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Skin and Soft Tissue lnfections si r Skin and Soft Tissue -., lnfections lntroduqtion Risk factors for skin and soft tissue infections (SSTIs) include breach of the epidermis associated with trauma (injection drugs, surgery, bites, Iacerations, abrasions). nontrauma (ulcers. tinea pedis), impaired lymphatic and venous drainage (chronic venous insufficiency, lymphedema), immunocom promising conditions (diabetes mellitus, neutropenia, cirrho sis, HIV and transplantation), peripheral arterial disease, and history of cellulitis. Infections can be characterized by anatomic involvement and presence or absence of pus. Nonpurulent spreading skin infections (usually caused by B hemolytic streptococci like Streptococcus pAogenes) include erysipelas, cellulitis, and necrotizing SSTIs; purulent skin infections (generally caused by staphylococci, including methicillin -resistant Staphylococcus oureus [MRSA] ) refer to folliculitis, abscesses (Figure 3). furuncles, and carbuncles. t I G U R E 4. Facial erysipelas manifested as severe malar and periorbital Table 5 includes other pathogens and their associated risk fac- erythema and swelling. Erysipelas is a dermatologic condition, which involves the tors for less common causes of skin infection. Complications inoculation of the skin and subcutaneous tissue with streptococcal bacteria causing edema and bright red erythema of the affected areas. include systemic inflammatory response (as in severe celluli Photo from the CDC Public Health lmage Library tis) or systemic toxin release (as in toxic shock syndrome).

tors for less common causes of skin infection. Complications inoculation of the skin and subcutaneous tissue with streptococcal bacteria causing edema and bright red erythema of the affected areas. include systemic inflammatory response (as in severe celluli Photo from the CDC Public Health lmage Library tis) or systemic toxin release (as in toxic shock syndrome). venous stasis dermatitis. Iymphedema, erythema nodosum, Erysipelas and Cellulitis deep venous thrombosis, lipodermatosclerosis, erythromelal Erysipelas refers to infection of the epidermis, upper dermis, gia, trauma-related inflammation, pyoderma gangrenosum, and superficial lymphatics. Usually involving the face or lower and hypersensitivity reactions. Approximately 5'2, of patients extremities, this infection is brightly erythematous and tender, with cellulitis have positive blood cultures, so they are not with distinct elevated borders and associated fever, lymphangi- routinely indicated; however, cultures should be performed tis, and regional lymphadenopathy (Figure 4). Cellulitis refers fbr those who are immunocompromised or have chronic to infection ir-rvolving the deeper dermis and subcutaneous fat lymphedema, exhibit severe sepsis or a possible necrotizing tissue. Inflammatory signs of infection are similar to erysipelas, component, or have unusual precipitating circumstances, but the area of involvement is less well demarcated (Figure 5). including immersion injury or animal bites. Culture of skin Although erysipelas and cellulitis are usually diagnosed tissue aspirate or biopsy should also be considered for these clinically, approximately one third of patients are misdiag patients. Radiographic imaging is unhelpful for primary nosed. Clinical mimics (Figure 6) include contact dermatitis,

venous stasis dermatitis. Iymphedema, erythema nodosum, Erysipelas and Cellulitis deep venous thrombosis, lipodermatosclerosis, erythromelal Erysipelas refers to infection of the epidermis, upper dermis, gia, trauma-related inflammation, pyoderma gangrenosum, and superficial lymphatics. Usually involving the face or lower and hypersensitivity reactions. Approximately 5'2, of patients extremities, this infection is brightly erythematous and tender, with cellulitis have positive blood cultures, so they are not with distinct elevated borders and associated fever, lymphangi- routinely indicated; however, cultures should be performed tis, and regional lymphadenopathy (Figure 4). Cellulitis refers fbr those who are immunocompromised or have chronic to infection ir-rvolving the deeper dermis and subcutaneous fat lymphedema, exhibit severe sepsis or a possible necrotizing tissue. Inflammatory signs of infection are similar to erysipelas, component, or have unusual precipitating circumstances, but the area of involvement is less well demarcated (Figure 5). including immersion injury or animal bites. Culture of skin Although erysipelas and cellulitis are usually diagnosed tissue aspirate or biopsy should also be considered for these clinically, approximately one third of patients are misdiag patients. Radiographic imaging is unhelpful for primary nosed. Clinical mimics (Figure 6) include contact dermatitis, FIGURE 5. Cellulitis, a rapidly spreading, deep, subcutaneous-based infection, FIGURE 3. Astaphylococcal abscessonthe posteriorthigh presenting asatender, is characterized by warmth, swelling, tenderness, and erythema that may be erythematous, fluctuant nodule topped by a central pustule. accompanied by lymphatic streaking and is predominately unilateral. 8

Skin and Soft Tissue lnfections Pathogen Risk Factor Comment Aeromonas hydrophila Contact with freshwater lakes, streams, Cellulitis nonspecific in clinical appearance; minor trauma rivers (including brackish water) to skin usually leads to inoculation of organism; can cause necrotizing infection Contact with leeches Vi brio vul nificus, Vibrio Contact with salt water or brackish water Cellulitis through direct inoculation into skin parahaemolyticus Contact with drippings from raw seafood Hallmark is hemorrhagic bullae in area of cellulitis Consumption of undercooked shellfish lngestion leads to bacteremia with secondary skin ( particu larly oysters) infection Liver cirrhosis or chronic liver disease Can cause necrotizing infection E nJsi p e I oth ri x rh u si o p ath i a e Contact with saltwater marine life (can Causes erysipeloid disease a lso i nfect freshwater fish ) Cellulitis usually involves the hand or arm, especially in those handling fish, shellfish, or, occasionally, poultry or meat contaminated with bacterium Stre ptobaci I I u s m o n i I ifo rm i s Bite or scratch from rat Initia ly fever, vomiting, headache, muscle/joint pai ns, I

Pathogen Risk Factor Comment Aeromonas hydrophila Contact with freshwater lakes, streams, Cellulitis nonspecific in clinical appearance; minor trauma rivers (including brackish water) to skin usually leads to inoculation of organism; can cause necrotizing infection Contact with leeches Vi brio vul nificus, Vibrio Contact with salt water or brackish water Cellulitis through direct inoculation into skin parahaemolyticus Contact with drippings from raw seafood Hallmark is hemorrhagic bullae in area of cellulitis Consumption of undercooked shellfish lngestion leads to bacteremia with secondary skin ( particu larly oysters) infection Liver cirrhosis or chronic liver disease Can cause necrotizing infection E nJsi p e I oth ri x rh u si o p ath i a e Contact with saltwater marine life (can Causes erysipeloid disease a lso i nfect freshwater fish ) Cellulitis usually involves the hand or arm, especially in those handling fish, shellfish, or, occasionally, poultry or meat contaminated with bacterium Stre ptobaci I I u s m o n i I ifo rm i s Bite or scratch from rat Initia ly fever, vomiting, headache, muscle/joint pai ns, I followed by maculopapular rash over extremities Pasteurella multocida Contact primarily with cats and dogs Cellulitis occurs as a result of cat scratch or cat or dog bite or lick Ca p n ocyto p h a g a ca n i m o rsu s Contact primarily with dogs Cellulitis and sepsis, particularly in patients with hyposplenism Bacillus anthracis Contact with infected animals or animal Edematous pruritic lesion with central eschar; spore- products. May be the result of forming organism bioterrorism Fra n ci se I I a tu I a re n si s Contact with or bite from infected animal U lcerog la nd u la r synd rome cha racterizedby u lcerative (pa rticu la rly cats); arth ropod bites lesion with central eschar and localized tender (particularly ticks) lym p h ad enopathy; co nstitutio na I sym ptoms ofte n p rese nt

