Contact Sports and Skin Infections

6 02 2012

(Welcome to guest blogger Rebecca Kreston, MSPH and thanks, Rebecca, for sharing this post from your blog: bodyhorrors!)

In honor of one of the most lucrative American events that happened just yesterday, I thought I’d explore sports and infectious diseases. Specifically, contact sports and skin infections!

Since starting this blog, I’ve gathered that readers just love reading about transmissible skin infections, so what could be better than watching the Super Bowl and knowing just exactly what kind of diseases could possibly be smeared between the players of the Patriots and Giants?

There is a glut of infectious diseases that one can acquire from dabbling in combat or contact sports such as American or Aussie-style football, rugby, wrestling, and sumo. In fact, skin infections are the most common injury associated with all sports (1). All that body bashing and face-to-face smearing in contact sports does wonders for spreading skin or cutaneous infections. A number of these ailments are common to us non-athletic mortals—athlete’s foot, jock rash and ringworm (or tinea corporis). Two diseases in particular, with the marvelous potential to initiate larger epidemics within and beyond the locker room, form the focus of this article.

Herpes gladiatorum is a wonderfully evocative name used to describe an athlete’s infection with herpes simplex virus 1 (HVS-1), a terribly contagious virus that many have the misfortune of being acquainted with; it’s estimated that 65% of people will become infected with the virus by the time they reach their 40s (2). Symptoms can include painful, blistery cold sores on the face and neck, along with a sore throat, infected lymph nodes and malaise.

It’s a tricky little bugger of a virus. It can remain dormant, hiding away in nerve cells known as sensory ganglia, only to spring out on one’s face or genitals during periods of physical or emotional stress or, say, when you’re sunbathing in tropical locales on vacation. It has an uncanny sense of knowing when to erupt at the most inappropriate of times, though I’ve been unable to track down any research examining the molecular basis of how it goes about conducting this remarkable mechanism.

Most people rightfully assume that HSV-1 infection is a rather personal, intimate matter: we hear about transmission between a mother and her child, between romancing couples and so on. This makes sense considering that it’s spread by respiratory droplets or direct contact with infected lesions; you’ve really got to get up close and personal in someone’s face if you want to get a sense of what HSV-1 infection feels like (2). But given social situations with a generous amount of skin-to-skin contact with many individuals—sports, for instance—the virus will happily engage in a bit of unplanned host-hopping. As such, it has a frustrating tendency to erupt into outbreaks in sports team and during competitions.

Many athletes may sport micro-abrasions and skin breaks stemming from turf burns, powerful body-to-body collisions, facial stubble or beard burn, and shaving. Depending upon the level of protective clothing and gear, these athletes can experience substantial exposure with their opponent’s infected HSV-1 lesions, not to mention the respiratory droplets, spit and mucus that may transmit other types of infections. Charming! Among teammates, a grab-bag of infections can also be spread by sharing towels, water bottles, clothing, equipment, and hygiene and cosmetic products.

HSV-1 is considered to be particularly endemic in rugby players due to the style of the sport and the lack of protective gear (3). Its rampant presence in rugby leagues has earned it the moniker “herpes rugbiorum” or “scrum pox” (“scrum strep”, caused by the bacterium Streptococcus pyogenes, can also plague rugby players).

In rugby, the “scrum” is a type of huddle maneuver used to return the ball into play. It is a sensational way to spread HSV-1: players in the forward position interlock their heads with their opponents in facing rows before the ball is launched between them. These forwards are the most likely of their teammates to contract scrum pox due to their prominent role in scrums and the increased prospect of serious face-to-face contact. The fact that rugby players do not use protective gear, including helmets, exposes a greater part of their body to physical contact and further increases their risk.

HSV-1 regularly rears its ulcerous face on wrestlers as well. A research group checking serum samples from wrestlers to determine previous HSV 1 exposure found that 29.8% of college wrestlers had reported previous HSV infection (4).

The level of intimacy required in grappling almost makes it inevitable that something is going to be transmitted between two athletes, whether that be sweat, saliva or HSV-1. Indeed, in a 1989 outbreak in high-school wrestling camp for boys, 34% of participants were diagnosed with HSV-1 (5). Lesions commonly appeared on regions of the body most likely to encounter direct skin-to-skin contact with their opponents – 73% on the head, 42% on the extremities and 28% on the trunk of the body.

