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Journal of Infection (2015) xx, 1e4

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11 Update on common childhood skin infections 72
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14 Q9 Arnold P. Oranje a,b,c,*, Flora B. de Waard-van der Spek d 75
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Maasstad Hospital, Rotterdam, The Netherlands 79
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Dermicis Skin Hospital, Alkmaar, The Netherlands 80
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Intermedica Hair Clinic, Boxmeer, The Netherlands 81
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Sint Franciscus Vlietland Group, Vlietland Hospital, Schiedam, The Netherlands 82
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Accepted 23 April 2015 84
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Available online - - - 85
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KEYWORDS Summary A literature review and clinical commentary on diagnosis and treatment of com- 89
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Skin infections; mon childhood bacterial, fungal and viral skin infections is presented including impetigo, 90
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Clinical clues and tricks; folliculitis, staphylococcal scalded skin syndrome, tinea capitis, warts and molluscum conta- 91
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Resistance to antibiotics giosum. 92
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2015 The British Infection Association. Published by Elsevier Ltd. All rights reserved. 93
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Introduction differs from that in normal skin. Probably and presumably 99
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this altered microbiome plays a pathogenic role in atopic 100
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40 eczema.4 101
At birth the skin is sterile. After one day colonisation occurs
The skin of AD patients is highly colonised by Staphylo- 102
41 with bacterial, viral and fungal commensals. Per cm2
coccus aureus and other staphylococcal species persisting 103
42 100e1,000,000 microorganisms are present.1 Recently the
in areas of dry skin as well in mildly affected skin. Those bac- 104
43 human cutaneous microbiome became in much scientific in-
teria form a biofilm. The current hypothesis is that staphyloc- 105
44 terest, although Anton van Leeuwenhoek already described
coccal antigens act as super-antigens causing exacerbations 106
45 it into 1683.2 The human microbiome is an ecosystem
of eczema. Therefore, increased staphylococci coloniza- 107
46 composed of trillions of microorganisms (bacteria, yeast,
tion/infection may be responsible for flares and reducing 108
47 viruses, fungi etc.), which colonise the stratum corneum.
bacterial load may result in clinical improvement. This may 109
48 The skin microbiome and consequent biofilms interact by
also explain why regular baths of diluted bleach (sodium hy- 110
49 playing a dominant role in the occlusion of sweat ducts,
pochlorite) and intranasal application of mupirocin ointment 111
50 leading to inflammation and pruritus.3 It was reported
reduces the severity of atopic dermatitis in children. 112
51 that the microbiome or biofilm in AD, rosacea and psoriasis
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* Corresponding author. Maasstad ziekenhuis Rotterdam, Dermicis Huidziekenhuis Alkmaar and Intermedica Haar kliniek Boxmeer, P.O. 117
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Box 8176, 3015 AD, Rotterdam, The Netherlands. Tel.: 31(0)6 5331 6268. Q2 118
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E-mail address: a.oranje@inter.nl.net (A.P. Oranje). 119
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http://dx.doi.org/10.1016/j.jinf.2015.04.030 121
60 0163-4453/ 2015 The British Infection Association. Published by Elsevier Ltd. All rights reserved. 122

Please cite this article in press as: Oranje AP, de Waard-van der Spek FB, Update on common childhood skin infections, J Infect (2015),
http://dx.doi.org/10.1016/j.jinf.2015.04.030
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2 A.P. Oranje, F.B. de Waard-van der Spek

