Pediatric Annals

Parasitic Infestations of the Skin

Roy M Colven, MD; Neil S Prose, MD

Abstract

Cutaneous parasites, or ectoparasites, primarily target the skin for their food source and habitat. This implies a relationship with the host that encompasses a significant portion of the parasite's life cycle, as opposed to most blood-sucking arthropods, which are better considered micropredators.1 Some endoparasites use the skin as a portal of entry enroute to internal systemic infection and may produce cutaneous manifestations (hookworm is such an example). Another endoparasite, the pinwortn, manifests most commonly as perianal and perineal itching, although its primary habitat is the gut where it generally produces no symptoms.

Of the ectoparasites infesting children in the United States, pediculosis (lice) and scabies are the most common. These will be the focus of this article. Less common ectoparasitic conditions (cercarial dermatitis and creeping eruption) will be discussed briefly. Other parasites can involve the skin, but are seen mainly in the tropics and only rarely in this country. They will not be discussed here.

SCABIES

Etiology and Life Cycle

Scabies is caused by the mite Sarcoptes scabiei var /tominis. The larger adult female is less than 0.5 mm in diameter and is white to translucent in color. Scabies is an obligate human parasite. Survival time away from the skin at room temperature is 24 to 36 hours.2 The adult female mite burrows into the stratum corneum where she mates with the male, deposits eggs, and then dies. The burrow, which is not restricted to the stratum corneum, is lengthened by 2 mm to 3 mm per day. Larvae hatch, bore out of the burrow, dig short molting pockets, and eventually develop into adult mites. The entire life span is 4 to 6 weeks. The mites prefer areas on the skin with relatively low density of pilosebaceous units. Thus, the face and scalp often are spared. In the common form of the infestation, there are only 10 to 15 female mites on the body at one time, in the crusted, or Norwegian, variant, at least hundreds of mites are present.3

Epidemiology

Scabies is found worldwide and spares no age, race, or socioeconomic strata. Cyclic variations in incidence have prompted theories regarding herd immunity. Scabies may confer a degree of immunity individually, both cell-mediated and humoral, although a protective effect is controversial. Thus, pandemics could arise with the emergence of an underimmune generation. Many other factors (eg, crowded living conditions, poor hygiene, and sexual promiscuity) may play a role in these pandemic cycles.3

Close contact with infested individuals is needed for transmission in the common form. Children and young adults are affected more often. Household member contact is important, whereas contact with children in school does not appear to play an important role in transmission. Infants less than 2 years of age have the highest incidence, a result of frequent handling by infested adults and older children.4 In young adults, scabies is frequently a sexually transmitted disease. Fomitic transmission from clothing or bed linen appears to play only a minor role.

Transmissibility also is related directly to mite numbers. Infestation can occur with casual and brief contact with an individual with crusted scabies.5 The skin debris from such patients contains numerous mites protected from desiccation, thus prolonging mite survival away from the skin for up to 10 days. Hospital and other institutional outbreaks have resulted from unrecognized cases. Crusted scabies is found in those with an altered response or appreciation of the mite on their skin. This includes those with the physical inability to scratch (eg, paresis or physical debilitation), those with a suppressed or altered sensation of pruritis (eg, neuropathy or dementia), or those with an altered immune response to…

Cutaneous parasites, or ectoparasites, primarily target the skin for their food source and habitat. This implies a relationship with the host that encompasses a significant portion of the parasite's life cycle, as opposed to most blood-sucking arthropods, which are better considered micropredators.1 Some endoparasites use the skin as a portal of entry enroute to internal systemic infection and may produce cutaneous manifestations (hookworm is such an example). Another endoparasite, the pinwortn, manifests most commonly as perianal and perineal itching, although its primary habitat is the gut where it generally produces no symptoms.

Of the ectoparasites infesting children in the United States, pediculosis (lice) and scabies are the most common. These will be the focus of this article. Less common ectoparasitic conditions (cercarial dermatitis and creeping eruption) will be discussed briefly. Other parasites can involve the skin, but are seen mainly in the tropics and only rarely in this country. They will not be discussed here.

