dogs eat?  Add this disease to the list of reasons that it’s not a good idea.  Don’t let your dogs defecate in children’s playgrounds because small children are not very discerning about what goes in their mouth.

References:

  1. Barbour AG, Everett JR, Andersen FL, et al. Hydatid disease screening: Sanpete County, Utah, 1971-1976. Am J Trop Med Hyg 1978 Jan; 27: 94-100.
  2. Bistow BN, Lee S, Shafir S, et al. Human echinococcosis mortality in the United States, 1990-2007. PLos Negl Trop Dis 2012 Feb; 6: e1524.
  3. Crellin JR, Andersen FL, Schantz PM, et al. Possible factors influencing distribution and prevalence of Echinococcus granulosus in Utah. Am J Epidemiol 1982 Sep; 116: 463-474.
  4. Donovan SM, Mickiewicz N, Myer RD, et al. Imported echinococcosis in southern California. Am J Trop Med Hyg 1995 Dec; 53: 668-671.
  5. Foreyt WJ, Drew ML, Atkinson M, et al. Echinococcus granulosus in gray wolves and ungulates in Idaho and Montana, USA. J Wildl Dis 2009 Oct; 45: 1208-1212.
  6. Himsworth CG, Jenkins E, Hill JE, et al. Emergence of sylvatic Echinococcus granulosus as a parasitic zoonosis of public health concern in an indigenous community in Canada. Am J Trop Med Hyg 2010 Apr; 82: 643-645.
  7. Loveless RM, Andersen FL, Ramsay MJ, et al. Echinococcus granulosus in dogs and sheep in central Utah, 1971-1976. Am J Vet Res 1978 Mar; 39: 499-502.
  8. Pappaioanou M, SchwabeCW, Sard DM. An evolving pattern of human hydatid disease transmission in the United States. Am J Trop Med Hyg 1977 Jul; 26: 732-742.
  9. Shaikenov BS, Torgerson PR, Usenbayer AE, et al. The changing epidemiology of echinococcosis in Kazakhstan due to transforming of farming practices. Acta Trop 2003 Feb; 85: 287-293.
  10. Torgerson PR, Budke CM. Echinococcosis- an international public health challenge. Res Vet Sci 2003 Jun; 74: 191-202.
  11. Yang YR, McManus DP, Huang Y, et al. Echinococcus granulosus infection and options for control of cystic echinococcosis in Tibetan communities of Western Sichuan Province, China. PLos Negl Trop Dis 2009 April; 3: e426.

Things that want to eat your brain

This is the fourth of 16 student posts, guest-authored by Eric Wika.

Let’s face it, it’s a dangerous world to be a brain. The brain is so soft and squishy it cannot even support its own weight. That’s right, even gravity itself is enough to take out an unprotected brain. Besides these passive threats, there are several factions out there that active try to damage your brain! Zombies are an ever present menace which wish to eat our brains. TV will rot our brains, drugs will fry our brains and bullies will offer to “beat your brains in”. It’s no wonder mother nature had to come up with the enormous bone braincase on top of your shoulders, it really is a dangerous place to be a brain!

And now, there’s even a new threat against our brain. Brain eating amoebas. Isn’t mother nature so adorable sometimes?!? Scientist have discovered an amoeba in river water that normally sits quite happily in its own environment eating bacteria. However, when it’s take out of its natural environment and shot up someone’s nose, it starts to eat the food source that’s readily available. That’s right, lunch time for brain eaters.

The amoeba is Naegleria fowleri, and has been reported recently in Louisiana. The Department of Health and Hospitals in the region had this to say about it.

Now if you think you may be infested with these brain loving parasites, let’s take a trip down Webmd.com to review what the natural history and symptoms of this tour of joy are. Remember standard disclaimers apply. If you go to the internet and use it as a replacement for real medical evaluation and treatment, then you are essentially leaving your medical health up to this guy, and come on, this guy can’t even figure out how to ROW.

