CM E

MRSA, Staphylococcal Scalded Skin Syndrome,

and Other Cutaneous Bacterial Emergencies
CM E EDUCATIONAL OBJECTIVES
1. State distinguishing clinical features
of important pediatric bacterial skin
emergencies.
2. Describe the evaluation of select
pediatric bacterial skin emergencies.
3. Identify and explain the manage-
ment of bacterial skin emergencies
in children, including important treat-
ment and infection control measures.

David R. Berk, MD, is Assistant Professor

of Dermatology and Pediatrics, Depart-
ment of Internal Medicine and Pediatrics,
Division of Dermatology, Washington
University School of Medicine and St. Louis
Children’s Hospital, St. Louis, MO.
Susan J. Bayliss, MD, is Professor of Der-
matology and Pediatrics, Director of Pediat-
ric Dermatology, Residency Program Direc-
tor, Department of Internal Medicine and
Pediatrics, Division of Dermatology, Wash-
ington University School of Medicine and St.
Louis Children’s Hospital, St. Louis, MO.
Address correspondence to: David R.
Berk, MD, Campus Box 8123, 4921 Parkview
Place, St. Louis, MO 63110; fax: 314-747-
8693; e-mail: dberk@dom.wustl.edu.
Dr. Berk and Dr. Bayliss have disclosed no
relevant financial relationships.
doi: 10.3928/00904481-20100922-02

David R. Berk, MD; and Susan J. Bayliss, MD

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3910Berk.indd 627 9/24/2010 4:21:45 PM


C
utaneous bacterial infections
are important to recognize in
pediatrics. Some may actually
be emergencies. These include localized
skin infections, such as methicillin-re-
sistant Staphylococcus aureus (MRSA)
infections, as well as more generalized
toxin-mediated diseases, such as toxic
shock syndrome (TSS) and staphylo-
coccal scalded skin syndrome (SSSS).
It is important for pediatricians to rec-
ognize and distinguish these cutaneous
bacterial emergencies so treatment and
appropriate infection control measures
can be promptly initiated.
MRSA
MRSA poses therapeutic and pub-
lic health challenges because of its
increasing incidence, enhanced viru-
lence, and frequent multidrug re-
sistance.1-3 MRSA infections most
commonly involve the skin and soft
tissues, typically manifesting as sup-
purative lesions such abscesses, fu-
runcles, folliculitis, or cellulitis (see
Figure 1, page 629).4-6 Infections may
occur at any site but especially on the
buttocks and lower extremities. Be-
cause pustular lesions commonly have
a necrotic center, they are often con-
fused with spider bites. Skin and soft-
tissue infections caused by MRSA
cannot be distinguished reliably on
clinical grounds from those caused by
methicillin-sensitive Staphylococcus
aureus.7 Risk factors include trauma
to the skin, contact with an individual
infected with MRSA, rectal and/or na-
sal colonization, crowded households,
childcare attendance, antibiotic usage
in the past year, contact sports, chronic
skin disease, and pets.3
The mecA gene provides MRSA
with its methicillin resistance.8 This
gene encodes penicillin-binding pro-
tein 2a, a transpeptidase with very
low affinity for beta-lactams. Penicil-
lin-binding protein 2a catalyzes the
transpeptidation reactions of peptido-
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3910Berk.indd 628
CM E
glycan, allowing cell wall synthesis
even in the presence of beta-lactams.
The mecA gene may be carried on
small-sized (eg, the staphylococcal
cassette chromosome mec type IV or
V of community-acquired MRSA) or
large-sized (eg, the staphylococcal
cassette chromosome mec type I, II, or
III of hospital-acquired MRSA) gene
cassettes. The latter can also confer
resistance to many non-beta-lactam
antibiotics.
