Impetigo is a common superficial infection of the skin characterized by honey-colored crusts or bullae, typically caused by Staphylococcus aureus, sometimes caused by Streptococcus pyogenes, or both.
INSIGHT 
Bacterial resistance such as community-acquired methicillin-resistant Staphylococcus aureus (MRSA) is becoming more prevalent; thus, treatment of infections must take evolving resistance patterns into account.
SYNONYMS Bullous impetigo, blistering distal dactylitis, impetigo contagiosa.
AGE Preschool children, young adults.
GENDER M = F.
INCIDENCE Common; up to 10% of dermatology visits.
SEASON Peak summer and fall.
ETIOLOGY Bullous impetigo is most often caused by Staphylococcus aureus phage group II strains which produce exfoliative toxin A or B. Vesiculopustular impetigo is often caused by Staphylococcus aureus or group A β-hemolytic Streptococcus species.
PREDISPOSING FACTORS Colonization of the skin and/or nares of the patient or patient’s family members, warm temperatures, high humidity, poor hygiene, atopic diathesis, skin trauma.
Crusted impetigo is caused by S. aureus or occasionally S. pyogenes at sites of skin trauma. Bullous impetigo is caused by an S. aureus exfoliative toxin A, which binds to desmoglein 1, cleaving its extracellular domain, resulting in an intraepidermal blister.
The skin lesions begin as erythematous areas, which may progress to superficial vesicles and bullae that rupture and form honey-colored crusts. The skin lesions are contagious and spread by person-to-person contact or fomites. Systemic symptoms are rare but can include fever and lymphadenopathy.
TYPE Macules, vesicles, bullae, crusts, and erosions (Fig. 20-1).
COLOR Pink, yellow “stuck-on” crusts. Pustules may appear whitish-yellow.
SIZE 1 to 3 cm.
SHAPE Round or oval.
ARRANGEMENT Discrete, confluent, or satellite lesions from autoinoculation.
DISTRIBUTION Face, arms, legs, buttocks, distal fingers (Fig. 20-2), toes.
In the early vesicular stage, impetigo may simulate varicella, herpes simplex, or candidiasis. The bullous stage may be confused with bullous insect bites, autoimmune bullous dermatoses, adverse drug reactions, or burns. The crusted stage may resemble eczematous dermatoses or tinea infections.
DERMATOPATHOLOGY Acantholytic cleft in the stratum granulosum with leukocytes; may also show scattered gram-positive cocci. Bacteria can be seen within the blister cavity of bullous lesions.
BACTERIAL CULTURE Group A streptococci and sometimes a mixed culture of streptococci and S. aureus can be cultured from lesions or nasopharynx. Use of a moistened culture swab to dissolve crusts may be necessary to isolate the pathogens.
Impetigo is a benign but recurrent and contagious condition. Untreated, it can persist for 3 to 6 weeks and continue to spread. Once treatment is initiated, the clinical response is swift and effective. In 5% of cases of β-hemolytic S. pyogenes impetigo (serotypes 1, 4, 12, 25, and 49), acute glomerulonephritis can ensue.
Preventive measures include antibacterial soaps, washes, and maintaining good hygiene.
For uncomplicated cases of impetigo, topical treatment is effective. Topical mupirocin, retapamulin, or fusidic acid ointments are highly effective in eliminating both S. aureus and Streptococcus. If bacterial nasal colonization is suspected or identified, the lower inner third of the nares should be treated to eradicate a chronic carriage state. All close household and/or family members should be treated at the same time because asymptomatic nasal carriage of the pathogenic bacteria can occur.
Systemic antibiotic therapy may be considered for moderate or refractory cases. The prevalence of MRSA has increased over the last decades; thus, traditional penicillin no longer seems as effective as β-lactamase-resistant penicillins (dicloxacillin), macrolides (erythromycin, clarithromycin), or cephalosporins. The risk of poststreptococcal glomerulonephritis is not decreased by administration of systemic antibiotics.
Ecthyma is a deep or ulcerative bacterial infection of the skin characterized by ulcers, typically occurring on the buttocks or legs of children.
SYNONYMS Ecthyma minor, ecthyma major.
AGE Children, adolescents, elderly.
