MRSA: to decolonize or not to decolonize?

Although the Dutch system of "search and destroy" has given the Netherlands one of the lowest rates of MRSA colonization and infection, testing everyone in a hospital for MRSA and subsequently treating is not generally recommended. Numerous studies have advocated colonization screening and mupirocin decolonization for outbreaks, but it has not been proven to reduce infections in endemic areas. This study from Kauffman, et al is widely cited and makes a few key points:
1) reduction of MRSA colonization is not necessarily correlated to reduction of MRSA infection in facilities without high infection rates
2) mupirocin resistance is increasing with prolonged use
3) intranasal mupirocin is only an effective decolonizer if all other colonized areas of the body are treated with mupirocin as well

Mupirocin is widely used, especially in dermatology, for recurrent superficial infections and wound healing in high-risk individuals. It will be interesting to follow the trend of mupirocin resistance amongst strains of MRSA. Mupirocin is by far the most effective agent in decolonization although new medications are under review. There are two types of mupirocin resistance, high-level (plasmid-mediated) and low-level (still mupirocin susceptible at the commonly used dosage). High-level resistance is most concerning and was shown to increase with widespread mupirocin use in the above study.

Kauffman CA, Bradley SF, Terpenning MS. Methicillin-resistant Staphylococcus aureus in long-term care facilities. Infect Control Hosp Epidemiol. 1990;11:600–603.

Scott and White to test all patients for MRSA

Now here's an interesting piece of news! Scott & White hospitals in Round Rock and Temple, TX are going to start testing all patients for MRSA colonization through nasal cultures. This will surely provide some interesting epidemiological data, but the bigger question is, what will they do with this information? Are they going to try to treat everyone who is colonized? Study after study does not recommend this unless the patient has recurring infections. This is going to be an important question in the coming years, should asymptomatic MRSA carriers be treated? The Netherlands maintains one of the world's lowest MRSA colonization and infection rates by screening for MRSA upon hospital admission and subsequently treating all colonizers. Does the US have the resources for this? Also, with mupirocin-resistant MRSA emergence, is it a waste of resources to treat patients who are asymptomatic? And would treatment involve just topical antibiotics? Antiseptic washes? Oral antibiotics? I'm eager to see how this information is handled and if hospital MRSA infection rates are decreased.

New type of tattoo ink

Laser tattoo removal is when the pigmented ink in the skin absorbs energy from the laser, breaks down, and is resorbed by the body's immune system. This requires a certain wavelength to target a certain color at a certain depth in the skin. Also, the energy should not be so much as to damage the surrounding skin. Some colors are easier to remove than others, and tattoos that are more skillfully applied at an even depth across the skin are easier to remove as well.

Freedom-2 is an interesting, relatively new product that allows for easier tattoo removal. Instead of the multiple laser treatments and incomplete removal, Freedom-2 advertises tattoo removal after just one laser treatment. They do this by using a biodegradable ink that is microencapsulated. These microcapsules are what make up the tattoo. When a laser's energy is applied to the capsules, they burst, releasing the biodegradable ink. This is assuming it is easier to burst open the capsule than it is to heat and destroy normal ink. Also, it should be easier for the body to dispose of the biodegradable ink than the normal ink.

It is featured as one of Time magazine's best new inventions, and is really a clever idea. However, keep in mind that this product is not FDA-regulated and has not been thoroughly studied in the literature. The material used for encapsulating is not listed on their web page, but it is always a risk that you may have an allergy to the product.

Exercising makes wounds heal faster

At least according to this study. It is a pretty straight forward look at wound size in a sedentary versus exercise group of mice. The exercise did not have a statistically significant effect on wound healing in young mice, but did in older mice. TNF alpha, monocyte chemoattractant, and keratinocyte chemoattractant were all decreased with exercise. These mainly cause inflammation at the wound site. From this data, it can be inferred that exercising reduces inflammation in the skin, which speeds up wound healing in mice. We'll see how this translates to humans, but it's an interesting study overall.

Why is the nose the most common site of BCCs?

A study out of Australia attempts to explain why basal cell carcinomas are most commonly found on the sides of the nose. Here is the news article I found. It seems like a reasonable theory that our curved eyeballs would reflect UV rays onto the side of our noses, making skin cancer more common there than on other parts of our face that are equally exposed to sunlight. Also, the medial canthus (inner corner of the eye) is a common place to see skin cancers, but looks like it is pretty well-shadowed to direct sun. According to this study, it receives a focused ray of UV radiation reflecting from the eye, which might explain its susceptibility to BCCs. The study uses models to show how 60-100% of UV radiation is reflected from the eye surface and where this reflected radiation is eventually absorbed, helping to explain why some areas of the face are more likely to get skin cancers.

Now we need a study discussing the effects of wearing sunglasses on the distribution of skin cancers as the flatter lenses should prevent as much reflection onto the face.

Birt B, Cowling I, Coyne S, Michael G. The effect of the eye's surface topography on the total irradiance of ultraviolet radiation on the inner canthus. J Photochem Photobiol B. 2007 Apr 2;87(1):27-36

Birt B, Cowling I, Coyne S. UVR reflections at the surface of the eye. J Photochem Photobiol B. 2004 Dec 2;77(1-3):71-7.

National Hairdressers Day

Hairdressers are particularly prone to hand dermatitis, and today seems like a great day to discuss why. The constant wet and dry of their hands drys the skin and weakens its protective barrier. With the addition of the large number of irritating chemicals and the possibility of developing allergies to other chemicals, hairdressers have pretty beaten up hands.

PPD (paraphenylendiamine) in black hair dye and glycerol monothioglycolate in hair perming solutions are two allergens that hair dressers come ac. People are exposed to them and over time can become sensitized. This means that the immune system recognizes the chemical as an allergen and mounts an immune response to it upon subsequent exposures.

PPD is also used in "black henna". Henna is naturally green and has not been reported as an allergen before. However, PPD is used to blacken the color, so someone can become sensitized to PPD without having used hair dye. This web page has a great picture of allergic contact dermatitis to black henna (PPD).

Vinyl gloves are effective at preventing PPD sensitization, but not glycerol monothioglycolate sensitization. How do you treat allergic contact dermatitis? Avoidance is the only way to prevent it. And topical steroids can be used to help current lesions heal.

Take home points:
1. Black hair dye, black henna tattoos, and perming solutions contain common allergens
2. People can become allergic to something with repeated exposure over time


Redlick F, DeKoven J. Allergic contact dermatitis to paraphenylendiamine in hair dye after sensitization from black henna tattoos: a report of 6 cases. CMAJ. 2007 Feb 13;176(4):445-6.

Fisher AA. Management of hairdressers sensitized to hair dyes or permanent wave solutions. Cutis. 1989 Apr;43(4):316-8.

CA MRSA in dermatology

Community-acquired methicillin Staphylococcus aureus (CA MRSA) is a relatively recent infection (the last decade). It is particularly relevant to dermatologists as these bacterial strains present most commonly as skin or soft tissue infections. With the recent media blitz surrounding MRSA, it is difficult to discern the medical facts from the news reports. The American Academy of Dermatology has some valuable Talking Points and FAQs that are useful to both patients and healthcare professionals alike.

Mineral makeup

I've heard lots of patients extol the virtues of mineral makeup, and from what I have seen, it appears to be very effective as a natural-appearing foundation. It is pretty amazing how well it covers up patchy skin pigmentation or redness on the face, but still looks natural. And as of yet, I have not seen any irritant or allergic contact reactions to the makeup. It's claim to fame is that it is almost solely made of finely pulverized natural minerals and does not contain fillers and preservatives. Since the fillers and preservatives are common allergens and irritants, the pure mineral makeup could be safer for sensitive skin. However, there is no regulatory body certifying the purity of this makeup so it is up to the consumer to check ingredients. There are lots of companies out there (as evidenced by a simple Google search), and it is difficult to know which ones are better and safer. As with sunscreens, there is concern over the safety of nanoparticles being applied to the skin as there would likely be increased absorption. The absorption of topical powdered minerals has not been studied, so I cannot comment on this either way. One of these weekends, I'm going to explore the makeup counters at the mall and see what sorts of products are out there and what ingredients they use...

I've been away

I've been away for a couple months doing rotations at other medical schools and have fallen behind on my posts. Many are in the works and I just haven't had time to read all the journal articles before posting. Now that I'm back, look for the daily posts.

Smallpox vaccine and eczema

This article discusses how the newest smallpox vaccine has been approved for testing in patients with eczema or atopic dermatitis.

Between 1 and 6 percent of patients vaccinated with the original smallpox vaccine had eczema vaccinatum (EV), where the live virus vaccine actually caused a smallpox infection. The mortality rate for EV is 1%. This article explains why people with atopic dermatitis may have this response. The vaccine is administered via the lower epidermis, which has proven to have the best immune response. Individuals with atopic dermatitis have an altered epidermis that does not produce the same quantity of anti viral and anti bacterial proteins. Further, with the dermatitis, there is an exagerrated Th2 response, but Th1 cells are the primary cell-mediated immune cells. Basically, patients with atopic dermatitis could not safely be vaccinated with the original vaccine. In fact, exposure to someone who was vaccinated was enough to give some patients EV. Because over 50% of the population has eczema or comes in direct contact with someone who does, it is an important step for a vaccine to reduce the risk of EV.