followed by maculopapular rash over extremities Pasteurella multocida Contact primarily with cats and dogs Cellulitis occurs as a result of cat scratch or cat or dog bite or lick Ca p n ocyto p h a g a ca n i m o rsu s Contact primarily with dogs Cellulitis and sepsis, particularly in patients with hyposplenism Bacillus anthracis Contact with infected animals or animal Edematous pruritic lesion with central eschar; spore- products. May be the result of forming organism bioterrorism Fra n ci se I I a tu I a re n si s Contact with or bite from infected animal U lcerog la nd u la r synd rome cha racterizedby u lcerative (pa rticu la rly cats); arth ropod bites lesion with central eschar and localized tender (particularly ticks) lym p h ad enopathy; co nstitutio na I sym ptoms ofte n p rese nt Burkholderia mallei Contact with tissues or bodily fluids of Pustules with suppurative localized lymph nodes or infected mules or horses ulcerative nodules at site of inoculation Cl o stri d i u m pe rf ri n g e n s Surgery or other significant trauma Necrotizing infection, often referred to as clostridial myonecrosis or gas gangrene Pseu d o mo n as ae ru gi nosa Hottub exposure Folliculitis Neutropenia Ecthyma gangrenosum >1 necrotic ulcer with erythematous border/ha lo; bacterem ia typica ly present I

Burkholderia mallei Contact with tissues or bodily fluids of Pustules with suppurative localized lymph nodes or infected mules or horses ulcerative nodules at site of inoculation Cl o stri d i u m pe rf ri n g e n s Surgery or other significant trauma Necrotizing infection, often referred to as clostridial myonecrosis or gas gangrene Pseu d o mo n as ae ru gi nosa Hottub exposure Folliculitis Neutropenia Ecthyma gangrenosum >1 necrotic ulcer with erythematous border/ha lo; bacterem ia typica ly present I Nail-puncture wound through sole of Moist environment of shoe enables colonization with tennis shoe Pseudomonas Mycobacterium marinum Contact with fresh water or salt watel Lesion is often trauma associated and often involves the including fish tanks and swimming pools upper extremity; papular lesions become ulcerative at site of inoculation; ascending lymphatic spread can be seen ("spo rotrich o id" a ppea ra nce); syste m ic toxicity usua ly I

Nail-puncture wound through sole of Moist environment of shoe enables colonization with tennis shoe Pseudomonas Mycobacterium marinum Contact with fresh water or salt watel Lesion is often trauma associated and often involves the including fish tanks and swimming pools upper extremity; papular lesions become ulcerative at site of inoculation; ascending lymphatic spread can be seen ("spo rotrich o id" a ppea ra nce); syste m ic toxicity usua ly I absent My co b a cte ri u m f o rtu itu m Exposure to freshwater footbaths/ Furuncle(s); postoperative wound infection pedicures at nail salons, particularly after razor shaving; surgery Sporothrix schenckii Contact with soil, moss, or other organic lnitial papule at the site of inoculation that may ulcerate; material during gardening, landscaping subsequent development of papules along proximal lymphatic channels

Sporothrix schenckii Contact with soil, moss, or other organic lnitial papule at the site of inoculation that may ulcerate; material during gardening, landscaping subsequent development of papules along proximal lymphatic channels diagnosis but may be useful when a deeper necrotizing infec- Table 6). An antibiotic such as vancomycin with coverage tion is suspected. against streptococci and MRSA is recommended when nonpu- For immunocompetent patients who have no systemic rulent cellulitis is associated with penetrating trauma, nasal signs or symptoms (mild infection), empiric oral therapy colonization or infection with MRSA elsewhere, or injection directed against streptococci is recommended as outlined in drug use. Treating predisposing factors (such as tinea pedis, Table 6. Treatment duration for uncomplicated infection can edema, and primary skin disorders) may decrease the risk for be as short as 5 days but should be extended as necessary until recurrent infection. Prophylactic antibiotics such as penicillin the infection improves. In patients with systemic signs (mod- can be considered in select patients with more than three epi- erate infection), intravenous treatment is recommended (see sodes of cellulitis annually. 9

Skin and Soft Tissue lnfections treatment may be adjusted based on culture and sensitivity results from lesion associated specimens. t(EY POtt{TS o Patients with mild cellulitis or erysipelas without sys- temic signs or symptoms should receive empiric oral therapy directed against streptococci (penicillin, cepha- losporin, dicloxacillin, or clindamycin). o Patients with moderate cellulitis or erysipelas with sys temic signs should receive empiric intravenous antibiot- ics (penicillin, ceftriaxone, cefazolin, clindamycin). o Patients with evidence of deeper necrotizing soft tissue infection such as bullae and desquamation (severe infection) should receive urgent surgical evaluation for debridement and empiric vancomycin plus piperacillin- tazobactam or a carbapenem like imipenem.

t(EY POtt{TS o Patients with mild cellulitis or erysipelas without sys- temic signs or symptoms should receive empiric oral therapy directed against streptococci (penicillin, cepha- losporin, dicloxacillin, or clindamycin). o Patients with moderate cellulitis or erysipelas with sys temic signs should receive empiric intravenous antibiot- ics (penicillin, ceftriaxone, cefazolin, clindamycin). o Patients with evidence of deeper necrotizing soft tissue infection such as bullae and desquamation (severe infection) should receive urgent surgical evaluation for debridement and empiric vancomycin plus piperacillin- tazobactam or a carbapenem like imipenem. Necrotizing Fasciitis Necrotizing soft tissue infections, which involve subdermal compartments such as fascia and possibly muscle, are uncommon but potentially life threatening. In necrotizing fasciitis (NF), infection usually spreads along the superficial fascia. These infections may be monomicrobial or polymicro bial, consisting of mixed aerobic and anaerobic bacteria, and are often associated with toxin production. In monomicro- bial infection, the classically associated pathogen is S. pyo- genes; other potential organisms are provided in Table 6. NF characteristically occurs in the setting of previous skin trauma or infection and most commonly affects the extremi- ties. Risk factors include diabetes, injection drug use, malig- nancy, immunosuppression, and liver disease. Patients with diabetes are at risk for NF of the perineum, a polymicrobial infection known as Fournier gangrene that usually results from antecedent genitourinary, traumatic, or anorectal infection. The initial presentation of NF resembles cellulitis before potentially rapid progression with edema, severe pain, hemor rhagic bullous lesions, skin necrosis, and local crepitus. Systemic toxicity manifests with fever, hypotension, tachycar F lG U R E 6. Common clinical mimics of erysipelas and cellulitis are shown. dia, mental status changes, and tachypnea. A hallmark of Chronic stasis dermatitis (top)presents as erythematous, scaling, and eczematous infection is "woody" induration discovered by palpation of patches or plaques associated with chronic venous insufficiency and chronic lower extremity edema, often bilateral. Acute stasis dermatitis appears as weeping involved subcutaneous tissues. Necrosis of local nerves may plaques with vesicles and crusting and may become secondarily infected with result in anesthesia. bacteria or Candida. Erythema nodosum (boftom) may also mimic erysipelas and Although elevated serum lactate levels may assist in cellulitis. Erythema nodosum most commonly presents as single or multiple tender the diagnosis of necrotizing infection, individual labora- nodules 0n extensor surfaces of the lower extremities. tory study results are nonspecific. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score is associ- Patients who are immunocompromised, who have sys- ated with an increased likelihood of necrotizing skin infec- temic inflammatory response syndrome and hypotension, or tion; it is derived from six variables: C reactive protein level who have evidence of deeper necrotizing infection such as bul (>15 mg/dl [150 mg/L]), total leukocyte count (>1s,000- lae and desquamation (severe infection) should receive urgent 25,000/prl [ts-ZS x 10e/L), hemoglobin level (<tt tS.S gldL surgical evaluation for debridement. Initial empiric broad- [tto tss g/L1), sodium level (<13s mEq/L h3s mmol/L]), spectrum antibiotic therapy should be started (see Table 6); creatinine level (>1.6 mg/dl [t+r pmol/L]), and glucose

