World Journal of Pediatrics

https://doi.org/10.1007/s12519-018-0150-x

REVIEW ARTICLE

Staphylococcal‑scalded skin syndrome: evaluation, diagnosis,

and management
Alexander K. C. Leung1 · Benjamin Barankin2 · Kin Fon Leong3

Received: 5 September 2017 / Revised: 22 November 2017 / Accepted: 23 November 2017

© Children’s Hospital, Zhejiang University School of Medicine 2018

Abstract
Background  Staphylococcal-scalded skin syndrome (SSSS), also known as Ritter disease, is a potentially life-threatening
disorder and a pediatric emergency. Early diagnosis and treatment is imperative to reduce the morbidity and mortality of
this condition. The purpose of this article is to familiarize physicians with the evaluation, diagnosis, and treatment of SSSS.
Data sources  A PubMed search was completed in Clinical Queries using the key terms “Staphylococcal scalded skin syn-
drome” and “Ritter disease”.
Results  SSSS is caused by toxigenic strains of Staphylococcus aureus. Hydrolysis of the amino-terminal extracellular domain
of desmoglein 1 by staphylococcal exfoliative toxins results in disruption of keratinocytes adhesion and cleavage within
the stratum granulosum which leads to bulla formation. The diagnosis is mainly clinical, based on the findings of tender
erythroderma, bullae, and desquamation with a scalded appearance especially in friction zones, periorificial scabs/crusting,
positive Nikolsky sign, and absence of mucosal involvement. Prompt empiric treatment with intravenous anti-staphylococcal
antibiotic such as nafcillin, oxacillin, or flucloxacillin is essential until cultures are available to guide therapy. Clarithromycin
or cefuroxime may be used should the patient have penicillin allergy. If the patient is not improving, critically ill, or in com-
munities where the prevalence of methicillin-resistant S. aureus is high, vancomycin should be used.
Conclusion  A high index of suspicion is essential for an accurate diagnosis to be made and treatment promptly initiated.

Keywords  Blisters · Desquamation · Erythroderma · Exfoliative toxins · Staphylococcus aureus

Introduction Epidemiology

Staphylococcal-scalded skin syndrome (SSSS), also known
as Ritter disease, is a superficial blistering skin disorder
caused by the exfoliative toxins of certain strains of Staphy-
lococcus aureus [1]. The condition was first described by
Ritter von Rittershain [2]. The term “staphylococcal scalded
skin syndrome” was defined by Melish and Glasgow [3].
* Alexander K. C. Leung
aleung@ucalgary.ca
1
Department of Pediatrics, The Alberta Children’s Hospital,
The University of Calgary, Calgary, #200, 233‑16th Avenue
NW, Calgary, AB T2M 0H5, Canada
2 tibility to infection and insufficient antibodies against toxins)
Toronto Dermatology Centre, Toronto, ON, Canada
3
The Pediatric Institute, Kuala Lumpur General Hospital,
Kuala Lumpur, Malaysia
The estimated prevalence ranges from 0.09 to 0.56 cases
per million people [4, 5]. The condition is most commonly
observed in neonates and children younger than 5  years
with a peak between 2 and 3 years of age [1, 6–8]. Lack of
protective antibodies to exfoliative toxins, immature renal
function with decreased renal clearance of these toxins, and
increased amount of desmoglein-1 in the skin at a young age
may account for the increased incidence at this age [7, 9, 10].
The male-to-female ratio is approximately equal in children
and 2:1 in adults, respectively [9, 11, 12]. African–American
children are less susceptible than Caucasian children [11, 12].
The disorder can also occur in older children and adults who
have chronic illness especially renal disease (decreased toxin
excretion), overwhelming staphylococcal infection (excessive
toxin production), and immunodeficiency (increased suscep-
[9, 13, 14]. The condition is more common during the summer
and autumn months [9]. The occurrence can be sporadic or as

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outbreaks due to asymptomatic carriers who spread the disease

to susceptible individuals [15].

