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84 INFECTIONS OF SKIN, SOFT TISSUES, JOINTS, AND BONES

84 INFECTIONS OF SKIN, SOFT TISSUES, JOINTS, AND BONES
Harrison’s Manual of Medicine

84

INFECTIONS OF SKIN, SOFT TISSUES, JOINTS, AND BONES

Skin and Soft Tissue Infections

Erysipelas

Cellulitis

Impetigo

Necrotizing Fasciitis

Myositis/Myonecrosis
Bone and Joint Infections

Infectious Arthritis

Osteomyelitis
Bibliography

SKIN AND SOFT TISSUE INFECTIONS
The etiologic agents of various types of skin and soft tissue infections are listed in Table 84-1. Antimicrobial agents used to treat several prominent infections are shown in Table 84-2.

Table 84-1 Skin and Soft Tissue Infections

Table 84-2 Treatment of Common Infections of the Skin

Erysipelas
Erysipelas, or lymphangitis of the dermis, features a fiery red, intensely painful, demarcated swelling of the face or extremities. Classic erysipelas is due to Streptococcus pyogenes and may be treated with penicillin. If the condition’s appearance is not sufficiently distinctive to exclude cellulitis, it is prudent to broaden coverage as described below for cellulitis.
Cellulitis
Cellulitis is an acute inflammatory condition of the skin caused either by indigenous flora colonizing the skin or by a wide variety of exogenous bacteria. These organisms can (1) be inoculated through small breaks in the skin (S. pyogenes) or via bites (Pasteurella, Eikenella, anaerobes); (2) originate in wounds, ulcers, or abscesses (Staphylococcus aureus); (3) be associated with sinusitis (Haemophilus influenzae); or (4) gain entry during immersion in water (Aeromonas, Vibrio vulnificus). Cellulitis is characterized by localized pain, erythema, swelling, and heat.

TREATMENT
If an etiologic agent is suggested by the pt’s history, treatment is directed at a specific pathogen or group of pathogens. Both blood and any abscess, open wound, or drainage should be cultured. In the absence of a specific etiology, treatment is directed at gram-positive pathogens. IV therapy with oxacillin (2 g q4–6h) or cefazolin (1–2 g q8h) is administered until signs of systemic toxicity have resolved and acute inflammation has improved substantially; oral treatment is then given to complete a 2-week course.

Impetigo
Impetigo begins as multiple pruritic erythematous lesions that evolve into yellow crusts. This infection may be caused by S. pyogenes (impetigo contagiosa) or S. aureus (bullous impetigo). It is important to recognize impetigo caused by S. pyogenes because of the risk of poststreptococcal glomerulonephritis. Treatment consists of dicloxacillin (500 mg PO qid), cephalexin (500 mg PO qid), or topical mupirocin ointment.
Necrotizing Fasciitis
This life-threatening infection of the fascia and soft tissues investing the muscles of the trunk or extremities may be caused by group A streptococci (often from apparent or inapparent infection via the skin), Clostridium perfringens (accompanying gas gangrene), or mixed aerobic and anaerobic bacteria (usually of GI origin). The infection presents acutely as pain, fever, and systemic toxicity, often with a paucity of cutaneous findings. Necrotizing fasciitis can extend to cutaneous structures, causing thrombosis, skin discoloration, crepitus, anesthesia, and bulla formation. As the infection extends rapidly along fascial planes and via veins and lymphatics, cutaneous and fascial necrosis and shock occur (e.g., streptococcal toxic shock syndrome). Early surgical exploration is critical to both diagnosis and therapy.

TREATMENT
Antibiotic therapy is directed at the offending pathogen; for group A streptococci and clostridia, experimental data suggest that a combination of clindamycin (600–900 mg IV q8h) and penicillin G (4 million U, IV q4h) may be superior to penicillin alone. When polymicrobial infection is suspected, therapy consists of a three-drug combination of either ampicillin (2 g IV q4h) plus clindamycin (600–900 mg IV q6–8h) plus ciprofloxacin (400 mg IV q12h) or vancomycin (1 g IV q12h) plus metronidazole (500 mg IV q6h) plus ciprofloxacin. Hyperbaric oxygen therapy may be useful in clostridial disease.

