Skin, wound and soft tissue infections

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1 Skin, wound and soft tissue infections Diseases: HAIR FOLLICULES: folliculitis, furuncle, carbuncle SEBACEOUS GLANDS: acne EPIDERMIS: intertrigo, impetigo, burn wounds, SSS (exfoliative dermatosis) DERMIS: erysipelas, bite wounds DERMIS& SUBCUTANEOUS FAT: cellulitis, skin abscesses FASCIA & MUSCLES: necrotizing soft tissue infections (type I & II), pyomyositis, viral myositis, rhabdomyolysis Folliculitis An infection in the hair follicles. Commonly moist and warm skin areas are affected (in the inner side of the thigh, in genital area and groin, in neck and underarms); usually self limiting and does not require treatment; antibacterial soaps are recommended. Deep folliculitis (sycosis) is a subacute or chronic pyogenic infection involving the whole depth of hair follicle. Lupoid sycosis means that the follicles are destroyed with clinically evident scarring. It occurs mostly in males after puberty and commonly involves the follicle of beard (sycosis barbae) and is caused by Staphylococcus aureus. Furuncle acute, usually necrotic infection of a hair follicle with Staphylococcus aureus (an abscess of hair follicle). Carbuncle deep infection of a group of contiguous hair follicles with Staphylococcus aureus that characterize intense inflammatory changes in the surrounding and underlying connective tissues including subcutaneous fat layer. Etiology and treatment: a) Staphylococcus aureus (most common) MSSA dicloxacillin, cephalexin; MRSA clindamycin, TMP- SMX, tetracyclines, linezolid; mupirocin ointment for recurrent infections in carriers b) Pseudomonas aeruginosa (hot tube folliculitis) ciprofoxacin c) yeast folliculitis (Pityrosporum, Candida (itching sensations are characteristic) ketoconazole cream d) herpetic folliculitis (HSV) acyclovir, valacyclovir, famcyclovir Acne vulgaris May be mild (few, occasional pimples), moderate (inflammatory papules), or severe (nodules and cysts). Treatment depends on the severity of the condition. Acne is primarily a hormonal condition driven by male or androgenic hormones, which typically become active during the teenage years. Sensitivity to such hormones, combined with bacteria on the skin, and fatty acids within oil glands, cause acne. Common sites for acne are the face, chest, shoulders, and back the sites of oil glands. As the infection is caused by bacteria colonizing skin (Propionibacterium acne most commonly) treatment include: tetracyclines, macrolides, clindamycin.

2 Intertrigo inflammation of skin folds (the opposed skin surfaces). Heat, moisture, friction and sweat retention induces maceration and inflammation of tissue areas. Commonest offenders are: Str. pyogenes, Candida spp., dermatophytes (Trichophyton, Epidermophyton), Corynebacterium minutissimum (cutaneous erythrasma), St. aureus, Pseudomonas aeruginosa, Proteus spp. but may also be allergic. Treatment include topical agents: bacitracin, polymyxin B, neomycin, mupirocin, sodium fusidate (depending on etiology); systemic treatment in severe cases: cephalosporins, quinolones, aminoglycosides, mupirocin topically, erythromycin (cutaneous erythrasma), antifungal ointments, creams etc. (imidazoles, fluconazole, itraconazole tec.) Impetigo Impetigo is a contagious superficial bacterial infection observed most frequently in children. It may be classified as primary impetigo (direct bacterial invasion of previously normal skin) or secondary impetigo (infection at sites of minor skin trauma such as abrasions, minor trauma, and insect bites, or underlying conditions such as eczema). Pyoderma and impetigo contagiosa are sometimes used as synonyms for primary impetigo. The infection usually occurs in warm, humid conditions and is easily spread among individuals in close contact; risk factors include poverty, crowding, poor hygiene, and underlying scabies. Carriage of group A Streptococcus (GAS) and Staphylococcus aureus predisposes to subsequent impetigo. Poststreptococcal glomerulonephritis and rheumatic fever following impetigo have also been