Bonus images for this chapter can be found online at

expertconsult.inkling.com

Bacterial Infections
14
Bacterial infections in the skin often have distinct morphologic Staphylococcus aureus is a normal inhabitant of the anterior
characteristics that should alert the clinician that a potentially nares in 20–40% of adults and also resides on the hands and
treatable and reversible condition exists. These cutaneous perineum in smaller numbers of individuals. Nasal carriers are
signs may be an indication of a generalized systemic process particularly prone to infections with S. aureus because of its
or simply an isolated superficial event. Immunodeficiencies continuous presence on the skin and nasal mucosa. Spread of
with low immunoglobulin levels, neutropenia, reduced neu- infection in the hospital setting is frequently traced to the
trophil migration or killing, and disease caused by the human hands of a health care worker. Proper handwashing technique
immunodeficiency virus (HIV) may be associated with severe is essential in preventing this nosocomial complication. HIV-
or refractory pyogenic infections. Patients with atopic derma- infected patients are at least twice as often nasal carriers, and
titis and syndromes with atopic-like dermatitis are also they tend to harbor S. aureus in higher frequency and density
predisposed to bacterial infections. The categorization of at other sites of the body, thus predisposing them to skin and
bacterial infections in this chapter first addresses diseases systemic infection.
caused by gram-positive bacteria, followed by those caused by Antibiotic resistance has become a clinically important con-
gram-negative bacteria, and then several miscellaneous dis- sideration in many infections. Methicillin-resistant Staphylococ-
eases caused by the rickettsiae, mycoplasmas, chlamydiae, and cus aureus (MRSA) is an important pathogen in nosocomial
spirochetes. and community-acquired skin infections. MRSA infection may
Centers for Disease Control and Prevention: STD treatment guidelines be suspected from knowledge of local patterns of resistance,
2010. MMWR 2010; 59(RR-12):1–110. lack of response to initial methicillin-sensitive S. aureus
Chon SY, et al: Antibiotic overuse and resistance in dermatology. (MSSA)–directed therapy (e.g., cefalexin), and factors predis-
Dermatol Ther 2012; 25:55–69. posing to colonization and infection with this organism. Pre-
Dawson AL, et al: Infectious skin diseases. Dermatol Clin 2012; disposing factors include age (>65), exposure to others with
30:141–151. MRSA infection, prior antibiotic therapy, trauma to the skin,
Drucker CR: Update on topical antibiotics in dermatology. Dermatol rectal or nasal colonization, crowded households, child care
Ther 2012; 25:6–11.
attendance, contact sports, chronic skin disease, pets, and
Dumville JC, et al: Preoperative skin antiseptics for preventing surgical
wound infections after clean surgery. Cochrane Database Syst Rev
recent hospitalization or chronic illness. In patients with risk
2013; 3:CD003949. factors, multidrug resistance is likely, and treatment with
Grice EA, et al: Topographical and temporal diversity of the human skin intravenous (IV) vancomycin or linezolid may be necessary.
microbiome. Science 2009; 324:1190. In community-acquired infection in patients without risk
Mistry RD: Skin and soft tissue infections. Pediatr Clin North Am 2013; factors, clindamycin, trimethoprim-sulfamethoxazole (TMP-
60:1063–1082. SMX, alone or combined with rifampin), doxycycline, or oral
Petry V, et al: Bacterial skin colonization and infections in linezolid often are effective. TMP-SMX and doxycycline do not
patients with atopic dermatitis. An Bras Dermatol 2012; cover group A streptococci; therefore, if a mixed infection is
87:729–734. suspected, adding cephalexin or penicillin is necessary, or
clindamycin alone will treat both pathogens. Definitive antibi-
otic therapy may be tailored to the antibiotic susceptibility of
the cultured organism.
INFECTIONS CAUSED BY
GRAM-POSITIVE ORGANISMS
Superficial pustular folliculitis
STAPHYLOCOCCAL INFECTIONS (impetigo of Bockhart)
The skin lesions induced by the gram-positive staphylococci Bockhart impetigo is a superficial folliculitis with thin-walled
usually appear as pustules, furuncles, or erosions with honey- pustules at the follicle orifices. Susceptible locations are the
colored crusts. However, bullae, widespread erythema and extremities and scalp, although it is also seen on the face,
desquamation, or vegetating pyodermas may also be indica- especially periorally. These fragile, yellowish white, domed
tors of Staphylococcus aureus infection. Purulent purpura may pustules develop in crops and heal in a few days. S. aureus is
indicate bacteremia or endocarditis caused by S. aureus or, in the most frequent cause. The infection may secondarily arise
immunocompromised patients, S. epidermidis. Two distinctive in scratches, insect bites, or other skin injuries.
cutaneous lesions that occur with endocarditis are the Osler
node and aneway lesion or spot. The Osler node is a painful,
erythematous nodule with a pale center located on the finger- Sycosis vulgaris (sycosis barbae)
tips. The aneway spot is a nontender, angular hemorrhagic
lesion of the soles and palms (Fig. 14-1). These lesions are Sycosis vulgaris, also known as “barber’s itch” or sycosis
likely caused by septic emboli. barbae, is a perifollicular, chronic, pustular staphylococcal
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14
Bacterial Infections

