Chapter 176. Superficial Cutaneous Infections and Pyodermas

Normal human skin is colonized soon after birth by a large number of bacteria that live as commensals on the epidermis and epidermal appendages (the skin microbiome). 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 microbiome of neonatal skin is similar to that of adults and includes many species of bacteria and fungi (see Chapter 175).

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 (STIs; see Chapter 179) depending on the organism, the anatomic location of infections, and on host factors.

Epidemiology

Staphylococci are classified into two major groups: (1) the coagulase-negative Staphylococci and (2) coagulase-positive (S. aureus) Staphylococci. Individuals carry a minimum of 10–24 combined temporary and resident strains of S. epidermidis, the most common coagulase-negative strain. S. epidermidis is a common colonizer of the skin but is capable of causing superficial and invasive infections (particularly about implants and catheters).

S. aureus permanently colonizes the anterior nares in approximately 20% of the population. Carriage is transient or intermittent in other individuals. Approximately 60% of healthy individuals have occasional carriage of S. aureus at some site.1 Other sites of colonization include the axillae, perineum, pharynx, and hands. Conditions predisposing to S. aureus colonization include atopic dermatitis, diabetes mellitus (insulin dependent), dialysis (hemo- and peritoneal), intravenous drug use, liver dysfunction, and human immunodeficiency virus (HIV) infection. Colonization by S. aureus is found at some body site in up to 37% of patients presenting with purulent community associated methicillin resistant S. aureus (MRSA) infections.2

S. aureus is an aggressive pathogen and the most common cause of primary pyodermas and STIs, as well as of secondary infections on disease-altered skin. S. aureus in pyodermas or STIs can invade the bloodstream, producing bacteremia, metastatic infection such as osteomyelitis, and acute infective endocarditis. Some strains of S. aureus also produce exotoxins, which can cause constellations of cutaneous and systemic symptoms such as staphylococcal scalded-skin syndrome (SSSS) and staphylococcal toxic shock syndrome (TSS).

Transfer of organisms to patients occurs predominantly via the hands of personnel rather than through the air. This appears to be particularly true in newborn nurseries. Any individuals with open staphylococcal infections are high-risk potential carriers and transmitters of infection. Nasal carriage of S. aureus appears to be a major risk factor for wound infection after cardiac surgery, resulting in higher mortality rates and longer postoperative stays.3 The rate of S. aureus bacteremia is also higher in nasal carriers of S. aureus.4 Good nursery technique, careful handling of patients, strict hand-washing procedures, and isolation of patients with open draining staphylococcal infections are important in the reduction of transmission of Staphylococci. In older adults, S. aureus accounts for 9% of nosocomial infections and follows only Escherichia coli, Pseudomonas aeruginosa, and Enterococci in prevalence.5

Etiology and Pathogenesis

Colonization by S. aureus may be transient or represent a prolonged carrier state. S. aureus produces many cellular components and extracellular products that may contribute to its pathogenicity. Host factors such as immunosuppression, glucocorticoid therapy, and atopy may play a major role in the pathogenesis of staphylococcal infections. Preexisting tissue injury or inflammation (surgical wound, burn, trauma, dermatitis, retained foreign body) is of major importance in the pathogenesis of staphylococcal disease.

Some strains produce one or more exoproteins, including the staphylococcal enterotoxins (SEA, SEB, SECn, SED, SEE, SEG, SEH, and SEI), and the exfoliative toxins (ETA and ETB), TSS toxin-1 (TSST-1), and leukocidin. These toxins have unique potent effects on immune cells and other biologic effects as well, ultimately inhibiting host immune response.

TSST-1 and the staphylococcal enterotoxins are also known as pyrogenic toxin superantigens. These molecules act by binding directly to constitutively expressed HLA-DR molecules (major histocompatibility complex II) on antigen-presenting cells without antigen processing. Although conventional antigens require recognition by all five elements of the T-cell-receptor complex, superantigens require only the variable region of the β-chain. As a result, 5%–30% of resting T cells may be activated, whereas the “normal” antigenic response is only 0.0001%–0.01% of T cells.6 Nonspecific T-cell activation leads to massive systemic release of cytokines, especially interleukin 2, interferon-γ, and tumor necrosis factor-β from T cells and interleukin 1 and tumor necrosis factor-α from macrophages.7 Superantigen stimulation of T cells also results in activation and expansion of lymphocytes expressing specific T cell-receptor variable region of the β-chain. They may activate B cells, leading to high levels of immunoglobulin E (IgE) or autoantibodies.8 Also, there is evidence that superantigens selectively induce cutaneous lymphocyte-associated antigen on T cells, thereby “homing” them to the skin.8

There are several other mechanisms by which S. aureus evades immune clearance. Approximately 60% of S. aureus strains secrete the chemotaxis inhibitory protein of Staphylococci, which inhibits neutrophil chemotaxis. Additionally, protein A, staphylokinase, capsular polysaccharide, fibrinogen binding protein, and clumping factor A all act to aid in avoidance of being opsonized and phagocytosed. Staphylokinase and aureolysin bind and cleave antimicrobial peptides, respectively, resulting in increased survival in vitro and probably in vivo.1

Drug Resistance

A major problem in treating staphylococcal infections has been the emergence of antibiotic-resistant strains. With ever-increasing use of penicillins, methicillin-resistant S. aureus (MRSA) strains have become a major epidemiologic problem since the 1980s. Resistance to methicillin indicates pan resistance to all β-lactam antibiotics. Recently, intermediate-level resistance of MRSA to vancomycin has emerged and constitutes a potential further problem in treatment. Although S. aureus infection prevalence has not changed much, the percentage of MRSA isolates of these infections has significantly increased in some countries. Today, MRSA can be divided into Hospital-Associated (HA) or Community-Associated (CA) MRSA. In many areas, the prevalence of CA-MRSA strains is over 50%.9

Attempts to eradicate MRSA have generally been unsuccessful. Treatment of anterior nares and wounds with mupirocin ointment has been shown to decrease S. aureus colonization but in one study did not decrease the rate of transmission to a roommate in a long-term care facility.10 Although there are many other reports of the use of topical mupirocin to reduce colonization of MRSA and methicillin-sensitive S. aureus, indiscriminate use of topical mupirocin must be avoided because significant mupirocin resistance has already emerged.