1 In this article a short overview of the common bacterial resistance, to fluoroquinolones, macrolides, clindamycin, 63
2 and other common infections of the skin is given together fusidic acid and mupirocin in S. aureus, and to macrolides 64
3 with an update of developments. and clindamycin in S. pyogenes. 65
4 Most cases of skin infections are treated by primary care 66
5 Q3 Impetigo: general aspects and resistance physicians. Clearance of S. aureus and/or S. pyogenes is the 67
6 main goal of treatment.6 In general treatment is applied 68
7 Impetigo is a common self-limiting superficial skin infection topically but uncontrolled over-the-counter use and treat- 69
8 lasting 1e3 weeks usually caused by staphylococci, less ment of ordinary wounds and minor infections promotes 70
9 frequently by streptococci or both. It mostly occurs in development of resistance to these agents. Fusidic acid 71
10 children aged 2e10 years, and sometimes in younger cream is effective against superficial infections and is often 72
11 children (particularly bullous impetigo) or older people. In first line treatment although it should not generally be used 73
12 infancy impetigo can be more serious, especially when it for longer than 10 consecutive days to reduce the risk of 74
13 occurs in the first months of life (neonatal impetigo).5 Both development of resistance. Retapumalin 2% ointment (see 75
14 primary and secondary cases occur, the latter is especially below) is effective in cases resistant to Fusidic acid cream. 76
15 common in atopic eczema, where staphylococci may play a Mupirocin 2% ointment is very effective against 77
16 triggering super-antigen role. While in moderate climates S. methicillin-resistant S. aureus (MRSA) colonisation. For 78
17 aureus is the most common pathogen, Streptococcus pyo- this reason and because there is therefore a need to mini- 79
18 genes is much more prevalent in tropical impetigo.6 mise development of resistance to it, it should be reserved 80
19 Impetigo occurs in about 1% of the children, but more for the elimination of nasal colonisation and not be used 81
20 often in tropical areas and secondary in atopic eczema. The more generally. However, mupirocin use does not always 82
21 following forms of impetigo are described: lead to emergence of resistance and an integrated under- 83
22 standing of the factors that lead to it is lacking.10 84
23 Bullous impetigo Overall current therapy of impetigo is not well stand- 85
24 ardised and there is no general agreement about guidelines 86
25 for treatment.11 The lack of evidence of superiority of oral 87
Bullous impetigo is caused almost exclusively by staphylo-
26 antibiotics over topical antibiotics may in part reflect the 88
cocci, most commonly group II, phage types 71, 3a, 3c or
27 relative absence of studies of extensive impetigo. Evidence 89
55. It can present as a few blisters (vesicles quickly
28 for the application of disinfectants in impetigo is also 90
developing in bullae and exfoliation of the skin) especially
29 lacking.8 91
in the body folds. Generalisation may occur and may
30 Local choice of drug varies in different regions. Van 92
develop into Staphylococcal Scalded Skin Syndrome (SSSS)
31 Bijnen et al. studied different national guidelines in Europe 93
(see below).7 Both conditions show a positive direct Nikol-
32 concluding that there is a lack of relevant national data on 94
sky sign (the outer epidermis separates easily from the
33 resistance.12,13 95
basal layer when slightly rubbed) in the erythematous
34 Mupirocin 2% nasal ointment is advised in the treatment 96
areas. In this clinical scenario and in contrast to other types
35 of atopic eczema combined with diluted bleach baths as 97
of impetigo, topical treatment is contra-indicated and sys-
36 maintenance treatment to diminish the staphylococcal 98
temic treatment is required, a fact which is often over-
37 load.14 In healthy adults Mupirocin nasal ointment is used 99
looked. By rubbing the skin you will induce a direct
38 for decolonisation of proven carriers. Wertheim et al. also 100
Nikolsky phenomenon making the exfoliation of the skin
39 conclude that it is less effective in decolinizing other sites 101
worse.
