Student guest post: Cancer isn’t contagious…or is it??

Student guest post by McKenzie Steger

Off the southeastern coast of Australia lies a small island that in the 1700 and 1800’s was inhabited by the very worst of Europe’s criminals and is now the only natural home in the world to a species named after the devil himself. Decades later beginning in 1996 Tasmanian devils were going about their nocturnal lifestyle in normal devilish fashion feasting on small mammals and birds, finding mates and reproducing, occasionally fighting with one another and so on. (1) Just as criminals divvied up their booty hundreds of years before, the devils were sharing something of their own—only something of much less value. It turns out they were transmitting to one another a rare and contagious form of cancer known as Devil Facial Tumor Disease or DFTD. Once infected, facial tumors developed and the devil faced 100% mortality most often due to inability to eat or airway obstruction. Over the last 17 years the result of this highly contagious and fatal cancer has been the elimination of over half of the devil population throughout Tasmania. (2)

mckenzie picture


DFTD is not alone when it comes to transmissible forms of cancer. For over six thousand years dogs, jackals, wolves, and coyotes across the globe have experienced their own “contagious” cancer in the form of canine transmissible venereal tumor—C TVT and also called Sticker’s sarcoma. (2) CTVT is generally considered the first known cell line to be malignant having been described in the mid 1800’s. These unique growths like DFTD can spread from one individual to the next, but in the case of CTVT this most commonly occurs during coitus, licking, and biting infected areas. CTVT lesions usually establish in the genitals or in close proximity as a result. CTVT is unique in that only an estimated 7% of cases metastasize unlike in DFTD cases where 65% of them result in metastasis. CTVT rarely results in severe clinical illness but instead nearly always regresses on its own. (3)

So what is it that makes DFTD and CTVT so “contagious”? Essentially it boils down to host immunity. In the case of DFTD, devils pass on tumor cells when they are in close physical contact with others during mating or fighting. The Tasmanian devil population simply lacks the genetic diversity to be able to immunologically recognize and ward off the tumor and thus, these highly virulent and metastatic cells set up camp in the new host tissue and invade in no time. Interestingly, studies have shown that the DFTD cells are unique, containing only 13 pairs of chromosomes instead of 14 like most cells. Technology has also shown the very same cell line that began the DFTD devastation—thought to be of Schwann cell origin—is the very same one being transmitted throughout devil populations today. (2)

In contrast, CTVT, a histiocytic tumor (4), affects mammals rather than marsupials which have much greater diversity within the population and a more advanced capability to detect foreign and potentially invasive cells. This is due to the MHC-1 molecules or multiple histocompatibility complexes that help the body’s immune system to recognize foreign substances. CTVT is so effective in transmission because it down regulates these MHC-1 molecules effectively “hiding” the invasive cells from the body’s immune system. At some point however, this mechanism is overcome and the CTVT is recognized and killed by the body in animals that are immunologically sound. (2)

What about transmissible cancer in humans? The good news is that no comparable strain of such a killer contagious cancer has been recognized in humans compared to what devils in the “land down under” are experiencing. The bad news is that there are technically forms of cancer affecting man that result from contagious agents. Estimations attribute 15% of tumors world-wide to contagious pathogens including mainly viruses but also bacteria and parasites as well. Most documentation of cancer transmission cases in humans are reported in individual case reports, however, highlighting the rarity and unlikelihood of this occurrence. (2) Nonetheless, it still occurs. Hepatitis B and C viruses, herpes viruses, human immunodeficiency virus (HIV), and papilloma viruses are just a few examples of viruses that can develop into cancer in patients or predispose them to tumor formation. Bacterial etiologies include members of the Chlamydia, Helicobacter, Borellia, and Campylobacter families. There are also a few select parasites classified as Group I and Group II carcinogens including members of the Schistosoma, Opisthorchis, and Clonorchis families. So really, “contagious cancer” in humans is due to contagious or infectious etiologies and not necessarily direct contact transmission. Although there are documented and potential exceptions including cancer spread through tissue grafts, organ transplants, papillomavirus transmission during sexual intercourse and other isolated events. (1)

At the end of the day, the presence, history, transmission, and pathogenesis of transmissible cancers in Tasmanian devils, dogs, and the few cases documented in humans provides insight regarding the immune mechanisms that do and those that do not allow cancer to develop. The key difference here is mammals verses marsupials and the reality that mammals have a more advanced immune system allowing them to better overcome cancer and other foreign invasions. A better understanding of both CTVT and DFTD has and will likely continue to allow researchers better insight into mechanisms of immune system invasion of various types of cancer. (1)



(2)   Welsh JS. Contagious Cancer. Oncologist. 2011 January; 16(1): 1–4. Published online 2011 January 6.

(3)   Belov K. Contagious cancer: Lessons from the devil and the dog. BioEssays: Volume 34 (4), pages 285–292, April 2012.



Student guest post: New Study Finds that the Flu has Multiple Ways of Spreading

Student guest post by Sean McCaul

Sean pic 1

Image Source:

The next time somebody in your office or household has the flu, you might want to consider keeping your distance.  A new study published this month in Nature Communications suggests that about half of the transmission of influenza A results from inhalation of microscopic infectious droplets created by the coughing and sneezing of people infected with the flu.  The flu virus hitches a ride in these droplets, and may infect nearby susceptible people who breathe them in.1

The influenza A virus generally causes fever, coughing, body aches, runny nose, sore throat, headache, and fatigue.  Vomiting and diarrhea may occur, but are more common in children.3 Fever and most other clinical signs usually resolve within 5 to 7 days, but coughing may last two weeks or more.2 Children under 2 years old and the elderly are at greatest risk for complications such as pneumonia, and over 90% of influenza deaths are in people over age 65.2

Seasonal outbreaks of influenza are common in the United States, and typically occur during winter months.  During and average outbreak, 5% to 20% of the people in a community may become ill with the flu, and up to half of the people in environments like schools and nursing homes may get sick.2

In adults with healthy immune systems, the flu virus is shed in highest numbers during the first 3 to 5 days of illness, making spread of the flu most likely during this time.  Children may shed the virus for up to 10 days, and people with weakened immune systems may shed the virus even longer.2 In a typical outbreak, a person sick with the flu passes the illness on to an average of 1 to 2 other people.1,2

Previously, influenza A viruses were thought to be transmitted primarily by direct contact and by larger (but still very tiny) droplets generated by coughing, sneezing, and talking.1,2,3  These droplets are capable of travelling 1 to 2 meters, where they may come to rest in the eyes, nose, or mouth of a susceptible person and cause them to become sick with the flu.  These droplets may also fall upon nearby surfaces and objects, where the flu virus can survive for hours.  A person touching these surfaces or objects may get the flu virus on their hands, and then transfer the virus to their eyes, nose or mouth and become ill.1,2