GENDER M = F.
INCIDENCE Common.
ETIOLOGY Group A streptococci or S. aureus, or both.
Skin bacteria grow in excoriations, insect bites, and sites of trauma, particularly in susceptible individuals like young children, persons with lymphedematous limbs, poor hygiene, or immunosuppression. The extension of bacteria into the dermis results in the deeper lesions of ecthyma in contrast to the superficial lesions of impetigo.
Lesions begin as excoriations or insect bites with superinfection leading to saucer-shaped ulcers with a raised margin and a “punched out” appearance. The lesions are pruritic and tender and heal slowly, usually with scar formation. Systemic symptoms and bacteremia are rarely seen.
TYPE Vesicle, pustule, ulcer, scar (Fig. 20-3).
COLOR Purple, yellowish-gray crust.
SIZE 0.5 to 3.0 cm.
SHAPE Round or oval with a “punched out” appearance.
PALPATION Indurated, tender.
DISTRIBUTION Ankles; dorsa of feet, thighs, buttocks.
Ecthyma can be confused with ecthyma gangrenosum and other ulcers such as from vasculitis.
Group A streptococci, staphylococci.
Lesions persist for weeks and are slow to heal. They often heal with a resultant scar. Bacteremia is rarely seen, thus cellulitis and osteomyelitis are uncommon.
Ecthyma should be treated with warm soaks to remove crusts. Systemic antibiotic therapy may be considered for moderate or refractory cases. The prevalence of MRSA has increased over the last decades; β-lactamase-resistant penicillins (dicloxacillin), macrolides (erythromycin, clarithromycin), or cephalosporins may be considered first-line agents for streptococcal infections, with trimethoprim-sulfamethoxazole, clindamycin, or tetracyclines (in appropriate age groups) useful for MRSA.
Folliculitis is a superficial or deep inflammation (often bacterial) of hair follicles. Different types occur on different regions of the body (Table 20-1).
| Location | Synonym | Etiology |
|---|---|---|
| Neck | Acne keloidalis nuchae, folliculitis keloidalis nuchae | Staphylococcus aureus, ingrown hairs, curly hairs |
| Back | Periporitis suppurativa | Candida albicans |
| Buttocks, body | Hot tub folliculitis, whirlpool folliculitis, pseudomonas folliculitis | Pseudomonas aeruginosa acquired from hot tubs |
| Face | Folliculitis barbae, sycosis barbae, pseudofolliculitis barbae | Staphylococcus aureus, ingrown hairs |
SYNONYMS Bockhart’s impetigo; sycosis barbae.
AGE All ages.
INCIDENCE Common.
ETIOLOGY Bacterial: S. aureus most common.
Folliculitis occurs when there is inflammation or infection of the hair follicle. The cause is most often bacterial (S. aureus, Pseudomonas) especially in skin that is occluded, macerated, or wet. It can be exacerbated by shaving, plucking or waxing hair, hot/humid weather, topical steroids, tar, or mineral oils.
Folliculitis begins with inflammation of the follicular ostium that may be symptomatic or pruritic. Deep-seated inflammation of the hair follicle may be more tender (see Furuncle). Systemic symptoms are not typically present.
TYPE Papules, pustules.
COLOR Pink, red, yellow, gray.
SIZE 1 to 5 mm.
ARRANGEMENT Confined to the ostium of the hair follicles (Fig. 20-4).
DISTRIBUTION Scalp, face, chest, back, buttocks, extremities.
GRAM STAIN Gram-positive cocci.
CULTURE S. aureus >> Candida albicans, Pseudomonas aeruginosa > Streptococcus, Proteus, or Staphylococcus epidermidis.
The differential diagnosis for folliculitis includes acne, rosacea, keratosis pilaris, flat warts, molluscum contagiosum, tinea barbae, tinea corporis, and pustular miliaria.
In the treatment of folliculitis, occlusive agents or precipitants (clothes, topical oils, etc.) should be removed.