SCABIES

Etiology and Life Cycle

Scabies is caused by the mite Sarcoptes scabiei var /tominis. The larger adult female is less than 0.5 mm in diameter and is white to translucent in color. Scabies is an obligate human parasite. Survival time away from the skin at room temperature is 24 to 36 hours.2 The adult female mite burrows into the stratum corneum where she mates with the male, deposits eggs, and then dies. The burrow, which is not restricted to the stratum corneum, is lengthened by 2 mm to 3 mm per day. Larvae hatch, bore out of the burrow, dig short molting pockets, and eventually develop into adult mites. The entire life span is 4 to 6 weeks. The mites prefer areas on the skin with relatively low density of pilosebaceous units. Thus, the face and scalp often are spared. In the common form of the infestation, there are only 10 to 15 female mites on the body at one time, in the crusted, or Norwegian, variant, at least hundreds of mites are present.3

Epidemiology

Scabies is found worldwide and spares no age, race, or socioeconomic strata. Cyclic variations in incidence have prompted theories regarding herd immunity. Scabies may confer a degree of immunity individually, both cell-mediated and humoral, although a protective effect is controversial. Thus, pandemics could arise with the emergence of an underimmune generation. Many other factors (eg, crowded living conditions, poor hygiene, and sexual promiscuity) may play a role in these pandemic cycles.3

Close contact with infested individuals is needed for transmission in the common form. Children and young adults are affected more often. Household member contact is important, whereas contact with children in school does not appear to play an important role in transmission. Infants less than 2 years of age have the highest incidence, a result of frequent handling by infested adults and older children.4 In young adults, scabies is frequently a sexually transmitted disease. Fomitic transmission from clothing or bed linen appears to play only a minor role.

Transmissibility also is related directly to mite numbers. Infestation can occur with casual and brief contact with an individual with crusted scabies.5 The skin debris from such patients contains numerous mites protected from desiccation, thus prolonging mite survival away from the skin for up to 10 days. Hospital and other institutional outbreaks have resulted from unrecognized cases. Crusted scabies is found in those with an altered response or appreciation of the mite on their skin. This includes those with the physical inability to scratch (eg, paresis or physical debilitation), those with a suppressed or altered sensation of pruritis (eg, neuropathy or dementia), or those with an altered immune response to the mite (eg, patients with acquired immunodeficiency syndrome [AIDS] or transplant patients on immunosuppressive drugs). For unclear reasons, crusted scabies also has a predilection for those with Down syndrome and mental retardation.

Clinical Presentation

Like all ectoparasites, itching is the most common presenting complaint in scabies. Interestingly, pruritus is minimal or absent in crusted scabies. Pruritus is more intense while in bed and when the patient is warm, although this pattern of itching is not specific to scabies. Infants may express severe pruritus as increased irritability.4

Pruritus and clinical lesions are related to allergic sensitization, Ukely to be antigens in the mite's saliva or mouth parts.5 Symptoms begin at least 3 to 4 weeks after the initial infestation, during which time sensitization occurs. Reinfestation soon after a cure initiates a brisk response.

Figure 1. Scabies infestation in an infant.

Figure 1. Scabies infestation in an infant.

The classic lesion of scabies is the burrow of the female mite. This is generally less than a centimeter long, irregularly linear, and dirty appearing. If found, it is considered pathognomonic. However, burrows are uncommon or absent in many cases. Further, secondary changes from excoriation may render them unidentifiable. The eroded red papule, 1 mm to 2 mm in diameter, is a more common lesion. Inflamed nodules and vesicles, particularly on the palms and soles, may be seen.