Engler RJ, Kenner J, Leung DY. Smallpox vaccination: Risk considerations for patients with atopic dermatitis. J Allergy Clin Immunol. 2002 Sep;110(3):357-65.

Sweaty palms... treatment with surgery

If iontophoresis and botox are not treating the hyperhidrosis, the effected area of skin can be excised (usually only used for axillae), denervated with a sympathectomy, or liposuction can be performed to remove the sweat glands at the dermal/subcutaneous border (usually only used in axillae). The surgeries should only have to be done once, but are significantly more involved than the prior treatments discussed. The article in the Canadian literature referenced yesterday has a nice discussion about when to use which treatment. And Emedicine has a good summary of the surgical procedures.

Boni R. Tumescent suction curettage in the treatment of axillary hyperhidrosis: experience in 63 patients. Dermatology 2006; 213:215– 217.

Sweaty palms... treatment with botox

Botulinum toxin A blocks the release of the neurotransmitter acetylcholine at the neuromuscular junction. This toxin, which is produced by the Clostridium botulinum bacteria, inhibits the stimulation of muscular cells, including those surrounding eccrine sweat glands. Blocking the secretion of sweat glands in this way has proven to be an effective treatment usually lasting 3-4 months. It does, however, require multiple injections. With 1.5 cm standard spacing, my palms would need about 50 injections each.

Solish N, Bertucci V, Dansereau A, Hong HC, Lynde C, Lupin M, Smith KC, Storwick G; Canadian Hyperhidrosis Advisory Committee. A comprehensive approach to the recognition, diagnosis, and severity-based treatment of focal hyperhidrosis: recommendations of the Canadian Hyperhidrosis Advisory Committee. Dermatol Surg. 2007 Aug;33(8):908-23.

Sweaty palms... treatment with iontophoresis

Finding studies proving the efficacy of iontophoresis for hyperhidrosis was not as difficult as figuring out how iontophoresis works. The hands and feet are placed in a water bath and a direct electric current is run through it. This is a popular treatment if topical aluminum salts have failed. Iontophoresis is also used to help with the cutaneous absorption of drugs.

This article (and others following it) have related the accumulation of hydrogen ions in the sweat glands to secretory damage. With the electric current, water becomes acidified and the ions more easily penetrate the skin because of the current. They collect in the sweat glands and damage them. It takes multiple treatments for hyperhidrosis treatment, as after one treatment, there was only a mild decrease in activity with choline stimulation.

Sato K, Timm DE, Sato F, Templeton EA, Meletiou DS, Toyomoto T, Soos G, Sato SK. Generation and transit pathway of H+ is critical for inhibition of palmar sweating by iontophoresis in water. J Appl Physiol. 1993 Nov;75(5):2258-64.

Sweaty palms

Hyperhidrosis is excess sweating via the eccrine glands beyond what is required for thermal regulation. There are various guidelines for how much sweat produced over a certain body area is normal, but clinically no one uses these. The guidelines are used more for research than for actually diagnosing the condition. The loose definition for hyperhidrosis is excess sweating that interferes with daily activities.

Today I was just going to discuss different causes of excess sweating and the quality of life implications. Over the next couple days I'll discuss two of the treatments.

Emedicine has a great article if you are interested in details. I thought hyperhidrosis would have more information on the internet, but most of what I found were ads for various treatments.

Localized essential hyperhidrosis usually presents in childhood or adolescence as localized excess eccrine sweat production of the palms, soles, and/or axillae. The exact cause is unknown, but it is believed to be triggered by overactive sympathetic innervation causing excessive stimulation of the glands. Palms and soles sweating is not associated with heat, but more so with anxiety, so the excess sweating should stop when the patient is asleep or sedated. Generalized excess sweating may be caused by systemic disease and should be further investigated. The Emedicine article has a list of disorders under the "Causes" subheading that can present with localized or generalized excessive sweating.

I helped treat a patient with hyperhidrosis of the palms and soles, and it was interesting to hear her perspective on how this has affected her life. She doesn't like to shake hands and can't wear shoes without socks. The thing she was most looking forward to after her treatment was to wear dress shoes! Although her disorder is completely benign, the quality of life implications can be socially debilitating. A friend of mine has trouble with yoga because of her sweaty soles, and people with axillary hyperhidrosis suffer from embarrassing sweat stains. Depending on a person's age and occupation, the effects of hyperhidrosis can vary in severity.

First line treatment is topical aluminum salts (used in anti-perspirants), which are drying to the skin.

Aamir Haider and Nowell Solish. Focal hyperhidrosis: diagnosis and management.
Can. Med. Assoc. J. 2005 172: 9.

UV protection from windows Part 2

I did some more research on UV protection of windows since I got stuck on window films the last time I posted about this.

I found a great review article discussing the photoprotective properties of glass and what is being done to increase broad spectrum UV protection.

Tuchinda C, Srivannaboon S, Lim HW. Photoprotection by window glass, automobile glass, and sunglasses.J Am Acad Dermatol. 2006 May;54(5):845-54.

I wish that everyone could have a copy of this article, as it has some useful tables, but here's my attempt at summarizing it.

Clear glass allows almost full (90%) visible light transmission and blocks about 30% of solar heat and 20% of UV radiation. Depending on the use of the glass (commercial v. residential) and how much visible light transmission is desired, different methods of fortifying clear glass are available. Here are some properties of glass and how they affect light transmission.

1. Thickness - minimal effect on light transmission
2. Double-glazing - moderate reduction in UV and heat radiation without sacrificing much visible light transmission
3. Tinting - more effective than double-glazing in UV and heat radiation, but sacrifices visible light transmission
4. Reflective coating - significant reduction of visible light, UV, and solar heat transmission
5. Low emissivity glass (coating of microscopically thin, transparent layers of silver between layers of antireflective metal oxide coatings) - significant reduction of UV and heat radiation without sacrificing much visible light transmission
6. Laminated glass (bonding two pieces of glass together with polyvinyl butyral) - dramatic reduction of UV radiation but only moderate reduction of solar heat while retaining good visible light transmission
7. UV-blocking coating - dramatic UV reduction with minimal solar heat and visible light transmission reduction

According to this article, using double glazed glass, where one piece is low-e glass and the other has the UV-blocking coat offers the best UV and heat insulation without sacrificing visible light and can block up to 99.9% of UV transmission. The thing to remember is that UV blocking is not uniform over all wavelengths. It is easier to block shorter wavelengths than longer ones. So the 0.1% of UV transmitted will not be a cross section of UV wavelengths, but will be predominantly UVA1 (long wavelength) waves.

According to this report from the government, a ten-window house can spend $75 more per window ($750) to get a more efficient frame with low-e double glazed glass instead of plain clear glass. The energy savings per year for heating/cooling are estimated at $319 per year. In less than 2.5 years, the energy savings would make up for the increased cost, not to mention the sun protection benefits. With housing design including more windows, the sun protection factor cannot be discounted.

New psoriasis drug in the news

The World Congress of Dermatology met this past week in Argentina, and this story made international news. It is about the new biologic drug used to treat psoriasis, Ustekinumab. I found this study detailing its mechanism of action

Reddy M, Davis C, Wong J, Marsters P, Pendley C, Prabhakar U. Modulation of CLA, IL-12R, CD40L, and IL-2Ralpha expression and inhibition of IL-12- and IL-23-induced cytokine secretion by CNTO 1275. Cell Immunol. 2007 May;247(1):1-11.

This drug works by targeting IL-12 and IL-23. Current medications such as Adalimumab (Humira), Etanercept (Enbrel), Efalizumab (Raptiva), and Infliximab (Remicade) work similarly by targeting other types of cell messangers. All but Efalizumab work by blocking TNF alpha, an inflammation-causing mediator. Efalizumab binds to CD11a and prevents T cell functioning. Because psoriasis is mediated by T cells, these biologic drugs can work. Further, IL-12 is one of the key mediators in T cell activation.

Part of the problem with the current biologics is that they are extremely expensive (which I'm sure Ustekinumab will be also), and they require weekly injections or infusions. This new drug promises to only require monthly self injections, which is far more convenient and less painful than the weekly administrations. It should also help reduce cost compared to a drug like remicade, which requires infusions at specialty pharmacies or a hospital.

Do eyebrows grow back?

According to this study

Fezza JP, Klippenstein KA, Wesley RE. Cilia regrowth of shaven eyebrows. Arch Facial Plast Surg. 1999 Jul-Sep;1(3):223-4.

eyebrow regrowth after complete shaving is possible. Five brave patients had one eyebrow shaven and within 4 months all but one had full regrowth. The fifth patient required an extra couple months for full regrowth. Because of the small sample size, no conclusions can be drawn as to the implications for widespread eyebrow shaving. However, this should debunk the commonly held myth that eyebrows don't grow back.

Ultraviolet-C rays

We don't hear much about UVC rays in the popular media or in the literature with relation to skin damage. This is because UVC is blocked by the ozone layer and has not been a significant player in skin damage. Most journal articles discussing UVC address its germicidal properties and use in laboratory research. But as the ozone layer continues to thin, UVC damage will become more significant in the pathogenesis of skin disease.