Luckily there’s a FAQ for brain eating amoebas. The first thing to do is to check your exposure history. This bug doesn’t take the midtown bus and arrive at the steps of your apartment. You have to come to it. It lives in lake water, ponds, untreated pools, well water and the like. If you (or more to the point your nose) hasn’t been to any of these places, then you’re in luck. If your nose doesn’t go to these places, the bug can’t have access to your juicy brain bits. If you use a neti pot   there are some extra precautions to take. (more on this later) If you do get this bug up your nose, that’s where the confusion begins. It’s been postulated that these bugs get confused by the chemicals your brain cells use to communicate with each other. The signal that brain cell 1 uses to say “Hey, let Frank know I smell a hotdog down here” gets to the amoeba and through some massive mess up in communication, that signal is misinterpreted as “hey, Naegleria, get your butt up here for some goodies!!!” Naegleria then does the logical thing and get’s it’s little amoeba butt through the olfactory nerve (the bit that smells stuff) and into your frontal lobe (the smart “decides what you’ll have for lunch” bit) and begins the chow down process. Once you get it it takes about 2 to 15 days to show symptoms, and most people unfortunately die 3 to 7 days after symptoms appear. Symptoms are very similar to that of viral meningitis, including headache, fever, stiff neck, loss of appetite, vomiting, altered mental state, seizures and coma. Luckily these are symptoms that generally get you prompt attention from the local doctors at your hospital.

There have been a few cases of this disease so far. About 400 cases have been reported worldwide, 35 of which have been from the US since 2001. Thankfully, it is pretty rare. Unfortunately that can be a double edged sword as rare diseases tend to take longer to diagnose, if they get diagnosed at all. One of the most common ways to get this disease is through the use of a neti pot. A neti pot for those fortunate enough to not be in the know, is a tool used for pouring water directly into your nose. If you ever get to the point where your sinuses are so bad you start thinking to yourself “wow, having water poured directly into my nose would suck WAY less than this”, then getting a neti pot is for you. Other than medieval torture, a neti pot is a great device for flushing out the sinuses. Using one involves getting water, mixing it with some salt, and pouring it right on in there. Here is a lovely set of instructions coupled with an equally lovely picture of a woman in full nose irrigation mode.

The trick, however, is you have to use CLEAN water. If you’re going to shove something up your nose, whether it’s water or if you’re in Total Recall trying to remove an alien probe from your brain, do yourself a favor and make sure it’s clean.

Now you may be thinking “I’m fine, the only water I stick up my nose is pure, clean tap water. I don’t use dirty well water or go swimming in icky lakes and streams. Unfortunately, in today’s world, that just ain’t good enough. See tap water isn’t sterile. It’s clean, it’s safe to drink, but it isn’t sterile. Drinking tap water with Naegleria in it won’t make you sick, but sticking it up your nose will. You can avoid this easily one of two ways. 1) boil water (don’t forget to cool it!) before using your neti pot, or 2) buy distilled water for use with your neti pot (it costs less that $1 per gallon at most grocery stores).

Remember, the only one who can protect your brain is you! Use your neti pot safely and don’t get your brain eaten!

What you don’t see can hurt your cat…and you too

This is the second of 16 student posts, guest-authored by Eileen Ball.

The beauty of dogs and cats as companions is that we don’t have to raise them to go out into the world and be successful.  As pet parents we can set the household “rules” according to what works for us and get on with enjoying our pets; hopefully for many years.   According 2011-2012 APPA National Pet Owners Survey cats have now surpassed dogs as the most common household pets in the United States.  Despite this fact  the same survey reports that in 2010 only 30% of US veterinary patients were cats.  As a companion animal veterinarian I find these statistics alarming and I fear that many well-intentioned pet owners are simply unaware of the risks that can accompany the joys of cat ownership.

A common perception is that indoor cats don’t need veterinary care.  In this sentence there two big factors that need to be addressed.  The first, and for me the most obvious, is that indoor cats need veterinary care too!  In a bit I’ll get to explaining that even without outdoor threats,  such as motor vehicles and big dogs, indoor cats and their owners face almost as many dangers as their outdoor brethren.    The other part of the eleven word sentence at the start of this paragraph that requires definition is the concept of “indoor cat.”    During my ten years as a practicing veterinarian I had many a conversation with an owner that started with the question “Is Fluffy indoor or outdoor?”  Followed by the owner confidently responding “indoor.”  As we moved forward in our discussion and I asked more about how Fluffy spent her day I’d often learn that Fluffy had access to the yard or deck and often spent long periods of time there.  There were alternative versions of the discussion where Fluffy didn’t physically go outside but the dog did as well as scenarios where mice, birds or bats came indoors even though they weren’t invited.  The reality is that In order for a cat to be considered 100%  indoor it would need to live in a biosphere.

