ACP medicine, 3rd Edition
Elizabeth A. Abel MD1
1Clinical Professor of Dermatology, Stanford University School of Medicine
The author has served as advisor or consultant to Amgen, Inc., Biogen Idec, Inc., Genentech, Inc., Abbott Laboratories, Ligand Pharmaceuticals, Inc., and 3M Co.
The drug ivermectin has not been approved by the FDA for uses des cribed in this chapter.
Ectoparasites may cause severely pruritic infectious diseases of the skin. With early detection and treatment, parasitic infestations can be cured and their spread to other persons prevented. The most common parasitic diseases of the skin that occur in nontropical environments are scabies, which is caused by itch mites, and pediculosis capitis, pediculosis corporis, and pediculosis pubis, which are caused by bloodsucking lice.
An increase in international travel, including vacation travel to tropical destinations and immigration from such areas, has led to the occurrence of parasitic disorders endemic to tropical regions in persons living in temperate climates. The differential diagnosis of skin disorders in patients treated at a tropical disease clinic in Paris over a 2-year period included cutaneous larva migrans, pyodermas, arthropod-reactive dermatitis, myiasis, tungiasis, urticaria, and cutaneous leishmaniasis.1 The prevalence of ectoparasitoses in the general population is usually low, but it can be high in vulnerable groups. Management of some infestations (e.g., scabies and head lice) can be complicated because resistance to insecticides is spreading and unpredictable.2
Scabies is caused by infestation with Sarcoptes scabiei, an ectoparasite that bores into the corneal layer of human skin, forming burrows in which it deposits its eggs. The incubation period is 2 to 6 weeks in a person who has not been previously exposed. During this time, the host develops delayed hypersensitivity to mite antigens. Upon reinfestation, symptoms occur in sensitized persons within 24 to 48 hours after exposure.3
The scabies mite does not survive for more than 48 hours away from the host. Therefore, most infestations are transmitted through direct personal skin-to-skin and sexual contact.3 However, transfer of organisms can occur by exposure to fomites such as contaminated bedding, clothing, or furniture and is a common cause of epidemics of scabies in nursing homes and other institutions.3,4
Scabies causes severe itching, which is usually worse at night. Characteristic sites of infestation are the webs of the fingers, the flexor aspects of the wrists, the axillae, the buttocks, the umbilicus, the penis and scrotum of males, and the breasts and nipples of females. The disease is more generalized in infants and children than in adults.
The burrow of the female Sarcoptes may be seen as an irregular zigzag line in the stratum corneum, with a black dot at one end that indicates the presence of the mite [see Figure 1]. Secondary lesions represent immunologic reactions to the mites and usually appear as small erythematous papules and vesicles with surrounding edema and scratch marks [see Figure 2]. The type and number of lesions depend predominantly on the immune status of the host. Occasionally, nodular lesions, which may resemble lesions of histiocytosis X (Langerhans cell granulomatosis) or lymphoma, occur as a hypersensitivity reaction to retained mite parts. Fewer lesions occur in people who practice good hygiene, and the condition may be masked in those who are using topical steroids. Secondary bacterial infection with impetiginization is common, especially in children and in elderly patients who actively excoriate their lesions.
Figure 1. Scabies Lesions
Typical scabies lesions are small erythematous papules and vesicles with surrounding edema.
Figure 2. Scabies Burrow
The burrow of the female Sarcoptes frequently appears as an irregular line several millimeters to a few centimeters long in the stratum corneum.
Atypical presentations of scabies have been described in immunosuppressed persons, including organ transplant recipients, patients with lymphoma or leukemia, and patients with AIDS. Itching and scratching, with elimination of mites and burrows, may be minimal in patients who lack an immunologic host response, allowing for thousands of mites to reproduce and thrive.3 Crusted scabies, which was originally described in Norway, is associated with widespread hyperkeratotic lesions and deep fissures in the skin. Crusted scabies can develop in patients with malnutrition or severe mental deficiency and in institutionalized patients. The condition is highly contagious because of the large number of mites present in the exfoliating skin.
A severe form of scabies with unusual clinical features consisting of crusted lesions and a widespread pruritic papular dermatitis has been described in HIV-infected patients.3,5 In these patients, multiple treatment applications may be needed because of the large mite population and the patients' impaired immunologic response.
A skin scraping that demonstrates the presence of mite eggs or mite products can confirm a diagnosis of scabies. A No. 15 surgical blade is used to scrape across one or more bur rows. Saline solution or mineral oil is used to remove scrapings from the blade. The scrapings are then placed on a glass slide with a coverslip and examined under a microscope at low-power magnification. The scraping is positive if the gravid female, eggs, or scy ba la (fecal pellets) are seen [see Figure 3]. The yield is greatest in burrows that are not yet excoriated, which may be difficult to find. For this reason, if the scraping is negative but the clinical suspicion of scabies is high, the patient should be treated empirically. Histopathologic examination of a skin biopsy sample is also diagnostic if it reveals the mite or the superficial skin burrow and its contents.6 In atypical or subtle cases of scabies, epiluminescence microscopy (ELM) or polymerase chain reaction may be useful in confirming the diagnosis.7,8 ELM, which allows visualization of the skin down to the superficial papillary dermis, is able to detect the presence of scabies within minutes, with no discomfort to the patient. PCR can amplify S. scabiei DNA when the number of mites is so few that diagnosis by standard means is inconclusive.
