Common skin infections in children
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《英国医生杂志》
1 Department of Dermatology, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LE1 5WW
Correspondence to: M J Sladden m.sladden@doctors.org.uk
Introduction
Molluscum contagiosum is a common, benign, self limiting viral infection of the skin. It generally affects children and is caused by a human specific poxvirus. Infection is rare in children under 1 year of age and typically occurs in the 2-5 year age group.4 Although the prevalence of molluscum contagiosum is not known, one of six Dutch children have visited their doctor for the condition.5
Infection follows autoinoculation or contact with affected people.6 The incubation period is from two weeks to six months. The condition is more common in young children and in children who swim, who bathe together, and who are immunosuppressed. Little evidence supports the view that lesions (mollusca) are more common in children with atopic dermatitis.
Mollusca present as multiple dome shaped pearly or flesh coloured papules with a central depression (umbilication), which usually appear on the trunk and flexural areas (fig 1). They vary in size from 1 mm to 10 mm, with growth occurring over several weeks.4 In patients who are immunocompetent, lesions may persist for six to eight weeks. The mean duration is at least eight months when new lesions appear due to continuous autoinoculation.6 Resolution is often preceded by inflammation. Uncomplicated lesions heal without scarring.
Fig 1 Typical multiple dome shaped pearly or flesh coloured papules of mollluscum contagiosum, with a central depression (umbilication)
Credit: DOIA
Whether doctors should treat molluscum contagiosum is controversial. As the condition is benign and typically resolves spontaneously, treatment is usually not necessary. Advocates of treatment state that intervention speeds resolution, reduces self inoculation and symptoms, limits spread, and prevents scarring. Often there is pressure from parents to treat their otherwise healthy children because of the stigma of visible lesions.7
Summary points
Molluscum contagiosum is a common, self limiting condition
Topical salicylic acid should be regarded as first line treatment for cutaneous viral warts
Mild impetigo is effectively treated with topical mupirocin or fusidic acid for seven days
Oral antibiotics should be reserved for recalcitrant, extensive impetigo with systemic symptoms
Tinea capitis should be considered in every child with a scaly scalp as the infection is common and the presentation diverse
Tinea capitis should be confirmed by mycological analysis before an eight week course of griseofulvin is started
Treatment
Many treatments for molluscum contagiosum have been reported, including physical destruction or manual extrusion of the lesions, cryotherapy, and curettage. Treatments are painful, and there is limited evidence that they are more effective than watchful waiting. One study found no difference in resolution of lesions after extrusion of the umbilicated core compared with destruction of the lesion using phenol, although treatment with phenol produced notably more scarring.6 Acidified nitrite cream has been reported as effective and painless.8 Topical imiquimod cream may be useful in widespread or recalcitrant mollusca, but it has not been tested in controlled trials.9
A Cochrane review is under way to evaluate treatments for molluscum contagiosum. Until there is clear evidence of safety and efficacy of active intervention, we recommend watchful waiting and reassurance of patients and parents.
Viral warts
Cutaneous staphylococcal and streptococcal infections are important in children. They cause a wide spectrum of illness depending on the site of infection, the organism, and the host's immunity.14 Impetigo is a superficial skin infection characterised by golden crusts (fig 3). It is caused by Staphylococcus aureus or Streptococcus pyogenes.
Fig 3 Impetigo, showing classic golden coloured crust
Credit: DOIA
Impetigo is the third most common skin disease in children, after dermatitis and viral warts, with a peak incidence at 2-6 years of age.15 16 Lesions are highly contagious and can spread rapidly by direct contact, through a family, nursery, or class.17 The condition is more common in children with atopic dermatitis, in those living in tropical climates, and in conditions of overcrowding and poor hygiene. Nasal carriage of organisms may predispose to recurrent infection in an individual.
Impetigo can occur either as a primary infection or secondary to another condition, such as atopic dermatitis or scabies, which disrupts the skin barrier. It can be classified clinically as impetigo contagiosa (non-bullous impetigo) or bullous impetigo. Impetigo contagiosa is caused by S aureus or S pyogenes. Bullous impetigo is invariably caused by toxin-producing S aureus.