described. Variants of impetigo include: Non-bullous impetigo is the most common form of impetigo. Lesions begin as papules that progress to vesicles surrounded by erythema. Subsequently they become pustules that enlarge and rapidly break down to form thick, adherent crusts with a characteristic golden appearance; this evolution usually occurs over about one week. Lesions usually involve the face and extremities. Multiple lesions may develop but tend to remain well localized. Regional lymphadenitis may occur, although systemic symptoms are usually absent. Bullous impetigo is a form of impetigo seen primarily in young children in which the vesicles enlarge to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust. Usually there are fewer lesions than in non bullous impetigo, and the trunk is more frequently affected. Bullous impetigo in an adult should prompt an investigation for previously undiagnosed human immunodeficiency virus (HIV) infection. Bullous impetigo is due to strains of S. aureus that produce exfoliative toxin A, a toxin that causes loss of cell adhesion in the superficial epidermis by targeting the protein desmoglein 1. This mechanism is related to the pathophysiology of pemphigus, in which autoantibodies are directed against the same protein. Ecthyma is an ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis. They consist of "punched-out" ulcers covered with yellow crust surrounded by raised violaceous margins. Etiology and treatment: a) Staphylococcus aureus is the principal pathogen b) β-hemolytic streptococci (primarily group A, but occasionally other serogroups such as C and G) account for a minority of cases, either alone or in combination with S. aureus. Treatment: topical therapy with mupirocin, fusidic acid; systemic antibiotics: penicillin, TMP-SMX, for MRSA doxycycline, clindamycin, erythromycin. Fluoroquinolones should NOT be used to treat impetigo, as MRSA resistance to this class is widespread and resistance can develop on therapy. Diagnosis: Gram stain and culture of pus or exudate is recommended to identify whether S. aureus and/or a beta-hemolytic Streptococcus is the cause. However, treatment may be initiated without these studies in patients with typical clinical presentations. What key enzymes does S. aureus have: *Catalase: converts toxic oxygen radicals from peripheral mononuclear cells (PMN) to non-toxic forms, deactivating them *Hyaluronidase: hydrolyzes mucopolysaccharides in the extracellular matrix of connective tissue *Beta-lactamases: mediate drug resistance *Lipases, nuclease What toxins does S. aureus have: *Alpha-toxin: membrane-damaging (hemolysin), dermonecrotic *Beta-toxin: membrane damaging, sphingomyelinase *Leukocidin: forms pores in phagocyte membranes *Epidermolytic toxins: exfoliatins (SSSS)

3 *TSST-1: related enterotoxins, causes TSS *Enterotoxins: heat-stable causes of food poisoning *ET, TSST, SE are superantigens: directly activate T cells to induce cytokines Streptococcal toxins and enzymes: *Pyrogenic exotoxin: scarlet fever *Hemolysins: affect PMNs also *Dnases, hyaluronidase, streptokinase, proteinases, etc: may help spread through tissue planes Burn wounds The spectrum of microorganisms causing infections in burn patients varies with time and location. The organisms causing burn wound infection typically appear at varying stages post-burn-injury. Immediately after burning, the microbial population of the burn wound is sparse and includes predominantly GP bacteria that survived the thermal insult, such as staphylococci located deep within sweat glands and hair follicles. Within the first week postburn, burn wounds are colonized with other microbes, such as GP and GN bacteria, and yeasts derived from the patient s normal gastrointestinal or upper respiratory tract flora, and from the hospital environment. The predominant GP organisms found in burn wound infections remain Staphylococcus aureus, followed by Enterococcus species. GN pathogens dominate after the fifth day of a typically protracted inhospital stay and have emerged as the most common etiologic agents of invasive