Lecture 12 - Vacation Dermatoses PDF

Lecture 12 – Vacation Dermatoses Cutaneous Larva Migrans (CLM) CLM usually occurs following skin exposure to warm, sandy soil contaminated with domestic cat or dog feces. The eruption presents as a red, itchy, serpiginous line, sometimes with blisters (Figure 12.1). It most commonly occurs on the...

Lecture 12 – Vacation Dermatoses Cutaneous Larva Migrans (CLM) CLM usually occurs following skin exposure to warm, sandy soil contaminated with domestic cat or dog feces. The eruption presents as a red, itchy, serpiginous line, sometimes with blisters (Figure 12.1). It most commonly occurs on the feet. The line extends by 1-2 cm each day. CLM is caused by a skin-penetrating hookworm that typically affects dogs and cats. The two most common organisms are Ancylostoma braziliense and Ancylostoma caninum. These organisms are unable to penetrate through the basement membrane, so they remain in the epidermis until they die. In cats and dogs, they can penetrate into the bloodstream and establish chronic infections in the intestines – this does NOT happen in humans. CLM will resolve on its own when the organism dies and is shed from the skin, but this may take months. Thus, it is often treated with anti-helminthic agents, namely, ivermectin or albendazole. Insect Bites and Stings Insect bites and stings are common during the spring, summer, and fall, but not in winter. Reactions to insect bites can be divided into three types: immediate reactions, delayed allergic reactions, and delayed toxic reactions. Immediate reactions develop immediately after the bite or sting and are due to mediators present in the insect venom. These reactions are specific to the insect, not to the patient. In other words, if an insect has a toxin that causes immediate reactions, essentially all patients should have a reaction. Immediate reactions usually involve pain, stinging, itching, swelling, and pinkness of the skin. The reactions should resolve within hours. If the insect does not have toxic venom, then victims should not have immediate reactions. A good example is a bee sting. Delayed allergic reactions develop hours to days after the bite or sting and may or may not occur following an immediate reaction (in fact, the patient is often not even aware they were bitten). Delayed allergic reactions present most commonly with itchy, red papules (Figure 12.2) (Figure 12.3). Most are due to allergy to substances in insect saliva. A good example is a mosquito bite. You may be unaware that you were bitten; then several hours later, an itchy red papule develops. Delayed toxic reactions develop minutes to days after the bite. The best examples are spider bites. These reactions can be localized or systemic. Localized reactions can manifest as ulcers (brown recluse bites) or as persistent inflammatory reactions (Figure 12.4). Systemic reactions usually manifest as neurologic symptoms (muscle spasms, pain, paralysis), as in a black widow spider bite, or as hematologic toxicity (hemolysis, clotting). Delayed toxic reactions are due to toxins the organism injects with the bite. These toxins are designed to digest or disable the spider’s typical prey, but the effects can also cause problems in humans if the toxin is injected. The pathogenesis of insect bite reactions is discussed above. It should be noted that most insects that feed on human blood (mosquitos, bed-bugs, ticks, etc.) do not cause immediate reactions but may cause delayed allergic reactions, while most insects that bite or sting as a defense mechanism (fire ants, bees, wasps, etc.) do cause immediate reactions. The best treatment is prevention. With stinging insects, prevention includes not provoking the insects, as they have no natural predilection to sting humans. The same is true for spiders. In terms of insects that feed on human blood, insect repellants are the best protection. The most effective insect repellant is DEET. The higher the concentration, the better and longer it works. It is very safe, with only a few case reports of neurologic toxicity after truly excessive use. As a general rule, 10% concentration is sufficient, and 30% concentration is about as high as would ever be needed for daily use. Avoiding perfume and brightly colored clothing can also be useful. For outdoor use, DEET can be applied to the skin, and permethrin can be applied to the clothing. This is an extremely effective strategy for preventing tick bites. For treatment of delayed allergic bite reactions, antihistamines and topical steroids are effective. Anaphylaxis, most often associated with stings from hymenoptera (bees and wasps), should be treated the same as any other cause of anaphylaxis (epinephrine and systemic steroids). Patients with this problem should be prescribed an EpiPen to carry at all times, which allows patients to rapidly self-inject epinephrine in the event of a sting or bite. Seabather’s Eruption and Swimmer’s Itch Seabather’s eruption occurs after recent swimming in the ocean/salt water. Swimmer’s itch occurs after swimming in fresh water. Seabather’s eruption begins within 24 hours of swimming in the ocean. It consists of itchy, red papules and macules in areas covered by the bathing suit that heal within 2 weeks. Swimmer’s itch usually begins within several hours of swimming in fresh water, often in one of the great lakes. It follows a similar time course to that of Seabather’s eruption, but it