Common Bacterial Skin Infections
DANIEL L. STULBERG, M.D., MARC A. PENROD, M.D., and
RICHARD A. BLATNY, M.D.
Utah Valley Family Practice Residency, Provo, Utah
Family physicians frequently treat bacterial skin
infections in the office and in the hospital. Common skin infections include
cellulitis, erysipelas, impetigo, folliculitis, and furuncles and carbuncles.
Cellulitis is an infection of the dermis and subcutaneous tissue that has
poorly demarcated borders and is usually caused by Streptococcus or
Staphylococcus species. Erysipelas is a superficial form of cellulitis with
sharply demarcated borders and is caused almost exclusively by Streptococcus.
Impetigo is also caused by Streptococcus or Staphylococcus and can lead to
lifting of the stratum corneum resulting in the commonly seen bullous effect.
Folliculitis is an inflammation of the hair follicles. When the infection is
bacterial rather than mechanical in nature, it is most commonly caused by
Staphylococcus. If the infection of the follicle is deeper and involves more
follicles, it moves into the furuncle and carbuncle stages and usually requires
incision and drainage. All of these infections are typically diagnosed by
clinical presentation and treated empirically. If antibiotics are required, one
that is active against gram-positive organisms such as penicillinase-resistant
penicillins, cephalosporins, macrolides, or fluoroquinolones should be chosen.
Children, patients who have diabetes, or patients who have immunodeficiencies
are more susceptible to gram-negative infections and may require treatment with
a second- or third-generation cephalosporin. (Am Fam Physician 2002;66:119-24.
Copyright© 2002 American Academy of Family Physicians.)
Bacterial skin infections are the 28th most common
diagnosis in hospitalized patients.1 Cellulitis, impetigo, and
folliculitis are the most common bacterial skin infections seen by the family
physician. The percentage of office visits for cellulitis was 2.2 percent, and
for impetigo, it was 0.3 percent, in a cohort of almost 320,000 health plan
members (data taken from primary physician diagnosis codes from January 1, 1999
to December 1, 1999 for Intermountain Health Care, Salt Lake City). Knowledge
of the presentation, histopathology, and microbiology for each type of
infection is important for proper care of the patient. The presentation,
etiology, and current management of these diseases are presented.
| Marking the
margins of erythema with ink is helpful in following the progression or
regression of cellulitis.
Cellulitis is a painful, erythematous infection of
the dermis and subcutaneous tissues that is characterized by warmth, edema, and
advancing borders (Table 1). Cellulitis commonly occurs near
breaks in the skin, such as surgical wounds, trauma, tinea infections
(Figure 1), or ulcerations, but occasionally presents in skin
that appears normal. Patients may have a fever and an elevated white blood cell
count. Cellulitis can occur on any part of the body. Among the patients in the
cohort above, the most common sites of cellulitis were the legs and digits,
followed by the face, feet, hands, torso, neck, and buttocks (data taken from
primary physician diagnosis codes from January 1, 1999 to December 1, 1999 for
health plan members of Intermountain Health Care, Salt Lake City).
In otherwise healthy adults, isolation of an
etiologic agent is difficult and unrewarding. If the patient has diabetes, an
immunocompromising disease, or persistent inflammation, blood cultures or
aspiration (some physicians inject sterile nonpreserved saline before
aspiration) of the area of maximal inflammation may be useful.2-4
For infection in patients without diabetes, empiric treatment with a
penicillinase-resistant penicillin, first-generation cephalosporin,
amoxicillin-clavulanate (Augmentin), macrolide, or fluoroquinolone (adults
only) is appropriate.5 Limited disease can be treated orally, but
more extensive disease requires parenteral therapy. Marking the margins of
erythema with ink is helpful in following the progression or regression of
cellulitis (Figure 2). Outpatient therapy with injected
ceftriaxone (Rocephin) provides 24 hours of parenteral coverage and may be an
option for some patients. The patient should be seen the following day to
reassess disease progression.
Descriptions of Bacterial
|| A network of furuncles
connected by sinus tracts
|| Painful, erythematous
infection of deep skin with poorly demarcated borders
|| Fiery red, painful
infection of superficial skin with sharply demarcated borders
|| Papular or pustular
inflammation of hair follicles
|| Painful, firm or fluctuant
abscess originating from a hair follicle
|| Large vessicles and/or
Most cases of superficial cellulitis improve within
one day, but patients who exhibit thickening of the dermis usually take several
days of parenteral antibiotics before significant improvement occurs.
