The Pap smear is no panacea, Katie Couric

Regular readers keeping up on infectious disease issues might have seen Seth Mnookin’s post yesterday, warning of an upcoming episode of the Katie Couric show  focusing on the HPV vaccine. Even though Mnookin previously spoke with a producer at length regarding this topic, the promo for the show certainly did not look promising:

“The HPV vaccine is considered a life-saving cancer preventer … but is it a potentially deadly dose for girls? Meet a mom who claims her daughter died after getting the HPV vaccine, and hear all sides of the HPV vaccine controversy.”

And indeed, reviews thus far show that unfortunately, Couric pretty much  mangled the issue and allowed heart-wrenching anecdotes to trump science (reminiscent of Jenny McCarthy’s appearance on Oprah). I won’t cover it all (you can view it here), but basically Couric allows stories about illness and death in the weeks following administration of the vaccine to go unchallenged, and brings on Dr. Diane Harper as her HPV expert (featured prominently in the anti-vaccine documentary “The Greater Good“). Dr. Harper believes the HPV vaccine is over-hyped, and that Pap screening is “100% accurate” so no HPV vaccine is really needed. This, frankly, is hogwash. Even with emphasis on screening, here in the U.S. we have 12,000 cases and 4,000 deaths from cervical cancer alone each year. (And in Mnookin’s post and in Matthew Herper’s Forbes post, both note that head and neck cancers can also be caused by HPV as well–but have no good screening process).

Even when HPV cervical infections are caught via screening, the treatment ain’t pretty. I’ve written before mentioning one such remedy–the LEEP procedure.  I had this done several years ago, after a Pap smear came back with abnormal cells and positive for HPV DNA:

“Next, a woman with abnormal cells can expect to undergo a LEEP procedure, where portions of your cervix are removed with a burning electric wire under local anesthetic, and the foul smoking remains of your cells are sucked up into the smoke shark, “a sleek, powerful, smoke-eating machine.” [And one gets to look forward to “coffee ground-like discharge” for up to several days following the procedure, due to the materials they use to stem the bleeding cervix]. After LEEP, side effects may include infection, hemorrhage and possibly cervical incompetence.  These are rare, but if we’re talking vaccine side effects versus possible outcomes from HPV infection, these types of outcomes need to be considered as well–not just death from cervical cancer.”

Being currently pregnant following such a procedure, cervical incompetence was something I was carefully monitored for. Nevertheless, it’s still been a huge source of stress throughout this pregnancy, as this is a significant cause of second-trimester miscarriage and there aren’t great, foolproof ways to detect it, or remedy it if it does occur. Harper acts as if finding HPV via Pap smears is like rainbows and unicorns, but it too has a risk-benefit equation, and I’d so much rather have received a vaccination than to have gone through that. And, some women’s treatments for HPV infections and cervical abnormalities are even more extreme than mine was.

This is why I had my now-almost-14-year-old daughter vaccinated for HPV, and why my pre-teen son will soon be getting his as well. There are multiple ways to prevent HPV-induced cancers, but the vaccine (in combination with routine Pap smears) is by far the least invasive and safest route, as multiple studies have confirmed.

Finally, the show was doubly disappointing because Couric has been such an outspoken advocate of colon cancer prevention, which was the cause of her husband’s death in 1998. While realizing this is a fluff talk show and not the kind of harder journalism she’s apparently now abandoned, she still failed to ask even the most basic of questions to the supposed HPV vaccine “victims” she featured on her show, nor to note during their segments that other possibilities may exist for the girls’ illnesses and death besides the HPV vaccine. In the second segment, Rosemary Mathis even admits blatantly doctor-shopping until one would “listen to her” about her daughter–in other words, give her a new diagnosis (vaccine injury). Why isn’t this even questioned? What did her previous doctors tell her about her daughter’s condition? Couric allowed ratings and anecdotes to trump actual science, potentially causing real harm to the public health. How disappointing that this is now part of her legacy.

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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

Source: http://www.discoverworld.ru/park-tasmanijskogo-dyavola-17528/

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)

Sources:

(1)   http://www.dpiw.tas.gov.au/inter.nsf/WebPages/BHAN-5358KH

(2)   Welsh JS. Contagious Cancer. Oncologist. 2011 January; 16(1): 1–4. Published online 2011 January 6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228048/

(3)   Belov K. Contagious cancer: Lessons from the devil and the dog. BioEssays: Volume 34 (4), pages 285–292, April 2012. http://onlinelibrary.wiley.com/doi/10.1002/bies.201100161/full

Picture: http://www.discoverworld.ru/park-tasmanijskogo-dyavola-17528/

 

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.

