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Bacterial skin infections
Bacterial infections of the skin are of three major categories:
(1) primary skin infection
(2) secondary infection of a primary skin disease (e.g., infected atopic dermatitis)
(3) reactive skin conditions resulting from bacterial infection (e.g., erythema nodosum
due to streptococcal pharyngitis).
Normal human skin is colonized soon after birth by a large number of bacteria that live as
commensals on the epidermis and epidermal appendages. Coagulase-negative staphylococci
(Staphylococcus epidermidis) are inoculated during vaginal passage and coryneform bacteria
take up residence on neonatal skin shortly after birth. Within several weeks after birth, the
flora of neonatal skin is similar to that of adults.
The majority of the primary and secondary pyodermas (cutaneous bacterial infections) are
caused by either S. aureus or group A streptococcus. These bacteria cause a broad clinical
spectrum of infection ranging from superficial pyodermas to invasive soft-tissue infections
depending on the organism, the anatomic location of infections and host factors.
STAPHYLOCOCCAL SKIN INFECTIONS
Epidemiology
Staphylococci are classified into two major groups: the coagulase-negative staphylococci
(S. epidermidis) and coagulase-positive (S. aureus) staphylococci. S. epidermidis is a
common colonizer of the skin but is capable of causing superficial and invasive infections.
S. aureus permanently colonizes the anterior nares in 20% of the population.
Other sites of
colonization include the axillae, perineum, pharynx, and hands. Conditions predisposing to
S. aureus colonization include atopic dermatitis, diabetes mellitus, dialysis, intravenous drug
use, liver dysfunction, and HIV infection.
S. aureus is an aggressive pathogen and the most common cause of primary pyodermas as
well as of secondary infections on disease-altered skin. S. aureus in pyodermas can invade
the bloodstream, producing bacteremia, metastatic infection such as osteomyelitis, and acute
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infective endocarditis. Some strains of S. aureus also produce exotoxins, which can cause a
group of cutaneous and systemic symptoms such as staphylococcal scalded-skin syndrome
(SSSS) and staphylococcal toxic shock syndrome (TSS).
Infections and Toxin Syndromes Involving the Skin and Soft Tissues Caused
by Staphylococcus aureus:
A- Superficial primary pyodermas
Impetigo
Ecthyma
Folliculitis
Furuncle (boil)
Carbuncle
Acute Paronychia
B- Secondary pyodermas: Impetiginization of dermatoses such as atopic dermatitis
C- Invasive infections
Pyomyositis
Cellulites & erysiplas
Bacteremia, septicemia
Disseminated intravascular coagulation associated with staphylococcal bacteremia
D- Staphylococcal toxin-associated syndromes
Staphylococcal scalded-skin syndromes SSSS
Staphylococcal toxic-shock syndrome
TSS
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Impetigo
:
Impetigo is a common contagious superficial infection of the skin caused by either
streptococcal or staphylococcal organisms, or both. It is most commonly observed during
childhood and in those living in warm, humid climates. Poor personal hygiene may
predispose individuals to impetigo. Additionally, impetigo is a common complication of
insect bites, scabies, and viral infections. Systemic symptoms are rare, but regional
lymphadenopathy may be present.
Two clinical patterns of impetigo are recognized: bullous and crusted. Bullous impetigo is
caused by S. aureus. Currently, crusted impetigo also is most commonly caused by S.
aureus and less often by group A streptococcus.
1. Non bullous crusted imetigo:
The non-bullous type of impetigo accounts for more than 70% of cases of this form of
pyoderma. It occurs in children of all ages as well as in adults. Impetigo usually involves the
exposed parts of the body like face, scalp and extremities.
The initial lesion is a transient vesicle or pustule that quickly evolves into a honey-colored
crusted plaque, surrounding erythema may be present. Constitutional symptoms are absent.
Regional lymphadenopathy may be present in up to 90% of patients with prolonged,
untreated infection. If untreated, the lesions may slowly enlarge and involve new sites over
several weeks. In some individuals, lesions resolve spontaneously. In others, the lesions
extend into the dermis, forming an ulcer (ecthyma).