How do you tell if a wrestler is right or left-handed? Check which side of their face, head, neck and arms has the greatest amount of lesions. Athletes will tend to prominently use the most powerful sides of their body, regardless of which sport, and it will be this side that can receive the greatest amount of skin-to-skin contact with opponents.

Getting a touch of HSV-1 and sharing it with your teammates may be the least of an athlete’s problems. In 2003, a ghastly outbreak of methicillin-resistant Staphylococcus aureus (MRSA) emerged during a college football camp in Connecticut (6). Ten players were infected, of whom two required hospitalization. The infection was discovered to have spread due to the combination of body shaving and turf burns from the artificial grass. Infections were most commonly located at the elbow, thigh, hip, chin, forearm and knee, parts of the body most likely to incur abrasions on the turf. Those players with turf burns had a seven-fold risk of acquiring MRSA infection than those who emerged from scrimmage and active play unscathed (6). Cornerbacks and wide receivers were particularly susceptible due to their frequent body contact during drills and scrimmage play.

A quick browse through the research literature pulls up dozens of MRSA outbreaks like this. In 2002, two college football players in Los Angeles were hospitalized due to MRSA infection (7). A one-year surveillance of a football team at an unnamed major university in the southeastern United States found that 19% of the players showed evidence of nasal colonization of the bacteria at the end of the football season; though the high prevalence of MRSA among these men did not yield any active skin and soft tissue infections, it goes to show how endemic of a problem this really is (8). In 2007, six football players on a Brooklyn high school football team showed evidence of MRSA skin and soft tissue infection; the players had just recently returned from a preseason training camp (9). The infections were serious enough that they generated abscesses requiring surgical incision and drainage.

MRSA colonization of football players is apparently becoming so commonplace that some researchers have suggested using them as human sentinels for public health surveillance of outbreaks within the surrounding community (10). It is regrettably becoming a rather conventional type of emerging infection in athletes.

These infections aren’t just unseemly looking but can be disfiguring, have long-lasting effects within the body and can temporarily disqualify an athlete from practice and competition to prevent localized outbreaks. Hell, some of them can kill ya! These outbreaks can ruin seasons for the team while for salaried athletes, these kinds of infections have serious economic, professional and personal repercussions. Medical professionals recommend that players abstain from play until they’ve started antiviral medications or antibiotics, they are free of systemic symptoms – fever, malaise and lymph node swelling – and until any moist lesions have subsided. Seems reasonable, no?

Infectious diseases are always context specific and spread through particular practices. In the case of contact sports, there are several variables at play that help to spread some nasty infections. While there isn’t a lot we can do about changing how a sport is played (or can we?), coaches and referees can keep an eye out for athletes who seem ill or are showing visible evidence of infection. Fighting against poor hygiene practices and ensuring that wounds are cleaned and dressed immediately can also keep these kinds of sticky situations in line. Game on!

RESOURCES
A mission statement and guidelines on how to deal with herpes gladiatorum from the Sports Medicine Advisory Committee at the National Federation of State High School Associations.
Wrestlers filed a “herpes lawsuit” in 2008 against their coach and trainer holding them responsible for a localized HSV-1 outbreak.
In 2008, researchers discovered a unique herpes strain that only affects sumo wrestlers.