 References:

  1. USDA/APHIS/VS (2004).  Scrapie Fact Sheet.  Retrieved from http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/fs_ahscrapie.pdf  – scrapie Fact sheet
  2. RSSS program http://www.aphis.usda.gov/publications/animal_health/content/printable_version/fs_scrafcp.pdf
  3. USDA/APHIS (2013). Chronic Wasting Disease.  Retrieved from http://www.aphis.usda.gov/animal_health/animal_diseases/cwd/history.shtml
  4. USDA/APHIS (2012).  About BSE. Retrieved from http://www.aphis.usda.gov/newsroom/hot_issues/bse/index.shtml  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

http://www.sciencedirect.com.proxy.lib.uiowa.edu/science/article/pii/S1474442205701927

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

Retrieved from  http://www.cdc.gov/ncidod/dvrd/cjd/

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 http://www.who.int/mediacentre/factsheets/fs180/en/

  1. http://commons.wikimedia.org/wiki/File:BOVINE_PRION_PROTEIN_1dx0_asym_r_500. – prion

picture

  1. http://commons.wikimedia.org/wiki/File:Histology_bse.jpg – histology picture

12. http://www.aphis.usda.gov/animal_health/videos/scrapie-narrated.mpg   (scrapie

Video hyperlink)

13.  BSE information – bseinfo.org   retrieved from

http://www.bseinfo.org/deactivationofprions.aspx

All photographs in this blog are for public domain found on http://creativecommons.org/

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.

References:

[1] NIH Website http://www.niaid.nih.gov/topics/lymedisease/understanding/pages/intro.aspx

[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 www.CDC.gov

[5] National Science Foundation http://www.nsf.gov/news/special_reports/ecoinf/lyme.jsp

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

[7] Ohio DNR http://www.ohiodnr.com/home_page/NewsReleases/tabid/18276/EntryId/3033/Acorn-Mast-Survey-Results-Show-Increases-for-White-Red-Oaks.aspx

[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.

[14} http://medicineworld.org/stories/lead/7-2010/protection-against-ticks-that-carry-lyme-disease.html

Student guest post: Seasonal Flu Vaccine: Why we need it

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Fifth one this year is by Nai-Chung Chang. 

Of the many health problems that everyone is bound to have at some point, influenza, or just “the flu,” is one of the most prominent. In fact, we call the time during which it is most prevalent the “flu season”. It has now become a regular occurrence in the U.S. to just get a shot before the flu season hits, and be free of it for the rest of the year. In some cases, like me, people just decide not to get the vaccine at all. I say to myself all the time: “It is just the flu. If I do get it, I’ll just take a nap, and I’ll be fine.” However, there are serious complications with influenza if the individual is afflicted with certain diseases, making the vaccine a necessity. Even in the general population, influenza infections could lead to serious health problems, at a lower rate, that could complicate the daily lives of individuals.

Influenza is a generic description of a variety of strains of influenza viruses, including influenza A (H1N1, H3N2), and influenza B. It is a widespread virus, and can infect both human and animals, albeit with different strains. (1) The influenza virus is difficult to completely control since it constantly undergoes different changes through antigenic drifts and shifts, small and abrupt changes in the virus constructs, respectively. (2) It causes fever, coughs, sore throat, runny nose, and a host of other symptoms that target different parts of the body. In extreme, severe cases, it may cause the death of the infected individuals. It can spread from person to person up to 6 feet away through coughing and sneezing, spraying droplets containing infectious particles into the air. The droplets either lands in the other individual’s mouth, or is inhaled into the lung. Influenza is very contagious, due to the fact that it can infect others prior to the development of symptoms, as well as a period after. In addition, there exist asymptomatic carriers that can infect others without knowing. There are vaccines provided every year prior to the start of the “flu season:” a period of time in which the population is most likely to acquire the disease. Once the symptoms develop, it can be treated with antiviral medicine, such as Tamiflu (oseltamivir) and Relenza (zanamivir).

In addition to the problems that a regular influenza infection can cause, in individuals with certain diseases, complications could develop from the interaction between the influenza virus and the disease currently affecting the patient. In asthma patients, the attacks are often triggered by respiratory virus infection, whether by the virus particle itself or the inflammation resulting from the influenza symptoms. Also, the influenza viruses could augment natural responses to allergenic particles resulting in a more severe than normal attack; influenza patients with asthma are often hospitalized as the result. (3) In patients with cardiovascular disease, influenza infections represent a high level risk. The infection could destabilize existing plaques (blocks in the artery) in atherosclerotic patients. In addition to the acute responses from the destabilization, influenza infections could also induce chronic inflammation in the body, as well as reduced clotting ability. (4) For patients with diabetes, infection with influenza represents a high risk of hospitalization and death. In diabetics, the immune system is weakened, making it difficult to fight of the disease. In addition, the infection can cause fluctuation in the level of blood sugar in the patients, through natural immune responses, or lack of desire to eat due to the effects of the influenza symptoms. There is also an increased risk of acquiring pneumonia as a complication of the infection. (5) As in the case with diabetics, patients with cancer and HIV/AIDS are also likely to have complications due to weakened immune systems from both treatment and disease.

