Patrick A. Murphy
Most skin infections are trivial and can be managed at home without medical assistance. Each year, however, approximately 5% of the population develop a skin infection that requires medical attention. The severity of these infections depends on the virulence of the infecting organisms and the state of host defenses. The most common infecting organisms are Streptococcus pyogenes and Staphylococcus aureus. In otherwise healthy people, these often cause only modest morbidity and respond rapidly to appropriate treatment. They can, however, cause serious infections, especially in diabetic patients, in patients with impaired blood supply to the infected site, impaired lymphatic or venous drainage of the site, and in patients with defects in leukocytic or immunologic defense mechanisms. Serious infection is also more likely when other bacteria, or combinations of bacteria, are involved, as occurs in bites or contaminated wounds.
Superficial Infections Caused by S. PYOGENES and S. AUREUS
Impetigo, ecthyma, and erysipelas are superficial infections usually caused by group A hemolytic streptococci (S. pyogenes) and S. aureus(1). These infections arise from breaks in the skin that are often so minor they are un-noticed.
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Impetigo
Impetigo occurs mostly among preschool children, especially in warm, humid climates or when personal hygiene is poor (2). Under these conditions, the disease is highly contagious and outbreaks may occur. Older children and adults are only occasionally affected.
Impetigo begins as a pruritic, focal, superficial eruption of small 1- to 2-mm vesicles, often on the face near the nares, chin, or lower extremities. There is usually no history of trauma. In several days, the vesicles change to pustules that break, become crusted, and have an erythematous base. Regional lymphadenopathy is common, but there are no constitutional symptoms. The process may spread because of scratching. Healing occurs without scarring. Impetigo may recur if personal hygiene is not improved.
Bullous impetigo is caused by strains of S. aureusthat secrete one of the epidermolytic toxins (3). Epidemics of bullous impetigo can occur among newborns, but only sporadic cases are seen in older children, and adult cases are uncommon. The process begins as a macular erythematous rash. The characteristic thin-walled, fluid-filled, superficial bullae appear within 1 to 3 days, range from 1 cm to several centimeters in diameter, and usually involve exposed areas of the body. These bullae rupture, desquamation occurs, and healing without scarring follows in about 7 days. In its most dramatic form, this process causes the scalded skin syndrome, a disease of small children in which there is extensive superficial desquamation.
Ecthyma
Ecthyma occurs under the same conditions of poor hygiene that promote impetigo. It is characterized by 3- to 10-mm discrete, ulcerating lesions with an adherent necrotic crust and surrounding erythema; a small amount of pus often underlies the crust. The ulcer is sufficiently deep to cause permanent scarring. Lesions are most common on the anterior tibial surface at sites of minor trauma or insect bites. Left untreated, the lesions tend to spread distally and there may be associated lymphadenopathy; systemic symptoms, however, are lacking. Cultures of pus may yield both S. pyogenes and S. aureus. There is evidence that S. aureus causes a majority of the cases. Lesions with a similar appearance may result from bacteremia with Pseudomonas aeruginosa.
Erysipelas
Erysipelas involves progressive, often rapid spread of infection through superficial layers of skin and lymphatics. It may occur after a minor wound in normal skin but is more likely when prior injury or disease has impaired the lymphatic or venous drainage of the skin or left extensive scarring, as, for example, in a patient with chronic venous insufficiency of the lower extremities or lymphedema of the arm after radical mastectomy. Most episodes of erysipelas are caused by S. pyogenes. A few are caused by S. aureus or other agents, such asPasteurella multocida or Erysipelothrix rhusiopathiae (see sections Bites, Cellulitis, Wound Infections, and Table 32.4), and these cannot always be distinguished clinically.
Erysipelas is characterized by a rapidly spreading area of marked erythema with warmth, local pain, an elevated sharp margin between involved and uninvolved skin, and firm edema that gives the skin a typical “orange peel” appearance. There may be seropurulent drainage at the inoculation site, but fluctuation and dermal necrosis are lacking. Erythema often extends centrally along superficial draining lymphatics; regional lymph nodes are often enlarged and tender. Systemic toxicity, chills, and fever are common. If it is untreated, metastatic infection may occur, and there is appreciable mortality. Facial infections are especially dangerous because of possible intracranial spread via draining lymphatics or veins. Extensive involvement of the trunk also carries an increased risk of death.