UV protection from windows

There are a two questions I want to address in this posting:

1. How much UV radiation to normal windows block?

Normal glass is good at filtering out lower wavelength UV waves (UVB), but UVA waves predominantly transmit through the glass.

2. Do the UV films and special UV windows actually make a difference?

In this study, the UV film added to the auto glass had a significant reduction in cytotoxicity compared to normal glass. The plain glass offered 29% protection while glass and film together offered 93% protection. This includes longer wavelength UVA. But this study only measured the resultant effects on cells and did not actually measure which and how much UV radiation went through the glass, making it difficult to draw conclusions about UVA v. UVB protection from the film.

Bernstein EF, Schwartz M, Viehmeyer R, Arocena MS, Sambuco CP, Ksenzenko SM. Measurement of protection afforded by ultraviolet-absorbing window film using an in vitro model of photodamage.Lasers Surg Med. 2006 Apr;38(4):337-42.

The Skin Cancer Foundation has a list of recommended window films for UV protection. I haven't been able to figure out how they chose these window films. On 3M's website, they say that all of their films listed here block 99.90% of UV radiation, but again, no details.

According to

Edlich RF, Winters KL, Cox MJ, Becker DG, Horowitz JH, Nichter LS, Britt LD, Long WB, Edlic EC.Use of UV-protective windows and window films to aid in the prevention of skin cancer. J Long Term Eff Med Implants. 2004;14(5):415-30.

the International Window Film Association offers certifications for certain levels of UV protection, but after checking out their website, I couldn't find any detailed standards.

And this article

J.A. Johnson and R.M. Fusaro, Broad-spectrum photoprotection: the roles of tinted auto windows, sunscreens and browning agents in the diagnosis and treatment of photosensitivity, Dermatology 185 (1992), pp. 237–241.

is able to correlate visible light transmitted to UV light transmitted. Basically concluding that the less visible light transmitted, the broader spectrum of UV protection available.

Basically it's hard to tell which window tints are better than others, but it is safe to assume that darker tints will block more UV radiation.

Psoriasis... is it contagious?

Today, my first day of a Pediatric Dermatology rotation, I was struck by the significant lack of public awareness about psoriasis. Almost 1 in 50 people have psoriasis. 125 million people worldwide have this condition, and everyone must know someone (if not a few someones) with psoriasis. Yet two patients came in on the same day requesting notes for their teachers stating that their skin condition is not contagious. If there is any way to make a shy adolescent who has so much psoriasis that he wears a baseball cap, long pants, and long sleeve shirts in the Texas heat any more uncomfortable, it is to imply that other kids may not be safe around him. The teacher did not trust either of these students' or their parents' retelling of the diagnoses. These kids know what they have because they are reminded with every pill they take and every ointment they use, not to mention the physical discomfort they endure.

I read this article talking about a drug-company sponsored public health website with a great section onpsoriasis. It is well done and informative. There are many other great websites out there with reliable information, including the National Psoriasis Foundation. I hope you take a few minutes to learn a little more about psoriasis.

Is tanning ever good for you? (Neonatal jaundice)

It is not uncommon for neonates to have high bilirubin levels, causing jaundice. This is because their livers are still immature and are not able to process heme at full capacity quite yet (decreased uptake and conjugation of bilirubin) and they have a higher red blood cell turnover rate than adults. The bilirubin deposits in the epithelium, causing the yellow tint in their eyes and skin. This could lead to more serious depositions in the nervous system, and possibly kerincterus.

The number one therapy is phototherapy, with blue, white, or green lights. Blue is best absorbed by the yellow bilirubin and helps metabolize it to water-soluble lumirubin, which can then be excreted. Green has a longer wavelength and may be better for protein-bound bilirubin. Phototherapy causes a systemic reduction in bilirubin levels.

Dennery PA, Seidman DS, Stevenson DK. Neonatal hyperbilirubinemia. N Engl J Med. 2001;344 :581 –590

Is tanning ever good for you? (Psoriasis and eczema)

UV light has anti-inflammatory effects that can help control both psoriasis and atopic dermatitis. This treatment is used in both children and adults and is thought to be particularly effective for acute onset conditions. PUVA, UVB, and narrow-band UVB have all been used. PUVA requires the ingestion of a psoralen pill before treatment, which increases photosensitivity to UVA waves. Narrow band UVB is thought to have fewer side effects than normal UVB treatment.

There are lots of studies on the effectiveness of PUVA and UVB for psoriasis and eczema treatments. But this study discusses the mechanism of action of PUVA v, NB-UVB v cyclosporin.

Erkin G, Ugur Y, Gurer CK, Asan E, Korkusuz P, Sahin S, Kolemen F. Effect of PUVA, narrow-band UVB and cyclosporin on inflammatory cells of the psoriatic plaque.
J Cutan Pathol. 2007 Mar;34(3):213-9.


- PUVA is the only treatment that decreased Langerhans cells (CD1a+) in the epidermis
- All 3 treatments decreased T lymphocytes (CD4+ and CD8+)
- All 3 treatments reduced expression of CD86, an inflammatory stimulator

Is tanning ever good for you? (Acne)

Narrow band blue light (420 nm) has anti-inflammatory effects on acne. It is less useful for comedonal acne, where inflammation is less prevalent. The light attacks the heme metabolism mechanism of Propionibacterium acnes, therefore killing the bacteria. This study showed the antinflammatory effects of the blue light also. There was reduced staining of IL-1alpha and ICAM-1, both indicators of an inflammatory response. And with the addition of low-dose narrow band-UVB (312 nm), the results were even better.

Shnitkind E, Yaping E, Geen S, Shalita AR, Lee WL. Anti-inflammatory properties of narrow-band blue light. J Drugs Dermatol. 2006 Jul-Aug;5(7):605-10.

Is tanning ever good for you? (Prurigo)

Prurigo nodularis is a disease where the patient experiences intense itching at discrete points and due to scratching, rubbing, and picking develops thickening of the skin in the form of nodules +/- pigmentary changes. The etiology of the intense itching is unknown. Historically this is a very difficult disease to treat, and topical steroids and antihistamines are most commonly used to control the itching.

Tamagawa-Mineoka R, Katoh N, Ueda E, Kishimoto S. Narrow-band ultraviolet B phototherapy in patients with recalcitrant nodular prurigo. J Dermatol. 2007 Oct;34(10):691-5.

This study shows that narrow-band UVB is an effective treatment for recalcitrant prurigo nodularis. It does not recommend phototherapy as a first line, but only for those patients who have failed topical steroids or antihistamines.

Is tanning ever good for you? (CTCL)

Cutaneous T-cell Lymphoma is a category of diseases encompassing all lymphomas that are limited to the skin. There are multiple types of CTCL with different histological and clinical features. Emedicine has a simple overview of the different types, how they present, and whether they are typically indolent or aggressive. Mycosis fungoides is the most common type of CTCL and is predominantly an indolent disease.

A lot of research has been done on light therapy for early-stage Mycosis fungoides, and this is generally accepted as an effective first-line treatment. Both PUVA and UVB have been shown effective, but PUVA is associated with more side effects (erythema, carcinogenicity, nausea). In this study narrowband UVB and PUVA are compared.

Diederen PV, van Weelden H, Sanders CJ, Toonstra J, van Vloten WA. Narrowband UVB and psoralen-UVA in the treatment of early-stage mycosis fungoides: a retrospective study. J Am Acad Dermatol. 2003 Feb;48(2):215-9.

Narrowband UVB was found to have similar treatment efficacy and disease-free periods as PUVA.

Proposed mechanisms of action for narrowband UVB:
- increases allo-activating and antigen-presenting capabilities of Langerhans cells
- increases Il-2 and IL-6 production by keratinocytes
- increases TNF
- suppresses neoplastic T cells
- upregulates immune system

Propsed mechanisms of action for PUVA:
- mitotic inhibition
- killing neoplastic T cells
- psoralen might damage cell organelles or alter the immune system

In this study, PUVB, UVB, and PUVA are compared.

El-Mofty M, El-Darouty M, Salonas M, Bosseila M, Sobeih S, Leheta T, Nada H, Tawdy A, Amin I, El-Enany G. Narrow band UVB (311 nm), psoralen UVB (311 nm) and PUVA therapy in the treatment of early-stage mycosis fungoides: a right-left comparative study.Photodermatol Photoimmunol Photomed. 2005 Dec;21(6):281-6.

PUVB was not shown to have a significant advantage over UVB.

Caution should be used with light therapy treatments because of the risk of later carcinogenicity.

Is tanning ever good for you? (Vitiligo)

Vitiligo is believed to be an autoimmune depigmentation disorder. The exact cause is unknown, but it is believed that the body's immune system attacks its melanocutes (pigment-producing cells). Our country's most popular vitiligo patient is probably Michael Jackson.

Light therapy is thought to have a dual mechanism of action on vitiligo. First its anti-inflammatory effects reduce the destruction of melanocytes. Second the UV stimulation activates the remaining melanocytes. Pigment is more likely to persist in hair follicles, which is why repigmentation occurs around them.

Yones SS et al. Randomized double-blind trial of treatment of vitiligo: Efficacy of psoralen–UV-A therapy vs narrowband–UV-B therapy. Arch Dermatol 2007 May; 143:578-84.