Antibiotics should be maintained for at least three days after the resolution
of acute inflammation.5 Adjunctive therapy includes the following:
cool compresses; appropriate analgesics for pain; tetanus immunization; and
immobilization and elevation of the affected extremity.6
A parenteral second- or third-generation
cephalosporin (with or without an aminoglycoside) should be considered in
patients who have diabetes, immunocompromised patients, those with unresponsive
infections, or in young children.5 The patient may also require a
plain radiograph of the area or surgical debridement to evaluate for gas
gangrene, osteomyelitis, or necrotizing fasciitis.6
Recurrent episodes of cellulitis or undergoing
surgery, such as mastectomy with lymph node dissection, can compromise venous
or lymphatic circulation and cause dermal fibrosis, lymphedema, epidermal
thickening, and repeated episodes of cellulitis. These patients may benefit
from prophylaxis with erythromycin, penicillin, or clindamycin
FIGURE 1. Cellulitis secondary to tinea infection.
FIGURE 2. Inked margins of cellulitis.
FIGURE 3. Erysipelas.
FIGURE 4. Nonbullous impetigo.
FIGURE 5. Ruptured bullous impetigo.
FIGURE 6. Folliculitis caused by contamination of
undertreated water in a hot tub or whirlpool.
Periorbital cellulitis is caused by the same
organisms that cause other forms of cellulitis and is treated with warm soaks,
oral antibiotics, and close follow-up.8 Children with periorbital or
orbital cellulitis often have underlying sinusitis.9 If the child is
febrile and appears toxic, blood cultures should be performed and lumbar
puncture considered. Haemophilus influenzae type b (Hib) in
young children was a significant concern until the widespread use of the Hib
vaccine and coverage with a parenteral third-generation cephalosporin was used
routinely. Recently, some researchers have recommended no longer routinely
covering for H. influenzae.8-10
Orbital cellulitis occurs when the infection passes
the orbital septum and is manifested by proptosis, orbital pain, restricted eye
movement, visual disturbances, and concomitant sinusitis. Complications include
abscess formation, persistent blindness, limited eye movement, diplopia, and,
rarely, meningitis.11 This ocular emergency requires intravenous
antibiotics, otorhinolaryngology, and ophthalmologic consultation.12
Perianal cellulitis is caused by group A
beta-hemolytic streptococcal infection and occurs most often in children. A
study13 of children with perianal cellulitis found a mean age of
onset of 4.25 years. Ninety percent of patients presented with dermatitis, 78
percent with itching, 52 percent with rectal pain, and 35 percent with
blood-streaked stools. Despite 10 days of oral antibiotics (primarily
penicillin or erythromycin), the recurrence rate was high at 39 percent. If
there is recurrence, the presence of an abscess should be considered, with
needle aspiration of the site for bacteriology being more accurate than a skin
Erysipelas (Figure 3), also known
as St. Anthony's fire, usually presents as an intensely erythematous infection
with clearly demarcated raised margins, and often with associated lymphatic
streaking (Table 1). Common sites are the legs and
face.15 Most cases do not have an inciting wound or skin lesion and
are preceded by influenza-like symptoms. The incidence of erysipelas is rising,
especially in young children, the elderly, persons with diabetes, alcoholic
persons, and patients with compromised immune systems or
Erysipelas is caused almost exclusively by
beta-hemolytic streptococcus and thus can be treated with standard dosages of
oral or intravenous penicillin. However, most physicians treat this infection
the same as cellulitis, which is outlined earlier. Adjunctive treatment and
complications are the same as for cellulitis.