So why should you take your indoor cat to the veterinarian on at least a yearly basis?   The first and most important reason is that your cat has the potential to carry parasites and diseases that can be transmitted to you and your family.  These include but are not limited to:  hookworms, roundworms, fleas, ticks, ringworm and Rabies.  According to the CDC approximately 14% of the US population has been infected with a type of roundworm called Toxocara.  Indoor cats are a potential source of exposure as they generally use litter boxes and they frequently contact surfaces such as countertops, bathroom vanities, kitchen tables and bedding.  Many cat owners have the misunderstanding that because their cats do not go outdoors they are not at risk.  This is simply not true.  There are lots of indoor/outdoor parasite sources such as mice, rats, other pets and people.  Hookworm and roundworm infections are easily and safely prevented with a variety of medications.  Your veterinarian can run a simple fecal test to see if your cat is infected with these or other parasites.  Another concern for cat owners is the transmission of a type of bacteria called Bartonella.   In most cases infected cats will show no symptoms, although in some it may cause gum disease, conjunctivitis (swollen membranes around the eyes) or respiratory disease.  Bartonella can spread from cats to humans.  It is the causative agent of Cat Scratch Disease in people.  Cats often get this bacteria from fleas and they can transmit it to humans via bites and scratches.  While parasites and Bartonella are a significant risk for healthy humans in those who don’t have a fully functioning immune system the risk is magnified even further.

The most important disease that you can protect your indoor cat from is Rabies.  This is a virus that is spread via saliva and is almost always deadly.  Rabies infection is common in skunks, raccoons, foxes and bats.  A bat getting into the house through an open window or a chimney is a very real risk for any animal or person in your house.  If you should happen to find a bat in the house with your cat (or other pets) you must assume that they were bitten.  Because of the thick fur that cats have it can be impossible to see a small bite wound.  Depending on local laws you may be required to vaccinate your cat for Rabies every 1-3 years.

There are other conditions such as ringworm and toxoplasmosis that cats can have without showing any signs.  People with healthy immune systems are not likely to show symptoms if they are exposed to these parasites but for others with HIV, cancer, pregnancy or a suppressed immune system serious consequences can occur.  When I think of ringworm without symptoms I always recall one of my patients, Miss Kitty, who was loved and adored by her entire family.  Miss Kitty and her humans were originally from Hawaii and had moved to Virginia where I was in practice.  Since Miss Kitty couldn’t travel from mainland US to Hawaii without quarantine the relatives in Hawaii decided to come to Virginia for Christmas.  Miss Kitty’s human grandmother happened to have breast cancer and was undergoing radiation.  The family had a great holiday.  Shortly after her return to Hawaii the grandmother developed circular, itchy scabs on her skin.  Her MD diagnosed it as ringworm and asked if she had any pets.  The grandmother said “no” and the MD presumed she had picked it up from the environment and started treating her.  It was a couple months later in conversation with Miss Kitty’s owner that I’d inquired about the holiday visit and the grandmother’s health.  Miss Kitty’s owner described the wonderful time that they’d had and mentioned that the grandmother had enjoyed the trip except for her persistent skin lesions.  A bell went off in my head and I decided to test Miss Kitty’s hair for ringworm.  Sure enough even though she’d never had a problem with her skin Miss Kitty was positive for ringworm.  Based on the species we cultured the grandmother’s MD was able to change treatment and get her skin cleared up quickly.

Finally, as most people who have shared their lives with both dogs and cats will agree, cats are not small dogs.  While the process of domestication for both dogs and cats has been ongoing for thousands of years it is estimated that the dog started the process 9-10,000 years before the cat.  For this reason cats tend to display a “survival of the fittest” instinct that we don’t see in dogs. Because of this instinct cats generally aren’t transparent when they don’t feel well.  Some cats are prone to chronic heart, thyroid  and kidney diseases that can often be detected with a thorough examination and some bloodwork.  Although most of these chronic conditions can’t be cured, with good veterinary guidance they can be well managed and allow you to share many happy years with your cat.

If your cat hasn’t been to the veterinarian in awhile I hope you will consider scheduling an appointment.  This can not only make life longer and better for your cat it can also protect you and your family from serious disease.

References:

American Pet Products Association 2011-2012 Pet Owners Survey

http://www.americanpetproducts.org/pubs_survey.asp

http://www.cdc.gov/parasites/toxocariasis/epi.html

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002581/

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002310/

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002411/

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001661/

http://catvets.com/cfpandpractitionersearch/

Bartonella Spp. In Pets and Effect on Human Health,  Chomel et al. Vol. 12 number 3, March 2006,  www.cdc.gov/eid