An important virulence factor for
MRSA is Panton-Valentine leukocidin
(PVL). PVL is uncommon among non-
MRSA isolates. PVL acts as a cytotox-
in, causing lysis of leukocytes and tis-
sue necrosis. In addition, PVL is more
often found in MRSA strains, which
contain staphylococcal cassette chro-
mosome mec type IV or V rather than
I, II, or III. PVL is encoded by the lukS-
PV and lukF-PV genes. Other virulence
factors for MRSA include alpha-hemo-
lysin and phenol soluble modulins.9
When possible, incision and drain-
age are a critical part of initial thera-
py for skin and soft tissue infections
suspected to be due to MRSA.10,11
Antibiotics should be considered as
an adjunctive therapy, especially for
cases with purulent drainage, rapid
progression, large abscess size, and
the presence of systemic manifesta-
tions or immunocompromise. Antibi-
otic therapy should be based on local
resistance patterns and the results of
cultures and susceptibility testing. In
general, non-beta-lactam antibiotics
should be used for cases that are ei-
ther suspected to be due to MRSA or
which do not respond to initial inci-
sion, drainage, and beta-lactam antibi-
otics. These agents include clindamy-
cin, trimethoprim/sulfamethoxazole,
tetracycline, linezolid, or vancomy-
cin. Decolonization measures, such
as intranasal mupirocin, dilute bleach
baths, and bathing with antimicrobial
soaps, can be helpful adjuncts.12
SSSS
SSSS is caused by infections with
epidermolytic (also known as exfolia-
tive) toxin (ET)-producing S. aureus.
SSSS preferentially affects newborns
and children younger than 5 years.13 The
nares, conjunctivae, perioral region,
umbilicus, and perineum are common
foci of infection. When involvement is
localized, infections manifest as bul-
lous impetigo. On the other hand, when
hematogenous spread of ET occurs, the
generalized form of SSSS develops.
Cutaneous findings include widespread
erythema, which may start on the head
and evolve into superficial skin peel-
ing, flaccid bullae, and denuded tender
skin (see Figure 2, page 630).14
Erythema arises abruptly, spreads
rapidly, and demonstrates characteris-
tic flexural and perioral prominence,
including radial perioral fissures. There
also may be a predilection for areas of
mechanical stress, such as shoulders,
buttocks, hands, and feet. Skin tender-
ness is a key feature. The Nikolsky sign,
defined as extension of blistering with
gentle pressure at the edge of a bulla,
may be elicited. Other features include
fever, malaise, irritability, purulent rhi-
norrhea, conjunctivitis, and poor oral
intake. The primary source of infection
is often around the head and neck area
or circumcision site. Rarely, SSSS may
result from ET derived from extracu-
taneous infections, such as pneumonia,
pyomyositis, endocarditis, urinary tract
infection, and septic arthritis.15
The predilection of SSSS for new-
borns and young children may be
caused by decreased renal clearance of
ET and/or the lack of anti-toxin anti-
bodies. Outbreaks in nurseries and in-
tensive care units are well described.16
Two types of ET mediate SSSS, in-
cluding ET-A and ET-B, both of which
are serine proteases.17,18 These two
ETs target desmoglein-1, a cell adhe-
sion protein located in desmosomes in
the superficial epidermis, explaining
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the superficial cleavage plane within
the stratum granulosum seen in le-
sions of SSSS. These ETs also pos-
sess superantigen activity.19 Strains of
ET-producing S. aureus usually belong
to phage groups 1, 2, or 3, especially
group 2 strains 71 and 55. ET-A is
chromosomally encoded, whereas ET-
B is plasmid derived.
SSSS is a clinical diagnosis that can
be confirmed by culturing S. aureus
from foci of infection, such as from
the nostrils, conjunctivae, umbilicus,
or nasopharynx.20 Culturing exfoliative
lesions and blisters is not helpful be-
cause these are induced by circulating
ET and, therefore, are typically sterile,
unless secondarily infected. Bacte-
remia is uncommon in children with
SSSS. Occasionally, a skin biopsy or
the painless removal and examination
of blisters roofs can help to confirm a
superficial cleavage plane, at the level
of the stratum granulosum.
The main differential diagnosis for
SSSS is toxic epidermal necrolysis
(TEN), a more life-threatening blister-
ing disease characterized by a signifi-
cantly lower cleavage plane below the
junction of the epidermis and dermis.
TEN is discussed later in this issue.
TEN involves full thickness necrosis
of the epidermis. Unlike SSSS, TEN
demonstrates characteristic mucosal
involvement. TEN is quite unusual in
infants. Other differential diagnoses
may include epidermolysis bullosa,
epidermolytic hyperkeratosis, thermal
burns, scarlet fever, toxic shock syn-
drome, Kawasaki disease, and nutri-
tional deficiencies.