Impetigo is most commonly seen in children aged two
to five years and is classified as bullous or nonbullous (Table
1). The nonbullous type predominates and presents with an erosion (sore),
cluster of erosions, or small vesicles or pustules that have an adherent or
oozing honey-yellow crust. The predilection for the very young can be
remembered by the common lay misnomer, "infant tigo." Impetigo usually appears
in areas where there is a break in the skin, such as a wound, herpes simplex
infection, or maceration associated with angular cheilitis (Figure 4), but Staphylococcus aureus can
directly invade the skin and cause a de novo infection.6
The bullous form of impetigo presents as a large
thin-walled bulla (2 to 5 cm) containing serous yellow fluid. It often ruptures
leaving a complete or partially denuded area with a ring or arc of remaining
bulla (Figure 5). More than one area may be involved and a
mix of bullous and nonbullous findings can exist. Nonbullous impetigo was
previously thought to be a group A streptococcal process and bullous impetigo
was primarily thought to be caused by S. aureus.
Studies16,17 now indicate that both forms of impetigo are
primarily caused by S. aureus with Streptococcus usually
being involved in the nonbullous form. If the infection is a toxin-producing,
phage group II, type 71 Staphylococcus (the same toxin seen in Staphylococcus
scalded skin syndrome, a medical emergency where large sheets of the upper
epidermis slough off), large bullae will form as the toxin produces intradermal
cleavage.18 Otherwise, smaller bullae develop and the honey-crusted
A study19 published in 1990 concluded
that topical mupirocin (Bactroban) ointment is as effective as oral
erythromycin in treating impetigo. However, because the lesions of bullous
impetigo can be large and both forms of impetigo can have satellite lesions, an
oral antibiotic with activity against S. aureus and group A
beta-hemolytic streptococcal infection is warranted in nonlocalized cases.
Because of developing resistance, erythromycin is no longer the drug of
choice.17 Azithromycin (Zithromax) for five days and cephalexin
(Keflex) for 10 days have been shown to be effective and
well-tolerated.20 Dicloxacillin (Pathocil), oxacillin (Prostaphlin),
first-generation cephalosporins, or amoxicillin-clavulanate are also acceptable
alternatives.5 Broad-spectrum fluoroquinolones have also been shown
to be effective, and several have been approved by the U.S. Food and Drug
Administration for treating skin and soft tissue infections.21 These
medications have excellent skin penetration and good bioavailability, but no
generic forms are currently available, and they are only approved for use in
As with other diseases involving Streptococci,
there is a small chance of developing glomerulonephritis, especially in
children aged two to six years. Presenting signs and symptoms of
glomerulonephritis include edema and hypertension; about one third of patients
have smoky or tea-colored urine. Streptococcal glomerulonephritis usually
resolves spontaneously although acute symptoms and problems may
Impetigo can be spread by direct person-to-person
contact, so appropriate hygiene is warranted. Nasal carriage of S. aureus has been implicated as a source of recurrent disease
and can be reduced by the topical application of mupirocin twice daily for five
Hair follicles can become inflamed by physical
injury, chemical irritation, or infection that leads to folliculitis
(Table 1). Classification is by the depth of involvement of
the hair follicle. The most common form is superficial folliculitis that
manifests as a tender or painless pustule that heals without
scarring.24 The hair shaft will frequently be seen in the center of
the pustule. Multiple or single lesions can appear on any skin bearing hair
including the head, neck, trunk, buttocks, and extremities. Associated systemic
symptoms or fever rarely exist. S. aureus is the most likely
pathogen; however, commensal organisms such as yeast and fungi occasionally
appear, especially in immunocompromised patients. These lesions typically
resolve spontaneously. Topical therapy with erythromycin, clindamycin,
mupirocin, or benzoyl peroxide can be administered to accelerate the healing
Staphylococci will occasionally invade the deeper
portion of the follicle, causing swelling and erythema with or without a
pustule at the skin surface. These lesions are painful and may scar. This
inflammation of the entire follicle or the deeper portion of the hair follicle
(isthmus and below) is called deep folliculitis. Oral antibiotics are usually
used in the treatment and include first-generation cephalosporins,
penicillinase-resistant penicillins, macrolides, and fluoroquinolones.
| Studies now
indicate that both forms of impetigo are primarily caused by Staphylococcus
aureus with Streptococcus usually being involved in the nonbullous
Gram-negative folliculitis usually involves the
face and affects patients with a history of long-term antibiotic therapy for
acne. Pathogens include Klebsiella, Enterobacter, and Proteus species. It can
be treated as severe acne with isotretinoin (Accutane), but use of isotretinoin
is associated with major side effects, including birth defects.26
"Hot tub" folliculitis is caused by Pseudomonas aeruginosa contamination of undertreated water in a
hot tub or whirlpool. Multiple pustular or papular perifollicular lesions
appear on the trunk and sometimes extremities within six to 72 hours after
exposure (Figure 6), and mild fever and malaise may occur.
