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OTHER CHILDHOOD VIRUSES

Hand, foot, and mouth disease

Hand, foot, and mouth disease is a common vesicular eruption in children and is primarily caused by coxsackievirus A16 but also by enterovirus 71. Gray-white oval vesicles, 3–8mm in diameter, on an erythematous base occur on the hands, feet, mouth, and buttocks (Figs 25.15 – 25.17). Young children are usually affected. Epidemics are common. One can try to culture the causative virus from the mouth, skin, or feces. Rarely, fatalities may occur (e.g. from interstitial pneumonitis, myocarditis, and encephalitis). No treatment is needed.

Figure 25.15 Hand, foot, and mouth disease. This viral infection (usually by coxsackievirus A16) of young children can produce 3–8-mm, gray-white, oval vesicles on the hands, feet, mouth, and buttocks.

Figure 25.16 Hand, foot, and mouth disease. Aphthae-like erosions occur in the mouth..

Figure 25.17 Hand, foot, and mouth disease. Silver-gray vesicles on the dorsal foot.

Figure 25.18 Chicken pox.

PRACTICE POINTS

Chicken pox

Etiology and pathogenesis

Chicken pox results from infection by the varicella zoster virus. Children are affected primarily, but the introduction of a vaccine has greatly reduced its incidence in developed countries. Because the vaccine is a live attenuated virus, immunocompromised patients should not be vaccinated. The best approach for them is to ensure that their close contacts have either had chicken pox or have received the vaccine. Breakthrough disease (defined as vaccinia >42 days after vaccination) does occur and is more likely in individuals who were vaccinated more than 4 years before exposure. Luckily, breakthrough disease is milder and less contagious than the wild type.

    Herpes zoster may also occur in children, even in infants, but is much less common than in adults and is discussed later in this chapter.

Clinical

Crops of several to hundreds of vesicles, each like a drop of water on an erythematous base, on the trunk, face, extremities, and oral mucosa, are characteristic (Fig.25.18). Headache, malaise, and fever may accompany the rash. The incubation period is 14–21 days. Lesions may heal, leaving depressed pox scars. The vesicles turn gray, pustular, then scabbed, with lesions at different stages being apparent over a period of days.

    The most severe complications of varicella in children that lead to death are secondary bacterial infections and pneumonia. Fever, localized swelling, or cellulitis after 2 days of varicella may indicate invasive group A streptococcal disease. Bullous impetigo may occasionally complicate chicken pox.

    Systemic involvement is more common in adults and may consist of pneumonia, hepatitis, glomerulonephritis, encephalitis, and arthritis. Maternal infection during pregnancy can cause severe damage to the fetus. Deaths in adults from chicken pox still occur.

Differential diagnosis

This is the differential diagnosis of a vesicular eruption in a child (Table 25.2).

Treatment

Adult patients benefit from aciclovir or its analogs if started within 24 – 48h of the onset of the rash. There is benefit to children if given within 24h of onset, but it is much less dramatic, as chicken pox is usually milder at this age. However, neonates, and immunosuppressed patients at any age, should be treated. Soaks to remove the crusting and acetaminophen (not aspirin, which runs the risk of Reye syndrome) are helpful. Aciclovir (40–80mg/kg per day given four times a day to infants and children exposed to chicken pox) greatly decreases or prevents the development of fever and vesicles but does not prevent seroconversion in the majority of cases.

    Varicella zoster immune globulin is recommended for postexposure prophylaxis in susceptible persons at risk and is effective if administered up to 96 h after exposure.

Herpes gingivostomatitis

Herpes labialis is extremely common in the general population (see later discussion of adult viral infections). Herpes gingivostomatitis refers to the initial infection of the lips and mouth by herpes simplex virus (HSV) (Fig.25.19); this primary infection usually occurs in childhood. HSV-1 is the predominant pathogen.

    Diffuse crusting and vesiculation of the lips or the oropharynx of a child is most typical. Fever and lymphadenopathy may occur. Some episodes are very mild and may be confused with aphthae or with hand, foot, and mouth disease; extensive oral mucous membrane herpetic infection may be difficult to distinguish clinically from Stevens–Johnson syndrome. Recurrent outbreaks may develop later, as later described under the heading Herpes labialis .