Myositis/Myonecrosis
Myositis/myonecrosis can arise spontaneously (S. aureus, S. pyogenes) or after penetrating trauma (Clostridium). Streptococcal necrotizing myositis can accompany necrotizing fasciitis and can cause a systemic toxic shock syndrome.
BONE AND JOINT INFECTIONS
Infectious Arthritis
Acute bacterial arthritis is a common medical problem affecting individuals of all ages and requiring prompt recognition and treatment. While bacteria are the most common causes of infectious arthritis, various fungi and viruses also infect joints.
ETIOLOGY AND PATHOGENESIS   Gonococcal infection is a common cause of septic arthritis (Chap. 83). Approximately 75% of nongonococcal pyoarthroses are due to gram-positive cocci. S. aureus is the most common pathogen; next most common are streptococci of groups A and G, viridans streptococci, pneumococci, and—in neonates—group B streptococci. Gram- negative bacilli account for 20% of infections, typically affecting pts with risk factors for gram-negative bacteremia. In general, infection occurs via hematogenous seeding of the synovium. Predisposing factors include infancy, immunosuppressive illness or therapy, diabetes mellitus, hemodialysis, alcoholism, IV drug use, and prior joint damage (including rheumatoid arthritis). Persons with HIV infection are at increased risk of septic arthritis due to pneumococci, salmonellae, and H. influenzae. Direct seeding of the joint may be attributable to trauma, arthroscopy, or surgery. An extraarticular focus of infection is identified in 25% of cases. Prosthetic joint infections are usually due to staphylococci (either coagulase-negative staphylococci or S. aureus) and occur in 1–4% of prosthetic joints over a 10-year period, with an increased rate in joints that have undergone revision. Other causes of acute infectious arthritis include rubella virus, hepatitis B virus, mumps virus, coxsackievirus, adenovirus, and parvovirus. Borrelia burgdorferi and Treponema pallidum may cause a more chronic, slowly progressive arthritis, as do Mycobacterium tuberculosis and fungal agents such as Coccidioides, Sporothrix, and Histoplasma. Candida and Blastomyces may cause acute or chronic arthritis.
CLINICAL MANIFESTATIONS   Acute bacterial arthritis presents as a monarticular process in ~90% of pts, involving the large joints (most commonly the knee and hip; next most commonly the ankle, wrist, elbow, and shoulder and the sternoclavicular and sacroiliac joints). Fever may be lacking in persons who have rheumatoid arthritis or who are receiving immunosuppressive therapy. In the hip or shoulder, effusion may be difficult to detect, and pain may be minimal. Symptoms are similar to those of cellulitis, bursitis, and acute osteomyelitis, and these infections must be distinguished from septic arthritis by their greater range of motion and less-than-circumferential swelling. Infection due to gram-positive cocci usually presents as an acute onset of swelling, pain, warmth, and limitation of movement. Gram-negative infections tend to be more indolent, and pts typically present after 3 weeks of illness, frequently with coexistent osteomyelitis. Infections of prosthetic joints are even more indolent, with presenting symptoms so mild that diagnosis may be delayed by several months; there is always accompanying osteomyelitis.
DIAGNOSIS   Analysis of aspirated synovial fluid is necessary for the diagnosis of bacterial joint infection. The fluid is usually turbid, with >25,000 WBCs/µL (typically >100,000/µL, with >90% neutrophils). Gram’s staining identifies the pathogen in 75% of gram-positive and 30–50% of gram-negative infections. Cultures of joint fluid are usually positive. Blood should also be cultured. In gonococcal infection, Gram’s staining rarely gives a positive result and synovial fluid culture is positive in only ~40% of cases. Culture of skin and mucosal lesions on special medium and PCR-based assays of synovial fluid will improve the diagnostic yield for gonococcal infection. Prosthetic joint infections are generally diagnosed by the finding of loosening of the implant or of osteomyelitis on radiographs; the diagnosis is confirmed by needle aspiration of the joint. The ESR and C-reactive protein levels are usually elevated.

TREATMENT
Optimal management requires IV antibiotic administration, drainage (usually by repeated daily aspiration), and avoidance of weight bearing. Open surgical drainage should be considered when the hip, shoulder, or sternoclavicular joint is infected; when fluid loculations occur; when cultures are persistently positive; or when effusion persists for >7 d. Prosthetic joints should be removed and replaced after antibiotic therapy. The choice of antibiotics is based initially on Gram’s stain and then on culture. An IV third-generation cephalosporin such as ceftriaxone (1–2 g q24h) provides adequate empirical coverage when Gram’s stain is unrevealing. Staphylococcal infections are initially treated IV with oxacillin (2 g q4h) for 4 weeks or—if methicillin- resistant S. aureus is suspected—with vancomycin (1 g q12h). Streptococcal arthritis due to a penicillin-susceptible organism is treated with penicillin G (2 million U q4h) for 2 weeks. Gram-negative septic arthritis is treated with a second- or third-generation cephalosporin (e.g., cefuroxime, 1.5 g IV q8h; or ceftriaxone, 1–2 g IV q12–24h) or a quinolone (e.g., levofloxacin, 500 mg IV q24h) for 3–4 weeks. Infection due to Pseudomonas aeruginosa is treated for at least 3 weeks with a combination of an extended-spectrum penicillin such as mezlocillin (3 g IV q4h) or ceftazidime (1 g IV q8h) plus an aminoglycoside such as tobramycin (1.7 mg/kg IV q8h). If tolerated, this regimen is continued for an additional 2–3 weeks; alternatively, oral ciprofloxacin (750 mg bid) may be substituted for the aminoglycoside. Gonococcal arthritis is treated initially with ceftriaxone (1 g IV/IM q24h). After signs of local and systemic inflammation begin to resolve, therapy may be switched to an oral agent (cefixime, 400 mg bid; or ciprofloxacin, 500 mg bid) to complete a 7- to 10-d course. Amoxicillin (500 mg PO tid) may be used to complete therapy against penicillin-susceptible isolates.

