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 ( .  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.


  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 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!

Atypical Typhus

This is the third of 16 student posts, guest-authored by Mary Egan.

Murine typhus has been in the news recently in Austin, TX, where in May of this year, two people were found to be positive and one died.  This rings a number of alarm bells for me, since I live in Texas, and specifically in Austin.  I know of another Austin veterinarian who got sick with murine typhus in 2008, when it was first noticed in Austin and investigated by the CDC.  I was also working as a relief vet at the Town Lake Animal Center, the municipal shelter, and at the Austin Humane Society, the main nonprofit adoption shelter which has a feral cat Trap-Neuter-Return surgery clinic, when the CDC investigators came to Austin.  They collected blood samples on local animals and also fleas.  Of course, at that time I wasn’t particularly interested in public health, just shelter medicine, and it didn’t really register.  Now I wish I could’ve gone back and tagged along to see more of what they were doing!

Murine typhus is an odd and off the radar disease.  It doesn’t help that murine and typhus are both words with multiple meanings.  Murine is a word that refers to mice, in Latin, murinus, or mouse, in Latin, mus.  It is also a type of eye drops and also a brand of ear wax remover.  How putting mice in your eyes or ears helps them is a mystery to me.  Murine also sounds very similar to marine, so it’s not unreasonable to start picturing typhus near the ocean, which is an odd coincidence, since murine typhus actually occurs primarily in coastal areas.

Typhus itself is a confusing word.  It comes from the Greek, and means hazy, which is how your brain feels if you’re infected.  It is not the same as typhoid fever, which is caused by Salmonella typhi, a bacteria that can cause food borne illness resulting in diarrhea and vomiting.  This is not that.

The typhus we are interested in is a tiny bacteria from the family Rickettsia.  And of course there is more than one type of typhus, to confuse the issue further.  Epidemic typhus is the ancient disease that has been a major player in history.  It was first noted in the Spanish blockade of Granada in 1489, and then killed more of Napoleon’s army than the Russians.   This is Rickettsia prowazekii, which is carried on lice and affects humans.  This is the typical typhus.  If you ever read just “typhus” it is referring to this type of typhus.  It has also been called jail fever, since many old jails were breeding grounds for lice, and the prisoners were more likely to die of infection than be hung for their misdeeds.  This typhus can cause a rash, fever, severe headache, joint pain, kidney failure, delirium, stupor, and even death in 10-60% of cases if it’s not treated.  A blood test will show if there are antibodies to typhus if you go to your doctor with these signs.  There is an effective treatment, a course of antibiotics that kills the rickettsia, and supportive care depending on how far along the disease had progressed.  It is possible for the agent to go underground, and then reappear later in life.  Then it is called Brill-Zinsser disease and is often a very mild form of epidemic typhus, still treated with antibiotics.

The typhus that showed up in Austin is murine typhus, also called Rickettsia typhi, and it is carried on fleas and primarily affects rats.  This is also called endemic typhus because it is pretty much always present on rats in the environment.  Humans historically get it as a side product of coming into contact with rats carrying the infected fleas.  This disease is usually not as severe as epidemic typhus, but can still cause all the same signs and symptoms, and rarely can lead to death if not treated.  Less than 2% die of murine typhus if it is not treated with antibiotics.

Murine typhus has a worldwide distribution, but in the United States it is usually seen near coastal areas in California, Hawaii, and Texas.  The 2008 cases were odd that they were in Austin, in central Texas.   In the previous 25 years, there had only been four cases total.  In 2008 there were 13 cases in the four months from March to July, and a total of 33 cases by October.  Of these, 70% of the people infected were hospitalized with myalgia, severe headache, and fever, and the most severe cases were treated for pneumonia, kidney failure, and coagulopathy.   There were no deaths.  This outbreak showed that aside from the normal rat-flea cycle, there are likely other cycles that involve domestic and feral cats, opossums, dogs, and the fleas that live on them.  And consequently, the fleas that live on domestic cats and dogs then live in the yards and homes of their owners, and then can live on the owners themselves.

The cases were clustered in the central Austin area, with a large percentage coming from one zip code that contains a large portion of the exceedingly popular Town Lake Hike and Bike Trail used by over 20,000 people daily, and the smaller but more wild Shoal Creek Trail.  There have been reports of coyote sightings and suspected killings of family pets in this zip code.  So there is ample space for wildlife within this urban environment.  This also means there are plenty of hosts for fleas.  And Austin in general and this neighborhood in particular is known for a slightly hippy, crunchy granola lifestyle preferring organic and natural everything, with easy access to the outdoors and hiking trails.  It is not surprising this outbreak occurred in this area.