For uncomplicated cases, folliculitis can be managed with antibacterial soaps and washes (benzoyl peroxide, chlorhexidine, or triclosan). For localized disease, topical antibiotics (mupirocin, bacitracin, erythromycin, or clindamycin) are highly effective. If bacterial nasal colonization is suspected or identified, the lower inner third of the nares should be treated to eradicate a chronic carriage state. All close household and/or family members should be treated at the same time because asymptomatic nasal carriage of the pathogenic bacteria can occur. Dilute bleach baths may also be useful for bacterial decolonization and prevention of recurrent folliculitis.
Systemic antibiotic therapy may be considered for moderate-to-severe, refractory, widespread, or recurrent cases. Despite rising bacterial-resistance rates, folliculitis continues to be responsive to β-lactam antibiotics (penicillins, cephalosporins), macrolides (erythromycin, clarithromycin), and lincosamides (clindamycin).
Furuncle is an acute, deep-seated, red, hot, tender inflammatory nodule that frequently evolves from a folliculitis. A carbuncle is a large lesion of coalescing furuncles.
SYNONYMS Boils, abscesses.
AGE Adolescents and young adults.
GENDER M > F.
INCIDENCE Common.
ETIOLOGY S. aureus most common. Anaerobic bacteria in the anogenital region.
Furuncles are inflammatory areas of pus involving the entire hair follicle and surrounding tissue. A contiguous collection of furuncles makes a carbuncle. The predisposing factor for both include chronic staphylococcal carrier state in nares, axillae or perineum, friction of collars or belts, obesity, poor hygiene, bactericidal defects (e.g., in chronic granulomatous disease), defects in chemotaxis, and in hyperimmunoglobulin E (IgE) syndrome, diabetes mellitus.
Furuncles result from folliculitis that becomes deeper and larger from friction or maceration. They begin as enlarging tender, red nodules that become painful, fluctuant, and then rupture. With numerous furuncles that coalesce, carbuncles can ensue. Systemic symptoms are rare but can include low-grade fever and malaise. Occasionally, lymphadenopathy or peripheral leukocytosis may also occur with widespread lesions.
TYPE Nodules, pustules, ulcers, scars.
COLOR Bright red (Fig. 20-5).
PALPATION Indurated, firm, tender.
ARRANGEMENT Scattered, discrete.
DISTRIBUTION Hair follicles and in areas subject to friction and sweating: neck, scalp, face, axillae, buttocks, thighs, and perineum.
DERMATOPATHOLOGY Subcutaneous dense neutrophilic infiltrate with a suppurative reaction around the hair follicle below the infundibulum, perifollicular necrosis, and fibrinoid debris.
SKIN CULTURE Incision and drainage of lesions for Gram stain, culture, and antibiotic sensitivity studies with identification of the bacteria (S. aureus >> anaerobic bacteria).
BLOOD CULTURE In rare cases with fever and/or constitutional symptoms; if blood culture is positive, systemic antibiotics may be necessary.
Furuncles and carbuncles can sometime be confused with ruptured cysts, hidradenitis suppurativa, or acne.
Furuncles and carbuncles resolve, but some need incision, drainage, and systemic antibiotic treatment. Some patients are subject to recurrent furunculosis and these patients and their family members need to be treated simultaneously and aggressively to eradicate recurrences. At times, furunculosis is complicated by bacteremia and possible hematogenous seeding of heart valves, joints, spine, long bones, and viscera (especially kidneys).
Simple furunculosis is treated by local application of heat, such as with warm compresses. Fluctuant lesions may require incision and drainage, particularly for carbuncles. No systemic antibiotics are needed except in patients with systemic symptoms, patients with furunculosis in the perinasal or periauricular regions, or in patients with immunosuppression or other significant comorbidities.
Furunculosis with surrounding cellulitis or with fever should be treated with systemic antibiotics. Most cases of folliculitis continue to be responsive to b-lactam antibiotics (penicillins, cephalosporins), macrolides (erythromycin, clarithromycin), and lincosamides (clindamycin), but consideration should be given to the increasing prevalence of MRSA and consideration of empiric antibiotics with MRSA coverage (e.g., trimethoprim-sulfamethoxazole, clindamycin) or for refractory disease.