Figure 3. Micrograph of Scabies Organism
Observation of the Sarcoptes scabiei or its eggs and feces confirms the diagnosis of scabies. Magnification is 400 times.
Clinical differential diagnosis includes drug eruption, papular urticaria, follicullitis, atopic dermatitis, dermatitis herpetiformis, and contact dermatitis, particularly from fiberglass. Crusted scabies may be mistaken for eczema. Papular urticaria is an intensely itchy eruption caused by a hypersensitivity reaction to bites from such insects as fleas, bedbugs, and animal scabies. Lesions occur as small papules that may have a central punctum, often occurring in groups on exposed skin.
After a cleansing bath or shower, the patient should allow the skin to dry and cool and then apply a scabicide over the entire body, excluding the face and scalp. Care must be taken to include skin folds such as toe webs and the skin under the nails. The medication is left in place for 8 to 12 hours, usually overnight. In the morning, the patient showers and changes clothes. All clothing worn within 2 days before treatment, in addition to towels and bed linens, is laundered in hot water or dry-cleaned. Chairs and mattresses should be vacuumed.
First-line treatment for uncomplicated scabies is permethrin 5% cream (Elimite, Acticin); other available scabicides include 1% lindane, or gamma benzene hexachloride, lotion or cream (Kwell, Gamene); 10% to 20% benzyl benzoate lotion; crotamiton cream (Eurax); and 6% precipitated sulfur ointment [see Table 1]. Ivermectin, although not approved by the Food and Drug Administration as a scabicide, has shown promising results in several trials.
Table 1 Drug Therapy for Scabies Infestations
Permethrin, a synthetic pyrethroid with low toxicity, has proved to be safe and effective for use in infants, children, and pregnant women.9Natural pyrethrins, which are derived from chrysanthemum flowers, have greater toxicity and less insecticidal activity than the synthetic pyrethroids. The low toxicity of the drug is a result of its rapid breakdown into inactive metabolites. Permethrin cream can be safely used in children and infants older than 2 months and in the elderly. Acticin is a form of per methrin in a base that has a lower viscosity to promote ease of application. Alternative scabicides that can be used for young children and pregnant or lactating women include crotamiton cream and sulfur ointment. Six-percent precipitated sulfur ointment is applied three times: at diagnosis, after 24 hours, and at 1 week. Crotamiton cream is applied for 2 or more consecutive days but is less effective than permethrin. Permethrin appears to be more effective than crotamiton in clinical and parasitic cure rates.9
Lindane is lipophilic and can accumulate in fat and bind to brain tissue. Toxic reactions may occur in patients who have increased absorption; infants and young children, who have a higher ratio of skin surface to body volume than do adults, are especially susceptible. Excessive treatment with lindane has been reported to cause central nervous system toxicity resulting in convulsions and seizures.10 In 2003, the FDA issued a label change for lindane emphasizing its use as second-line therapy; treatment with lindane should be considered only if other medications have failed or cannot be tolerated (information on lindane can be found on the Internet, athttp://www.fda.gov/cder/drug/infopage/lindane/default.htm). Lindane lotion should be used with caution in persons weighing less than 110 lb; its use in infants is not recommended.11 Nevertheless, low cost, ease of application, and experience with the drug have made lindane one of the most commonly prescribed scabicides; the FDA considers the benefits of lindane to outweigh the risks when the medication is used as directed.
Oral ivermectin is another treatment option that has been found to be safe and effective in children as young as 6 months12 and in HIV-positive patients. A single oral dose of 200 µg/kg of ivermectin was used to treat uncomplicated scabies in 11 otherwise healthy patients and in 11 patients with HIV infection.13 Clearing was documented by negative skin scrapings at 2 weeks and 4 weeks after treatment, and cure was achieved in all of the otherwise healthy patients and in eight of the HIV-infected patients. Advantages of an oral medication are its ease of use, lack of treatment-associated dermatitis, and increased compliance. In a comparative study of oral ivermectin and topical permethrin, a single application of permethrin was found to be superior to a single dose of ivermectin. Two doses of ivermectin were required for eradication of scabies. The lack of ovicidal activity of ivermectin may explain the difference in effectiveness between the two drugs.14 Ivermectin is toxic to invertebrate nerve and muscle cells but may not be effective against younger stages of the parasite that do not have a developed nervous system. Permethrin acts at early stages of the life cycle of the parasite, and topical application ensures adequate drug concentration in the skin.14
Oral ivermectin has been used successfully to control outbreaks of scabies infestations in institutional settings4,15; it may prove to be the treatment of choice in nursing homes and other institutions in which topical therapy is impractical.