    Oral antiviral agents may be used for treatment (see Table 25.5 for dosages). Soaks twice daily to reduce crusting are helpful. Petrolatum or an antibiotic ointment locally will decrease crusting and pain, and speed healing.

Molluscum contagiosum

Etiology and pathogenesis

The molluscum contagiosum virus (MCV) is the last remaining member of the Poxviridae family to specifically infect humans. MCV is a large, brick-shaped virus that contains double-stranded DNA. Extensive large lesions may occur in patients with HIV infection. They may be widespread and therapeutically difficult in atopic eczema. Additionally, several case reports describe the development of multiple mollusca in eczematous skin treated with tacrolimus. Swimming in pools is correlated with incidence. Those lesions on the lower abdomen in adults may be transmitted during sexual contact, but genital lesions in children are innocently obtained in most cases.

Figure 25.19 Herpes gingivostomatitis. These lesions can be extremely painful. Oral antiviral therapy is indicated.

Clinical

Grouped, pink to flesh-colored, smooth papules with a central dell, most visible during cryotherapy, are characteristic (Fig.25.20). In children, they may occur anywhere, although the groin, buttocks, and larger flexures are often the main site. In an adult, the lower abdomen, groin, and penis are characteristic sites. In HIV-positive patients, who commonly develop these papules, the face and beard area are especially involved. Eczematous changes may occasionally (or annular erythema rarely) surround the lesions (Fig.25.21). Lesions on the eyelid may cause a significant conjunctivitis. Transmission seems to be significantly enhanced by mechanical trauma (e.g. scratching or shaving).

Figure 25.20 Molluscum contagiosum papules are pink to flesh-colored and smooth with a central dell (brought out nicely during cryotherapy). Affected children often have a history of spending much time in the swimming pool. (a) Note the linearity. (b) Close-up showing the characteristic whitish areas.

Figure 25.21 Molluscum with eczema. Eczematous changes are common around molluscum lesions. They often occur a few weeks before the lesions resolve, except in patients with atopic dermatitis.

Figure 25.22 Eczema herpeticum.

Differential diagnosis

These lesions are usually readily diagnosed but may be confused with the following.

Treatment

Treatment is often not needed in this benign disease, the normal course of which is spontaneous resolution. Treatment is appropriate if the lesions are limited and the patient both wishes and seems able to tolerate therapy. However, conservative observation may be best for younger children or the child with hundreds of lesions.

    One simple approach is to have the parent wrap clear tape around a finger, with the sticky side out, and to press against each lesion 20 times. This can, in a painless manner, tape-strip out the core. Another painless approach is to apply cantharidin in the doctor's office (e.g. every 2–3 weeks) and have the parent wash it off 1–4h later. Blisters at each site will result. Curettage is also highly effective, but the young child may tolerate it poorly. EMLA, applied and occluded for an hour before curettage, is especially helpful with young children (don't let them watch!). Cryotherapy (e.g. every 2 weeks) works well for the older child or the adult. The use of an otoscope cone helps focus the spray. Imiquimod applied topically three times per week cleared a significant proportion of subjects in one study.

PRACTICE POINTS

^aThis is a partial list, as over 100 human papillomavirus types have been identified.

Figure 25.23 Multiple warts in the beard area. This is often a difficult clinical problem, as shaving spreads the warts during treatment and destructive measures must be used with caution on the face. Often curettage after local infiltration with lidocaine performed every 2–3 weeks is effective.

Eczema herpeticum

Multiple eroded lesions on the face and neck are common in eczema herpeticum, which represents herpes simplex infection of eczematous skin (Fig. 25.22). Occasionally, other skin conditions may become secondarily infected by herpes simplex. For a more full discussion, see Chapter 6.

Verruca vulgaris

Etiology and pathogenesis

Warts (or verrucas) are caused by the human papillomavirus (HPV). HPV is a DNA virus that infects epidermal cells, causing hyperproliferation. Verrucous papules result. Currently, over 100 types of HPV have been identified. Although not usually identified in clinical practice, several types commonly cause specific types of warts (Table 25.3). Warts are benign, but many neoplastic lesions may result from HPV infection (e.g. cervical cancer and verrucous carcinoma).