So what does all this mean?  Diseases which were previously uncommon are now becoming more common due to changes in lifestyle.  People want to live close to nature and have trails to walk their dogs.  There is nothing wrong with that.  It’s the parasite hitchhikers their pets pick up and bring home that’s the problem.  And changes in behavior where dogs are now not only in the house, but often in the bed with their owners, means that those fleas have a chance to bite humans.  That doesn’t mean you shouldn’t walk your dog on the trail.  But it does mean you need to use protection.  Spray yourself and your clothes with a flea killing insecticide such as DEET when out walking.  Wear boots, long pants, and long sleeved shirts.  Use appropriate flea control on your pets.  Kill fleas in your yard or home with appropriate premises control measures.  It’s great to be one with nature, you just don’t want that nature to bite back with a case of murine typhus.


1.  Adjemian J, Parks S, McElroy K, Campbell J, Eremeeva ME, Nicholson WL, et al. Murine typhus in Austin, Texas, USA. Emerg Infect Dis. 2010 Mar.   Accessed June 13, 2012.  Available at:

2.  James C.  Two cases of typhus in Travis County.  KXAN web site.  Accessed June 13, 2012.  Available at:

3.  Typhus.  Wikipedia website.  Accessed June 13, 2012.  Available at:

4.  Murine typhus.  Texas Department of State Health Services website.  Accessed June 13, 2012.  Available at:

5.  Conlon J.  The historical impact of epidemic typhus.  Accessed June 13, 2012.  Available at:

6.  Google map of 78703 zip code.  Google maps website.  Accessed June 13, 2012.  Available at:,Austin,+TX+78703&gl=us&ei=i7DTT9vPJsLQ2AX54riFDw&sa=X&oi=local_group&ct=image&ved=0CHQQtgM

7.  Gonzales R.  Santa Ana announces flea-borne typhus alert.  Orange County Register website.   Accessed June 13, 2012.Available at:

8.  Roving pack of coyotes mauls pets.  KXAN website.  Accessed June 13, 2012.  Available at:

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.


American Pet Products Association 2011-2012 Pet Owners Survey

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













Bugs in your berry juice

This is the first of 16 student posts, guest-authored by Riva Ben-Ezra.

Acai fruit comes from the Brazilian Amazon forests and is one of the main dietary staples of the native population.  It has been touted as having potent antioxidant properties 1,2 as well as being a stimulant for weight loss3, a cancer cure and an anti-aging miracle drug.  Whether these claims are true or not remains to be seen4,5; however the FDA has clamped down on Acai products claiming to perform health benefits without classifying themselves as drugs (see here, here and here).

Something that the FDA has not taken into consideration, however, is the presence of triatomines in Acai juice.  Triatomines are blood-sucking insects that have been found in South America (mainly Brazil), Texas and Mexico.6 These bugs can carry a protozoan parasite called Trypanosoma cruzi, which is the causative agent for Chagas disease.6  Chagas disease is considered a “Neglected Disease” by the CDC because:

These infections are considered neglected because relatively little attention has been devoted to their surveillance, prevention, and/or treatment.

Chagas disease can be divided into two phases: acute and chronic.  In the acute phase, the most common symptoms are fever and swelling where the parasite feces entered the patient.  The chronic phase is hallmarked by the development of cardiomyopathies, arrhythmias, and megaesophagus or megacolon. 6 The disease can “hibernate” in the body and re-activate during times of stress or immunosuppression.   The WHO estimates that 10,000,000 people worldwide have been infected with Trypanosoma cruzi, and the CDC estimates that approximately 300,000 of those people are living in the United States.  The most common methods of becoming infected include:

  • being bitten by a triatomines insect
  • receiving a contaminated blood transfusion
  • transferring it through the placenta to a fetus
  • receiving a contaminated organ transplant, and
  • ingesting contaminated food

Since 2009, the last option mentioned above was considered to be rare.  However, in the past three years, several studies have been published confirming the transmission of Chagas disease through contaminated food in Brazil, Venezuela and Colombia (not the US).7  The suspected or confirmed culprits include acai juice/paste, orange juice, guava juice, sugarcane juice, and other (unknown) meal items.7  An epidemiological trace-back to discover the source of the protozoa on infected food revealed the presence of feces from either triatomine bugs or other animals such as opossum, marsupial or rodent8 9 already infected with the protozoa7.  From observing the processing of Acai fruit and sugar cane, it was revealed that conditions are frequently unsanitary and that there are many instances when the triatomine bugs are ground up with the fruit to make juice.10  In 2007, the Brazilian authorities drafted a guidance document to control foodborne transmission of Trypanosoma cruzi, but as evidenced by the data above, there is little compliance with these recommendations.7
Triatomine bug

Triatomine bug, Trypanosoma cruzi vector, defecating on the wound after taking a blood meal.