From the variety of complications that could result from influenza infections, one can now see that it is extremely important for an individual to receive the vaccines when available. In some places, vaccines are often offered free of charge, especially in workplaces that have high exposure risks, such as hospitals and research facilities. In addition to reducing the likelihood of being affected by influenza, flu vaccines have shown to have reduced the development and progression of other diseases such as chronic obstructive pulmonary disease (COPD). (6) For individuals with HIV/AIDS, vaccines are especially important since they are more vulnerable to infections. In addition, they must be aware of the type of vaccines they are using, since certain vaccines do not work sufficiently in people with immune-deficient issues. However, there exist other treatments for the prevention of the disease, such as chemoprophylaxis, that would allow these individuals to be properly protected against possibilities of infection. (7) With the prevalence of the influenza virus in both the U.S. and globally, it is important that an individual keep up with the most current vaccines, as they are designed to combat the most common forms that would appear that flu season, since the strains changes every year.

References:

  1. CDC. Seasonal Influenza (Flu). http://www.cdc.gov/flu/index.htm
  2. CDC. How the Flu Virus Can Change. http://www.cdc.gov/flu/about/viruses/change.htm
  3. Glezen, W. Paul. Asthma, influenza, and vaccination. Journal of Allergy and Clinical Immunology 188(6): 1199-1206.
  4. Madjid M, Nagahvi M, Litovsky S, Casscells SW, Influenza and Cardiovascular Disease. Circulation 108:2730-2736.
  5. CDC. Flu and People with Diabetes. http://www.cdc.gov/flu/diabetes/index.htm
  6. Poole PJ, Chacko E, Wood-Baker RWB, Cates CJ. Influenza vaccine for patients with chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews.
  7. CDC. HIV/AIDS and the Flu. http://www.cdc.gov/flu/protect/hiv-flu.htm

Student guest post: Cholesterol, a bacterium, and gallbladder cancer

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Fourth one this round is by Kristen Coleman. 

If you are anything like me, you have been told countless reasons over the years why we must watch what we eat, keep our cholesterol intake down, and try to work out. It shouldn’t really come as a surprise then that I, since I am a public health student after all, aim to convince you of yet another reason why a healthy diet and exercise are valuable. What is this huge reason to avoid Big Macs and think about taking the stairs instead of the elevator you ask? Well, it may help you to prevent gall bladder cancer, is all.

All of this begins with gallstone formation. Gallstones are hard deposits, usually of cholesterol, that become lodged in your gallbladder over time. Your gallbladder is an organ that helps to aid in digestion through the storage and release of bile which helps to break down fats in your small intestine. The gallbladder is located on the right side of the body attached to the liver. The process of gallstone formation is called cholelithiasis. In this process, cholesterol, which is not very soluble, becomes clustered together in droplets in the bile called micelles. This cholesterol droplet then hardens into the crystals that make up a gallstone. Obesity causes bile to transit the gallbladder less rapidly and increased cholesterol in the diet means there is more cholesterol available to form stones. It does not require and active imagination then, to understand how obesity and high cholesterol intake contribute to stone formation, but how does this all tie into cancer you ask? http://www.umm.edu/patiented/articles/what_gallstones_gallbladder_disease_000010_1.htm

It all comes down to infection with a bacterium known as Salmonella typhi. Yes, this is the same bacterium that causes Typhoid fever and was the malady that afflicted the famous Typhoid Mary. While many people may become infected with S. typhi over the course of their lives, those individuals with gallstones are 6-15 times more likely to become carriers of S. typhi in the gallbladder. This is important because those people with a chronic infection of S. typhi have been shown to have 3-200 times higher risk of developing gallbladder cancer then non-carriers. Furthermore, chronic carriers have a 1-6% lifetime risk of developing gallbladder cancer. In fact, gallbladder cancer is so linked to S. typhi infection that gallbladder removal, called cholecystectomy, is recommended for those people with gallstone disease who live in high risk areas. Where is a high risk area? Most developing countries of the world are high risk areas for S. typhi, especially countries in Asia, Africa, and Latin America. This means that travelers from the USA and other developed countries to these regions are at risk for developing the infection. However, even at home in the USA, low risk doesn’t mean no risk, and we should be vigilant against emergence of this bacterium.  

In conclusion for all my gallbladder-containing friends out there (I make this distinction because I, myself, am no longer at risk for gallbladder cancer since I had mine removed in 2006 after a bout with gallstone disease) stay aware of your cholesterol levels and pay attention to making sure you have a healthy diet because, like every health care professional will tell you, it might just save your life….perhaps in a way you don’t expect!

