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MRSA, Staphylococcal Scalded Skin Syndrome,

and Other Cutaneous Bacterial Emergencies

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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 management of bacterial skin emergencies
in children, including important treatment and infection control measures.

David R. Berk, MD, is Assistant Professor

of Dermatology and Pediatrics, Department of Internal Medicine and Pediatrics,
Division of Dermatology, Washington
University School of Medicine and St. Louis
Childrens Hospital, St. Louis, MO.
Susan J. Bayliss, MD, is Professor of Dermatology and Pediatrics, Director of Pediatric Dermatology, Residency Program Director, Department of Internal Medicine and
Pediatrics, Division of Dermatology, Washington University School of Medicine and St.
Louis Childrens Hospital, St. Louis, MO.
Address correspondence to: David R.
Berk, MD, Campus Box 8123, 4921 Parkview
Place, St. Louis, MO 63110; fax: 314-7478693; e-mail: [email protected].
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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utaneous bacterial infections

are important to recognize in
pediatrics. Some may actually
be emergencies. These include localized
skin infections, such as methicillin-resistant Staphylococcus aureus (MRSA)
infections, as well as more generalized
toxin-mediated diseases, such as toxic
shock syndrome (TSS) and staphylococcal scalded skin syndrome (SSSS).
It is important for pediatricians to recognize and distinguish these cutaneous
bacterial emergencies so treatment and
appropriate infection control measures
can be promptly initiated.
MRSA
MRSA poses therapeutic and public health challenges because of its
increasing incidence, enhanced virulence, and frequent multidrug resistance.1-3 MRSA infections most
commonly involve the skin and soft
tissues, typically manifesting as suppurative lesions such abscesses, furuncles, folliculitis, or cellulitis (see
Figure 1, page 629).4-6 Infections may
occur at any site but especially on the
buttocks and lower extremities. Because pustular lesions commonly have
a necrotic center, they are often confused with spider bites. Skin and softtissue 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 nasal 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 protein 2a, a transpeptidase with very
low affinity for beta-lactams. Penicillin-binding protein 2a catalyzes the
transpeptidation reactions of peptido-

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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 nonMRSA isolates. PVL acts as a cytotoxin, causing lysis of leukocytes and tissue necrosis. In addition, PVL is more
often found in MRSA strains, which
contain staphylococcal cassette chromosome mec type IV or V rather than
I, II, or III. PVL is encoded by the lukSPV and lukF-PV genes. Other virulence
factors for MRSA include alpha-hemolysin and phenol soluble modulins.9
When possible, incision and drainage are a critical part of initial therapy 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 manifestations or immunocompromise. Antibiotic 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 either suspected to be due to MRSA or
which do not respond to initial incision, drainage, and beta-lactam antibiotics. These agents include clindamycin, trimethoprim/sulfamethoxazole,
tetracycline, linezolid, or vancomycin. 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 exfoliative) 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 bullous 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 peeling, flaccid bullae, and denuded tender
skin (see Figure 2, page 630).14
Erythema arises abruptly, spreads
rapidly, and demonstrates characteristic 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 tenderness 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 rhinorrhea, 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 extracutaneous infections, such as pneumonia,
pyomyositis, endocarditis, urinary tract
infection, and septic arthritis.15
The predilection of SSSS for newborns and young children may be
caused by decreased renal clearance of
ET and/or the lack of anti-toxin antibodies. Outbreaks in nurseries and intensive care units are well described.16
Two types of ET mediate SSSS, including ET-A and ET-B, both of which
are serine proteases.17,18 These two
ETs target desmoglein-1, a cell adhesion protein located in desmosomes in
the superficial epidermis, explaining

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the superficial cleavage plane within
the stratum granulosum seen in lesions of SSSS. These ETs also possess 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 ETB 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 because these are induced by circulating
ET and, therefore, are typically sterile,
unless secondarily infected. Bacteremia 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 blistering disease characterized by a significantly 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 syndrome, Kawasaki disease, and nutritional deficiencies.
Treatment of generalized SSSS includes 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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Figure 1. Children with abscesses (A) and carbuncles (B) typical of methicillin-resistant Staphylococcus
aureus.

adjustments made based on local resistance patterns and sensitivities of

obtained cultures. Skin care generally
consists of bland emollients (petroleum 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 necessary initially when the skin is too tender to touch but is used an adjunct later.
Other important measures include contact 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 sepsis, secondary infections, electrolyte
imbalances, fluid losses, and hypothermia. 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 rapidly to treatment, with complete recovery 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 immunocompromise 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, nonbullous impetigo demonstrates the classic honey-colored crust and commonly
affects the face, especially around the
nose. The differential diagnosis sometimes includes herpes simplex infection.
In contrast, bullous impetigo is the localized version of SSSS and is, therefore,
always caused by S. aureus. Clinically,
bullous impetigo presents with flaccid 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 often 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 mediated by the same ET-A and -B, and typically 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 staphylococcal vaginal infection or colonization
by phage group 1 S. aureus. Historically, it was associated with the usage of
superabsorbent tampons.25
Non-menstrual TSS is also caused
by S. aureus, and may be associated

with upper airway infections, burns,

postpartum infections, cutaneous infections, surgical procedures, and
nasal packing.26 Staphylococcal TSS
is mediated by toxic shock syndrome
toxin-1 and staphylococcal enterotoxins-A, -B, and -C. These toxins act
as superantigens, directly activating
T cells, resulting in massive cytokine
release.27 TSS toxin-1 may also decrease clearance of endotoxins from
gut flora.