Impetigo contagiosa
Impetigo contagiosa is the most common form of impetigo. Lesions begin as vesicles or pustules that rapidly evolve into gold-crusted plaques, often 2 cm in diameter. They usually affect the face and extremities and heal without scarring. Constitutional symptoms are absent. Satellite lesions may occur due to autoinoculation.
Bullous impetigo
Bullous impetigo is characterised by flaccid, fluid filled vesicles and blisters (bullae). These are painful, spread rapidly, and produce systemic symptoms. Lesions are often multiple, particularly around the oronasal orifices, and grouped in body folds. To confirm the diagnosis and to target treatment, Gram's stain, culture, and sensitivity testing should be carried out on the exudate from lesions.
Treatment
Treatments for impetigo include topical and systemic antibiotics and topical antiseptics.18 Good evidence shows that topical mupirocin and fusidic acid are safe and effective treatments for mild impetigo.18 In mild cases they are probably as effective as oral antibiotics.18 To minimise the development of resistant organisms, use topical antibiotics that are available in cream form only, which are not available as systemic preparations.
Oral antibiotics
Oral antibiotics may be better than topical preparations for more serious or extensive disease; they are easier to use but have more side effects than topical agents. Flucloxacillin is considered the treatment of choice for impetigo.19 Macrolides, cephalosporins, and coamoxiclav are also reported to be effective, but evidence is limited because the studies have not been performed.18 Selection of systemic antibiotic is determined by factors such as local epidemiology of resistance, patients' allergy or intolerance, and proved bacterial sensitivity after microbiological assessment.
If oral antibiotics are needed, we recommend as first line treatment a seven day course of flucloxacillin. In cases of allergy to penicillin, erythromycin (or similar macrolide) is suitable, but in some patients this causes gastrointestinal disturbance, and resistance to erythromycin is increasing. For impetigo caused by erythromycin resistant organisms, cephalosporins such as cephalexin are effective, although 10% of patients who are sensitive to penicillin are also sensitive to cephalosporins. Coamoxiclav (amoxicillin and clavulanic acid) is effective in infections caused by lactamase producing strains of S aureus. Bacteriological culture is important before changing to this drug.
Topical antiseptics
Although no clear evidence supports the role of topical antiseptics in impetigo, they do help to soften crusts and clear exudate in mild disease. In more severe cases they may be a useful adjunct to antibiotics.
We suggest using topical mupirocin or fusidic acid for seven days in clinically mild impetigo. Oral antibiotics should be reserved for recalcitrant, extensive, systemic disease.
Tinea capitis (scalp ringworm)
Hayden GF. Skin diseases encountered in a pediatric clinic. A one-year prospective study. Am J Dis Childhood 1985;139: 36-8.
Tunnessen WW. A survey of skin disorders seen in pediatric general and dermatology clinics. Pediatr Dermatol 1984;1: 219-22.
Findlay GH, Vismer HF, Sophianos T. The spectrum of pediatric dermatology. Analysis 10,000 cases. Br J Dermatol 1974;91: 379-87.
Rogers M, Barnetson RSC. Diseases of the skin. In: Campbell AGM, McIntosh N, eds. Forfar and Arneil's textbook of pediatrics. 5 th ed. New York: Churchill Livingstone, 1998: 1633-5.
Koning S, Bruijnzeels MA, van Suijlekom-Smit LWA, van der Wouden JC. Molluscum contagiosum in Dutch general practice. Br J Gen Pract 1994;44: 417-9.
Weller R, O'Callaghan CJ, MacSween RM, White MI. Scarring in molluscum contagiosum: comparison of physical expression and phenol ablation. BMJ 1999;319: 1540.
Van der Wouden JC, Gajadin S, Berger MY, Butler CC, Koning S, Menke J, et al. Interventions for molluscum contagiosum in children. Cochrane Library: 2004, Issue 2. Chichester: Wiley.