This study was really well done and presents good evidence that narrowband UVB is more effective in vitiligo treatment. Although the data was not quite statistically significant (p=0.06 instead of p<0.05) between the two groups, there was some difference. Any study on vitiligo therapy will be inherently flawed because of the subjective nature in judging repigmentation, but the methods included examination under Wood's lamp, comparison of nonlesional skin and repigmented skin color, patient survey, and a quality of life index. The amazing thing is that all 50 patients showed improvement. Although the Nb-UVB patients had better color match, fewer side effects, and more repigmentation.

Controlled UV exposure is a proven treatment for vitiligo.

Hair transplants in areas of scarring

The question came up today about whether or not hair transplants are feasible in areas of scarring. I found a number of studies addressing surgical repair of cicatricial (scarring) alopecia, in which the hair follicles are destroyed and replaced with scar tissue, so these studies should be relevant for any type of scarring on the scalp.

The older studies discuss surgical techniques including free flaps and tissue expansion. Tissue expansion involves using silicon implants to stretch skin where there is hair growth and create enough skin with naturally occurring hair follicles to use as a flap and replace the scarred scalp. It is difficult to just transplant hair/follicles into the scarred skin because of the decreased blood supply in scar tissue relative to normal scalp. This has a double-edged effect on the graft survival rate. Decreased blood supply means it is harder for the hair follicles to survive and grow, but also, the traumatized skin is more susceptible to infection and necrosis. Using flaps and skin grafts is risky because the procedure involves traumatized blood vessels for both the grafting site and the grafted skin, making it difficult for the new skin to survive.

New techniques use lasers to help with both preparation of the scarred skin and hair implantation, eliminating the need for a skin graft (which is really the riskiest part of the old procedures). A carbon dioxide laser was used to burn tiny holes into the scarred scalp, causing angiogenesis and increased blood supply to the scalp. In this case report, the success of the hair transplantation was attributed to the new vasculature. In another study, an Er:YAG laser was used to form the implantation holes for the hair follicles. Using the laser minimized trauma to the implantation site and was credited with a successful transplantation.

In summary, technology for hair transplants in scarred skin is quickly evolving into less risky and more successful procedures.

Kwon OS, Kim MH, Park SH, Chung JH, Eun HC, Oh JK. Staged hair transplantation in cicatricial alopecia after carbon dioxide laser-assisted scar tissue remodeling. Arch Dermatol. 2007 Apr;143(4):457-60.

Neidel FG, Fuchs M, Krahl D. Laser-assisted autologous hair transplantation with the Er:YAG laser. J Cutan Laser Ther. 1999 Dec;1(4):229-31.

Pressure sores in the WSJ

The Wall Street Journal talked about the measures hospitals and nursing facilities are taking to prevent pressure ulcers in this article. They are using fancy mattresses, playing music every 2 hours to remind nursing staff to turn the patients, and doing thorough skin checks more often. This is great news for patients, as ulcers are slow-healing, easily-infected, and preventable. They are also a significant part of the Medicare budget. But not for long. Medicare and some private insurers are slowly implementing a plan to stop paying for preventable conditions, such as pressure sores. I hope that they plan to increase compensation to facilities for the added cost of increased man hours and equipment. These are necessary and important measures to maintain a patient's quality of life, whether or not the improvement in care is cost-induced.

Do you have cancer? (Alopecia Areata)

A lot of kids with alopecia areata get asked that question. Why else would a child be losing his or her hair?
Alopecia areata is an autoimmune skin disease where your lymphocytes attack your own hair follicles. This results in patchy loss of hair all over the body, including head hair, eyebrows, arms, and legs. It is usually a disease of childhood and presents as round patches of smooth hair loss. For most people, the hair grows back and another patch may appear somewhere else. Eventually, most kids grow out of it. But for some, it progresses to alopecia totalis (complete loss of head hair) or alopecia universalis (complete loss of body hair).

Treatments include topical or intralesional steroids, but these are not cures and do not have great efficacy rates.

Because AA is not known well among the public, this can be a difficult disease for kids and adults alike. There were a number of campers with AA last week, and they had lots of stories about being stared at in public, kids making fun of them, and people asking them if they had cancer. They discussed different hair accessories (like hats and bandanas) to cover up their heads. For this group of campers in particular, I think it is therapeutic to be around other kids like themselves and to talk about they're good days and bad days with AA.

The National AA Foundation has a great website, check it out.

Whole-body peel (Erythroderma)

Non-bullous, Congenital Icthyosiform Erythroderma (CIE) is caused by an autosomal recessive hereditary deficiency of an enzyme involved in skin regeneration. The mutated or missing enzyme varies depending on which type of CIE the patient has, but it always leads to a build up of thick, dry skin. Either the patients are regenerating skin too fast or they are shedding epidermal cells too slowly. The transglutiminase-1 gene, the 12R-lipoxygenase gene, or the lipoxygenase-3 gene may be affected.

The patients appear red with partially adherent white scales. They are at high risk for infection because of the fissures they get in the thickened skin. Also, the thick skin can make it difficult to move joints, to the point where patients can end up in wheelchairs because their skin is just too tight and thick.

This is an incredibly difficult disease for kids and their families to deal with. It requires diligence to keep the kids well-moisturized and clean, but also the emotional effects of this disease are huge. Essentially, these kids are always peeling. Their beds and clothes are peppered with scaled off skin. There is also an odor to the hyperkeratotic skin. Patients are prone to overheating and alopecia (loss of hair).

Unfortunately there is no cure. Patients can only treat symptomatically by moisturizing and keeping their skin as supple and clean as possible.

There seems to be a lot of research done on prenatal testing for CIE. Skin samples can be taken of the fetus that are then analyzed for hyperkeratosis, particularly around hair follicles. Parents have even terminated pregnancies based on the positive diagnosis. The study below found that it is difficult to judge the presence or absence of the disease based on skin samples for two main reasons: 1. the random sample may be from an area that is less affected (as was the case in one of their patients) and 2. normal epidermal growth does not occur until the 24th week, at the end of the 2nd trimester

Holbrook KA, Dale BA, Williams ML, Perry TB, Hoff MS, Hamilton EF, Fisher C, Senikas V.The expression of congenital ichthyosiform erythroderma in second trimester fetuses of the same family: morphologic and biochemical studies.J Invest Dermatol. 1988 Dec;91(6):521-31.

OMIM has a nice summary of the disease.

A world without sun (Xeroderma pigmentosum)

Xeroderma pigmentosum is a hereditary deficiency in part of the nuclear repair enzymes, inhibiting the body's ability to repair damage caused by UV rays. UV rays cause pyrimidine dimers to form in our DNA and endonucleases, DNA polymerases, and ligases work to repair the damage. If any of these enzymes are decreased, ineffective, or all together missing, the DNA will not be repaired properly. Increased DNA mutations lead to increased risks of malignant growth.

This past week I had the chance to hang out with a kid who has XP and take a small glimpse into her world. She spends all of her time between 7 AM and 8 PM in doors. If she had to go outside, she would suit up in a jacket, jeans, close-toed shoes, gloves, and a hat/hood that looked like a bee keeper's hood but it was opaque. In the 90+ degree heat, this was less than comfortable. She was diagnosed as a baby when, after 10 minutes outside in the shade, she was severely sunburned. Ever since then, she has lived in this inside world. I can't imagine it is easy being a kid with all that pent up energy and not being allowed to run around outside or play with the other kids. But it is a necessity. These kids can get skin cancer from a very young age and the only protection is UV avoidance.

Wikipedia has a nice list of literary and film references about people with XP. Also, the XP family support group has tips on how to protect yourself against UV damage. From special clothes to window tints to avoiding sun at airports, theme parks, etc, the support group has lots of interesting strategies for avoiding the sun.

CAMP

I was a camp counselor for a group of kids with skin disorders last week (hence the lack of posts). As an ode to my campers, I'm going to do a few days of posts dedicated to their skin conditions and address how these conditions have affected their lives. Middle school is a tough time as is, but when you have a disease that everyone can see, a tough time can become tougher. These girls are remarkably mature, caring, and sensitive, and it was a pleasure getting to know them.

I think people would be less judgmental if they understood what kinds of conditions kids like these have, and hopefully this series of posts will bring together some useful information and helpful links.

Pets as Staph carriers

Many studies have been done showing that dogs, cats, and horses can be colonized or infected with methicillin-resistant staph aureus (MRSA).

Here are some definitions:
1. colonized- one carries the bacteria, but doesn't have any adverse effects from it. it just lives benignly usually in the nose or other mucosal surfaces
2. infected- the bacteria is causing adverse effects

MRSA is particularly dangerous because it is often resistant to multiple antibiotics and can be hard to treat. It is spread easily through hospitals and the community. And apparently, it can be spread via pets.

From what I've read, it looks like dogs and cats can pick up human strains of MRSA from their owners and either be colonized or infected. They can then pass the bacteria back to humans they contact (licking, petting, rubbing noses). What makes this particularly dangerous is that there are genes in bacteria that allow them to be resistant to different antibiotics. For example, the mecA gene makes Staph aureus resistant to methicillin. Well, these genes can be transferred from one bacteria to another. Dogs' natural flora includes Staph intermedius, which has been shown to have a high resistance to multiple drugs. And if dogs are harboring all these bacteria, they can breed MRSA strains that are resistant to multiple antibiotics, transfer them to humans, and make an infection that is very difficult to treat.