References:

  1. University of Maryland Medical Center. Gallstones and gallbladder disease. Online http://www.umm.edu/patiented/articles/what_gallstones_gallbladder_disease_000010_1.htm
  2. Ferreccio, Catterina. Salmonella typhi and Gallbladder Cancer. http://link.springer.com/chapter/10.1007/978-94-007-2585-0_5#page-1

Center for Disease Control online source. http://www.cdc.gov/nczved/divisions/dfbmd/diseases/typhoid_fever/

Student guest post: Challenges and Progresses in HIV Vaccine Research

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Third one this round is by Jack Walsh. 

The Human Immunodeficiency Virus (HIV) infection is one of the most significant global health challenges of this 21st century. Since the isolation of the virus in 1983, it has infected 70 million people among whom 35 million have died of Acquired Immunodeficiency Syndrome (AIDS).1 Although important progresses have been made in slowing down the pandemic and reducing the morbidity and mortality related to HIV/AIDS with the highly active antiretroviral therapy (HAART) drugs, there are still difficulties in stopping the dissemination of the infection. It is estimated that for every person gaining access to HART, there are two new others infected by the virus.2 An effective and safe vaccine is therefore needed to prevent HIV from spreading, but the development of the vaccine has been proven to be an enormous scientific challenge.

HIV presents particularities that make it very difficult for researchers to find a vaccine. It is a lentivirus from the Retroviridae family, slowly progressive using an enzyme (called reverse transcriptase) for the transformation of its genome or genetic material (RNA in this case) into a new one (proviral DNA) integrated in that of the human host using another enzyme known as integrase. One of the most fascinating characteristics of the virus is its genetic variability in both an infected individual and geographically. In a same person, new mutations can be introduced in almost every new copy, creating up to millions of new particles every day. One antibody could then neutralize one virion, but not another.3 Additionally, super-infection in an individual already HIV infected results in new recombinants increasing further viral genetic diversity. The virus also presents two different types, HIV-1 worldwide and HIV-2 confined to West Africa. HIV-1 is further subdivided into subtypes or clades differently distributed on the globe and further diversified within each clade. Moreover, by integrating proviral DNA in the genome of memory cells of the immune system (CD4+ T cells) the HIV can escape the immune surveillance. To complicate the development of an effective vaccine, the virus envelope is able to hide receptor site to antibody that could potentially inhibit its effect (neutralizing antibodies). This explained the inefficiency of antibodies generated by vaccines targeting the glycoprotein 120 (gp120) located on the surface of virus developed in early vaccine trials.4

However, despite these challenges, encouraging progresses in the development of an effective HIV vaccine have been made. The first HIV vaccine trial was opened at the National Institutes of Health (NIH) Clinical Center in 1987, including 138 healthy volunteers. Other large scale trials included participants from North America and The Netherlands (1998), then Africa and Asia (1999).5 Three main approaches have been used in the development of an HIV vaccine: 1) the induction of neutralizing antibodies against HIV using the virus envelope proteins (gp120 or 140), 2) the use of viral vectors to stimulate responses form killer cells (CD8 T-cells or T cell that would recognize antigens on virus surface of the virus-infected cell, binds to it, and kill it), and 3) the optimization of cellular immunity (activation of killer cells) and humoral immunity (production of antibody) with prime-boosts (administration of one type of vaccine, such as a live-vector vaccine, followed by or together with a second type of vaccine, usually a recombinant).6 Also, to cope with the genetic variability of the virus, multiple strategies are explored, such as mixing envelope immunogens from several HIV subtypes or clades. Unfortunately, most of the tested vaccine models did not significantly reduce HIV infection in participants, except an envelope-based subunits’ vaccine tested in Thailand which showed significant decline by about 30% in HIV infection in 2009.7 Though modest, the results clearly show that HIV/AIDS is a vaccine preventable disease. More recently in 2012, a Spanish study showed promising results in the development of a therapeutic HIV vaccine effective in reducing the viral load by 90% after 12 weeks of therapy, awkwardly the vaccine lost effectiveness within a year.8 Just a few days ago, the Duke Human Vaccine Institute team published an important study, in which it has been able for the first time to map the co-evolutions of antibodies and virus in an infected individual, whose immune system launched a broad attack against the pathogen, using new technologies. They also identified the viral surface glycoprotein, which initiated the neutralizing antibody development.9

Despite two decades of disappointing results on HIV vaccine research, we now have started to see encouraging advances. For the first time a candidate vaccine was successful in significantly reducing the HIV infection. Furthermore, an important progress has been made very recently in identifying neutralizing antibodies initialization and mapping. The study provides crucial insights for the development of a vaccine that could mimic the actual antibody development and elicit non-strain specific antibodies. Progress towards finding an effective vaccine is slow, but we can optimistically say that the future is promising.