The recent study, published on June 4, 2013, used a mathematical model of influenza virus transmission to evaluate the data from two previously published studies of the effectiveness of hand hygiene and facemasks for the reduction of transmission of influenza A viruses.   It suggests that the flu virus may survive in very tiny droplets created by coughing and sneezing that can remain suspended in the air as an aerosol long enough to be inhaled by nearby susceptible people.   The study shows that aerosols are an important route of transmission of the virus, and may account for as much as 50% of the spread of the flu.1

Sean pic 2

Image Source:

How you get the flu may determine, in part, how ill you get.  Influenza researchers have long suspected that inhalation of aerosols containing the flu virus can lead to more severe illness than exposure to the flu virus by direct contact or by the settling of larger droplets in the eyes, mouth or nose of susceptible people.  This is thought to be because larger droplets are trapped by the defense mechanisms of the upper respiratory tract, such as the large surface area of the nasal turbinates and the mucus lining the nose, pharynx, and trachea.  Smaller droplets, meanwhile, are capable of being inhaled deep into the lungs, resulting in infection in the lower respiratory tract which can cause more severe disease.  The current study found that there was an increased risk for fever plus cough in people suspected to have contracted the flu by inhalation of infective aerosols, which is consistent with current ideas regarding the importance of the route of infection.1

Understanding the routes of transmission of influenza is also important for designing control measures to reduce the spread of this disease.    Interventions such as increased hand hygiene and facemasks help to limit transmission of influenza by larger droplets produced by coughing and sneezing, but may offer little protection from inhaled aerosols.1 Additional methods for controlling the spread of influenza through aerosols, such as improved ventilation of enclosed spaces, ultraviolet lights (which are capable of killing the flu virus), and minimizing exposure to those infected with the flu could reduce the risk of becoming sick.1

So, what can you do avoid getting the flu?  The most effective way is to get vaccinated before flu season.  In the United States, flu season can start as early as October, though the peak months for flu are January and February, and sometimes even later.3 Because the flu strains circulating through the population change from year to year, you should be vaccinated each year.  The vaccine is developed to prevent illness caused by the flu strains likely to cause outbreaks during the flu season, but may not prevent illness from novel or unanticipated strains causing outbreaks.  Some people, such as babies less than 6 months old and those with allergies to eggs should not receive the flu vaccine.3  So the CDC recommends that you take additional preventive measures, such as good hand hygiene, avoid close contact with people who are sick with the flu, avoid touching your eyes, nose, and mouth, and practice good health habits such as remaining well hydrated, eating a healthy diet, exercising, and getting plenty of rest.5

If you do get the flu, what can you do to avoid infecting your family, friends, and colleagues?  First, avoid close contact with others.  Stay home from school or work if at all possible, and don’t run errands while you are sick.  In this way, you can avoid exposing others to your illness.  Second, cover your nose and mouth when you cough or sneeze.  Experts recommend that you cough and sneeze into a cloth or into your elbow, so that you don’t contaminate your hands, which are commonly implicated in the spread of the flu.  This simple practice can reduce the amount of infectious material you spread into your environment.  Practice good hand hygiene, particularly before touching doorknobs and other items that may leave the virus where others are likely to become exposed.5


  1. Cowling, B.J., Dennis, K.M., Fang, V.J., Suntarattiwong, P., Olsen, S.J., Levy, J., Uyeki, T.M., Leung, G.M., Malik Peiris, J.S., Chotpitayasunondh, T., Nishiura, H., & Simmerman, J.M. (2013).  Aerosol Transmission is an Important Mode of Influenza A Virus Spread.  Nature Communications, DOI: 10.1038/ncomms2922  LINK
  2. Bridges, C.B., Fry, A., Fukuda, Shindo, N., & Stohr, K. (2010).  Influenza (Seasonal).  In Heymann, D.L. (Ed.).  Control of Communicable Diseases Manual.  American Public Health Association, Unbound™ Mobile Platform
  3. Centers for Disease Control (February 13, 2013), Key Facts About Influenza (Flu) and Flu Vaccine, accessed at , June 8, 2013
  4. Centers for Disease Control (May 6, 2013), What You Should Know for the 2013-2014 Flu Season, accessed at, June 8, 2013
  5. Centers for Disease Control (January 11, 2013) Preventing the Flu: Good Health Habits Can Help Stop Germs, accessed at, June 8, 2013
  6. Flu Virus Image:  Tom Yulsman (May 26, 2009), U.S. and Other Countries Fail to Adequately Monitor Pigs for Flu, accessed at, June 8, 2013
  7. Sneeze Image:  Ben Mauk, photo credit Andrew Davidhazy/RIT (November 28, 2012), Why Do Bright Lights Make Me Sneeze?, accessed at, June 8, 2013

Student guest post: Captain, our sensors have detected Prions moving into the Medula Oblangata!

Student guest post by Bradley Christensen

No, this isn’t a clip from a science fiction movie.  Although dramatic, this does occur in the brains of some people and animals around on our home planet.  What is a prion you ask?  Prions are almost as mysterious to the scientists that research them as they are to me, you and the neighbor down the street.  Prion is a term used to describe an abnormal and particularly destructive strand of protein found in the brain.  Proteins are the building blocks of the muscles and tissues of our bodies that work combine together to perform different functions.  Prions are in their most basic form just an abnormal protein.  They create damage by causing neighboring proteins (in the brain tissue) to become abnormal and misshapen as well.  Like a house of cards, the structure of the brain tissue begins to break down.  When pathologists look at tissue samples from brains affected by prions, they find multiple holes like cutting through a section of sponge.  Thus giving this condition the medical term “spongiform encephalopathy.“
Brad pic 1

Microscopic picture of affected brain tissue from Wikipedia commons

Brad pic 2

 Computerized model of prion from Wikipedia commons

Diseases caused by prions are generally termed TSE (transmissible spongiform encephalopathy).  Some of these diseases occur spontaneously and some are transferred from one infected animal (or human) to another.  We know that the prion can occur be passed from mother to offspring, through bodily fluids, or by ingestion [8] of or exposure to brain or spinal tissue of an infected animal [6] or man (Zombie fanatics, may I please have your attention back.)

Prions are unique because like cancer cells, the body can’t recognize them as abnormal and mount an immune response against them.  Also, we have not developed an effective way of testing for prions until after the patient has already died. A third concern is that prions cannot be destroyed or controlled by chemicals, medications and treatments that we have available for other diseases. They are very hardy and seem to be unaffected by traditional and even extreme means of disinfection like ionizing or ultraviolet radiation and even formalin.

The Prion Family

TSE’s have been found in humans, cervids (elk, deer, moose), mink, sheep and goats, and even cats.  Listed below are several.

Scrapie (sheep and goats)

Brad pic 3Scrapie was first discovered in the United States in 1947[2] and causes progressive neurologic and behavioral changes in sheep and goats that eventually lead to death.  There is no treatment and the only way to diagnose is post mortem examinations of brain tissue however, a test has been developed to identify susceptible live animals.  Scrapie is thought to be transferred from mother to offspring during pregnancy.