Immunity

The primary defense against S. aureus infections is the innate immunity provided by neutrophils.11 A major component of the innate response is antimicrobial peptides. These peptides can be found in various locales and include dermicidin, LL-37, protegrin, α-defensins and β-defensins, lactoferricin, and cascocidin. However, S. aureus also has the ability to thwart the immune system in several ways. One of the main virulence factors of S. aureus is the production of adhesins that facilitate binding to host epithelial cell surfaces. The almost universal presence in adults of circulating antibodies to one or more cell-wall antigens or extracellular toxins substantiates the high prevalence of staphylococcal infections. However, these antibodies are not the primary determinants of resistance to such infections. Recent evidence demonstrates that S. aureus can invade and survive in many types of host cells, suggesting that a cell-mediated immune response may be required for killing intracellular organisms.

Clinical Findings

Superficial Staphylococcal Pyodermas

Pyodermas are infections in the epidermis, just below the stratum corneum or in hair follicles. In industrialized nations, S. aureus is the most common cause of superficial pyodermas (Box 176-1), but group A Streptococcus continues to be a common cause of pyoderma in developing countries. If untreated, pyodermas can extend to the dermis, resulting in ecthyma and furuncle formation.

Impetigo

Two clinical patterns of impetigo are recognized: (1) bullous and (2) nonbullous. Bullous impetigo is caused by S. aureus. Currently, in industrialized nations, nonbullous impetigo is most commonly caused by S. aureus and less often by group A Streptococcus. Group A Streptococcus remains a common cause of nonbullous impetigo in developing nations.

Nonbullous Impetigo

The nonbullous 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. Intact skin is usually resistant to colonization or impetiginization, possibly due to absence of fibronectin receptors for teichoic acid moieties on S. aureus and group A Streptococcus. Production of bacteriocins, produced by certain S. aureus strains (phage group 71) and highly bactericidal to group A Streptococcus, may be responsible for the isolation of only S. aureus from some lesions initially caused by Streptococci.

History

In a typical sequence, S. aureus spreads from nose to normal skin (approximately 11 days later) and then develop into skin lesions (after another 11 days). Lesions commonly arise on the skin of the face (especially around the nares) or extremities after trauma. Nasal carriers of S. aureus can present with a very localized type of impetigo confined to the anterior nares and the adjacent lip area (Fig. 176-1); pruritus or soreness of the area is a common complaint (Fig. 176-2). Conditions that disrupt the integrity of the epidermis, providing a portal of entry of impetiginization, include insect bites, epidermal dermatophytoses, herpes simplex, varicella, abrasions, lacerations, and thermal burns.

Differential Diagnosis

See Box 176-2 for differential diagnosis of nonbullous impetigo.

Cutaneous Lesions

The initial lesion is a transient vesicle or pustule (see Fig. 176-2) that quickly evolves into a honey-colored crusted plaque that can enlarge to greater than 2 cm in diameter (see Fig. 176-1). 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 (see Section “Staphylococcal Ecthyma”).

Bullous Impetigo

Three types of skin eruptions can be produced by phage group II S. aureus, particularly strains 77 and 55: (1) bullous impetigo, (2) exfoliative disease (SSSS), and (3) nonstreptococcal scarlatiniform eruption (staphylococcal scarlet fever). All three represent varying cutaneous responses to extracellular exfoliative toxins (“exfoliatin”) types A and B produced by these Staphylococci (see Chapter 177). Exfoliative toxin A acts as a serine protease of desmoglein 1, the desmosomal cadherin that is also the target of autoantibodies in pemphigus foliaceus.12

In a study of bullous impetigo, 51% of patients had concurrent S. aureus cultured from the nose or throat, and 79% of cultures grew the same strain from both sites.

Cutaneous Lesions

Bullous impetigo occurs more commonly in the newborn and in older infants, and is characterized by the rapid progression of vesicles to flaccid bullae (Fig. 176-3). Decades ago, extensive bullous impetigo (archaic term: pemphigus neonatorum or Ritter disease) occurred in epidemics within neonatal nurseries.

Bullae usually arise on areas of grossly normal skin. The Nikolsky sign (sheet-like removal of epidermis by shearing pressure) is not present. Bullae initially contain clear yellow fluid that subsequently becomes dark yellow and turbid (see Fig. 176-3A), and their margins are sharply demarcated without an erythematous halo. The bullae are superficial, and within a day or two, they rupture and collapse, at times forming thin, light-brown to golden-yellow crusts (see Fig. 176-3B). So-called bullous varicella represents superinfection by S. aureus (phage group II) of varicella lesions (bullous impetiginization).

Laboratory Tests

Gram stain of exudates from bullous impetigo reveals Gram-positive cocci in clusters. S. aureus belonging to phage group II can be cultured from the contents of intact bullae.

Histologically, the lesions of bullous impetigo show vesicle formation in the subcorneal or granular region, occasional acantholytic cells within the blister, spongiosis, edema of the papillary dermis, and a mixed infiltrate of lymphocytes and neutrophils around blood vessels of the superficial plexus.

Differential Diagnosis

See Box 176-3 for differential diagnosis of bullous impetigo.

Prognosis and Clinical Course

If untreated, invasive infection can complicate S. aureus impetigo with cellulitis, lymphangitis, and bacteremia, resulting in osteomyelitis, septic arthritis, pneumonitis, and septicemia. Exfoliatin production can lead to SSSS in infants and in adults who are immunocompromised or have impaired renal function.

Treatment

See Box 176-4. Local treatment with mupirocin ointment or cream, removal of crusts, and good hygiene is sufficient to cure most mild to moderate cases.13 Retapamulin 1% ointment is also effective for localized impetigo and secondarily impetiginized dermatitis as well, although decreased efficacy against MRSA was noted in some trials.14 Fusidic acid is an equally effective topical agent for localized impetigo and has very few adverse effects topically. However, it is currently unavailable in the United States.15 Systemic antibiotics may be required in extensive cases. The frequency of isolation of group A Streptococcus makes such therapy a reasonable approach in most patients who have a significant degree of involvement. There is no role for general disinfectant treatments or bacitracin.16

Staphylococcal impetigo responds quite promptly to appropriate treatment. In an adult with extensive or bullous lesions, dicloxacillin (or similar penicillinase-resistant semisynthetic penicillin), 250–500 mg orally (PO) four times daily (qid), or erythromycin (in the penicillin-allergic patient), 250–500 mg PO qid, should be given. Treatment should be continued for 5–7 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) has been shown to be equally as effective as dicloxacillin for skin infections in adults and children. For impetigo caused by erythromycin-resistant S. aureus, which is commonly isolated from impetigo lesions of children, amoxicillin plus clavulanic acid [25 mg/kg/day given three times a day (tid)], cephalexin (40–50 mg/kg/day), cefaclor (20 mg/kg/day given tid), cefprozil (20 mg/kg once daily), or clindamycin (15 mg/kg/day tid or qid) given for 10 days are effective alternative therapies. If CA-MRSA is likely, consider the following therapies: TMP-SMX and rifampin (100%), clindamycin (95%), and tetracycline (92%). Inducible resistance to clindamycin should be excluded by performing a D-zone disk-diffusion test.

