Impetigo 

Impetigo is an acute, contagious, superficial pyogenic skin infection that occurs most commonly in children, especially those who live in hot humid climates.

Bullous impetigo is caused almost exclusively by Staphylococcus aureus, whereas nonbullous impetigo is caused by S aureus,group A Streptococcus (Streptococcus pyogenes), or a combination of both.

Impetigo most often develops at a site of minor trauma or insult in which the integrity of the skin is disrupted.

Nonbullous impetigo can affect all ages, but it most commonly affects children aged 2-5 years.

Bullous impetigo affects all ages, but, historically, it occurs more often in newborns and older infants.

Patients with impetigo may report a history of minor trauma, insect bites, scabies, herpes simplex, varicella, or eczema at the site of infection, and any history of preexisting skin disease should raise the clinician's index of suspicion.

The lesions are usually painless, although patients may report burning and pruritus.

Constitutional symptoms are usually absent.

Nonbullous impetigo Lesions first begin as thin-walled vesicles or

pustules on an erythematous base. The lesions promptly rupture, releasing their

serum, which dries and forms a light brown, honey-colored crust.

Skin on any part of the body can be involved, but the face and extremities are affected most commonly.

Bullous impetigoThe vesicles do not rupture as easily or

quickly as in nonbullous lesions, but they do enlarge into bullae that are usually 1-2 cm in diameter. The bullae initially contain a clear yellow fluid that subsequently turns cloudy and dark yellow.

In contrast to nonbullous impetigo, bullous impetigo may involve the buccal mucous membranes, but regional lymphadenopathy is rare.

Bullous impetigo S aureus phage group II type 71 is the

predominant causative organism.Nonbullous impetigoStreptococci are the most common primary

cause when both organisms are present.

DifferentialsErythema Multiforme

(Stevens-Johnson Syndrome) Herpes Simplex Herpes Zoster Pediculosis Staphylococcal Infections Varicella-Zoster Virus

Impetigo can usually be diagnosed based on the clinical picture.

The presence of gram-positive cocci in chains indicates S pyogenes.

Gram-positive cocci in clusters indicate S aureus.If acute glomerulonephritis presents in a patient

with a recent history of impetigo, use a titer of antibodies to streptococcal components (eg, antideoxyribonuclease [DNAse] B, antihyaluronidase, and antistreptolysin O [ASO] titers) to identify a possible etiology for the renal findings.

Topical therapy Topical mupirocin Systemic therapy The drug preferred for impetigo caused by S

pyogenes is penicillin. Substitute clindamycin in patients who are

allergic to penicillin. In cases caused by S aureus, clindamycin or

cephalexin may be used.

ComplicationsAcute poststreptococcal glomerulonephritis

(AGN) is a rare but potential complication of nonbullous impetigo.

It occurs in less than 1% of cases, depending on the nephritogenic potential of the S pyogenes strain involved.

M-60 and M-49 cause AGN in 70% and 25% .

Other complications (rare) Cellulitis Erysipelas Scarlet fever Erythema multiforme Urticaria

Ecthyma

Ecthyma is an ulcerative pyoderma of the skin caused by group A beta-hemolytic streptococci.

Because ecthyma extends into the dermis, it is often referred to as a deeper form of impetigo.

Preexisting tissue damage (eg, excoriations, insect bites, dermatitis) and immunocompromised states (eg, diabetes, neutropenia) predispose patients to the development of ecthyma.

Lesions are painful and can have associated lymphadenopathy.

Secondary lymphangitis and cellulitis can occur. Ecthyma does heal with scarring. The rate of poststreptococcal glomerulonephritis

is approximately 1%.

Ecthyma usually arises on the lower extremities of children, persons with diabetes, and neglected elderly patients.

Ecthyma begins as a vesicle or pustule overlying an inflamed area of skin that deepens into a dermal ulceration with overlying crust. The crust of ecthyma lesions is gray-yellow and is thicker and harder than the crust of impetigo.

A shallow, punched-out ulceration is apparent when adherent crust is removed.

The deep dermal ulcer has a raised and indurated surrounding margin.

Important factors contribute to the development of streptococcal pyodermas or ecthyma.

High temperature and humidityCrowded living conditions Poor hygiene

DifferentialsEcthyma Gangrenosum Insect Bites Leishmaniasis Lymphomatoid Papulosis Mycobacterium Marinum

Infection of the Skin Papulonecrotic Tuberculids Pyoderma Gangrenosum Sporotrichosis

Consider topical therapy with mupirocin ointment for localized ecthyma.

More extensive ecthyma lesions require oral antibiotics.

Penicillin should be adequate to treat ecthyma.Oral antistaphylococcal agents (eg,

dicloxacillin, cephalexin, erythromycin, clindamycin) have been used to cover possible secondary Staphylococcus aureus infections.

Erysipelas

Historically, erysipelas occurred on the face and was caused by Streptococcus pyogenes.

However, a shift in the distribution and etiology of erysipelas has occurred, with most erysipelas infections now occurring on the legs and with non–group A streptococci sometimes being identified as the etiologic agents.

Bacterial inoculation into an area of skin trauma is the initial event in developing erysipelas.

Thus, local factors, such as venous insufficiency, stasis ulcerations, inflammatory dermatoses, dermatophyte infections, insect bites, and surgical incisions, have been implicated as portals of entry.

The source of the bacteria in facial erysipelas is often the host's nasopharynx, and a history of recent streptococcal pharyngitis has been reported in up to one third of cases.

Preexisting lymphedema is a clear-cut risk factor for erysipelas.

In erysipelas, the infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin "streaking" and regional lymph node swelling and tenderness.

The peak incidence has been reported to be in patients aged 60-80 years, especially in patients who are considered high-risk and immunocompromised or those with lymphatic drainage problems (eg, after mastectomy, pelvic surgery, bypass grafting).

Prodromal symptoms, such as malaise, chills, and high fever, often begin before the onset of the skin lesions and usually are present within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are typical complaints.

Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque.

The lesion classically exhibits raised sharply demarcated advancing margins.

Local signs of inflammation, such as warmth, edema, and tenderness, are universal.

Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy.

More severe infections may exhibit numerous vesicles and bullae along with petechiae and even frank necrosis.

Streptococci are the primary cause of erysipelas. Most facial infections are attributed to group A streptococci, with an increasing percentage of lower extremity infections being caused by non–group A streptococci.

Routine blood and tissue cultures are not cost-effective because they have an extremely low yield and results have a minimal impact on management. Cultures are perhaps best reserved for very immunosuppressed hosts in whom an atypical etiologic agent might be more likely.

Elevation and rest of the affected limb are recommended in erysipelas treatment to reduce local swelling, inflammation, and pain.

Streptococci cause most cases of erysipelas; thus, penicillin has remained first-line therapy.Penicillin administered orally or intramuscularly is sufficient for most cases of classic erysipelas and should be given for 10-20 days.

A first-generation cephalosporin or macrolide, such as erythromycin or azithromycin, may be used if the patient has an allergy to penicillin.