The USDA began actively monitoring this disease in 2003 and started the RSSS (Regulatory Scrapie Slaughter Surveillance) program.[3] This is a voluntary program that allows flock owners to test and identify susceptible animals and are compensated for having these animals removed from the flocks.   Animals are also tested at the time of slaughter and any infected animals are traced back to the producers and allow them to further identify infected or exposed animals in their flocks for voluntary removal.   Research is ongoing to find better ways to detect infected live animals.   In laboratory environments, scientists have been able to transmit scrapie to other species but there is no evidence linking its potential spread to humans [2].

Chronic Wasting Disease (CWD)

brad pic 4

CWD was first seen in the U.S. in 1967 but it wasn’t until 1978 that a prion was discovered to be the cause [3].  Similar to other TSE’s, this disease cause a progressively fatal neurologic disease in deer, elk and moose.  Much less is known about this disease but it is thought to be spread by direct contact with saliva feces or urine from infected animals.  Through surveillance programs started in 2002 [3], this disease has been found in both wild and domestic deer, elk and moose in multiple states.  Research and control is much more difficult since the vast majority of these species are wild.  There is no evidence of this condition being spread to humans.

Bovine Spongioform Encephalopathy (BSE)  “Mad Cow Disease”

BSE or Mad Cow Disease has been a hot topic over the past 15 years since its possible link to humans.  Just like scrapie and CWD in their prospective animals, BSE causes a fatal TSE in cows.  The name “Mad Cow dbrad pic 5isease” came from the symptoms that are observed in some cows with this disease.   This prion disease is transmitted through ingestion of brain or nervous system tissues of infected animals.  It used to be common practice to feed ground bone meal from deceased animals to live animals as a source of mineral but since the discovery of this disease transmission, the practice has been almost universally discontinued.  Unlike TSE’s in other species, the medical and research community has discovered a link between cows and man.[5]

Human prion diseases – CJD (Creutzfeldt-Jakob Disease), Kuru, vCJD.

There are several types and descriptions of prion diseases in people.  These TSE’s are much more studied and researched because they affect humans.  All of these conditions are a TSE but have variations based on how they are transmitted and differences in symptoms.  CJD has been seen since the 1920’s [7] and Kuru was discovered in cannibalistic tribes in New Guinea in 1957 [8].   The occurrence of prion diseases in humans varies from sporadic (unknown cause), iatrogenic (inadvertent transplant of infected tissue like corneal grafts), to genetic predisposition (familial CJD) and even ingestion of infected tissues (Kuru – human cannibalism and variant CJD – infected cattle).  The onset and length of symptomatic disease and death in humans varies between these types of prion diseases but are always fatal.

Overall, prion disease in humans is rare with 1-2 deaths per 1 million people in the population worldwide but it does tend to be more common after the age of 50 with 3.4 deaths per 1 millions [7].

brad pic 6Am I going to get this disease? 

Probably not.  Statistically, TSE is rare in humans.  You are much more likely to develop any number of common types of cancer or even be struck by lightning than to develop prion disease.

Then why are prions a concern?

They are scary because they look normal to your body, we can’t test for them while the person or animal is still alive and they are not susceptible to any types of treatments that we have available.  TSE is rare in people but always fatal.

Is there anything I can do to protect myself? 

If you’re a cannibal, please seek intervention right away.  Wild game hunters, the CDC recommends that you consult state health departments regarding precautions in states that have cases of CWD.  You should generally avoid hunting sick or abnormal appearing animals, reduce exposure to brain or spinal tissues and where gloves.  Overall there is little you can do to personally limit your risk.

Is anyone trying to protect us? 

Definitely.  Massive amounts of research has been underway all over the world to try and understand prions and find ways to test and combat them.  The WHO (World Health Organization) has created guidelines regarding food supply, human tissue handing and use for research and medical purposes as well as handling of.  The United States also has very rigorous regulations and monitoring in cattle populations in our country.  At this time, we are considered BSE free country and our food supply safe.  Other countries are following suit to protect the food supply on a global basis.

Where do I learn more?

There are many good resources but there are many bad ones too.  Good places to consult is the CDC (Centers for Disease Control), APHIS (Animal and Plant Health Inspection Service) or your local and state public health services.

Should I avoid contact with types of animals that can have prion disease? 

No, except in the normal precautions around wildlife.  We have no evidence that prions are transmitted from animals to humans other than with BSE as mentioned above.  You are at more risk of being trampled by an animal than catching prions from it.


  1. USDA/APHIS/VS (2004).  Scrapie Fact Sheet.  Retrieved from  – scrapie Fact sheet
  2. RSSS program
  3. USDA/APHIS (2013). Chronic Wasting Disease.  Retrieved from
  4. USDA/APHIS (2012).  About BSE. Retrieved from  BSE aphis
  5. Will RG, Ironside JW, Zeidler M, Cousens SN, Estibeiro K, Alperovitch A, Poser S, Pocchiari M, Hofman A , Smith PG (1996) Apr. 6. A new variant of Creutzfeldt-Jakob Disease in UK.  Lancet 347(9006):921-5
  6. 6.      Johnson, Richard T. (2005).  Prion Diseases. The Lancet Neurology, Vol. 4, Iss. 10, 635-42

7.  Centers for Disease Control and Prevention (CDC) (2012). Creutzfeldt-Jakob Disease.

Retrieved from

8.   Gajdusek, V. Z. (1957). Degenerative disease of the nervous system in New Guinea: the

Endemic occurrence of “kuru” in the native population.  N Engl J Med, 257, 974-978

9.   World Health Organization (WHO) (2012). Variant Creutzfeldt-Jakob Disease.

Retrieved from

  1. – prion


  1. – histology picture

12.   (scrapie

Video hyperlink)

13.  BSE information –   retrieved from

All photographs in this blog are for public domain found on

Student guest post: A taste of Lyme

Student guest post by Kyle Malter

In many areas of the country there is a vile blood sucker that lurks in our forests, our parks and even our backyards.  What concerns us is not what this creature takes but rather what it leaves in our body after it bites us:  corkscrew shaped bacteria called spirochetes and with the name Borrelia burgdorferi.  When the bacteria invade our bodies and cause problems along the way we call it Lyme disease.

It is Lyme, not “Lymes” disease, and here’s how it got that name. In the early 1970’s a large number of cases emerged involving children with a “bulls-eye” rash followed by arthritis and they were concentrated in a small area in and near Lyme, Connecticut.  Initially, the cause of the disease was unknown.  A clue to the mystery was that most of the kids lived near a wooded area.  After more investigation, ticks that feed on deer were identified as likely suspects.  The medical community learned that the “deer tick” transmitted the spirochete bacteria which was likely infecting the children and causing symptoms.  A researcher named Willy Burgdorfer helped identify the organism and in honor of his contribution the bacterium was named Borrelia burgdorferi. [1]  Wouldn’t it be fun to have a nasty bacteria named after you?