(There's no reference here because hopefully I'll be able to add the paper I'm working on as a reference when it's done :)

Does antibiotic ointment really help wounds heal?

Not any better than plain old Vaseline.

According to...

Smack DP, Harrington AC, Dunn C, Howard RS, Szkutnik AJ, Krivda SJ. Infection and allergy incidence in ambulatory surgery patients using white petrolatum vs. bacitracin ointment. A randomized controlled trial. JAMA 1996;276:972-7.

... bacitracin (an antibiotic used in triple antibiotic ointment or Polysporin) usage after outpatient dermatologic procedures has a statistically similar rate of infection to white petrolatum (AKA Vaseline) usage. In fact, white petrolatum not only kept infection rates very low, but it also had no allergic reactions, unlike bacitracin.

1 oz of bacitracin ointment costs about $3
13 oz of white petrolatum costs about $3

It appears that these ointments serve as an occlusive dressing and keep the wound clean and moist.

I'm using Neosporin, but my wound keeps getting worse!

I saw two patients today with the same complaint and the same problem. Neosporin is an antibiotic ointment containing neomycin, an aminoglycoside antibiotic. Neomycin can be used topically or orally, but it is most commonly used as a topical medication. Neosporin is mainly used as an agent to help with wound healing. So why did these two patients have what appeared to be normal wounds that were actually getting worse when they used Neosporin?

Neomycin is one of the top 10 topical allergens in the US. The allergic reaction usually presents as a red, raw area similar to eczema. It will look like the wound is spreading or getting worse instead of healing. Just stop using the Neosporin and be sure to avoid all ointments (like triple antibiotic ointment) that contain Neomycin as well. Also, people who are allergic to Neomycin show a high incidence of allergic reactions to Bacitracin, another topical antibiotic (usually sold as Polysporin). Finally, it's important to remember that you had this allergic reaction to Neosporin because you may be allergic to oral medications that are in the same class of drugs. But when you take the oral aminoglycosides, you could have an eczematous reaction over your whole body or even have anaphylactic shock. Look back at my previous post about Vaseline being used for wound healing. It's a great alternative for people who are allergic to Neomycin or Bacitracin.



Hopefully my paper will be accepted and I'll use it as the reference here :)

How good are clothes at protecting you from the sun?

There are actually a number of studies looking at the UV protection factor (UPF) of clothing. Europe even has a standardized method of determining the UPF of clothing using spectrophotometry. It is recommended by the European guidelines that clothing have a UPF of 30 or higher for sun wear.

Summary:
1. Cotton, linen, and viscose are not great at sun protection
2. With UV-protective coating, the UPF of viscose greatly increases
3. Water can either increase OR decrease the UPF of clothing, depending on the material
4. Cotton's UPF can be increased via washing with soap and water (tightens the weave) or by washing with the UV-protective coating

I found one study that measured the UPF of various summer clothes. Clothing made from cotton, linen, and viscose were most likely to have UPF less than 30. But if they were black, navy-blue, white, green, or beige, they had higher UPF values in general. These were clothes taken from the summer collection of a department store. I don't really understand how white clothes can have higher UPF ratings unless the material is actually thicker or more tightly woven because it is white.

BGambichler T, Rotterdam S, Altmeyer P, Hoffmann K. Protection against ultraviolet radiation by commercial summer clothing: need for standardised testing and labelling. MC Dermatol. 2001;1:6.

In a study comparing normal viscose with viscose that is treated with special UV-protective coating, a statistically significant difference was found between the two. The UV protective coating was found to be effective in raising the UPF of the lightweight fabric, suggesting that wider usage of the coating is in order. Also, the in vivo (in life) and in vitro (in the laboratory) measurements of UPF varied depending on the material and whether or not it was treated. So the UPF measurement is not necessarily accurate, depending on the material.

Hoffmann K, Kaspar K, Gambichler T, Altmeyer P.In vitro and in vivo determination of the UV protection factor for lightweight cotton and viscose summer fabrics: a preliminary study.J Am Acad Dermatol. 2000 Dec;43(6):1009-16.

This next study looks at the effect of water on the UPF of clothing. For linen, viscose, and polyester fabrics, UPF significantly increased when wet. For the cotton fabrics and the polyester + TiO2 fabrics, UPF significantly decreased. For the modal + TiO2 fabrics and the polyester crepe + TiO2 fabrics, UPF significantly increased. Material should be tested both wet and dry to elucidate the effects of moisture on UPF.

Gambichler T, Hatch KL, Avermaete A, Altmeyer P, Hoffmann K.Influence of wetness on the ultraviolet protection factor (UPF) of textiles: in vitro and in vivo measurements.Photodermatol Photoimmunol Photomed. 2002 Feb;18(1):29-35.

"Laundering with detergent and water improves UPF slightly by causing fabric shrinkage. Dyeing fabrics or adding a UV-absorbing agent during laundering substantially reduces UV transmission and increases UPF. More UVA is transmitted through the fabrics than UVB."

Wang SQ, Kopf AW, Marx J, Bogdan A, Polsky D, Bart RS.Reduction of ultraviolet transmission through cotton T-shirt fabrics with low ultraviolet protection by various laundering methods and dyeing: clinical implications.J Am Acad Dermatol. 2001 May;44(5):767-74.

Sunscreen causes cancer??? Part 2

Benzophenones are another agent used in sunscreen that have been linked to carcinogenic effects. I found two studies addressing this issue.

Rhodes MC, Bucher JR, Peckham JC, Kissling GE, Hejtmancik MR, Chhabra RS Carcinogenesis studies of benzophenone in rats and mice.Food Chem Toxicol. 2007 May;45(5):843-51.

Toxicology and carcinogenesis studies of benzophenone (CAS No. 119-61-9) in F344/N rats and B6C3F1 mice (feed studies). Natl Toxicol Program Tech Rep Ser. 2006 Feb;(533):1-264.

These studies did show increased rates of cancer, particularly liver cancer... in MICE and RATS... WHEN THEY ATE BENZOPHENONE.

So, I would avoid feeding rates or mice benzophenone and avoid eating it myself. The FDA is funding more studies for benzophenone and other sunscreen additive research. It looks like we need a topical, human study to really judge the carcinogenicity.

Sunscreen causes cancer???

According to this article, 84% of sunscreens are causing cancer and...

As NewsTarget readers have known for a long time, sunscreen products are a hoax, and they actually cause cancer instead of preventing it. The more consumers use sunscreen products, the greater their chance of someday being diagnosed with cancer. Part of this is due to sunscreen's effect of blocking ultraviolet radiation (UV light), which generates the powerful anti-cancer nutrient Vitamin D in human skin. Vitamin D is quite simply the world's best anti-cancer medicine, and recent studies have shown that it can prevent nearly four out of five cancers in women (ALL cancers, including breast cancer, cervical cancer, lung cancer, brain tumors, multiple myeloma and even skin cancer).

Three issues here...

1. UV light can damage skin. UV light damages cellular DNA and inhibits normal base-pairing. This can lead to mutations and neoplastic behavior. UV light has been proven over and over to be a cause of skin cancer. Further, patients with xeroderma pigmentosa, a genetic disorder where parts of the DNA's repair mechanism are mutated, have a high rate of skin cancer. This supports the assertion that UV-caused DNA damage can lead to skin cancer.

2. Dangers of sunscreen
The Australian government did an excellent review of the literature on potentially hazardous components of sunscreen. (Australia has the highest incidence of skin cancer, and coincidentally, is very interested in sunscreen.) Zinc oxide and titanium dioxide have been used in sunscreen for many years. They are broad spectrum UVA and UVB blockers, and are really a great choice for sun protection.
But because they are opaque, and it is no longer the 80s, people don't want to use them. The nanosized zinc oxide and titanium dioxide offer sun protection without the opacity. The concern is that the nano particles will be absorbed into the dermis and, with the application of light and heat, will become toxic.

I'm not going to reference each article individually, you can follow the link to the Australian document. But nanoparticles of titanium dioxide have been shown to produce OH radicals when exposed to UVA light. These OH radicals can harm viable cells, cause DNA mutations, and potentially lead to cancer, according to in vitro experiments. However, this has never been studied in vivo (in actual skin samples). It has only been studied in non-epidermal cells. The unique part about our epidermis is that the stratum corneum has a waxy layer that helps keep moisture in and toxins out. The epidermis is constantly regenerating, but the replicating cells are below the stratum corneum. So, as long as the nanoparticles do not go below the stratum corneum, our replicating cells are safe. And these replicating cells are the ones who are in danger of turning cancerous. A cancer is just a replicating cell that starts replicating out of control. All the studies examining how deep the nanoparticles penetrate show the same thing... THE NANOPARTICLES DO NOT PENETRATE PAST THE STRATUM CORNEUM. This means that they cannot cause cancer. One loophole is that hair follicles go all the way down past the epidermis into the dermis. But the studies looking at titanium dioxide penetration of hair follicles shows that the particles stay in the upper follicle and do not absorb into the dermis.

We need a study that uses human skin samples, micronized titanium dioxide, and sun exposure, and that tests for both penetration and cellular damage short term and skin cancer long term.

3. Vitamin D is good, but you don't need all that much sunlight to produce adequate amounts of it. UVB is involved in the production of vitamin D and then the kidneys and liver convert it to its active form. The Vitamin D then helps absorb calcium from the intestinal tract.