Fig. 14-1 Janeway lesion in subacute bacterial endocarditis. Fig. 14-3 Staphylococcal folliculitis.

patients with acquired immunodeficiency syndrome (AIDS)

and may be a cause of pruritus. An atypical, plaquelike form
has been reported.

Treatment
Deep lesions of folliculitis represent small follicular abscesses
and must be drained. Superficial pustules will rupture and
drain spontaneously. Many patients will heal with drainage
and topical therapy. Bacitracin (Bactroban) or retapamulin
ointment and topical clindamycin (Cleocin) solution are effec-
tive topical agents. Skin surface staphylococcal carriage in
abrasions and eczematous areas may be addressed with these
topical antibiotics, topical chlorhexidine, or bleach baths ( 1 2
cup bleach added to tub of bathwater). If drainage and topical
therapy fail, or if there is accompanying soft tissue infection,
a first-generation cephalosporin or penicillinase-resistant pen-
Fig. 14-2 Sycosis barbae. icillin (e.g., dicloxacillin) is indicated, unless MRSA is sus-
pected (see earlier). When the inflammation is acute, hot wet
infection of the bearded region characterized by inflammatory soaks with aluminum acetate (Burow) solution diluted 1 : 20
papules and pustules, and a tendency to recurrence (Fig. 14-2). (Domeboro) are beneficial. An anhydrous formulation of alu-
The disease begins with erythema and burning or itching, minum chloride (Drysol, Xerac-AC) is effective when used
usually on the upper lip near the nose. In 1 or 2 days, one or once nightly for chronic folliculitis, especially of the buttocks.
more pinhead-sized pustules, pierced by hairs, develop. These Antibiotic ophthalmic ointments are used for blepharitis.
rupture after shaving or washing and leave an erythematous
spot, which is later the site of a fresh crop of pustules. In this
manner, the infection persists and gradually spreads, at times Furunculosis
extending deep into the follicles. A hairless, atrophic scar bor-
dered by pustules and crusts may result. Marginal blepharitis A furuncle, or boil, is an acute, round, tender, circumscribed,
with conjunctivitis is usually present in severe cases of sycosis. perifollicular staphylococcal abscess that generally ends in
Sycosis vulgaris is to be distinguished from tinea, acne vul- central suppuration (Fig. 14-4). A carbuncle is merely two or
garis, pseudofolliculitis barbae, and herpetic sycosis. Tinea more confluent furuncles, with separate heads.
barbae rarely affects the upper lip, which is a common location The lesions begin in hair follicles and often continue for a
for sycosis. In tinea barbae, involvement is usually in the sub- prolonged period by autoinoculation. Some lesions disappear
maxillary region or on the chin, and spores and hyphae are before rupture, but most undergo central necrosis and rupture
found in the hairs. Pseudofolliculitis barbae manifests torpid through the skin, discharging purulent, necrotic debris. Sites
papules at sites of ingrowing beard hairs in black men. In of predilection are the nape, axillae, and buttocks, but boils
herpes simplex virus (HSV) infection, duration is usually only may occur anywhere.
a few days, and even in persistent cases there are vesicles, The integrity of the skin surface may be impaired by irrita-
which help to differentiate HSV from sycosis vulgaris. tion, pressure, friction, hyperhidrosis, dermatitis, dermato-
phytosis, shaving, and other factors. Local barrier compromise
predisposes to infection by providing a portal of entry for the
Folliculitis ubiquitous S. aureus. The proximate cause is either contagion
or autoinoculation from a carrier focus, usually in the nose or
Staphylococcal folliculitis may affect areas such as the eye- groin.
lashes, axillae, pubis, and thighs (Fig. 14-3). On the pubis, it Certain systemic disorders may predispose to furunculosis:
may be transmitted among sexual partners, and “mini” epi- alcoholism; malnutrition; blood dyscrasias; disorders of
demics of folliculitis and furunculosis of the genital and gluteal neutrophil function; iatrogenic or other immunosuppression
areas may be considered a sexually transmitted disease (STD). (e.g., AIDS); and diabetes (Fig. 14-5). Patients with several of
Staphylococcal folliculitis has also been reported frequently in these diseases, as well as those receiving renal dialysis or
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 Fig. 14-4 antibiotics are administered. A penicillinase-resistant penicil-
Staphylococcal lin or first-generation cephalosporin should be given orally in
abscess. a dose of 1–2 g/day, according to the severity of the case.
Methicillin-resistant and even vancomycin-resistant strains
occur and, if suspected, are treated with trimethoprim-