Management
Bacterial cultures of the lesions of impetigo, bullous impetigo, and ecthyma usually are not helpful. Impetigo and ecthyma may reveal mixed cultures of S. pyogenes and S. aureus, or either agent alone, whereas lesions of bullous impetigo are often sterile. Blood cultures should be obtained when erysipelas is extensive or is associated with marked systemic toxicity (e.g., temperature greater than 102°F [39°C], shaking chills, severe malaise). Attempts to isolate an organism by culturing sterile saline that has been injected and withdrawn through a fine needle at the edge of the lesion have a low yield and are not useful. If there is seropurulent drainage from the lesions, it should be cultured.
Antimicrobial therapy is required for most of these infections (Tables 32.1 and 32.2). Minor cases of impetigo, with no systemic symptoms and few local symptoms, can be treated with antibacterial ointments such as bacitracin. Topical mupirocin (Bactroban) was recommended previously, but resistance develops very rapidly and it is no longer recommended. If the rash is spreading rapidly, or there are many cases in a school or a village, it is probably wise to use a systemic antibiotic.
Impetigo and ecthyma are treated similarly. Dicloxacillin, cephalexin, and other penicillinase-resistant β-lactams are usually effective oral antimicrobials. Erythromycin is also frequently effective. These simple antibiotics probably work because most of the cases are partially or solely attributable to streptococci. Adjunctive therapy includes careful daily soaking of lesions to remove crusted debris using warm water with an iodophor (a soap that releases iodine in a nontoxic, nonstaining form, such as
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Betadine skin cleanser) or with a soap that contains hexachlorophene (e.g., pHisoHex). Prevention depends primarily on improved personal hygiene; the most important preventive measure is careful frequent skin cleansing with soap and water.
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TABLE 32.1 Antibiotic Selection for Superficial and Pustular Skin Infectionsa |
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Treatment of bullous impetigo should be directed at penicillin-resistant staphylococci. Oral dicloxacillin and cephalexin are the standard initial treatment, but in some communities as many as 50% of S. aureus are resistant. If these antibiotics fail, the patient should be treated with a regimen which covers methicillin-resistant S. aureus (MRSA, see Pustular Infections Caused by S. aureus).
Minor episodes of erysipelas may be treated with oral penicillin V or erythromycin. Application of moist heat to the affected area appears to hasten clearing of the infection. Serious episodes are those with marked systemic toxicity, extensive lesions, or facial lesions and those occurring in compromised hosts (e.g., diabetics). Such patients have an appreciable mortality, and they require hospitalization and intravenous treatment with penicillin G (Tables 32.1 and 32.2).
Special attention should also be paid to patients with atherosclerotic peripheral vascular disease who have infections of their lower extremities. Such patients should be put at bed rest, or at least couch rest. The leg should be at approximately the same height as the heart. If the leg is elevated too much, the blood pressure in distal arteries may become so low that blood does not reach the toes. If the leg is too dependent, it may become edematous. Either eventuality will result in difficulty in clearing infection. Sustained pressure on any part of the leg or foot should be avoided because it is likely to result in a decubitus ulcer.
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TABLE 32.2 Antibiotic Dosage and Schedule for Skin Infections Caused by Streptococcus pyogenes and Staphylococcus aureusin Adults |
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Patients with chronic edema caused by damage to the veins or lymphatics of an extremity may experience repeated episodes of erysipelas or cellulitis that cause further damage. More than 95% of such infections are caused by hemolytic streptococci. While Group A causes some cases, most are due to streptococci of other Lancefield types—B, C, F, or G. Fortunately, hemolytic streptococci have not (yet) developed resistance to penicillin G. Patients who have numerous recurrent infections should receive continuous antibiotic prophylaxis with penicillin V (250 mg twice daily), benzathine penicillin (600,000 units intramuscularly monthly), or erythromycin (250 mg twice daily). Reduction of chronic edema by use of fitted pressure stockings or by administration of diuretics helps reduce susceptibility to this infection.
Superficial skin infections respond rapidly to appropriate therapy. Systemic toxicity and erythema associated with erysipelas usually abate within 3 or 4 days, and discrete skin lesions show marked healing within 10 days. During this period, activity should be restricted in accord with the extent of the infection. Minor lesions require no restrictions. Patients with any form of impetigo should avoid contact with infants and small children until lesions heal.