So, given the fact that people can and do become infected with Trypanosoma cruzi through eating contaminated fruit and other foods, and given the fact that the WHO, EFSA, and the CDC all recognize that oral transmission of Chagas disease is an emerging infectious disease, how have our regulators addressed this risk?

The simple answer is: not at all.

In the United States, fruit juice must be processed under a food safety system called HACCP- Hazard Analysis and Critical Control Points.  HACCP requires the manufacturer to identify the possible hazards associated with the production of this food, and preventing those hazards from being present in the final product.  The FDA’s Guidance for Industry: Juice HACCP Hazards and Controls Guidance was published in 2004 as a response to an outbreak of E. coli 0157:H7 in apple juice11,12.  It states:

The HACCP regulation requires you to use treatments capable of consistently achieving at least a 5-log reduction (using ten as the base number) in the level of the pertinent microorganism in your juice…The “pertinent microorganism” is the most resistant microorganism of public health significance that is likely to occur in the juice and is the pathogen that you must target for the 5-log pathogen reduction treatment (21 CFR 120.24(a)). By choosing the most resistant pathogen as your target, you are also treating the product for all other pathogens that are less resistant to the means of treatment.  One way to identify the pertinent microorganism for your juice is to consider whether there have been any illness outbreaks associated with this type of juice, and what microorganisms have caused the outbreaks. If certain pathogens have been demonstrated, i.e., through outbreaks, to be potential contaminants in certain juices, then the pertinent microorganism for your process typically should be one of these pathogens.

Sounds good, however further on it lists the various hazards that may be present in fruit juice, and it does not include the protozoan parasite Trypanosoma cruzi.  It also does not require pasteurization for all fruit juices, the only known method to destroy Trypanosoma cruzi.10  The FDA permits other methods to create a 5-log reduction such as high-pressure, UV radiation, or surface sanitation; none of which have been shown to be effective in destroying Trypanosoma cruzi.

The CDC published an article entitled “Preventing Health Risks Associated with Drinking Unpasteurized or Untreated Juice” on their web site.  Their recommendations are as follows:

Untreated (raw) juice has not been treated in any way to kill pathogens that may be present. This type of juice may be found in the refrigerated sections of grocery stores, health-food stores, cider mills, and farm markets. Another form of untreated juice is untreated cider. One way to make this cider safer is to heat it to at least 170° F. Prepackaged, untreated juice must bear a warning label that looks similar to this one:


To minimize health risk, young children, the elderly and people with weakened immune systems should not consume packaged juice that bears the above warning label or any other form of juice that is known to be untreated (e.g. untreated juice served by the glass at a roadside cider stand). Anyone who wishes to reduce their risk may follow this recommendation.
If it is unclear that a juice has been treated to destroy harmful bacteria, avoid drinking it.

This is definitely a step in the right direction-however, not only high-risk individuals can become infected with Trypanosoma cruzi, and the recommendations should reflect that.

Looking at other countries, we find a variety of responses.

The Codex General Standard for Fruit Juices and Nectars does not include any reference to pasteurization or other treatment to control the transmission of Trypanosoma cruzi in fruit juice.  The Code of Hygienic Practice for Fresh Fruits and Vegetables does address the general notion of prevention of contamination during harvesting and storage.


The Australia New Zealand Food Authority discussed the possibility of requiring orange juice to be pasteurized or to require a label stating that the product is unpasteurized as in the US, and recommended similar requirements as the FDA in 2001.  As of 2008, however, the Fruit Juice Standard does not require any form of pathogen reduction treatment or labeling.


The European Union, similar to Australia, does not have any requirement for pathogen reduction treatment or labeling within their legislation.  They do require HACCP for all factories manufacturing fruit juice and with that should be the listing of the presence of Trypanosoma cruzi as a hazard to be eliminated.


The Canadian Food Inspection Agency published the “Code of Practice for the Production and Distribution of Unpasteurized Apple and Other Fruit Juice/Cider in Canada” which addresses the possibility of fecal contamination of the fruit used to make juice and outlines procedures to minimize the presence of microbial contamination in the final product.  It also requires manufacturers to label unpasteurized products as such.  In their Holiday Food Safety Tips for consumers, they write:

  • When making punch or serving cider, check the product label to make sure the juice or cider has been pasteurized.
  • If the juice or cider has not been pasteurized, bring it to a rolling boil and then cool before serving.
  • Unpasteurized fruit juice and cider may contain bacteria like Salmonella and E. coli that can cause serious illness, especially in children, seniors and people with weakened immune systems.