Staphylococcal Infections
sulfamethoxazole double strength twice daily, clindamycin
300 to 450 mg three times daily, or doxycycline or minocycline
100 mg two times daily. In patients with staphylococcal infec-
tions unresponsive to these usual measures, antibiotic-resistant
strains should be suspected and sensitivities checked. Mupi-
rocin ointment applied to the anterior nares daily for 5 days
and bleach baths may help prevent recurrence.
When the furuncle has become localized and shows definite
fluctuation, incision with drainage is indicated. The cavity
should be packed with iodoform or petrolatum gauze. In these
cases, oral antibiotics are not usually necessary. Indications for
antibiotics in addition to drainage are high fever, lesion larger
than 5 cm or located in a critical location or difficult-to-drain
area, multiple furuncles, or signs and symptoms persisting
after drainage.
In boils of the external auditory canal, upper lip, and nose,
incision and drainage are generally only performed if antibi-
otic therapy fails. In these patients, antibiotic ointment should
be applied and antibiotics given internally. Warm saline-
solution compresses should be applied liberally.

Chronic furunculosis
Fig. 14-5 Staphylococcal
abscess in a diabetic Despite treatment, recurrences of some boils may be antici-
patient. pated. Usually, no underlying predisposing disease is present;
rather, autoinoculation and intrafamilial spread among colo-
nized individuals are responsible.
One of the most important factors in prevention is to avoid
autoinoculation. It is important to emphasize that the nasal
carrier state predisposes to chronic furunculosis. The skin
surface in the region of the furuncles may be a source of colo-
nization, especially if there are cuts, excoriation, or eczematous
changes. In addition, the hazard of contamination from the
perianal and intertriginous areas must be considered. In
general, indications for elimination of the carriage state are
recurrent infection, evidence of spread to others, and high-risk
individuals in the household.
Routine precautions to take in attempting to break the cycle
of recurrent furunculosis include a daily chlorhexidine wash,
with special attention to the axillae, groin, and perianal area;
laundering of bedding and clothing on a daily basis initially;
use of bleach baths; and frequent handwashing. Additionally,
the application of mupirocin ointment twice daily to the nares
of patients and family members every fourth week has been
isotretinoin or acitretin therapy, are often nasal carriers of found to be effective. Rifampin (600 mg/day) for 10 days,
S. aureus. Additionally, atopic dermatitis also predisposes to combined with dicloxacillin for MSSA or TMP-SMX for MRSA,
the S. aureus carrier state, which helps explain the observed or low-dose (150 mg/day) clindamycin for 3 months is also
increases in the incidence of infections in these diseases. effective in eradicating the nasal carriage state. The use of
bacitracin ointment inside the nares twice daily throughout
Hospital furunculosis the course of isotretinoin therapy eliminates, or greatly
reduces, the risk of inducing nasal carriage of S. aureus and
Epidemics of staphylococcal infections occur in hospitals. thus staphylococcal infections.
Marked resistance to antibacterial agents in these cases is
common. Attempts to control these outbreaks center on metic-
ulous handwashing. In nurseries, a fall in neonatal coloniza- Pyogenic paronychia
tion and infections with S. aureus and non–group A streptococci
may be achieved by using a 4% solution of chlorhexidine for Paronychia is an inflammatory reaction involving the folds of
skin and umbilical cord care. the skin surrounding the fingernail. It is characterized by
acute or chronic purulent, tender, and painful swellings of
Treatment the tissues around the nail, caused by an abscess in the nail-
fold. When the infection becomes chronic, horizontal ridges
When the lesions are incipient and acutely inflamed, incision appear at the base of the nail. With recurrent bouts, new