 

References

[1] World Health Organization (WHO), Global Health Observatory (GHO). HIV/AIDS, Global situation and trends. 2012. http://www.who.int/gho/hiv/en/

2 Letvin, Norman L. “Progress and obstacles in the development of an AIDS vaccine.” Nature Reviews Immunology 6.12 (2006): 930-939.

3Letvin NL. Progress Toward an HIV Vaccine. Annu. Rev. Med. 2005. 56:213–23

4Marc GP, OsmanovSK, Kieny MP. “A review of vaccine research and development: the human immunodeficiency virus (HIV).” Vaccine 24.19 (2006): 4062-4081.

5 National Institute of Allergy and Infectious Diseases (NIAID). History of HIV Vaccine Research. 2012. http://www.niaid.nih.gov/topics/hivaids/research/vaccines/Pages/history.aspx

6 Ross, Anna Laura, et al. “Progress towards development of an HIV vaccine: report of the AIDS Vaccine 2009 Conference.” The Lancet infectious diseases 10.5 (2010): 305-316.

7 Rerks-Ngarm, Supachai, et al. “Vaccination with ALVAC and AIDSVAX to prevent HIV-1 infection in Thailand.” New England Journal of Medicine 361.23 (2009): 2209-2220.

8 García, Felipe, et al. “A Dendritic Cell–Based Vaccine Elicits T Cell Responses Associated with Control of HIV-1 Replication.” Science translational medicine 5.166 (2013): 166ra2-166ra2.

9 Liao HX et al. Co-evolution of a broadly neutralizing HIV-1 antibody and founder virus. Nature 2013. Epub April 3, 2013

Student Guest Post: Arsenic, Benzene, and Now Clostridium? Smokers are Inhaling More Than Just Chemicals in Their Cigarettes

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Second one this round is by Jonathan Yuska. 

If you happen to be one of the 46 million individuals who have not been swayed to quit smoking by the countless anti-cigarette ads in print and on television, here is one more piece of evidence that may have you second thinking that next puff. On top of the more than 3,000 chemicals and heavy metals already identified in ordinary cigarettes1, upwards of a million microorganisms per cigarette have also been found to live and thrive in virtually all cigarettes in the United States2. Microbes such as Bacillus (which is linked to the notorious anthrax disease), Clostridium, and Pseudomonas—to name a few—likely contaminate the tobacco leaves early at the farm level and are able to flourish during curing and manufacturing to be viable in the cigarette at the time of the consumer’s use. While some of the bacteria are capable of causing no more than a stomachache, others (and their respective endotoxins) have been linked to pneumonia and chronic lung inflammation—a widely recognized risk factor for cancer1,2. While cigarette smoking is a well-established cause of cancer in and of itself, the role microorganisms have in the toxicity of cigarette smoke should not go underplayed. With increasing evidence supporting the vast illness causing biodiversity found in cigarettes, hopefully more individuals will be aware of the dangerous contaminants they are welcoming into their bodies and call for greater sanitary measures to be taken to potentially create a less harmful cigarette product.

Approximately 23 different species of bacteria have been found in cigarette tobacco, many of which have been linked to serious illness in humans. For example, Pseudomonas aeruginosawhich is the leading cause of nosocomial pneumonia and often found in soil or sand—was found to be present in nearly all cigarettes tested in a study that looked at the presence of cigarette bacteria in the most commonly smoked brands, like Marlboro2. Another study interested in understanding the cause of severe lung inflammation in United States troops during Operation Iraqi Freedom found eight different species of Bacillus (five of which were never seen before) contaminating the soldier’s cigarettes3. Regardless of the actual bacteria within the cigarettes, the endotoxins derived from the bacteria that remain well after the bacteria have died have been shown to be a powerful inducer of lung inflammation (chronic inflammation is recognized as a powerful risk factor for cancer). It is theorized that the bacteria and their respective endotoxins may have an additive or multiplicative effect with tobacco smoke’s natural ability to cause pulmonary inflammation, though the amount of the effect that can be attributed is still up to debate2.

Research has shown that more than 90 percent of cigarettes are contaminated with some form of bacteria, and these bacteria are believed to originate early in the cigarette manufacturing process1. Similar to other crop cultivation, tobacco is grown in large fields where animal manure is used to provide the nutrients needed for a hearty crop. Some of the bacteria from the manure are believed to adhere to the tobacco leaves during the plant’s development. Curing the tobacco, which is essential in the cigarette manufacturing process to develop an ignitable, flavorful product, further facilitates bacterial growth because it is often done in moist, warm conditions3. Unlike other agriculture crops grown for consumption, tobacco has no regulations associated with its sanitation, and as a result, tobacco products can contain soil residues and insecticides in addition to a vast array of deleterious bacteria. Efforts to sanitize tobacco through an antimicrobial wash have been proven to be effective in reducing contaminants; however, since so little mainstream attention has been given to microbes in cigarettes, no sanitation process is currently being used by the cigarette industry2.