Treatment of generalized SSSS in-
cludes hospitalization for most young
children, with intravenous antibiotics
and close monitoring of electrolytes,
temperature, and hemodynamics.20,21
Typical empiric antibiotic choices
should include a penicillinase-resistant
penicillin, first- or second-generation
cephalosporin, and clindamycin, with
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3910Berk.indd 629
CM E
A B
Figure 1. Children with abscesses (A) and carbuncles (B) typical of methicillin-resistant Staphylococcus
aureus.
adjustments made based on local re-
sistance patterns and sensitivities of
obtained cultures. Skin care generally
consists of bland emollients (petro-
leum jelly) and minimal handling of
patients. Mupirocin can be used at foci
of infection. Gentle cleansing may help
prevent secondary infection. Removal
of dried skin with bathing is not neces-
sary initially when the skin is too ten-
der to touch but is used an adjunct later.
Other important measures include con-
tact isolation and pain management.
Corticosteriods should be avoided.
The prognosis of SSSS is usually
good in children and is more guarded
in infants. Complications include sep-
sis, secondary infections, electrolyte
imbalances, fluid losses, and hypother-
mia. Compared with TEN, the higher
blister cleavage plane in SSSS confers
a better prognosis, causing less water
loss and temperature instability. The
mortality rate in SSSS is less than 5%.
In many cases, patients respond rapid-
ly to treatment, with complete recov-
ery within 2 or 3 weeks. Because the
cleavage plane in SSSS is superficial,
lesions heal without scarring. SSSS is
more life-threatening in newborns as
well as adults, especially those with
underlying diseases, such as immuno-
compromise or renal failure.22
BULLOUS IMPETIGO
Impetigo is a contagious, superficial
skin infection that occurs in bullous or
non-bullous forms.23,24 Most cases are
non-bullous, caused by streptococci,
staphylococci, or both. Clinically, non-
bullous impetigo demonstrates the clas-
sic honey-colored crust and commonly
affects the face, especially around the
nose. The differential diagnosis some-
times includes herpes simplex infection.
In contrast, bullous impetigo is the local-
ized version of SSSS and is, therefore,
always caused by S. aureus. Clinically,
bullous impetigo presents with flac-
cid bullae and tender erosions, without
much surrounding erythema (see Figure
3, page 630). A rim of scale may be seen
at edge of erosions, where the blister has
become denuded. Bullous impetigo of-
ten occurs in infancy, particularly in the
diaper area. Treatment includes topical
mupirocin or, for more widespread or
severe cases, oral antibiotics. Similar to
SSSS, bullous impetigo is characterized
by a superficial cleavage plane, is medi-
ated by the same ET-A and -B, and typi-
cally does not scar.
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Figure 2. Child demonstrating superficial skin peeling, denuded tender skin (A), flexural prominence, and periorificial crusting (B) typical of staphylococcal
scalded skin syndrome.
STAPHYLOCOCCAL TSS
Staphylococcal TSS is a systemic
toxin-mediated disorder that may occur
in menstrual or non-menstrual forms.
The menstrual form tends to occur in
young, healthy women with staphylo-
coccal vaginal infection or colonization
by phage group 1 S. aureus. Historical-
ly, it was associated with the usage of
superabsorbent tampons.25
Non-menstrual TSS is also caused
by S. aureus, and may be associated
Figure 3. Flaccid bullae in the diaper area of a newborn with bullous impetigo.
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3910Berk.indd 630
CM E
A B
with upper airway infections, burns,
postpartum infections, cutaneous in-
fections, surgical procedures, and
nasal packing.26 Staphylococcal TSS
is mediated by toxic shock syndrome
toxin-1 and staphylococcal enterotox-
ins-A, -B, and -C. These toxins act
as superantigens, directly activating
T cells, resulting in massive cytokine
release.27 TSS toxin-1 may also de-
crease clearance of endotoxins from
gut flora.
Clinical features are similar for
menstrual and non-menstrual TSS. It
starts with the abrupt onset of high
fever, abdominal distress, myalgias,
and headache, followed by shock and
multisystem organ failure.25,26,28-30
Within 1 to 3 days of disease onset,
patients develop a widespread scar-
latiniform eruption or erythema with
flexural accentuation. Other common
findings include pharyngitis, conjunc-
tival and mucosal membrane hyper-
ermia, strawberry tongue, and gener-
alized edema, especially of the hands
and feet. A pruritic, maculopapular
erythema occurs within 1 to 2 weeks,
with a predilection for the palms and
soles, sparing the face.