Staphylococcal Ecthyma

Ecthyma is a cutaneous pyoderma characterized by thickly crusted erosions or ulcerations. Ecthyma is usually a consequence of neglected impetigo and classically evolves in impetigo occluded by footwear and clothing. Thus, it is a lesion, typically occurring in the homeless and soldiers in combat on maneuver in a humid and hot climate. S. aureus and/or group A Streptococcus can be isolated on culture. Untreated staphylococcal or streptococcal impetigo can extend more deeply, penetrating the epidermis, producing a shallow crusted ulcer (Fig. 176-4). Ecthymatous lesions can evolve from a primary pyoderma or within a preexisting dermatosis or site of trauma. Ecthyma gangrenosum is a cutaneous ulcer caused by P. aeruginosa and resembles staphylococcal or streptococcal ecthyma (see Chapter 180).

Ecthyma occurs most commonly on the lower extremities of children, or neglected elderly patients, or individuals with diabetes. Poor hygiene and neglect are key elements in pathogenesis.

The ulcer has a “punched-out” appearance when the dirty grayish-yellow crust and purulent material are debrided. The margin of the ulcer is indurated, raised, and violaceous (see Fig. 176-4), 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. Problems of spread by autoinoculation or by insect vectors and of poststreptococcal sequela (glomerulonephritis) are the same as with impetigo.

Management of ecthyma is usually systemic and includes the same agents used for staphylococcal impetigo (see Box 176-4).

Folliculitis

Folliculitis is a pyoderma that begins within the hair follicle, and is classified according to the depth of invasion (superficial and deep), and microbial etiology (Box 176-5).

Superficial Folliculitis

Superficial folliculitis has also been termed follicular or Bockhart impetigo. A small, fragile, dome-shaped pustule occurs at the infundibulum (ostium or opening) of a hair follicle, often on the scalps of children and in the beard area (Fig. 176-5), axillae, extremities, and buttocks of adults. Isolated staphylococcal folliculitis is common on the buttock of adults. Periporitis staphylogenes refers to secondary infection of miliaria of the neonate by S. aureus. Staphylococcal blepharitis is an S. aureus infection of the eyelids, presenting with scaling or crusting of the eyelid margins, often with associated conjunctivitis; the differential diagnosis includes seborrheic dermatitis and rosacea of the eyelid.

S. aureus folliculitis must be differentiated from other folliculocentric infections. Also, three noninfectious, inflammatory, follicular disorders are more common in black men: (1) pseudofolliculitis barbae, which occurs on the lower beard area (Fig. 176-6); (2) folliculitis keloidalis or acne keloidalis nuchae, on the nape of the neck; and (3) perifolliculitis capitis, on the scalp. S. aureus can cause secondary infection in these inflammatory disorders. Exposure to mineral oils, tar products, and cutting oils can cause an irritant folliculitis. Acne vulgaris, drug-induced acneiform eruptions, rosacea, hidradenitis suppurativa, acne necrotica of the scalp, and eosinophilic folliculitis of HIV disease must be distinguished from infectious folliculitis as well. Also, “hot tub” folliculitis may be caused by P. aeruginosa (see Chapter 180).

Deep Folliculitis

Sycosis barbae is a deep folliculitis with perifollicular inflammation occurring in the bearded areas of the face and upper lip (Fig. 176-7). If untreated, the lesions may become more deeply seated and chronic. Local treatment with warm saline compresses and local antibiotics (mupirocin or topical clindamycin) may be sufficient to control infection. More extensive cases require systemic antibiotic therapy. Dermatophytic folliculitis must be differentiated from S. aureus folliculitis. In fungal infections, hairs are usually broken or loosened, and there are suppurative or granulomatous nodules rather than pustules. Also, in dermatophytic folliculitis plucking of hairs is usually painless (see Chapter 188).

Lupoid sycosis is a deep, chronic form of sycosis barbae associated with scarring, usually occurring as a circinate lesion. A central cicatrix surrounded by pustules and papules gives the appearance of lupus vulgaris (see Chapter 184).

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, and infiltrated lesion that develops when suppuration occurs in thick inelastic skin when multiple, closely set furuncles coalesce.

Furuncles

Furuncles arise in hair-bearing sites, particularly in regions subject to friction, occlusion, and perspiration, such as the neck, face, axillae, and buttocks. They may complicate preexisting lesions such as atopic dermatitis, excoriations, abrasions, scabies, or pediculosis, but occur more often in the absence of any local predisposing causes. In addition, a variety of systemic host factors is associated with furunculosis: obesity, blood dyscrasias, defects in neutrophil function (defects in chemotaxis associated with eczema and high levels of IgE, defects in intracellular killing of organisms as in chronic granulomatous disease of childhood), treatment with glucocorticoids and cytotoxic agents, and immunoglobulin deficiency states. The process is often more extensive in patients with diabetes. The majority of patients with problems of furunculosis appear to be otherwise healthy.

Cutaneous Lesions

A furuncle starts as a hard, tender, red folliculocentric nodule in hair-bearing skin that enlarges and becomes painful and fluctuant after several days (i.e., undergoes abscess formation; Fig. 176-8A). 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 (see Fig. 176-8B).

Differential Diagnosis

See Box 176-6 for differential diagnosis of furunculosis.

Carbuncles

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 (Fig. 176-9). 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 lesion soon develops a yellow–gray irregular crater at the center, which may then heal slowly by granulating, although the area may remain deeply violaceous for a prolonged period. The resulting permanent scar is often dense and readily evident.

Laboratory Tests

Extensive furunculosis or a carbuncle may be associated with leukocytosis. S. aureus is almost always the cause with CA-MRSA being more than likely in most geographic locations. Histologic examination of a furuncle shows a dense polymorphonuclear inflammatory process in the dermis and subcutaneous fat. In carbuncles, multiple abscesses, separated by connective-tissue trabeculae, infiltrate the dermis and pass along the edges of the hair follicles, reaching the surface through openings in the undermined epidermis. The diagnosis is made on the basis of the clinical appearance. Gram stain of pus, clusters of Gram-positive cocci, or isolation of S. aureus on culture confirms the diagnosis.