Recurrent furunculosis may be difficult to control. This may be related to persistent staphylococci in the nares, perineum, and body folds. Effective control can sometimes be obtained with frequent showers (not baths), antibacterial soaps, and washes (benzoyl peroxide, chlorhexidine, or triclosan); topical mupirocin antibiotic ointment for skin lesions and nasal passages is effective in eliminating S. aureus. Dilute bleach baths are also effective for reducing bacterial colonization. All close household and/or family members should be treated at the same time because asymptomatic nasal carriage of the pathogenic bacteria can occur. Systemic antibiotics at lower doses on a daily basis prophylactically may be needed to avoid relapses for particularly refractory cases.
Cellulitis is an acute, spreading infection of dermal and subcutaneous tissues, characterized by a red, hot, tender area of skin, often at the site of bacterial entry.
INSIGHT 
Bilateral or multifocal cellulitis is exceedingly rare; in all such cases, other possible diagnoses should be considered, with allergic contact dermatitis at the top of the list.
AGE Children younger than 3 years; adults 45 to 65 years.
GENDER M > F.
INCIDENCE Common, up to 3/100 individuals.
ETIOLOGY Bacterial: Group A streptococci, or S. aureus. Less commonly, Haemophilus influenza, pneumococci, or Neisseria meningitidis.
Break in the skin from puncture, laceration, abrasion, surgical site, underlying dermatosis (tinea pedis, atopic dermatitis), or impaired circulation (lymphedema, peripheral vascular disease, diabetes) allows bacterial entry and proliferation in the soft tissues with a marked inflammatory response. In children, H. influenzae enters through the middle ear or nasal mucosa, though less common in vaccinated children.
Cellulitis occurs 1 to 3 days after a break in the skin (wound, trauma) as a red, tender, hot swelling of the skin and underlying tissues. Rarely bullae may develop. Systemic symptoms such as malaise, anorexia, fever, chills can co-occur or precede skin changes; an associated bacteremia may be present.
TYPE Plaque, edema, bullae.
COLOR Red, purple (H. influenzae).
SIZE Few to several centimeters.
PALPATION Firm, hot, tender.
DISTRIBUTION Children: cheek, periorbital area (Fig. 20-6), head, neck. Adults: extremities.
Lymphadenopathy Can be enlarged and tender regionally.
The differential diagnosis of cellulitis includes atopic dermatitis, contact dermatitis, urticaria, erysipelas, impetigo, insect bites, vaccination reactions, fixed drug eruptions, annular erythema, stasis dermatitis, superficial thrombophlebitis or deep vein thrombosis, and panniculitis.
DERMATOPATHOLOGY Dermal inflammation with lymphocytes and neutrophils. Edema of the lymphatics and blood vessels. Special stains for organisms can be performed, but are only positive in the minority of cases.
COMPLETE BLOOD COUNT White cell count and sedimentation rate may be elevated.
SKIN CULTURES Cultures of the skin can be aspirated or biopsied at the leading edge of inflammation. Positive cultures are obtained in only up to 40% of cases.
BLOOD CULTURES Positive bacterial cultures are obtained in fewer than 25% of cases.
The prognosis for cellulitis is good if early detection and treatment is initiated. Complications are rare, but include acute glomerulonephritis (Streptococcus), lymphadenitis, and subacute bacterial endocarditis. Facial, orbital, and periorbital cellulitis require special attention, early recognition, and systemic treatment because of the risk of serious visual impairment in untreated cases.
Identifying the organism that is causing the cellulitis can aid in choosing the correct antibiotic coverage. Mild cases of staphylococcal and streptococcal cellulitis can be treated on an outpatient basis with a 10-day course of oral antibiotics with good gram-positive coverage. For severe refractory cases, facial and/or periorbital cellulitis, hospitalization and intravenous (IV) antibiotics may be necessary. For cases of purulent cellulitis, empiric coverage of MRSA is warranted given the increased prevalence of this organism.
For cellulitis affecting an extremity, supportive measures such as elevation and compression to relieve swelling are useful.
Erysipelas is a dermal and lymphatic infection of the skin most often caused by group A β-hemolytic streptococci.
SYNONYM St. Anthony’s fire.
AGE Young children. Elderly.
GENDER Children: M > F. Elderly: F > M.
INCIDENCE Uncommon.
SEASON Increased in summer.