should be strictly avoided, and warm compresses and oral ridges appear.
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 Fig. 14-6 Fig. 14-8
14 Staphylococcal
paronychia.
Botryomycosis.
Bacterial Infections

warts may mimic paronychia. Subungual black macules, fol-

Fig. 14-7 lowed by edema, pain, and swelling, have been reported as a
Streptococcal sign of osteomyelitis caused by S. aureus or Streptococcus iri-
paronychia and
dans, in children with atopic dermatitis.
impetigo.
Treatment of pyogenic paronychia consists mostly of protec-
tion against trauma and concentrated efforts to keep the
affected fingernails meticulously dry. Rubber or plastic gloves
over cotton gloves should be used whenever the hand must
be placed in water. Acutely inflamed pyogenic abscesses
should be incised and drained. The abscess may often be
opened by pushing the nailfold away from the nail plate. In
acute suppurative paronychia, especially if stains show pyo-
genic cocci, a semisynthetic penicillin or a cephalosporin with
excellent staphylococcal activity should be given orally. If
these are ineffective, MRSA or a mixed–anaerobic bacteria
infection should be suspected. TMP-SMX for the latter or treat-
ment dictated by the sensitivity of the cultured organism will
improve cure rates. Rarely, long-term antibiotic therapy may
The primary predisposing factor that is identifiable is sepa- be required.
ration of the eponychium from the nail plate. The separation While Candida is the most frequently recovered organism in
is usually caused by trauma as a result of moisture-induced chronic paronychia, topical or oral antifungals lead to cure in
maceration of the nailfolds from frequent wetting of the hands. only about 50% of cases. If topical corticosteroids are used to
The relationship is close enough to justify treating chronic decrease inflammation and allow for tissue repair, cure results
paronychia as a work-related condition in bartenders, food more reliably (almost 80% in one study). Often, an antifungal
servers, nurses, and others who often wet their hands. The liquid such as miconazole is combined with a topical cortico-
moist grooves of the nail and nailfold become secondarily steroid cream or ointment.
invaded by pyogenic cocci and yeasts. The causative bacteria
are usually S. aureus, Streptococcus pyogenes, Pseudomonas
species, Proteus species, or anaerobes. The pathogenic yeast is Botryomycosis
most frequently Candida albicans.
The bacteria usually cause acute abscess formation (Staphy- Botryomycosis is an uncommon, chronic, indolent disorder
lococcus Fig. 14-6) or erythema and swelling (Streptococcus Fig. characterized by nodular, crusted, purulent lesions (Fig. 14-8).
14-7), and C. albicans most frequently causes a chronic swell- Sinuses that discharge sulfur granules are present. These heal
ing. If an abscess is suspected, applying light pressure with with atrophic scars. The granules most frequently yield S.
the index finger against the distal volar aspect of the affected aureus on culture, although cases caused by Pseudomonas aeru-
digit will better demonstrate the extent of the collected pus by ginosa, Escherichia coli, Proteus, acteroides, and Streptococcus
inducing a well-demarcated blanching. Smears of purulent have been reported. Botryomycosis often occurs in patients
material will help confirm the clinical impression. Myrmecial with altered immune function, such as those with neutrophilic
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defects. Other predisposing factors include diabetes, HIV is noted. The exudate dries to form loosely stratified, golden-
infection, alcoholism, and ob syndrome. Appropriate antibi- yellow crusts, which accumulate layer upon layer until they
otics, surgical drainage, and surgical excision are methods are thick and friable. The crusts can usually be removed
used to treat botryomycosis. readily, leaving a smooth, red, moist surface that soon collects
droplets of fresh exudate again; these are spread to other parts