Prognosis and Clinical Course

The major problems with furunculosis and carbuncles are bacteremic spread of infection and recurrence. Lesions about the lips and nose raise the specter of spread via the facial and angular emissary veins to the cavernous sinus. Invasion of the bloodstream may occur from furuncles or carbuncles at any time, in an unpredictable fashion, resulting in metastatic infection such as osteomyelitis, acute endocarditis, or brain abscess. Manipulation of such lesions is particularly dangerous and may facilitate spread of infection via the bloodstream. Fortunately, these complications are not common. Recurrent furunculosis is a troublesome process that may continue for many years.

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 MRSA impetigo; see Box 176-4). For severe infections or infections in a dangerous area, maximal antibiotic dosage should be employed by the parenteral route. CA-MRSA should be suspected in all serious purulent infections. Vancomycin (1.0–2.0 g intravenously daily in divided doses) or other systemic parenteral agents that have anti-CA-MRSA activity are indicated for these patients. Antibiotic treatment should be continued for at least 1 week.

When the lesions are large, painful, and fluctuant, then incision and drainage are the most important actions that one should take in a timely manner. If the infection is recurrent or complicated by comorbidities, a culture can be sent. Antimicrobial therapy should be continued until all evidence of inflammation has regressed and altered appropriately as culture results become available. Draining lesions should be covered to prevent autoinoculation and diligent hand washing performed. Patients with recurrent furunculosis present a special and frequently exasperating problem (Box 176-7).

Abscess

As discussed in Section “Furuncles and Carbuncles,” abscesses caused by S. aureus commonly occur in folliculocentric infections—that is, folliculitis, furuncles, and carbuncles. Abscesses can also occur at sites of trauma, foreign bodies, burns, or sites of insertion of intravenous catheters. The initial lesion is an erythematous nodule. If untreated, the lesion often enlarges, with the formation of a pus-filled cavity (Fig. 176-10). CA-MRSA should be suspected in all patients with abscess.

The initial and most important treatment of an abscess is incision and drainage. Antibiotic usage after incision and drainage is only recommended if the lesion is severe or associated with cellulitis, there are signs of systemic illness, there are comorbid factors or immune suppression, the patient is very young or very old, if the abscess is in a body location that is difficult to drain, there is associated septic phlebitis, or there is no response to incision and drainage alone.9

Botryomycosis

(See Chapter 185, Table 185-1).

Botryomycosis is a rare pyogenic disease, possibly related to a balance between numbers of organisms and host defenses, presenting as a purulent chronic, subcutaneous infection. Predisposing factors include trauma, immunosuppression (HIV disease, hyper-IgE syndrome), chronic alcoholism, and diabetes mellitus. Lesions (usually solitary) can occur in skin, bone, and liver.

Cutaneous botryomycosis usually presents as a solitary lesion or a few lesions, often occurring in the genital area. The lesion has the gross appearance of a ruptured epidermal inclusion cyst (an erythematous circumscribed tender nodule), or prurigo nodularis (Fig. 176-11). In the majority of reported cases, a foreign body (fish bone, broom straw, etc.) has played a role in initiating or perpetuating the lesion. For diagnosis and treatment, see Chapter 185.

Staphylococcal Paronychia

Individuals exposed to hand trauma or chronic moisture are predisposed to staphylococcal paronychia, as well as to other causes of paronychia (e.g., Candida, Pseudomonas, Streptococcus, dermatophytes). S. aureus is the major infectious cause of acute paronychia, usually around the fingernails, often originating from a break in the skin, such as a hangnail. Clinically, skin and soft tissue of the proximal and lateral nail fold are red, hot, and tender, and, if not treated, can progress to abscess formation (Fig. 176-12).

In contrast, chronic or recurrent paronychia caused by Candida albicans is an infection of the space created by separation of the proximal dorsal nail plate and the undersurface of the proximal nail fold. Candidal paronychia is most common in individuals who have their hands in water for a great deal of time (see Chapter 189).

Management of paronychia caused by S. aureus includes oral and topical antibiotics, and incision and drainage of abscesses.

Staphylococcal Whitlow (Felon)

A whitlow is a purulent infection or abscess involving the bulbous distal end of the finger. The most common causes are S. aureus and herpes simplex virus. The portal of entry of S. aureus is a traumatic injury or possible extension of an acute paronychia. This infection is usually very painful. An obvious portal of entry is often apparent. The finger bulb is red, hot, tender, and edematous, with possible abscess formation (Fig. 176-13). In contrast, individuals with herpetic whitlows usually have a history of lesions occurring in the same site and present with grouped hemorrhagic vesicles, which may become confluent and form a single bulla (see Chapter 193). Management of a staphylococcal whitlow requires surgical drainage of loculated abscess(es) within the tissue and intravenous antibiotic therapy. X-ray examination of the involved finger is indicated to determine the presence of osteomyelitis. CA-MRSA should be suspected in all cases.

Syndromes Caused by Staphylococcal Exotoxins

SSSS, staphylococcal scarlatiniform eruption, TSS, recalcitrant erythematous, desquamating disorders (red disorders), and recurrent toxin-mediated perineal erythema are syndromes caused by staphylococcal exotoxins and are discussed in Chapter 177.

General Features

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. Although the carriage rate of group A Streptococcus on normal skin is less than 1%, a variety of skin lesions and puerperal sepsis may also be the source of intrahospital spread of infection. Group A Streptococci introduced into the operating room in the form of a minor skin infection, or even through perianal carriage by a surgeon or anesthetist, may be responsible for an epidemic of streptococcal wound infections.

The major factor in the spread from a carrier or an infected person is the proximity to the individual disseminating the organisms. Because many patients with group A streptococcal (GAS) skin infections harbor the same organism in their pharynxes, they are, for both reasons, potential sources for spread of infection in a hospital. Particular care must be taken to prevent spread of infection by isolating such patients until antibiotic therapy has rendered them noncontagious.

