Infectious DiseasesInfectious DiseasesSkin & soft Tissues Skin & soft Tissues InfectionsInfections

Rowa’ Al-Ramahi

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DEFINITIONDEFINITION

Bacterial infections of the skin can be classified as primary or secondary. Primary bacterial infections are usually caused by a single bacterial species and involve areas of generally healthy skin (e.g., impetigo, erysipelas). Secondary infections, however, develop in areas of previously damaged skin and are frequently polymicrobic.

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DEFINITIONDEFINITION

The conditions that may predispose a patient to the development of skin and soft-tissue infections (SSTIs) include (1) a high concentration of bacteria, (2) excessive moisture of the skin, (3) inadequate blood supply, (4) availability of bacterial nutrients, and (5) damage to the corneal layer allowing for bacterial penetration.

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The majority of SSTIs are caused by gram-positive organisms and, less commonly, gram-negative bacteria present on the skin surface. Staphylococcus aureus and Streptococcus pyogenes account for the majority of SSTIs. Community-associated methicillin-resistant S. aureus (CA-MRSA) has recently emerged and it is often isolated in otherwise healthy patients.

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`ERYSIPELAS

Erysipelas (Saint Anthony’s fire) is an infection of the superficial layers of the skin and cutaneous lymphatics. The infection is almost always caused by β-hemolytic streptococci, with S. pyogenes (Group A streptococci) responsible for most infections.

The lower extremities are the most common sites for erysipelas. Patients often experience flu-like symptoms (fever and malaise) prior to the appearance of the lesions. The infected area is painful, often a burning pain.

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ERYSIPELAS

Erysipelas lesions are bright red and edematous with lymphatic streaking and clearly demarcated raised margins. Leukocytosis is common, and C-reactive protein is generally elevated.

Mild to moderate cases of erysipelas in adults are treated with intramuscular procaine penicillin G or penicillin VK. For more serious infections, aqueous penicillin G, 2 million to 8 million units daily, should be administered IV. Penicillin-allergic patients can be treated with clindamycin or erythromycin.

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IMPETIGO

Impetigo is a superficial skin infection that is seen most commonly in children. It is highly communicable and spreads through close contact. Most cases are caused by S. pyogenes, but S. aureus either alone or in combination with S. pyogenes has emerged as a principal cause of impetigo.

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CLINICAL PRESENTATION

Exposed skin, especially the face, is the most common site for impetigo.

Pruritus is common, and scratching of the lesions may further spread infection through excoriation of the skin. Other systemic signs of infection are minimal.

Weakness, fever, and diarrhea are sometimes seen with bullous impetigo.

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CLINICAL PRESENTATION

Nonbullous impetigo manifests initially as small, fluid-filled vesicles. These lesions rapidly develop into pus-filled blisters that readily rupture. Purulent discharge from the lesions dries to form golden yellow crusts that are characteristic of impetigo.

In the bullous form of impetigo, the lesions begin as vesicles and turn into bullae containing clear yellow fluid. Bullae soon rupture, forming thin, light brown crusts.

Regional lymph nodes may be enlarged.

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TREATMENT

Penicillinase-resistant penicillins (such as dicloxacillin) are the agents of first choice because of the increased isolation of S. aureus. First-generation cephalosporins (such as cephalexin) are also effective. Penicillin may be used for impetigo caused by S. pyogenes. It may be administered as either a single intramuscular dose of benzathine penicillin G (300,000 to 600,000 units in children, 1.2 million units in adults) or as oral penicillin VK given for 7 to 10 days. Penicillin-allergic patients can be treated with oral clindamycin.

The duration of therapy is 7 to 10 days.

ointment is also effective.

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CELLULITIS

Cellulitis is an acute, spreading infectious process that initially affects the epidermis and dermis and may subsequently spread within the superficial fascia. This process is characterized by inflammation but with little or no necrosis or suppuration of soft tissue.

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CELLULITIS

Cellulitis is most often caused by S. pyogenes or by S. aureus.