Necrotizing Fasciitis Necrotizing soft tissue infections, which involve subdermal compartments such as fascia and possibly muscle, are uncommon but potentially life threatening. In necrotizing fasciitis (NF), infection usually spreads along the superficial fascia. These infections may be monomicrobial or polymicro bial, consisting of mixed aerobic and anaerobic bacteria, and are often associated with toxin production. In monomicro- bial infection, the classically associated pathogen is S. pyo- genes; other potential organisms are provided in Table 6. NF characteristically occurs in the setting of previous skin trauma or infection and most commonly affects the extremi- ties. Risk factors include diabetes, injection drug use, malig- nancy, immunosuppression, and liver disease. Patients with diabetes are at risk for NF of the perineum, a polymicrobial infection known as Fournier gangrene that usually results from antecedent genitourinary, traumatic, or anorectal infection. The initial presentation of NF resembles cellulitis before potentially rapid progression with edema, severe pain, hemor rhagic bullous lesions, skin necrosis, and local crepitus. Systemic toxicity manifests with fever, hypotension, tachycar F lG U R E 6. Common clinical mimics of erysipelas and cellulitis are shown. dia, mental status changes, and tachypnea. A hallmark of Chronic stasis dermatitis (top)presents as erythematous, scaling, and eczematous infection is "woody" induration discovered by palpation of patches or plaques associated with chronic venous insufficiency and chronic lower extremity edema, often bilateral. Acute stasis dermatitis appears as weeping involved subcutaneous tissues. Necrosis of local nerves may plaques with vesicles and crusting and may become secondarily infected with result in anesthesia. bacteria or Candida. Erythema nodosum (boftom) may also mimic erysipelas and Although elevated serum lactate levels may assist in cellulitis. Erythema nodosum most commonly presents as single or multiple tender the diagnosis of necrotizing infection, individual labora- nodules 0n extensor surfaces of the lower extremities. tory study results are nonspecific. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score is associ- Patients who are immunocompromised, who have sys- ated with an increased likelihood of necrotizing skin infec- temic inflammatory response syndrome and hypotension, or tion; it is derived from six variables: C reactive protein level who have evidence of deeper necrotizing infection such as bul (>15 mg/dl [150 mg/L]), total leukocyte count (>1s,000- lae and desquamation (severe infection) should receive urgent 25,000/prl [ts-ZS x 10e/L), hemoglobin level (<tt tS.S gldL surgical evaluation for debridement. Initial empiric broad- [tto tss g/L1), sodium level (<13s mEq/L h3s mmol/L]), spectrum antibiotic therapy should be started (see Table 6); creatinine level (>1.6 mg/dl [t+r pmol/L]), and glucose 10

Skin and Soft Tissue lnfections TABLE 6. Treatment of Skin lnfections lnfection Treatment Erysipelas or cellulitis Mild: Oral penicillin, cephalosporin, dicloxacillin, clindamycin Moderate: ntravenous penicil in, ceftriaxone, cefazolin, clinda mycinu I I Severe: Surgical assessment for possible necrotizing component and empiric intravenous vancomycin plus piperacillin-tazobactam, imipenem, or meropenem Necrotizing fasciitis Polymicrobial infection: Surgical assessmenVdebridement and combination therapy such as vancomycin plus pi peracil lin-tazobactam or imipenem or meropenem

Severe: Surgical assessment for possible necrotizing component and empiric intravenous vancomycin plus piperacillin-tazobactam, imipenem, or meropenem Necrotizing fasciitis Polymicrobial infection: Surgical assessmenVdebridement and combination therapy such as vancomycin plus pi peracil lin-tazobactam or imipenem or meropenem Streptococcus pyogenes or C/ostridium species: Surgical assessment/debridement and penicillin plus clindamycin Aeromonas hydrophila: Surgical assessment/debridement and ciprofloxacin plus doxycycline Vibrio vulnificus: Surgical assessmenVdebridement and ceftazidime, ceftriaxone, or cefotaxime plus doxycycline Folliculitis Staphylococcus aureus: Usually self-limited; can use topical mupirocin, clindamycin, or retapamulin; systemic antibiotics usually not needed Pseudomonas aeruginosa (i.e., hot tub folliculitis): Usually self-limited; oral ciprofloxacin usually reserved for immunosuppressed host or for persistent or severe infection Furuncle, carbuncle, Mild: lncision and drainage; consider adjunctive oral anti-MRSA antibiotic like trimethoprim-sulfamethoxazole or abscess Moderate: lncision and drainage plus empiric trimethoprim-sulfamethoxazole or doxycycline pending culture and susceptibilities Severe: lncision and drainage plus empiric vancomycin, daptomycin, linezolid, telavancin, or ceftaroline pending culture and susceptibilities M RSA = meth ici I li n-resistant Staphy/ococcus aureus. "lnducible resistance (resistance appearing after exposure to an agent) may be seen with clindamycin