The overall incidence of streptococcal disease has surged since the mid-1980s.17 Reports of invasive GAS infections often associated with shock and multiorgan failure have increased globally. Localized epidemics continue to appear and, during such outbreaks, the carrier and infection rates in the community increase. After recovery (without antibiotic treatment) from streptococcal pharyngitis, some individuals may carry the organism for prolonged periods. The carrier state may also occur in the absence of overt antecedent infection. Fifteen percent to twenty percent of schoolchildren carry group A Streptococci in the throat. Some have hypothesized that the genetic predisposition to develop psoriasis may have been associated with an improved survival outcome in times of epidemic streptococcal infections.18

Etiology and Pathogenesis

The Lancefield classification of streptococcal groups (A–T) is based on the C carbohydrate antigens of the cell wall. Although essentially all GAS strains are β-hemolytic Streptococci, not all Streptococci producing β-hemolysis belong to group A. Because serologic grouping of Streptococci is not generally available, a reasonably accurate presumptive test for group A Streptococci is necessary. Bacitracin disk (“Taxos S”) sensitivity has been widely used; group A Streptococci are, almost without exception, susceptible to the low concentration of bacitracin contained in the disk, whereas Streptococci of other groups are often resistant. Subtyping of group A Streptococci can be performed according to their M protein antigenicity (see below). Certain M protein serotypes appear to correlate with greater virulence of the organism. The M protein inhibits phagocytosis, promotes adherence to host cells and allows bacterial growth in human blood.19 The M protein is highly polymorphic, with more than 150 variants coded for by the emm gene. Other virulence factors are cell surface molecules, including the hyaluronic acid capsule, C5a peptidase, opacity factor, and streptococcal inhibitor of complement. Secreted proteins playing a role in virulence include streptolysins O and S, cysteine proteinase, pyrogenic exotoxins, streptokinase, hyaluronidase, and other enzymes. It should be noted that horizontal gene transfer in GAS strains is a very common event. This transfer results in the rapid development of new and more virulent strains.20

The primary invasive streptococcal pyodermas are due almost exclusively to group A Streptococcus, which is usually considerably more invasive than of other Streptococci. Nonsuppurative postinfectious complications have been limited mostly to those produced by group A Streptococcus. Thus, GAS infections merit antibiotic treatment and eradication.

The hallmarks of invasive GAS infection are profuse edema, rapid spread through tissue planes, and a relatively thin exudative response. Infection may spread via the lymphatic or hematogenous routes and result in a fulminant clinical course.

The presence of Streptococci of groups other than A in skin lesions may represent either surface colonization or actual secondary infection in preexisting dermatoses. Group C and group G Streptococci have occasionally been implicated in impetiginous lesions, secondarily infected dermatitis, wound infections with lymphangitis, and even in erysipelas and cellulitis (see Chapter 178). Streptococci of groups B and D have been isolated from infections of skin lesions secondary to ischemia or venous stasis and have particularly involved the perineal area and operative wound sites. As with most secondary infections, those due to group B and group D Streptococci are frequently mixed infections with enteric bacteria or S. aureus. Group B Streptococci may cause cellulitis and otitis in neonates and, sometimes, in adults. Group L Streptococci (often carried by pigs, cattle, and poultry) have been responsible for impetigo, secondarily infected wounds, and paronychias in meat handlers.

The incidence of invasive complications (lymphangitis, suppurative lymphadenitis, bacteremia) of streptococcal infections of the skin has decreased in the antibiotic era. Other than these pyogenic complications, a variety of nonsuppurative complications (acute rheumatic fever, acute glomerulonephritis, erythema nodosum) may follow GAS infections. Distinct differences exist between acute rheumatic fever and acute glomerulonephritis in the site of the antecedent infection, the length of the latent period, and the streptococcal serotypes involved. Acute rheumatic fever may be a complication of GAS pharyngitis or tonsillitis, but it does not occur after streptococcal skin infections. In contrast, acute nephritis may follow infection of either the skin or the upper respiratory tract. The latent period between streptococcal pharyngitis and the onset of rheumatic fever is 2–3 weeks; whereas the latent period for pharyngitis-associated nephritis is approximately 10 days. A longer latent period of approximately 3 weeks is characteristic of acute nephritis associated with streptococcal pyoderma.

Group A Streptococci are classified into over 80 subtypes, based on the antigenicity of their M proteins (fibrillar structures extending out from the cell surface). Although there is no strong evidence of an association between infection with any specific group A serotypes and the subsequent development of rheumatic fever as yet, several serotypes (particularly mucoid strains of types 1, 3, and 18) have been implicated in a few outbreaks of streptococcal sore throat complicated by this sequela.21 However, there is a clear relationship between infection with certain serotypes and the subsequent occurrence of nephritis—the so-called nephritogenic serotypes. Type 12 is the classic serotype responsible for pharyngitis-associated acute nephritis, but other serotypes, such as 1, 4, 25, and 49, have been implicated. The pyoderma-associated nephritogenic strains generally belong to different serotypes: types 2, 49, 42, 55, 56, 57, and 60.22,23 Unlike the pharyngitis strains, the pyoderma serotypes produce lipoproteinase or opacity factor, illustrating a fundamental difference between the two.17 The skin rather than the pharynx is the principal site of antecedent streptococcal infection causing nephritis, and impetigo is now the most common form of such predisposing skin infections.

The frequency of acute glomerulonephritis after infection with a known nephritogenic strain is 10%–15%; the frequency of rheumatic fever after an unrecognized or inadequately treated pharyngeal infection by any serotype of group A Streptococcus is 2%–3% or less. The distinction between nephritogenic and other strains of Streptococci that might be associated with rheumatic fever can be seen in studies from Trinidad, a hyperendemic area for pyoderma-associated nephritis. There the streptococcal serotypes causing outbreaks of nephritis differed from the serotypes associated with sporadically occurring cases of acute rheumatic fever in the same population.21

It has been suggested that several biologic properties are associated with broad categories of group A Streptococci. Most M proteins fall into one of two antigenic classes based on the presence (class I) or absence (class II) of a highly conserved antigenic domain. Almost all rheumatic fever outbreak-associated strains belong to serotypes of class I and require a precursor nasopharyngeal infection. However, because many class I serotypes are associated with impetigo as well, and because class II serotypes are responsible for both upper respiratory and skin infections, the class of M protein alone is not a determinant of tissue tropism. Current evidence indicates differences among class I organisms that may relate to their capacities to induce rheumatic fever: class I nasopharyngeal isolates appear to lack human IgG-binding activity, whereas nearly all impetigo isolates of the same class bear human IgG receptors.24

As in S. aureus, there are several GAS superantigens that have been identified. These include streptococcal pyrogenic exotoxin (or erythrogenic exotoxin) A–C, F, and G–J, streptococcal superantigen, and streptococcal mitogenic exotoxin Z. These superantigens are associated with disease.25