    Children are affected primarily, and the incubation period is usually from several weeks to a month. Warts may be acquired in a variety of ways Figs 25.23 – 25.26), for example stepping on keratinaceous debris left by someone with plantar warts; autoinoculation through picking, biting, or sucking; sexual transmission of anogenital warts; maternal–neonatal transmission during delivery; hand-holding or touch during playing, for common warts; and autoinoculation via shaving the beard in men or the legs in women. Immunosuppressed patients may be plagued by many large warts (Fig. 25.27).

Clinical

Common warts appear as solitary or multiple hyperkeratotic or verrucous papules on the hands or fingers of children and adolescents. The normal skin lines are obscured. Periungual lesions (Fig. 25.28) are common in children, and if they depress the nail matrix, a groove in the nail plate may result. Subungual lesions may lift the nail (Fig. 25.29). Autoinoculation (often erroneously termed koebnerization) may be seen, with linear lesions occurring in the path of a scratch. Occasionally, warts will regress spontaneously, presumably as a result of attack by the body's immune system. In that case, the wart will turn black and necrotic, and fall off within several weeks (Fig. 25.30).

Figure 25.24 Verruca vulgaris. Solitary or multiple hyperkeratotic or verrucous papules on the hands or fingers of a child or adolescent are characteristic. The normal skin lines are obscured. In this patient, the wart probably appeared on the finger first and then spread to the lip.

Figure 25.25 Multiple warts on the face.

Figure 25.26 The shaved legs of teenage women are commonly affected by flat warts. The razor seems to spread the infection. Tiny papules around many of the hairs are seen.

    Flat (plane) warts appear as tan, brown, or pink, flat-topped papules. They often resemble nevi (Fig. 25.31). Sometimes, they cover the legs of a woman who shaves her legs (see Fig. 25.26); they are also common on the face in children.

    Most warts are exophytic (grow outward), but plantar warts are endophytic (grow inward) because the pressure of walking drives them into the sole (Fig. 25.32). These lesions must be distinguished from corns and may be removed by paring with a sharp blade. Paring a wart reveals black dots, whereas paring a corn reveals a translucent center (Figs 25.33 and 25.34). An area of multiple, confluent plantar warts has been termed a mosaic wart.

Figure 25.27 Multiple verrucas in an immunocompromised patient.

Figure 25.28 Periungual warts about the nails are common in children. Their presence may depress the matrix, causing a groove in the nail. Care must be taken to not damage the matrix when treating such verrucas, else permanent damage to the nail may result.

    Condyloma on the anogenital mucosa may be filiform or verrucous (Fig. 25.35). Perianal lesions can become quite large. Condyloma acuminatum and bowenoid papulosis are discussed in Chapter 20.

    Some lesions appear more like seborrheic keratoses. Filiform warts have multiple tiny projections and resemble a horse's tail (Fig. 25.36). The development of warts in the shape of a circle (doughnut wart) or semicircle (Fig. 25.37) may follow cryotherapy. Multiple lesions may proliferate in the immunocompromised patient (see Fig. 25.27).

Figure 25.29 Subungual wart lifting the nail. The differential diagnosis should include squamous cell carcinoma or keratoacanthoma. Rarely, an amelanotic melanoma will be confused as a wart of the nail. If there is any question of the diagnosis, or the lesion resists treatment, a biopsy should be done.

Figure 25.30 Regressing wart. Spontaneous blackening of a wart is a sign of imminent regression. Erythema and pruritus may precede this color change. After turning black, as shown here on the sole, the wart just peels and falls off.

Figure 25.31 Flat warts. Also known as verruca plana, flat warts present as pink, flesh-colored, or tan, flat-topped, slightly elevated papules common on the forehead, face, dorsa of the hands, and legs. The lesions are typically caused by human papillomavirus (HPV)-3.

Differential diagnosis

See Table 25.4.