Topical ivermectin has also been investigated for treatment of scabies. A total of 75 patients were found to be cured, on the basis of clinical and parasitologic examinations, within 48 hours after a single application of ivermectin. Postscabies itching, which persisted in 50% of the patients, was effectively treated by a second application of ivermectin within 5 days.16
Postscabies itch is thought to represent a hypersensitivity reaction to the mite or mite products and is not caused by active infestation. The pruritus may persist for weeks to months and can be treated with an antipruritic or anti-inflammatory agent, such as a low-potency to midpotency corticosteroid cream, in addition to oral antihistamines. Overtreatment with the scabicide may result in a primary irritant dermatitis that may be confused with persistent infestation. The use of bland emollients and a corticosteroid cream and avoidance of skin irritants may reduce the dermatitis. Patients should be evaluated at 4 weeks, which is the time required for viable eggs to mature to the adult stage, to determine the efficacy of treatment. If lesions are healed and no new outbreaks have occurred, the patient is considered cured.3
Overuse and misuse of certain scabicides, notably lindane, have decreased their efficacy. Differing resistance patterns have been identified within a single city; more commonly, resistance corresponds to local or regional patterns.2 If treatment failure occurs with one scabicide, the use of a different scabicide may be indicated. For example, treatment failure with topical permethrin may prompt the consideration of lindane as a second-line therapy. Pyrethroids are effective in cases of lindane-resistant scabies.17 Treatment failures can also occur in cases involving impetiginized or crusted scabies. In these cases, treatment with the appropriate oral antibiotic is initiated along with application of the scabicide and is followed within a week by a second application of the scabicide. Keratolytics are useful as an aid in removal of the crusts.
Oral ivermectin has been used to treat resistant scabies.18 Although it has not been approved by the FDA for this purpose, oral ivermectin is rapidly gaining acceptance as an effective therapy for resistant scabies. Combination treatment with one or two doses of ivermectin 8 days apart, in addition to permethrin and mechanical removal of subungual debris, has been advocated for outbreaks of crusted scabies in the geriatric population.19
In Europe, combination therapy with oral ivermectin, 200 mg/kg, and benzylbenzoate, 15% solution applied twice daily for 3 days, was found to be more effective than either agent alone for the treatment of crusted scabies in patients with HIV.20 In the United States, a combination of oral ivermectin, total body therapy with permethrin cream, and keratolytic agents to hasten removal of crusts was used successfully to treat crusted scabies in patients with HIV.21
Cases of apparent resistant scabies may be the result of reinfestation. Therefore, family members and sexual partners of persons with scabies should be treated because they may be asymptomatic carriers. Scabies occurring in patients and personnel in long-term health care facilities may be difficult to diagnose and manage. In this setting, it is extremely important to treat all nursing contacts, as well as family members and other visitors of affected patients. In addition to the patients with scabies, other patients in the facility need to be assessed, and care must be coordinated to treat all affected persons simultaneously. In cases of crusted scabies, the head and neck must be treated, as well as subungual areas, which may also harbor the mites.4
Animal scabies is a common disorder in farm animals and domestic animals—especially dogs, in which the external ear is frequently infested with a species-specific mite. In persons who handle affected animals, an extremely pruritic papular eruption can develop that differs from ordinary scabies in several ways: distribution of lesions is proximal, with involvement of the thighs, abdomen, and forearms. Burrows are usually absent. The course is self-limited, provided there is no reexposure. Other persons in the household do not have to be treated, because human-to-human transmission of animal scabies does not occur.
The Cheyletiella mite is an ectoparasite that resides in the fur of dogs, cats, and rabbits. Persons who hold infested house pets, especially cats, are susceptible to a dermatitis from the mite bites. However, the mites do not live on humans, so diagnosis requires a high index of suspicion. Lesions may appear as urticarial papules, vesicles, or bullae on the arms, trunk, and legs. Cases most commonly occur in the fall or winter. An important part of the overall treatment of Cheyletiella infestation is treatment of the household pets by a veterinarian.22
The three types of bloodsucking lice that cause pediculosis are Pediculus humanus var. capitis (head louse), Pediculus humanus var. corporis(body louse), and Phthirus pubis (pubic, or crab, louse). The first two types are closely related. The third is a separate genus and is distinctive not only in appearance and location on the body but also in its characteristic attachment to the skin for long periods. Any form of pediculosis causes intense pruritus, which is aggravated by scratching and is often complicated by secondary bacterial infection.23
The most common infestation is pediculosis capitis. Infestations of P. captitis have been reported worldwide, and an estimated 12 million cases occur annually in the United States alone.23 Pediculosis corporis, which is usually less prevalent than pediculosis captitis, becomes widespread under conditions of overcrowding and poor sanitation or in wartime. In pediculosis capitis and pediculosis corporis, the lice may be transmitted directly from person to person or indirectly through contact with contaminated personal objects such as combs and brushes, clothing, and bedding. Pediculosis pubis (also called crabs) is usually transmitted sexually; only occasionally are the lice transmitted through contact with fomites such as contaminated bedding or toilet seats. Epidemiologic data indicate that P. capitis infestations are more frequent in the warmer months, whereas P. pubis infestations occur more frequently in the cooler months.24
The natural history of lice is important because it suggests specific preventive measures. The life expectancy of the organism is about 1 month. Eggs live up to 10 days but need the body heat of the host to hatch. Eggs ordinarily hatch in 7 to 8 days, and organisms reach adulthood and attain sexual reproductive capacity in 3 to 4 weeks. Lice can survive 48 hours without a blood meal.
