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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).
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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
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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).
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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
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Etiology and Pathogenesis
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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.
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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.
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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
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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
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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
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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.
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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.
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Superficial Staphylococcal Pyodermas
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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.
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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.
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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.
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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.
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Differential Diagnosis
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See Box 176-2 for differential diagnosis of nonbullous impetigo.
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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”).
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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
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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.
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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.
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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).
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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.
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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.
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Differential Diagnosis
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See Box 176-3 for differential diagnosis of bullous impetigo.
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Prognosis and Clinical Course
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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.
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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
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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.
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Staphylococcal Ecthyma
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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).
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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.
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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.
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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.
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Management of ecthyma is usually systemic and includes the same agents used for staphylococcal impetigo (see Box 176-4).
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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).
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Superficial Folliculitis
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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.
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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).
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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).
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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).
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Furuncles and Carbuncles
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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.
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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.
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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).
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Differential Diagnosis
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See Box 176-6 for differential diagnosis of furunculosis.
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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.
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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.
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Prognosis and Clinical Course
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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.
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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.
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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).
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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.
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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
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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.
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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.
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Staphylococcal Paronychia
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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).
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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).
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Management of paronychia caused by S. aureus includes oral and topical antibiotics, and incision and drainage of abscesses.
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Staphylococcal Whitlow (Felon)
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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.
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Syndromes Caused by Staphylococcal Exotoxins
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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.