involves skin not covered by the bathing suit. Seabather’s eruption is caused by the stings of immature nematocysts of thimble jellyfish larvae and anemone larvae (found in the tropics and Florida). These larvae get trapped under your bathing suit, and the nematocysts cause the pruritic eruption. Swimmer’s itch is caused by schistosome larvae. These larvae penetrate the skin and die in the dermis. Humans are not their natural host (waterfowl are), and therefore, they cannot survive in humans. The larvae die in the skin, and after the initial symptoms from skin penetration, the rest of the symptoms and rash are a foreign body reaction against the dead larvae in the skin. Both dermatoses can be treated symptomatically with topical steroids and antihistamines. Both will resolve spontaneously within 2-4 weeks. Hot Tub Folliculitis Hot tub folliculitis starts one to several days after exposure to an inadequately chlorinated swimming pool or hot tub that is contaminated with Pseudomonas aeruginosa. Hot tub folliculitis usually develops as red follicular-based papules that may or may not be slightly itchy. They may involve skin covered by the bathing suit (Figure 12.5) or skin in contact with the wall of the offending pool or hot tub. The most classic setting is the use of a hot tub that has not been used for at least several days. Patients may have low grade fevers and malaise, but these symptoms are actually relatively uncommon in this disease. Hot tub folliculitis usually occurs when there is Pseudomonas contamination of a recreational water source. The organism can usually be cultured from the water and occasionally from the patient’s skin. It is unclear how the organism is able to penetrate the adnexal structure to cause clinical disease. Hot tub folliculitis spontaneously resolves within 10-14 days in immunocompetent patients. Treatment is not necessary. If the patient feels systemically ill or is quite anxious about the diagnosis, an antibiotic with good Pseudomonas coverage can be given for a short period. In immunosuppressed patients, hot tub folliculitis can progress to significant infection. These patients should be treated with aggressive anti-pseudomonal antibiotics. Sunburn Sunburn is more common in younger and more lightly pigmented individuals, although it can occur in anyone. Sunburn is manifested by erythema and pain of the affected skin (Figure 12.6). It typically first becomes noticeable anywhere from 4 to 24 hours after the relevant exposure. There are often sharp cut-offs where clothing was protecting the skin. The more severe the burn, the longer it will take to resolve, with a mild burn resolving in 1 day and a severe burn possibly taking weeks to fully resolve. Extremely severe burns may lead to blistering. Significant sunburns usually lead to desquamation of the involved skin as the burn resolves. In severe burns, permanent lentigines can appear in the burned skin. Sunburns are manifestations of epidermal damage from UV radiation, specifically UVB, which damages the epidermis in two ways. First, it directly interacts with keratinocyte DNA, leading to DNA damage, which then leads to inflammation. Second, free radicals are generated by interactions with membrane and cytoplasmic molecules, and the oxidative effects of these free radicals cause further inflammation. A suntan obtained from natural sunlight offers protection in two ways. First, more epidermal melanin is produced. Melanin absorbs the UV radiation, preventing its toxic effects. Second, the epidermis thickens, so that less of the UV radiation penetrates to the deeper epidermis, which is where the worst damage is done. As a generalization, the increased melanin production is due to UVA and the increased epidermal thickness is due to UVB. In general, UVB rays are considered “burning rays”, while UVA rays are considered “tanning rays”. The amount of UVB reaching the earth’s surface is about 1/20th the amount of UVA reaching the surface. In addition, the amount of UVB reaching the surface dramatically varies at different times of the day and year. The amount of UVA reaching the surface is fairly constant. Prevention of sunburning through use of sunscreens (see lecture 6) and protective clothing, and avoidance of excessive sun exposure is by far the best course. However, when a sunburn does occur, several things can be done to minimize the symptoms. First, application of a medium- to high-potency topical steroid every 6-8 hours is useful. The cream can be kept in the refrigerator between uses, as it feels better going on if it is cool. Second, non-steroidal anti-inflammatories taken at anti-inflammatory doses (ibuprofen 2400 mg/day, divided into 3 or 4 doses) are also useful. Finally, the skin should be kept well-moisturized, as this can decrease the severity of the desquamation. Avoidance of further sun exposure is an obvious necessity. Of special note, a suntan obtained in tanning beds does not give the same sunburn protection as a tan obtained from natural sunlight. This is because tanning beds emit UVA almost exclusively. As noted above, UVA leads to increased melanin production (i.e., a suntan, the desired effect), but UVB is necessary for epidermal thickening to occur. Without epidermal thickening, the protection is minor compared to that afforded by the combination of epidermal thickening and increased melanin production. Phytophotodermatitis Phytophotodermatitis usually occurs