REFERENCES
1. BB Adams. (2010) Skin Infections in Athletes. Expert Rev Dermatol. 5(5): 567-577
2. R Sharma et al. (2011) Herpes Simplex in Emergency Medicine. Accessed online on Feb 2, 2012. Link.
3. BB Adams. (2000) Transmission of cutaneous infections in athletes. Br J Sports Med. 34(6): 413–414
4. B.J. Anderson (2008) Managing Herpes Gladiatorum Outbreaks in Competitive Wrestling: The 2007 Minnesota Experience. Curr Sports Med Rep. 7(6): 323-7
5. Belongia EA, Goodman JL, Holland EJ, et al. (1991) An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med. 325(13): 906-10
6. EM Begier et al. (2004) A High-Morbidity Outbreak of Methicillin-Resistant Staphylococcus aureus among Players on a College Football Team, Facilitated by Cosmetic Body Shaving and Turf Burns. Clin Infect Dis. 39(10): 1446-1453
7. DM Nguyen et al. (2005) Recurring Methicillin-resistant Staphylococcus aureus Infections in a Football Team Emerg Infect Dis. 11(4): 526-32
8. CB Creech (2010) One-year surveillance of methicillin-resistant Staphylococcus aureus nasal colonization and skin and soft tissue infections in collegiate athletes. Arch Pediatr Adolesc Med. 164(7): 615-20
9. Centers for Disease Control & Prevention (CDC). (2009) Methicillin-resistant Staphylococcus aureus among players on a high school football team–New York City, 2007. MMWR Morb Mortal Wkly Rep. 58(3): 52-5
10. B Barr, M Felkner & PM Diamond. (2006) High school athletic departments as sentinel surveillance sites for community-associated methicillin-resistant staphylococcal infections. Tex Med. 102(4):56-61

Image courtesy of Textbook of Bacteriology

Image courtesy of Medscape

Image courtesy of Abragad

Image courtesy of Andrew Bradley/ABC News

Image courtesy of PodiatryToday


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Rare Diseases Matter

2 02 2012

(We welcome David Bradley Science Writer as our guest blogger. Thanks, David!)

Pharmaceutical research and development has improved our quality of life and boosted life expectancy significantly over the last few decades.

We are living longer, healthier lives thanks to medical science. Although there are concerns about drug resistance and so-called superbugs, vaccination, antibiotics and antiviral drugs are incredibly successful at keeping diseases at bay and reducing significantly the risk of death from infection following a surgical operation.

In addition, important medical advances have made cancer treatable and reduced the risk of dying from heart disease significantly. The emergence of diseases of old age, such as Alzheimer’s disease, reflect not a failure on the part of medicine, but the fact that so many people reach old age rather than dying young of the illnesses to which our ancestors succumbed for lack of medicine.

There remain, nevertheless, many lesser-known and rare diseases for which there are no treatments. The US Rare Diseases Act of 2002 defined rare diseases based on prevalence. Any condition afflicting fewer than 200,000 people in the US (about 1 in 1,500) was labeled rare.

The Europeans by contrast defined these diseases based on how much of a threat to life they represent. Whatever the definition, the pharmaceutical industry is beginning to home in on these rare diseases, which is obviously good news for sufferers.

Orphanet, which as the name might suggest is an online portal for information about rare diseases and orphan drugs, suggests that, “There is no disease so rare that it does not deserve attention.”

Moreover, just because a disease is labeled rare does not mean that there are not large numbers of people affected. There might be 10,000 patients with any given “rare” disease in the US alone. The numbers might be in the millions if we consider worldwide incidence.

Orphanet’s Segolene Ayme told me: “The true prevalence of rare diseases is unknown, there is no source of data at population level.” In fact, the data are often skewed towards more conservative estimates of disease incidence, although for some genetic diseases, the numbers may truly amount to a few dozen people rather than tens of thousands.

The list of rare diseases is vast and continues to grow as new health problems are identified for the first time as distinct diseases and disorders. On that growing list are Aarskog syndrome, Gaucher’s disease, tyrosinemia type 1, Kahler’s disease, Q fever, Takayasu arteritis , Waardenburg anophthalmia syndrome and Zygomycosis.

Andreas Zaby of the Berlin School of Economics and Law, in Germany, has analysed the impact of legislation aimed at stimulating R&D into these and other diseases. He says there is a great deal of room for improvement in addressing the problem of rare diseases and suggests that the creation of expert networks could help. He adds that specialist care facilities and reference centers for research and treatment are urgently needed if medicine in these areas is to move forward.

Coordination by the World Health Organization could be the answer to helping medical science tackle a vast range of diseases, each of which afflicts a limited number of people but taken as a whole cause misery and suffering for millions worldwide.

Rare Disease Day is 29 February. Let’s all make some noise for those who are too often ignored.

Image courtesy of rarediseaseday.org


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All Hallows Eve

31 10 2011

Behold, it is a dark and thunderous night (but please, no rain, or the toilet paper will be impossible to lob over the tree limbs).