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Complications
Streptococcal skin infections do not cause rheumatic fever, but they may cause acute glomerulonephritis if the streptococcal strain is nephritogenic. Nephritis is not prevented by antimicrobial therapy. The average latency period between initial symptoms of a streptococcal skin infection and the onset of glomerulonephritis is 2 weeks. If a nephritogenic strain is known to be in the community, initial and 14-day followup evaluation should include a urinalysis. Most patients who develop poststreptococcal glomerulonephritis are asymptomatic, but in some, glomerulonephritis is first suggested by gross hematuria; acute hypertension; and signs of salt and water retention, such as dependent edema or congestive heart fail-ure (CHF).
Bacteremia with metastatic infection may complicate neglected or severe episodes of erysipelas. Metastatic infection should be considered in patients with severe disease that responds poorly to treatment or if findings develop that are suggestive of distant localized infection. Possible metastatic infections include meningitis, endocarditis, septic arthritis, infection of pre-existing pleural effusions or ascites, and solid organ abscesses (e.g., liver, spleen).
Pustular Infections Caused by S. Aureus
These include folliculitis, furunculosis, hidradenitis suppurativa, and carbuncles. They represent increasingly severe effects of the infection of hair follicles, sebaceous glands, or sweat glands by S. aureus, the result being inflammation and abscess formation.
Folliculitis
Folliculitis involves minor inflammation of individual hair follicles, often with formation of small superficial pustules. There is little pain or surrounding erythema. In some people, lesions recur for months or even years. A common area of involvement is the bearded part of the face, where minor trauma from shaving may be a contributing factor.
Furunculosis
Deeper infection of follicles or cutaneous glands leads to formation of pustular furuncles. Boils are large furuncles. They range in diameter from about 5 mm to 2 or 3 cm and occur most commonly on hairy areas exposed to friction, trauma, or maceration (e.g., buttocks, neck, face, axillae, groin, forearms, thighs, upper back). Furunculosis may also complicate the acne of adolescence. Furuncles begin with pruritus, local tenderness, and erythema, followed by swelling and marked local pain. As pus forms in the center of the lesion, the overlying skin becomes thin, the lesion becomes elevated, pain increases, and spontaneous drainage of pus ultimately occurs, usually with prompt relief of pain and rapid healing. Furunculosis may be recurrent in some people, especially diabetics and chronic nasal carriers ofS. aureus.
Hidradenitis Suppurativa
Hidradenitis suppurativa is a noninfectious skin disease characterized by obstruction of the ducts of apocrine sweat glands in the axilla, perineum, or groin. The process begins at puberty when these glands become active, and it comes to light when staphylococcal infection of one or several of the obstructed glands occurs. Such episodes initially respond well to antimicrobials, but because antimicrobials do nothing for the primary condition, the infections recur. After several years, infection becomes chronic, with multiple scars and numerous draining abscesses and sinus tracts. By this time, the bacterial flora is usually gram negative, with Proteus and Pseudomonas commonly found.
Carbuncles
A carbuncle is a coalescent mass of deeply infected follicles or sebaceous glands with multiple interconnecting sinus tracts and cutaneous openings that drain pus ineffectively. Carbuncles usually occur in the thick skin on the back of the neck or upper back. Once formed, the lesions steadily worsen, with increasing pain, erythema, swelling, purulent drainage, and lateral enlargement; they vary in diameter from 3 to 10 cm or larger. Fever and systemic toxicity are common, and bacteremia may be present. Carbuncles occur with increased frequency in diabetics and may cause a major increase in the severity of diabetes. Patients who are normally sustained on an oral agent or who were not previously known to be diabetic may present in ketosis.
Management
Bacterial cultures of typical pustular lesions are usually unnecessary because virtually all are caused by S. aureus and most isolates prove resistant to penicillin G. Increasingly, these infections are caused by MRSA, and cultures should be done if standard treatment fails.
Minimal lesions, such as folliculitis, require little therapy. Careful, twice-daily cleansing with a mild soap, preferably one containing hexachlorophene, and avoidance of minor trauma and irritants, such as cosmetics or abrasive soaps, are usually sufficient.