40 such as the perineum and pharynx.15 102
Bullous impetigo can occur in neonates, but is most
41 Retapamulin cream is a semisynthetic novel pleuro- 103
common between the ages of 2e5 years. In neonates it may
42 mutilin antibacterial that is the most recently developed 104
be life-threatening. Treatment with skin substitutes with
43 topical drug.16 It is a selective bacterial protein synthesis 105
intensive care in a burns centre is often indicated in such
44 inhibitor which interacts with the 50S subunit of the bacte- 106
cases.8
45 rial ribosome in a manner distinct from other antibiotics.17 107
46 This agent has in vitro activity against staphylococci and 108
47 Crusted impetigo streptococci resistant to other classes of agents, including 109
48 MRSA and is thought to have a low potential for develop- 110
49 Crusted impetigo is caused by staphylococci, group A ment of mutational resistance. 111
50 streptococci or by a mixed infection. It can present with 112
51 small blisters (vesicles) which quickly turn into crusts as 113
52 secondary efflorescences. The crusts are yellow and blisters Folliculitis and furunculosis 114
53 are small and break easily. Some strains of streptococci 115
54 may also infect the heart or more commonly the kidneys in Folliculitis is a common skin disorder in which hair follicles 116
55 serious infections leading to serious sequelae. Even in a become infected and inflamed. S. aureus is the commonest 117
56 small country like Holland the incidence may differ from cause but it also be due to other microorganisms, including 118
57 region to region for reasons unknown.9 fungi and yeasts, and sometimes by an inflammation from 119
58 ingrown hairs. The condition is classified as either superfi- 120
59 Therapy of impetigo cial or deep, based on how much of the hair follicle it 121
60 involves. Deep folliculitis is usually more severe. Some indi- 122
61 Treatment of superficial bacterial infections has been viduals are particularly susceptible. It may also be persis- 123
62 compromised by the development of antimicrobial tent and severe in particular in people with diabetes 124

Please cite this article in press as: Oranje AP, de Waard-van der Spek FB, Update on common childhood skin infections, J Infect (2015),
http://dx.doi.org/10.1016/j.jinf.2015.04.030
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Q10 Update on common childhood skin infections 3

1 mellitus, anaemia or MRSA carriage themselves or in other presenting as emergencies are frequently mismanaged with 63
2 family members. Treatment is the same as described for surgical incision and oral antibiotics whereas the treatment 64
3 impetigo. Pseudomonas folliculitis is a community- of choice is oral griseofulvin. 65
4 acquired skin infection associated with playing in whirl- Fungi can spread from one person to another causing 66
5 pools and hot tubs and use of nylon towels as recently clinically silent fungal carriage on the scalp and from pet 67
6 observed in Japan.18 animals to people. Avoidance of close physical contact and 68
7 sharing of personal objects, such as combs and hairbrushes 69
8 Staphylococcal scalded skin syndrome with siblings and playmates may be advisable. 70
9 71
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Staphylococcal scalded skin syndrome (SSSS) is a rare toxin- Warts and similar lesions 72
11 73
mediated skin disease caused by skin-splitting toxins of S.
12 Warts and similar lesions are very common in childhood. 74
aureus (colonization or infection). The skin is affected,
13 Human papilloma virus (HPV) causes warts and Molluscum 75
but the mucous membranes are spared. It is primarily
14 contagiosum is caused by pox virus infection. These 76
seen in infants and children younger than 5 years, but oc-
15 conditions are generally self-limiting and disappear spon- 77
curs also in adults with impaired immune status (such in
16 taneously within 3 years or less in most cases. 78
HIV infection). Usually the therapy is supportive, with
17 79
appropriate antibiotics and if skin involvement is extensive
18 80
19
such patients are often best treated at burns centres. The HPV infections (common warts and 81
mortality rate is low, but in neonates it may lead to meta- condylomata acuminata)
20 82
bolic imbalance, and skin-substitute therapy may be
21 83
extremely helpful. Baartmans et al. described 7 infants
22 Different HPV strains cause different types of warts. Four 84
with SSSS and stressed the value of skin substitutes such
23 main types of HPV-induced warts are described: Verruca 85
as Omiderm and Suprathel as adjuvant treatment.8
24 vulgaris e the common wart, plane verrucae e flat topped 86
25 warts, plantar verrucae e on the soles of the feet and 87
26 Fungal infections condylomata acuminata e or anogenital warts. 88
27 The occurrence of condylomata acuminata in a child 89
28 Superficial fungal infections of the skin and nails are raises the question of sexual abuse but common warts can 90