Ormerod AD, White MI, Shah SA, Benjamin N. Molluscum contagiosum effectively treated with a topical acidified nitrite, nitric oxide liberating cream. Br J Dermatol 1999;141; 1051-3.
Bayerl C, Feller G, Goerdt S. Experience in treating molluscum contagiosum in children with imiquimod 5% cream. Br J Dermatol 2003;149(suppl): 25-9.
Sterling JC, Kurtz JB. Viral infections. In: Champion RH, Burton JL, Burns DA, Breathnach SM, eds. Rook textbook of dermatology. 6th ed. Oxford: Blackwell, 1998.
Gibbs S, Harvey I, Sterling JC, Stark R. Local treatments for cutaneous warts. Cochrane Database Syst Rev 2003;(3): CD001781.
Williams HC, Pottier A, Strachan D. The descriptive epidemiology of warts in British schoolchildren. Br J Dermatol 1993;128: 504-11.
Gibbs S, Harvey I, Sterling J, Stark R. Local treatments for cutaneous warts: systematic review. BMJ 2002;325: 461.
Resnick S. Staphylococcal and streptococcal skin infections: pyodermas and toxin-mediated syndromes. In: Harper JO, A. Prose N, eds. Textbook of pediatric dermatology. Oxford: Blackwell, 2000: 369-77.
Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Ped Annals 1993;22: 235-40.
Bruijnzeels MA, van Suijlekom-Smit LWA, van der Velden J, van der Wouden JC. The child in general practice. Dutch national survey of morbidity and interventions in general practice. Rotterdam: Erasmus University Rotterdam, 1993.
Hlady WG, Middaugh JP. An epidemic of bullous impetigo in a newborn nursery due to Staphylococcus aureus: epidemiology and control measures. Alaska Med 1986;28: 99-103.
Koning S, Verhagen AP, van Suijlekom-Smit LWA, Morris A, Butler CC, van der Wouden JC. Interventions for impetigo. Cochrane Database Syst Rev 2004;2: CD003261.
Feingold DS. Staphylococcal and streptococcal pyodermas. Semin Dermatol 1993;12: 331-5.
González U, Seaton T, Bergus G, Torres JM, Jacobson J. Systemic antifungal therapy for tinea capitis in children. Cochrane Library, 2004: Issue 2. Chichester: Wiley.
Aly R. Ecology and epidemiology of dermatophyte infections. J Am Acad Dermatol 1994;31: S21-5.
Higgins EM, Fuller LC, Smith CH. Guidelines for the management of tinea capitis. Br J Dermatol 2000;143: 53-8.
Bronson DM, Desai DR, Barskey S. An epidemic of infection with Trichophyton tonsurans revealed in a twenty year survey of fungal pathogens in Chicago. J Am Acad Dermatol 1983;8: 322-30.
Fuller LC, Child FJ, Midgley G, Higgins EM. Diagnosis and management of scalp ringworm. BMJ 2003;326: 539-41.
Fuller LC, Child FC, Midgley G, Higgins EM. Scalp ringworm in south-east London and an analysis of a cohort of patients from a paediatric dermatology department. Br J Dermatol 2003;148: 985-8.
Caceres-Rios H, Rueda M, Ballona R, Bustamante B. Comparison of terbinafine and griseofulvin in the treatment of tinea capitis. J Am Acad Dermatol 2000;42: 80-4.
Fuller LC, Smith CH, Cerio R, Marsden RA, Midgley G, Beard AL, et al. A randomized comparison of 4 weeks of terbinafine vs. 8 weeks of griseofulvin for the treatment of tinea capitis. Br J Dermatol 2001;144: 321-7.