This study...

Valrance ME, Brunet AH, Welsh J.VDR Dependent Inhibition of Mammary Tumor Growth by EB1089 and UV Radiation in vivo.Endocrinology. 2007 Jul 12

... and many others like it, show that certain tumors containing vitamin D receptors do respond to vitamin D therapy. However, vitamin D does not prevent these tumors. It is being studied as a therapeutic (not preventative) agent for specific cancers with the specific receptor.

For now, I'm going to continue wearing my micronized titanium dioxide sunscreen.

Vaseline is flammable

Petrolatum is a favorite of dermatologists everywhere. It is virtually non-allergenic and non-irritating, holds moisture in skin well, and does not require preservatives. It is particularly popular as white petrolatum, Vaseline, or in some lip balms. It is sold over the counter as well as via prescription in the form of ointments. Ointments are often white petrolatum with medicine that are applied topically to the eyes or skin. This is great... unless you use home oxygen. Although the flashpoint of white petrolatum is 199 deg Celsius, you can't be too careful when using pressurized, high concentration oxygen. Petrolatum is a petroleum based product and can catch fire with a spark and oxygen. All preparations using petrolatum should be avoided on the face, scalp, and eyes when oxygen is in use. Also, it should not be used as a lubricant for endotracheal tubes (because you can develop lipoid pneumonia if the vaseline gets in your lungs too). Laser treatments and plastic surgery cases using petrolatum and oxygen should be done with caution.

Common preparations:
vaseline
ointments (check the ingredients)
lip balms (check the ingredients)

Petrolatum is not going to spontaneously combust and is generally safe. But for people in special situations... home oxygen, laser treatments, and the operating room, it is something to consider.

Chocolate and acne

I found this article about diet and acne. It is based on the study below where researchers looked for a relationship between low-glycemic index foods and acne. It also addressed the popular association between acne and chocolate.

Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA.A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am J Clin Nutr. 2007 Jul;86(1):107-15.

This looked like a well-done study comparing a LGL (low glycemic load) diet group of 15-25 year old males with a normal diet group. The study was blinded to both the participants and the dermatologists who graded their acne. Of course, acne severity can be subjective, but the group also had independent raters who did sort of a quality control on the acne gradings.

The study addresses hyperinsulinemia, high androgen levels, acne, and the relationship to diet. The LGL diet group was given foods with a slower glucose release, like complex carbs, whole grains, and proteins. Not only was there a statistically significant difference in number of lesions and inflammatory response, but there was also a significant weight loss in the LGL diet group. The negatives of this study are that it was a relatively small sample group, unigender, and a narrow age range. But, for this population, acne severity was decreased by following the low glycemic load diet.

The basis for this is that high glucose levels in the blood cause a high insulin level. This was shown over time to decrease insulin sensitivity. Hyperinsulinemia is associated with increased androgen bioavailability and free concentrations of insulin-like growth factor I. So people gain weight and get acne.


Fulton J, Plewig G, Kligman A. Effect of chocolate on acne vulgaris. JAMA 1969;210:2071–4.

This is the study showing that acne and chocolate are not related. But the study design has been criticized because the placebo candy bar had similar nutritional contents to the chocolate bar.

My conclusion based on these studies is that maintaining a diet high in complex carbs and protein is good for weight, insulin resistance, and acne; but the exact mechanism of the effect on acne needs to be investigated further.

BUG WEEK: Day 7.5- I forgot about tick-borne encephalitis

After 3 hours of lecture today on meningitis, meningoencephalitis, and encephalitis, I became aware of an omission on one of my posts. On 7/15 I listed the diseases carried by the Ixodes tick (AKA black-legged tick AKA deer tick), but I left out a strain of Flavivirus, which can cause tick-borne encephalitis. The interesting thing about this is that all other viral causes of encephalitis are transmitted by mosquito bites. West Nile virus is also a Flavivirus, and is probably the most commonly known strain in the US. (especially after the New York outbreak a few years ago)

Meningitis is inflammation of the meninges, which is one of the protective tissue layers of the central nervous system (brain and spinal cord). Encephalitis is inflammation of the brain tissue. Meningoencephalitis is both. TBE can present as any of the three. You'll have a patient with a fever, altered mental status, and mosquito or tick bites. They don't necessarily get the stiff neck that people with bacterial meningitis do.

Anyway, there are no skin findings and treatment is supportive, meaning there is no cure, but it is something to think about if you're in tick-infested country. Also, there is a rare association with neurological side effects similar to amyotrophic lateral sclerosis (Lou Gehrig's disease). I couldn't find much research on it, but it does exist in case reports. ALS is a neurodegenerative disorder where the motor neurons in both the central and peripheral nervous systems start to die. It is one of the only neurodegenerative disorders that has both upper and lower motor neuron symptoms.

Müller WK, Hilgenstock F. An uncommon case of amyotrophic lateral sclerosis with isolation of a virus from the CSF. J Neurol. 1975 Dec 2;211(1):11-23.Links

An atypical case of amyotrophic lateral sclerosis (ALS) is described, characterized by early manifestation, a long lasting course with asymmetry of the lesions, absence of bulbar symptoms in the presence of an otherwise very advanced symptomatology, and constant signs of an inflammatory reaction in the CSF which was the reason to initiate extensive virological studies, including procedures for virus isolation. A virus belonging to the TbE complex of arbovirus group B (tick-borne flavivures), was finally isolated from the CSF. About 70% of the ALS cases in Hamburg/W. Germany, examined for antibodies, apparently had contact with this virus. The antibody pattern found made it possible to explain this exceptional case.

I could only find a couple articles written specifically on this topic since 1975. They think that some of the antibodies produced in reaction to the virus end up attacking motor neuron cells.

This concludes BUG WEEK 2007.

BUG WEEK: Day 7- The Brown Recluse

The brown recluse (Loxosceles reclusa)is the last one I wanted to cover before BUG WEEK 2007 ended. Actually, there will probably be another bug week... or maybe just a worm week... or half week (I don't think I could do a full week of worms).

The brown recluse is interesting to me for a couple reasons. The first is that it has a painless bite. The second is that it is in Texas (like me).

As the name implies, the spider is both brown and reclusive. It lives in wood sheds, garages, attics, etc. Basically any place where it can be left alone. We come across them when we decide to clean up these places. It's back is supposed to look like a violin, which it does sometimes. It is found in the midwest and the Gulf of Mexico states (except Florida).

It has skin findings! (sometimes) Most bites are relatively mild and could cause some inflammation, which should be treated with ice packs. If it starts to turn dusky and the wound is not healing, it might be necrotic. This is rare, but serious. The necrotic (dying) tissue can spread and take a while to heal. In some cases, multi system organ failure can occur. Dapsone has been used with mixed results to decrease necrosis.

Elston DM, Miller SD, Young RJ, Eggers J, McGlasson D, Schmidt WH, Bush A. Comparison of colchicine, dapsone, triamcinolone, and diphenhydramine therapy for the treatment of brown recluse spider envenomation: a double-blind, controlled study in a rabbit model.Arch Dermatol. 2005 May;141(5):595-7.

This study basically said that none of the agents helped with necrosis or eschar formation in the rabbits


These bites are very rare and often overdiagnosed. The following conditions should be kept on your differential diagnosis as they present similarly and are far more common:
1. Staph or Strep infections
2. Pyoderma gangrenosum
3. Herpes
4. Diabetic ulcer
5. Squamous cell carcinoma
6. Deep fungal infections
7. Chemical burns
8. Localized vasculitis
9. Sporotrichosis
10. Site of tick bite in Lyme disease

I actually saw a patient with a lesion that could be any one of these things today. Brown recluse bite was not in the top 10 of our differential.

BUG WEEK: Day 6- How to treat head lice

Robinson D, Leo N, Prociv P, Barker SC.Potential role of head lice, Pediculus humanus capitis, as vectors of Rickettsia prowazekii. Parasitol Res. 2003 Jun;90(3):209-11.

Head lice are the same species as body lice and can transmit disease! However, there have been no cases that I could find of an isolated head lice infestation that caused the transmittal of infection. The article above makes the excellent point that when one has a body lice infection, one will also have a head lice infection, so it is difficult to tell which ones are transmitting disease. I suspect that head lice treatment guidelines will continue to be lax as long as there are no elementary school kids who come down with typhus.

Head lice don't live on pets or clothes, and they require human blood to survive. You can see the nits (the eggs that are near the hair root) much easier than you can see the actual louse. So when people do lice checks, they're not actually looking for little bugs running around on your scalp, but they are trying to see little clearish oval eggs attached to your hair.

I've never had lice, but it seems pretty popular with the under-12 crowd. All that hat-sharing, head-to-head contact, and shared nap space makes for the perfect environment for a lice infestation. Judging from a quick Google search, there's big money in the lice-removal market. Combs, medicinal shampoos, and non-chemical treatments are all over the place. But what do the doctors recommend????

