Ask Emily

23 02 2012

Why does our skin break out in a rash with some viral infections like measles or Fifth disease?

These sorts of rashes are technically known as viral exanthems (the word derives from the Greek word “exanthema,” meaning “breaking out”).

The skin responds to infection with a rash for one of three reasons: the infectious agent releases a toxin that causes the rash, the infectious agent damages the skin and causes a rash, or the immune response results in the skin outbreak.

The skin responds in only a few ways to these challenges, although the pattern of the response can vary from virus to virus (bacteria and some other infectious organisms can also trigger a rash).

The response is the body’s attempt to deal with the presence of viral particles that find their way to the epidermis, or skin. In general, the upshot of the immune response is an area of inflammation. Because viruses cause a systemic or body-wide infection, viral rashes often cover much of the body.

Although the basic pathway to the rash is similar among viruses, the specific pattern of the rash can help distinguish the virus involved. For example, Fifth disease, so-named because it was the fifth virus in a series to be identified as causing a rash, produces a “slapped-cheek” ruddy appearance on the face and may cause a lacy, rather flat rash elsewhere on the body.

A measles rash, on the other hand, starts as an eruption of raised or flat spots behind the ears and around the hairline before spreading body-wide.

One thing to recognize is that not every rash is a viral rash or a benign viral rash, although most viral rashes will resolve on their own. Usually, a fever accompanies a viral rash. If a rash develops, you should be aware of the following warning signs that signal a call to your doctor:

  • If you suspect you have shingles. This highly uncomfortable rash tends to trace along the nerve routes under the skin but can spread out from those, as well. Starting antivirals within the first 24 hours may ward off a more intense recurrence or a permanent pain syndrome called postherpetic neuralgia.
  • If you suspect measles. Infection with this highly contagious virus should be reported immediately.
  • What you think is a rash from a severe allergic reaction or a rash that arises coincident with taking a new medication.
  • The rash accompanies a high fever, spreads rapidly, and starts to look like purple bruising. This pattern is indicative of meningitis.
  • Any rash involving a very high fever, pain, dizziness or fainting, difficulty breathing, or a very young child or that is painful.
  • Any rash that you find worrisome, including for reasons of persistence or timing with something such as exposure to infection, a new medication, or new food.

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

By Emily Willingham

Image courtesy of HowStuffWorks


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Ask Emily

26 01 2012

I’ve just read that there’s a kind of tuberculosis making a comeback that doesn’t respond to any known TB drugs. How does that happen and can anything be done to treat it or stop its spread?

Tuberculosis (TB) is a bacterial infection, usually of the lungs, although it can invade other tissues.

A healthy person may be infected but not show symptoms, but someone with an active infection may have a cough with blood in the sputum, night sweats, weight loss, and fever. The bacteria spread through coughs or sneezes.

As with seemingly all infections we treat with antibiotics, the TB bacterium has evolved to evade the arsenal of medications we throw at it.

While many cases still resolve after the long-term antibiotic treatment required (6 months or more), often people with the infection begin to feel better or get tired of the unpleasant side effects and will cease the therapy.

As with other similar situations with antibiotics, this premature cessation of therapy can give resistant bacteria the upper hand. The outcome is different grades of TB infection, based on the level of resistance. TB that resists most but not all drugs is multidrug-resistant. TB that resists all but drugs of last resort is extensively drug-resistant, and TB that responds to no antibiotics at all is totally drug-resistant (TDR).

That last form of TB strikes fear into the hearts of epidemiologists and public health officials because it is an infectious disease nightmare.

For a series of reasons ranging from an inability of low-resource countries to test for and detect TB to a lapse in treatment adherence because of poor healthcare management and patient follow-up, the most resistant forms of TB often emerge in areas poorly equipped to control it. Thus, when a report surfaced in January 2012 that a research team had identified 12 cases of TDR TB in India, on the heels of 15 identified cases in Iran in 2006, the worldwide response was, essentially, anxiety and fear.

The fear is that if this TDR form of TB gains a stronger foothold in overcrowded conditions where people walk ill and undiagnosed, it would be a plane flight away from toeholds anywhere else in the world. While humanity dealt with incurable and fatal TB for millennia before antibiotics started to fight back in the 1940s, this resurgence at a time when technology can take a disease around the world in a matter of hours adds a whole new dimension to the threat.

There is, of course, already the threat on the ground in India, where one of the cases is a 13-year-old girl and another of the people in the cohort has died from the disease. But lest anyone think that in their comfortable home in the West they are sheltered from threat, the news the day I wrote this contained reports of a student with TB in Fort Wayne, Indiana, which precipitated notification to 100 students who may have come in contact with their classmate. Another student in Westlake, Ohio, also had been diagnosed with TB, precipitating community action to make people aware of symptoms and prevention of spread.

The communities in these cases benefited from a public health surveillance program that moved into action once each diagnosis was made. But in India, the result has led to public health chaos, with officials arguing over whether or not some of the cases truly were TDR TB. That does not change the fact that TDR TB has already been identified in Iran, or the economic and healthcare gaps that will only continue to contribute to the likelihood of its spread.