Gupta AK, Adam P, Dlova N, Lynde CW, Hofstader S, Morar N, et al. Therapeutic options for the treatment of tinea capitis caused by Trichophyton species: griseofulvin versus the new oral antifungal agents, terbinafine, itraconazole, and fluconazole. Pediatr Dermatol 2001;18: 433-8.(Michael J Sladden, specia)
Correspondence to: M J Sladden m.sladden@doctors.org.uk
Introduction
Molluscum contagiosum is a common, benign, self limiting viral infection of the skin. It generally affects children and is caused by a human specific poxvirus. Infection is rare in children under 1 year of age and typically occurs in the 2-5 year age group.4 Although the prevalence of molluscum contagiosum is not known, one of six Dutch children have visited their doctor for the condition.5
Infection follows autoinoculation or contact with affected people.6 The incubation period is from two weeks to six months. The condition is more common in young children and in children who swim, who bathe together, and who are immunosuppressed. Little evidence supports the view that lesions (mollusca) are more common in children with atopic dermatitis.
Mollusca present as multiple dome shaped pearly or flesh coloured papules with a central depression (umbilication), which usually appear on the trunk and flexural areas (fig 1). They vary in size from 1 mm to 10 mm, with growth occurring over several weeks.4 In patients who are immunocompetent, lesions may persist for six to eight weeks. The mean duration is at least eight months when new lesions appear due to continuous autoinoculation.6 Resolution is often preceded by inflammation. Uncomplicated lesions heal without scarring.
Fig 1 Typical multiple dome shaped pearly or flesh coloured papules of mollluscum contagiosum, with a central depression (umbilication)
Credit: DOIA
Whether doctors should treat molluscum contagiosum is controversial. As the condition is benign and typically resolves spontaneously, treatment is usually not necessary. Advocates of treatment state that intervention speeds resolution, reduces self inoculation and symptoms, limits spread, and prevents scarring. Often there is pressure from parents to treat their otherwise healthy children because of the stigma of visible lesions.7
Summary points
Molluscum contagiosum is a common, self limiting condition
Topical salicylic acid should be regarded as first line treatment for cutaneous viral warts
Mild impetigo is effectively treated with topical mupirocin or fusidic acid for seven days
Oral antibiotics should be reserved for recalcitrant, extensive impetigo with systemic symptoms
Tinea capitis should be considered in every child with a scaly scalp as the infection is common and the presentation diverse
Tinea capitis should be confirmed by mycological analysis before an eight week course of griseofulvin is started
Treatment
Many treatments for molluscum contagiosum have been reported, including physical destruction or manual extrusion of the lesions, cryotherapy, and curettage. Treatments are painful, and there is limited evidence that they are more effective than watchful waiting. One study found no difference in resolution of lesions after extrusion of the umbilicated core compared with destruction of the lesion using phenol, although treatment with phenol produced notably more scarring.6 Acidified nitrite cream has been reported as effective and painless.8 Topical imiquimod cream may be useful in widespread or recalcitrant mollusca, but it has not been tested in controlled trials.9
A Cochrane review is under way to evaluate treatments for molluscum contagiosum. Until there is clear evidence of safety and efficacy of active intervention, we recommend watchful waiting and reassurance of patients and parents.
Viral warts
Cutaneous staphylococcal and streptococcal infections are important in children. They cause a wide spectrum of illness depending on the site of infection, the organism, and the host's immunity.14 Impetigo is a superficial skin infection characterised by golden crusts (fig 3). It is caused by Staphylococcus aureus or Streptococcus pyogenes.
Fig 3 Impetigo, showing classic golden coloured crust
Credit: DOIA
Impetigo is the third most common skin disease in children, after dermatitis and viral warts, with a peak incidence at 2-6 years of age.15 16 Lesions are highly contagious and can spread rapidly by direct contact, through a family, nursery, or class.17 The condition is more common in children with atopic dermatitis, in those living in tropical climates, and in conditions of overcrowding and poor hygiene. Nasal carriage of organisms may predispose to recurrent infection in an individual.
Impetigo can occur either as a primary infection or secondary to another condition, such as atopic dermatitis or scabies, which disrupts the skin barrier. It can be classified clinically as impetigo contagiosa (non-bullous impetigo) or bullous impetigo. Impetigo contagiosa is caused by S aureus or S pyogenes. Bullous impetigo is invariably caused by toxin-producing S aureus.