Secondary lesions may dominate the picture and are important to recognize. These include linear excoriations, eczematous changes (wider erythema with weepiness and scaling), secondary bacterial infection, and scarring. Corticosteroid use, either topically or systemically, is not uncommon owing to misdiagnosis and leads to less inflammation and pruritus, and an unusual distribution and extent of lesions.6

The distribution of lesions in older children is similar to that in adults. The head and neck tend to be spared, although exceptions to this, particularly in warmer climates, are found. The periaxillary areas, periareolar areas, abdomen, buttocks, thighs, wrist creases, finger web spaces, ankles, insteps of the feet, and in the male, the external genitalia are common sites of predilection. Lesions tend to be symmetric.

Scabies in infants and small children has notable differences.4 Generalized involvement, including head, neck, palms, and soles, is much more common (Figure 1). Papules and vesiculopustules are the typical primary lesions. Scabietic nodules are seen frequently. Bullae and bullous pustules are uncommon and usually indicate secondary bacterial infection by staphylococcus. Neonates, due to ineffective motor and immature immune responses, tend to have increased numbers of mites with diffuse involvement. Eczematization occurs and often confuses the picture.7 Poor feeding and failure to thrive may result.

Figure 2. Female scabies mite with eggs and feces. (Photo courtesy of Robin L. Hornung.)

Figure 2. Female scabies mite with eggs and feces. (Photo courtesy of Robin L. Hornung.)

In crusted scabies, the mite burden is enormous, unchecked by limited physical or immunologìcal responses. Pruritus is often absent, although it can be severe. Warty aerai hyperkeratosis with nail thickening and a generalized papular eruption or diffuse erythema with scaling describes the typical case.5 Fortunately, this is rare in children, although it has been described in a child with AIDS,8 in one after bone marrow transplantation, and in one with presumed psoriasis but no underlying immune deficiency.

Diagnosis

A high index of suspicion of any pruritic skin rash is key in recognizing scabies. Demonstration of mites, eggs, or feces is definitive. More recent appearing papules or burrows with minimal excoriation are the best lesions to scrape. A drop of mineral oil is first placed on a glass slide, and the edge of a no. 15 blade is dipped into the oil. This allows adherence of scrapings to the blade. Several lesions should be scraped, wiping the blade off in the oil on the slide after each lesion. A cover slip is placed over the slide, which is scanned under low power (Figure 2). If no mites or their products are seen and the clinical suspicion is high, one should scrape again in several different areas. If still negative, other possible causes of the rash need be considered. If the clinical picture is classic, but the mineral oil prep unrevealing, one may consider a therapeutic trial of a scabicide.

The differential diagnosis of scabies in the pediatrie population includes: atopic dermatitis, other arthropod bites, contact dermatitis, pyoderma, pruritus due to underlying systemic disease, pediculosis, drug eruption, histiocytosis X, and acropustulosis of infancy.4

Treatment

Management of scabies should be directed toward treatment of the patient and control of reinfestation. One percent gamma benzene hexacholoride or Iindane (Kwell, Reed & Camrick, Jersey City, New Jersey), a mainstay of scabies therapy, has largely been replaced by 5% permethrin (Elimite, Herbert Laboratories, Irvine, California).9 Systemic toxicity has been associated with Iindane in infants, and neurotoxicity has been described after accidental ingestion of the drug. Additionally, there are reports of resistance to Iindane in cases that subsequently responded to permethrin.10 Clinical efficacy of a single application of permethrin was higher compared with Iindane or crotamiton (Eurax, Westwood-Squibb Pharmaceuticals Ine, Buffalo, New York) cream. Crotamiton usually requires more than one application and is not considered a highly effective scabicide.9 Table 1 gives details of prescribing and using permethrin 5% and Iindane.