Streptococcus pyogenes or C/ostridium species: Surgical assessment/debridement and penicillin plus clindamycin Aeromonas hydrophila: Surgical assessment/debridement and ciprofloxacin plus doxycycline Vibrio vulnificus: Surgical assessmenVdebridement and ceftazidime, ceftriaxone, or cefotaxime plus doxycycline Folliculitis Staphylococcus aureus: Usually self-limited; can use topical mupirocin, clindamycin, or retapamulin; systemic antibiotics usually not needed Pseudomonas aeruginosa (i.e., hot tub folliculitis): Usually self-limited; oral ciprofloxacin usually reserved for immunosuppressed host or for persistent or severe infection Furuncle, carbuncle, Mild: lncision and drainage; consider adjunctive oral anti-MRSA antibiotic like trimethoprim-sulfamethoxazole or abscess Moderate: lncision and drainage plus empiric trimethoprim-sulfamethoxazole or doxycycline pending culture and susceptibilities Severe: lncision and drainage plus empiric vancomycin, daptomycin, linezolid, telavancin, or ceftaroline pending culture and susceptibilities M RSA = meth ici I li n-resistant Staphy/ococcus aureus. "lnducible resistance (resistance appearing after exposure to an agent) may be seen with clindamycin level (>t80 mg/dl [10 mmol/L]). ffris tool was developed to rEY POIilT improve diagnostic accuracy; the reported positive and neg o Empiric antibiotic treatment for necrotizing cellulitis ative predictive values are 92"/,, and 96%, respectively. includes broad spectrum coverage for aerobic and Subsequent analysis of the sensitivity of this score has shown anaerobic gram-negative and gram-positive organisms it may not be optimal for ruling out NF, so operative debride- (including methic i llin - resistant Staphy lo cocc us au re us) ment should be pursued in patients with a high index of' such as a carbapenem or piperacillin-tazobactam plus clinical suspicion. vancomycin or daptomycin. Plain radiographs, CT scans, and MRI may demonstrate gas and swelling in soft tissues. Surgical exploration can con firm the diagnosis of NF and should not be delayed when the diagnosis is highly suspected, particularly because early surgi Purulent Skin lnfections cal management can improve mortality. Blood culture(s) Folliculitis results from superflcial inflatnmation or infection obtained before surgery and antibiotic administration or deep of the hair follicle. It typically presents as pruritic perifollicular intraoperative specimen culture can establish the microbio- erythematous papules and pustules on the face, scalp, tmnk, logic cause. and thigh; however, it can appear on any hair bearing area of In confirmed NF, repeated surgical debridement is typi- skin (Figure 7). Risk factors for folliculitis are occlusive dress- cally required. Pending culture results, initial empiric antibi- ings or clothing, increased sweating, obesity, and long-term otic treatment includes broad-spectrum coverage for aerobic topical glucocorticoid use. Folliculitis can be noninfectious and anaerobic gram-negative and gram-positive organisms (HlV-associated eosinophilic folliculitis) or infectious. Tl-re (including MRSA) such as a carbapenem or piperacillin- most frequent cause of infectious folliculitis is S. ou,-eus. tazobactam plus vancomycin or daptomycin. Some experts Other common infectious causes are gram-negative bacteria also recommend adding empiric clindamycin because of its (Kleb s iella or Ente robocte r specie s) fro m prolo nged antibiot ic suppression of toxin production by staphylococci and strepto treatment for acne and Pseudomonas aeruginosa, which is cocci. See Table 6 for treatment of NF caused by S. pyogenes, V. associated with hot tubs (Figure 8). Other infectious causes uulnificus, A. hydrophila, or clostridial species. Antimicrobial are the yeast Malassezia: viral folliculitis from herpes simplex discontinuation can be considered when the patient is afebrile, or varicella zoster; and Demodex folliculitis, which is caused clinically stable, and surgical debridement is no longer by a mite. Folliculitis is typically diagnosed from history and required. clinical presentation. Mild cases of staphylococcal folliculitis

level (>t80 mg/dl [10 mmol/L]). ffris tool was developed to rEY POIilT improve diagnostic accuracy; the reported positive and neg o Empiric antibiotic treatment for necrotizing cellulitis ative predictive values are 92"/,, and 96%, respectively. includes broad spectrum coverage for aerobic and Subsequent analysis of the sensitivity of this score has shown anaerobic gram-negative and gram-positive organisms it may not be optimal for ruling out NF, so operative debride- (including methic i llin - resistant Staphy lo cocc us au re us) ment should be pursued in patients with a high index of' such as a carbapenem or piperacillin-tazobactam plus clinical suspicion. vancomycin or daptomycin. Plain radiographs, CT scans, and MRI may demonstrate gas and swelling in soft tissues. Surgical exploration can con firm the diagnosis of NF and should not be delayed when the diagnosis is highly suspected, particularly because early surgi Purulent Skin lnfections cal management can improve mortality. Blood culture(s) Folliculitis results from superflcial inflatnmation or infection obtained before surgery and antibiotic administration or deep of the hair follicle. It typically presents as pruritic perifollicular intraoperative specimen culture can establish the microbio- erythematous papules and pustules on the face, scalp, tmnk, logic cause. and thigh; however, it can appear on any hair bearing area of In confirmed NF, repeated surgical debridement is typi- skin (Figure 7). Risk factors for folliculitis are occlusive dress- cally required. Pending culture results, initial empiric antibi- ings or clothing, increased sweating, obesity, and long-term otic treatment includes broad-spectrum coverage for aerobic topical glucocorticoid use. Folliculitis can be noninfectious and anaerobic gram-negative and gram-positive organisms (HlV-associated eosinophilic folliculitis) or infectious. Tl-re (including MRSA) such as a carbapenem or piperacillin- most frequent cause of infectious folliculitis is S. ou,-eus. tazobactam plus vancomycin or daptomycin. Some experts Other common infectious causes are gram-negative bacteria also recommend adding empiric clindamycin because of its (Kleb s iella or Ente robocte r specie s) fro m prolo nged antibiot ic suppression of toxin production by staphylococci and strepto treatment for acne and Pseudomonas aeruginosa, which is cocci. See Table 6 for treatment of NF caused by S. pyogenes, V. associated with hot tubs (Figure 8). Other infectious causes uulnificus, A. hydrophila, or clostridial species. Antimicrobial are the yeast Malassezia: viral folliculitis from herpes simplex discontinuation can be considered when the patient is afebrile, or varicella zoster; and Demodex folliculitis, which is caused clinically stable, and surgical debridement is no longer by a mite. Folliculitis is typically diagnosed from history and required. clinical presentation. Mild cases of staphylococcal folliculitis 11

Skin and Soft Tissue lnfections drainage. However, based on recent studies that show improved cure rates, some experts recommend careful consid- eration of adjunctive antibiotics for uncomplicated abscesses rather than incision and drainage alone. For patients with moderate infections who have systemic signs of infection, empiric oral treatment directed against MRSA is recom- mended (see Table 6). Empiric treatment with parenteral ther- apy is also recommended in immunocompromised patients, patients with hypotension and systemic inflammatory response syndrome (severe infection), or patients in whom incision and drainage plus oral antibiotics fail. Treatment is adjusted based on sensitivities from culture of the purulent drainage. If MRSA is the cause of multiple recurrences of purulent tIGURE 7. Pink papules and pustules centered on hairfollicles, characteristic skin infection, decolonization with topical intranasal mupi of folliculitis. rocin, chlorhexidine washes, and decontamination of personal items such as clothes, towels, and sheets should be considered. are usually self-limited, but topical antibiotics can be used (see Other diagnoses such as hidradenitis suppurativa, pilonidal Table 6). Systemic antibiotics, with coverage against S. oureus, cysts, or a foreign body should be considered when no micro may be required for extensive, refractory or recurrent follicu- bial cause is identified. litis. Pseudomonas folliculitis is usually self-limited, although Newer antibiotics for SSTIs caused by MRSA include tedi- oral ciprofloxacin can be used for immunosuppressed persons zolid, delafloxacin, omadacycline, oritavancin, and dalba- or persistent or severe infections. vancin. Use ofthese antibiotics is recommended in consultation Abscesses are erythematous, nodular, localized collec- with infectious disease specialists. tions of pus within the dermis and subcutaneous fat (see IEY POITTS Figure 3). Furuncles (boils) are hair follicle-associated o Primary treatment for abscesses, furuncles, and car- HVC abscesses that extend into the dermis and subcutaneous tis- buncles is incision and drainage; however, some experts sue. These inflammatory nodules are typically seen on the recommend careful consideration of adjunctive antibi- face, neck, and axilla. Infection that extends subcutaneously to otics for mild uncomplicated abscesses based on recent involve several furuncles is known as a carbuncle. This coales- studies that show improved cure rates compared with cence of abscesses can result in systemic signs of infection. incision and drainage alone. Primary treatment for abscesses, furuncles, and carbun- cles is incision and drainage. Gram stain and culture should be . For moderate and severe purulent infections associated obtained from the purulent drainage when antibiotic admin- with systemic symptoms, Gram stain and culture istration is planned. According to the 2014lnfectious Diseases should be performed on the purulent drainage followed Society of America (IDSA) guidelines, mild infections without by empiric oral antibiotic treatment for moderate infec- systemic symptoms do not require antibiotic therapy after tions (trimethoprim-sulfamethoxazole or doxycycline) and empiric intravenous antibiotics for severe infections (vancomycin, daptomycin, linezolid, telavancin, or cef- taroline).