Impetigo contagiosa
Impetigo contagiosa is the most common form of impetigo. Lesions begin as vesicles or pustules that rapidly evolve into gold-crusted plaques, often 2 cm in diameter. They usually affect the face and extremities and heal without scarring. Constitutional symptoms are absent. Satellite lesions may occur due to autoinoculation.
Bullous impetigo
Bullous impetigo is characterised by flaccid, fluid filled vesicles and blisters (bullae). These are painful, spread rapidly, and produce systemic symptoms. Lesions are often multiple, particularly around the oronasal orifices, and grouped in body folds. To confirm the diagnosis and to target treatment, Gram's stain, culture, and sensitivity testing should be carried out on the exudate from lesions.
Treatment
Treatments for impetigo include topical and systemic antibiotics and topical antiseptics.18 Good evidence shows that topical mupirocin and fusidic acid are safe and effective treatments for mild impetigo.18 In mild cases they are probably as effective as oral antibiotics.18 To minimise the development of resistant organisms, use topical antibiotics that are available in cream form only, which are not available as systemic preparations.
Oral antibiotics
Oral antibiotics may be better than topical preparations for more serious or extensive disease; they are easier to use but have more side effects than topical agents. Flucloxacillin is considered the treatment of choice for impetigo.19 Macrolides, cephalosporins, and coamoxiclav are also reported to be effective, but evidence is limited because the studies have not been performed.18 Selection of systemic antibiotic is determined by factors such as local epidemiology of resistance, patients' allergy or intolerance, and proved bacterial sensitivity after microbiological assessment.
If oral antibiotics are needed, we recommend as first line treatment a seven day course of flucloxacillin. In cases of allergy to penicillin, erythromycin (or similar macrolide) is suitable, but in some patients this causes gastrointestinal disturbance, and resistance to erythromycin is increasing. For impetigo caused by erythromycin resistant organisms, cephalosporins such as cephalexin are effective, although 10% of patients who are sensitive to penicillin are also sensitive to cephalosporins. Coamoxiclav (amoxicillin and clavulanic acid) is effective in infections caused by lactamase producing strains of S aureus. Bacteriological culture is important before changing to this drug.
Topical antiseptics
Although no clear evidence supports the role of topical antiseptics in impetigo, they do help to soften crusts and clear exudate in mild disease. In more severe cases they may be a useful adjunct to antibiotics.
We suggest using topical mupirocin or fusidic acid for seven days in clinically mild impetigo. Oral antibiotics should be reserved for recalcitrant, extensive, systemic disease.
Tinea capitis (scalp ringworm)
Hayden GF. Skin diseases encountered in a pediatric clinic. A one-year prospective study. Am J Dis Childhood 1985;139: 36-8.
Tunnessen WW. A survey of skin disorders seen in pediatric general and dermatology clinics. Pediatr Dermatol 1984;1: 219-22.
Findlay GH, Vismer HF, Sophianos T. The spectrum of pediatric dermatology. Analysis 10,000 cases. Br J Dermatol 1974;91: 379-87.
Rogers M, Barnetson RSC. Diseases of the skin. In: Campbell AGM, McIntosh N, eds. Forfar and Arneil's textbook of pediatrics. 5 th ed. New York: Churchill Livingstone, 1998: 1633-5.
Koning S, Bruijnzeels MA, van Suijlekom-Smit LWA, van der Wouden JC. Molluscum contagiosum in Dutch general practice. Br J Gen Pract 1994;44: 417-9.
Weller R, O'Callaghan CJ, MacSween RM, White MI. Scarring in molluscum contagiosum: comparison of physical expression and phenol ablation. BMJ 1999;319: 1540.
Van der Wouden JC, Gajadin S, Berger MY, Butler CC, Koning S, Menke J, et al. Interventions for molluscum contagiosum in children. Cochrane Library: 2004, Issue 2. Chichester: Wiley.