Here are the basics of lice removal:
1. treat with an agent that will kill the lice and help loosen the nits
a. pyrethroids- over the counter, permethrin and pyrethin are most common, documented increasing resistance, relatively few side effects
b. lindane- over the counter, documented increasing resistance, associated with some CNS side effects (seizures)
c. malathion- prescription, 98% ovicidal (should only require 1 or 2 treatments), no known serious side effects, flammable (so monitor children after treatment), no known resistance
2. manually remove the nits and lice
3. wash clothes, sheets, and other heads that the infected head may have come in contact with

The American Academy of Pediatricians recommends the use of over the counter pediculicides first (permethrin 1%) and malathion for resistant cases. Also, once treated, patients are safe to return to school, even if they still have nits in their hair. Interestingly enough, the main societal cost associated with lice is the lost school time by the kids and the lost work time by the parents who have to stay home with them. The AAP believes that the "no nit" policy is obsolete and that the treatments are effective enough to prevent outbreak. Also, they think that lice screening and the "no nit" policy are out of proportion to the medical significance of a head lice infestation. The children should, however, be discouraged from head-to-head contact with others.

The National Pediculosis Association disagrees. They are not proponents of pesticidal treatments as they can be dangerous depending on the medical condition of the patient, are often overused, and are not 100% effective. They have chosen to endorse the Licemeister comb. Really all you need is a comb with teeth that are as close together as possible (this is to physically drag the nits off your hair), but having one with a cool name couldn't hurt.

Although I would tend to agree with the AAP over the NPA, I must admit that the NPA website is full of wonderful treasures. There's a page with a bunch of educational videos, you can even observe an effective comb out! And my personal favorite is the lice e-card. I believe I have some e-cards to send now...

BUG WEEK: Day 5- I'm feeling Lousey

Pediculus humanus... body or head louse...

The body louse lives in the seams of clothes and is associated with war, famine, close living quarters, and elementary school. Today's post actually covers a disease of great historical significance. Please, read on...

1. Borreliae recurrentis-- humans are the reservoir, but lice are the vectors
- recurring fevers, just like the other Borrelia infections


2. Rickettsia prowazekii-- humans are the reservoir, but lice are the vectors
- TYPHUS!
- there are a few different types of typhus, each of which has different vectors, but epidemic typhus, which is transmitted by body louse, is the most serious
- the louse bite an infected person, the bacteria multiply within the louse belly, then it is excreted in feces when the louse is feeding on the next human, the human scratches the itchy louse bite, and any broken skin has now become a site of inefction
- a one to two week incubation period is followed by sustained high fevers, muscle aches, vasculitis, multiple organ disease, AND SKIN FINDINGS!
- also heart failure, shock, and death.
- early light rose colored macules start on trunk and spread to extremities, they blanche early, but later turn dull and red, they can spread everywhere but the palms and soles
- of course, with any vasculitis, you can get petechiae as well
- Wikipedia has a nice summary of the historical significance of typhus (all the historical figures killed by this disease and all the wars that it appeared in... which is pretty much every war up to World War II, when we got a vaccine)

BUG WEEK: Day 4- Tick talk (cont.)

Yesterday just about wore me out with all the tick stuff. But we shall press on...

Ixodes ticks also carry:
1. Ehrlichia-- no skin findings, presents as fever, HA, jt point, malaise... your classic fever of unknown origin
- the tick is the vector and the reservoir includes dogs, foxes, coyotes, deer, and rodents
- seen in the NE US
- infects macrophages, difficult to culture, but can possibly see microorganism in cells on blood smear

2. Babesia-- no skin findings, hemoprotozoan parasite (often confused with malaria), most infections are asymptomatic, but can produce fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia after a 1 to 4 week incubation period
- the tick is the vector and reservoir
- seen in the NE and Midwest as well as CA and WA
- infects red blood cells, can be seen on blood smear

The soft tick Ornithodoros carries:
1. Borreliae hermsii-- no skin findings AND the tick falls off by itself, so most people don't know they had a bite at all
- presents a lot like Ehrlichiosis with recurring fevers
- western US


Hard ticks can also transmit...
1. ROCKY MOUNTAIN SPOTTED FEVER (Rickettsia rickettsii)--finally some skin findings!
- contrary to popular belief, it is most common in the Appalachians, but is seen in the Rocky Mountains, Central and South America
- can be very severe
- stages of disease: fever, malaise, muscle aches -> classic palms and soles rash -> systemic vasculitis
- the tick is the vector and rodents or dogs are the reservoir



The lone star tick (Amblyomma americanum) is pretty distinctive with that big colored dot on its back. It has one ill-defined disease association...
1. Southern Tick-Associated Rash Illness (STARI) (this one I didn't learn about in school, but found on the CDC's web page)-- skin findings again!
- it looks just like erythema migrans and can be easily confused for Lyme disease
- but the CDC says that the lone star tick does not carry Borrelia burgdorferi
- my lit search only came up with 3 articles on pubmed

Masters E, Granter S, Duray P, Cordes P. Physician-diagnosed erythema migrans and erythema migrans-like rashes following Lone Star tick bites.
Arch Dermatol. 1998 Aug;134(8):955-60.

- this one claims to have isolated B. burgdoferi in lone star ticks infesting the farm of a person with a tick bite and erythema migrans, so it looks like lone star ticks could transmit lyme disease. it also looks like no one cares to find out more since there is not much research on this topic
- these ticks are in the southeast and mid south


Finally, the last tick-borne illness...
The hard tick Hyalomma carries one virus...
1. Crimean-Congo Hemorrhagic Fever from the Nairovirus (of the Bunyavirus family)-- some skin findings!
- petechiae, flushing, jaundice can all be found (which kind of go with the hemorrhagic fever thing)
- the tick is both reservoir and vector
- most commonly found in Eastern Europe, particularly Russia (but also in China and India)
- it presents like a lot of the other diseases discussed today with high fever, joint pains, headache, and vomiting

That's all for the ticks!

BUG WEEK: Day 3- Tick talk

Often a fair amount of time elapses before people realize they have a tick on them. This goes back to yesterday's post, where I listed the most common bug bites that are painless. (Technically, ticks aren't even bugs. They have eight legs, making them arachnids. Bugs have 6 legs.) Unlike bed bugs, ticks do not usually elicit an allergic response, so there's no itchiness to alert one to the presence of the feeding tick. There are a few things I want to talk about with ticks...
1. The different types of skin reactions they elicit
2. The different diseases that they carry and transmit
3. The regions of the country where you will find certain ticks
4. How long they have to be attached to transmit disease
5. When to give antibiotic prophylaxis
Hopefully I'll get through everything tonight.

There are two kinds of ticks: hard ticks (Ixodae) and soft ticks (Argasidae). Mostly hard ticks are responsible for disease transmission. I'm going to try to minimize the tick pictures I post because I think they're gross.


Erythema chronicum migrans is associated with Lyme disease. You see multiple large red patches that are clear in the middle. The skin reaction is in the early stages of the disease and resolves on its own. So you may see a patient within the first few weeks of infection that has the skin findings, but after that, you'll have to elicit the history about the skin findings. Judging by how long it takes to get into see a dermatologist these days, I bet you're more likely to see patients who had the rash when they made the appointment, but it resolved before they made it into the office. I got the picture from DermAtlas

LYME DISEASE (Borreliae burgdoferi)- The most well known of all the tick-borne diseases. So, I didn't realize that there was a commercially-available Lyme disease vaccine between 1998 and 2002 (LYMErix). It contained a surface antigen of the bacteria that caused antibody production in humans. The neat part about the vaccine is that the antibodies actually fight the bacteria in the tick instead of in the human. When the tick attaches to the human, it does not transmit the bacteria until it regurgitates some blood and saliva. This doesn't happen until 18-24 hours after the original bite. During this time, the antibody immune response is going on inside the tick, so that when it regurgitates, it should not have active bacteria in the regurgitant. I guess that living in Florida and Texas aren't close enough to the tick belt to get you the vaccine. But it looks like I didn't miss much, since they took the vaccine off the market because of reports of a vaccine-induced, treatment-resistant, chronic arthritis.


The ticks responsible for Lyme disease are from the Ixodes genus and are commonly known as black-legged ticks. They are merely the vector for transport, as they acquire the disease from white-footed mice, deer, and other mammals. When the infected tick bites humans, it transmits the disease 18-24 hours after biting. You have almost a full day to find the tick before it transmits disease! This disease is most common in the northeast and Wisconsin, but it can be found in the Northwest as well.

It can present clinically as a relapsing fever with general symptoms of malaise and muscles aches or it can present as classic Lyme disease. This involves three stages. The first is relapsing fever with erythema migrans. The second is disseminated disease which could include arthritis, carditis, and neurologic disease. This happens after the little spirochetes screw their way down to the blood stream and spread throughout the body. The third stage is chronic arthritis. This is if you don't treat it. Treatment is with doxycycline or penicillin. Antibiotic prophylaxis after a tick bite is quite controversial.

RB Nadelman, J Nowakowski and D Fish et al., Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite, N Engl J Med 345 (2001), pp. 79–84.

This study showed that one dose of Doxycycline 200 mg was effective in preventing Lyme disease. They did not claim to prevent all cases, but they did have statistically significant results between the placebo and doxy groups. They showed an efficacy of treatment of 87%, but the 95% confidence interval is 25-98%. Confidence intervals this wide weaken the results of the study.

Maraspin V, Lotric-Furlan S, Strle F. Development of erythema migrans in spite of treatment with antibiotics after a tick bite. 2002 Jul 31;114(13-14):616-9.