Signs of Lyme disease can vary from a mild rash to serious pain and disability. If infected, a “bull’s-eye” rash occurs in most people because of the inflammation left in the trail of the migrating bacteria. They move from the bite site away leaving the classic target appearance.  When this bug spirals though your joints, organs and tissues it can cause damage and a wide range of symptoms including fever, headache, lethargy, stiffness and general soreness.   In some cases, more serious and long-term problems with swollen joints, arthritis, Bell’s palsy, and even heart disease can result.   The symptoms can come and go and may last a lifetime.  [1] This is one serious problem if you have the disease-spreading tick in your environment.  Most people refer to the species as the “deer tick” or the “black-legged tick” although the proper name is Ixodes. Don’t forget about your dogs either.  They are also commonly infected in endemic states, can get permanent arthritis, and can rarely even die from the disease. [2]

Lyme disease has been diagnosed in all 50 states but is heavily concentrated in the northeast and upper Mid-West. [3] Approximately 96% of cases come from only 13 states. [4] CDC data by state, maps and disease forecast models show a clearly increasing trend.  Why such a steep increase in the number of cases?  There are probably many reasons.  First, surveillance is probably higher now than it was 15 years ago.  We simply weren’t looking for it as much then.  Another contributor is the increased population of the white-footed mouse in some regions. [5] This rodent is a reservoir for the bacteria meaning they harbor the bug until the tick larva come for a meal.  They are like a bank filled with Borrelia ready for every tick to make a withdrawal.  Once the tick has the bug in its gut, it is a loaded gun.

The recent increase in the white-footed mouse population may be the result of a cascade of events. “Change one thing. Change everything.”[6] Ohio reported two recent “banner years” for acorn production with a 36% increase in white oak acorns between 2011 and 2012.[7] A more abundant supply of “mouse food” in the way of acorns could result in more mice because they replicate much more efficiently.  More white-footed mice means more banks filled with Borrelia.  Ticks have a much better chance of making a withdrawal with every meal.  More ticks with Borrelia means more animals and humans infected.   So that’s how more acorns could mean more Lyme disease.

If you are unsure if Lyme bacteria are in your area just ask your dog.  Some studies suggest that dogs that live in your area may be able to predict your risk level. [8] [9] [10]  For those in the northeast and upper Mid-West you don’t have to ask.  It is ubiquitous in these parts of the country. Veterinarians in many non-endemic states are now screening dogs yearly to see if they have ever been infected with Borrelia.   If some dogs in your region are positive you should be more vigilant.  The CDC will keep track as well so check their Lyme page annually.

Preventing Lyme disease can be a very big challenge.  For dogs, very effective vaccines are available to protect them. [11] [12] So if this is such a potentially devastating disease in people why don’t we have a vaccine for humans?  Well, we did.  In the late 1990’s a vaccine was approved by the FDA to aid in the prevention of Lyme disease in humans.  While the safety and efficacy during the approval studies were good, there were skeptics and strong opponents in the public and medical community.  Some people claimed that the vaccine caused Lyme disease rather than prevent it.  Ultimately, the vaccine manufacturer withdrew it from the market citing poor demand. [12] Allen Steere, the man who discovered Lyme disease, also led one of the SmithKline Beecham (SKB) Lyme vaccine trials.  He said, “the withdrawal of the SKB vaccine . . . represents the most painful event in our Lyme disease history . . . the vaccine was really withdrawn because of fear and lawsuits, not because of scientific findings” [13]  Some advocates are attempting to rekindle efforts to make a vaccine for Lyme disease available again while others are opposed to the idea.

Tick prevention is our best strategy to prevent Lyme disease. Without a tick bite you cannot get Lyme disease.  In fact, even if an Ixodes tick bites you, it takes at least 24-48 hours of attachment to transmit the bacteria into your body. The National Institutes of Health suggest that you follow their fashion advice and tuck in your shirt into your light colored pants, tuck your pants into your socks and then put tape around the bottom. [1] I’ve never seen this method utilized in a public place but I’m sure you will end up on the “People of Wal-Mart” site if you try it.  The CDC recommends pyrethrins on your clothing and DEET on your skin and clothing to repel ticks. [4] The EPA also has a nice online tool.  Check yourself everyday for ticks during peak months.  Deer ticks are tiny so take some time and inspect your nooks and crannies.  The nymph stage, the second smallest tick in this picture,  is the one that usually infects people.  Again, don’t forget about your dog. While he can’t give you Lyme disease, he is also susceptible to it. Ask your veterinarian which flea and tick preventative is right for your pets.

Kyle picture

Lyme disease is no longer just a Lyme, Connecticut problem.  If it is not yet in your backyard, it could be soon. Lyme disease can have lifelong, debilitating consequences. Arm yourself with information and your body with tick protection.  We are not defenseless.  Protect yourself.   Protect your dog.  Please.


[1] NIH Website

[2] Littman MP. Lyme nephritis. J Vet Emerg Crit Care (San Antonio). 2013 Mar-Apr;23(2):163-73

[3] Smith BG, Cruz AI Jr, Milewski MD, Shapiro ED. Lyme disease and the orthopaedic implications of lyme arthritis. J Am Acad Orthop Surg. 2011 Feb;19(2):91-100

[4] Centers for Disease Control and Prevention

[5] National Science Foundation

[6] Townsend, Tracy A., “Change One Thing, Change Everything: Understanding the Rhetorical Triangle” (2013). Rhetoric Unit. Paper 3.

[7] Ohio DNR

[8] J M Lindenmayer, D Marshall, and A B Onderdonk.  Dogs as sentinels for Lyme disease in Massachusetts. American Journal of Public Health November 1991: Vol. 81, No. 11, pp. 1448-1455.

[9] Olson, Canines as Sentinels for Lyme Disease in San Diego County, California, Journal of Veterinary Diagnostic Investigation March 2000 vol. 12 no. 2 126-129

[10] Faith D. Smith, Rachel Ballantyne, Eric R. Morgan, Richard Wall Estimating Lyme disease risk using pet dogs as sentinels Comparative Immunology, Microbiology and Infectious Diseases, Volume 35, Issue 2, March 2012, Pages 163–167

[11] Levy et al. Use of a C6 ELISA test to evaluate the efficacy of a wholecell bacterin for the prevention of naturally transmitted canine Borrelia burgdorferi infection. Vet Ther. 2002 Winter;3(4):420-4

[12] Aronowitz RA. The rise and fall of the lyme disease vaccines: a cautionary tale for risk interventions in American medicine and public health. Milbank Q. 2012 Jun;90(2):250-77.

[13] Steere, A.C. 2006. Lyme Borreliosis in 2005, 30 Years after Initial Observations in Lyme Connecticut. Wien Klin Wochenschr 118(21–22):625–33.


Student guest post: Chirp, Chirp, Sneeze!