Acute cellulitis with mixed aerobic-anaerobic flora generally occurs in diabetes, where the skin is near a traumatic site or surgical incision, at sites of surgical incisions to the abdomen or perineum, or when host defenses are compromised.

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CLINICAL PRESENTATION

Cellulitis is characterized by erythema and edema of the skin. The lesion, which may be extensive, is painful and nonelevated and has poorly defined margins.

Tender lymphadenopathy associated with lymphatic involvement is common. Malaise, fever, and chills are also commonly present. There is usually a history of an antecedent wound from minor trauma, an ulcer, or surgery.

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CLINICAL PRESENTATION

A Gram stain of a smear obtained by injection and aspiration of 0.5 mL of saline (using a small-gauge needle) into the advancing edge of the erythematous lesion may help in making the microbiologic diagnosis, but often yields negative results.

Blood cultures are useful as bacteremia may be present in 30% of cases.

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TREATMENT

The goal of therapy of acute bacterial cellulitis is rapid eradication of the infection and prevention of further complications.

Local care of cellulitis includes elevation and immobilization of the involved area to decrease local swelling.

As streptococcal cellulitis is indistinguishable clinically from staphylococcal cellulitis, administration of a semisynthetic penicillin (nafcillin or oxacillin) or first-generation cephalosporin (cefazolin) is recommended until a definitive diagnosis, by skin or blood cultures, can be made. 17

TREATMENT

Mild to moderate infections not associated with systemic symptoms may be treated orally with dicloxacillin or cephalexin.

If documented to be a mild cellulitis secondary to streptococci, oral penicillin VK, or intramuscular procaine penicillin may be administered. More severe streptococcal infections should be treated with IV antibiotics (such as ceftriaxone 50 to 100 mg/kg as a single dose).

The usual duration of therapy for cellulitis is 5 to 10 days. 18

In penicillin-allergic patients, oral or parenteral clindamycin may be used. Alternatively, a first-generation cephalosporin such as cefazolin (1 to 2 g IV every 6 to 8 hours) may be used cautiously for patients who have not experienced immediate or anaphylactic penicillin reactions and are penicillin skin test negative.

In severe cases in which cephalosporins cannot be used because of documented methicillin resistance or severe allergic reactions to β-lactam antibiotics, IV vancomycin should be administered.

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Initial therapy with trimethoprim–sulfamethoxazole, doxycycline or clindamycin appears to be effective for CA-MRSA and should be considered in geographic areas in which CA-MRSA are commonly encountered.

Alternative agents for documented infections with resistant gram-positive bacteria such as methicillin- resistant staphylococci and vancomycin-resistant enterococci include linezolid, quinupristin/dalfopristin, daptomycin, and tigecycline and telavancin.

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For cellulitis caused by gram-negative bacilli or a mixture of microorganisms, immediate antimicrobial chemotherapy as determined by Gram stain is essential, along with appropriate surgical excision of necrotic tissue and drainage.

Gram-negative cellulitis may be treated appropriately with an aminoglycoside or first- or second-generation cephalosporin. If gram positive aerobic bacteria are also present, penicillin G or a penicillinase resistant penicillin should be added to the regimen.

Therapy should be 10 to 14 days in duration.

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DIABETIC FOOT INFECTIONS

Three key factors are involved in the causation of diabetic foot problems: neuropathy, ischemia, and immunologic defects. Any of these disorders can occur in isolation; however, they frequently occur together.

There are three major types of diabetic foot infections: deep abscesses, cellulitis of the dorsum, and mal perforans ulcers of the sole of the foot. Osteomyelitis may occur in 30% to 40% of infections.

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DIABETIC FOOT INFECTIONS

Diabetic foot infections are typically polymicrobic. Staphylococci (especially S. aureus) and streptococci are the most common pathogens, although gram-negative bacilli and anaerobes occur in 50% of cases. Common isolates include E coli, Klepsiella spp., Proteus spp., Pseudomonas aeruginosa, Bacteroides fragilis & Peptostreptococcus spp.

Patients with peripheral neuropathy often do not experience pain but seek medical attention for swelling or erythema. Lesions vary in size and clinical features. A foul-smelling odor suggests anaerobic organisms. Temperature may be mildly elevated or normal.