Furuncles should be managed initially by gentle application of warm moist heat (as moist compresses or baths) for about 30 minutes four times a day. Traditionally, compresses contain hyper-osmotic solutions of substances such as glycerin and magnesium sulfate to “draw the pus out,” and they probably work. The patient should
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be instructed to avoid squeezing or pressing on the furuncle. Lesions less than 1 cm in diameter often drain spontaneously after 1 to 3 days and require no further treatment. Larger lesions, painful lesions, and lesions that do not drain spontaneously should be drained surgically when they are fluctuant. This can be done in the office by making a single incision into the abscess with a scalpel, after first infiltrating the incision line with 0.5% or 1.0% lidocaine for local anesthesia. Lifting the anesthetized skin with a forceps when the incision is made helps avoid pain caused by downward pressure from the scalpel. Packing with iodoform gauze for 1 or 2 days may be needed to control oozing of serosanguineous discharge after surgical drainage. Antimicrobial therapy is required only for extensive lesions such as multiple furuncles, carbuncles, or lesions associated with marked surrounding inflammation, or in diabetic patients. In such cases, oral dicloxacillin or cephalexin (Tables 32.1 and 32.2) should be given until signs of inflammation subside completely, which may take 2 weeks or longer. When antibiotics are given, indurated furuncles often resolve without becoming fluctuant. Progression on treatment suggests MRSA infection.
Currently many community-acquired strains of S. aureus are methicillin-resistant, and some of them are highly virulent. Such strains can cause epidemic furunculosis in baseball, football, and basketball players, and in athletic locker rooms of high schools and gymnasiums (4). The common factors are minor skin trauma, frequent skin-to-skin contact, and shared towels and clothing. It is difficult to predict which oral agent will be effective in such circumstances, and cultures are, therefore, very helpful. Most MRSA strains are resistant to clindamycin and quinolones, although these drugs are still effective if the organisms are sensitive. Almost all strains are sensitive to linezolid, but this drug is exceedingly expensive ($1,000 or more per course). Most, but not all strains can be treated with trimethoprim/sulfamethoxazole, which is very inexpensive. If all else fails, it may be necessary to install a line, and treat with intravenous vancomycin; in many instances that can be done in an ambulatory setting.
Carbuncles require surgical drainage, which usually can be done in an outpatient facility. Patients with severe systemic toxicity, such as diabetics with carbuncles, require hospital admission and parenteral therapy with a penicillinase-resistant penicillin; vancomycin is an effective alternative for those who are allergic to penicillin, or for MRSA strains.
Recurrent furunculosis may prove a frustrating problem. Management of individual episodes is as described previously, but other steps should also be taken to eliminate colonization with staphylococci. The anterior nares should be cultured. Patients whose nasal cultures contain S. aureus should be treated by application of mupirocin ointment to the anterior nares twice daily for 5 days. Alternatively, bacitracin ointment or gentamicin ointment may be applied three or four times daily for 14 days. During topical treatment, bacterial contamination of skin should be meticulously controlled by having the patient bathe and shampoo twice daily with a chlorhexidine soap or lotion, and by changing underclothing and bed and bath linens daily.
Recurrent furunculosis may occur in certain disorders that impair host defenses. Tests for diabetes mellitus should be made; if they are positive, control of blood glucose may prove beneficial (see Chapter 79). Defects in polymorphonuclear leukocyte function are a rare cause of recurrent furunculosis but should be considered in young patients who show an increased incidence or severity of infections caused by staphylococci. Gram-negative bacteria and fungi may be cultured from the furuncles of such patients. If an unusual problem, such as a leukocyte defect, is suspected, the patient should be referred to a medical center with the capability to investigate such disorders.
Hidradenitis suppurativa is a difficult problem that requires prolonged, often lifelong treatment by multiple methods. These include selective surgical drainage of abscesses; elimination of irritants such as tight clothing, antiperspirants, and shaving of the axillae; careful, frequent cleansing of skin with antiseptic agents; local application of heat; and intermittent or long-term systemic antimicrobial therapy. The only curative therapy is surgical removal of all involved skin, which is easier said than done. Management of such patients is best supervised by a dermatologist (see Chapter 115).