Student guest post by Julia Wiederholt

I don’t think there is a single person that can claim to have never had the joyous experience (sarcasm intended) of suffering from the influenza.  We all recognize the common symptoms that accompany this infectious little virus taking up residence in our bodies: the chills accompanying a fever, the total body ache, the nausea, and overall feeling of malaise.  Typically this virus comes and goes within a week without serious side effects.  When novel strains of the influenza pop up however, there can be more serious complications as your body lacks a sufficient immune recognition of the virus.  An example of a new strain of influenza that presents a great risk for the human population is the H7N9 influenza, also known as Avian Influenza A.

H7N9 was first recognized earlier this year in China and thankfully has yet to be reported in the US. The majority of the people infected have had direct contact with poultry or an environment that has contained infected poultry.  Some of the people diagnosed however, report having had no direct contact with poultry opening up the possibility of human to human transfer of the disease.  The infected poultry have shown no obvious symptoms of being infected, but when humans become infected it can cause severe respiratory problems and fever.  As of May this year, LiveScience reported that there have been a total of 131 reported human cases of H7N9 with 32 reported deaths.

While all of that may not sound too impressive, here’s what makes H7N9 such a concern as an emerging infectious disease.  The first major concern regarding this specific influenza is the fact that it is the first time the H7N9 virus has been reported in humans.  The H in the name H7N9 stands for hemaglutinin, which is the attachment protein found on influenza viruses.  This protein not only enables the virus to attach to the cells it is trying to infect, it also is provides the host’s immune system a way of recognizing the virus as a foreign threat.  The fact that this is the first time this specific virus has been found to infect humans means that we lack any prior immunity to it and are therefore, more susceptible.

Another factor that raises the alarm for this influenza is the fact that the infected poultry that have been found so far have shown no outward signs of being sick.  This is a huge concern because it makes controlling the spread of the disease much more difficult.  When poultry and livestock exhibit obvious signs of being infected, it allows the infected to be separated out from the healthy and either isolated or culled to prevent further spread of the disease.  In some cases, the disease may have already spread amongst all of the animals in the vicinity requiring the entire herd or flock to be culled.  When it is difficult to distinguish between healthy and infected animals however, any evidence that the disease has been found within the animals will more than likely lead to the entire herd or flock being culled.  This not only results in greater economic losses for the poultry farmers but also a higher number of people being exposed to infected animals before realizing the danger that is present.

Possibly the greatest concern with H7N9 is the fact that it could be jumping from person to person.  The original thought was that the only way it had been spreading was from direct contact with sick poultry, which would limit the at risk human population to people coming into contact with the infected birds.  Some of the people who have been diagnosed with H7N9 however, are claiming to have had no contact with poultry suggesting that the disease may be capable of human to human transmission.  This would greatly increase the reproductive rate of the disease because people would no longer need to come into contact with poultry to be exposed to it.  The reproductive rate, commonly referred to in scientific communities as the Ro, is a way of measuring the predicted number of new infections that one infectious case is likely to create.  Another factor that suggests the possibility of human to human transfer is the fact that there have been three reported family clusters of H7N9.  While this does not necessarily mean that the virus is capable of sustained human to human transfer, it is highly suggestive that human to human transmission has occurred in these particular instances and that with the right (or depending on how you look at it, wrong) mutation, it could transfer between humans with ease.

While all of these things explain why H7N9 is being watched so closely and why it is important to have a healthy respect for just how dangerous it could be, there’s no reason for people to start panicking quite yet.  As mentioned earlier, this strain of influenza has only been reported in people that either live in or have recently traveled to China.  Unless you are planning to travel out of the country in the near future, there is no reason to become overly concerned about H7N9 at the moment.  Also, the majority of the cases have either had direct contact with infected poultry or close contact with someone who has had contact with poultry.  This means that unless the virus becomes proficient at human to human transmission, the majority of the population is at a low risk.

For the germaphobes out there that are still freaking out over the possibility of catching H7N9, there are several ways to reduce the risk of catching it, or any other influenza for that matter.  Good hygiene practices such as frequently washing your hands and avoiding touching your face will help minimize the risk of introducing the influenza virus into your body.  Eating a well-balanced diet and getting plenty of rest will help keep your immune system in tip top shape in the event of a virus managing to get past your innate defense mechanisms.  In regards to reducing the risk of catching a zoonotic strain of influenza, practices such as thoroughly washing your hands after handling any animals and avoiding contact with sick poultry or livestock will reduce the risk of transmission.  So rest at ease, the world isn’t coming to an end due to H7N9…at least not yet.


Cong Dai, Min Jiang, “Understanding H7N9 Avian Flu,” BMJ, Available online 3 May 2013.  <>.

“Frequently Asked Questions on Human Infection Caused by the Avian Influenza A (H7N9) Virus.”

World Health Organization. WHO, 30 Apr. 2013. Web. 12 June 2013. <


Guang-Wu Chen, Michael M.C. Lai, Suh-Chin Wu, Shih-Cheng Chang, Li-Min Huang, Shin-Ru Shih, “Is avian influenza A (H7N9) virus staggering its way to humans?”, Journal of the Formosan Medical Association, Available online 3 June 2013, ISSN 0929-6646, 10.1016/j.jfma.2013.04.015. <>.

“H7N9: Frequently Asked Questions.” Centers for Disease Control and Prevention. Centers for Disease

Control and Prevention, 22 Apr. 2013. Web. 12 June 2013. <


Kannan Tharakaraman, Akila Jayaraman, Rahul Raman, Karthik Viswanathan, Nathan W. Stebbins, David Johnson, Zachary Shriver, V. Sasisekharan, Ram Sasisekharan, “Glycan Receptor Binding of the Influenza A Virus H7N9 Hemagglutinin,” Cell, Available online 6 June 2013, ISSN 0092-8674, 10.1016/j.cell.2013.05.034. <>.

Rettner, Rachael. “H7N9 Bird Flu Cases Declining, Health Officials Say.” LiveScience. N.p., 10 May

2013. Web. 12 June 2013. <



Student guest post: Mission Impossible: Fighting Zoonotic Infections in Nicaragua

Student guest post by Brandon Woods

A Dangerous Paradise

From jungles with jaguars to crystal blue lakes with freshwater sharks, Nicaragua is one of the most beautiful and dangerous countries in Central America. The brilliant biodiversity attracts millions of tourists each year and the looming volcanoes that pepper the landscape can be an exciting yet unsettling sight. However, in reality much of the danger in Nicaragua comes from the risk of infectious diseases. For example, if you’re planning to travel to this tropical paradise anytime soon, the Center for Disease Control (CDC) states that international travelers are at risk of contracting Typhoid fever, hepatitis A, hepatitis B, Leishmaniasis, malaria, dengue, rabies, and more! As a dual degree veterinary medical and public health student, I am fascinated by these infectious diseases and want to learn how they interact with the environment, people and animals. Many of the diseases that the CDC listed are called zoonotic diseases, or diseases that are transmissible between animals and humans. Other zoonotic diseases you may know include ringworm, Lyme disease, and Cat scratch disease. Whether you own a pet, like to travel, or simply enjoy spending time outdoors, you are at risk of infection because these zoonotic diseases are increasingly emerging worldwide and are becoming a serious public health threat. During the spring break of my first year of veterinary school, I traveled to Nicaragua on a mission trip and got first-hand experiences of these frightening infectious diseases.