Ormerod AD, White MI, Shah SA, Benjamin N. Molluscum contagiosum effectively treated with a topical acidified nitrite, nitric oxide liberating cream. Br J Dermatol 1999;141; 1051-3.
Bayerl C, Feller G, Goerdt S. Experience in treating molluscum contagiosum in children with imiquimod 5% cream. Br J Dermatol 2003;149(suppl): 25-9.
Sterling JC, Kurtz JB. Viral infections. In: Champion RH, Burton JL, Burns DA, Breathnach SM, eds. Rook textbook of dermatology. 6th ed. Oxford: Blackwell, 1998.
Gibbs S, Harvey I, Sterling JC, Stark R. Local treatments for cutaneous warts. Cochrane Database Syst Rev 2003;(3): CD001781.
Williams HC, Pottier A, Strachan D. The descriptive epidemiology of warts in British schoolchildren. Br J Dermatol 1993;128: 504-11.
Gibbs S, Harvey I, Sterling J, Stark R. Local treatments for cutaneous warts: systematic review. BMJ 2002;325: 461.
Resnick S. Staphylococcal and streptococcal skin infections: pyodermas and toxin-mediated syndromes. In: Harper JO, A. Prose N, eds. Textbook of pediatric dermatology. Oxford: Blackwell, 2000: 369-77.
Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Ped Annals 1993;22: 235-40.
Bruijnzeels MA, van Suijlekom-Smit LWA, van der Velden J, van der Wouden JC. The child in general practice. Dutch national survey of morbidity and interventions in general practice. Rotterdam: Erasmus University Rotterdam, 1993.
Hlady WG, Middaugh JP. An epidemic of bullous impetigo in a newborn nursery due to Staphylococcus aureus: epidemiology and control measures. Alaska Med 1986;28: 99-103.
Koning S, Verhagen AP, van Suijlekom-Smit LWA, Morris A, Butler CC, van der Wouden JC. Interventions for impetigo. Cochrane Database Syst Rev 2004;2: CD003261.
Feingold DS. Staphylococcal and streptococcal pyodermas. Semin Dermatol 1993;12: 331-5.
González U, Seaton T, Bergus G, Torres JM, Jacobson J. Systemic antifungal therapy for tinea capitis in children. Cochrane Library, 2004: Issue 2. Chichester: Wiley.
Aly R. Ecology and epidemiology of dermatophyte infections. J Am Acad Dermatol 1994;31: S21-5.
Higgins EM, Fuller LC, Smith CH. Guidelines for the management of tinea capitis. Br J Dermatol 2000;143: 53-8.
Bronson DM, Desai DR, Barskey S. An epidemic of infection with Trichophyton tonsurans revealed in a twenty year survey of fungal pathogens in Chicago. J Am Acad Dermatol 1983;8: 322-30.
Fuller LC, Child FJ, Midgley G, Higgins EM. Diagnosis and management of scalp ringworm. BMJ 2003;326: 539-41.
Fuller LC, Child FC, Midgley G, Higgins EM. Scalp ringworm in south-east London and an analysis of a cohort of patients from a paediatric dermatology department. Br J Dermatol 2003;148: 985-8.
Caceres-Rios H, Rueda M, Ballona R, Bustamante B. Comparison of terbinafine and griseofulvin in the treatment of tinea capitis. J Am Acad Dermatol 2000;42: 80-4.
Fuller LC, Smith CH, Cerio R, Marsden RA, Midgley G, Beard AL, et al. A randomized comparison of 4 weeks of terbinafine vs. 8 weeks of griseofulvin for the treatment of tinea capitis. Br J Dermatol 2001;144: 321-7.
Gupta AK, Adam P, Dlova N, Lynde CW, Hofstader S, Morar N, et al. Therapeutic options for the treatment of tinea capitis caused by Trichophyton species: griseofulvin versus the new oral antifungal agents, terbinafine, itraconazole, and fluconazole. Pediatr Dermatol 2001;18: 433-8.(Michael J Sladden, specia)