Microbiology and pathophysiology

SSSS is caused by toxigenic strains of S. aureus most often

belonging to phage group 2, types 3A, 3B, 3C, 55, and 71
[12, 16–18]. S. aureus belonging to phage group 1 and 3
may also be responsible [11, 17]. These organisms produce
two exotoxins (exfoliative toxins A and B). Only 5% of S.
aureus isolates produce these toxins [9, 19, 20]. Recently, a
new clone of S. aureus causing SSSS and impetigo has been
identified by multilocus sequence typing (MLST). The clone
belongs to ST121. Approximately 95% of staphylococcal
strains that belong to this clone habor genes for both exfo-
liative toxins A and B [21]. The exfoliative toxins spread
hematogenously to reach the stratum granulosum of the epi-
dermis, where they act locally to produce the characteristic
skin lesions [22].
Exfoliative toxin A and exfoliative toxin B are serine pro-
teases that target and cleave desmoglein 1 [12]. Exfoliative
toxin A is heat stable and chromosomally encoded, whereas
exfoliative toxin B is heat-labile and plasmid derived [11,
16, 18]. Desmoglein 1 is a desmosomal cadherin which
mediates keratinocytes adhesion in the stratum granulosum Fig. 1  Diffuse erythroderma and desquamation in a child with staphy-
[1]. Hydrolysis of the amino-terminal extracellular domain lococcal scalded skin syndrome on day 5 after the onset
of desmoglein 1 by staphylococcal exfoliative toxins results
in disruption of keratinocytes adhesion and cleavage within pharyngitis, and otitis media), a circumcision site (post-
the stratum granulosum which leads to bulla formation and operative infection), and in neonates, the umbilical area
subsequent diffuse, sheet-like desquamation [11]. (omphalitis), and the diaper area (e.g., pustules, impetigo,
Desmoglein 1 is found in the upper epidermis but not in and cellulitis). It should be noted that clinical staphylococcal
the mucosal membrane [23]. On the other hand, desmoglein infection may or may not be present. The incubation period
3 is present in the mucosal membrane as well as the lower from skin infection to the appearance of the syndrome ranges
epidermis [24]. Desmoglein 3 compensates for the lysis of from 1 to 10 days [16]. A prodrome of general malaise, irri-
desmoglein 1 and helps to maintain cellular adhesion in the tability, and fever may be present [9, 18].
mucosal membrane and lower epidermis [13]. This explains The syndrome starts abruptly with widespread tender
why the mucosal membrane and lower epidermis are not erythroderma and tissue paper-like wrinkling of the skin
affected in SSSS [13]. accentuated in flexural and periorificial area [16, 20, 22].
The affected skin may have a texture of gooseflesh or coarse
Histology sandpaper before becoming red and wrinkled [13]. Mucosal
membranes are characteristically spared [6, 10, 24]. Within
Histopathological examination of the lesion shows a sub- 24–48 hours, fluid-filled blisters develop within the ery-
corneal split along the granular cell layer which may contain thematous areas [18]. These blisters enlarge to form bullae
acantholytic cells [18, 22, 25]. Inflammatory cell infiltrate which are thin-walled, flaccid, and rupture easily. Affected
and cell necrosis are characteristically absent [18]. skin may peel off in sheets (desquamation) due to the loss
of the roof of the bullae, leaving a moist erythematous area,
giving rise to the scalded appearance (Fig. 1) [18, 24]. Based
Clinical manifestations and complications on our experience, erythema is usually more subtle and less
well appreciated in dark-skinned individuals. Gentle pres-
Usually, SSSS starts with a local infection by a S. aureus sure on apparently normal skin results in separation of the
strain that produces exfoliative toxins which cause epidermal upper epidermis (Nikolsky sign) [6]. Facial edema, perior-
damage at distant sites [16, 19]. The primary source of infec- ificial scabs/crusting (Fig. 2), and peeling in friction zones
tion is usually the head and neck region (e.g., conjunctivitis, are other characteristic features [10, 13].