One to 3 weeks after disease on-
set, full thickness desquamation of the
palms (especially subungually), soles,
and perineum occurs. Nail and hair
shedding may occur later. Particularly
concerning complications include re-
spiratory distress syndrome, which is
more common in children, as well as
disseminated intravascular coagula-
tion, myocardial dysfunction, and renal
failure. Positive blood cultures are un-
common (< 15%), and mortality is less
than 3%. Diagnosis is based on clinical
criteria (see Sidebar 1, page 631).
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Figure 4. Papular, sandpaper-like plaques with streptococcal infections.
The differential diagnosis of staph-
ylococcal TSS includes streptococcal
toxic shock syndrome, scarlet fever,
Kawasaki disease, Rocky Mountain
spotted fever, viral exanthems, and
drug reactions, such as TEN. Unlike
many of the differential diagnoses,
staphylococcal TSS is always charac-
terized by shock and multiorgan fail-
ure. Skin biopsies in staphylococcal
TSS reveal non-specific findings and
are usually unnecessary, but can help
eliminate some conditions in the differ-
ential diagnosis, such as TEN.
The mainstay of treatment of staphy-
lococcal TSS includes rapid identifica-
tion and drainage of infections, as well
as removal of foreign bodies that could
harbor infection (eg, meshes, tampons,
nasal packing). In addition, intravenous
penicillinase-resistant antistaphylococ-
cal antibiotics and supportive care are
necessary. Antibiotics that inhibit toxin
production, including clindamycin, flu-
oroquinolones, and rifampin, are some-
times recommended.
STREPTOCOCCAL TSS
Streptococcal toxic shock syndrome
(STSS) is caused by infection with
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3910Berk.indd 631
CM E
particular toxin-producing strains of
Streptococcus pyogenes, including M
protein types 1, 3, 12 and 28.31 Impor-
tant toxins in the pathogenesis include
streptococcal pyrogenic exotoxin-A,
-B, and -C, streptococcal superanti-
gen, and mitogenic factor.27 Unlike
staphylococcal TSS, STTS is more of-
ten associated with a focal tissue infec-
tion and bacteremia, as well as a more
fulminant course and greater lethality
(mortality of 30% to 60%).32,33
Moreover, patients with STSS typi-
cally present with severe pain, usually
affecting a leg and often out of propor-
tion to objective findings, such as ede-
ma and erythema. Necrotizing fasciitis
or myonecrosis are possible.33,34 Some
patients with STSS have prodromal
influenza-like symptoms. Nausea and
vomiting are less common than in staph-
ylococcal TSS. Very soon after presen-
tation, patients quickly develop shock
and multiorgan failure, such as renal
failure, respiratory distress syndrome,
and disseminated intravascular coagu-
lation. Bullae are uncommon and are
associated with poor prognosis. Some
patients demonstrate erythroderma and
desquamation 1 to 2 weeks after disease
SIDEBAR 1.
CDC Case Definition
for SSSS
Clinical Criteria
• Temperature > 38.9°C
• Diffuse macular erythroderma
• Desquamation, 1 to 2 weeks after onset,
particularly palmoplantar
• Hypotension for age
• Multisystem involvement, three or more
of the following:
Gastrointestinal
Muscular
Mucous membranes
Renal
Hepatic
Hematologic
Central nervous system
Laboratory Criteria
Negative test results for the following (if
obtained):
• Throat, CSF, blood cultures (although
blood may be positive for S. aureus)
• Serological tests for Rocky Mountain
spotted fever, measles, or leptospirosis
‘Probable’ disease: Laboratory criteria +
4 out of 5 clinical criteria
‘Confirmed’ disease: Laboratory criteria
+ all 5 clinical criteria (unless patient
dies before desquamation)
Source: www.cdc.gov/ncphi/disss/nndss/casedef/toxicss-
current.htm
onset, although this is less common than
in staphylococcal TSS. A strawberry
tongue is rare in STSS. More than half
of cases demonstrate positive blood cul-
tures. Clinical criteria are summarized in
Sidebar 2 (see page 632).