Complications
Staphylococcal skin infections may spread to other sites. This is especially true in patients with extensive inflammation and systemic toxicity, such as those with carbuncles, in whom bacteremia is common. Even an innocent-appearing furuncle can cause metastatic infection, especially in patients with a focus of increased susceptibility, such as a ventricular septal defect, an artificial heart valve, or an arthritic joint. Patients at risk for bacteremia who have such susceptible foci or whose systemic complaints (fever, focal pain) persist despite antimicrobial treatment, should be carefully examined for possible metastatic infection.
Cellulitis and Wound Infections
Any break in the skin can become infected. This includes not only obvious trauma, such as lacerations, burns, abrasions, and animal or human bites, but also minor injuries such as scratches and insect bites. The features of the resultant infection vary widely and depend on the nature of the wound, the type of infecting organism, and the defensive responses of the infected person. In many instances, early
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appropriate management given on an ambulatory basis is sufficient. In others, recognition of serious infection and prompt hospitalization for vigorous medical or surgical treatment are of prime importance. Table 32.3 describes findings that require hospitalization or surgical intervention. Table 32.4 lists organisms that can cause life-threatening forms of cellulitis. The most important are Vibrio vulnificus, associated with injuries sustained in brackish water, and Aeromonas hydrophila, associated with injuries in fresh water. Both organisms cause severe, rapidly spreading, necrotic cellulitis, with hemorrhagic bulla formation and frequent bacteremia. The most useful treatment is doxycycline, which is not commonly used for cellulitis unless these diagnoses are suspected.
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TABLE 32.3 Wound Infections: Findings That Necessitate Hospitalization or Surgical Intervention |
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Cellulitis Caused by S. pyogenes and S. aureus
Acute cellulitis is a spreading infection of subcutaneous tissues. The infection plane is below the epidermis and above the deep fascia, in subcutaneous fat. The involved area, which enlarges steadily, is painful, tender, and intensely erythematous. Chills and fever are common, and bacteremia may occur. The lesion differs from erysipelas in that its margin is not as sharply demarcated, nor is it elevated. There may be purulent or serous drainage at the inoculation site; in severe cases, patches of involved skin may become necrotic.
The most common causes of acute cellulitis are S. pyogenes and S. aureus. Studies based on full-thickness biopsies of skin and subcutaneous fat show that more than 95% of cases are streptococcal (5). Finding gram-positive cocci in drainage from the wound is presumptive evidence that they are causative. Cellulitis may progress rapidly, especially when it involves an area of chronic edema. Lower extremity infection in patients with peripheral arterial insufficiency can cause tissue necrosis and secondary in-fection.
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TABLE 32.4 Causes of Life-Threatening Bacterial Cellulitis |
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Management of cellulitis should include culture of any wound drainage (as described for erysipelas) and prompt antimicrobial therapy. In mild cases, treatment may be given on an ambulatory basis. Generally, the antimicrobial is designed to cover infections by penicillin-resistant staphylococci as well as penicillin-sensitive streptococci. However, since the overwhelming majority of cellulitis is streptococcal, this is probably unnecessary. Oral dicloxacillin or cephalexin is adequate for infections caused by either type of organism; erythromycin is a suitable alternative for patients who are allergic to penicillin (Tables 32.1 and 32.2). Local application of moist heat is a useful adjunct to antibiotic treatment; care should be taken, however, to avoid causing burns, especially in patients with impaired sensitivity to pain. Improvement is usually apparent in 3 or 4 days; during this period, patients should rest the involved area (with elevation when the cellulitis involves an extremity). Patients should be told to report promptly any worsening of the infection or of constitutional symptoms. Severe infections require hospitalization and parenteral treatment with a penicillinase-resistant β-lactam such as nafcillin, or vancomycin. This includes patients with extensive lesions, lesions of the face, or serious toxicity.
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Necrotizing Fasciitis
Most patients with an acutely swollen, painful leg have cellulitis. A very few have a much more serious infection in which the primary infectious process is in the plane of the deep fascia. The infection spreads rapidly and widely in this plane, and a whole limb may be involved in a few hours. Initially, the patient is febrile and toxic out of proportion to the visible changes in the skin, which may be minor or nonexistent. The infection causes thrombosis of small blood vessels as they cross the fascia to supply blood to the skin. The overlying skin becomes dusky blue and edematous, ultimately developing hemorrhagic bullae.