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World Journal of Pediatrics
Complications of SSSS include secondary infection (cel-
lulitis, sepsis, pneumonia), dehydration, electrolyte imbal-
ance, and hypothermia [25, 26].
Diagnosis and differential diagnosis
The diagnosis is mainly clinical, based on the findings
of tender erythroderma, bullae, and desquamation with a
scalded appearance especially in friction zones, periorifi-
cial scabs/crusting, positive Nikolsky sign, and absence of
mucosal involvement. The diagnosis can be confirmed by
culturing S. aureus from any suspected primary focus of
infection, such as the nasopharynx, conjunctiva, umbilicus,
and diaper area [1]. Culturing exfoliative lesions and bul-
lae are not helpful, because they are caused by circulating
exofoliative toxins and S. aureus does not occur in the skin
lesions [26]. Blood culture is usually negative in children,
but may be positive in adults [16]. Phage typing of the iso-
lated S. aureus or polymerase chain reaction (PCR) serum
test for exofoliative toxins is usually not necessary except for
academic purposes [12]. A skin biopsy is usually not neces-
sary, but if performed, may show superficial intraepidermal
separation along the granular cell layer [22, 25].
Differential diagnosis of SSSS includes toxic epidermal
necrolysis, Stevens–Johnson syndrome, bullous impetigo,
epidermolysis bullosa, bullous mastocytosis, bullous pem-
phigoid, pemphigus vulgaris, scalding thermal burn, Kawa-
saki disease, scarlet fever, and peeling skin syndrome.
Toxic epidermal necrolysis is characterized by a sud-
den onset of cutaneous erythema and inflammatory bullous
lesions on the skin with full thickness epidermal detachment
involving > 30% of the total body surface area accompa-
nied by involvement of two or more mucosal surfaces [27].
The condition is more commonly seen in older children and
adults. Nikolsky sign can only be elicited in affected areas.
Fig. 2  Perioral crusting and exfoliating erythematous lesions in a
child with staphylococcal scalded skin syndrome on day 5 after the
onset
Most cases are clearly linked to medications such as sul-
fonamides, penicillins, cephalosporins, quinolones, anticon-
vulsants, and non-steroidal anti-inflammatory agents [27].
Histopathologic examination shows full thickness epider-
mal necrosis of keratinocytes and vacuolar change along the
epidermal basal layer with adjacent subepidermal vesicle/
blister.
Patients with Stevens–Johnson syndrome have clinical
features similar to those seen in toxic epidermal necrolysis
except that the full thickness epidermal detachment is less
than 10% of the total body surface area [28, 29]. Patients
with full thickness epidermal detachment between 10 and
30% of the total body surface area are classified as hav-
ing Stevens–Johnson syndrome–toxic epidermal necrolysis
overlap [28, 29].
Bullous impetigo is caused by toxigenic strains of S.
aureus, mainly from phage group 2 [30]. These organisms
produce exfoliative toxins specific for desmoglein 1 and
restricted to the area of infection. S. aureus can be cultured
from the skin lesion. The condition is seen primarily in
newborns and infants [30]. In bullous impetigo, the bulla
is sharply demarcated without surrounding or generalized
erythema and forms at the initial site of infection and not in
other areas of the body. Rupture of the bulla usually reveals a
moist, erythematous base that dries to form a shiny lacquer-
like appearance. A pathognomonic finding is a narrow rim
of scale at the edge of the ruptured lesion [30]. The Nikolsky
sign is characteristically negative.
Epidermolysis bullosa is a heterogeneous group of con-
nective tissue disorders characterized by blisters in skin
and mucosal membranes in response to trivial rubbing and
frictional trauma [31]. The condition is due to impaired epi-
dermal or dermo-epidermal adhesion. Epidermolysis bul-
losa is classified into several categories, each with many
subtypes based on the precise level at which the separation
or blistering occurs, namely, epidermolysis bullosa simplex,
junctional epidermolysis bullosa, dystrophic epidermolysis
bullosa, epidermolysis bullosa acquisita, and Kindler syn-
drome [32].
Bullous mastocytosis is a variant of cutaneous masto-
cytosis characterized by generalized, yellowish/reddish/
brownish, thickened skin with doughy/leathery feel and a
fine “cobblestone” or “peau d’ orange” appearance due to
diffuse mast cell infiltration [33]. Affected patients have
widespread bullae which may occur spontaneously or fol-
lowing mild trauma [33]. The bullae may rupture, leaving
erosions and crusts. The condition is very pruritic and usu-
ally occurs in the first year of life.
Bullous pemphigoid and pemphigus vulgaris are diseases
of an aging population, in contrast to SSSS which occurs in
a much younger age group. Bullous pemphigoid and pem-
phigus vulgaris are characterized by bullous lesions which
are tense in bullous pemphigoid and flaccid in pemphigus
13