2. Bullous impetigo:
It is characterized by localized bullae arising on normal skin. The bullae are easily ruptured
and form shallow erosions with an adjacent yellow-brown crust. The bullous lesion is caused
by an exfoliative toxin produced by the bacteria that causes cleavage within the granular cell
layer of the epidermis.
Prognosis:
Untreated, invasive infection can complicate S. aureus
impetigo with cellulitis, lymphangitis, and bacteremia, resulting in osteomyelitis, septic
arthritis, pneumonitis, and septicemia.
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Treatment:
Local treatment with mupirocin ointment or cream, removal of crusts, and good hygiene is
sufficient to cure most mild to moderate cases Systemic antibiotics may be required in
extensive cases.
Staphylococcal impetigo responds quite promptly to appropriate treatment. In an adult with
extensive or bullous lesions, dicloxacillin 250 to 500 mg orally (PO) four times daily (qid),
or erythromycin (in the penicillin-allergic patient), 250 to 500 mg PO qid, should be given.
Treatment should be continued for 5 to 7 days (10 days if streptococci are isolated). Also, a
single course of oral azithromycin (in adults 500 mg on the first day, 250 mg daily on the
next 4 days).
cephalexin (40 to 50 mg/kg/day) or clindamycin (15 mg/kg/day tid or qid) given for 10 days
are effective alternative therapies.
Ecthyma:
Ecthyma is characterized by thickly crusted erosions or ulcerations nearly always on the
shin and feet. S. aureus and/or group A streptococcus can be isolated on culture.
Ecthyma occurs most commonly on the lower extremities of children, or neglected elderly
patients, or individuals with diabetes.
The ulcer has a “punched out” appearance when the dirty grayish-yellow crust and purulent
material are débrided. The margin of the ulcer is indurated, raised, and violaceous and the
granulating base extends deeply into the dermis. Untreated ecthymatous lesions enlarge over
weeks to months to a diameter of 2-3 cm or more.
The lesions are slow to heal, requiring several weeks of antibiotic treatment for resolution. It
usually leaves a scar after healing.
Management of ecthyma is the same as for staphylococcal impetigo
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Folliculitis:
Folliculitis is a pyoderma that begins within the hair follicle, and is classified according
to the depth of invasion (superficial and deep).
A/ Superficial folliculitis (Bockhart impetigo): A small, fragile, dome-shaped pustule
occurs at the infundibulum (opening) of a hair follicle, often on the scalps of children and in
the beard area, axillae, extremities, and buttocks of adults.
B/ Deep folliculitis (Sycosis barbae): is a deep folliculitis with perifollicular inflammation
occurring in the bearded areas of the face and upper lip. If untreated, the lesions may become
more deeply seated and chronic.
Furuncles and Carbuncles:
A furuncle or boil is a deep-seated inflammatory nodule that develops around a hair follicle,
usually from a preceding, more superficial folliculitis and often evolving into an abscess. A
carbuncle is a more extensive, deeper, communicating, infiltrated lesion that develops when
closely set furuncles coalesce.
Furuncles arise in hair-bearing sites, particularly in regions subject to friction, occlusion, and
perspiration, such as the neck, face, axillae, and buttocks.
A furuncle starts as a hard, tender, red folliculo-centric nodule that enlarges and becomes
painful and fluctuant after several days i.e., undergoes abscess formation. Rupture occurs,
with discharge of pus and often a core of necrotic material. The pain surrounding the lesion
then subsides, and the redness and edema diminish over several days to several weeks.
Furuncles may occur as solitary lesions or as multiple lesions in sites such as the buttocks
A carbuncle is a larger, more serious inflammatory lesion with a deeper base,
characteristically occurring as an extremely painful lesion at the nape of the neck, the back,
or thighs. Fever and malaise are often present, and the patient may appear quite ill. The
involved area is red and indurated, and multiple pustules soon appear on the surface,
draining externally around multiple hair follicles. The resulting permanent scar is often
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dense and readily evident. The major problems with furunculosis and carbuncles are
bacteremic spread of infection and recurrence.
Lesions about the lips and nose can spread via the facial and angular emissary veins to the
cavernous sinus (lead to cavernous sinus thrombosis). Fortunately, these complications are
not common.