Necrotizing fasciitis is a surgical emergency; the fascia is dead over wide areas, and it must be removed back to normal bleeding tissue. Diagnosis is primarily clinical, although computed tomographic scans may show gas or edema, or both, in the plane of the deep fascia. Treatment involves long incisions with much undermining of skin edges to allow removal of necrotic material. The wounds are drained and left open to heal by secondary intention. Multiple subsequent débridements usually are necessary.
There are two distinct bacterial causes. Group A S. pyogenes can cause this syndrome as a single organism (6). Formerly there were epidemics of streptococcal gangrene in hospitals; presently, streptococci are the “flesh-eating bacteria” of the popular media. Streptococci do not form gas, so computed tomography shows only edema. The other kind of necrotizing fasciitis was described by Fournier and is called Fournier gangrene (7). It is caused by a mixed fecal flora involving several bacteria—aerobic gram-negative rods and both gram-positive and gram-negative anaerobes. This flora typically produces abundant gas. Streptococcal fasciitis can start anywhere; Fournier gangrene usually starts near the perineum. These cases are treated in hospital with broad-spectrum antimicrobials as an adjunct to surgery; if a streptococcus is responsible, treatment can be simplified to penicillin.
Secondarily Infected Ulcers
Cutaneous ulcers are caused by a wide variety of conditions (see Chapter 95). By far the most common cause is chronic venous insufficiency, most typically associated with ulceration of the medial side of the leg, just above the ankle.
Management of the ulcer is generally aimed at the underlying cause and seeks to improve blood flow, reduce edema, and avoid pressure and trauma (see Chapter 95).
Control of secondary infection is also important. Superficial colonization with a variety of bacteria is unavoidable and without consequence; however, infection that is deeper or laterally invasive prevents healing and may interfere with other treatments, such as skin grafting. It should be remembered that infection is almost never the primary cause of an ulcer. Ulcers will not respond to antimicrobials if the primary problem is vascular insufficiency. Infection is best controlled by repeated careful cleaning and local debridement. Systemic antimicrobials should be used only after other methods have failed to control surrounding infection. The choice of antimicrobial should be based on cultures of the wound or its purulent drainage. Local antibacterials are sometimes helpful. Those effective against a broad spectrum of bacterial agents include polymyxin–bacitracin–neomycin ointment, topical nitrofurazone (Furacin ointment), and the silver sulfadiazine ointment commonly used to treat burns. These should be applied three times daily until healing occurs or it is apparent that they are ineffective. Soaking with 3% acetic acid three to four times daily is helpful in controlling bacterial growth in ulcers colonized with P. aeruginosa.
There is good evidence that local application of fibro-blast growth factors speeds healing of ulcers, but the proteins are recombinant and very expensive.
Cutaneous Diphtheria
Cutaneous ulcers and other skin lesions may become secondarily infected with Corynebacterium diphtheriae, causing cutaneous diphtheria. Although the cutaneous lesion may appear benign, myocarditis or neuropathy develops in approximately 3% of cases. Outbreaks have occurred in the northwest and southern parts of the United States, primarily among Native Americans or indigent urban residents (8). The presence of cutaneous diphtheria in a community should increase suspicion that skin wounds may harbor this agent. The diagnosis should be suspected when existing wounds develop a gray-yellow or gray-brown covering membrane and surrounding erythema. Typically, the membrane can easily be removed to reveal a clean base. Other minor skin lesions may also become infected. Typical organisms can be seen in methylene blue stains of smears from the wound and confirmed by culture on Loeffler or tellurite agar. Presumptive cases should be reported to public health officials and treated with equine diphtheria antitoxin (20,000 to 40,000 units intramuscularly or intravenously after testing for hypersensitivity to horse serum) and either erythromycin (1.5 grams per day, orally) or procaine penicillin (1.2 million units per day, intramuscularly) for 7 to 10 days. Because horse serum is frequently allergenic, attempts are being made to synthesize a human soluble receptor that binds diphtheria toxin.