29 common in humans, but in children nail infections are also present in the perineal area and the condition may be a 91
30 rare, while infections of the scalp and the skin are common. result of perinatal vertical transmission, indirect trans- 92
31 There has been limited recent progress in the treatment mission through contaminated objects or surfaces, auto- 93
32 and diagnosis of these infections. Topical treatment alone inoculation, as well as sexual transmission. Available 94
33 is usually effective except when the scalp is affected. topical treatment include imiquimod, podophyllin, bi- 95
34 Diagnostic improvements are imminent for dermatophyto- chloroacetic acid and trichloroacetic acid. Surgical treat- 96
35 ses with the advent of molecular techniques for rapid ments include excision, cryotherapy and electrosurgery.20 A 97
36 identification. new treatment which shows promise is sinecatechin (green 98
37 tea).21 Intralesional treatment with mycobacterial vaccines 99
38 for condylomata acuminata has been reported.22 Wide- 100
39 Tinea capitis spread use of HPV vaccine containing anogenital wart- 101
40 causing viral types 6 and 11 may reduce circulation of these 102
41 Tinea capitis or scalp ringworm infection is caused by fungi strains in the population. 103
42 that grow into or upon hairs. It is common in young children 104
43 and very rare in adults. It is very common in temperate Molluscum contagiosum 105
44 climates, but occurs worldwide and currently it is endemic 106
45 in the UK, the Netherlands, Belgium and Germany and 107
Molluscum contagiosum, caused by a pox virus, is a very
46 probably other countries. Spontaneous cure occurs in 108
common condition affecting at least 40% of children. The
47 puberty when the sebaceous gland activity changes. Topical 109
condition is self-limiting and the standard advice usually is
48 treatment is ineffective and not recommended for the 110
to wait for the lesions to resolve spontaneously. Mild
49 management of tinea capitis because these agents do not 111
treatments consist of Dermal Honey ointment or daily
50 reach the fungi deep in the skin, around the hair follicles. 112
application of potassium hydroxide 5%. These authors
51 The treatment of choice remains oral griseofulvin, a drug in 113
have found sinecatechin (green tea) application to be
52 use since 1958; absorption is improved when taken with 114
effective although this treatment is licensed as drug for
53 fatty food and these authors recommend a high dose of Q4 115
genital warts (condylomata acuminata).
54 20 mg/kg daily for 3 months. Oral terbinafine is probably 116
55 more effective against trichophyton species and itracona- 117
56 zole is another treatment option which may be considered References 118
57 based on results of laboratory identification of the fungi.19 119
58 If left untreated, tinea capitis may develop into deep 120
59 suppurating infiltrates leading to destructing of hairs and 1. Oranje AP, de Waard-van der Spk FB. Handbook paediatric 121
60 hair follicles resulting in scarring alopecia called Kerion dermatology (original: Handboek Kinderdermatologie [dutch], 122
61 Celsi. Lesions can be associated with regional lymphade- third edition). 2009. 123
62 nopathy are often mistaken for bacterial infections. Cases 2. Anonymous. www.History-of-the-Microscope.org; 2010. Q5 124

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http://dx.doi.org/10.1016/j.jinf.2015.04.030
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1 3. Allen HB, Vaze ND, Choi C, Hailu T, Tulbert BH, Cusack CA, 13. Rumsfield J, West DP, Aronson IK. Topical mupirocin in the 34
2 et al. The presence and impact of biofilm-producing staphylo- treatment of bacterial skin infections. Drug Intell Clin Pharm 35
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7 6. Bowen AC, Tong S, Chatfield MD, Carapetis JR. The microbi- Verbrugh HA, Vos MC. Effect of mupirocin treatment on nasal, 40
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19 the incidence of impetigo. Environ Res 2009;109:590e3. 19. Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and manage- 52
20 10. Hetem DJ, Bonten MJ. Clinical relevance of mupirocin resis- ment of tinea infections. Am Fam Physician 2014;90:702e10. 53
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23 11. Koning S, van der Sande R, Verhagen AP, van Suijlekom- 250e5. 56
Smit LW, Morris AD, Butler CC, et al. Interventions for impe- 21. Karnes JB, Usatine RP. Management of external genital warts.
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tigo. Cochrane Database Syst Rev 2012;1:CD003261. Am Fam Physician 2014;90:312e8.
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12. Van Bijnen EM, Paget J, den Heijer CD, Stobberingh EE, 22. Kumar P, Dar L, Saldiwal S, Varma S, Datt Upadhyay A,
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Please cite this article in press as: Oranje AP, de Waard-van der Spek FB, Update on common childhood skin infections, J Infect (2015),
http://dx.doi.org/10.1016/j.jinf.2015.04.030