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TREATMENT

The goal of therapy is preservation of as much normal limb function as possible while preventing infectious complications. Most infections can be successfully treated on an outpatient basis with wound care and antibiotics.

Necrotic tissue must be thoroughly debrided, with wound drainage and amputation as required.

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TREATMENT

Diabetic glycemic control should be maximized to ensure optimal healing.

The patient should initially be restricted to bed rest, leg elevation, and control of edema, if present.

Amoxicillin-clavulanate is the agent of choice for oral outpatient treatment; however, this agent does not cover P. aeruginosa. Fluoroquinolones with metronidazole or clindamycin are reasonable alternatives.

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Serious polymicrobic infections may be treated with agents used for anaerobic cellulitis.

Monotherapy with broad-spectrum parenteral antimicrobials, along with appropriate medical and/or surgical management, is often effective in treating moderate to severe infections (including those in which osteomyelitis is present).

In penicillin-allergic patients, metronidazole or clindamycin plus either a fluoroquinolone, aztreonam, or, possibly, a third-generation cephalosporin is appropriate.

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Vancomycin is used frequently in severe infections with gram-positive pathogens. With increasing staphylococcal resistance, linezolid, quinupristin/dalfopristin, daptomycin, and tigecycline are alternatives.

Treatment of soft-tissue infections in diabetic patients should generally be at least 7 to 14 days in duration, although some infections may require an additional 1 to 2 weeks of therapy. However, in cases of underlying osteomyelitis, treatment should continue for 6 to 12 weeks.

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INFECTED PRESSURE ULCERS

A pressure sore is also called a “decubitus ulcer” and “bed sore”.

Many factors are thought to predispose patients to the formation of pressure ulcers: paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age.

Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture; however, there is still debate as to the exact pathophysiology of pressure sore formation.

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INFECTED PRESSURE ULCERS

The areas of highest pressure are generated over the bony prominences.

Most pressure sores are colonized by bacteria; however, bacteria frequently infect healthy tissue. A large variety of aerobic gram-positive and gram negative bacteria, as well as anaerobes, are frequently isolated.

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CLINICAL PRESENTATION More than 95% of all pressure sores are located on the

lower part of the body.

Clinical infection is recognized by the presence of redness, heat, and pain. Purulent discharge, foul odor, and systemic signs (fever and leukocytosis) may be present.

Pressure sores vary greatly in their severity, ranging from an abrasion to large lesions that can penetrate into the deep fascia involving both bone and muscle.

Without treatment, an initial, small, localized area of ulceration can rapidly progress to 5 to 6 cm within days.

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PREVENTION AND TREATMENT

The goal of therapy is to clean and decontaminate the ulcer to promote wound healing by permitting the formation of healthy granulation tissue or to prepare the wound for an operative procedure.

The main factors to be considered for successful wound care are (1) relief of pressure; (2) debridement of necrotic tissue; (3) wound cleansing; (4) dressing selection; and (5) prevention, diagnosis, and treatment of infection.

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PREVENTION AND TREATMENT

Prevention is the single most important aspect in the management of pressure sores. Friction and shearing forces can be minimized by proper positioning. Skin care and prevention of soilage are important, with the intent being to keep the surface relatively free from moisture. Relief of pressure (even for 5 minutes once every 2 hours) is probably the single most important factor in preventing pressure sore formation.

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Medical management is generally indicated for lesions that are of moderate size and of relatively shallow depth (stage 1 or 2 lesions) and are not located over a bony prominence.

Debridement can be accomplished by surgical or mechanical means (wet to- dry dressing changes). Other effective therapies are hydrotherapy, wound irrigation, and dextranomers.

Pressure sores should be cleaned with normal saline.

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A number of agents have been used to disinfect pressure sores (e.g., povidone-iodine, iodophor, sodium hypochlorite, hydrogen peroxide, and acetic acid) as well as other types of open wounds; however, these agents should be avoided as they impair healing.