Misperceptions about how much risk the bacteria pose to the smoker is one reason so little attention has been given to microbes in cigarettes.  Some critics believe that bacteria in cigarettes pose no harm because the cigarette flakes are prevented from entering the lungs because of the built-in filter within the cigarette. Some further argue that the viable bacteria found in the tobacco are destroyed or heavily reduced in number by the heat of the cigarette. Though, the validity of these observations are derailed by the fact in the process of transportation, or even minor jostling, tobacco flakes are often seen lying freely on the mouth end of the filter. Thus, loose tobacco on filters could transfer bacteria to the mouths and lungs of smokers before the cigarette is even lit. Additionally, some extremely fine tobacco microparticulates are able to pass through the cigarette filters currently being used and can be inhaled deep into the lungs to cause inflammation2,5. The harsh, high temperature conditions of cigarette smoking also does little in eliminating the bacteria that are able to produce robust heat resistant endospores such as the bacterial species Bacillus and Clostridium1. It is clear that more attention should be given to dismiss the misperceptions of bacterial risk associated with cigarettes so that effective sanitary regulations can be applied to tobacco similar to other widely consumed foodstuffs.

If the more than 3,000 chemicals and heavy metals that have been identified in ordinary cigarettes have not influenced you to quit smoking, hopefully the realization that one cigarette can contain roughly 1,000,000 microorganisms will have you second thinking the habit the next time you light up. Microorganisms that have been linked to serious illness in humans like pneumonia and chronic inflammation are thought to contaminate tobacco leaves early in the manufacturing process, and these organisms thrive and multiply to be viable bacteria in the consumer cigarette. While cigarettes themselves are recognized as a serious cause of ill health, the role microorganisms have in their toxicity should not be underplayed. With a better understanding of the vast bacterial biodiversity within cigarettes, sanitary regulations that eliminate bacterial contamination should be mandated to potentially make a less harmful tobacco product. Though until then, people should recognize the dangerous bacterial contaminants they are welcoming into their bodies every time they light up.

Sources:

1.   Sapkota, Amy R., Sibel Berger, and Timothy M. Vogel. “Human Pathogens

Abundant in the Bacterial Metagenome of Cigarettes.” National Center for Biotechnology Information. 22 Oct. 2009. U.S. National Library of Medicine. 13 Apr. 2013 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854762/>.

2.  Pauly, J. L., J. D. Waight, and G. M. Paszkiewicz. “Tobacco flakes on cigarette filters

grow bacteria: A potential health risk to the smoker?” Tobacco Control. 18 Oct. 2007. 13 Apr. 2013 <http://tobaccocontrol.bmj.com/content/17/Suppl_1/i49.long>.

3. Rooney, Alejandro P., James L. Swezey, Donald T. Wicklow, and Matthew J. McAtee.

“Bacterial Species Diversity in Cigarettes Linked to an Investigation of Severe Pneumonitis in U.S. Military Personnel Deployed in Operation Iraqi Freedom.” Current Microbiology 51 (2005): 46-52.

4. “How to Grow Tobacco.” How To Grow Stuff. 23 Nov. 2007. 13 Apr. 2013

<http://www.howtogrowstuff.com/how-to-grow-tobacco/>.

5. Pauly, John L., and Geraldine Paszkiewicz. “Cigarette Smoke, Bacteria, Mold,

Microbial Toxins, and Chronic Lung Inflammation.” National Center for Biotechnology Information. 09 July 2011. U.S. National Library of Medicine. 13 Apr. 2013 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136185/>.

 

 

Student guest post: The Fallacious Fad of Foregoing Vaccinations

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. First one this year is by Dana Lowry.

Humans have a long history of illness and death from infectious diseases. It wasn’t until the 1790s that we had a solution. Edward Jenner recognized that milkmaids never contracted smallpox but suffered from a more mild disease, cowpox. Jenner took pus from a cowpox lesion on a milkmaid’s hand and placed it in an incision he made in an eight year-old boy’s arm. He then exposed the boy to smallpox; the boy didn’t contract the disease, proving he was immune. Jenner experimented on several other children, including his own 11-month old son, and his theory of passing on immunity proved to be successful. The Latin term for cow is vacca, which is where Jenner coined the term “vaccine”. Jenner’s discovery eventually led to the eradication of smallpox from the U.S. in 1949 and from the world in 1979. For over a century, vaccines were limited to preventing smallpox but as we know today, vaccines prevent a large number of diseases.