It is—BOM BOM BOM  . . . All Hallows Eve. The night that invites superstition, just as the dawn invites the dew.

What superstitions have we, this 31st of October? Let’s share—

Parents in remote villages in India believe a measles infection indicates a visit from God, and to vaccinate would deprive their child of that visit. They also believe the vaccine will cause the number “666” to appear on their child’s body.

Spitting three times, or saying “pooh, pooh, pooh” after the birth of a healthy baby will, according to some, ward off the evil eye and protect the babe from demons.

Should you want to get back at the kid who stole your cupcake, surreptitiously rubbing a toad on his skin will cause an outbreak of warts (bwahahahahah).

Hordes of healthcare workers believe a full moon brings chaos and disruptive patients to the Emergency Department and that Fridays, particularly Friday the 13th, bring excessive trauma cases and even more chaos. And, should anyone suggest a shift is “quiet,” all of hell will actually break loose.

In parts of Ukraine, mothers will not bathe children infected with chickenpox until all lesions are crusted over, believing it not safe for the child.

A few baseball players believe peeing on their hands will toughen them up (the hands, not the guys). At least one NHL player repeatedly dunked his hockey stick in the toilet to break scoring slumps and another talked to the net posts to make them his friends, believing they would cause opponents’ pucks to bounce off the posts during games.

In Louisiana, a few years back, some believed that a nosebleed could be stopped by putting cobwebs up the nose, yellow paper under the top lip, or by crisscrossing two match sticks in one’s hair and sprinkling salt in the hair. Teething woes were fixed by tying an animal bone or alligator tooth to a string and hanging it around the neck, although garlic in a pouch would do in a pinch.

One can dive deep to find superstitions, or it’s as easy as asking relatives. Superstitions abound, and the magical thinking is practiced by a surprising number of Americans.

Just what do you believe, on this All Hallows Eve? Will you step on a crack, and risk breaking your mother’s back?

By Trish Parnell

Image courtesy of Totally Severe


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Ask Emily

29 09 2011

Are there really worms living in our eyelashes?

Well, no, not worms, exactly. Exactly speaking, they are arachnids. And unless you’re in the estimated 5% free of these microscopic critters, there’s likely more than one living in that forest of hairs lining your eyes. I know, there’s a major ewww factor involved for a lot of people, especially when you see images of these things. By the way, obtaining those images appears to involve extracting the microscopic mites from hair follicles using “Krazy Glue” (see below).

Clocking in at a tiny 0.1  to 0.44 mm, the mites, if you’ve got ‘em, move around mostly at night on their four pairs of legs and dine sumptuously on surface skin cells (and yes, they poop). Many people walk around oblivious to their presence, but if the mites do cause symptoms, they generally are of the irritation sort, such as itching and scaling skin on the eyelids. These mites may not stay confined to the eye area and have been found in people who have rosacea, although whether or not they’re causative in that skin disorder remains unclear.

As with many organisms we host, it may be that disease or infection gives them a greater opportunity for colonization, especially if the immune system is suppressed or overtasked. They’ve also been implicated in conditions involving dry eyes, facial inflammation, and an eye disorder called blepharitis.

We’ve known about our cohabitation with these mites since at least 1840, when the primary species that inhabits us, Demodex folliculorum, was identified. It may make or may not make you feel better to know that this mite is the only parasite that hangs out in this specific area. Their presence appears to increase with age, with one study finding it in 84% of a population with an average age of 61 years, but in 100% of those older than age 70. They don’t seem to care at all whether you’re male or female. In spite of their ubiquity, though, these parasites are by no means off the hook when it comes to implications of their involvement in disease. As one publication has noted—and it’s worth quoting here—

As old-fashioned as mites may seem, and as low-tech is their removal from the follicle with Krazy Glue on a glass slide, the reader is cautioned that one of the great minds in dermatology suspected Demodex to be an unindicted coconspirator in several still poorly understood skin disorders. One could do worse than to further consider the possibility.

I supposed one could.