vulgaris [34]. In bullous pemphigoid, the bullae tend to be
stable and unlikely to erode. Lesions tend to occur on the
flexural areas; involvement of mucosal surfaces is rare [34].
Nikolsky sign is typically negative [34]. In contrast, mucosal
erosions are common in pemphigus vulgaris. Sites of pre-
dilection include the chest and back. Blisters rupture easily.
Nikolsky sign is often positive [34].
SSSS may mimic a scalding thermal burn [35, 36]. The
diagnosis is usually obvious by a careful history taking. In
case of doubt, the child should be hospitalized and observed
for the development of new lesions which, if present, favor
the diagnosis of SSSS [36]. If suspicion remains, isolation
and phage typing of S. aureus from pharyngeal, nasal, or
cutaneous swabs may confirm the diagnosis [36].
Kawasaki disease is characterized by fever for at least
5 days, conjunctival injection, oral mucosal changes, swell-
ing and edema of the hands, polymorphous rash, and cervi-
cal lymphadenopathy [37]. Desquamation of the fingers and
toes is common 2–3 weeks after the onset of fever. Bullous
and vesicular eruptions are characteristically absent [37].
Scarlet fever is characterized by fever, scarletiniform
rash, beefy red pharynx, enlarged and erythematous ton-
sil, pharyngeal exudates, enlarged tender anterior cervical
lymph nodes, and strawberry tongue [28]. Typically, the rash
blanches on pressure, has the texture of gooseflesh or coarse
sandpaper, and is better felt than seen. The rash may be more
prominent in flexor skin creases, especially in the antecubital
fossae (Pastia’s lines). Bullous and vesicular eruptions are
characteristically absent.
Peeling skin syndrome is a heterogeneous group of auto-
somal recessive disorders characterized by superficial pain-
less peeling with blistering of the skin without mucosal
involvement [38]. Two major forms of peeling skin syn-
drome are recognized, namely, acral peeling skin syndrome
and generalized peeling skin syndrome. The latter is sub-
classified into generalized noninflammatory (type A) peel-
ing skin syndrome and generalized (type B) inflammatory
peeling skin syndrome.
Management
Prompt empiric treatment with intravenous anti-staphylo-
coccal antibiotic such as nafcillin, oxacillin, or flucloxacil-
lin is essential until cultures are available to guide therapy
[7, 17, 20, 39]. Clarithromycin or cefuroxime may be used
should the patient have penicillin allergy [9]. If the patient
is not improving, critically ill, or in communities where the
prevalence of methicillin-resistant S. aureus (MRSA) is
high, vancomycin should be used [1]. Some authors suggest
the use of clindamycin as an adjunct because of its capacity
to inhibit production of exofoliative toxins [6, 40]. Pending
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World Journal of Pediatrics
response to treatment, oral antibiotics can be substituted
within a few days.
Supportive measures include proper wound care, main-
tenance of fluid and electrolyte balance, nutritional sup-
port, and use of paracetamol or ibuprofen for pain and fever
when necessary [7, 9]. Non-steroidal anti-inflammatory
drugs (NSAIDs) should not be given for pain, because they
may impair renal function [9]. Topical antibiotics such as
mupirocin and fusidic acid can be used as an adjunct at the
affected areas as well as at the site of colonization in an
attempt to eradicate colonization [7, 39]. The use of corti-
costeroids should be discouraged; the use of which is associ-
ated with a worsening of the disease [18, 26].
Prognosis
Most cases resolve without sequelae within 2–3 weeks of
proper treatment [26]. Skin lesions heal without scarring as
the cleavage plane is very superficial [11, 22]. In the pedi-
atric age group, the mortality is approximately 4% and is
associated with extensive skin involvement, overwhelming
sepsis, and fluid and electrolyte imbalance [18, 22]. In the