drainage. However, based on recent studies that show improved cure rates, some experts recommend careful consid- eration of adjunctive antibiotics for uncomplicated abscesses rather than incision and drainage alone. For patients with moderate infections who have systemic signs of infection, empiric oral treatment directed against MRSA is recom- mended (see Table 6). Empiric treatment with parenteral ther- apy is also recommended in immunocompromised patients, patients with hypotension and systemic inflammatory response syndrome (severe infection), or patients in whom incision and drainage plus oral antibiotics fail. Treatment is adjusted based on sensitivities from culture of the purulent drainage. If MRSA is the cause of multiple recurrences of purulent tIGURE 7. Pink papules and pustules centered on hairfollicles, characteristic skin infection, decolonization with topical intranasal mupi of folliculitis. rocin, chlorhexidine washes, and decontamination of personal items such as clothes, towels, and sheets should be considered. are usually self-limited, but topical antibiotics can be used (see Other diagnoses such as hidradenitis suppurativa, pilonidal Table 6). Systemic antibiotics, with coverage against S. oureus, cysts, or a foreign body should be considered when no micro may be required for extensive, refractory or recurrent follicu- bial cause is identified. litis. Pseudomonas folliculitis is usually self-limited, although Newer antibiotics for SSTIs caused by MRSA include tedi- oral ciprofloxacin can be used for immunosuppressed persons zolid, delafloxacin, omadacycline, oritavancin, and dalba- or persistent or severe infections. vancin. Use ofthese antibiotics is recommended in consultation Abscesses are erythematous, nodular, localized collec- with infectious disease specialists. tions of pus within the dermis and subcutaneous fat (see IEY POITTS Figure 3). Furuncles (boils) are hair follicle-associated o Primary treatment for abscesses, furuncles, and car- HVC abscesses that extend into the dermis and subcutaneous tis- buncles is incision and drainage; however, some experts sue. These inflammatory nodules are typically seen on the recommend careful consideration of adjunctive antibi- face, neck, and axilla. Infection that extends subcutaneously to otics for mild uncomplicated abscesses based on recent involve several furuncles is known as a carbuncle. This coales- studies that show improved cure rates compared with cence of abscesses can result in systemic signs of infection. incision and drainage alone. Primary treatment for abscesses, furuncles, and carbun- cles is incision and drainage. Gram stain and culture should be . For moderate and severe purulent infections associated obtained from the purulent drainage when antibiotic admin- with systemic symptoms, Gram stain and culture istration is planned. According to the 2014lnfectious Diseases should be performed on the purulent drainage followed Society of America (IDSA) guidelines, mild infections without by empiric oral antibiotic treatment for moderate infec- systemic symptoms do not require antibiotic therapy after tions (trimethoprim-sulfamethoxazole or doxycycline) and empiric intravenous antibiotics for severe infections (vancomycin, daptomycin, linezolid, telavancin, or cef- taroline). Animal Bites Bites from cats and dogs represent approximately I% of emer- gency department visits in the United States; most wounds (about 80%)will not become infected. Cat bites are more likely to become infected because of deeper puncture wounds cre- ated by cats' sharp, slender teeth. The microbiologz of infection depends on the microbiota of the animal's mouth and of the patient's skin. Mixed aerobes and anaerobes, including staphy- lococci, streptococci, Bacteroides species, PorphAromonas species, Fusobacterium species, and Pasteurella species, typi- cally compose the bacteria in bite wounds. Capnocytophaga FIGURE 8. Erythematous papules with flare seen in hot tub folliculitis. The skin conimorsus is a common constituent of canine microbiota and under the bathing suit is characteristically involved. can cause severe infections in patients with asplenia.

Animal Bites Bites from cats and dogs represent approximately I% of emer- gency department visits in the United States; most wounds (about 80%)will not become infected. Cat bites are more likely to become infected because of deeper puncture wounds cre- ated by cats' sharp, slender teeth. The microbiologz of infection depends on the microbiota of the animal's mouth and of the patient's skin. Mixed aerobes and anaerobes, including staphy- lococci, streptococci, Bacteroides species, PorphAromonas species, Fusobacterium species, and Pasteurella species, typi- cally compose the bacteria in bite wounds. Capnocytophaga FIGURE 8. Erythematous papules with flare seen in hot tub folliculitis. The skin conimorsus is a common constituent of canine microbiota and under the bathing suit is characteristically involved. can cause severe infections in patients with asplenia. 12