Antibody Response and Immunity

The immune response to GAS infection depends to a large measure on the site of infection. Streptococcal infection is usually defined as a positive throat culture with a serologic response to group A Streptococcus and the streptococcal carrier state by a positive throat culture and no serologic response. After streptococcal pharyngitis, specific antibodies develop to many of the extracellular enzymes of the Streptococci. Eighty-five percent of patients with acute rheumatic fever and a proven preceding streptococcal infection have an elevated or increasing antistreptolysin O titer. The serologic demonstration of an antecedent streptococcal infection in this situation can be increased to virtually 100% by the simultaneous testing for several other antibodies (antihyaluronidase, anti-DNase B). Antibodies to extracellular products, with the exception of antibody to the erythrogenic toxin of scarlet fever, appear to have no effect on the manifestations of illness. Streptococcal immunity is type specific (but not group specific), long lasting, and depends on the production of bactericidal antibodies to the specific M proteins of the over 80 different serotypes of group A organisms. Although recurrent pharyngeal infections caused by the same serotype are most unusual, repeated clinical infections caused by different types are not uncommon. Early treatment of streptococcal upper respiratory tract disease with antibiotics may suppress the appearance of type-specific antibody (and immunity), as well as the development of antibody to the extracellular products of the organism.

In contrast to pharyngeal infections, the antistreptolysin O response with streptococcal skin infections or pyoderma-associated nephritis is weak. To define the latter serologically, anti-DNase B titers are much more reliable. Although pyoderma strains of Streptococci produce M proteins, and although type-specific antibody may develop in patients with pyoderma-associated nephritis, the frequency of production of such antibodies and their role in protection against reinfection are unclear. Although pharyngeal reinfection with the same streptococcal serotype is probably unusual, some evidence suggests that the same serotype can be associated with repeated episodes of pyoderma.

Specific diseases caused by group A (and other) Streptococci are listed in Box 176-8. Streptococcal pyodermas include all types of superficial streptococcal skin infections except erysipelas—that is, impetigo, ecthyma, and secondary infections of preexisting skin lesions (e.g., insect bites, abrasions, eczema). Streptococcal intertrigo such as streptococcal perianal “cellulitis” can occur primarily or secondarily in underlying conditions such as inverse psoriasis.

Impetigo

Epidemiology

Impetigo caused by group A Streptococcus is a highly communicable infection and occurs predominantly in preschool-aged children (usually before the age of 2 years except in highly endemic areas). It is more common in warmer, more humid climates than in temperate zones. Its peak seasonal incidence is in the later summer and early fall. Nongroup A (groups B, C, and G) Streptococci may be responsible for rare cases of impetigo; group B Streptococci are associated with impetigo in the newborn. Whereas, many different serotypes of group A Streptococci may cause pharyngitis, a limited number of newly described types predominate in impetigo (types 49, 52, 53, 55, 56, 57, 59, and 61).

Etiology and Pathogenesis

Group A Streptococci appear on normal skin of children approximately 10 days before the development of impetigo, and they are not recovered from the nose and throat of the same patients until 14–20 days after skin acquisition of the organism. Streptococci are recovered from the respiratory tract of approximately 30% of children with skin lesions, but there is no clinical evidence of streptococcal pharyngitis. Thus, the sequence of spread in a given patient is from normal skin to lesions and eventually to the respiratory tract.26 In contrast, the sequence of spread of S. aureus (in cases of impetigo in which it is the only organism isolated) is from nose, to normal skin, to skin lesions (see Section “Impetigo”).

When exposed to an infectious contact, preexisting lesions, such as scabies, varicella, or eczema, predispose to the appearance of infected lesions. Crowding, poor hygiene, and neglected minor skin trauma contribute to the spread of streptococcal impetigo in families. Minor outbreaks have also occurred among athletes involved in contact sports. Although the majority of cases occur in children, particularly of preschool age, young adults are also affected. The inflammatory process of impetigo is superficial, with a unilocular vesicopustule located between the stratum corneum above and the stratum granulosum below. This is usually situated near the opening of a hair follicle. Organisms, as well as leukocytes and cell debris, fill the vesicle.

Clinical Findings

Cutaneous Lesions

Impetigo caused by group A Streptococcus presents as a crusted superficial infection of the skin; an initial vesicular phase has been described but is rarely detected. Lesions are clinically indistinguishable from impetigo caused by S. aureus, with the exception of bullous impetigo (see Section “Nonbullous Impetigo” and Figs. 176-1, 176-2, and 176-3). Pruritus and burning may occur, but the lesions are usually painless. Systemic response is minimal unless complications occur.

Laboratory Tests

A slight leukocytosis may occur. A Gram-stained smear of early vesicle fluid reveals Gram-positive cocci in chains. Culture of the weeping area or of the area beneath an unroofed crust reveals group A Streptococci or a mixture of Streptococci and S. aureus (particularly from older crusted lesions).

Prognosis and Clinical Course

If untreated, the process may persist and new lesions may develop over the course of several weeks; thereafter, the infection tends to resolve spontaneously unless there is some underlying cutaneous disorder such as eczema. If untreated, some lesions become chronic and deeper, such as ecthyma (see Section “Staphylococcal Ecthyma”). Complicating erysipelas, cellulitis, or bacteremia are unusual. The major serious sequela is acute poststreptococcal glomerulonephritis.

Treatment

Topical treatment (removal of dirt, crusts, and debris by soaking with soap and water) is a valuable adjunct. Mupirocin ointment appears to be as effective as parenteral or oral penicillin for treatment of impetigo.27 Retapamulin 1% ointment is also effective for localized impetigo and secondarily impetiginized dermatitis as well, although decreased efficacy against MRSA was noted in some trials.14

In superficial pyodermas known to be caused by group A Streptococcus, penicillin is the drug of choice, administered either as a single injection of long-acting benzathine penicillin (300,000–600,000 units for children; 1.2 million units for adults) or orally (25,000–100,000 units/kg/day in divided doses q6h for 10 days). Although penicillin treatment clears the lesions of GAS impetigo and prevents recurrence for a short time, Streptococci can persist on or newly colonize unaffected skin in spite of this therapy. Erythromycin (30–50 mg/kg/day PO in divided doses q6h for children; 250–500 mg PO q6h for adults administered for 10 days) is a suitable alternative drug in patients allergic to penicillin. However, it should be noted that 20% or more of GAS strains became resistant to erythromycin in areas (Japan, Finland) where this antibiotic had been extensively used for a variety of indications.28 There is still no evidence to suggest that treatment of GAS pyoderma can prevent subsequent nephritis in any individual. Although the latent period after impetigo is longer than that after pharyngeal infection, the mildness of the illness delays or negates the seeking of medical attention.