Staphylococcal Infections
of the body by fingers or towels. As the lesions spread periph-
Blastomycosis-like pyoderma erally and the skin clears centrally, large circles are formed by
fusion of the spreading lesions to produce gyrate patterns. In
Large, verrucous plaques with elevated borders and multiple streptococcal-induced impetigo, regional lymphadenopathy is
pustules occur. Most patients with blastomycosis-like pyo- common, but not serious.
derma have some underlying systemic or local host compro- Most studies find 50–70% of cases are caused by S. aureus,
mise. Bacteria such as S. aureus, P. aeruginosa, Proteus, E. coli, with the remainder from either S. pyogenes or a combination
or streptococci may be isolated. Antibiotics appropriate for the of these two organisms. Streptococci may represent an early
organism isolated are curative; however, response may be pathogen in the development of impetigo, with staphylococci
delayed and prolonged therapy required. Acitretin may also replacing streptococci as the lesion matures. Group B strepto-
be useful. cocci are associated with newborn impetigo, and groups C and
G are rarely isolated from impetigo, unlike the usual group A.
Impetigo occurs most frequently in early childhood (Fig.
Pyomyositis 14-10), although all ages may be affected. It occurs in the tem-
perate zone, mostly during the summer in hot, humid weather.
Staphylococcus aureus abscess formation within the deep, large, Common sources of infection for children are pets, dirty fin-
striated muscles usually presents with fever and muscle pain. gernails, and other children in schools, day care centers, or
It is typically hematogenous in origin. Pyomyositis is more crowded housing areas; sources for adults include infected
common in the tropics, where it may affect adults but most children and self-inoculation from nasal or perineal carriage.
frequently occurs in children. In temperate climates, it occurs Impetigo often complicates pediculosis capitis, scabies, HSV,
in children and patients with AIDS. The most frequent site in insect bites, poison ivy, eczema, and other exudative, pustular,
tropical disease is the thigh, whereas in HIV-infected patients, or itching skin diseases.
the deltoid muscle is most often involved, followed closely by Group A β-hemolytic streptococcal skin infections are some-
the quadriceps. Swelling and occasionally erythema or yellow times followed by acute glomerulonephritis (AGN). Nephrito-
or purplish discoloration are visible signs of pyomyositis, but genic streptococci are generally associated with impetigo
these are late findings. Non–S. aureus infections may also cause rather than with upper respiratory tract infections. There is no
this same clinical picture. Magnetic resonance imaging (MRI) evidence that AGN occurs with staphylococcal impetigo. The
with gadolinium injection will help delineate the extent of important factor predisposing to AGN is the serotype of the
disease. Drainage of the abscess and appropriate systemic streptococcus producing the impetigo. Type 49, 55, 57, and 60
antibiotics are the recommended treatment. strains and strain M-type 2 are related to nephritis.
The incidence of AGN with impetigo varies from about 2%
to 5% (10–15% with nephritogenic strains of streptococcus)
Impetigo contagiosa and occurs most frequently in childhood, generally before age
6. The prognosis in children is mostly excellent, but in adults
Impetigo contagiosa is a staphylococcal, streptococcal, or com- it is not as good. Treatment, however early and appropriate,
bined infection characterized by discrete, thin-walled vesicles is not believed to reduce the risk of AGN.
that rapidly become pustular and then rupture. Impetigo Impetigo may simulate several diseases. The circinate
occurs most frequently on the exposed parts of the body: the patches are frequently mistaken for ringworm, but clinically
face, hands, neck, and extremities (Fig. 14-9). Impetigo on the are quite different. Impetigo is characterized by superficial,
scalp is a frequent complication of pediculosis capitis. very weepy lesions covered by thick, bright-yellow or orange
The disease begins with 2-mm erythematous macules, which crusts with loose edges, which do not resemble the scaling
may shortly develop into vesicles or bullae. As soon as these patches with peripheral erythema seen in tinea. Impetigo may
lesions rupture, a thin, straw-colored, seropurulent discharge be mistaken for Toxicodendron dermatitis, but it is more crusted
and pustular and more likely to involve the nostrils, corners
of the mouth, and ears. Impetigo is not associated with the