ETIOLOGY Group A streptococci > groups G, B, C, or D streptococci, S. aureus, Streptococcus pneumoniae, Klebsiella pneumoniae, Yersinia enterocolitica, H. influenzae type B.
Group A streptococci enters the dermis and lymphatics from an external break in the skin or pharynx, or, less likely, through internal hematogenous spread.
Two to five days after a break in the skin, a red, hot, tender well-demarcated erythematous plaque begins to form and enlarge around the inoculation site. Fever, chills, malaise, nausea, lymphadenopathy, and lymphatic streaking may be present and may precede the skin changes.
TYPE Plaques > bullae, necrosis. Sharply demarcated borders.
COLOR Bright red (Fig. 20-7).
PALPATION Firm, hot, tender.
DISTRIBUTION Bridge of nose, cheeks, face, scalp, lower extremities.
FEVER Malaise, nausea.
LYMPHADENOPATHY With, or without, lymphatic streaking.
Erysipelas can be confused with cellulitis, lupus, sunburn, contact dermatitis, urticaria, or dermatomyositis.
DERMATOPATHOLOGY Edema of the dermis and a dermal neutrophilic infiltrate. Special stains, direct immunofluorescence, and latex agglutination tests can detect streptococci within biopsy specimens.
SKIN CULTURE Tissue or wound swab cultures may grow organism.
BLOOD CULTURE Positive in only 5% of cases.
OTHER Anti-DNase B and antistreptolysin O titers are good indicators of streptococcal infections. Peripheral leukocytosis may also be present.
Once identified and treated, erysipelas has a good prognosis. Complications are rare, occurring in patients with underlying disease (lymphedema, chronic cutaneous ulcers).
The treatment of choice for streptococcal erysipelas is a 10- to 14-day course of penicillin. Penicillin-allergic individuals can be treated with macrolides (erythromycin, clarithromycin) but macrolide-resistant S. pyogenes strains have been reported.
Refractory or recurrent cases of erysipelas may require hospitalization and IV or intramuscular antibiotics. Patients with local circulatory problems (lymphedema) and recurrent erysipelas may need daily prophylactic penicillin.
Perianal streptococcal infection is characterized by bright red perianal dermatitis that leads to pruritus, pain, fissures, and can lead to behavioral defecation disorders.
SYNONYMS Perianal streptococcal cellulitis, streptococcal perianal disease.
AGE Children younger than 4 years.
GENDER M > F.
INCIDENCE Uncommon.
ETIOLOGY Group A streptococci.
Perianal streptococcal dermatitis may be precipitated by group A streptococcal pharyngitis or act as the infectious precipitant for a flare of guttate or recurrent psoriasis.
Perianal streptococcal infection typically presents as well-demarcated bright red perianal erythema extending 2 to 3 cm around the anus with itching or pain. No systemic symptoms are usually present.
TYPE Plaque.
COLOR Bright red.
SIZE Few to several centimeters.
DISTRIBUTION Perianal area (Fig. 20-8).
Perianal streptococcal infection can be clinically confused with psoriasis, candidiasis, contact dermatitis, seborrheic dermatitis, atopic dermatitis, pinworm infection, inflammatory bowel disease, early Kawasaki’s disease, or sexual abuse.
SKIN CULTURE Perianal area will grow β-hemolytic streptococcus.
Perianal streptococcal infection has a good prognosis when properly treated, but relapses (seen in up to 40% of cases) occur requiring retreatment. Untreated cases can lead to perianal irritation or pruritus, perianal fissures, painful defecation, streaks of blood on the stool, soiling of undergarments, and behavioral defecating disabilities.
The treatments for perianal streptococcal infection include a 10-day course of penicillin or 7-day course of oral cephalosporin. Penicillin-allergic individuals can be treated with macrolides (erythromycin, clarithromycin) but macrolide-resistant S. pyogenes strains have been reported.
Scarlet fever is a group A streptococcal infection of the tonsils, pharynx, or skin, associated with a characteristic toxin-mediated diffuse erythematous exanthem.
SYNONYMS Scarlatina, surgical scarlet.
AGE 1 to 10 years.
INCIDENCE Uncommon.
SEASON Seen more commonly in late fall, winter, and early spring.
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