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Bed Nets and Bug Spray

Planning for this trip was time-intensive and reminded me of planning for my semester study abroad adventure to Tasmania, Australia. However, unlike my semester Down Under, this trip was coordinated through the national non-profit Christian Veterinary Mission (CVM) whose goal has been to help veterinarians serve others and live out their Christian faith for more than 30 years. Out of all the fundraising and logistics meetings we had, the meeting that stands out the most was when the Iowa State University travel nurse described the laundry list of potential pathogens we could encounter. Our team of 8 veterinary students, 3 veterinarians, and 1 pharmacist would be treating animals in a remote village called Espavel in the jungles of eastern Nicaragua. When I saw that my destination was in the middle of the red zone for malaria on the CDC map, my eyebrows escalated and my stomach dropped.

I was going to fly to an unstable, earthquake-prone country of approximately 5.7 million Spanish-speaking people where malaria was endemic. My Spanish was scarce, but my drive to serve was strong. After I heard that malaria was essentially eliminated from Nicaragua, my blood pressure dropped a few millimeters of mercury. Approximately 84% of the Nicaraguan population is at risk of contracting malaria, according to a UCLA study. However, Nicaragua has experienced a 97% decrease in reported malaria cases between 2000 and 2010. This significant decrease in prevalence was a result of Nicaragua partnering with the Pan American Health Organization (PAHO) in 2006 which heavily implemented stronger surveillance, prevention, vector control, and treatment. Despite this progress, I learned from my undergraduate Lyme disease Honors project that there are always numerous challenges to completely eliminate vector-borne diseases like malaria. For instance, controlling mosquito breeding populations is particularly vexing due to the complex ecology of the parasite life-cycle. In addition, you may have heard about the controversy surrounding toxic pesticides like DDT. My colleagues and I were fortunate for our DEET bug spray and Permethrin treated clothes and bed nets that we brought after skyping our host-country missionaries. I was also relieved that our trip in March 2013 was during the dry season and not during the September-to-January rainy season, when disease transmission is highest.

Rambunctious Rabies

Escaping the endless hours in the frigid, formaldehyde laden anatomy lab and flying to a third-world tropical country to practice preventative medicine was slightly shocking, but totally worth it. On our first day, we drove through the littered streets of Catarina to an outdoor shelter where we set up a temporary clinic. The local children brought their pet dogs and we treated them with Ivermectin and other anti-parasitic medication. Many animals were very thin and infested with fleas and ticks. However, it was rewarding to interact with the children and walk them through a brochure that described both healthy animal care and the Gospel of Jesus Christ. Then suddenly one of my colleagues was bitten by a dog! He was trying to give a rambunctious mixed-breed a pill to protect against heartworm disease and the next thing he knew, the dog bit him in the hand. He quickly washed the wound with soap and water and bandaged it. Fortunately, everyone on our veterinary team was already vaccinated for rabies prior to the trip because it’s a requirement to enter veterinary school. He also followed up with post-exposure rabies prophylaxis when he returned home.Brandon picture 2

Rabies is one of the deadliest and most notorious zoonotic diseases in the world. Rabies is endemic to Nicaragua, often occurs in poor rural communities, and the most common source of transmission is when a dog bites a human and delivers the fatal RNA virus. According to the World Health Organization, potentially any mammal can contract rabies, and common reservoirs in the USA include skunks, foxes, raccoons, and bats. Although rabies cases can be successfully treated, it still persists worldwide killing more than 55, 000 people each year. The Center for Food Security and Public Health (CFSPH) at Iowa State University is an excellent resource that provides more information on rabies and preventing zoonotic diseases. Reducing the prevalence of rabies globally requires a multinational effort and the World Rabies Day Initiative was founded solely for this mission and has already collaborated with 150 countries and vaccinated over 7.7 million dogs.

Tasting Iguana and Tackling Typhoid

It’s a good thing I like rice and beans, because that was the bread and butter of most of my meals every day. Hiking to farms builds an appetite and one day we had to traverse across a narrow blank that stretched precariously over a ravine. After we arrived, we vaccinated over 100 head of cattle for clostridium, anthrax, and Dectomax. Dectomax is an injectable drug used to control parasites like hookworms, round worms, grubs and mites. When we returned to the main village and got out of the blazing 90+ degree sun, the crispy, plantain chips with a glass of freshly squeezed tamarind juice was an irresistible snack. However, the most memorable meal of all was the morning the villagers surprised us with two 5 foot long iguanas! A few hours later, I was savoring some delicious iguana meat seasoned with local spices and vegetables. Cooking wild reptiles is foreign to us in the developed world; likewise, the way many Nicaraguans prepare their food is also different.

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Sayings like, “Don’t drink the water,” or ‘Boil it, cook it, peel it or forget it,” come to mind when traveling abroad, and they couldn’t ring more true for my experience. Food-borne illnesses are another great example of how veterinary medicine and public health overlap. I’m enrolled in the dual DVM-MPH degree program at the University of Iowa’s College of Public Health and learned that food-borne epidemics are a major focus of research in epidemiology. From mild cases of spoiled potato salad on romantic picnics to church dinner outbreaks from contaminated home-made ice cream, food-borne illnesses can range in their severity depending on your pre-existing health and the dose and type of microorganism ingested. One of the Nicaraguan diseases that I was vaccinated for before my trip was a food-borne illness known as Typhoid fever. Thankfully I avoided this illness; however, I couldn’t escape the wrath of Montezuma’s revenge, or traveler’s diarrhea, most commonly caused by enterotoxigenic Escherichia coli.

Typhoid fever is transmitted through contaminated food or water and is unique among food-borne pathogens because it only affects humans. In fact, some individuals can unwittingly become carriers of the bacterium and transmit the disease to others through improperly prepared food, like the infamous Typhoid Mary. This disease is caused by the bacterium Salmonella typhi, which is one of over 2,300 species of Salmonella and can be treated with antibiotics, according to the USDA. Other Salmonella species are also common among household, cold-blooded critters like turtles, frogs, iguanas, and snakes, so it’s important to always wash your hands after handling these pets.  Like malaria and rabies, Typhoid fever presents challenges for eradication in developing countries where poverty limits accessibility to clean water, pasteurization, and proper sanitation and hygiene. For example, I had never taken a well-water bucket shower before, and although the murky water felt refreshing after a long days’ work, I came to more deeply appreciate the luxuries of everyday plumbing and electricity.