Pediculosis capitis is confined to the scalp and is most prevalent in women and children. Louse infestation may present as scalp pruritus, excoriations, cervical lymphadenopathy, or conjunctivitis.23 Examination of the itchy scalp may reveal the lice, which look like tiny black dots that are barely visible to the naked eye, and lice eggs (nits), which are white and are attached to the hair shafts [see Figure 4]. Except in conditions of increased warmth and high humidity, viable nits are attached close to the scalp. Those that occur several millimeters away from the surface on hairs that have grown out are empty egg cases. The hair may become matted because of exudation and secondary infection of lesions. Visual examination may not detect infestation; the use of a louse comb is recommended because it is four times more efficient than visual examination alone in the diagnosis of active pediculosis capitis.25
Figure 4. Micrograph of Pediculus Humanus
Pediculosis capitis is caused by infestation of the scalp with Pediculus humanus var. capitis. Magnification is 10 times.
Pediculosis corporis, also called vagabond disease, affects areas of the body covered by clothing. Body lice live in the seams of clothing, and they attach to the body only to feed [see Figure 5]. They may serve as vectors of infectious disease under conditions of overcrowding or poor hygiene, as in wartime or during natural disasters. Characteristic lesions include erythematous macules and wheals. Lesions are most common on the shoulders, buttocks, and abdomen; furunculosis is an occasional complication. Excoriations and secondary infection may result from intense scratching. After the eggs hatch, the organisms reach adulthood in 10 days and complete their life cycle in approximately 1 month. Adult lice lay about 10 eggs a day.
Figure 5. Pediculosis Corporis
Pediculosis corporis is caused by infestation with Pediculus humanus var. corporis organisms, which live in the seams of clothing.
Pediculosis pubis, which is caused by infestation with Phthirus pubis [see Figure 6], tends to be limited to the pubic area but occasionally affects the axillae, eyelashes, or other hairy parts of the body. Examination will reveal lice attached to the skin and lice eggs attached to the hair shafts [see Figure 7]. Blue macules, which are caused by the lice's sucking blood from the dermis, may be seen on the thighs or pubic area.
Figure 6. Micrograph of Pediculosis Pubis
Pediculosis pubis, also called crabs, is caused by infestation with Phthirus pubis. Magnification is 100 times.
Figure 7. Pediculosis Pubis
Lice attached to the skin and lice eggs attached to the hair shafts can be seen on a patient with pediculosis pubis.
Over-the-counter preparations available for the treatment of pediculosis capitis include synergized pyrethrin products, such as RID, R&C Spray, A-200, and a 1% permethrin cream rinse (Nix) [see Table 2]. These products are cosmetically acceptable and require only 10 minutes to apply but may not always be effective. Repeat treatment in 7 to 10 days is advisable because the initial treatment does not kill all the eggs. If pyrethrin or permethrin fails to eradicate the infestation, the treatment of choice is malathion.26 Malathion, which was recently reintroduced in the United States as a prescription medication for head lice, is an effective, fast-acting pediculicide and ovicide; it has not been associated with treatment resistance or notable adverse effects.27,28 In children, proper use of malathion is safe; however, serious side effects can occur with ingestion.29
Table 2 Drug Therapy for Pediculosis Infestations
One of the most widely used remedies for pediculosis capitis in the United States is 1% lindane (Kwell, Gamene). However, potentially serious adverse effects associated with lindane shampoo prompted the FDA to issue a label change for this medication; treatment with lindane is now indicated only if other medications have failed or cannot be tolerated.11,27 For the treatment of pediculosis capitis, 2 tbsp (30 ml) of the shampoo is applied to affected and adjacent areas of the scalp for at least 4 minutes, followed by thorough rinsing and drying. Adherent nits may be removed with a fine-tooth comb. Distilled white vinegar can be used to soften the nit cementing material to aid in removal of the nits.
Resistance to lindane has emerged over the past 2 decades,30 and treatment of lice infestation has been complicated by the development of resistance to permethrin.28 Mechanical methods of removing head lice and nits31 and application of occlusive oils or ointments32 have been advocated for treatment of resistant head lice. Oral ivermectin has been administered as a single dose of 12 mg (2 to 6 mg tablets), followed by a second dose 7 to 10 days later.23 Current evidence suggests that permethrin, pyrethrin, and malathion are equally effective in the treatment of head lice; the best choice of therapy depends on local resistance.33
Pediculosis Pubis and Pediculosis Corpis
To treat hairy areas of the body infested with P. pubis, a cleansing bath or shower should first be taken and the skin dried with a towel. One ounce of lindane cream or lotion is applied to the affected and surrounding areas and left on for 12 to 24 hours. To discourage percutaneous absorption, the lotion should be applied only after the skin has become cool and dry. Lotions containing pyrethrins and piperonyl butoxide are acceptable alternatives, and their use is preferred in select patients and children (see below).11 After another bath or shower, freshly laundered clothing should be donned; bedsheets and towels should also be changed. Lindane may be applied a second time after 1 week if infestation continues. Lindane should not be applied to the face and eyelids, because it causes irritation; eyelash infestation may be treated by local application of 0.25% physostigmine ophthalmic ointment. An alternative treatment for eyelash infestation that is effective and nonirritating is the application of a thick layer of petrolatum twice a day, followed by mechanical removal of the nits.