Cutaneous Anthrax
Until recently, cutaneous anthrax was a curiosity seen occasionally in agricultural areas and in factories where workers handled imported hides or wool. Now that anthrax has been used by bioterrorists, it is not clear how
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common it may become in the future. The cutaneous form of the disease occurs when anthrax spores become implanted under the skin, germinate, and begin to multiply. The disease is usually found on exposed skin of the hands and arms, sometimes on the face. The anthrax bacilli make two toxins: (a) an edema-forming toxin that poisons capillary endothelium and produces leaky capillaries, and (b) a lethal toxin that poisons most cells by inducing apoptosis (programmed cell death). These two toxins account for the distinctive features of the disease. At the site of initial implantation, the skin rapidly becomes black and necrotic. The lesion is roughly circular, and diameters range from 1 to 3 cm. Although anthrax is described as causing a “malignant pustule,” it is more like a vesicle, because the fluid contains bacteria but very few cells. There may be secondary vesicles around the primary one. Spreading from the primary site is an area of pronounced edema that may extend 10 cm or more from the primary lesion. There may be regional lymph node enlargement. Fever and systemic toxicity are rare except in neglected cases.
Cutaneous anthrax must be distinguished primarily from the vastly more common boil (see Pustular Infections Caused by S. aureus). Anthrax lesions are curiously painless and may itch. Big boils are very painful, as are the associated nodes. A boil may develop a black or dark red crust of coagulated blood if it has been picked at, but the anthrax lesion is black from the beginning. Edema around boils is less pronounced than that around anthrax lesions. Gram stains from boils show pus, sheets of polymorphonuclear cells, and gram-positive cocci in clusters. Gram stains from anthrax vesicle fluid show big (8 µm) gram-positive rods with few or no cells. The organisms are easily differentiated on culture, but the laboratory should be warned what it may be dealing with.
Without treatment, the mortality rate of cutaneous anthrax is approximately 25%. The most suitable antimicrobials for adults are quinolones (e.g., ciprofloxacin 500 mg orally twice daily) and tetracyclines (e.g., doxycycline 100 mg orally twice daily), given for 60 days. Penicillins, cephalosporins, and vancomycin are commonly used in children. Patients with cutaneous anthrax lesions on the head or neck or with extensive edema or signs of systemic toxicity should be hospitalized for intravenous therapy with a multidrug regimen. With treatment, the mortality rate should be under 5%.
Bites
Bite wounds become infected with the oral, salivary, or dental flora of the biting person or animal and may cause serious local or systemic infections. Initial management before signs of infection appear is of primary importance in preventing certain infections (9). Appropriate prophylaxis for tetanus is required for all bite wounds (see Chapter 18).
Human bites are contaminated with a complex variety of aerobic and anaerobic oral bacteria. Without treatment, a severe necrotizing cellulitis often results. Minor lesions that break the skin should be washed thoroughly and tre-ated with a combination of amoxicillin 875 mg and clavulanic acid (Augmentin) orally twice daily. Oral clindamycin (150 to 300 mg three times a day) is appropriate for patients who are allergic to penicillin. Antimicrobials should be continued for 7 to 10 days. More severe wounds, including wounds of the hands and knuckles, require meticulous debridement and possible tendon repairs. These injuries should be referred for surgical management.
Dog bites carry the risk of local soft tissue infection with various organisms, including P. multocida, and raise concern about rabies. Minor abrasions, shallow punctures, and superficial lacerations require no therapy for local infection other than thorough cleansing with soap and water. Puncture wounds should be irrigated vigorously with sterile saline injected through a 20-gauge needle. More extensive or deeper bites require surgical management for debridement. Amoxicillin and clavulanic acid, as described previously, should be given for bites of the hands or face. The same treatment is appropriate for patients who have signs of soft tissue infection when first seen. Patients with hand infection require surgical management and intensive antimicrobial therapy.
Rabies precautions should be taken with all dog bites, including bites by domestic pets, even though the risk of rabies from domestic pets—especially when biting was provoked—is very small. The dog should be quarantined for 10 days. If the dog's owner cannot be identified, the local health department should be called to take charge of the dog. If its owner is known and can prove that the dog was vaccinated against rabies, it may be observed at its home. If it remains well, there is no risk of rabies. If the dog develops neurologic symptoms or dies, its brain should be examined immediately; prophylaxis is required if evidence of rabies is found. If the dog escapes after biting, and especially if the bite was unprovoked, rabies prophylaxis with human rabies immune globulin and human diploid cell rabies vaccine is indicated (seeChapter 18).