Lesions in the immunocompetent patient typically resolve spontaneously within a
period of seven to 10 days.25 Treatment is directed at prevention by
appropriately cleaning the whirlpool or hot tub and maintaining appropriate
chlorine levels (bromine and copper solutions are less common alternatives) in
Furuncles and Carbuncles
Furuncles and carbuncles occur as a follicular
infection progresses deeper and extends out from the follicle (Table 1). Commonly known as an abscess or boil, a furuncle is a
tender, erythematous, firm or fluctuant mass of walled-off purulent material,
arising from the hair follicle. These lesions may occur anywhere on the body,
but have a predilection for areas exposed to friction. Furuncles rarely appear
before puberty. The pathogen is usually S. aureus. Typically,
the furuncle will develop into a fluctuant mass and eventually open to the skin
surface, allowing the purulent contents to drain, either spontaneously or
following incision of the furuncle.
carriage of Staphylococcus aureus has been implicated as a source of
recurrent impetigo and can be reduced by the topical application of mupirocin.
Carbuncles are an aggregate of infected hair
follicles that form broad, swollen, erythematous, deep, and painful masses that
usually open and drain through multiple tracts. Constitutional symptoms,
including fever and malaise, are commonly associated with these lesions but are
rarely found with furuncles. With both of these lesions, gentle incision and
drainage is indicated when lesions "point" (fluctuant or boggy with a thin
shiny appearance of the overlying skin); caution should be taken to not incise
deeper than the pseudo capsule that has been built at the site of infection.
Loculations should be broken with a hemostat. The wound may be packed (usually
with iodoform gauze) to encourage further drainage. In severe cases, parenteral
antibiotics such as cloxacillin (Tegopen), or a first-generation cephalosporin
such as cefazolin (Ancef), are required.27 The physician should be
aware of the potential for gas-containing abscesses or necrotizing fasciitis,
which require immediate surgical debridement.
The majority of bacterial skin infections are
caused by the gram-positive bacteria Staphylococcus and Streptococcus species.
Antibiotics are used empirically with consideration for resistance patterns.
Current antibiotic recommendations include penicillinase-resistant penicillins,
first-generation cephalosporins, azithromycin, clarithromycin,
amoxicillin-clavulanic acid, or a second-generation fluoroquinolone in the
skeletally mature patient. Gram-negative coverage with a second-, third-, or
fourth-generation cephalosporin is usually indicated in children under three
years and in patients with diabetes or who are immunocompromised.
The photographs in Figures 1, 2, 4, and 5 were
provided by Utah Valley Family Practice Residency, Provo, Utah. The photographs
in Figures 3 and 6 were provided by Richard Usatine, M.D., of the University of
California-Los Angeles, Los Angeles, Calif.
The authors indicate that they do not have any
conflicts of interest. Sources of funding: none reported.
This article is one in a series coordinated by Daniel
L. Sulberg, M.D., director of dermatology curriculum at the Utah Valley Family
Practice Residency, Provo, Utah. .
DANIEL L. STULBERG, M.D., is director of dermatology
curriculum at the Utah Valley Family Practice Residency in Provo, Utah. Dr.
Stulberg received his medical degree from the University of Michigan Medical
School, Ann Arbor, where he also completed a family practice residency. He also
publishes a bimonthly e-mail dermatology quiz.
MARC A. PENROD, M.D., is a third-year and chief resident
at the Utah Valley Family Practice Residency. He received his medical degree
from the University of Virginia School of Medicine, Charlottesville.
RICHARD A. BLATNY, M.D., is in private family practice in
Fairbury, Neb. He received his medical degree from the University of Nebraska
College of Medicine, Omaha. Dr. Blatny completed a family practice residency at
the Utah Valley Family Practice Residency.
Address correspondence to Daniel L. Stulberg, M.D.,
Utah Valley Family Practice Residency, 1134 N. 500 West, Provo, UT 84604
(e-mail: firstname.lastname@example.org). Reprints are
not available from the authors.
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