Neurologic complications can ensue from absorption of lindane after extensive or prolonged topical application [see Scabies, above]; severe adverse reactions have also occurred after a single use (information on lindane can be found on the Internet, athttp://www.fda.gov/cder/drug/infopage/lindane/default.htm). Careful consideration should be given before prescribing lindane to patients with conditions that increase the risk of seizure (e.g., HIV infection, history of past seizure, or severe hepatic cirrhosis) or whose concomitant medications include drugs that lower risk of seizure. Alternative treatments are indicated in infants (who are especially susceptible), young children, pregnant women, and the elderly.
A combination of pyrethrins with piperonyl butoxide (RID or A-200) has been shown to be considerably less toxic than lindane in animal experiments and in clinical experience. However, this combination irritates the eyes and mucous membranes and may also cause allergic contact dermatitis in susceptible people.
General Treatment Measures
All family members should be carefully examined for pediculosis and treated, if necessary, to avoid spread or reinfection of previously treated persons. In the case of pediculosis pubis, sexual contacts should be examined and treated. Because sexually transmitted diseases are frequently present in persons infested with P. pubis, a serologic test for syphilis and screening for HIV are usually done. To prevent spread of pediculosis, contaminated clothing and other articles, such as towels and bedding, should be boiled, machine washed in hot water, and placed in a dryer using a 20-minute hot cycle or should be dry-cleaned. Items such as combs and brushes may be cleaned with medicated shampoo or soaked in 5% Lysol. To eradicate P. corporis, the patient's clothing must be put through the same decontamination process as that used for P. pubis. A hot iron with pressure applied, especially to the seams of clothing, may also be used to kill P. corporis. Systemic antibiotics should be prescribed for concomitant secondary bacterial infections such as furunculosis and impetigo, both of which are commonly associated with pediculosis capitis.
Fleas are small (approximately 3 mm), bloodsucking, wingless ectoparasites of the insect order Siphonaptera. Fleas are medically significant because they are vectors of infectious disease [see 7:XI Infections Due to Brucella, Francisella, Yersinia Pestis, and Bartonella and 7:XVII Infections Due to Rickettsia, Ehrlichia, and Coxiella]. They can also cause considerable cutaneous symptoms, particularly if the symptoms are associated with an allergic hypersensitivity reaction, as seen in papular urticaria. There are approximately 250 species of flea, 20 of which can infest humans. Two common species that infest cats and dogs are Ctenocephalides felis and C. canis. They are not host specific and can therefore infest humans as well. Pulex irritans, the house flea, infests humans and in most places is not a problem for pets. Flea bites appear as erythematous edematous papules with hemorrhagic puncta in clusters or groups on the lower extremities, especially on the ankles. Occasionally, vesicles and bullae appear, as well as larger urticarial lesions. Secondary impetiginization may occur because of scratching.34
Fleas are difficult to eradicate because of their unpredictable life cycle, which consists of egg, larva, pupa, and adult stages. The eggs are laid on the host but can drop to the ground; onto carpets, pet bedding, and furniture; and into floor cracks. Eggs hatch in 2 to 21 days into larvae. A larva molts twice and, in the third larval stage, spins a cocoon, in which it becomes a pupa. Within 7 days to 1 year or more, the adult emerges, depending on various trigger factors (e.g., a vibration caused by a nearby pet or human). The life cycle from egg to adult generally ranges from 14 to 21 days but, under ideal conditions, can be as long as 20 months.34
Eradication of the fleas may require consultation with a veterinarian. Pets must be treated more than once with topical agents to kill the eggs, larvae, and pupae, as well as the residual fleas. Systemic agents are available to protect pets from reinfestation. A household flea spray should be combined with a fogger to fumigate the house. A proper extermination procedure includes vacuuming the furniture and vacuuming or steam cleaning carpets or rugs. The yard should be sprayed and cleared of organic debris. Treatment of flea bites consists of cool-water compresses, application of a corticosteroid cream and an antipruritic lotion, and oral antihistamines in the case of allergic hypersensitivity reaction. Systemic antibiotics are prescribed for secondary bacterial infection.
Cutaneous infestation by the sandflea Tunga penetrans is endemic in Central and South America, parts of Mexico, tropical Africa, Pakistan, and the west coast of India. Isolated cases have been reported in the United States, Australia, and New Zealand. Tungiasis is more prevalent in poverty-stricken areas and is associated with domestic animals such as pigs, dogs, and cattle, which serve as intermediaries in the biologic life cycle.35 The female adult sandflea exists in sandy soils and requires a warm-blooded host to complete its life cycle. The organism penetrates the stratum corneum, resulting in erythematous nodules with a central dark spot. Common sites of skin involvement are the soles of the feet, the web spaces between fingers and toes, the ankles, the perineal area, and the buttocks.
Infestation can be prevented by wearing shoes and proper clothing and by the use of insecticides.