Although many developing countries still suffer from the burden of preventable infectious diseases, the U.S. has greatly increased the life expectancy and quality of life through the use of vaccines. In the 1940s, the U.S. recommended vaccines for diphtheria, pertussis and tetanus; polio was added in the 1950s. In the 1970s, measles, mumps and rubella (MMR) were added to list. Today in the U.S., immunizations are recommended for 17 vaccine-preventable diseases during one’s lifetime and more are available for individuals traveling outside of the U.S. Many of these vaccinations are combined so they can prevent multiple diseases from one series of immunizations. The increase in life expectancy in the 20th century is largely attributable to vaccines. For each birth cohort vaccinated, 33,000 lives are saved, 14 million cases of disease are prevented, healthcare costs are reduced by $9.9 billion and $33.4 billion is saved in indirect costs. The Bill Gates Foundation believes that vaccines are one of the most cost-effective investments in global health, saving about 2.5 million lives each year. One child dies every 20 seconds from vaccine-preventable diseases while tens of thousands of other children suffer from severe illnesses and permanently disabling diseases.

Despite the facts, less and less parents are choosing to vaccinate their children today because of fears that vaccines are unsafe. Much of the controversy started with Dr. Andrew Wakefield, a former British surgeon and medical researcher. Wakefield published a paper in 1998 linking the MMR vaccine to autism and bowel disease. Wakefield’s entire study was found to be fraudulent and the infamous paper was retracted in 2010. But, what got more attention than a retracted science paper was Jenny McCarthy sharing her personal life story of how her son got autism from a vaccine on the Oprah Show. Unfortunately, more moms keep up-to-date with Oprah and popular news rather than science and still do not know the truth behind Wakefield’s falsified study; therefore, the autism myth continues.

Furthermore, parents argue “herd immunity”. If your children are effectively vaccinated then why would I have to worry about mine? First, many vaccine-preventable diseases still exist in other countries and can easily be brought into our country; second, some individuals do not build immunity to the disease even after vaccination. The more and more parents that opt out of vaccinations, the less protection their children have from the rest of the “herd”. Additionally, parents argue that their children should contract diseases “naturally” through the environment to build immunity. Parents don’t fully understand the severity of these diseases because many have been virtually eradicated through the successful use of vaccines. Though some crippling effects of polio still linger, it is rare to come across someone wearing braces or using a wheelchair as a result of a polio infection in the U.S. Many vaccine-preventable diseases can cause death during the initial acute illness and if the individual survives, he or she may be left with chronic effects that last a lifetime. Polio can lead to temporary or permanent paralysis, deformities in the hips, ankles and feet; measles, mumps and varicella can all lead to brain damage and mumps is known to cause deafness; hepatitis B can cause permanent liver damage and even liver cancer. The list of damaging effects goes on and on.

In some areas throughout the U.S., as many as 1 in 20 kindergarteners have not been vaccinated. As the antivaccination fad grows in American so do the infectious disease rates. Measles was said to be eliminated from the U.S. in 2000 but an average of about 60 cases of measles occurs each year, typically from traveling. However, in 2011, there were 17 measles outbreaks in U.S. communities and the number of cases jumped to 222. In 2012, the U.S. had one of the largest pertussis outbreaks in nearly 50 years. Nationwide, over 85,000 vaccine-preventable diseases occur each year. I am not arguing that vaccines have no potential side effects and have never caused adverse effects or even death in children. However, I do think vaccines have done considerably more good than harm. So I urge parents, before deciding to withhold your children from vaccinations, look into the facts and make a decision based on science – not popular news. Although outbreaks of disease have been conquered in the past, many vaccine-preventable diseases remain throughout the world and the U.S. is not immune to future outbreaks.

 

HIV In-Home Testing Kits: Increased Awareness or Increased Problems?

Fifth of five student guest posts by Jonathan Yuska

The saying, “The more you know, the more you can control,” is no more meaningful than when used in the context of HIV detection and prevention. Public health advocates endlessly stress the need for knowing one’s status; and one would assume that any way in which the most amount of people can be tested would be beneficial for the population1. The Food and Drug Administration shared this same idea when they overwhelmingly approved the first ever over-the-counter (OTC) HIV testing kit in 20052; which in theory, sounds like a promising way to reduce the possible 350,000 HIV cases that remain undiagnosed in this country3. Though, some medical staff are still weary of this type of diagnostic method for reasons such that it breaks the linkage between the patient and long-term care. The debate on whether HIV testing should be—shall we say—left only to the professionals or put in the hands of everyday citizens is only just beginning; though, here are some points you may want to consider when making your own opinion on HIV home testing.

The OraQuick ADVANCE is one example of an in-home testing kit that provides the user with an accurate (sensitivity of 99.3% and specificity of 99.8%) and rapid means of HIV detection with nearly no invasiveness. In just 20 minutes and a swab of the mouth, individuals who may have been living their entire life unaware they are HIV positive, now can take that knowledge as empowerment to manage their health safely and finally receive the appropriate care they may desperately have needed. Supporters of in-home kits believe it offers a choice of what to do with the knowledge of being diagnosed and dismisses possible stigmatizations associated with being tested since testing can be done in the privacy of one’s own home. Proponents also feel that HIV home testing may become the new norm before engaging in intimacy and suggest testing kits come in boxes of two so partners can test each other4. The OTC HIV testing kits are hoped to slow down the more than 40,000 new infections3 that occur every year in the United States; though, some that believe kits such as OraQuick will make little difference in reducing the HIV infection crisis in the populations that need it most.