adult population, the mortality is greater than 60% which
may be attributed to the underlying condition predisposing
to the illness [12, 18].
Conclusions
SSSS is a superficial blistering skin disorder caused by the
exfoliative toxins of certain strains of S. aureus. The condi-
tion is most commonly observed in neonates and children
younger than 5 years with a peak between 2 and 3 years of
age. Affected skin may peel off in sheets giving rise to the
scalded appearance. Gentle pressure on apparently normal
skin results in separation of the upper epidermis (Nikolsky
sign). Facial edema, periorificial scabs/crusting, and peeling
in friction zones are other characteristic features. Prompt
empiric treatment with intravenous anti-staphylococcal anti-
biotic such as nafcillin, oxacillin, or flucloxacillin is essen-
tial until cultures are available to guide therapy. Supportive
measures include proper wound care, maintenance of fluid
and electrolyte balance, nutritional support, and use of par-
acetamol or ibuprofen for pain and fever when necessary.
Author contributions  AKCL wrote the first draft of the manuscript, as
well as a statement of whether an honorarium, grant, or other form of
payment was given to anyone to produce the manuscript. AKCL, BB,
and KFL contributed to drafting and revising the manuscript. We have
seen and approved the final version submitted for publication and take
full responsibility for the manuscript.
World Journal of Pediatrics
Funding  None. There is no honorarium, grant, or other form of pay-
ment given to any of the author/coauthor.
Compliance with ethical standards  skin syndrome due to burn wound infection. Ann Burns Fire Dis-
Ethical approval  Not applicable.
Conflict of interest  No financial or non-financial benefits have been re-
ceived or will be received from any party related directly or indirectly
to the subject of this article.
References
1. Davidson J, Polly S, Hayes PJ, Fisher KR, Talati AJ, Patel T.
Recurrent staphylococcal scalded skin syndrome in an extremely
low-birth-weight neonate. AJP Rep. 2017;7:e134–7.
2. Ritter von Rittershain G. Die exfoliativa dermatitis jungerer Saul-
inge. Centralz Kinderheilk. 1878;2:3–23.
3. Melish ME, Glasgow LA. The staphylococcal scalded skin syn-
drome. N Engl Med. 1970;282:1114–9.
4. Lamand V, Dauwalder O, Tristan A, Casalegno JS, Meugnier
H, Bes M, et al. Epidemiological data of staphylococcal scalded
skin syndrome in France from 1997 to 2007 and microbiological
characteristics of Staphylococcus aureus associated strains. Clin
Microbiol Infect. 2012;18:e514–21.
5. Mockenhaupt M, Idzko M, Grosber M, Schöpf E, Norgauer J. Epi-
demiology of staphylococcal scalded skin syndrome in Germany.
J Invest Dermatol. 2005;124:700–3.
6. Arora P, Kalra VK, Rane S, McGrath EJ, Zegarra-Linares R, Chawla S.
Staphylococcal scalded skin syndrome in a preterm newborn present-
ing within first 24 h of life. BMJ Case Rep. 2011;2011:bcr0820114733.
7. Mishra AK, Yadav P, Mishra A. A systemic review on staphylo-
coccal scalded skin syndrome (SSSS): a rare and critical disease
of neonates. Open Microbiol J. 2016;10:150–9.
8. Oliveira AR, Aires S, Faria C, Santos E. Staphylococcal scalded
skin syndrome. BMJ Case Rep. 2013;2013:bcr2013009478.
9. Handler MZ, Schwartz RA. Staphylococcal scalded skin syn-
drome: diagnosis and management in children and adults. J Eur
Acad Dermatol Venereol. 2014;28:1418–23.
10. Jeyakumari D, Gopal R, Eswaran M, Maheshkumar C. Staphy-
lococcal scalded skin syndrome in a newborn. J Glob Infect Dis.
2009;1:45–7.
11. Berk D. Staphylococcal scalded skin syndrome. Clinical decision
support: pediatrics. Wilmington, delaware: decision support in
medicine, LLC., 2015, electronic database. http://www.decisi​ onsu​
pport​inmed​icine​.com. Accessed 13 Nov 2017.
12. Manders SM. In: Heyman WR, Anderson BE, Hivnor C, et al,
editors. Clinical Decision Support: Dermatology. Wilmington,