Collaboration is Key

An empowering lesson that continues to inspire me was when I participated in a humanitarian collaboration. Before our departure, we communicated with another mission team from an Arkansas Baptist church that would work at the same time as our Iowa State Christian veterinary mission team would work over spring break. The goal of the Arkansas team was to provide humanitarian care while the goal of the Iowa State team was to provide veterinary care. For instance, the Arkansas team brought donated shoes and eyeglasses, provided nutrition education and had a dentist and nurse that pulled teeth. On the other hand, the Iowa State team vaccinated dogs, cats, horses, cattle, and pigs, performed surgeries and provided agricultural advice to farmers. Even though the two teams set up separate clinics to work on different species, we still felt united as one team because we traveled together, ate meals together, and worshiped together.

Brandon picture 4

One sunny afternoon, we asked the human dentist to come over to our animal clinic to pull a rotten tooth out of a horses’ mouth. The dentist had hardly been around horses in his life, let alone stuck his hand in one’s mouth before, but after the novelty wore off, he quickly agreed to help our team. The sedated horse was lying on its side surrounded by curious villagers and veterinary students. The dentist was nervous and the 3 inch long decayed molar kept wiggling out of his grip. Finally, he extracted the tooth and everyone was amazed and overjoyed. It’s a simple story like this that showcases the successful collaboration between veterinarians and other medical professionals that is the goal of the One Health Initiative or the new concept of interdisciplinary healthcare collaboration. In order for us to eradicate these infectious diseases and save lives, it is vital that veterinarians, physicians, dentists, and epidemiologists collaborate and communicate to find solutions.

A Future Fighting Infections

Going on this short-term veterinary mission trip put me in harm’s way, but it gave me real-life experience with infectious diseases, deepened my faith, and strengthened my clinical skills. It was bittersweet to say adios to my amigos, but I know I’ll return to that perilous paradise.  I enjoyed the international fieldwork and cross-cultural partnership because it embodies the One Health Initiative that I highly esteem. From hiking in the jungle on my 23rd birthday to taste-testing iguana to teaching children about pet care and the Word of God, this trip was a remarkable adventure that has forged a new trail for me. I don’t believe it’s an impossible mission, and I am committed to pursue veterinary public health as a career and control zoonotic diseases in developing countries.

All photos courtesy and copyright Brandon Woods. 


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.

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(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.

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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.

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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.

“HIV and AIDS Statistics: Worldwide.” Statistics: Worldwide. AmfAR, Nov. 2012. Web. 10 June 2013. <>.
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. <>.
“Schistosomiasis: Epidemiological Situation.” World Health Organization. N.p., n.d. Web. 10 June 2013. <>.
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. <>.
“South Africa: ‘Over 25% of Schoolgirls HIV Positive'” BBC News. BBC, 14 Mar. 2013. Web. 10 June 2013. <>.
Temple, Bliss. Schistosoma Haematobium (blood Flukes). Schistosomiasis Haematobium (blood Flukes). Stanford University, May 2004. Web. 10 June 2013. <>.

Student guest post: A Push for Pasteurization

Student guest post by Molly Stafne

Nothing could be worse than watching your seven-year-old lying in a hospital bed fighting for his life after being diagnosed with hemolytic uremic syndrome. Unfortunately, Mary McGonigle-Martin experienced it first hand as her son, Chris, fought for his life after being poisoned by E. coli 0157:H7 found in contaminated raw milk. Like many mothers, Mary was coerced into believing the inaccurate “facts” given to her by the farm she purchased raw milk from. Too often across the US, parents are given incorrect information about the safety of the milk they drink and unfortunately, it is often children that pay the price.

Few people today know of a time when they didn’t have the choice to drink anything but raw milk. Now there is an overwhelming argument that pasteurization is decreasing the nutritional value and safety of the milk. During the 1800s, Louis Pasteur developed the germ theory which claimed that germs outside the body, like those found in raw milk, have the ability to cause infection. As a result, he developed the process of pasteurization which is used in many foods we consume today, including milk, to kill bacteria. In the past couple decades, many consumers have decided that they would rather consume more natural and organic foods rather than those that were produced by more modern methods. It is frequently believed that these natural foods, such as raw milk, are healthier which is not the case.

Pasteurizing milk has had many benefits through history. One of its major contributions is the massive reduction in human tuberculosis cases as the bacteria that causes bovine tuberculosis can also infect humans. Bovine tuberculosis can be spread to humans through contact with an infected animal but most commonly through ingestion of raw milk. Although the prevalence of tuberculosis in humans in the US has significantly reduced since pasteurization began, there are still a number of other zoonotic pathogens that can be transmissible from milk to humans including salmonella, campylobacter, listeria, and E. coli 0157:H7, all of which can have dangerous or unpleasant consequences or even potentially be fatal. E. coli is possibly the most dangerous since it only needs less than 100 organisms to cause infection. It can lead to a dangerous condition called hemolytic uremic syndrome (HUS) which may cause kidney failure. According to the CDC, there have been 148 dairy product-associated outbreaks from 1998 – 2011 that were a result of consumption of raw milk or cheese which resulted in 2,384 illnesses, 284 hospitalizations, and 2 deaths. Today, milk is heated to 161°F for 15 seconds to destroy the bacteria. This is called high temp, short time pasteurization. Another form of pasteurization is low temp, long time, 145°F for 30 minutes.

Proponents of raw milk often argue it has a greater nutritional value than pasteurized milk. There have been numerous studies that have de-bunked this myth according to the CDC. Many factors are involved when determining the nutritional value of a product. One thing that is analyzed is how readily a body breaks down and utilizes a nutrient. If a mineral or vitamin is passed through the body quickly, any loss would be irrelevant. A second analysis would be the percent contribution of the nutrient to the recommended daily intake. If people don’t rely on a certain product as the main source of an essential nutrient, the loss of the nutrient is almost negligible. It is true that some nutrients or enzymes are slightly reduced during pasteurization. For example, lysine is the most relevant essential amino acid found in milk. After heating the milk, only 1-4% loss of the amino acid was observed1,5,7. But like what was previously alluded to, reduction of nutrients like vitamin C is not considered a significant concern as milk is not a major source of vitamin C. It would take 20 liters of milk to consume the daily requirement of vitamin C, regardless if it was raw or pasteurized milk3. The availability of nutritionally relevant vitamins such as B2 or B12 were found to be affected minimally or not at all by most common heat treatments2,5. Finally, while milk is a significant source of calcium and phosphorus, neither were affected by heating the milk3.

Another raw milk marketing tool some farmers use is to claim that their cattle are grass fed. When cattle were first domesticated, they were raised on a grass diet. As the understanding of animal nutrition grew, farmers discovered that cattle would gain weight faster if they fed them grain which is economically beneficial. Proponents of grass fed cattle argue that grain is not their natural food and the growth at a faster than normal rate is unhealthy. A grass-fed animal does not mean the animal is healthier. Nutritionally speaking, it was hypothesized that grass fed cattle have a lower milk fat content. The amount of grain does play some role in the fat development but energy and dietary protein intake and the current state of pasture the cattle are being grazed on must also be accounted for. In addition, milk fat content is also determined by the genetics of the individual animal, whether or not it currently has or had infections in her udder, and her stage of lactation3.