Practically, however, the majority of cases of nonbullous impetigo are caused by S. aureus, and topical or systemic antimicrobial treatment should be directed at that pathogen (see Box 176-4).

Streptococcal Ecthyma

See Section “Staphylococcal Ecthyma.”

Intertriginous Streptococcal Infections

Streptococcal pyodermas occur much less commonly in occluded sites such as the perineum/perianal region, vulva/vagina, axillae (Fig. 176-14), inframammary region, groin, preputial sac, and web spaces of the feet. Perianal (group A) streptococcal “cellulitis” occurs principally in children, presenting with intense perianal erythema (Fig. 176-15), pain on defecation, blood-streaked stools associated with anal fissures, and chronicity if untreated.29 It is often confused with psoriasis, candidiasis, seborrheic dermatitis, inflammatory bowel disease, pinworm infection, or a behavioral problem. The infection can also involve the penis and vulva. Treatment options include oral antibiotics or topical mupirocin. Guttate psoriasis has also occurred in children, associated with perianal streptococcal infection.30

Blistering Distal Dactylitis

Group A Streptococcus is responsible for the majority of cases of blistering distal dactylitis, also called bulla repens, usually occurring in children and adolescents. However, group B Streptococcus can also cause this infection. A large, tense blister develops, filled with seropurulent fluid, over the volar skin pad of distal fingers or toes (Fig. 176-16). The blisters are often surrounded by an erythematous base. The lesion may be more proximally located on the finger or extend to involve the nail folds. Group A Streptococcus may be cultured from the vesicle fluid. Blistering distal dactylitis may be treated with oral penicillins or erythromycin and release of subungual pus is often required. Staphylococcal blistering distal dactylitis has been reported with an identical clinical picture.31

Acute Lymphangitis

Acute lymphangitis is an inflammatory process involving the subcutaneous lymphatic channels. It is most often caused by group A Streptococci, but occasionally may be caused by S. aureus; rarely, STIs with other organisms, such as Pasteurella multocida or herpes simplex virus may be associated with acute lymphangitis.

Clinical Findings

History

The portal of entry is commonly a wound on an extremity, an infected blister, or a paronychia. The systemic manifestations of infection may occur either before any evidence of infection that is present at the site of inoculation or after the initial lesion has subsided. The patient may notice pain over an area of redness proximal to the original break in the skin. Systemic symptoms are often more prominent than expected from the degree of local pain and erythema.

An unusual spread of streptococcal infection of the thumb (paronychia) or of the interdigital webs between the thumb and index finger may occur occasionally. Lymphatic drainage from this area can bypass the lymph nodes at the elbow and drain into the axillary nodes, which, in turn, communicate with the subpectoral nodes and the pleural lymphatics. As a consequence, subpectoral abscesses and pleural effusion can develop. The subpectoral infection may dissect downward and appear over the lower chest and upper abdomen as an area of cellulitis. This is a very serious illness. The clinical clues to the development of this sequence of events are provided by the location of the original infection on the thumb or medial surface of the index finger and the early occurrence of axillary pain.

Cutaneous Lesions

Red linear streaks, which may be a few millimeters to several centimeters in width, extend from the local lesion toward the regional lymph nodes, which are usually enlarged and tender (Fig. 176-17).

Differential Diagnosis

In the upper extremities, acute lymphangitis usually can be differentiated from subacute or chronic sporotrichoid syndrome caused by organisms such as Sporothrix schenckii. In the lower extremities, superficial thrombophlebitis may produce somewhat similar linear areas of tender erythema. The absence of a portal of entry and of tender regional adenopathy is helpful in distinguishing this process from lymphangitis.

Laboratory Tests

The peripheral white blood cell count is elevated, with a marked increase in polymorphonuclear cells. The offending organism cannot be cultured from the skin, as the infection is restricted to the lymphatic channels. However, the primary portal of entry or a suppurative lymph node, if overt infection is present, may reveal the etiologic agent.

Prognosis and Clinical Course

The frequent development of bacteremia with metastatic infection in various organs makes this a potentially serious disease. The infection responds readily to penicillin therapy if instituted promptly.

Invasive Streptococcal Infections

Erysipelas, cellulitis, and streptococcal gangrene are invasive streptococcal infections and are discussed in Chapter 178.

Streptococcal Toxin Syndromes

Scarlet fever and toxic streptococcal syndromes are streptococcal toxin syndromes and are discussed in Chapter 177.

Cutaneous Manifestations of Subacute Bacterial Endocarditis

(See Chapter 181)

Poststreptococcal (Group A) Nonsuppurative Cutaneous Sequelae

Erythema Nodosum

(See Chapter 70)

Erythema Marginatum (Cutaneous Lesions of Acute Rheumatic Fever)

(See Chapter 160)

Purpura Fulminans

(See Chapters 144 and 181)

Other Skin Lesions Accompanying or Following Group A Streptococcal Infections

Erythema Multiforme-Like Lesions

Round erythematous macules, up to 1.5 cm in diameter, some developing bright borders and subsequently showing clearing in the center, may occur during bacteremia caused by group A Streptococci (or S. aureus) in infants and young children (see Chapter 39).

Acute Guttate Psoriasis

Rarely, erythematous, papulosquamous, guttate psoriasiform lesions may develop during or after GAS pharyngitis, perianal streptococcal infection, or other skin infections. Children appear to be most commonly affected. Clearing of the lesions may occur within weeks of antimicrobial therapy of the streptococcal infection. Although the temporal relation of the two processes is striking, a direct causal connection has not been established. There is no strong evidence to support the use of antibiotics in the treatment of guttate psoriasis.

Management of Group A Streptococcal Skin Infections

General Principles

Penicillin G is the drug of choice in the treatment of known GAS skin infections. When the etiology is not known immediately (e.g., in cellulitis) and when S. aureus is also a distinct consideration, a semisynthetic penicillin (nafcillin or oxacillin) should be employed initially. Penicillin treatment should be continued for at least 10 days to ensure eradication of the infection. Prophylactic penicillin therapy is indicated for close family contacts (particularly children) of patients with streptococcal pharyngitis.

Antimicrobial Therapy

Mild instances of infections, such as impetigo, scarlet fever, or certain cases of erysipelas and cellulitis, may be treated with oral penicillin V (250–500 mg qid). When staphylococcal infection is suspected, dicloxacillin (250–500 mg PO qid) should be substituted. In adults allergic to penicillin, erythromycin (250–500 mg PO qid) is a reasonable alternative. Other alternatives include azithromycin, clarithromycin, and clindamycin (Box 176-9).