Simultaneous treatment of close contacts within the last month, including babysitters, day-care workers, all household members, and in sexually active patients, sexual partners (whether symptoms exist or not), is recommended to prevent reinfestation. Underwear, sleepwear, and bed sheets should be laundered in hot water and dried on a hot cycle.11

Adjunctive use of antihistamines (diphenhydramine or hydroxyzine) and topical hydrocortisone 1% is recommended when pruritis is significant. "Hie patient should expect pruritus for up to several weeks posttreatment. Antibiotics generally are not needed when secondary infection is localized; this will clear with scabicidal therapy and antipruritics. Staphylococcal and streptococcal coverage is indicated for wider area infection, for bullous impetigo, and especially if fever accompanies secondary infection. Antibiotics to consider include dicloxaciflin, cephalexin, or erythromycin.

PEDICULOSIS

Etiology

Two species of lice, Prfurus pubis (the crab or pubic louse) and Pediculus hummus, which includes the subspecies copias and humanus (head and body lice), cause the three variations of infestation collectively known as pediculosis.

Head and body lice are morphologically identical and are capable of interbreeding, but prefer separate territories.3 The larger female measures 3 mm to 4 mm and is grayish in color. Ttie eggs, or nits, are slightly less than 1 mm and are cemented to the base of scalp hair or ¿lothing fibers. The body louse lives most of its life on clothing, only crawling onto skin to feed.

The pubic louse, distinct in appearance with its broad, brownish body and larger grasping claws, is well designed to move from hair to hair in areas of particular hair density and thickness. This includes not only the pubic hair, but also the beard, axillary hair, eyelashes, and eyebrows. Scalp margin and, in one infant, generalized scalp involvement have been described.12 In contrast to head and body lice, which move quite ably while off the skin, pubic lice move poorly away from their habitat.

Table

TABLE 1Scablcldes

TABLE 1

Scablcldes

Lice live for 5 to 6 weeks, with the adult female laying 5 to 10 eggs per day. Nymphs hatch in 8 days and mature in 10 days. Survival time away from the host is up to 10 days for head and body lice and 1 day for the pubic louse. All lice feed directly from dermal blood vessels using penetrating and sucking mouth parts.

Epidemiology

Pediculosis Capitis, The head louse is found worldwide and in all races. Curiously, North American blacks are rarely infested, although African and South American blacks are susceptible. This may have to do with the adaptation of the African and South American varieties of head louse to grasping the oval cross section of Negroid hair.3

Transmission is usually from direct head to head contact. Sharing of combs, brushes, and hats probably also play a role. Overcrowded living conditions, including in schools, contributes most to transmission. Poor hygiene does not appear to be a factor. School-aged children are the most frequent hosts, and girls are more commonly infested than boys. The prevalence in US schools is estimated at 10% to 40%. 13 Incidence is higher in late summer and early fall.

As with the other human lice species, there is no acquired immunity, and the phenomenon of herd immunity is not seen. In contrast to scabies, immune suppressed individuals are not more susceptible and do not manifest the infestation with unusual severity.

Pediculosis Corporis. Body lice also are distributed worldwide. In developed countries, the prevalence is highest in the homeless population. Both overcrowding and poor hygiene, particularly in changing and laundering clothing, contribute to transmission and maintaining a suitable habitat.13 The body louse can serve as a vector for transmission of epidemic typhus, trench fever, and relapsing fever.

Pubis. Infestation by pubic lice is primarily a sexually transmitted disease. In children without pubic or axillary hair, these lice can be found in eyelashes, eyebrows, and scalp margins. Infestation in children is a result of close, although not necessarily sexual, contact, usually with a parent.12 Sexual abuse has been identified in cases.

Clinical Presentation

As with scabies, itching is the most common presenting symptom with infestation by lice. Patients, parents, or school officials often have identified visible lice or nits before coming to the clinician. Secondary lesions of excoriations or bacterial infection may dominate the picture. The pruritus is due to allergic sensitization to louse salivary antigens, which takes 8 to 10 days to develop.6 Characteristics of the variants of pediculosis are described below.

Pediculosis Capitis. Scalp pruritus is present in sensitized patients. Nits are cemented at the base of the hair close to the warmer scalp surface (Figure 3). Nits can look like dandruff or hair casts. The main difference is nits are difficult to remove with the fingertips. The nape of the neck commonly will show pruritic papules. Posterior auricular and posterior cervical nodes are not infrequent.