Do you have a question for Emily? Send it to: pkids@pkids.org

By Emily Willingham

Image courtesy of Wikimedia Commons


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World Rabies Day – 28 September

26 09 2011

Anyone who’s read Old Yeller knows (spoiler alert!) what happens to the title dog in the book. In this day of vaccinations against rabies, though, many people don’t give rabies more than the thought required to take their pets to the vet.

Yet rabies is still around, present in many mammals, including raccoons, skunks, bats, and foxes, and contact with any infected animal can mean infection for you or an unvaccinated furry pet.

In fact, about 55,000 people still die every year from rabies, which translates into a death every 10 minutes.

To make people more aware of the continued threat and precautions to take, national and international health organizations have designated September 28, 2011, as World Rabies Day.

Rabies is a viral disease. The virus attacks the central nervous system—the brain and spinal cord—and eventually is fatal (although there are extremely rare cases of survival). Symptoms, according the Centers for Disease Control and Prevention, are non-specific in the beginning—a fever, a headache, a general feeling of being unwell. But eventually, they progress to neurological symptoms, including hallucinations, confusion, paralysis, difficulty swallowing, and hydrophobia (as the disease is called in Old Yeller). Once these symptoms are present, death is only days away.

Usually, rabies is transmitted through a bite, transferred via the saliva of the infected animal, although rarely it transfers through other routes, such as via the air or transplantation of infected organs. The virus itself triggers no symptoms for up to 12 weeks even as it multiplies and invades the brain and spinal cord. When symptoms finally show up, an infected organism dies within about seven days.

Vaccines against rabies are available for animals, but worldwide, dogs remain the most common source of rabies infection in people, and children are at greatest risk. Vaccination could reduce or eliminate this risk, and a goal of the World Rabies Day campaign is to ensure more widespread vaccination of dogs. Since the campaign began in 2007, 4.6 million dogs have been vaccinated thanks to awareness events. This year’s goal is to grow that number even more.

Vaccinations also exist for people, especially post-exposure vaccinations. They once had a dire reputation as painful shots administered in the stomach, but now they’re shots in the arm and no more painful than other vaccinations. These shots include a shot given the day of exposure followed by more shots in an arm muscle on days 3, 7, and 14, according to the CDC. However, there is a short window of time for these vaccines to be effective; they must be administered preferably within a day of exposure. For people who have already had rabies vaccinations, a briefer round of further shots is required.

What should you do if you think you’ve come into contact with a rabies-infected animal? The CDC has a few guidelines:

  • Consider the situation urgent but not an emergency. Get medical help as soon as you can.
  • Wash a wound immediately with soap and water, which decreases the chance of infection.
  • Get immediate medical attention for acute trauma from a wound before worrying about rabies infection.
  • Once immediate considerations are addressed, your doctor and the relevant health department will determine if you need vaccination.

Remember, above all, keep your pets vaccinated against rabies, and stay away from wild animals, especially those known to carry the virus. For more information, see the World Rabies Day website.

By Emily Willingham

Image courtesy of secad.ie


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HPV Vaccine: The Anti-Cancer Vax

15 09 2011

Have you or a loved one ever had an abnormal Pap smear result? If precancerous cells were identified, the cause was almost undoubtedly infection with human papillomavirus (HPV). Almost all cases of cervical cancer arise because of infection with this virus. Yet a vaccine can prevent infection with the strains that most commonly cause cervical cancer.

A vaccine against cancer. It’s true.

For the vaccine to work, though, a woman must have it before HPV infects her. You may find it difficult to look at your daughter, especially a pre-teen daughter, and think of that scenario. But the fact is that even if your daughter avoids all sexual contact until, say, her wedding night, she can still contract HPV from her partner. It happens to be the most common sexually transmitted infection.

About 20 million Americans have an HPV infection, and 6 million people become newly infected every year. Half of the people who are ever sexually active pick up an HPV infection in a lifetime. That means your daughter, even if she waits until her wedding night, has a 1 in 2 chance of contracting the virus. Unless it’s a strain that causes genital warts, HPV usually produces no symptoms, and the infected person doesn’t even know they’ve been infected.

Until the cancer shows up.

And it can show up in more places than the cervix. This virus, you see, favors a certain kind of tissue, one that happens to be present in several parts of you. This tissue, a type of epithelium, is a thin layer of the skin and mucous membranes. It’s available for viral invasion in the cervix, vagina, vulva, anus, and the mouth and pharynx. In fact, HPV is poised to replace tobacco as the major cause of oral cancers in the United States.