infection. Pseudomonas aeruginosa remains the most frequent GN microorganism isolated from burn wounds, followed by E. coli. With severe burn-associated immune deficiency and/or delayed or inadequate treatment, microbial invasion of viable tissue occurs, which represents the hallmark of an invasive burn wound infection. Fungi (e.g. Candida, Aspergillus, Fusarium, Mucor species) and multi-resistant organisms (e.g. MRSA, VRE, Acinetobacter) appear late in chronological appearance, and typically occur after use of broad-spectrum antibiotics and/or a prolonged hospital stay. Candida sp. is the most common fungus isolated from burn wounds and the fourth most common cause of burn wound infections overall, and HSV-1 remains the most common viral organism in burn wounds. Chronologic appearance and characteristics of organisms in burns Organism, chronology Characteristics Commensal skin organisms (gram Streptococcus and Staphylococcus species primarily positive) result in early Other sources are upper respiratory tract and environment colonization of burns Topical antimicrobials help decrease colonization 2 to 4 days post-burn, gram-negative bacteria colonize wound Patient skin, upper respiratory tract, gastrointestinal tract, and Gram-negative species dominant >5 hospital environment are typical sources days Pseudomonas aeruginosa, Acinetobacter baumannii, E. coli, Klebsiella pneumoniae, Enterobacter cloacae Yeast and fungi colonization follows If gram-negative cover is initiated, Majority are Candida species, other fungi are increasing in yeast often appears frequency MRSA, VRE, multi-drug-resistant Pseudomonas and Acinetobacter species, and fungi Finally, more resistant bacteria and fungi invade the wound Usually secondary to broad-spectrum antibiotics, or inadequate host response or therapeutic measures (excision burn, topical and systemic antibiotics) Transition from colonization to invasion DIAGNOSIS: When burn wound infection is suspected qualitative wound cultures can identify the presence of flora, but quantitative wound cultures (number of bacteria per gram of tissue) are required to confirm the diagnosis of burn wound infection. In an infected burn wound, bacteria are present at concentrations >10 5 bacteria per gram of tissue. The presence of bacteria at concentrations >10 5 bacteria per gram of tissue in adjacent unburned tissue defines invasive burn wound infection. Systemic symptoms are usually present in patients with burn wound sepsis related to invasive burn wound infection. Wound colonization Surface wound cultures are useful for identifying predominant organisms of the burn wound flora. Swab cultures assist in the surveillance of the bacterial flora colonizing burn patients. Burn wounds are swabbed on admission, and again if there are any concerning changes in appearance. Colonization is present when bacteria are cultured from the burn wound surface at concentrations <10 5 bacteria per

4 gram tissue, in the absence of clinical or histopathologic evidence of infection or invasion of unburned tissue. Colonization does not generally impair wound healing. Noninvasive infection Noninvasive burn wound infection is present when there are typical clinical features of infection without systemic signs, and the bacterial count is >10 5 bacteria per gram of tissue (or recovery of mold or yeast by culture) obtained from a burn wound or eschar with no invasive component (i.e. no microbial invasion into unburned tissue) as identified by tissue histopathology. This bacterial burden results in impaired skin and tissue graft take, and promotes systemic infection. Invasive infection Invasive burn wound infection is present when there are typical clinical features consistent with burn wound infection associated with systemic signs, and bacterial count is >10 5 bacteria per gram of tissue obtained from a burn wound or eschar with an invasive component (i.e. microbial or fungal invasion into unburned tissue) identified by tissue histopathology. Necrotizing infections, which are aggressive infections involving the deeper tissues with the