Because varicella is a risk factor for
invasive S. pyogenes, clinicians treating
patients with varicella should have a high
index of suspicion if there is persistent
or recurrent fevers (beyond day 4).35
Treatment of STSS involves sup-
portive management in an intensive
care unit, early surgical debridement,
and intravenous antibiotics. Clinda-
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SIDEBAR 2.
CDC Case Definition for
Streptococcal TSS
Clinical Case Definition
• Hypotension for age/shock
• At least two of the following:
Renal impairment
Coagulopathy
Hepatic involvement
Adult respiratory distress syndrome
Generalized erythematous rash with or
without desquamation
Soft-tissue necrosis (eg, necrotizing
fasciitis or myositis, or gangrene)
Laboratory Criteria
• Isolation of group A beta-hemolytic
Streptococcus
‘Probable’ disease: Clinical case defini-
tion + isolation of group A beta-hemo-
lytic Streptococcus from a non-sterile site
‘Confirmed’ disease: Clinical case defini-
tion + isolation of group A beta-he-
molytic Streptococcus from a normally
sterile site
Source: www.cdc.gov/ncphi/disss/nndss/casedef/strepto-
coccalcurrent.htm
mycin is often used with the intent of
impairing toxin production. Because of
the extent of invasive infection and the
required debridement, morbidity and
disfigurement often occur in survivors.
SCARLET FEVER
Scarlet fever is caused by infection
with particular S. pyogenes strains that
produce streptococcal pyrogenic (eryth-
rogenic) exotoxin-A, -B, or -C.36 Strep-
tococcal tonsillopharyngitis is usually
the source of infection. Wound infec-
tions, burns, pelvic infections, food-
borne outbreaks, and cellulitis are other
possible sources.37
Most patients abruptly develop fe-
ver and sore throat, followed 1 to 2 days
later by a scarlatiniform rash. Headache,
malaise, myalgias, vomiting, abdominal
pain, lymphadenopathy, and leukocytosis
are common. Erythematous macules and
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3910Berk.indd 632
CM E
petechiae (Forschheimer’s spots) may be
present on the palate, as well as a “white
strawberry tongue” that sloughs to be-
come a “red strawberry tongue.”38,39
The rash of scarlet fever is char-
acterized by blanchable, confluent,
erythematous macules and patches, as
well as tiny papules with a dry, sand-
paper-like texture (see Figure 4, page
631). Lesions often start on the upper
trunk, then generalize over days, spar-
ing the palms and soles, and involving
the legs last. Pastia’s lines refer to ac-
centuation of erythema with linear pe-
techiae in skin folds. Accentuation is
also common at dependent sites. Facial
flushing with circumoral pallor is com-
mon. The rash fades within a week and
is followed a week later by a superfi-
cial desquamation, especially in skin
folds, on the face and in sheets from the
hands and feet (may take 2 to 6 weeks).
Beau’s lines (transverse nail grooves)
and telogen effluvium (hair loss) may
present after the illness. Early compli-
cations may include pneumonia, otitis
media, bacteremia, and osteomyelitis.
Later complications may include glo-
merulonephritis and rheumatic fever.
The differential diagnosis of scarlet
fever includes Kawasaki disease, SSSS,
staphylococcal and streptococcal TSS,
mononucleosis, fifth disease, rubella,
rubeola, other viral exanthems, juvenile
rheumatoid arthritis, and drug reac-
tions. Similar rashes can also be seen
with pharyngeal infections with S. au-
reus, Arcanobacterium haemolyticum,
or Haemophilus influenzae. Cultures of
infected areas should be obtained. Skin
biopsies are nonspecific and are not
generally helpful.
Before the discovery of antibiot-
ics, the mortality of scarlet fever was
approximately 20%.40 The antibiotic
of choice for scarlet fever is penicil-
lin. Treatment is important to relieve
symptoms, to minimize spreading the
infection to others, and to avoid com-
plications, such as rheumatic fever.
REFERENCES
1. Cohen PR. Community-acquired methi-
cillin-resistant Staphylococcus aureus
skin infections: implications for patients
and practitioners. Am J Clin Dermatol.
2007;8(5):259-270.