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

By Emily Willingham

Video courtesy of IBNLive


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Ask Emily

29 12 2011

Do cold viruses mutate, or are we simply encountering new viruses with each new infection?

If you’re in situations that expose you to frequent cold viruses, I’ve got some bad news for you. First, what we collectively call the “common cold” is a non-medical way of saying “general upper respiratory infection.” Those sniffles and coughs don’t trace to a single virus or even to a single group of viruses. In fact, more than 200 different viruses can cause what we think of as a cold, and they fall into various classes. The most common is the rhinovirus (rhino refers to the nose). These cause up to 40% of colds. The other two types are coronaviruses and respiratory syncytial virus, which is fairly harmless in healthy people but can be dangerous, particularly for premature infants. Coronaviruses made the news when one turned up as the culprit in the SARS outbreak earlier this decade.

Every time we encounter and do battle with one of these viruses, we develop immunity to that specific microbe. But there are another couple of hundred of them out there, waiting to get into our nasal passages with someone else’s cough or sneeze. In addition, it doesn’t take a lot of viral particles to cause an infection, so trace exposures can still lead to illness.

That’s not even the bad news, though. While people probably muse aloud every time they get the sniffles, wondering why scientists have yet to come up with a cure or a vaccine for the common cold, the fact is, a single vaccine is unlikely. Rhinoviruses, for example, are quite complex and mutate fairly rapidly, evading any immunity we’ve built up to previously encountered strains. In that way, it’s like influenza viruses, which reassort around the globe each year and usually turn up as different strains in each new season.

One thing is certain: You won’t get a cold virus just from being cold. You might be more susceptible to infection if you’re stressed or tired or have allergies.

Some people may think they have the flu, but the difference between an influenza virus infection and a cold virus infection is usually quite stark: a flu infection hits hard and fast, often within hours, with a high fever, extreme fatigue, chills, and possibly gastrointestinal involvement. A cold builds up more slowly, peaking after a few days, and fever is relatively uncommon.

Is there anything you can do to at least ease the symptoms of this incurable but usually benign blight on humanity?  Washing hands is one way to avoid picking up a nasty cold virus, but once symptoms develop, your options are limited. Antibiotics are useless against any viral infection. Vaporizers, fluids, some TLC, and time are your best weapons against riding out infection with any of the viruses that cause the common cold.

And go ahead and resign yourself to the idea that even when you’re over this one, new versions linger out there, waiting to find their way up your nose.

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

By Emily Willingham 

Image courtesy of Your Translation Service 


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Ask Emily

27 10 2011

I got a flu vaccine one year and ended up getting the flu anyway. Doesn’t that mean the vaccine doesn’t work?

Influenza viruses are notorious for constantly changing. Making vaccines against them is also notoriously difficult because it requires several months of advance preparation before the viral doses can be ready.

If you’ve heard of “bird flu,” you may realize that flu viruses flourish pretty well in the bird-related environment, and vaccine developers grow their viruses within fertilized chicken eggs (that’s why you’ll be asked if you’re allergic to egg proteins). Every vaccine requires about three eggs to yield sufficient (killed) virus, which translates into millions of chicken eggs (i.e., making 300 million vaccine doses would require 900 million eggs).

It also translates into six months of lead time for producing the viruses required to make the vaccine. To find out more about the current year’s strain selection, visit the Centers for Disease Control and Prevention site, which offer comprehensive information about influenza vaccines.

That advanced lead time means a delay between growing the viral strains authorities have determined may be most prevalent in the upcoming flu season and the actual arrival of the current season’s viruses. Experts can keep an eye on how flu goes in the southern hemisphere’s winter and use that as a gauge for which strains may be most prominent during winter in the northern hemisphere, but there’s no real guarantee that the viral strains pinpointed as most likely for a given season will turn out to be an accurate prediction.

The global surveillance network consists of 130 centers in 101 countries monitoring which strains are most prevalent. These are the people who try to predict months ahead of time which patterns of infection will prevail in a given geographic area.

So, it’s possible to be vaccinated against the flu and still get the flu. Why? Because if you’re exposed to a circulating strain that’s not included in this year’s vaccination mix, then you’re not vaccinated against catching that particular form of the virus. The good news is, the predictions generally turn out to be pretty on target, preventing most people who receive a vaccine from developing influenza.

Keep in mind that even if the vaccine misses a circulating strain, if you choose not to be vaccinated, you can contract influenza more than once in a season if you’re exposed to two different circulating strains.

Final answer? Yes, you can receive a flu vaccine and still come down with the flu. But that doesn’t mean the vaccine didn’t work. It did work against the strain it targeted, and if it hadn’t, you might’ve had to go through that misery more than once. So, get the influenza vaccine as indicated. It will certainly prevent infection from the strains it targets, and at the least can save you half the misery of flu season.

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

By Emily Willingham

Image courtesy of pittsburghhotplate.com


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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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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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