potential to cause extensive tissue necrosis, can occur. Systemic antimicrobial therapy is reserved for patients demonstrating sepsis or septic shock to limit the risk of super-infection with resistant microorganisms. Antibiotic choices are dependent on the antibiogram: cephalosporins, piperacillin/tazobactam or carbapenems ± vancomycin or clindamycin if there is suspicion for MRSA, ± an aminoglycoside if there is suspicion for multidrug resistant Pseudomonas aeruginosa or fluoroquinolone for burns involving the lower extremity or feet or burns in patients with diabetes. Local burn wound care Local management of infected burn wounds includes cleansing, debridement, topical antimicrobial agents (e.g. silver sulfadiazine, combination antibiotics, chlorhexidine), and dressings (e.g. compresses, biosynthetics, biologics). The treatment for unexcised deep burn wounds is always excision; the required depth of excision depends on the depth of microbial invasion. SOFT TISSUE INFECTIONS DUE TO DOG AND CAT BITES The predominant pathogens in animal bite wounds are the oral flora of the biting animal and human skin flora. About 85 percent of bites harbor potential pathogens, and the average wound yields five types of bacterial isolates; 60 percent have mixed aerobic and anaerobic bacteria. Skin flora such as staphylococci and streptococci are isolated in about 40 percent of bites. Pasteurella species are isolated from 50 percent of dog bite wounds and 75 percent of cat bite wounds. Capnocytophaga canimorsus, a fastidious gram-negative rod, can cause bacteremia and fatal sepsis after animal bites, especially in asplenic patients or those with underlying hepatic disease. Anaerobes isolated from dog and cat bite wounds include Bacteroides, fusobacteria, Porphyromonas, Prevotella, propionibacteria, and peptostreptococci. Eikenella corrodens is associated with human bites. Bite wounds may also be accompanied by bacteremia, even if they do not appear grossly infected; blood cultures should be obtained in the setting of fever or other signs of systemic infection. Sepsis and its complications can also occur, particularly among immunocompromised hosts. Empiric oral antibiotic therapy for animal bites: doxycycline, TMP-SMX, penicillin, amoxycillin/clavulanate, cefalosporins, quinolones (levofloxacin, moxifloxacin), metronidazole, clindamycin. Pasteurella multocida treatment options: β lactams, tetracyclines, quinolones Cellulitis and skin abscess including erysipelas Cellulitis, abscess, or both are among the most common skin and soft tissue infections. Cellulitis (which includes erysipelas characteristic lymphatic involvement) manifests as an area of skin erythema, edema, and warmth; it develops as a result of bacterial entry via breaches in the skin barrier. A skin abscess is a collection of pus within the dermis or subcutaneous space. Differences between erysipelas and cellulitis caused by streptococci: Erysipelas Caused by Str. pyogenes Involves upper subcutaneous tissue and lymphatic vessels History antecedent throat infection Common site: face with bridge of nose and cheeks Well defined margins Vesicle or bulla formation Self limiting Cellulitis Caused by Str. pyogenes and rarely by St. aureus Involves deeper subcutaneous tissue An intertrigo or deep fissures portal of entry Common site: legs Indistinct margins Bulla formation in severe In untreated necrosis can supervene

5 The most common cause of cellulitis is β-hemolytic streptococci (groups A, B, C, G, and F), most commonly Streptococcus pyogenes (especially cellulitis of lower extremities associated with chronic venous stasis); Streptococci group B are associated with cellulitis in newborn. S. aureus (including MRSA strains) is a notable but less common cause (e.g. recurrent cellulitis). GN aerobic bacilli are identified in a minority of cases. The vast majority of erysipelas cases are caused by β-hemolytic streptococci. Less common causes of cellulitis include Haemophilus influenzae (buccal, orbital, head, neck cellulitis in children), clostridia and non-spore-forming anaerobes (crepitant