Myiasis is caused by the larvae (maggots) of feeding flies of the order Diptera. The larvae may invade the skin primarily36 or become secondarily implanted in a preexisting skin wound.37 Many species of the genus Cuterebra can cause myiasis, but in North America, C. cuterebra and C. dermatobia cause furuncular cutaneous infestations. Mosquitoes act as vectors by transporting fly eggs from infected animals to human hosts.38 The skin lesions appear as nonhealing single or multiple nodules on the upper trunk, usually at the site of a painful bite wound. Skin lesions may be misdiagnosed as cellulitis, boils, or sebaceous cysts. Myiasis is commonly reported in travelers to endemic areas such as Central and South America and tropical and subtropical Africa. Preventive measures include the use of insect repellents, the wearing of protective clothing to prevent mosquito bites, and the avoidance of direct skin contact with sand that may be infested with eggs. Furuncular myiasis is effectively treated by removal of the larvae by incision and drainage with debridement. Antibiotics are prescribed for secondary bacterial infection. Occlusion with such agents as liquid paraffin, lubricating jelly, and even the fatty portion of raw bacon has been suggested to cause suffocation of the larvae or migration of the larvae from the wound.39
CUTANEOUS LARVA MIGRANS
Cutaneous larva migrans is caused by penetration and migration of larval hookworms (usually Ancylostoma braziliense) within the skin. Patients are usually travelers returning from seawater beaches in tropical areas and commonly present to the dermatologist with pruritic skin lesions. The abdomen or feet are most often involved, with a characteristic eruption consisting of one or several erythematous linear to serpiginous thin lines in the skin.
Optimal management is controversial, and most treatment trials have been of low quality; however, it is generally agreed that the most effective agents in treating cutaneous larva migrans are topical or oral anthelmintics, including albendazole, thiabendazole, and ivermectin. Regimens include topical thiabendazole (10% to 15% cream) three times daily for 5 to 10 days; oral albendazole, 400 mg daily for 3 to 5 days; oral ivermectin, single dose of 12 mg; and oral thiabendazole, 50 mg/kg weekly for 2 to 3 weeks. Topical thiabendazole (10% cream) is effective and safe in children,40,41 but it is difficult to obtain. Systemic therapy, either with albendazole or ivermectin, may be preferable to topical therapies. Oral albendazole has a high cure rate and appears to be effective in cases of multiple lesions.42,43 Oral ivermectin is effective and reportedly safe.43 Oral thiabendazole has been reported to cure long-standing cutaneous larva migrans, but it may cause side effects such as headaches, nausea, and vomiting.44
Seabather's eruption, also known as sea lice by laypersons, is an acute pruritic dermatitis that occurs within 24 hours of seawater exposure and resolves spontaneously after 3 to 5 days.45 Lesions affect areas of the skin covered by swimwear, particularly those that are subjected to pressure or friction, such as the waistline, axillae, neck, and inner thighs [see Figure 8]. The larvae of the thimble jellyfish Linuche unguiculata, which are washed ashore by ocean currents, have been identified as the cause of seabather eruption in southern Florida and the Caribbean.46 Similar outbreaks on Long Island, New York, are thought to be caused by larvae of the sea anemone Edwardsiella lineata.47Treatment is symptomatic and includes antihistamines, topical antipruritic agents, and steroids.
Figure 8. Seabather's Eruption
Seabather's eruption is characterized by the development of pruritic papules on areas covered by the patient's bathing suit.
Cercarial dermatitis, known as swimmer's itch, is caused by an avian schistosome, Microbilharzia variglandis. The skin eruption appears approximately 12 hours after contact with seawater as a pruritic papulovesicular dermatitis on exposed skin sites.48 The inflammatory response is attributed to dermatologic penetration by cercariae, which are the free-swimming larvae of M. variglandis and other bird schistosomes.
Treatment is symptomatic and includes antihistamines, topical antipruritic agents, topical corticosteroids, and antibiotic treatment of superimposed bacterial infection.
CUTANEOUS AND MUCOCUTANEOUS LEISHMANIASIS
There are distinctive skin lesions associated with the cutaneous and mucocutaneous forms of leishmaniasis [see Figure 9]. Leishmaniasis is caused by an obligate intracellular parasite introduced by the Phlebotomus sandfly, which feeds on infected animals. Leishmania braziliensisand L. mexicana are the most common causes of American, or New World, leishmaniasis. L. donovani causes Old World leishmaniasis, which is endemic in Asia and West Africa [see Section 7:XXXIV Protozoan Infections]. Infection by L. major is the cause of cutaneous leishmaniasis in United States military personnel returning from Afghanistan and Iraq.49
Figure 9. Ulcerations of Leishmaniasis
Leishmaniasis can present as chronic cutaneous ulcerations.
Cutaneous leishmaniasis—the initial, or primary, form of the disease—appears as a localized, usually single, lesion involving the mouth and nose. A red-brown papule develops at the site of inoculation into a nodule that becomes verrucous or ulcerates, and satellite nodules may form. Spontaneous healing with an atrophic scar occurs in most cases. Old World leishmaniasis is usually limited to the skin, whereas New World leishmaniasis can cause mutilating mucocutaneous involvement.50 After a period of months to years, the mucocutaneous, or secondary, form of the disease may develop, depending on host immunologic factors. Lesions in this stage range from edema of the lips and nose to perforation of the nasal cartilage. A rare form, disseminated cutaneous leishmaniasis, which has widespread nodules resembling lepromatous leprosy, may occur in immunosuppressed patients.