Pediculosis Corporis. Infested hosts experience itching, particularly at night. Persistent scratching can result in lichenification and hyperpigmentation known as "vagabond's skin."13 Lice and nits are uncommonly found on the skin. However; inspection of clothing, particularly in seams, will reveal both.

Pediculosis Pubis. Nighttime itching again is the most common symptom. Lice often are identified clinging to the base of hairs. Nits and reddish feces also may be seen. Bluish macules (maculae ceruleae) may develop and are felt to be due to the bite of the pubic louse, although their pathogenesis is unclear.3 In the children of adult patients with pubic lice, eyelash involvement may occur. It is estimated that a third or more of sexually active patients with pubic lice will have a second sexually transmitted disease.14 A thorough sexual history and examination is essential.

Figure 3. Numerous nits in pediculosis capitis. (Photo courtesy of Galloway Collection, Duke University Medical Center.)

Figure 3. Numerous nits in pediculosis capitis. (Photo courtesy of Galloway Collection, Duke University Medical Center.)

Figure 4. Close up of nit, with emerging nymph, cemented to hair shaft. (Photo courtesy of Robin L. Hornung.)

Figure 4. Close up of nit, with emerging nymph, cemented to hair shaft. (Photo courtesy of Robin L. Hornung.)

Diagnosis

Close inspection, enhanced with a hand lens, will identify lice or nits (Figure 4). The differential diagnosis includes eczema, seborrheic dermatitis, and urticaria.

Treatment

General Measures. Pediculosis, like scabies, is a household and community illness. Treatment needs to be directed toward the patient, his or her personal effects (including clothing and bed linen), and his or her contacts. Machine washing and hot cycle drying clothes and bed sheets is effective for killing lice and nits living off of the patient. Often, this is all that is required for the treatment of pediculosis corporis. There is no evidence to support routine environmental cleaning with a pediculocide or other insecticide.2 The exceptions are cleansing wigs, hairbrushes, and combs used by a patient or contacts of a patient with pediculosis capitis. Treatment of close contacts, in contrast to scabies, should be directed by the presence of lice or nits.

Pediculocides. A number of pediculocides are available (Table 2); some of the more effective ones can be purchased over the counter. Gamma benzene hexachloride (lindane) 1% shampoo had long been the drug of choice for head lice. In recent years, however, evidence of resistance, frequent need of a second application, and potential toxicity from frequent use or accidental ingestion have placed lindane below more effective and safer products.13

One of these is permethrin 1% (Nix, Burroughs Wellcome Co, Research Triangle Park, North Carolina). It is formulated in a creme rinse and used after regular shampooing, left on for 10 minutes, then rinsed off. Although PDA-approved for treatment of head lice only, it also can be used for pubic lice. Repeat treatment for the latter may be required 1 week later. Repeat treatment for head lice is generally unnecessary. Permethrin 1% is safe for use in pregnant or lactating women and in infants.

Pyrethrins with piperonyl butoxide (Rid Shampoo [Pfizer Consumer Health Care, Parsippany, New Jerseyl, R&C Shampoo [Reed & Camrick, Jersey City, New Jersey], A-200 Shampoo [SmithKline Beecham Consumer Brands, Pittsburgh, Pennsylvania], and others) is also a safe product with pediculocidal and ovicidal effects. Comparative trials, however, show lower efficacy than with permethrin.13 Second applications are recommended. Shampoos and lotions are available.

Malathion 0.5% (Ovide, Gen Derm, Lincolnshire, Illinois in the United States) has long been used in the United Kingdom for all types of lice infestation. Its efficacy is similar to lindane and pyrethrins. Its disadvantage is the need to leave it on for 8 to 12 hours.

All pediculocides should be avoided on eyelashes. Application of petrolatum 3 to 4 times a day for 8 to 10 days is effective. Nit removal is also effective, but is painful and therefore not practical in small children.