2. Elston DM.Community-acquired methicillin-
resistant Staphylococcus aureus. J Am Acad
Dermatol. 2007;56(1):1-16; quiz 17-20.
3. Kil EH, Heymann WR, Weinberg JM. Methi-
cillin-resistant Staphylococcus aureus: an up-
date for the dermatologist, Part 1: Epidemiol-
ogy. Cutis. 2008;81(3):227-233.
4. Gorwitz RJ. A review of community-associ-
ated methicillin-resistant Staphylococcus au-
reus skin and soft tissue infections. Pediatr
Infect Dis J. 2008;27(1):1-7.
5. Groner A, Laing-Grayman D, Silverberg NB.
Outpatient pediatric community-acquired
methicillin-resistant Staphylococcus aure-
us: a polymorphous clinical disease. Cutis.
2008;81(2):115-122.
6. Kil EH, Heymann WR, Weinberg JM. Methi-
cillin-resistant Staphylococcus aureus: an
update for the dermatologist, Part 2: Patho-
genesis and cutaneous manifestations. Cutis.
2008;81(3):247-254.
7. Miller LG, Perdreau-Remington F, Bayer AS,
et al. Clinical and epidemiologic characteris-
tics cannot distinguish community-associated
methicillin-resistant Staphylococcus aureus
infection from methicillin-susceptible S. au-
reus infection: a prospective investigation.
Clin Infect Dis. 2007;44(4):471-482.
8. Inglis B, Matthews PR, Stewart PR. The ex-
pression in Staphylococcus aureus of cloned
DNA encoding methicillin resistance. J Gen
Microbiol. 1988;134(6):1465-1469.
9. Hamilton SM, Bryant AE, Carroll KC, et al.
In vitro production of panton-valentine leu-
kocidin among strains of methicillin-resistant
Staphylococcus aureus causing diverse infec-
tions. Clin Infect Dis. 2007;45(12):1550-1558.
10. Elston DM. Practical management tips for
methicillin-resistant Staphylococcus aureus.
Cutis. 2008;81(4):311-313.
11. Kil EH, Heymann WR, Weinberg JM. Methi-
cillin-resistant Staphylococcus aureus: an
update for the dermatologist, Part 3: Clinical
management. Cutis. 2008;81(4):327-335.
12. Kluytmans J, van Belkum A, Verbrugh
H.Nasal carriage of Staphylococcus aureus:
epidemiology, underlying mechanisms,
and associated risks. Clin Microbiol Rev.
1997;10(3):505-520.
13. Ladhani S, Evans RW. Staphylococcal
scalded skin syndrome. Arch Dis Child.
1998;78(1):85-88.
14. Chang P, Mukundan D. Picture of the month.
Staphylococcal scalded skin syndrome. Arch Pe-
diatr Adolesc Med. 2008;162(12):1189-1190.
15. Sladden MJ, Mortimer NJ, Elston G, Newey
M, Harman KE. Staphylococcal scalded skin
syndrome as a complication of septic arthritis.
Clin Exp Dermatol. 2007;32(6):754-755.
PEDIATRIC ANNALS 39:10 | OCTOBER 2010
9/24/2010 4:21:54 PM

16. El Helali N, Carbonne A, Naas T, Kerneis S,
Fresco O, Giovangrandi Y, Fortineau N, Nor-
dmann P, Astagneau P. Nosocomial outbreak
of staphylococcal scalded skin syndrome in
neonates: epidemiological investigation and
control. J Hosp Infect. 2005;61(2):130-138.
17. Yamasaki O, Yamaguchi T, Sugai M, Chapuis-
Cellier C, Arnaud F, Vandenesch F, Etienne
J, Lina G. Clinical manifestations of staphy-
lococcal scalded-skin syndrome depend on
serotypes of exfoliative toxins. J Clin Micro-
biol. 2005;43(4):1890-183.
18. Nishifuji K, Sugai M, Amagai M. Staphylo-
coccal exfoliative toxins: “molecular scis-
sors” of bacteria that attack the cutaneous
defense barrier in mammals. J Dermatol Sci.
2008;49(1):21-31.
19. Gentilhomme E, Faure M, Piemont Y, Binder P,
Thivolet J. Action of staphylococcal exfoliative
toxins on epidermal cell cultures and organo-
typic skin. J Dermatol. 1990;17(9):526-532.