The differential diagnosis includes various inflammatory and neoplastic disorders, including squamous cell carcinoma. Diagnosis is made by skin biopsy with histopathologic examination. Cultures from skin biopsy may be inconclusive; PCR shows promise as a sensitive single diagnostic test.51 Appropriate therapy depends on species identification. A pentavalent antimony compound, such as sodium stibogluconate, is the drug of choice for New World leishmaniasis, which tends to be more aggres sive. Lesions acquired in the Middle East and North Africa may spontaneously involute or may respond to local therapy, including cryosurgery, heat therapy, or intralesional injection of antimonials.
Delusions of Parasitosis
Patients with delusions of parasitosis express the conviction that there are scabies, insects, lice, fleas, worms, or other vermin infesting their skin and producing a crawling, itching, or prickling sensation.52 They may have excoriations or skin inflammation and erosions consistent with factitial dermatitis. Frequently, patients will bring small containers filled with lint, hairs, pieces of skin, fibers, or other debris for examination. Despite the lack of objective evidence for infestation—including negative results from clinical examination, microscopic examination of skin scrapings, and skin biopsy—the delusions persist. Associated underlying psychiatric disturbances may range from a phobic-obsessive state or anxiety reaction to a frank psychosis with either depression or paranoia. Not infrequently, the delusion is shared by the spouse or other family members, as in the classic folie à deux or folie à famille. The patient usually functions in a highly organized manner in other aspects of his or her life. Such patients typically resist seeking psychiatric evaluation.
Treatment with pimozide, a high-potency antipsychotic neuroleptic of the diphenylbutylpiperidine group, has been used successfully.52 The effectiveness of the drug may be mediated by its ability to specifically block central dopamine receptors. As is characteristic of high-potency antipsychotic drugs, pimozide has fewer cardiovascular and anticholinergic effects but greater neurologic toxicity, especially with long-term use, than does low-potency antipsychotic drugs. Tardive dyskinesia, an extrapyramidal syndrome characterized by involuntary movements of facial muscles and extremities, may occur in 10% to 20% of patients on antipsychotic drugs. Other side effects may include skin discoloration, dermatitis, and blurred vision. Thorough medical and psychiatric evaluation should be obtained before antipsychotic medication is instituted.
- Lucchina LC, Wilson ME, Drake LA: Dermatology and the recently returned traveler: infectious diseases with dermatologic manifestations. Int J Dermatol 36:167, 1997
- Heukelbach J, Feldmeier H: Ectoparasites: the underestimated realm. Lancet 363:889, 2004
- Chouela E, Abeldano A, Pellerano G, et al: Diagnosis and treatment of scabies: a practical guide. Am J Clin Dermatol 3:9, 2002
- Scheinfeld N: Controlling scabies in institutional settings: a review of medications, treatment models, and implementation. Am J Clin Dermatol 5:31, 2004
- Schlesinger I, Oelrich DM, Tyring SK: Crusted (Norwegian) scabies in patients with AIDS: the range of clinical presentations. South Med J 87:352, 1994
- Head ES, Macdonald EM, Ewert A, et al: Sarcoptes scabieiin histopathologic sections of skin in human scabies. Arch Dermatol 126:1475, 1990
- Argenziano G, Fabbrocini G, Delfino M: Epiluminescence microscopy: a new approach to in vivo detection of Sarcoptes scabiei. Arch Dermatol 133:751, 1997
- Bezold G, Lange M, Schiener R, et al: Hidden scabies: diagnosis by polymerase chain reaction. Br J Dermatol 144:614, 2001
- Walker GJ, Johnstone PW: Interventions for treating scabies. Cochrane Database Syst Rev (3):CD000320, 2000
- Fischer TF: Lindane toxicity in a 24-year-old woman. Ann Emerg Med 24:972, 1994
- Labeling changes for lindane. FDA Consum 37:6, 2003
- Brooks PA, Grace RF: Ivermectin is better than benzyl benzoate for childhood scabies in developing countries. J Paediatr Child Health 38:401, 2002
- Meinking TL, Taplin D, Hermida JL, et al: The treatment of scabies with ivermectin. N Engl J Med 333:26, 1995
- Usha V, Gopalakrishnan Nair TV: A comparative study of oral ivermectin and topical permethrin cream in the treatment of scabies. J Am Acad Dermatol 42:236, 2000
- Leppard B, Naburi AE: The use of ivermectin in controlling an outbreak of scabies in a prison. Br J Dermatol 143:520, 2000
- Youssef MYM, Sadaka HAH, Eissa MM, et al: Topical application of ivermectin for human ectoparasites. Am J Trop Hyg 53:652, 1995