Prevention of Spread

Patients hospitalized with GAS infections should be isolated until the organisms have been eradicated by antibiotic treatment. Individuals with recurrent episodes of GAS infections can be treated with dicloxacillin or erythromycin, 250 mg twice daily (penicillin-allergic individuals), as secondary prophylaxis.

Soft-Tissue Streptococcal Infections

(See Chapter 178)

Cutaneous Infections Caused by Micrococcus: Pitted Keratolysis

Pitted keratolysis involves the stratum corneum of the web spaces and plantar surface. Originally named keratoma plantare sulcatum by Castellani in 1910, this disease has become more commonly called by its current name after Taplin and Zaias coined it in 1967. The disease was first seen in those who went barefooted during the rainy season.

Etiology and Pathogenesis

The likely causative organism is Micrococcus sedentarius, which is a Gram-positive Staphylococcus-related bacterium that invades the stratum corneum softened by sweat and moisture. Corynebacterium sp. may also be involved. Pitted keratolysis tends to be much more severe in tropical climates than in temperate ones.

Pitted keratolysis occurs in adults and children of both sexes, but adult males with sweaty feet are most susceptible (96% of cases).32 Sliminess of the skin, often manifest by the foot sticking to the socks, is also a common complaint (70% of cases). The feet are typically very malodorous (89%) and may be mildly pruritic (8%).

Clinical Manifestations

Pitted keratolysis presents as a superficial erosion of the stratum corneum, composed of numerous small crateriform pits coalescing to form a large discrete defect with serpiginous borders on the plantar surface of the foot. The pits are usually larger than 0.7 mm in diameter, but at times are smaller than 0.5 mm. The pits have elongated configurations along the plantar furrows and are located predominantly on the pressure-bearing areas, such as the ventral aspect of the toe, ball of the foot, and the heel, but they are also seen on nonpressure-bearing areas.32 The web spaces between the toes are also commonly involved sites, and may be the only manifestation (Fig. 176-18). The diagnosis is made clinically.

Differential Diagnosis

Interdigital tinea pedis can present with erosive lesions in the web spaces. Erythrasma in the web spaces is usually hyperkeratotic but can be erosive.

Laboratory Findings

Gram staining of scrapings may detect the microorganism more readily than potassium hydroxide examination. Histologically, the organisms are present in the walls and bases of the crateriform defects in the upper layer of the stratum corneum. The organisms appear as coccoid and filamentous forms with branches and septa.

Treatment

Prophylactic measures are aimed at keeping the feet as dry as possible. Inert antiseptic foot powders often help. Aluminum chloride 20% solution is an effective astringent. A benzoyl peroxide wash and 5% gel are effective therapy in most cases as well. Other commonly used topical adjunctive agents include clindamycin and erythromycin solutions. Systemic use of these agents can be attempted in severe cases.33

Infections Caused by Corynebacterium

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. It is commonly misdiagnosed as tinea cruris for many months before proper diagnosis is made.

Etiology and Epidemiology

Corynebacterium minutissimum, the etiologic agent of erythrasma, is a short, Gram-positive rod with subterminal granules. The infection is more common in tropical than in temperate climates. In a study in a temperate climate, 20% of randomly selected subjects were found to have erythrasma by Wood's lamp examination. The generalized disease is much more common in the tropics. Erythrasma is more common in men and may occur in asymptomatic form in the genitocrural area.

Clinical Findings

History

Symptoms vary from a completely asymptomatic form, through a genitocrural form with considerable pruritus, to a generalized form with scaly lamellated plaques on the trunk, inguinal area, and web spaces of the feet. When pruritic, irritation of lesions may cause secondary changes of excoriations and lichenification.

Cutaneous Lesions

The most common site of involvement is the web spaces of the feet, where erythrasma presents as a hyperkeratotic white macerated plaque (Fig. 176-19), 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 (Fig. 176-20). In these sites, the patches have a relatively uniform appearance as compared with tinea corporis or cruris, which often have central clearing.

Wood's lamp examination of erythrasma reveals a coral-red fluorescence caused by coproporphyrin III. The fluorescence may persist after eradication of the Corynebacterium as the pigment is within a thick stratum corneum.

Differential Diagnosis

Tinea versicolor is distinguished from erythrasma by the lesions on the trunk being most numerous at nonintertriginous sites. Tinea cruris tends to have an active scaling border with central clearing. Inverse psoriasis usually presents as sharply demarcated plaques with a shiny red color in the intergluteal cleft, inguinal folds, and axillae.

Laboratory Findings

Culture of the specific Corynebacterium in abundance from the lesion corroborates the diagnosis. Gram-stained imprints of the horny layer of the skin show rod-like, Gram-positive organisms in large numbers.

The diagnosis is strongly suggested by the location and superficial character of the process, but must be confirmed by demonstration of the characteristic “coral-red” fluorescence with Wood's lamp illumination.

Prognosis and Clinical Course

The disease may remain asymptomatic for years or may undergo periodic exacerbations. Relapses occasionally occur even after successful antibiotic treatment.

Treatment

For localized erythrasma, especially of the web spaces of the feet, benzoyl peroxide wash and 5% gel are effective in most cases. Clindamycin or erythromycin (2% solution) or azole creams are several of the many effective topical agents. Fusidic acid has been used outside the United States. For widespread involvement, oral erythromycin is effective. A 1-g single dose of clarithromycin has been used successfully.34 For secondary prophylaxis, an antibacterial benzoyl peroxide bar when showering is effective.

Trichomycosis Axillaris and Pubis

Trichomycosis axillaris, a bacterial infection of the hair shaft (not fungal as the name implies), is characterized by what appears to be nodular thickenings on the hair shaft, composed of colonies of aerobic Corynebacterium. The condition occurs both in the axillae and pubic areas, and not just in the axillae, as the name implies. The bacteria produce various pigments, giving the nodules a range of colors. The concretions on the hair shaft are usually a tan color but may be reddish, yellow, or black (Fig. 176-21). Lesions are most dense and may be present only in the central portion of the axillary hair. Trichomycosis is asymptomatic except for the patient's concern regarding the lesions themselves and because they are malodorous.

The diagnosis is usually made on the basis of the physical findings. The concretions can be visualized using a potassium hydroxide preparation. Pediculosis pubis infestation with multiple eggs on the hair shaft should be ruled out.

The involved hair can be removed by shaving. Benzoyl peroxide wash and gel are effective as treatment and prevention against recurrence of trichomycosis. Topical clindamycin or erythromycin solutions can be used as well.