Figure 3. Flaccid bullae in the diaper area of a newborn with bullous impetigo.

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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 scarlatiniform eruption or erythema with
flexural accentuation. Other common
findings include pharyngitis, conjunctival and mucosal membrane hyperermia, strawberry tongue, and generalized 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 onset, full thickness desquamation of the
palms (especially subungually), soles,
and perineum occurs. Nail and hair
shedding may occur later. Particularly
concerning complications include respiratory distress syndrome, which is
more common in children, as well as
disseminated intravascular coagulation, myocardial dysfunction, and renal
failure. Positive blood cultures are uncommon (< 15%), and mortality is less
than 3%. Diagnosis is based on clinical
criteria (see Sidebar 1, page 631).

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SIDEBAR 1.

CDC Case Definition

for SSSS
Clinical Criteria
Temperature > 38.9C
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
Figure 4. Papular, sandpaper-like plaques with streptococcal infections.

Hematologic
Central nervous system

Laboratory Criteria
The differential diagnosis of staphylococcal 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 characterized by shock and multiorgan failure. Skin biopsies in staphylococcal
TSS reveal non-specific findings and
are usually unnecessary, but can help
eliminate some conditions in the differential diagnosis, such as TEN.
The mainstay of treatment of staphylococcal TSS includes rapid identification 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 antistaphylococcal antibiotics and supportive care are
necessary. Antibiotics that inhibit toxin
production, including clindamycin, fluoroquinolones, and rifampin, are sometimes recommended.
STREPTOCOCCAL TSS
Streptococcal toxic shock syndrome
(STSS) is caused by infection with

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particular toxin-producing strains of

Streptococcus pyogenes, including M
protein types 1, 3, 12 and 28.31 Important toxins in the pathogenesis include
streptococcal pyrogenic exotoxin-A,
-B, and -C, streptococcal superantigen, and mitogenic factor.27 Unlike
staphylococcal TSS, STTS is more often associated with a focal tissue infection and bacteremia, as well as a more
fulminant course and greater lethality
(mortality of 30% to 60%).32,33
Moreover, patients with STSS typically present with severe pain, usually
affecting a leg and often out of proportion to objective findings, such as edema 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 staphylococcal TSS. Very soon after presentation, patients quickly develop shock
and multiorgan failure, such as renal
failure, respiratory distress syndrome,
and disseminated intravascular coagulation. Bullae are uncommon and are
associated with poor prognosis. Some
patients demonstrate erythroderma and
desquamation 1 to 2 weeks after disease

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/toxicsscurrent.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 cultures. 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 supportive 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 definition + isolation of group A beta-hemolytic Streptococcus from a non-sterile site
Confirmed disease: Clinical case definition + isolation of group A beta-hemolytic Streptococcus from a normally
sterile site
Source: www.cdc.gov/ncphi/disss/nndss/casedef/streptococcalcurrent.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 (erythrogenic) exotoxin-A, -B, or -C.36 Streptococcal tonsillopharyngitis is usually
the source of infection. Wound infections, burns, pelvic infections, foodborne outbreaks, and cellulitis are other
possible sources.37
Most patients abruptly develop fever 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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petechiae (Forschheimers spots) may be

present on the palate, as well as a white
strawberry tongue that sloughs to become a red strawberry tongue.38,39
The rash of scarlet fever is characterized by blanchable, confluent,
erythematous macules and patches, as
well as tiny papules with a dry, sandpaper-like texture (see Figure 4, page
631). Lesions often start on the upper
trunk, then generalize over days, sparing the palms and soles, and involving
the legs last. Pastias lines refer to accentuation of erythema with linear petechiae in skin folds. Accentuation is
also common at dependent sites. Facial
flushing with circumoral pallor is common. The rash fades within a week and
is followed a week later by a superficial desquamation, especially in skin
folds, on the face and in sheets from the
hands and feet (may take 2 to 6 weeks).
Beaus lines (transverse nail grooves)
and telogen effluvium (hair loss) may
present after the illness. Early complications may include pneumonia, otitis
media, bacteremia, and osteomyelitis.
Later complications may include glomerulonephritis 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 reactions. Similar rashes can also be seen
with pharyngeal infections with S. aureus, 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 antibiotics, the mortality of scarlet fever was
approximately 20%.40 The antibiotic
of choice for scarlet fever is penicillin. Treatment is important to relieve
symptoms, to minimize spreading the
infection to others, and to avoid complications, such as rheumatic fever.

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