The virus can even sometimes pass from mother to child, causing recurrent respiratory papillomatosis, or warts in the throat that must be removed periodically and can sometimes become cancerous. It strikes about 2000 children each year in the United States.

How does a virus cause cancer? To understand that, you must first understand cancer. You may know that cells reproduce by dividing, and that cancer occurs when cells divide out of control. Behind most cancers is a malfunction in the molecules that tell cells to stop dividing. These molecules operate in a chain reaction of signaling, like a series of well-timed stoplights along a boulevard. If one starts sending an inappropriate “go” signal or fails to send a “stop” signal, the cell divides, making more cells just like it that also lack the right signals. If your body’s immune system doesn’t halt this inappropriate growth, we call it cancer.

The blueprint for building these “stop” molecules is in your genes, in your DNA sequences. As a virus, HPV also requires a blueprint to make more viruses. Viruses use the division machinery of the host cell—in you—to achieve reproduction by stealthily inserting their own DNA blueprint into the host DNA.

Sometimes, when it’s finished with the host, a virus leaves a little bit of its DNA behind. If that leftover DNA is in the middle of the blueprint for a “stop” molecule, the cell won’t even notice. It will use the contaminated instructions to build a molecule, one that no longer functions in stopping cell division. The result can be cancer.

Of the 150 HPV types or strains, about 40 of which pass through sexual contact, two in particular are associated with cancer, types 16 and 18. They are the ones that may persist for years and eventually change the cellular blueprint. The vaccines developed against those two strains are, therefore, anti-cancer vaccines.

Without a successful viral infection, viral DNA can’t disrupt your DNA. That’s what the HPV vaccine achieves against the two strains responsible for about 70% of cervical cancers. Recent high-profile people have made claims about negative effects of this vaccine, claims that have been thoroughly debunked. The Centers for Disease Control and Prevention as always offers accurate information about the side effects associated with available HPV vaccines.

This achievement against cancer, including prevention of almost 100% of precancerous cervical changes related to types 16 and 18, is important.

Worldwide, a half million women receive a cervical cancer diagnosis each year, and 250,000 women die from it. These women are somebody’s daughter, wife, sister, friend. Women from all kinds of backgrounds, with all kinds of sexual histories.

Women whose precancerous cervical changes are identified in time often still must undergo uncomfortable and sometimes painful procedures to get rid of the precancerous cells. These invasive procedures include cone biopsies that require shots to numb the cervix and removal of a chunk of tissue from it. Cone biopsies carry a risk of causing infertility or miscarriage or preterm delivery. A vaccine for your daughter could prevent it all.

HPV doesn’t care if your daughter has had sex before. It’s equally oblivious to whether the epithelium it infects is in the cervix or in the mouth or pharynx or in an adult or a child. What it does respond to is antibodies that a body makes in response to the vaccine stimulus.

Even if your daughter’s first and only sex partner passes along one of the cancer-associated strains, if she’s been vaccinated, her antibodies will take that virus out cold. It’s a straightforward prevention against a lifetime of worry—and a premature death.

For more info: Facts about the HPV vaccine from the National Cancer Institute

By Emily Willingham

Image courtesy of CDC


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Using CAM? Tell Your Doc

12 09 2011

According to some estimates, one in three adults in the United States uses complementary or alternative medicine (CAM). CAM encompasses anything that’s not part of conventional medicine, such as herbal supplements and acupuncture.

In spite of this widespread use, however, many people neglect to tell their physicians about their CAM use. Some may think their doctor won’t approve or think the CAM treatments irrelevant to conventional medical care.

As many as 60% may not divulge this information, and in many cases, it’s because their doctor didn’t ask for it.

Leaving your physician in the dark on your CAM use—or, if it’s your child, any CAM your child may use—can be dangerous. It’s important to let your doctor know everything about your personal healthcare practices, whether it’s vitamins, herbal treatments, chiropracty, or acupuncture.