Treatment

Flat warts may not need treatment, but if indicated, a topical salicylic acid preparation applied daily, or tape stripping (as discussed earlier for molluscum contagiosum), may be employed. Topical tretinoin or benzoyl peroxide may also be tried. These interventions may have benefit merely because they irritate the wart.

Figure 25.32 Plantar wart. A hyperkeratotic, verrucous papule or plaque beneath a pressure point on the sole of the foot is characteristic. Human papillomavirus (HPV) types 1 (myrmecia), 2 (mosaic), and 4 are most common. Because plantar warts are driven into the skin by the pressure of walking or standing, they are usually the most treatment-resistant.

Figure 25.33 Paring a wart is an excellent way of differentiating it from a corn. Multiple black dots are seen, which represent thrombosed capillaries.

Figure 25.34 A pared corn shows a translucent core.

Figure 25.35 Condyloma, perianal. The possibility of sexual abuse must be considered and is more likely if the child is 3 years old or more. Younger children (as shown here) are more likely to have received the virus from the mother during pregnancy or delivery. Alternative modes of inoculation include transfer from the patient’s own hand warts or their parent’s hand warts.

Figure 25.36 Filiform warts are common on the face and neck of adults. Their shape is reminiscent of a horse’s tail.

Figure 25.37 It is not uncommon for warts to recur at the edges of cryotherapy, creating the shape of a doughnut. (The lesion pictured here perhaps resembles more a crescent roll.)

    For common warts, no intervention is often the best option, especially if the child is young and will not cooperate with any painful interventions. Topical salicylic acid preparations may be recommended to the parent. They should be applied daily for several months. Topical imiquimod is useful for genital warts but less helpful for other patterns.

    Formalin soaks (4% solution, 20 min daily, with a greasy barrier to protect the thinner skin of the toe webs) can be usefully combined with a salicylic acid gel for mosaic warts, which are generally rather unresponsive to therapy and unsuitable for destructive modalities.

    If more aggressive therapy is indicated, cryotherapy (see Chapter 5 for details of this technique) every 1–3 weeks cures 40–60% within 3 months (Fig. 25.38). Cure rates drop significantly if freezing is done every 4 weeks. One large study compared treatment performed every 1, 2, and 3 weeks and found that success correlated with the number of treatments, not the time interval. Therefore freezing every 1–2 weeks is more likely to cure the patient sooner than cryotherapy performed every 3 weeks. A single freeze–thaw cycle appears to be just as effective as two, except perhaps on the soles. It must be emphasized to the patient that one or two treatments are often not enough. The warts must be treated every 1–3 weeks until gone. This often takes five or more treatments. Because of the endophytic nature of plantar warts, paring prior to freezing is recommended. Topical salicylic acid plaster daily with paring by the patient is helpful as well. This may be done for the week prior to the next visit. Alternative destructive therapies include application of trichloroacetic or bichloroacetic acid, or the blistering agent cantharidin (Fig. 25.39).

Figure 25.38 (a) Wart with black dots in a characteristic place, characteristic because the virus is often acquired by stepping on it barefoot. (b) Cryotherapy of wart. Note that the patient needs to accept a series of freezings: one is usually not enough.

Figure 25.39 Cantharidin is a blistering agent that may be painlessly applied to the child’s wart in the office. Unfortunately, koebnerization and spreading of the wart occasionally occur, as shown here.

    If this approach fails, the following options may be employed. Blunt dissection (surgical removal) of warts was more common prior to the introduction of laser therapy. Nowadays, the CO₂ laser is used to bloodlessly remove the wart. A small scar may result. Alternatively, the pulsed dye laser has also been used in some cases. Intralesional bleomycin may be used for plantar warts. The area should be scrubbed initially with chlorhexidine or povidone–iodine to prevent subsequent infection. The procedure is quite painful, so the area is usually anesthetized with lidocaine. Bacterial lymphangitis or cellulitis may be a complication.

    Cimetidine (30–40mg/kg per day divided into three or four doses) was shown to be effective in approximately 80% of children in an open study, but a double-blind, placebo-controlled study showed no difference from placebo.

PRACTICE POINTS

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.