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trunk and neck of adolescents. Systemic steroids and chemotherapy (EGFR
inhibitors) patients who are immunodeficient can have folliculitis caused by
gram-negative bacteria or fungi. Performing a culture of the pus expressed
from an intact pustule establishes the diagnosis and guides therapy.
It is very important to recognize that vesicular eruption of herpes simplex
virus (HSV) or varicella zoster virus (VZV) can also look pustular if the
eruption has been present for a few days. Neutrophils infiltrate the vesicles
and make them look pustular. Therefore, in neonates with pustular
eruptions, and any child with recurrent localized areas of grouped pustules,
HSV should be considered.
Disseminated Gonococcal Infections (See also Chapter 94
Infectious Disease Emergencies )
Localized genitourinary or oral infection with Neisseria gonorrhoeae can
rarely disseminate to the skin, presenting with erythematous papules,
petechiae, or vesicle-pustules on a hemorrhagic base. These cutaneous
lesions usually develop on the trunk but may occur anywhere on the
extremities. Disseminated N. gonorrhoeae should be considered in sexually
active or sexually abused children, especially if the partner has a history of
vaginal or penile discharge.
Diagnosis can be made by culture of vesiculopustular skin lesions, blood
culture, or positive culture of oral or genital sites. Gram stains of pustules
show gram-negative diplococci and can help support the clinical diagnosis,
although Neisseria meningitidis may have the same appearance on Gram
stain. Based on resistance patterns, recommended current therapy is
ceftriaxone until clinical improvement is seen, at which point it can be
changed to an oral antibiotic, such as cefixime, ciprofloxacin, ofloxacin, or
levofloxacin, for a total of a 7-day course. Quinolones should not be used
for infections in men who have intercourse with men or in those with a
history of recent foreign travel or partners’ travel, or infections acquired in
other areas with increased resistance. Concomitant sexually transmitted
diseases should be tested for and treated empirically.

Furunculosis
Furunculosis is an acute purulent abscess extending from the dermis into
the subcutis. Furuncles manifest as painful red or purple fluctuant nodules


with or without a pustule on top ( Fig. 66.2 ). Furunculosis is most
commonly caused by SA and can be methicillin-sensitive or resistant
(MRSA). Diagnosis is clinical but can be aided by ultrasound if it is unclear
if there is fluctuance. Therapy is with incision and drainage and adding
antibiotic coverage is controversial. The literature suggests antibiotics are
not necessary for simple abscesses except in young children unless there is
associated cellulitis, the lesion has failed incision and drainage previously,
the patient is immunosuppressed or showing signs of sepsis, or the lesion is
particularly difficult to drain. Cultures can be sent from the purulent
drainage in order to confirm the diagnosis and measure the antibiotic
sensitivities. Empiric therapy should be guided by local resistance patterns
but is usually with clindamycin, trimethoprim-sulfamethoxazole, or
doxycycline (if age appropriate) in order to cover for MRSA.
Recurrence of furunculosis is common. Reinfection from the patient’s
local environment can come from sources such as close contacts, pets,
athletic equipment, or stuffed animals. Reinfection may occur because of
reinoculation from the patient’s own nares. Decolonization is challenging
but nasal decolonization may be effective with intranasal mupirocin two
times daily for 5 days for the patient and any close contacts. Four percent
chlorhexidine washes or dilute sodium hypochlorite (¼ cup in 20 to 40
gallons of water for 15 minutes) baths can be used to decolonize the skin.


FIGURE 66.1 Folliculitis. (Reprinted with permission from Burkhart C, Morrell D,
Goldsmith LA, et al. VisualDx: Essential Pediatric Dermatology . Philadelphia, PA:

Lippincott Williams & Wilkins; 2009.)

Bullous Impetigo
Bullous impetigo is caused by a localized staphylococcal infection that
produces an exfoliative toxin that cleaves the skin connection desmoglein 1
(DGS1). This allows fluid to build up within the epidermis and forms bullae
( Fig. 66.3 ). When the bullae rupture, the roof of the bulla and the fluid
dries to the skin giving the classic “honey-colored” crusting. SA
colonization is most common in the nares and perianal areas and thus
impetigo is more common on the face and perineum. Culture of the blister
fluid will yield the pathogen and establish sensitivities for therapy.
Localized bullous impetigo can often be treated with topical antibiotics
such as mupirocin, bacitracin, or retapamulin. Systemic antibiotics should
be used for more widespread or severe infections or those in
immunosuppressed hosts, including neonates.


FIGURE 66.2 Furuncle. Note pustule with surrounding erythema and induration.
(Image courtesy of Lee R. In: Elder DE, ed. Lever’s Histopathology of the Skin . 11th
ed. Philadelphia, PA: Wolters Kluwer; 2014. With permission.)