This study showed a 0.14% rate of erythema migrans after prophylaxis, which sounds pretty good to me, but it doesn't seem like everyone agrees...

D Volkman, Prophylaxis of tick bites, Lancet Infect Dis 7 (2007), pp. 370–371.

Volkman was pretty adamant that the NEJM study was flawed in how it measured its outcomes.

Anyway, it seems like the consensus is to prophylax for Lyme disease as it shows good results and is low-risk. But this can be tailored depending on where in the country you are.

OK, that's enough for today. I'll do more tick-borne diseases tomorrow.

BUG WEEK: Day 2- Is this a bug bite?

Usually you can tell when you get a bug bite because you feel the pinch of the bite. But there are a few bugs/arachnids that inject a cytotoxin or numbing poison while biting so that you cannot feel the pinch of the bite. They are:
1. bed bugs
2. brown recluse
3. ticks

We'll just discuss bed bugs today...


BED BUGS (Cimex lectularius)


- blood-sucking, but do not transmit disease, can get multiple bites from one bug, nocturnal
- superficial bites, produce wheal +/- pustules and itching, usually in groupings
- look similar to bites from fleas, body lice, and scabies
- prefer humans, but can be transmitted on dogs and cats, clothing, and luggage
- look for excrement on the seams of the mattress and look for bugs up near head of bed around mattress frame or box spring
- treat with topical steroids for itching and topical antibiotics if pustules or broken skin
- although relatively harmless, they can give people delusional parasitosis (make you feel itchy, even when there aren't bugs on you)... which I think I have after reading all about bed bugs

BUG WEEK: Day 1- How to remove a tick

Today I had a great lecture about the basic bugs that cause dermatological lesions. In spite of making me feel itchy all over, I actually learned a lot. In fact, it inspired me to dedicate a week to the creepy crawlies of dermatology.

But today, I have a very specific topic... HOW TO REMOVE A TICK. There was some discussion of this at lecture today, where the experienced opinion is that heat should be applied to the tick in the form of a heated paper clip in order to cause its release of the skin. However, my friends and I were discussing this apparently controversial topic, and it was brought to my attention that heating the ticks stresses it and causes it to regurgitate material into the skin before letting go. The method my freind recommended was to grab the tick as close to the skin as possible and just pull it out. She just completed a back country trip in Minnesota, which involved many a tick, so she had considerable experience in this area. My concern with just pulling the tick out is that there will likely be foreign material left in the skin. Which is worse, some mouth parts or regurgitated tick saliva in your skin?

I decided to do a lit search on pubmed...

Removal of ticks: a review of the literature
Health Protection Agency Centre for Infections, London, UK

Oteo JA, Martínez de Artola V, Gómez-Cadiñanos R, Casas JM, Blanco JR, Rosel Evaluation of methods of tick removal in human ixodidiasis. L.Rev Clin Esp. 1996 Sep;196(9):584-7.

The current opinion is that the tick should be grasped as close to the skin as possible, preferably with curved forceps and pulled straight out with constant force. This minimizes the chance for foreign material to remain in the skin and because the tick is removed immediately, it will not have the chance to regurgitate any material. If the barbed mouth piece is left behind, the chances for secondary infection and allergic response are increased. Multiple studies have been done on tick removal with measured outcomes including rates of complications (transmitted diseases and secondary infections) as well as retained mouth parts.

1. suffocating the tick- because ticks have a low respiratory rate, it usually takes a while to suffocate them, giving the tick more time to transmit disease
2. chemical irritants- in the studies, the ticks did not consistently detach
3. heat- in the studies, the ticks did not consistently detach
4. unscrewing the tick- higher likelihood of retained mouth parts
5. commercially available devices with grooves, like this one were better for immature ticks, but left behind mouth parts of mature ticks
6. forcep or finger removal of tick from point of attachment- RECOMMENDED METHOD

The WHO and the CDC recommend the forcep removal method. Here is an image and text from the CDC web page.

Remove a tick from your skin as soon as you notice it. Use fine-tipped tweezers to firmly
grasp the tick very close to your skin. With a steady motion, pull the tick’s body away from your skin. Then clean your skin with soap and warm water. Throw the dead tick away with your household trash.

Avoid crushing the tick’s body. Do not be alarmed if the tick’s mouthparts remain in the skin. Once the mouthparts are removed from the rest of the tick, it can no longer transmit the Lyme disease bacteria. If you accidentally crush the tick, clean your skin with soap and warm water or alcohol.

Don’t use petroleum jelly, a hot match, nail polish, or other products to remove a tick.

Who goes to the dermatologist?

Rising Skin Cancer Rates Are More Likely To Affect Wealthy People, Says 12-year Review

I read this article in the Science Daily, and the title and following quote intrigued me.

Women living in affluent areas were 29 per cent more likely than people living in disadvantaged areas to suffer from basal cell carcinoma and nearly two and a half times more likely to suffer from malignant melanoma.

Men displayed a similar pattern. They were 41 per cent more likely to suffer from basal cell carcinoma if they lived in an affluent area and two and a half times more likely to suffer from malignant melanoma.

The article referred to a study published last month.

Hoey et al. Skin cancer trends in Northern Ireland and consequences for provision of dermatology services. British Journal of Dermatology. 156, pp1301-1307. June 2007.

I found these statements particularly interesting as I am currently reviewing data for a local Moh's surgeon, and, as I ran through the data, I wondered about the socioeconomic effects on treating and diagnosing skin cancer. There are a number of day laborers working in industry in this area who are contract employees and likely do not have particularly good health insurance. I'm guessing that, even though they are high-risk for sun damaged skin, going to the dermatologist for yearly skin checks is not high on their priority lists. I wanted to look at the socioeconomic status versus likelihood for multiple lesions or recurrence rates. But this population is so hard to access because they simply do not visit the dermatologist. And, if they do, it is at a late stage, and they are less likely to follow up for regular skin checks, so recurrence rates are difficult to record.

So any study using data from patients who voluntarily went to the dermatologist is naturally skewed towards more affluent patients. Even in Ireland, where the majority of citizens are covered by public or private health insurance, this does not imply equivalent care. There are still both public and private health care options, and I cannot help but assume that public health care options are harder and more expensive to access. Working in a public hospital in the U.S., one realizes how difficult it is to even get an appointment with a specialist such as a dermatologist.

Anyways, my point is that statements like this are very misleading. After reviewing the article, it appears that the researchers divided their already-diagnosed-with-skin-cancer sample population based on their economic districts. Of course there will be fewer people from the poorer neighborhoods. Of course more affluent people have more time and better access to healthcare, causing their increased diagnosis of skin cancer. We need a study comparing incidence rates of skin cancer amongst varying socioeconomic classes. That would be a much better representation of the effect of affluence on skin cancer rates.

Lasers, Lasers

Light Amplification by Stimulated Emission of Radiation

I underestimated both the depth and breadth of this topic. It started as a self-serving interest in how laser hair removal works, but it ended up as a review of Physics 101. Anyways, here's what I've got so far...
Lasers produce a ocused beam of light through the synchronized release of photons. They are named for the substance that is being activated (usually through electrical energy). As the electrons fall back to their original energy levels, they release energy. Most is released as heat (lasers are very inefficient) and some is released as light. Laser light is coherent (waves trave in a synchronized fashion), collimated (no light divergence... hence, the laser pointer), and monochromatic.

The most popular laser types used in medicine are:
1. Argon laser: it targets pigmentation... so the hemoglobin in red blood cells and the melanin in hair follicles and skin are all damaged by this laser
2. Carbon dioxide laser: excites both intra- and extracellular water
3. Nd:YAG laser: it targets pigmentation (just like the argon laser), BUT it has a 1064 nm wavelength, causing deeper penetration

Laser properties and their applications:
1. Wavelength- determines depth of penetration and selects what biologic component will absorb it--- characteristic of the specific type of laser
2. Irradiance (power density) = laser energy (watts) x 100/ surface area of laser beam (cm^2), literally the density of your energy source--- you need to know this to achieve the same effect using different manufacturer lasers
3. Energy fluence (energy per pulse) = irradiance x exposure (sec) = joules /cm^2--- you need to know this to achieve the same energy over a large lesion


So the laser has to do two things for it to zap the hair follicle: penetrate to the dermis (requiring a wavelength between 630-100 nm) and target the melanin in the follicle. Because it is unknown which part of the follicle needs to be removed to prevent recurrent hair growth, the whole thing is zapped right now. Shorter wavelength lasers will also affect pigment in the epidermis. For fair skin, this is not a problem, but for pigmented skin there is a significant risk for permanent hypopigmentation. Using a longer pulse also helps target laser energy to the follicle, as melanosomes respond better to shorter pulses.

Here's my brief summary:
The closest to 1100 nm wavelength lasers without going over will give the least epidermal side effects (hypopigmentation, fibrosis, vesiculation).
The longer pulses will help target follicles over melanosomes.
Ideal conditions are pale skin with dark hair.
Argon and Nd:YAG lasers are used for photothermolysis.


Alster TS, Bryan H, Williams CM. Long-pulsed Nd:YAG laser-assisted hair removal in pigmented skin: a clinical and histological evaluation. Arch Dermatol. 2001 Jul;137(7):885-9.

Lasers in Skin Disease by Ronald Wheeland