Osteomyelitis
ETIOLOGY AND PATHOGENESIS   Osteomyelitis, an infection of bone, is caused most commonly by pyogenic bacteria and mycobacteria. Microorganisms enter the bone by hematogenous spread or directly via a wound or from an adjacent site of infection. The metaphyses of long bones in children (tibia, femur, humerus) and the vertebrae in adults are the most frequently involved sites. More than 95% of cases of hematogenous osteomyelitis are caused by a single organism, with S. aureus responsible for ~50% of the total number. Other common pathogens in adults include gram-negative bacillary organisms (Pseudomonas, Serratia, Salmonella, Escherichia coli). Tuberculosis, brucellosis, histoplasmosis, coccidioidomycosis, and blastomycosis are less frequent causes of osteomyelitis. Infections due to a contiguous focus of infection (e.g., diabetic foot ulcers) are often polymicrobial and are more likely to involve gram-negative and anaerobic bacteria. In addition, S. aureus is the principal cause of postoperative infections, and coagulase-negative staphylococci often cause prosthetic device–associated infections.
CLINICAL MANIFESTATIONS   Half of pts with osteomyelitis present with vague pain in the affected limb or the back (or in vertebral osteomyelitis, with pain due to nerve root irritation) of 1–3 months’ duration with little or no fever. Children may experience an acute onset of fever, irritability, and lethargy, with local inflammation of ❤ weeks’ duration. Findings on physical exam may include point tenderness, muscle spasm, and draining sinus (especially with chronic osteomyelitis or an infected prosthetic joint).
DIAGNOSIS   Osteomyelitis is diagnosed by culture of appropriate specimens. If blood cultures are negative, pus obtained by needle aspiration from bone or bone biopsy should be cultured. Cultures from superficial sites are not reliable. Findings on plain films do not become positive for at least 10 d, and lytic lesions may not be visible for 2–6 weeks. Radionuclide bone scan may become positive within 2 d of infection. CT or MRI may become positive early and may aid in the localization of lesions and the demonstration of sequestra and soft tissue collections. The ESR is usually elevated but falls in response to therapy.

TREATMENT
With prompt treatment, <5% of pts with acute hematogenous osteomyelitis develop chronic disease. Antibiotics should be given only after appropriate specimens have been obtained for culture. For acute hematogenous osteomyelitis, IV antibiotics active against the organisms identified should be given for 4–6 weeks. Surgical debridement should be considered if there is a poor response to therapy in the first 48 h or if there is undrained pus or septic arthritis. In vertebral osteomyelitis, surgery is also necessary in cases of spinal instability, new or progressive neurologic deficits, or large undrainable soft tissue abscesses. Chronic osteomyelitis requires complete drainage, debridement of sequestra, and removal of any prosthetic material as well as a 4- to 6-week course of antibiotics whose selection is based on culture of the bone. Skin flaps and bone grafts may facilitate healing. If the identity of the infecting organism(s) is known, antibiotic therapy should begin several days before surgery. Appropriate therapy for S. aureus or empirical therapy in the absence of a positive culture includes oxacillin (2 g IV q4h) or cefazolin (2 g IV q8h). Treatment of gram-negative osteomyelitis must be based on identification of the organism and determination of its susceptibility. Because Pseudomonas and Enterobacter show a propensity to develop resistance during therapy, osteomyelitis due to these organisms should be treated with a combination of an aminoglycoside (e.g., tobramycin for Pseudomonas infection and gentamicin for Enterobacter at doses of 1.7 mg/kg q8h) and a b-lactam antibiotic (e.g., mezlocillin, 3 g q4h). A quinolone (e.g., ciprofloxacin, 400 mg IV q12h; or levofloxacin, 500 mg IV q24h) may be substituted for the b-lactam antibiotic against Pseudomonas or used alone against Enterobacter. For other gram-negative bacillary infections of bone, treatment is based on susceptibility of the organism and ordinarily consists of a single agent, such as a cephalosporin (e.g., cefazolin, 2 g IV q8h; or ceftriaxone, 1 g IV q12h) or a fluoroquinolone (e.g., ciprofloxacin, 400 mg IV q12h). When sensitivity of the organism allows, oral ciprofloxacin (750 mg q12h) or levofloxacin (500 mg q24h) may be given after or instead of IV therapy.

Bibliography

For a more detailed discussion, see Maguire JH: Osteomyelitis, Chap. 129, p. 825; Stevens DL: Infections of the Skin, Muscle, and Soft Tissues, Chap. 128, p. 821; Wessels MR: Streptococcal and Enterococcal Infections, Chap. 140, p. 901; and Thaler SJ, Maguire JH: Infectious Arthritis, Chap. 323, p. 1998, in HPIM-15.

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