Bites by domestic cats should be managed in the same way as dog bites. Cats are not routinely vaccinated against rabies and are now a greater hazard than domestic dogs. Bites by wild animals carry a greater risk of rabies, and rabies prophylaxis is usually required unless the animal's brain can be examined. Wild animals with the greatest risk of carrying rabies are raccoons, skunks, foxes, coyotes, and bats. The risk of rabies with rodent bites, including squirrel bites, is very small.
It is recommended that the practitioner seek the help of the local or state health department when dealing with animal bites. Officials with knowledge of disease activity in local animal populations may be able to determine whether a particular exposure is trivial or serious and can also
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arrange fluorescent antibody testing and viral cultures if the animal is available. Not every animal that appears neurologically impaired has rabies; other causes of animal encephalitis are also found.
Puncture Wounds
Puncture wounds usually involve the feet or hands and may introduce infecting bacteria that cannot be removed by washing or debridement. In all instances, patients should receive appropriate prophylaxis for tetanus (see Chapter 18). Low-risk wounds (i.e., those not likely to be contaminated by soil or fecal material and in which the wound site is in healthy, well-vascularized tissue) need only be thoroughly washed and observed for several days for signs of developing infection. Should infection develop, any wound drainage should be cultured and treatment begun with dicloxacillin orally 250 mg three times daily or amoxicillin-clavulanate (see earlier discussion) for presumptive staphylococcal or streptococcal infection. The wound site should also be soaked in warm soapy water for 30 minutes at least four times a day.
Higher-risk wounds (i.e., those likely to be contaminated with fecal material, soil, or foreign debris and those occurring in a diabetic person or in an extremity with an inadequate blood supply) should be treated from the outset with a broad-spectrum antimicrobial. In adults, a quinolone such as ciprofloxacin 750 mg every 12 hours with or without metronidazole 500 mg every 8 hours. In children, probably a third generation cephalosporin or a carbapenem. The wound site should be rested and treated with warm soaks as described for low-risk wounds. The patient should promptly report any evidence of inflammation, swelling, or persisting pain. If purulent drainage develops, it should be cultured. Antimicrobial management should be altered if bacteria resistant to the current treatment are isolated. If pus develops, surgical drainage usually is required.
Felon
A felon is an infection of the pulp of the distal phalanx of a finger; it usually occurs after a recognized local wound. Abscess formation and tissue necrosis are common, and bony or articular involvement may occur. If the felon is neglected or inadequately treated, severe damage, including loss of function, may occur. The most common causative agents are S. aureus and S. pyogenes, although gram-negative bacilli may also be recovered. Treatment involves surgical drainage by a physician who is familiar with the procedure. Concurrent antibiotic therapy should be guided by Gram staining and culture of infected material. If Gram staining and culture are persistently negative, the diagnosis of herpetic whitlow (Chapter 117) should be considered.
Paronychia
A paronychia is an infection, often chronic or recurrent, that involves tissue immediately adjacent to a fingernail or toenail. The affected tissue is warm, tensely swollen, erythematous, and painful. When infection is chronic, the nail may become ridged or discolored and may be lost. Paronychia occurs most often in people who bite their nails, or whose hands are frequently in water (e.g., dishwashers, mothers of infants). Diabetics also have an increased risk for this infection. Candida species appear to play an etiologic role, although a variety of bacteria usually are present. Management involves keeping hands as dry as possible (e.g., using waterproof gloves for dishwashing) and applying an anticandidal medication (e.g., nystatin cream) or a broad-spectrum antifungal agent (clotrimazole or miconazole cream) two times a day for several weeks. If localized swelling does not respond to these measures, drainage may be helpful. This can be done by sliding an 18-gauge needle, bevel down, along the nail into the involved area. Lifting the skin from the nail with the needle usually achieves drainage and relief of pain.
The major cause of paronychia of the toe (usually a great toe) is an ingrown toenail. Chapter 73 describes the diagnosis and management of this problem.
Intertriginous Infections
Chapter 116 describes approaches to diagnosis of infections involving moist intertriginous areas (toe webs, axillae, groin area).
Specific References
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.