Tuesday, July 31, 2007

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.

Sunday, July 29, 2007

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 :)

Wednesday, July 25, 2007

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.

Tuesday, July 24, 2007

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.

Monday, July 23, 2007

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.

Sunday, July 22, 2007

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.

Friday, July 20, 2007

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.

Thursday, July 19, 2007

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.

Wednesday, July 18, 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.

Tuesday, July 17, 2007

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...

Monday, July 16, 2007

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)

Sunday, July 15, 2007

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!

Saturday, July 14, 2007

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.

Friday, July 13, 2007

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

Thursday, July 12, 2007

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.

Wednesday, July 11, 2007

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.

Friday, July 6, 2007

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

Tuesday, July 3, 2007

Screening Sunscreens

Screening Sunscreens, an article in the Washington Post

They discussed the importance of skin care in the sun and different methods of sun protection. I've always been a little unclear on sunscreen and what to look for, so I decided to do some research myself.

Important definitions:
1. UVA
-long- wave solar rays of 320-400 nanometers
-penetrate skin more deeply
-less likely to cause sunburn
-more likely to cause wrinkling and leathering

2. UVB
-short-wave solar rays of 290-320 nm
-more likely to cause sunburn
-main rays associated with basal cell and squamous cell carcinoma

3. Sunscreens: chemically absorb UV rays
-octylcrylene, benzophenones, avobenzone indicate increased UVA protection

4. Sunblocks: physically deflect UV rays
-titanium dioxide and zinc oxide indicate increased UVA blocking
-micronized preparations are less conspicuous

5. SPF (sun protection factor): measures the length of time a product protects against skin reddening from UVB, compared to how long the skin takes to redden without protection. If it takes 10 minutes without protection to begin reddening, using an SPF 15 sunscreen theoretically prevents reddening 15 times longer -- about 2.5 hours.
-this is only a measure of UVB protection, there is no standard for UVA protection
yet
-reapply every two hours to maintain the SPF and immediately after
sweating/swimming/toweling off
-the dermatologist I am working with recommends SPF 30 or higher, which blocks 97%
of UVB rays

6. Broad-spectrum protection: indicates that a product has UVA and UVB protection
-does not indicate spectrum of UVA coverage
-avobenzone, titanium dioxide, and zinc oxide indicate full UVA spectrum coverage

Both UVA and UVB rays are linked to skin cancer. The main mechanisms include:
1. altered cell signaling
2. decreased immune responese
3. increased DNA damage

Most studies I found could not identify which of these factors were greater predilections for skin cancer, making it difficult to blame one or the other for skin cancer. The study below used an animal model to show that UVB caused melanoma, but the mechanism of action remains unclear. Sunscreen companies and dermatologists continue to act under the impression that UVA and UVB are equal contributors to skin cancer. An interesting note... tanning bed manufacturers have acted on this evidence, however, and their newer beds emit a higher fraction of UVA rays.


De Fabo EC, Noonan FP, Fears T, Merlino G. Ultraviolet B but not ultraviolet A radiation initiates melanoma. Cancer Res. 2004 Sep 15;64(18):6372-6.



A number of articles address different methods of assessing a sunscreen's ability to block UVA rays. Although the following article seemed to have a promising method, it was published in 2000 without any forthcoming results. The in vitro assessment seemed to be ideal, as human and animal testing could be avoided. Similar studies assessing different methods of quantifying UVA coverage have been conducted over the last ten years, with no conclusive results. One thing that can be agreed upon is that SPF is not an indicator of UVA spectrum coverage.

Diffey BL, Tanner PR, Matts PJ, Nash JF. In vitro assessment of the broad-spectrum ultraviolet protection of sunscreen products. J Am Acad Dermatol. 2000 Dec;43(6):1024-35.

Something else to consider is the interaction between all of these chemicals, their shelf lives, and their photostability. More studies are beginning to address these issues, and a good example of a chemical stability and photostability study is belo They directly tested photostability, but indirectly tested chemical stability by including different UV-filtering combinations.

Gaspar LR, Maia Campos PM. Evaluation of the photostability of different UV filter combinations in a sunscreen. Int J Pharm. 2006 Jan 13;307(2):123-8.

Look here for a comprehensive analysis of the current sunscreens/blocks out there. I liked this analysis because they looked for active ingredients as well as photostability.