Fig. 14-10 Impetigo of

early childhood.

Fig. 14-9 Impetigo.

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 eyelid puffiness, the linear lesions, or the itchiness typically Fig. 14-11 Bullous
14 present in dermatitis and caused by poison ivy or oak. In
ecthyma, the lesions are crusted ulcers, not erosions.
impetigo.

Treatment
Bacterial Infections

Systemic antibiotics combined with topical therapy are recom-

mended for patients with impetigo contagiosa. Because most
cases are caused by Staphylococcus, a semisynthetic penicillin
or a first-generation cephalosporin is recommended, unless
MRSA is suspected, as detailed earlier. All treatment should
be given for 7 days. It is necessary to soak off the crusts fre-
quently, after which an antibacterial ointment should be
applied. If the lesions are localized, especially if facial, and are
present in an otherwise healthy child, topical therapy may be
effective as the sole treatment.
Applying antibiotic ointment as a prophylactic to sites of
skin trauma will prevent impetigo in high-risk children attend-
ing day care centers. In one study, infections were reduced by
47% with antibiotic ointment versus 15% with placebo. Addi-
tionally, if recurrent staphylococcal impetigo develops, a
culture of the anterior nares may yield this organism. Such
carrier states may be treated by application of mupirocin oint-
ment to the anterior nares twice daily or by a 10-day course of
rifampin, 600 mg/day, combined with dicloxacillin (for MSSA)
or TMP-SMX (for MRSA).