Treatment of Nits. In general, effective killing of lice treats most, though not alt nits. Viable nits contribute to pediculocide treatment failures. Of the above pediculocides, only permethrin appears to be effectively ovicidal after a single treatment. The others often require a second application to kill newly hatched nymphs and remaining nits. Once treated, nonviable nits eventually fall off after regular interval shampooing. However, many schools will not allow children who have been treated for lice to return to school if nits, even dead ones, are still present.15 Nit combs are included with most pediculocides, although complete mechanical removal of nits is difficult. A solution of vinegar may be used prior to nit combing to help dissolve the bonding substance of the nit. A creme rinse containing formic acid (Step 2, Gen Derm, Lincolnshire, Illinois) is available and when used immediately after the pediculocide appears to enhance mechanical removal.16

Table

TABLE 2Pedlculocldes

TABLE 2

Pedlculocldes

CERCARIAL DERMATITIS

Aiso known as swimmer's itch, cercarial dermatitis is caused by nonhuman schistosomes in which humans are accidental and dead-end hosts.17 Of three types of cercarial dermatitis, only two are seen in the United States, rreshwater or sea birds are the natural definitive hosts, and species of snails are the intermediate hosts. The free-swimming cercariae, the larval forms of the adult fluke, prefer warm shallow water with abundant aquatic vegetation that harbors the snails.

The cercariae bore into the exposed skin of bathers. Initially, a tingling sensation is felt by the bather for approximately 1 hour after swimming. Faint erythema may be present. The cercariae die within a day in the epidermis or superficial dermis and elicit a delayed hypersensitivity response. A pruritic papular, vesiculopapular, or urticarial rash ensues after 1 2 hours and may last up to 2 weeks. Resolution is spontaneous, and the only potential complication is secondary bacterial infection. Associated eosinophilia, as might be seen in invasive schistosomiasis, has been reported.

The differential diagnosis includes scabies, Rhus (poison ivy or poison oak) or other contact dermatitis, arthropod reactions, and seabather's eruption (below). The distribution and swimming history should easily distinguish swimmer's itch.

Figure 5. Wandering track of cutaneous larva migrane or creeping eruption. (Photo courtesy of Galloway Collection, Duke University Medical Center.)

Figure 5. Wandering track of cutaneous larva migrane or creeping eruption. (Photo courtesy of Galloway Collection, Duke University Medical Center.)

Other than symptomatic relief with antihistamines and treatment of secondary infection, no treatment is necessary. Topical and even systemic corticosteroids have been used for extreme pruritus with rash. Prevention is accomplished by avoiding known infested waters. Application before swimming of niclosamide lotion, an antihelminthic and molluscicide, has been used.

SEABATHER'S ERUPTION

Although technically not an ectoparasite, seabather's eruption or "sea lice" may have a variety of causes, including jellyfish larvae and toxic algae, and often is confused with cercarial dermatitis.18 In contrast to swimmer's itch, seabather's eruption usually occurs underneath the bathing suit. Otherwise, the lesions are similar. A rash occurs 4 to 24 hours after ocean exposure. Spontaneous resolution occurs within 1 to 2 weeks. Treatment is generally not necessary. Antihistamines and judicious use of topical steroids (1% hydrocortisone) may provide symptom relief Prompt removal of the bathing suit and showering with fresh water may prevent stings from trapped jellyfish that have not discharged their nematocysts.

CREEPING ERUPTION

Cutaneous larva migrans is another term for this migrating rash caused by the larval form of several nematode (round worm) species.19 The most common in the United States (primarily central and southeast) is Ancylostoma brazjiiense, the dog hookworm. Humans are accidental and dead-end hosts. Ova in dog feces hatch into infective larvae, which penetrate bare skin, typically feet, hands, and buttocks. Moist, warm sandy soil in shaded areas, for example a child's sandbox, is the typical habitat for the larvae. After a variable amount of time, localized pruritus develops. Soon thereafter, a wandering, serpentine erythematous line a few millimeters wide and advancing a few to several millimeters per day develops. Vesicles and subsequent crusting along the track are typical. Several larval tracks may occur simultaneously and tend to remain within a localized area (Figure 5).