Why? Well, drugs are often either synthetic mimics of natural compounds or derived from natural compounds, as are herbal supplements. Just like drugs, herbal supplements can have active ingredients that may interact with other compounds, including those your doctor may prescribe. For example, grapefruit seed extract, a popular CAM intervention, can interfere with many medications’ effects, including the blood thinner coumadin.

There may be hidden reasons, such as an instability of your cervical spine, that would make it important to avoid certain chiropractic manipulations.

In addition to these fundamental medical reasons to tell your doctor everything you’re doing for your health—or your child’s, it’s also important for less tangible reasons. Your health professional may be able, for example, to help you decide which CAM therapy is a good fit for your needs, point you to good information about a target CAM intervention, or discuss the benefits and risks with you.

In addition, sharing with your health professional makes you all a part of a healthcare team taking care of you, with you in the driver’s seat.

The National Institutes of Health has provided a few tips for people who’d like to talk more with their healthcare providers about CAM therapies. These include:

  • Starting the conversation yourself. Take the initiative to talk about your healthcare practices.
  • Have a list available of the therapies—CAM or otherwise—you’re using, including dosing and frequency. This information should be included on any patient histories you complete, right along with prescription medications or therapies you use.
  • Make a list of any questions you may have about a specific CAM intervention, and ask those questions.
  • Don’t hesitate to take notes or ask for clarification as you converse with your healthcare provider.

The most important thing to remember is, CAM therapies are like any other intervention: They can interact with other treatments you’re taking, sometimes negatively, and that’s fundamental information your healthcare provider needs to have, about you or your child.

By Emily Willingham

Image courtesy of AAFP and Karen Woo


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A Thoughtful Choice

25 08 2011

I remember lining up at school in the ‘60s to get vaccinated against smallpox and a few other diseases for which there were vaccines.

I also remember the years when my brothers and I took turns at getting measles, mumps and other diseases for which there were no vaccines.

In the end, we three were fortunate—no permanent harm from our maladies.

Fast-forward 30 years. My daughter was four months old when she was diagnosed with hepatitis B. She had not been vaccinated and subsequently developed a chronic infection.

It all sounds mundane when read as words on a screen. But in those early years, the heartache and anger I felt at having my daughter’s life so affected by something that was preventable . . . well, it was almost more than I could bear.

But again, we were fortunate. After years of infection, her body turned around and got control of the disease. Although we have bloodwork done every year to keep an eye on things, she has a good chance of living the rest of her life free of complications from this infection.

Over the years, I’ve met other parents whose children were affected by vaccine-preventable diseases. Some, like Kelly and Shannon, chose not to vaccinate their kids and ended up with horrible consequences. Kelly’s son Matthew was hospitalized for Hib and they came within a breath of losing him. Shannon did lose her daughter Abigale to pneumococcal disease, and almost lost her son. He recovered and was released from the hospital, at which time they had a funeral for their daughter.

Because of my job, I talk to and hear from many families with similar stories. Some children have died, some remain permanently affected, and some have managed to recover.

Also because of my job, I hear from parents who believe vaccines are not safe, and that natural infections are the safer choice. I understand and have experienced the emotions we as parents feel when something happens to our children. In a way, I was lucky. I knew exactly what caused my daughter’s problems. A simple test provided a definite diagnosis.

If we can’t identify the cause of our children’s pain or suffering, we feel like we can’t fix it and we can’t rest until we know the truth. When the cause can’t be found, we latch onto if onlys. What could we have done differently to keep our kids safe? If only we hadn’t taken her to grandpa’s when she didn’t feel good. If only we hadn’t vaccinated him on that particular day. If only. The problem is, the if onlys are guesses and no more reliable routes to the facts than playing Eenie Meenie Miney Mo.

The deeper I go into the world of infections and disease prevention, the more obvious it is to me that the only way to find the facts is to follow the science. Now granted, one study will pop up that refutes another, but I’ve learned that when multiple, replicable studies all reach the same conclusion, then I can safely say I’ve found the facts.

In our family, we vaccinate because for us, it is the thoughtful choice.

By Trish Parnell

Originally posted on Parents Who Protect


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End Polio Now

15 08 2011

What do Donald Sutherland, Joni Mitchell, Robert McNamara, and Arthur C. Clarke have in common?