Treatment: Simple furunculosis may be aided by local application of moist heat. A
carbuncle or a furuncle with surrounding cellulitis, or one with associated fever, should be
treated with a systemic antibiotic (as for impetigo). For severe infections or infections in a
dangerous area, maximal antibiotic dosage should be employed by the parenteral route.
Antibiotic treatment should be continued for at least 1 week.
When the lesions are large, painful, and fluctuant then incision and drainage is critical. If
the infection is recurrent or complicated by co-morbidities, a culture can be sent. Draining
lesions should be covered to prevent autoinoculation and diligent hand washing performed.
STREPTOCOCCAL SKIN INFECTIONS
Epidemiology: Group A streptococci are usually spread by transfer of organisms from an
infected person (or carrier) through close personal contact. The major source of such spread
is from patients with infections in the upper respiratory tract. Approximately 10% of the
normal population carry group A streptococcus asymptomatically—a higher percentage of
adults than of children in the oropharynx and less commonly in the nares and anus.
Infections and Toxin Syndromes Caused by Group A Streptococci:
A/ Superficial pyodermas
Impetigo
Ecthyma
Blistering distal dactylitis
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Perianal streptococcal cellulitis
Streptococcal vulvovaginitis
Streptococcal intertrigo
B/ Invasive infections
Acute lymphangitis
Erysipelas
Cellulitis
Streptococcal gangrene
Bacteremia, septicemia
C/ Toxin-associated syndrome:
Scarlet fever
Streptococcal toxic-shock-like syndrome
D/ Reactive complications:
Rheumatic fever
Glomerulonephritis
Erythema nodosum
Erythema multiforme
Guttate psoriasis
Vasculitis
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Cellulitis:
It represents an infection of the soft tissues and may be caused by group A beta hemolytic
Streptococcus or Staphylococcus aureus. It is often associated with impaired lymphatic
drainage and may be seen in patients who have undergone surgical procedures. Local
trauma, abrasions and dermatoses such as stasis dermatitis and tinea pedis are other
predisposing factors. Cellulitis is a common complication of intravenous drug abuse.
Clinically, cellulitis is characterized by an area of rapidly spreading erythema. The
borders are less distinct than in erysipelas and areas of involvement are warm to
touch. Associated features include tenderness, fever, malaise and an elevated white
blood cell count.
Erysipelas:
is a distinctive variant of cellulitis that involves the lymphatic vessels and superficial layers
of the skin; it is caused mostly by group A streptococcus. Erysipelas can be distinguished
from cellulitis by its sharp margins and its plaque-like elevation of involved skin. The
legs and face are the most common sites of involvement and the cutaneous findings are often
preceded by fever, chills, nausea, vomiting, headache and arthralgias. Recurrences of both
erysipelas and cellulitis are fairly common.
In most patients, the diagnosis of cellulitis or erysipelas is made on the basis of clinical
findings. For adults, treatment with systemic antibiotics that offer coverage for both
staphylococcal and streptococcal organisms is recommended. intravenous penicilinase-
resistant penicillins & 1
st
generation cephalosporin are usually effective.
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ERYTHRASMA
Erythrasma is a common superficial bacterial infection of the skin characterized by well-
defined but irregular reddish brown patches, occurring in the intertriginous areas, or by
fissuring and white maceration in the toe clefts. Corynebacterium minutissimum, the
etiologic agent of erythrasma, is a short, Gram-positive rod with subterminal granules.
Clinical Findings:
The most common site of involvement is the web spaces of the feet, where erythrasma
presents as a hyperkeratotic white macerated plaque , especially between the fourth and fifth
toes. In the genitocrural, axillary, and inframammary regions, the lesions present as well-
demarcated, reddish-brown, superficial, finely scaly, and finely wrinkled patches In these
sites, the patches have a relatively uniform appearance.
Wood's lamp examination of erythrasma reveals a coral-red fluorescence caused by
coproporphyrin III.
Treatment:
For localized erythrasma, especially of the web spaces of the feet, benzoyl peroxide wash or
5% gel are effective in most cases. Clindamycin (2%solution) or azole creams (topical
antifungal) are several of the many effective topical agents. For widespread involvement,
oral erythromycin is effective. A 1 gram single dose of clarithromycin has been used
successfully.
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