Bullous impetigo
The bullous variety of impetigo occurs characteristically in
newborns, although it may occur at any age. The neonatal type
is highly contagious and is a threat in nurseries. In most cases,
the disease begins between the fourth and tenth days of life
with the appearance of bullae, which may appear on any part
of the body. Common early sites are the face and hands.
Constitutional symptoms are absent at first, but weakness
and fever or a subnormal temperature may be present later.
Diarrhea with green stools frequently occurs. Bacteremia,
pneumonia, or meningitis may develop rapidly, with fatal
termination. Fig. 14-12 Staphylococcal scalded skin syndrome.
In warm climates particularly, adults may have bullous
impetigo (Fig. 14-11), most often in the axillae or groins, but
also on the hands. Usually, no scalp lesions are present. The A and B, elaborated by the staphylococcus in remote sites.
lesions are strikingly large, fragile bullae, suggestive of pem- Usually, staphylococci are present at a distant focus, such as
phigus. When these rupture, they leave circinate, weepy, or the pharynx, nose, ear, or conjunctiva. Septicemia or a cutane-
crusted lesions, and in this stage it may be called impetigo ous infection may also be the causative focus.
circinata. Children with bullous impetigo may give a history Clinical manifestations of SSSS begin abruptly with fever,
of an insect bite at the site of onset of lesions. The majority are skin tenderness, and erythema involving the neck, groins, and
caused by phage types 71 or 55 coagulase-positive S. aureus or axillae (Fig. 14-12). There is sparing of the palms, soles, and
a related group 2 phage type. Bullous impetigo may be an mucous membranes. Nikolsky’s sign is positive. Generalized
early manifestation of HIV infection. exfoliation follows within the next hours to days, with large
sheets of epidermis separating. Group 2 S. aureus, usually
phage types 71 or 55, is the causative agent in most cases. If
Staphylococcal scalded skin syndrome taken, cultures should be obtained from the mucous mem-
branes because the skin erythema and desquamation are
Staphylococcal scalded skin syndrome (SSSS) is a generalized, caused by the distant effects of the exfoliative toxins, unlike in
confluent, superficially exfoliative disease, occurring most bullous impetigo, where S. aureus is present in the lesions.
often in neonates and young children. It occurs rarely in Rapid diagnosis of SSSS can be made by examining frozen
adults, usually with renal compromise or immunosuppression sections of a blister roof and observing that the full thickness
as a predisposing factor. SSSS is a febrile, rapidly evolving, of the epidermis is not necrotic, as in TEN, but rather is cleaved
desquamative infectious disease in which the skin exfoliates below the granular layer. The exfoliative toxins A, B, and D
in sheets. Skin does not separate at the dermoepidermal junc- specifically cleave desmoglein 1, the antigenic target of
tion, as in toxic (drug-induced) epidermal necrolysis (TEN), autoantibodies in pemphigus foliaceus, thus accounting
but within the granular layer. The lesions are thus much more for the clinical and histologic similarity to pemphigus observed
superficial and less severe than in TEN, and healing is much in SSSS and bullous impetigo. Treatment of choice is a
more rapid. They also extend far beyond areas of actual staph- penicillinase-resistant penicillin such as dicloxacillin com-
ylococcal infection, by action of the exfoliative exotoxins types bined with fluid therapy and general supportive measures. If
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MRSA is cultured and response is sluggish, antibiotics directed
according to the susceptibility of the recovered organism are
needed. The prognosis is good in children, but mortality in
adults can reach 60%.