Delaware: Decision Support in Medicine, LLC, 2015, 2nd edi-
tion, electronic database. http://www.decis​ionsu​pport​inmed​icine​
.com. Accessed 14 Nov 2017.
13. Patel NN, Patel DN. Staphylococcal scalded skin syndrome. Am
J Med. 2010;123:505–7.
14. Redding KS, Jones EH, Patel T, Skinner RB. Staphylococcal
scalded skin syndrome in pregnancy. Cutis. 2015;96:e7–9.
15. Dudley M, Parsh B. Recognizing staphylococcal scalded skin
syndrome. Nursing. 2016;46:68.
16. Gupta A, Jacobs N. Visual diagnosis: 2-week-old has a red, peel-
ing rash. Pediatr Rev. 2013;34:e9–12.
17. Haveman LM, Fleer A, Gerards LJ. Staphylococcal scalded skin
syndrome in two very low birth weight infants. J Perinat Med.
2003;31:515–9.
18. Patel GK, Finlay AY. Staphylococcal scalded skin syn-
drome: diagnosis and management. Am J Clin Dermatol.
2003;4:165–75.
19. Farroha A, Frew Q, Jabir S, Dziewulski P. Staphylococcal scalded
asters. 2012;25:140–2.
20. Hennigan K, Riley C. Staphylococcal scalded skin syndrome: a
case review. Neonatal Netw. 2016;35:8–12.
21. Doudoulakakis A, Spiliopoulou I, Spyridis N, Giormezis N, Kop-
sidas J, Militsopoulou M, et al. Emergence of a Staphylococcus
aureus clone resistant to mupirocin and fusidic acid carrying exo-
toxin genes and causing mainly skin infections. J Clin Microbiol.
2017;55:2529–37.
22. Kouakou K, Dainguy ME, Kassi K. Staphylococcal scalded
skin syndrome in neonate. Case Rep Dermatol Med.
2015;2015:901968.
23. Jindal S, Bhobhe M, Jerajani H. An infant with skin rash. Indian
Pediatr. 2012;49:853–4.
24. Aalfs AS, Oktarina DA, Diercks GF, Jonkman MF, Pas HH.
Staphylococcal scalded skin syndrome: loss of desmoglein 1 in
patient skin. Eur J Dermatol. 2010;20:451–6.
25. Aydin D, Alsbjørn B. Severe case of staphylococcal scalded skin
syndrome in a 5-year-old child—case report. Clin Case Rep.
2016;4:416–9.
26. Berk DR, Bayliss SJ. MRSA, staphylococcal scalded skin syn-
drome, and other cutaneous bacterial emergencies. Pediatr Ann.
2010;39:627–33.
27. Leung AK, Barankin B. A girl with widespread blistering, scab-
bing, and swelling: Stevens–Johnson syndrome. Consult Pediatr.
2013;13:216–9.
28. Leung AK, Kellner JD. Group A beta-hemolytic streptococcal
pharyngitis in children. Adv Ther. 2004;21:277–87.
29. Mockenhaupt M. The current understanding of Steven-Johnson
syndrome and toxic epidermal necrolysis. Expert Rev Clin Immu-
nol. 2011;7:803–13.
30. Leung AK, Barankin B. Tender honey-colored lesion with “stuck-
on” crust: Impetigo. Consult Pediatr. 2013;12:83–5.
31. Hon KL, Li JJ, Cheng BL, Luk DC, Murrell DF, Leung AK. Age
and etiology of childhood epidermolysis bullosa mortality. J Der-
matol Treat. 2015;26:178–82.
32. Watkins J. Diagnosis, treatment and management of epidermolysis
bullosa. Br J Nurs. 2016;25(8):428–31.
33. Verma KK, Bhat R, Singh MK. Bullous mastocytosis
treated with oral betamethasone therapy. Indian J Pediatr.
2004;71(3):261–3.
34. Kayani M, Aslam AM. Bullous pemphigoid and pemphigus vul-
garis. BMJ. 2017;357:j2169.
35. Murphy S. Non accidental injury vs staphylococcal scalded skin
syndrome. A case study. Emerg Nurse. 2001;9:26–30.
36. Porzionato A, Aprile A. Staphylococcal scalded skin syn-
drome mimicking child abuse by burning. Forensic Sci Int.
2007;168:e1–4.
37. Leung AK. Kawasaki disease. In: Leung AK, editor. Com-
mon problems in ambulatory pediatrics: specific clinical prob-
lems, vol. 1. New York: Nova Science Publishers Inc; 2011. p.
385–90.
38. Sprecher E, Samuelov L. Peeling skin syndrome. In: Post TW,
editors. UpToDate. Waltham, MA. Accessed 14 Nov 2017.
39. Johnston GA. Treatment of bullous impetigo and the staphylococ-
cal scalded skin syndrome in infants. Expert Rev Anti Infect Ther.
2004;2:439–46.
40. Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC,
Treat JR. Antibiotic sensitivity and resistance patterns in pedi-
atric staphylococcal scalded skin syndrome. Pediatr Dermatol.
2014;31:305–8.
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