cellulitis), Streptococcus pneumoniae (orbital cellulitis); Pseudomonas aeruginosa (cellulitis associated with penetrating injury), Erysipelothrix rhusiopathiae (butchers, fish men), Mycobacterium marinum & M. ulcerans (cellulitis associated with aquariums and swimming pools). Skin abscess The most common cause of skin abscess is S. aureus MSSA or MRSA, which occurs in up to 75 percent of cases. A skin abscess can be caused by more than one pathogen; isolation of multiple organisms (including S. aureus together with S. pyogenes and GN rods with anaerobes) is more common in patients with skin abscess involving the perioral, perirectal, or vulvovaginal areas. Organisms of oral origin, including anaerobes, are seen most frequently among intravenous drug users. Unusual causes of skin abscess include nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis. Most abscesses are due to infection. However, sterile abscesses can occur in the setting of injected irritants. Examples include injected drugs (particularly oil-based ones) that may not be fully absorbed and so remain at the site of injection, causing local irritation. Sterile abscesses can turn into hard, solid lesions as they scar. The diagnosis of cellulitis, erysipelas, and skin abscess is usually based upon clinical manifestations. Patients with drainable abscess should undergo incision and drainage, with culture and susceptibility testing of debrided material. Treatment Cellulitis Patients with nonpurulent cellulitis should be managed with empiric therapy for infection due to β-hemolytic streptococci and MSSA. Common options are cephalosporins Erysipelas Patients with erysipelas should be managed with empiric therapy for infection due to betahemolytic streptococci cephalosporins, anti-staphylococcal penicillins (e.g. flucloxacillin). Patients with mild infection may be treated with oral penicillin or amoxicillin. In the setting of β-lactam allergy, cephalexin (if the patient can tolerate cephalosporins), clindamycin, or linezolid may be used. Options for oral treatment of MRSA: clindamycin, TMP-SMX, doxycycline, linezoild. Parenteral antimicrobial therapy for treatment of skin and soft tissue infections due to MRSA in adults: vancomycin, daptomycin, Linezolid, Tedizolid, Telavancin (derived from vancomycin), ceftaroline. NECROTIZING SOFT TISSUE INFECTIONS A. CLOSTRIDIAL B. NON-CLOSTRIDIAL CLOSTRIDIAL MYONECROSIS Clostridial myonecrosis (gas gangrene) is a life-threatening muscle infection that develops either contiguously from an area of trauma or hematogenously from the gastrointestinal tract with muscle seeding. Early recognition and aggressive treatment are essential. There are two major presentations of clostridial gas gangrene: traumatic and spontaneous. Traumatic gas gangrene is most commonly caused by Clostridium perfringens; spontaneous gangrene is most commonly caused by Clostridium septicum. Clostridium species are widespread in nature due to their ability to form endospores. They are commonly found in soil and marine sediments as well as human and animal intestinal tracts. Categories of clostridial soft tissue infections include: wound contamination, anaerobic cellulitis, myonecrosis (gas gangrene), and necrotizing fasciitis. Wound contamination with soil containing clostridial spores or vegetative organisms may occur, although contamination with clostridial species in the absence of devitalized tissue does not necessarily lead to infection. Anaerobic cellulitis occurs in the setting of modest quantities of devitalized tissue that support the growth of C. perfringens or other clostridial strains. Gas is produced locally and extends along fascial planes; bacteremia and invasion of healthy tissue (including muscle) does not occur. Mortality is low in the setting of appropriate management, including prompt removal of the devitalized tissue. Myonecrosis (clostridial gas gangrene) may be distinguished from the above infections by the progressive invasion and destruction of healthy muscle tissue. There are two major presentations of clostridial gas gangrene: traumatic and spontaneous.