Skin and Soft Tissue Infections Wound management includes assessment and irrigation l(EY POI tTS (cantinued) with sterile normal saline. Assessment allows for characteriza o Assessment for tetanus and rabies prophylaxis is essen tion of wound extent and dimensions; signs of inflammation tial in patients with animal bite wounds. and infection, including edema, erythema, pain, necrosis, lymphangitis, and pus; and local neurovascular involvement. o Pre-emptive amoxicillin-clavulanate is recommended Surgical evaluation for possible debridement and removal of for patients who are immunosuppressed and for wounds foreign bodies is particularly important with hand bites. with associated edema or lymphatic or venous insuffi- Culture of deep intraoperative tissue and antibiotic suscepti ciency; crush injury; joint or bone involvement; deep bilities of isolated organisms allows for pathogen directed punctures; or moderate to severe injuries, especial$ therapy. Radiographs may demonstrate fracture, other bony involving the face, genitalia, or hand. involvement, or foreign bodies. Assessment for tetanus and rabies prophylaxis is essential. With the exception of facial wounds, primary wound closure is not generally pursued. Human Bites The severity of the wound and the immune status of the Intentional biting of others, self-inflicted wounds such as tl-rose patient are deciding factors for beginning early antibiotic occurring from fingernail biting, and clenched-fist injuries prophylaxis without clinical signs of infection. Because of its after a punch to another person's mouth are the most common activity against pathogens associated with animal bite wounds, causes of human bite wounds. These wounds are at risk fbr a 3 to 5 day course of amoxicillin clavulanate is recorn- inf'ection with human skin and mouth organisn-rs. Tl-rese mended for patients who are immunosuppressed, including organisms comprise aerobic organisms, including staphylo- patients with cirrhosis and asplenia. Pre-emptive antibiotic cocci, streptococci, and Eikenella corrodens, and anaerobic therapy is also recommended for wounds with associated organisms, including Peptostreptococcus, Fusobacteri u nr. and edema or lymphatic or venous insufficienCy; crush injury; Preuotellaspecies. Short-course (3-S days) prophylactic antibi- joint or bone involvement; deep punctures; or moderate to otic therapy with amoxicillin-clavulanate is recommended for severe injuries, especially involving the face, genitalia, or hand. human bites that perfbrate the skin. The management of If a patient is allergic to penicillin. a combination of trimetho- infected wounds is similar to that fbr animal bites, including prim sulfamethoxazole, or a fluoroquinolone, or doxycycline empiric MRSA coverage in patients at increased risk for MRSA plus clindamycin or metronidazole can be used. infection. Hand involvement warrants surgical e'valuation. In For clinically infected bite wounds, antibiotics are rec- addition to tetanus prophylaxis assessment, evaluation fbr ommended after tissue wound cultures (and blood cultures, if potential exposure to hepatitis B and C viruses, I.llV and other systemic signs of infection are present) are obtained. For out- bodily fluid transmitted pathogens is warranted. patient management of mildly infected wounds, oral antibiot KEY POIilTS ics are recommended. The duration of antibiotic therapy is o Short-course prophylactic antibiotic therapy with usually less than 2 weeks unless bone or joint involvement dictates a more prolonged course. Intravenous therapy is indi- amoxicillin clavulanate is recommended for human bites that perforate the skin. cated for severe infections with systemic involvement, includ- ing sepsis; severe injuries, particularly those associated with . In addition to assessment fbr tetanus prophylaxis, evalu- tendon, nerve, vascular, or crush injuries; and hand infec ation of human bites for potential exposure to hepatitis tions. Intravenous antibiotic options include B-lactam/B- B and C viruses, HIV and other bodily fluid-transmitted

Wound management includes assessment and irrigation l(EY POI tTS (cantinued) with sterile normal saline. Assessment allows for characteriza o Assessment for tetanus and rabies prophylaxis is essen tion of wound extent and dimensions; signs of inflammation tial in patients with animal bite wounds. and infection, including edema, erythema, pain, necrosis, lymphangitis, and pus; and local neurovascular involvement. o Pre-emptive amoxicillin-clavulanate is recommended Surgical evaluation for possible debridement and removal of for patients who are immunosuppressed and for wounds foreign bodies is particularly important with hand bites. with associated edema or lymphatic or venous insuffi- Culture of deep intraoperative tissue and antibiotic suscepti ciency; crush injury; joint or bone involvement; deep bilities of isolated organisms allows for pathogen directed punctures; or moderate to severe injuries, especial$ therapy. Radiographs may demonstrate fracture, other bony involving the face, genitalia, or hand. involvement, or foreign bodies. Assessment for tetanus and rabies prophylaxis is essential. With the exception of facial wounds, primary wound closure is not generally pursued. Human Bites The severity of the wound and the immune status of the Intentional biting of others, self-inflicted wounds such as tl-rose patient are deciding factors for beginning early antibiotic occurring from fingernail biting, and clenched-fist injuries prophylaxis without clinical signs of infection. Because of its after a punch to another person's mouth are the most common activity against pathogens associated with animal bite wounds, causes of human bite wounds. These wounds are at risk fbr a 3 to 5 day course of amoxicillin clavulanate is recorn- inf'ection with human skin and mouth organisn-rs. Tl-rese mended for patients who are immunosuppressed, including organisms comprise aerobic organisms, including staphylo- patients with cirrhosis and asplenia. Pre-emptive antibiotic cocci, streptococci, and Eikenella corrodens, and anaerobic therapy is also recommended for wounds with associated organisms, including Peptostreptococcus, Fusobacteri u nr. and edema or lymphatic or venous insufficienCy; crush injury; Preuotellaspecies. Short-course (3-S days) prophylactic antibi- joint or bone involvement; deep punctures; or moderate to otic therapy with amoxicillin-clavulanate is recommended for severe injuries, especially involving the face, genitalia, or hand. human bites that perfbrate the skin. The management of If a patient is allergic to penicillin. a combination of trimetho- infected wounds is similar to that fbr animal bites, including prim sulfamethoxazole, or a fluoroquinolone, or doxycycline empiric MRSA coverage in patients at increased risk for MRSA plus clindamycin or metronidazole can be used. infection. Hand involvement warrants surgical e'valuation. In For clinically infected bite wounds, antibiotics are rec- addition to tetanus prophylaxis assessment, evaluation fbr ommended after tissue wound cultures (and blood cultures, if potential exposure to hepatitis B and C viruses, I.llV and other systemic signs of infection are present) are obtained. For out- bodily fluid transmitted pathogens is warranted. patient management of mildly infected wounds, oral antibiot KEY POIilTS ics are recommended. The duration of antibiotic therapy is o Short-course prophylactic antibiotic therapy with usually less than 2 weeks unless bone or joint involvement dictates a more prolonged course. Intravenous therapy is indi- amoxicillin clavulanate is recommended for human bites that perforate the skin. cated for severe infections with systemic involvement, includ- ing sepsis; severe injuries, particularly those associated with . In addition to assessment fbr tetanus prophylaxis, evalu- tendon, nerve, vascular, or crush injuries; and hand infec ation of human bites for potential exposure to hepatitis tions. Intravenous antibiotic options include B-lactam/B- B and C viruses, HIV and other bodily fluid-transmitted lactamase inhibitor combinations (ampicillin sulbactam, pathogens is warranted. piperacillin tazobactam), carbapenems (imipenem, merope- nem, ertapenem), or ceftriaxone or a fluoroquinolone plus clindamycin or metronidazole. Empiric MRSA coverage can Diabetic Foot I nfestions be included in patients with severe infections or risk factors Foot inf'ections typically result after trauma in persons n,ith for MRSA infection (nasal colonization, recent hospitaliza- diabetes who have vasculopathy, neuropathy, suboptimal tion, recent antibiotic use, hemodialysis, injection drug use, glucose control, and immunologic deficits. Additional risk close contact with MRSA infection, incarceration, previous factors fbr inf'ection include presence of an ulcer fbr greater MRSA inf.ection, HIV contact sport participation) until its than 1 month, recurrent ulcers, lower extremity amputa- presence is excluded. Surgical consultation is usually tion, kidney function impairment, walking barefo<.rt. aud a obtained. positive probe-to-bone test in the wound. Inf.ection is diag nosed when pus or two or more inflammatory sigtrs I(EY POITTS (warmth, induration, erythema, pain, and tenderness) are o Bite wound management includes irrigation with sterile present. normal saline; except for facial wounds, primary closure Following debridement of overlying callous or necrotic is not generally pursued. tissue as necessary, infections should be classified according to (Continued) severity and extent. Mild infections involve only skin and