In addition, grass-fed cattle don’t necessarily carry a lower bacterial load. Even at the most sanitary facilities, milk is often contaminated by fecal material carrying pathogens during the milking process. According to Dr. Jim Kazmierczak, a Public Health Veterinarian with the Wisconsin Department of Health Services, there have been numerous studies that proved grass-fed cattle shed E. coli 0157:H7 in the feces longer than grain-fed cattle4 and that “cattle fed a forage diet were 0157:H7 culture-positive longer and with higher numbers of bacteria in their feces than cattle fed a grain diet.6” This means that E. coli 0157:H7 remained alive in their feces longer than grain-fed cattle.  In addition to being found in fecal material, E. coli 0157:H7 can be found where cattle are grazing, can live on different environmental reservoirs for many months, such as gates, walkways, or water troughs, and is found more frequently during the summer.

We are blessed in the US to have a relatively safe food supply. Sure there will be occasional food-borne illness outbreaks but we are fortunate to have the technology, sanitary methods, and capabilities to keep the food we consume free from diseases to the best of our abilities. The invention of pasteurization reduced the number of illnesses and deaths caused by contaminated dairy products while maintaining the integrity and nutritional value of the milk. But there is a misconception of pasteurized milk across the country that has led to people making deadly decisions. Mary McGonigle-Martin would have never given her child raw milk had she known that it had the potential to harm or kill him. The risks are high when consuming raw milk and people need to be properly informed before their put their families and themselves in unnecessary danger.

1. Andersson, I., and Öste, R. (1995). Nutritional quality of heat processed liquid milk. In P. F. Fox (Ed.), Heat-induced changes in milk (2nd ed.) (pp. 279e307). Brussels: International Dairy Federation.

2. Burton, H. (1984). Reviews of the progress of dairy science: the bacteriological, chemical, biochemical and physical changes that occur in milk at temperatures of 100e150 _C. Journal of Dairy Research, 51, 341e363.

3. Claeys, W. L., et. Al (2013). Raw or heated cow milk consumption: Review of risks and benefits.

4. Hovde, C. J., et al. (1999). Effect of cattle diet on Escherichia coli O157:H7 acid resistance. Appl Environ Microbiol 65:3233–32

5. Schaafsma, G. (1989). Effects of heat treatment on the nutritional value of milk. Bulletin of the International Dairy Federation, 238, 68e70.

6. Van Baale, M. J., at al. (2004). Effect of Forage or Grain Diets with or without Monensin on Ruminal Persistence and Fecal Escherichia coli O157:H7 in Cattle. Appl Envir Microbiol 70:5336-5342.

7. Walstra, P., and Jeness, R. (1984). Dairy chemistry and physics (p. 467). New York: John Wiley & Sons.

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.

Student guest post: Tuberculosis: A Real Problem With No Real Solution

Student guest post by Jack Hamersky

After successfully completing a job interview I had the opportunity to take the next step in my employment process: taking a Tuberculosis or TB test.  I have received the test before but never really understood the point of testing for a disease no one ever sees in my community. I always thought, “Why not focus all this effort and money on more prevalent infectious agents such as Ebola or HIV?” You know, focus on something important.  So, as the nurse called me in from the waiting room I began to curse that hard little bubble that would soon be forming under my skin, and the inconvenience it would be to have to come back to this same clinic to have it read.

This same type of experience is known throughout the United States and other developed countries.  However, many people like myself, do not know the importance of this test.  They might not know that this test is a crucial part of the much larger goal of eradicating a deadly and common worldwide disease.

What is tuberculosis and why is it even important?

Tuberculosis is a contagious disease that is found in both animals and humans. The human form of the disease is caused by a group of three bacteria: Mycobacterium bovis, Mycobacterium avium, and Mycobacterium tuberculosis.  This disease can come in two forms: latent and active.  The active form of tuberculosis causes pockets of pus called granulomatous lesions in lungs and has a death rate around 50%. It is estimated that TB infects around one third of the human population on earth and is the second leading cause of death by infectious disease, behind HIV, killing around million people annually, according to the Center for Disease Control and Prevention; CDC (4).  The greatest prevalence of TB occurs in developing countries and their low socioeconomic populations.  This is likely due to the limited availability of health care, poor nutrition, and overcrowding conditions these people face on a daily basis.  Immunosuppressed individuals, such as people infected with HIV, are also more likely to contract tuberculosis.  TB is also very hard to treat and many forms of the disease are resistant to antibiotics.

Another reason TB is so dangerous is the threat of Mycobacterium bovis. M. bovis is another strain of tuberculosis that mainly infects cattle, cervids (deer like animals), elephants, bison, etc (7,10). What makes this bacterium interesting is its been known to infect people through the consumption of raw (unpasteurized) milk or products that were made from that raw milk (1,5,7,10). This zoonotic microorganism is responsible for two percent of all new cases of TB in the US (7) with an even a greater percentage worldwide (6).  The zoonotic nature of M. Bovis allows for it to hide in wildlife populations which act as a reservoir for the disease (6,9). The good news is a campaign to eradicate M. Bovis from the US food supply began in 1993(5). The bad news is that TB remains endemic in wildlife and agricultural animal populations worldwide. The program in the United States has been a success and most of the United States is considered Bovine Tuberculosis free.  However some states, such as Michigan, still find M. bovis in their wild deer herds making the continual threat of reemergence a reality.

So what have we done about this problem?

The United States government has taken a leading role in the fight against TB. It formed the Advisory Council for the Elimination of Tuberculosis to address the growing resurgence of TB in the 1980’s (5). It also passed legislation like the Comprehensive Tuberculosis Elimination Act which called for the increase of federal funding, education, and international collaboration in the fight against TB.  Other non-governmental advancements have taken place over the years too.  A vaccine was created and is now available throughout the world.  Known as BCG, this vaccine is good at protecting children against the disease, however, it loses its effectiveness as children grow older and has not shown promising results in adults (8).  This, coupled with the increasing amount of antibiotic resistant cases (known as Multi Drug Resistant Tuberculosis or MDR TB) once again proves the fight to eradication or even control might be more of an uphill battle then we once thought.

So how is the fight to end TB going?

Over the past few decades we have made progress and in 2011, the World Health Organization reported “The absolute number to TB cases has been falling since 2006”. However, in that same report, the WHO also stated, even though TB cases had dropped, “In 2009 there were almost 10 million children who were orphans as a result of parental deaths caused by TB” (12,13).  As long as there TB is left to reside in our low income populations and in animal reservoirs it will continue to plague millions worldwide.

So where do we go from here?

The continuation and strengthening of surveillance and research projects worldwide is the key to combat tuberculosis.  The more we know about the disease and its ecology the better prepared we will be to face the challenges we may encounter during its eradication process.  Will we ever get to total world eradication of tuberculosis?  This writer thinks so but to quote the great Robert Frost it seems that “we have miles to go before we can sleep”.