6 Traumatic gas gangrene with vascular compromise (particularly deep penetrating injuries such as knife wounds, gunshot wounds, and crush injuries) create an anaerobic environment that is ideal for proliferation of clostridia. Traumatic injury accounts for about 70 percent of gas gangrene cases, and about 80 percent of these are caused by C. perfringens. Other pathogens include C. septicum, C. novyi, C. histolyticum, C. bifermentans, C. tertium, and C. fallax. Traumatic gas gangrene may have other microbes isolated from the site of trauma; however, clostridia are the major players in terms of destruction of tissue. In gas gangrene, muscle necrosis is severe, and polymorphonuclear leukocytes (PMNs) are notably absent from infected tissues. This is in contrast to soft tissue infections caused by organisms such as Staphylococcus aureus, in which significant influx of PMNs localizes the infection without adjacent tissue or vascular destruction. In the setting of clostridial infection, PMNs arriving at the site of infection adhere to and accumulate along the endothelium of capillaries, small arterioles, and postcapillary venules but do not cross the vascular endothelium into infected tissue. Many extracellular toxins are produced by C. perfringens; of these, alpha and theta toxins have been implicated in pathogenesis: Alpha toxin is a hemolytic toxin with both phospholipase C (PLC) and sphingomyelinase activities. Theta toxin (also known as perfringolysin O) that is largely responsible for both the widespread tissue necrosis and the characteristic absence of tissue inflammatory response. Alpha toxin potently stimulates platelet aggregation and upregulates adherence molecules on PMN and endothelial cells. Experimental intramuscular alpha toxin injection causes a rapid, irreversible decline in muscle blood flow and concomitant ischemic necrosis of tissue due to the formation of occlusive intravascular aggregates composed of activated platelets, leukocytes, and fibrin. The perfusion deficits expand the anaerobic environment and contribute to the rapidly advancing margins of tissue destruction characteristic of clostridial gas gangrene. Shock associated with gas gangrene may be attributable to both direct and indirect effects of alpha and theta toxins. Alpha toxin directly suppresses myocardial contractility and may contribute to profound hypotension via a sudden reduction in cardiac output. Theta toxin causes markedly reduced systemic vascular resistance combined with a markedly increased cardiac output. Diagnosis: Blood (both aerobic and anaerobic bottles) and tissue cultures should be obtained; definitive diagnosis of gas gangrene requires demonstration of large, gram-variable rods at the site of injury. Clostridia can appear both GP and GN when stained directly from infected tissues but stain as GP rods when obtained from culture media. Drainage from surgical procedures is characteristically absent of frank pus, and microscopy demonstrates presence of organisms but absence of neutrophils. Treatment of traumatic gas gangrene consists of surgical debridement, antibiotic therapy, and supportive measures. Patients with trauma who have not received tetanus immunization for 10 years should receive a booster vaccine against tetanus. Antibiotic agents with excellent in vitro activity against C. perfringens include: penicillin, clindamycin, tetracycline, chloramphenicol, metronidazole, and a number of cephalosporins. Spontaneous gas gangrene generally occurs via hematogenous seeding of muscle with bacteria (usually C. septicum) from a gastrointestinal tract portal of entry. C. septicum can grow in normal tissues; it does not require anaerobic conditions. Spontaneous gas gangrene can also occur in patients who have congenital or cyclic neutropenia and among patients with prior radiation therapy to the abdomen. The diagnosis of spontaneous gas gangrene is frequently missed or delayed because it is not entertained. Necrotizing soft tissue infections are comprised of two distinct bacteriologic entities: type I (polymicrobial infection) type II (group A streptococcal infection). In type I infection (polymicrobial), at least one anaerobic species (most commonly Bacteroides, Clostridium, or Peptostreptococcus) is isolated in combination with one or more facultative anaerobic streptococci (Peptostreptococcus) and members of the Enterobacteriaceae (e.g. Escherichia coli, Enterobacter, Klebsiella, Proteus). An obligate aerobe, such as P. aeruginosa, is only rarely a component of such a mixed infection. Necrotizing fasciitis of the head and neck is usually caused by mouth anaerobes, such as Fusobacteria, anaerobic streptococci, Bacteroides, and spirochetes. Fournier's gangrene is caused by facultative organisms (E. coli, Klebsiella, enterococci) along with anaerobes (Bacteroides, Fusobacterium, Clostridium, anaerobic or microaerophilic streptococci). Cervical necrotizing fasciitis of the neck can result from a breach in oropharynx mucous membrane integrity following surgery or instrumentation or in the setting of odontogenic infection. Bacterial penetration into the fascial compartments of the head and neck region can also result in Ludwig's angina, a rapidly expanding inflammation in the submandibular and sublingual spaces. Necrotizing infection of the male perineum, known as Fournier's gangrene, can result from a breach in the

7 integrity of the gastrointestinal or urethral mucosa. Infection can occur in all age groups but is most common in older men. Necrotizing infection involving the labia and perineum can also occur in females, particularly in the setting of diabetes. Meleney's synergistic gangrene is a rare infection that occurs in postoperative patients. It is characterized by a slowly expanding indolent ulceration that is confined to the superficial fascia. It results from a synergistic interaction between S. aureus and microaerophilic streptococci. In type II (GAS, monomicrobic), necrotizing fasciitis is generally monomicrobic, most commonly caused by group A Streptococcus (also known as hemolytic streptococcal gangrene). Necrotizing fasciitis is an infection of the deeper tissues that results in progressive destruction of the muscle fascia and overlying subcutaneous fat; muscle tissue is frequently spared because of its generous blood supply. Infection typically spreads along the muscle fascia due to its relatively poor blood supply; initially, the overlying tissue can appear unaffected. It is this feature that makes necrotizing fasciitis difficult to diagnose without surgical intervention. Aeromonas hydrophila has been associated with traumatic lesions in fresh water, and Vibrio vulnificus can cause necrotizing fasciitis in association with seawater injuries (Gulf coast and South Atlantic seaboard) or among patients with cirrhosis who ingest raw oysters. There are also case reports of monomicrobial necrotizing soft tissue infections due to other organisms, including Haemophilus influenzae. Pyomyositis (muscle abscess, usually caused by Staphylococcus aureus) like clostridial myonecrosis, pyomyositis can occur following trauma or can develop spontaneously. They differ in that pyomyositis is not routinely associated with systemic toxicity or presence of gas in tissue on radiographic imaging. The two are distinguished by Gram stain and culture. Viral myositis Viral infection such as acute influenza type A can produce skeletal muscle injury. It differs from clostridial myonecrosis in that the muscle pain is diffuse rather than localized, and it is not routinely associated with systemic toxicity or gas in tissues. Rhabdomyolysis (muscle necrosis) both rhabdomyolysis and clostridial myonecrosis are associated with muscle pain; rhabdomyolysis has many causes including trauma, drugs, toxins, and metabolic disorders. Clostridial necrosis is distinguished by the presence of gas in tissues and Gram stain findings. Antibiotic therapy. In general, empiric treatment of necrotizing infection should consist of broad spectrum antimicrobial therapy, including activity against GP, GN, and anaerobic organisms; special consideration for group A Streptococcus (GAS) and Clostridium species should be taken. Regimens include administration of: carbapenem or β-lactam/β-lactamase inhibitor, plus clindamycin plus an agent with activity against MRSA such as vancomycin, daptomycin, or linezolid.