A short, 2-week trial of topical antibiotic (silver sulfadiazine or triple antibiotic [Bacitracin/Neomycin/Polymyxin]) is recommended for a clean ulcer that is not healing or is producing a moderate amount of exudate despite appropriate care.

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DOG BITESDOG BITESPatients at risk of acquiring an

infection after a bite have had a puncture wound, have not sought medical attention within 12 hours of injury, and are older than 50 years.

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The infected dog bite is usually characterized by a localized cellulitis and pain at the site of injury. The cellulitis usually spreads proximally from the initial site of injury. If Pasteurella multocida is present, a rapidly progressing cellulitis with a gray malodorous discharge may be encountered.

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Most infections are polymicrobial, and the most frequently isolated organisms are Pasteurella spp., streptococci, staphylococci, Moraxella, and Neisseria. The most common anaerobes are Fusobacterium spp., Bacteroides spp., Porphyromonas, and Prevotella.

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Wounds should be thoroughly irrigated with a sterile saline solution. Proper irrigation will reduce the bacterial count in the wound.

The role of antimicrobials for noninfected dog bite wounds remains controversial because only 20% of wounds become infected. Antibiotic recommendations for empiric treatment include a 3- to 5-day course of therapy.

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Amoxicillin–clavulanic acid is commonly recommended for oral outpatient therapy. Alternative agents include doxycycline and the combination of penicillin VK and dicloxacillin.

Trimethoprim–sulfamethoxazole and fluoroquinolones are recommended as alternatives for infections caused by P. multocida or those allergic to penicillins (but not in children or pregnant women). Macrolides or azolides may be considered an alternative in growing children or pregnant women.

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Treatment options for patients requiring IV therapy include β-lactam–β- lactamase inhibitors (ampicillin– sulbactam and piperacillin– tazobactam), second-generation cephalosporins wit antianaerobic activity (cefoxitin), and carbapenems.

If the immunization history of a patient with anything other than a clean minor wound is not known, tetanus/diphtheria toxoids should be administered. Both tetanus/diphtheria toxoids and tetanus immunoglobulin should be administered to patients who have never been immunized.

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If a patient has been exposed to rabies, the treatment objectives consist of thorough irrigation of the wound, tetanus prophylaxis, antibiotic prophylaxis (if indicated), and immunization. Postexposure prophylaxis immunization consists of both passive antibody administration and vaccine administration.

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CAT BITESCAT BITESApproximately 30% to 50% of cat bites

become infected. These infections are frequently caused by P. multocida, which has been isolated in the oropharynx of 50% to 70% of healthy cats.

The management of cat bites is similar to that discussed for dog bites. Antibiotic therapy with penicillin is the mainstay, and therapy is as described for dog bites.

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HUMAN BITESHUMAN BITESInfections can occur in 10% to 50% of

patients with human bites.

Infections caused by these injuries are most often caused by the normal oral flora, which includes both aerobic and anaerobic microorganisms. The most frequent aerobic organisms are Streptococcus spp., Staphylococcus spp., and Eikenella corrodens. The most commo anaerobic organisms are Fusobacterium, Prevotella, Porphyromonas, and Peptostreptococcus spp.

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Management of bite wounds consists of aggressive irrigation and topical wound dressing, surgical debridement, and immobilization of the affected area. Primary closure for human bites is not generally recommended. Tetanus toxoid and antitoxin may be indicated.

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If the biter is human immunodeficiency virus (HIV) positive, the victim should have a baseline HIV status determined and then repeated in 3 and 6 months. The bite should be thoroughly irrigated with a virucidal agent such as povidone–iodine. Victims may be offered antiretroviral chemoprophylaxis.

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Patients with noninfected bite injuries should be given prophylactic antibiotic therapy for 3 to 5 days. Amoxicillin– clavulanic acid (500 mg every 8 hours) is commonly recommended.

Alternatives for penicillin-allergic patients include fluoroquinolones or trimethoprim–sulfamethoxazole in combination with clindamycin or metronidazole. First-generation cephalosporins, macrolides, clindamycin alone, or aminoglycosides are not recommended, as the sensitivity to E. corrodens is variable.

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