- Purvis RS, Tyring SK: An outbreak of lindane-resistant scabies treated successfully with permethrin 5% cream. J Am Acad Dermatol 26(pt 1):1015, 1991
- Cook AM, Romanelli F: Ivermectin for the treatment of resistant scabies. Ann Pharmacother 37:279, 2003
- Paasch U, Haustein U-F: Management of endemic outbreaks of scabies with allethrin, permethrin, and ivermectin. Int J Dermatol 39:463, 2000
- Alberici F, Pagani L, Ratti G, et al: Ivermectin alone or in combination with benzyl benzoate in the treatment of human immunodeficiency virus-associated scabies. Br J Dermatol 142:969, 2000
- Taplin D, Meinking TL: Treatment of HIV-related scabies with emphasis on the efficacy of ivermectin. Semin Cutan Med Surg 16:235, 1997
- Lee BW: Cheyletielladermatitis: a report of fourteen cases. Cutis 47:111, 1991
- Ko CJ, Elston DM: Pediculosis. J Am Acad Dermatol 50:1, 2004
- Minouni D, Ankol OE, Gdalevich M, et al: Seasonality trends of Pediculosis capitisand Phthirus pubis in a young adult population: follow-up of 20 years. J Eur Acad Dermatol Venereol 16:257, 2002
- Mumcuoglu KY, Friger M, Ioffe-Uspensky I, et al: Louse comb versus direct visual examination for the diagnosis of head louse infestations. Pediatr Dermatol 18:9, 2001
- Jones KN, English JC 3rd: Review of common therapeutic options in the United States for the treatment of pediculosis capitis. Clin Infect Dis 36:1355, 2003
- Burkhart CG: Relationship of treatment-resistant head lice to the safety and efficacy of pediculicides. Mayo Clin Proc 79:661, 2004
- Yoon KS, Gao JR, Lee SH, et al: Permethrin-resistant human head lice, Pediculus capitis, and their treatment. Arch Dermatol 139:994, 2003
- Frankowski BL: American Academy of Pediatrics guidelines for the prevention and treatment of head lice. Am J Manag Care 10:S269, 2004
- Forrester MB, Sievert JS, Stanley SK: Epidemiology of lindane exposures for pediculosis reported to poison centers in Texas, 1998–2002. J Toxicol Clin Toxicol 42:55, 2004
- Roberts RJ, Casey D, Morgan DA, et al: Comparison of wet combing with malathion for treatment of head lice in the UK: a pragmatic randomised controlled trial. Lancet 356:540, 2000
- Mumcuoglu KY: Prevention and treatment of head lice in children. Paediatr Drugs 1:211, 1999
- Dodd CS: Interventions for treating headlice. Cochrane Database Syst Rev (3):CD001165
- Hutchins ME, Burnett JW: Fleas. Cutis 51:241, 1993
- Campos Macias P, Mendez Sashida P: Cutaneous infestation by Tunga penetrans. Int J Dermatol 39:296, 2000
- Jelinek T, Nothdurft HD, Rieder N, et al: Cutaneous myiasis: review of 13 cases in travelers from tropical countries. Int J Dermatol 34:624, 1995
- Sherman RA: Wound myiasis in urban and suburban United States. Arch Intern Med 160:2004, 2000
- Maier H, Honigsmann H: Furuncular myiasis caused by Dermatobia hominis, the human botfly. J Am Acad Dermatol 50:S26, 2004
- Brewer TF, Wilson ME, Gonzalez MD, et al: Bacon therapy and furuncular myiasis. JAMA 270:2087, 1993
- Jelinek T, Maiwald H, Nothdurft HD, et al: Cutaneous larva migrans in travelers: synopsis of histories, symptoms, and treatment of 98 patients. Clin Infect Dis 19:1062, 1994
- Simon MW, Simon NP: Cutaneous larva migrans. Pediatr Emerg Care 19:350, 2003
- Rizzitelli G, Scarabelli G, Veraldi S: Albendazole: a new therapeutic regimen in cutaneous larva migrans. Int J Dermatol 36:700, 1977
- Caumes E, Carriere J, Datry A, et al: A randomized trial of ivermectin versus albendazole for the treatment of cutaneous larva migrans. Am J Trop Med Hyg 49:641, 1993
- Richey TK, Gentry RH, Fitzpatrick JE, et al: Persistent cutaneous larva migrans due to Ancylostomaspecies. South Med J 89:609, 1996
- Tomchik RS, Russell MT, Szmant AM, et al: Clinical perspectives on seabather's eruption, also known as “sea lice.” JAMA 269:1669, 1993
- Segura-Puertas L, Ramos ME, Aramburo C, et al: One Linuchemystery solved: all three stages of the coronate scyphomedusa Linuche unguiculata cause seabather's eruption. J Am Acad Dermatol 44:624, 2001
- Freudenthal AR, Joseph PR: Seabather's eruption. N Engl J Med 329:542, 1993
- Verbrugge LM, Rainey JJ, Reimink RL: Swimmer's itch: incidence and risk factors. Am J Public Health 94:738, 2004
- Update: cutaneous leishmaniasis in U.S. military personnel: Southwest/Central Asia, 2002–2004. MMWR Morb Mortal Wkly Rep 53:264, 2004
- Koff AB, Rosen T: Treatment of cutaneous leishmaniasis. J Am Acad Dermatol 31:693, 1994
- Faber WR, Oskam L, van Gool T, et al: Value of diagnostic techniques for cutaneous leishmaniasis. J Am Acad Dermatol 49:70, 2003
- Driscoll MS, Rothe MJ, Grant-Kels JM, et al: Delusional parasitosis: a dermatologic, psychiatric, and pharmacologic approach. J Am Acad Dermatol 29:1023, 1993
Editors: Dale, David C.; Federman, Daniel D.