The HIV home testing kit is hoped to attract those at highest risk including young, low-income and education, non-white males who neither frequent medical care facilities nor are tested regularly on their HIV status5. Surveys conducted by the National Center for Health Statistics have shown that 79% of persons in these types of populations would indeed use home HIV tests if available; though, when participants in the survey were told the price of testing kits was $40, the approval rate of the kits dropped to 40%2. This raises some speculation on whether OTC kits will actually access these sorts of populations without first lowering the price to purchase them.

Rather than accessing those at highest risk, some naysayers anticipate the tests will predominantly appeal only to those “worry well” or hypochondriac individuals who continually test negative or new couples that want to verify their HIV statuses before sexual intimacy begins. Though, what one does with the knowledge of having tested negative for HIV is still under question. It may be seen that negative results actually promotes more risky sexual behaviors—since they were able to “get away” with it in the past—such as having intercourse without protection. This sort of risky behavior may expose the individual to a whole host of other sexually transmitted diseases2.

Issues with the proper usage of kits may also pose a problem in accurately diagnosing those who have been recently infected with HIV which could lead to false-negative results. Individuals participating in unsafe practices may be unaware of the 8-week “window period” needed for in-home tests to detect HIV antibodies (human antibody component is needed to determine HIV status in at-home tests [RNA tests commonly used by clinics can detect HIV within 9 to 11 days post infection]) and unwittingly spread their infection to others6.

False-positive results from in-home tests may also cause a great deal of damage to the validity of proven HIV detection methods as well as the likelihood of individuals to repeat HIV testing after receiving highly upsetting untrue news. False positive outcomes from tests are most common in populations with a low occurrence of disease in the first place—like in HIV—where the occurrence of unknown cases is roughly 0.2%. The ability to perfectly detect such a small percentage of people infected even with a test that is highly sensitive and specific is extremely unlikely and the predictive value of the test will be noticeably low2.

Lastly and most obviously is the disconnect from care that occurs from in-home diagnostic kits. Public testing focuses on linking HIV-positive patients with counseling and treatment; though, when this diagnosis is done in private, a person’s anxiety may force them to exile where they never seek treatment and may even contemplate suicide1. It is important to note that diagnosing patients is only half of the battle, linking them to the appropriate care is the other half—something home testing inherently does not do.

“The more you know, the more you can control” is a saying that is at the heart of reducing the amount of HIV transmissions person-to-person by knowing one’s status. HIV home testing kits such as OraQuick sounds like a promising way to reduce the number of transmissions since they are quick and convenient for the user, but whether these tests will actually reach those individuals who are at greatest risk is doubtful. At home kits may also promote risky behaviors, increase the numbers of false-positives and –negatives, and deteriorate the linkage to care that is vital to those with new diagnoses.

Will in-home HIV testing kits be the assistance needed in decreasing the HIV transmission concern—some professionals are questionable. Now after reviewing the facts on HIV home testing, what is your stance on the subject?

Sources:

1. Chesney, Margaret A., and Ashley W. Smith. “Critical Delays in HIV Testing and

Care.” American Behavioral Scientist. Apr. 1999. 17 Feb. 2013             <http://abs.sagepub.com/content/42/7/1162.short>.

2. Walensky, Rochelle P., and David Paltiel. “Rapid HIV Testing at Home: Does It Solve

a Problem or Create One?” Annals of Internal Medicine (2006): 459-562.

3. Fleming, P. L. “HIV Prevalence in the United States, 2000.” Feb. 2002. 18 Feb. 2013

<http://stdpreventiontraining.jhmi.edu/docs/Fleming%20et%20al_HIVPrev_Seattle_CROI_2002.pdf>.

4. McNeil, Donald G. “Another Use for Rapid Home H.I.V. Test: Screening Sexual

Partners.” The New York Times. 5 Oct. 2012. 18 Feb. 2013 <file:///Users/ska020/Desktop/Another%20Use%20for%20Home%20H.I.V.%20Test%20-%20Screening%20Partners%20-%20NYTimes.com.webarchive>.

5. Phillips, Kathryn A. “Potential Use of Home HIV Testing.” The New England Journal

of Medicine. 11 May 1995. 18 Feb. 2013 <http://www.nejm.org/doi/full/10.1056/NEJM199505113321918>.

6. “Possible Exposure to HIV?” How long it takes to test HIV positive after infection.

Stop AIDS Project. 18 Feb. 2013 <http://stopaids.org/resources/possible-exposure-hiv/time-it-takes-test-positive>.