following a beach vacation or a cruise. Phytophotodermatitis usually presents as asymptomatic, brown hyperpigmentation on the hands, chest, or abdomen resulting from a photosensitizing plant substance (usually lime juice) that gets on the skin while the skin is exposed to sunlight. Erythema with stinging occasionally precedes the discoloration, but the patient rarely recalls any symptoms or redness. The discoloration often does not appear until 1-2 weeks post-exposure and may persist for up to 2 years. The most common patterns are a vertical, linear streak on the chest (from a drop of drink containing lime juice running down the chest) (Figure 12.7), a ring shape or straight line on the upper abdomen (from the bottom of a glass or other object with liquid on it resting on this area) (Figure 12.8), or an irregular macule on the dorsal hand (from a splash or drip of the drink) (Figure 12.9). Patients typically recall drinking a beverage with lime (gin and tonic, cola with lime, beer with lime, etc.), but do not recall any of the beverage getting on their skin. Phytophotodermatitis is due to chemicals called furocoumarins found in the rinds of several citrus fruits (especially limes) and a few vegetables (especially celery). Furocoumarins, when photoactivated, cause clinical disease by causing both non-oxidative DNA cross-linking and oxidative DNA damage. There is no effective treatment for phytophotodermatitis. Usually, once the cause of the pigmentation is explained, the patient is satisfied and happy that it is not a serious disease. They should be reassured that the pigmentation will normalize over time, but it may take up to 2 years. Poison Ivy and Poison Oak 50% - 70% of individuals are allergic to poison ivy. It is more common in the summer and fall than in the spring and winter. On the first exposure (sensitization phase) to poison ivy and oak, there is no rash. On the second exposure, there is elicitation (the rash). Exposure can occur via contact with a living plant, a dead plant or plant part, contact with smoke from burning plants, or contact with an object that has touched a plant. The allergenic substance in the plants is the sap, called urushiol, which can remain allergenic for weeks or even months after being transferred to another object or after the plant has died. Urushiol is an oily substance present on the surface of the plant as well as in the stems, roots, and leaves. The classic manifestation of poison ivy or oak is an erythematous, edematous eruption with vesicles arranged in a “streaky” configuration (Figure 12.10). Depending on the mechanism of exposure, however, the actual configuration of the rash can be extremely variable. The eruption typically begins from 6 hours to 6 days after exposure in a previously sensitized individual. Particularly sensitive individuals can have both sensitization and elicitation occur from the same exposure. In this setting, the allergen persists in the skin while sensitization progresses, and once complete, an elicitation reaction can occur against the remaining allergen in the skin. In this setting, the eruption can develop up to 3 weeks after the exposure. Poison ivy and oak both cause allergic contact dermatitis. The allergenic substances, a pentadecacatechol urushiol in poison ivy and a heptadecacatechol urushiol in poison oak, are potent sensitizers. On initial exposure, the allergen is taken up by antigen presenting cells, transported to the regional lymph nodes, and presented to lymphocytes. Lymphocytes expressing the correct T-cell receptors are activated by interacting with activated antigen presenting cells and their relevant allergens, generating memory T-cells. On re-exposure to the allergen, the allergen is expressed by antigen presenting cells, but before they migrate to the local lymph nodes, trafficking memory T-cells recognize the presented antigen in the skin and begin to react, leading to the clinical disease. Washing the skin within 30 minutes of exposure can lessen or eliminate the reaction that will occur. Beyond 30 minutes post-exposure, washing has little benefit. Following exposure, the rapidity and severity of the response depend on the magnitude of exposure and the degree of sensitivity of the patient. Large exposure areas develop a reaction more quickly than areas with little exposure. This is one explanation for why some patients will continue to develop new areas of involvement for up to one week after the eruption first starts. The other explanation of this phenomenon of delayed spread is that the patient may be contacting an object (glove, chair, clothing, pet) that has urushiol residue on its surface. Blister fluid is not allergenic, and patients cannot spread poison ivy by scratching. This may seem to be the case because an area will often itch before the rash appears; thus, the patient notes that they scratch an area, and then a rash appears there. They assume that the scratching caused the rash, but in reality, the rash would have appeared regardless of whether or not they scratched the area. The treatment of choice for significant poison ivy is systemic steroids. The initial dose should be 1-2 mg/kg tapered over a 3 week period. If tapered too rapidly, the patient will likely have a “rebound” flare that is worse than the original poison ivy. Antibiotics should be used if there is any concern about possible superinfection. Cool, moist compresses can relieve symptoms.