8 C & S, culture and sensitivity; I & D, incision and drainage Summary Skin layer Disease Etiology Treatment Hair follicles Folliculitis MSSA anti-staphylococcal penicillins (nafcillin, oxacillin, cloxacillin, dicloxacillin), tetracyclines, macrolides, clindamycin, TMP- SMX MRSA clindamycin, TMP-SMX, doxycycline, linezoild, macrolides Pseudomonas aeruginosa gentamycin/neomycin cream, polymyxin B spray, ciprofloxacin oral Pityrosporum, Candida itraconazole, ketoconazole cream HSV acyclovir, valacyclovir, famcyclovir Sebaceous glands Acne Propionibacterium acne amoxycillin/clavulanate, ampicillin, tetracycline, minocycline, doxycycline, erythromycin, clindamycin, metronidazole Dermis Intertrigo Str. pyogenes penicillin drug of choice; macrolides Candida, dermatophytes itraconazole, ketoconazole cream MRSA, MSSA clindamycin, doxycycline, Cutaneous erythrasma Corynebacterium minutissimum linezoild, TMP-SMX macrolides, tetracyclines

9 Impetigo: non-bullous bullous ecthyma Str. pyogenes St. aureus penicillin, macrolides topical therapy with mupirocin, fusidic acid; systemic antibiotics: penicillin, TMP-SMX, doxycycline, clindamycin, erythromycin Burn wounds early staphylococci cloxacillin or nafcillin, vancomycin, clindamycin, tetracyclines, TMP-SMX 5 days Bite wounds cat/dogs human Pseudomonas aeruginosa, Acinetobacter spp., E. coli, Enterobacter, Klebsiella MRSA VRE multi-resistant GN rods Candida, molds Pasteurella multocida Capnocytophaga canimorsus Eikenella corrodens systemic treatment: cephalosporins, amoxycillin/clavulanate, ampicillin/sulbactam, piperacillin/tazobactam, carbapenems, monobactams, aminoglycosides, quinolones clindamycin, TMP-SMX, doxycycline, linezoild linezolid quinolones, aminoglycosides itraconazole, ketoconazole, amphotericin B β lactams, tetracyclines, quinolones penicillin G drug of choice; amoxycillin/clavulanate, ampicillin/sulbactam, cephalosporins (III gen.), tetracyclines, clindamycin penicillins, cephalosporins, tetracyclines Erysipelas Str. pyogenes penicillin drug of choice; cloxacillin or nafcillin, macrolides uncommon cause S. aureus MSSA, MRSA macrolides, pristinamycin, vancomycin Cellulitis less common Str. pyogenes, St. aureus penicillin, dicloxacillin, cephalexin, clindamycin, doxycycline, macrolides, quinolones, daptomycin, vancomycin H. influenzae ampicillin/sulbactam, cephalosporins (II & III gen.), macrolides, quinolones Clostridia non-spore-forming anaerobes Str. pneumoniae Pseudomonas aeruginosa Mycobacterium marinum, ulcerans Erysipelothrix rhusiopathiae penicillin, cefoxitin, amoxycillin/clavulanate, ampicillin/sulbactam, cephalosporins, clindamycin metronidazole, chloramphenicol, carbapenems penicillin, cephalosporins, macrolides, tetracyclines, vancomycin piperacillin/tazobactam, carbapenems, aminoglycosides, quinolones ceftazidime, cefepime or fluoroquinolone

10 abscesses less common Vibrio vulnificus, Aeromonas hydrophila MRSA, MSSA Str. pyogenes doxycycline, ceftazidime, quinolones penicillin, dicloxacillin, cephalexin, clindamycin, doxycycline, macrolides, quinolones, daptomycin, vancomycin Fascia/muscles necrotizing clostridial (gas gangrene) traumatic spontaneous type I (polymicrobic) Fournier s gangrene cervical necrotizing fasciitis Meleney s gangrene GN rods anaerobes C. perfringens C. septicum anaerobe+streptococci+gn rods anaerobes (Bacteroides, Fusobactrium, Clostridium spp., Peptostreptococci, intestinal rods oral anaerobes (Peptostreptococcus, Prophyromonas, Veilonella, Prevotella, Fusobacterium, Actinomyces, Propionibacterium) + facultative anaerobic bacteria (streptococci, staphylococci) St. aureus, Peptosptreptococci, streptococci cephalosporins, piperacillin/tazobactam, carbapenems, aminoglycosides, quinolones amoxycillin/clavulanate, ampicillin/sulbactam, cephalosporins, clindamycin amoxycillin/clavulanate, ampicillin/sulbactam, ticarcillin, cephalosporins, clindamycin metronidazole, chloramphenicol, cefoxitin, carbapenems (imipenem, meropenem, doripenem, ertapenem)