Creeping eruption usually resolves within 1 month, but the course is variable. Eosinophilia and pulmonary infiltrates with eosinophilic sputum (Loffler's syndrome) can complicate creeping eruption.

Treatment is with either topical or oral thiabendazole (Mintezol), a suspension of 500 mg/cc applied twice daily for 5 to 10 days or 22 mg/kg given orally twice daily for 5 days, respectively.

REFERENCES

1. Matkel EK, Voge M, John DT. Metal :Parasitology. Philadelphia. Pa: WB Saunders Co; 1992.

2. Blondell RD. Parasites of the skin and hair. Prim Care. 1991; 18:167-183.

3. Bums DPi. Diseases caused by arthropods and other noxious animals. In: Champion RH, Burton JL, Ebling F]G, eds. Textbook of Dermatology- London, England: Blackwll Scientific Publications; 1992:1265-1324.

4. Palier AS. Scabies in infants and small children. Semin Dermtool. 1993:12:3-8.

5. O'Donnell BF, O'Loughlin S, Poweil FC. Management of crusted scabies. Iiu ] Deimaiol. 1990; 29:2 58- 266.

6. Orkin M, Maibach H. Scabies. In: Holmes KK. Mardh P-A, Sparling PF, Wiesner PJ, eds. Senuilti Transmitted Diseases. New York, NY: McOraw-Hil! Book Co; 199O473479.

7. Sterling GB, Janniger CK, Kihiczak G. Neonatal scabies. CHOJ. 1990:45:229-231.

T. Jucowics P, Ramon ME, Don PC, Scone RK, Bamji M. Norwegian !cables in an infant with acquired immunodeficiency syndrome. Arch Dermoidi. 1989; 125:16701671.

9. Otkin M. Maibach HI. Scabies therapy- 1993. Semin Dermotol. 1993:12:22-25.

10. Purvis RS, Tyring SK. An outbreak d" lindane-resislant scabies treated successfully with petmeihnn 5% cream. } Am Acad Dermatd. 1991;25:1015-1016.

11. Centers for Disease Control and Prevention. 1993 sexually transmitted disease guidelines. MMWK. 1993;42:94-97.

12. Silburt BS, Parsons WL Scalp Infestation by Phthina pubis in a 6-week-old infent. Pediair Dermata. 1990:7:205-207.

13. Meinking TL, Taplin D. Advances in pediculosis, scabies, and orhec mite infestations. AAi Dermaul. 1990:5:131-152.

14- Felman YM, Nikitas JA. Sexually transmitted diseases: pediculosis pubis. Cuto. 1980;25:482-489.

15. Parish LC, Witkowski JA, Millikan LE Pediculosis capitis and the stubborn nit. Int J Dermtuol. 1989;64:69-70.

16. DeFelkeJ, Rumsfield J, Berstein JE, et al. Clinical evaluation of an arter-pediculocide nit removal system. Im } DermoioJ. 1989;28:468-470.

1 7. Chapman A, Ekeland C, Tominaga J. Rash and pruritis after a camping trip. PEOKUT In^rtDis }. 1993;! 2:966-969.

18. Tomchik RS, Russell MT, Szmant AM, Black NA. Clinical perspectives on seabathers eruption, also known as 'sea lice.' JAMA. 1993;269:1669-1672.

19. Davies HD, Sakuk P, Keystone JS. Creeping eruption: a review of clinical presentation and management of 60 cases presenting to a tropical disease clinic. Arch Dermofd. 1993;! 29:588- 591.

TABLE 1

Scablcldes

TABLE 2

Pedlculocldes

10.3928/0090-4481-19940801-10

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