lactamase inhibitor combinations (ampicillin sulbactam, pathogens is warranted. piperacillin tazobactam), carbapenems (imipenem, merope- nem, ertapenem), or ceftriaxone or a fluoroquinolone plus clindamycin or metronidazole. Empiric MRSA coverage can Diabetic Foot I nfestions be included in patients with severe infections or risk factors Foot inf'ections typically result after trauma in persons n,ith for MRSA infection (nasal colonization, recent hospitaliza- diabetes who have vasculopathy, neuropathy, suboptimal tion, recent antibiotic use, hemodialysis, injection drug use, glucose control, and immunologic deficits. Additional risk close contact with MRSA infection, incarceration, previous factors fbr inf'ection include presence of an ulcer fbr greater MRSA inf.ection, HIV contact sport participation) until its than 1 month, recurrent ulcers, lower extremity amputa- presence is excluded. Surgical consultation is usually tion, kidney function impairment, walking barefo<.rt. aud a obtained. positive probe-to-bone test in the wound. Inf.ection is diag nosed when pus or two or more inflammatory sigtrs I(EY POITTS (warmth, induration, erythema, pain, and tenderness) are o Bite wound management includes irrigation with sterile present. normal saline; except for facial wounds, primary closure Following debridement of overlying callous or necrotic is not generally pursued. tissue as necessary, infections should be classified according to (Continued) severity and extent. Mild infections involve only skin and 13

Community-Acquired Pneumonia subcutaneous tissue with erythema confined to 2 cm beyond XtY POlt{TS (confinuedl the ulcer. Moderate infections extend deeper than subcutane- o Deep-tissue culture (curettage or biopsy) is indicated ous tissue (e.g., abscess, fasciitis, and osteomyelitis), or the before antibiotic therapy for moderate or severe diabetic erythen,a is more extensive. Severe infections are associated foot infections and complicated mild infections (presence with systemic signs such as fever, tachycardia, tachypnea,leu- of pus or MRSA risk factors). kocytosis, and hypotension or metabolic complications such o Plain imaging is recommended for all patients with new as acidosis, worsening kidney function, and hyperglycemia. The affected foot or limb should also be assessed for arterial diabetic foot infections; additional imaging with ultra ischemia, venous insuffi ciency, neuropathy, and biomechani- sonography or MRI is recommended when abscess or cal abnormalities such as Charcot arthropathy or hammer toe. bone involvement is suspected. Evidence of critical ischemia can be considered a proxy for severe infection. Uninfected wounds should not be cultured or treated Toxic Shock Syndrome with antibiotics. Mild infections are typically caused by aero- S. oureus- and S. pAogenes-associated exotoxins result in bic staphylococci (non-MRSA) and streptococci and can be cytokine production that can result in toxic shock syndrome empirically treated with a short course (Z t+ days) of oral (TSS) (Table 7). Staphylococcal TSS is associated with tampon antibiotics, such as cephalexin, clindamycin, amoxicillin- use, nasal packings, surgical wounds, skin ulcers, burns, cath clavulanate, or dicloxacillin. For mild infections with pus or eters, and injection drug use. Streptococcal TSS is associated MRSA risk factors, wound cultures should be obtained by with skin and soft tissue infection, particularly NFl. Bacteremia curettage or biopsy of deep tissue before initiating antibiotics. and mortality rates are higher with streptococcal than staphy- Doxycycline or trimethoprim sulfamethoxazole can also be lococcal TSS. Source control typically requires surgical used with a B-lactam antibiotic. For moderate and severe debridement. Antibiotics for streptococcal TSS consist of peni- infections, polymicrobial coverage of staphylococci (including cillin plus clindamycin, the latter added to eradicate the high MRSA), streptococci, aerobic gram-negative bacilli, and anaer- inoculum of bacteria present and to suppress toxin produc- obes is recommended. Following deep-tissue culture, initial tion. If methicillin-susceptible S. oureus is the cause, nafcillin antibiotic regimens include B-lactam/p-lactamase inhibitor or oxacillin and clindamycin are recommended; for MRSA, combinations, carbapenems, or metronidazole plus a fluoro- vancomycin and clindamycin are recommended (for intoler- quinolone or third-generation cephalosporin in addition to ance to vancomycin, daptomycin or ceftaroline may be used). an anti-MRSA agent (vancomycin, daptomycin, linezolid). Linezolid can be used if clindamycin resistance is present. Antibiotic choices are guided by culture results. Moderate to Although the2Ol4lDSA guidelines do not recommend routine severe infections are usually treated with a longer course of adjunctive intravenous immune globulin use in TSS, some antibiotics (Z-+ weeks); if osteomyelitis is present, approxi- experts favor its administration in streptococcal TSS based on mately 6 weeks of antibiotic therapy is administered after reported mortality benefits. surgical debridement. A positive probe-to-bone test in a diabetic foot wound rEY POIl{TS is associated with increased risk for osteomyelitis. Surgical o Source control for toxic shock syndrome typically consultation can evaluate the need for debridement, resec- requires surgical debridement. tion, amputation, or revascularization. Plain imaging is rec- o Streptococcal toxic shock syndrome is treated with ommended for all patients with new foot infections to assess penicillin and clindamycin. for soft tissue gas, foreign body, and bony involvement; additional imaging with ultrasonography (for abscess) or o Infection with methicillin-susceptible Staphylococcus MRI (for bone involvement) is recommended when clinically aureus is treated with nafcillin or oxacillin and clinda- indicated. CT with intravenous contrast or a labeled leuko- mycin; vancomycin plus clindamycin is preferred for cyte scan combined with a radionuclide bone scan can be infection with methicillin-resistant S. aureus. considered when MRI is not possible. Wound care, glycemic control, and off-loading areas of biomechanical stress are essential. Community-Acquired I( EV PO I T{TS