20. Ladhani S, Joannou CL. Difficulties in diag-
nosis and management of the staphylococcal
scalded skin syndrome. Pediatr Infect Dis J.
2000;19(9):819-821.
21. Patel GK, Finlay AY. Staphylococcal scalded
skin syndrome: diagnosis and management.
Am J Clin Dermatol. 2003;4(3):165-175.
22. Cribier B, Piemont Y, Grosshans E. Staphy-
lococcal scalded skin syndrome in adults. A
clinical review illustrated with a new case. J
Am Acad Dermatol. 1994;30(2 Pt 2):319-324.
23. Darmstadt GL, Lane AT. Impetigo: an over-
PEDIATRIC ANNALS 39:10 | OCTOBER 2010
3910Berk.indd 633
CM E
view. Pediatr Dermatol. 1994;11(4):293-303.
24. Geria AN, Schwartz RA. Impetigo update:
new challenges in the era of methicillin resis-
tance. Cutis. 2010;85(2):65-70.
25. Shands KN, Schmid GP, Dan BB, et al. Toxic-
shock syndrome in menstruating women: as-
sociation with tampon use and Staphylococ-
cus aureus and clinical features in 52 cases. N
Engl J Med. 1980;303(25):1436-1442.
26. Reingold AL, Hargrett NT, Dan BB, Shands
KN, Strickland BY, Broome CV. Nonmenstru-
al toxic shock syndrome: a review of 130 cases.
Ann Intern Med. 1982;96(6 Pt 2):871-874.
27. McCormick JK, Yarwood JM, Schlievert PM.
Toxic shock syndrome and bacterial supe-
rantigens: an update. Annu Rev Microbiol.
2001;55:77-104.
28. Davis JP, Chesney PJ, Wand PJ, LaVenture M.
Toxic-shock syndrome: epidemiologic fea-
tures, recurrence, risk factors, and prevention.
N Engl J Med. 1980;303(25):1429-1435.
29. Tofte RW, Williams DN. Toxic shock syn-
drome. Evidence of a broad clinical spectrum.
JAMA. 1981;246(19):2163-2167.
30. Chesney PJ, Davis JP, Purdy WK, Wand PJ,
Chesney RW. Clinical manifestations of toxic
shock syndrome. JAMA. 1981;246(7):741-748.
31. The Working Group on Severe Streptococcal
Infections.Defining the group A streptococcal
toxic shock syndrome. Rationale and consen-
sus definition. JAMA. 1993;269(3):390-391.
32. Wolf JE, Rabinowitz LG. Streptococcal
toxic shock-like syndrome. Arch Dermatol.
1995;131(1):73-77.
33. Stevens DL. Streptococcal toxic shock syn-
drome associated with necrotizing fasciitis.
Annu Rev Med. 2000;51:271-288.
34. Wilson GJ, Talkington DF, Gruber W, Ed-
wards K, Dermody TS. Group A streptococ-
cal necrotizing fasciitis following varicella in
children: case reports and review. Clin Infect
Dis. 1995;20(5):1333-1338.
35. Lesko SM, O’Brien KL, Schwartz B, Vezina
R, Mitchell AA. Invasive group A streptococ-
cal infection and nonsteroidal antiinflamma-
tory drug use among children with primary
varicella. Pediatrics. 2001;107(5):1108-1115.
36. Cunningham MW. Pathogenesis of group A
streptococcal infections. Clin Microbiol Rev.
2000;13(3):470-511.
37. Yang SG, Dong HJ, Li FR, et al. Report and
analysis of a scarlet fever outbreak among
adults through food-borne transmission in
China. J Infect. 2007;55(5):419-424.
38. Manders SM. Toxin-mediated streptococcal
and staphylococcal disease. J Am Acad Der-
matol. 1998;39(3):383-398.
39. Bialecki C, Feder HM Jr, Grant-Kels JM. The
six classic childhood exanthems: a review and
update. J Am Acad Dermatol. 1989;21(5 Pt
1):891-903.
40. Quinn RW. Comprehensive review of morbid-
ity and mortality trends for rheumatic fever,
streptococcal disease, and scarlet fever: the
decline of rheumatic fever. Rev Infect Dis.
1989;11(6):928-953.
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