Again, similar to the CDC recommendations, they do not address the fact that healthy people can become infected with Trypanosoma cruzi by drink unpasteurized juice.

Returning to Acai berries, what is the take-home message for you, the consumer?


  • Make sure you only drink pasteurized juice.
  • Don’t use skin products with Acai berries in them unless the product has undergone a heat treatment.
  • Don’t accept claims that Acai berries cure disease.
  • When travelling to Latin and South America, be sure to eat food from a reliable source and do not eat fruit that has not been pasteurized.




1. Lichtenthler R, Rodrigues R, Maia JGS, Papagiannopoulos M, Fabricius H, Marx F. Total oxidant scavenging capacities of euterpe oleracea mart. (açaí) fruits. Int J Food Sci Nutr. 2005;56(1):53-64.

2. Jensen G, Wu X, Patterson K, et al. In vitro and in vivo antioxidant and anti-inflammatory capacities of an antioxidant-rich fruit and berry juice blend. results of a pilot and randomized, double-blinded, placebo-controlled, crossover study. J Agric Food Chem. 2008;56(18):8326-8333.

3. Udani J, Singh B, Singh V, Barrett M. Effects of açai (euterpe oleracea mart.) berry preparation on metabolic parameters in a healthy overweight population: A pilot study. Nutrition journal. 2011;10:45-45.

4. Are some of the more exotic berry types, such as goji and açaí berries, better for health than the more common berries such as strawberries, blueberries and raspberries? Mayo Clinic health letter. 2010;28(11):8-8.

5. Marcason W. What is the açaí berry and are there health benefits? J Am Diet Assoc. 2009;109(11):1968-1968.

6. Pereira K, Schmidt F, Guaraldo AMA, Franco RMB, Dias V, Passos LAC. Chagas’ disease as a foodborne illness. J Food Prot. 2009;72(2):441-446.

7. Shikanai Yasuda M, Carvalho N. Oral transmission of chagas disease. Clinical infectious diseases. 2012;54(6):845-852.

8. de Noya B. Large urban outbreak of orally acquired acute chagas disease at a school in caracas, venezuela. J Infect Dis. 2010;201(9):1308-1315.

9. Miles M. Orally acquired chagas disease: Lessons from an urban school outbreak. J Infect Dis. 2010;201(9):1282-1284.

10. Barbosa R, Dias V, Pereira K, et al. Survival in vitro and virulence of trypanosoma cruzi in açaí pulp in experimental acute chagas disease. J Food Prot. 2012;75(3):601-606.

11. Cody SH, Glynn MK, Farrar JA, et al. An outbreak of escherichia coli O157:H7 infection from unpasteurized commercial apple juice. Ann Intern Med. 1999;130(3):202-209.

12. Vojdani J, Beuchat L, Tauxe R. Juice-associated outbreaks of human illness in the united states, 1995 through 2005. J Food Prot. 2008;71(2):356-364.


Student posts 2012

As long-term readers know, I’ve previously featured student posts on various topics of their own choosing. I’m doing it again this year with my summer course on Applied Infectious Disease Epidemiology. In this course, students learn to take the theories and information from a basic ID epi course and apply them to real-world experiences–analyzing math models, determining the cause of an outbreak, and designing their own studies to test a research hypothesis, for example. As part of the course, communication is also a big segment, examining how information (and misinformation) is communicated over the internet and beyond, and learning how to work with media. Their final assignment is to write a blog post at a level laymen will understand on the topic of their choice. The first posts will begin to pop up tomorrow–enjoy, but please be kind (and constructive!) with any comments or criticisms.

ASM 2012!

ASM 2012 is almost upon us! Who’s going? Who’s presenting? Who wants to meet up and what are good days for it? Leave suggestions and pimp your own presentations below in the comments.

I will be convening a session on Sunday, June 17th on science communication, “Sound Bites to Superbugs”.

Sound Bites to Superbugs: How to Communicate Risk to the Public and Physicians
3:00 p.m. – 5:30 p.m.

TARA C. SMITH; University of Iowa, Iowa City, IA

Invited Speakers:
ROBYN WILSON; The Ohio State University; Columbus, OH
JOSH ROSENAU; National Center for Science Education, Oakland CA
JAMES HUGHES; Emory University, Atlanta, GA
TARA C. SMITH; University of Iowa, Iowa City, IA

Science denial is prominent in many areas of expertise. When individuals deny health and medical information, consequences can be serious. Anti-vaccination sentiment has increased and led to outbreaks of preventable disease. In this session, attendees will learn how to communicate risk effectively to the general public; to understand why individuals do not accept scientific evidence; and to work with physicians to facilitate increased understanding.