Staphylococcal Infections
Gram-positive toxic shock syndromes
Toxic shock syndrome (TSS) is an acute, febrile, multisystem
illness, with one of its major diagnostic criteria being a wide-
spread macular erythematous eruption. It is usually caused by
toxin-producing strains of S. aureus, most of which were ini-
tially isolated from the cervical mucosa in menstruating young
women. Currently, cases are most often caused by infections
in wounds, catheters, contraceptive diaphragms, or nasal
packing. Mortality in these nonmenstrual cases is higher (up
to 20%) compared with menstrual-related cases (<5%), prob-
ably as a result of delayed diagnoses. Also, a similar syndrome
has been defined in which the cause is group A, or rarely
group B, streptococci. This latter multiorgan disease has
systemic components similar to classic staphylococcal TSS;
however, the infection is usually a rapidly progressive,
destructive soft tissue infection such as necrotizing fasciitis.
Women with an underlying chronic illness, recently recovered
from varicella, or using nonsteroidal anti-inflammatory drugs
(NSAIDs) are predisposed. It has a case-fatality rate of 30%.
The streptococci are usually of M-types 1 and 3, with 80% of
the isolates producing pyrogenic exotoxin A.
The Centers for Disease Control and Prevention (CDC) case
definition of staphylococcal TSS includes a temperature of
38.9 C (102 F) or higher, an erythematous eruption, desqua-
mation of the palms and soles 1–2 weeks after onset
(Fig. 14-13), hypotension, and involvement of three or more Fig. 14-13 Desquamation of the palms and soles.
other systems: gastrointestinal (GI; vomiting, diarrhea), mus-
cular (myalgias, increased creatinine kinase level), mucous
membrane (hyperemia), renal (pyuria without infection or Treatment of TSS consists of systemic antibiotics such as
raised creatinine or blood urea nitrogen levels), hepatic vancomycin, which may be combined with nafcillin, 1–1.5 g
(increased bilrubin/serum glutamic oxaloacetic transami- intravenously every 4 h in critically ill patients; vigorous
nase/serum glutamic pyruvic transaminase), hematologic fluid therapy to treat shock; and drainage of the S. aureus–
(platelets <100 000/mm3), or central nervous system (CNS; dis- infected site.
orientation). In addition, serologic tests for Rocky Mountain
spotted fever, leptospirosis, and rubeola, and cultures of Agarwal V, et al: Pyomyositis. Neuroimaging Clin North Am 2011;
blood, urine, and cerebrospinal fluid should be negative. Pro- 21:975–983.
Al-Najar M, et al: Primary extensive pyomyositis in an
calcitonin, an indicator of severe bacterial infection, may be a
immunocompetent patient. Clin Rheumatol 2010; 29:1469–1472.
biologic marker for the toxic shock syndromes. Bulbar con- Antoniou T, et al: Prevalence of community-associated methicillin-
junctival hyperemia and palmar edema are two additional resistant Staphylococcus aureus colonization in men who have sex
clinical clues. Streptococcal TSS is defined by isolation of with men. Int J STD AIDS 2009; 20:180.
group A β-hemolytic streptococci, hypotension, and two or Atanaskova N, et al: Innovative management of recurrent furunculosis.
more of the following: renal impairment, coagulopathy, Dermatol Clin 2010; 28:479.
hepatic involvement, acute respiratory distress syndrome, a Bangert S, et al: Bacterial resistance and impetigo treatment trends.
generalized erythematous macular eruption that may desqua- Pediatr Dermatol 2012; 29:243–248.
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 Elston DM: How to handle a CA-MRSA outbreak. Dermatol Clin 2009; Fig. 14-14 Ecthyma.
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Scarlet fever
Van Rijen M, et al: Mupirocin ointment for preventing Staphylococcus
aureus infections in nasal carriers. Cochrane Database Syst Rev 2008; Scarlet fever is a diffuse, erythematous exanthem that occurs
4:CD006216. during the course of streptococcal pharyngitis. It affects pri-
marily children, who develop the eruption 24–48 h after onset
of pharyngeal symptoms. The tonsils are red, edematous, and
covered with exudate. The tongue has a white coating through
STREPTOCOCCAL SKIN INFECTIONS which reddened, hypertrophied papillae project, giving the
so-called white strawberry tongue appearance. By the fourth
Specific diseases caused by direct infection with Streptococcus or fifth day the coating disappears, the tongue is bright red,
pyogenes and its toxins, as discussed in this chapter, also have and the red strawberry tongue remains.
immune-mediated consequences, including acute rheumatic The cutaneous eruption begins on the neck, then spreads to
fever, chronic rheumatic heart disease, and acute poststrepto- the trunk and finally the extremities (Fig. 14-15). Within the
coccal glomerulonephritis. The last two only occur after phar- widespread erythema are 1–2 mm papules, which give the
yngitis or tonsillitis. Although most of such complications skin a rough, sandpaper quality. There is accentuation over
occur in resource-poor countries, the global burden of these the skinfolds, and a linear petechial eruption, called Pastia
sequelae is significant. lines, is often present in the antecubital and axillary folds.
There is facial flushing and circumoral pallor. A branny des-
quamation occurs as the eruption fades, with peeling of the
Ecthyma palms and soles taking place about 2 weeks after the acute
illness. The latter may be the only evidence that the disease
Ecthyma is an ulcerative staphylococcal or streptococcal pyo- has occurred.
derma, almost always of the shins or dorsal feet. The disease The eruption is produced by erythrogenic exotoxin-
begins with a vesicle or vesicopustule, which enlarges and in producing group A streptococci. Cultures of the pharynx will
a few days becomes thickly crusted. When the crust is removed, recover these organisms. Rarely, scarlet fever may be related
there is a superficial, saucer-shaped ulcer with a raw base and to a surgical wound or burn infection with streptococci. An
elevated edges (Fig. 14-14). In urban areas, these lesions are elevated antistreptolysin O titer may provide evidence of
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