Polio. They all survived polio.

This disease, which may be thousands of years old, was clinically described in the 18th century as a “debility of the lower extremities.” Later, in the U.S., it was labeled infantile paralysis.

Fast-forward a couple of centuries to the 1950s, when Dr. Jonas Salk developed the first polio vaccine and right on his heels was Dr. Albert Sabin, with another vaccine that became widely used. Cases of polio plummeted in most countries, but each year there were still hundreds of thousands of kids infected.

Fresh from the success of smallpox eradication, an opportunity to do the same to polio was envisioned and energies were renewed in 1988, when the World Health Assembly launched the Global Polio Eradication Initiative.

Twenty years later, the World Health Organization reports on the success of the Initiative:

“Polio cases have decreased by over 99% since 1988, from an estimated 350,000 cases in more than 125 endemic countries then, to 1604 reported cases in 2009 . . .”

That’s pretty good. But, polio keeps flaring up. Areas and countries that were once polio-free have seen the virus imported by those not protected through vaccination. In 2009-2010, 23 countries saw such activity. Seems we’re moving in the wrong direction.

Dr. Bruce Aylward explains how we’ll stop polio—for good.

We’re on a fine edge. Tilt one way and we eradicate polio from the world. Tilt the other, and we’ll never see the end of it.

Help spread the word. Blog about it. Tweet about it. Every kid deserves to grow up free of this disease.

By Trish Parnell


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Ask Emily

28 07 2011

What causes ear wax?

You do! Ear wax comes in two types. One is a thick, yellow wax, known as the “wet” type. The other is a greyish, flaky kind of wax, known as the “dry” type and most common among people of Asian origin and American Indians. Either way, its job is to clean, disinfect, and moisturize your ears, which makes it sound like a beauty product.

In reality, it is a health product that your body makes as a line of defense against things that might harm you, from bacteria to fungi to, yes, insects. For this reason, unless your ear wax is causing a health problem, medical folk recommend that you just leave it alone. It will cycle through and out of your ear, renewing as it goes.

Which type you have—wet or dry—depends on a single mutation in a single gene. Researchers have noted that Asians, especially people from East Asia, have ear wax that is dry and whitish. People whose ancestors are from Europe and Africa almost invariably have ear wax that is sticky and brown or yellow. If a person doesn’t dump cholesterol and other smooth fatty things into their ear wax, then the wax will consist primarily of dead skin flakes, the dry type.

Whether or not you make one or the other traces back to a single change in a single gene. This gene encodes a protein that makes ear wax . . . wet. With the single change in the genetic alphabet, a person doesn’t make wet wax. Researchers have even used this single change to trace the course of human migration throughout the world. Who knew ear wax could be so informative and useful?

I know that a fever is when my body’s temp goes up, but why does it go up? Why is THAT the reaction to whatever is going on in my body?

Let’s start by talking about bedbugs. One of the potential treatments for a bedbug infestation is to turn up the heat in the house to a level that bedbugs can’t survive. Turns out, the little bloodsuckers aren’t too fond of high temperatures. Many things that invade your body are like those bedbugs. They’re pretty comfortable at your normal temperature, but high heat can disable the molecules that keep them functioning. That’s why, when your body’s defense system recognizes an invader, one response may be fever.

Cells that detect these invaders can send out chemical signals with a great name: pyrogens. Pyro, of course, refers to fire or flame, and these chemicals travel to the brain’s thermostat center. There, they signal the brain to readjust the body’s temperature . . . kicking it up a few notches.

To a point, this higher temperature is thought to make things uncomfortable for microbes while not harming you too much. When a strong fever response takes things too far, fever can be harmful, but you might be surprised at exactly how high a fever needs to be to cause harm to you. According to the experts, a fever won’t cause brain damage unless it exceeds a very specific 107.6 F (42 C).

This general defense—it doesn’t target the specific invader; instead, it just relies on wholesale heating—is one of your body’s first responses to infectious invaders like bacteria or viruses. Meanwhile, your body is likely also getting to work on more specific tactics to deal with the unwanted intruders.

Do you have a question for Emily? Send it to: pkids@pkids.org

By Emily Willingham

Image courtesy of CuriousGeoff


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