subcutaneous tissue with erythema confined to 2 cm beyond XtY POlt{TS (confinuedl the ulcer. Moderate infections extend deeper than subcutane- o Deep-tissue culture (curettage or biopsy) is indicated ous tissue (e.g., abscess, fasciitis, and osteomyelitis), or the before antibiotic therapy for moderate or severe diabetic erythen,a is more extensive. Severe infections are associated foot infections and complicated mild infections (presence with systemic signs such as fever, tachycardia, tachypnea,leu- of pus or MRSA risk factors). kocytosis, and hypotension or metabolic complications such o Plain imaging is recommended for all patients with new as acidosis, worsening kidney function, and hyperglycemia. The affected foot or limb should also be assessed for arterial diabetic foot infections; additional imaging with ultra ischemia, venous insuffi ciency, neuropathy, and biomechani- sonography or MRI is recommended when abscess or cal abnormalities such as Charcot arthropathy or hammer toe. bone involvement is suspected. Evidence of critical ischemia can be considered a proxy for severe infection. Uninfected wounds should not be cultured or treated Toxic Shock Syndrome with antibiotics. Mild infections are typically caused by aero- S. oureus- and S. pAogenes-associated exotoxins result in bic staphylococci (non-MRSA) and streptococci and can be cytokine production that can result in toxic shock syndrome empirically treated with a short course (Z t+ days) of oral (TSS) (Table 7). Staphylococcal TSS is associated with tampon antibiotics, such as cephalexin, clindamycin, amoxicillin- use, nasal packings, surgical wounds, skin ulcers, burns, cath clavulanate, or dicloxacillin. For mild infections with pus or eters, and injection drug use. Streptococcal TSS is associated MRSA risk factors, wound cultures should be obtained by with skin and soft tissue infection, particularly NFl. Bacteremia curettage or biopsy of deep tissue before initiating antibiotics. and mortality rates are higher with streptococcal than staphy- Doxycycline or trimethoprim sulfamethoxazole can also be lococcal TSS. Source control typically requires surgical used with a B-lactam antibiotic. For moderate and severe debridement. Antibiotics for streptococcal TSS consist of peni- infections, polymicrobial coverage of staphylococci (including cillin plus clindamycin, the latter added to eradicate the high MRSA), streptococci, aerobic gram-negative bacilli, and anaer- inoculum of bacteria present and to suppress toxin produc- obes is recommended. Following deep-tissue culture, initial tion. If methicillin-susceptible S. oureus is the cause, nafcillin antibiotic regimens include B-lactam/p-lactamase inhibitor or oxacillin and clindamycin are recommended; for MRSA, combinations, carbapenems, or metronidazole plus a fluoro- vancomycin and clindamycin are recommended (for intoler- quinolone or third-generation cephalosporin in addition to ance to vancomycin, daptomycin or ceftaroline may be used). an anti-MRSA agent (vancomycin, daptomycin, linezolid). Linezolid can be used if clindamycin resistance is present. Antibiotic choices are guided by culture results. Moderate to Although the2Ol4lDSA guidelines do not recommend routine severe infections are usually treated with a longer course of adjunctive intravenous immune globulin use in TSS, some antibiotics (Z-+ weeks); if osteomyelitis is present, approxi- experts favor its administration in streptococcal TSS based on mately 6 weeks of antibiotic therapy is administered after reported mortality benefits. surgical debridement. A positive probe-to-bone test in a diabetic foot wound rEY POIl{TS is associated with increased risk for osteomyelitis. Surgical o Source control for toxic shock syndrome typically consultation can evaluate the need for debridement, resec- requires surgical debridement. tion, amputation, or revascularization. Plain imaging is rec- o Streptococcal toxic shock syndrome is treated with ommended for all patients with new foot infections to assess penicillin and clindamycin. for soft tissue gas, foreign body, and bony involvement; additional imaging with ultrasonography (for abscess) or o Infection with methicillin-susceptible Staphylococcus MRI (for bone involvement) is recommended when clinically aureus is treated with nafcillin or oxacillin and clinda- indicated. CT with intravenous contrast or a labeled leuko- mycin; vancomycin plus clindamycin is preferred for cyte scan combined with a radionuclide bone scan can be infection with methicillin-resistant S. aureus. considered when MRI is not possible. Wound care, glycemic control, and off-loading areas of biomechanical stress are essential. Community-Acquired I( EV PO I T{TS o Diabetic foot infection is diagnosed when pus or two or Pneumonia more inflammatory signs (warmth, induration, er5rthema, Epidemiology pain, and tenderness) are present. Community-acquired pneumonia (CAP) is a leading cause of HVC . Uninfected diabetic foot wounds should not be cultured infection and hospitalization in the United States. The spec- or treated with antibiotics. trum of illness due to CAP ranges from mild disease, with (Continued) approximately 50"1, of patients managed in the ambulatory

o Diabetic foot infection is diagnosed when pus or two or Pneumonia more inflammatory signs (warmth, induration, er5rthema, Epidemiology pain, and tenderness) are present. Community-acquired pneumonia (CAP) is a leading cause of HVC . Uninfected diabetic foot wounds should not be cultured infection and hospitalization in the United States. The spec- or treated with antibiotics. trum of illness due to CAP ranges from mild disease, with (Continued) approximately 50"1, of patients managed in the ambulatory 14

I I I I t Community-Acquired Pneumonia I I I TABLE 7. Diagnostic Criteria for Toxic Shock Syndrome I \ i I I Staphylococcal TSS" Streptococcal TSSb I I Fever >38.9 'C (102.0 "F) Definite case i I I i lsolation of GABHS from a sterile site (blood, cerebrospinal I i fluid, operative wound) I I Systolic blood pressure <90 mm Hg Probable case I lsolation of GABHS from a nonsterile site (throat, vagina, skin lesion) I I Diffuse macular rash with subsequent desquamation, especially Hypotension (systolic pressure <90 mm Hg) I i on palms and soles I I lnvolvement of three or more of the following organ systems: The presen ce of >2 of the following findings: I I i Gastroi ntesti nal ( nausea, vomitin g, d ia rrhea) Kidney (acute kidney injury or failure) i Muscular (severe myalgia or fivefold or greater increase in Liver (el evated a m i n otra nsfe rase conce ntrati o n s ) t I serum creatine kinase level) i Skin (erythematous macular rash, soft tissue necrosis) i Mucous membrane (hyperemia of the vagina, conjunctivae, or i

\ i I I Staphylococcal TSS" Streptococcal TSSb I I Fever >38.9 'C (102.0 "F) Definite case i I I i lsolation of GABHS from a sterile site (blood, cerebrospinal I i fluid, operative wound) I I Systolic blood pressure <90 mm Hg Probable case I lsolation of GABHS from a nonsterile site (throat, vagina, skin lesion) I I Diffuse macular rash with subsequent desquamation, especially Hypotension (systolic pressure <90 mm Hg) I i on palms and soles I I lnvolvement of three or more of the following organ systems: The presen ce of >2 of the following findings: I I i Gastroi ntesti nal ( nausea, vomitin g, d ia rrhea) Kidney (acute kidney injury or failure) i Muscular (severe myalgia or fivefold or greater increase in Liver (el evated a m i n otra nsfe rase conce ntrati o n s ) t I serum creatine kinase level) i Skin (erythematous macular rash, soft tissue necrosis) i Mucous membrane (hyperemia of the vagina, conjunctivae, or i I pharynx) Blood (coag u lopathy, incl ud i ng th rombocytopen ia and ; disseminated intravascular coagu lation) Kidney (blood urea nitrogen or serum creatinine level at least Pu lmonary (acute respi ratory d istress synd rome) , twice the upper limit of normal) Liver ( bil i ru bi n, aspa rtate ami notra nsferase, or a lani ne I

I pharynx) Blood (coag u lopathy, incl ud i ng th rombocytopen ia and ; disseminated intravascular coagu lation) Kidney (blood urea nitrogen or serum creatinine level at least Pu lmonary (acute respi ratory d istress synd rome) , twice the upper limit of normal) Liver ( bil i ru bi n, aspa rtate ami notra nsferase, or a lani ne I I aminotransferase concentration twice the upper limit of normal) Blood (platelet count <1 00,000/pL [1 00 x 1 Oell]) Central nervous system (disorientation without focal neurologic signs) Negative results on serologic testing for Rocky Mountain spotted fever, leptospirosis, and measles; negative blood or cerebrospinal fluid cultures for organisms other than Staphylococcus aureus GABHS = group A B-hemolytic streptococci; TSS = toxic shock syndrome. "Diagnosis is considered confirmed when fever, hypotension, and rash with involvement of three or more organ systems listed and negative serologic and cerebrospinal fluid results listed are all present. bA definite case is defined by the isolation of GABHS from a sterile site; hypotension with systolic blood pressure <90 mm Hg; plus the presence of two or more of the clinical findings listed. Reprinted with permission from Oue YA, Moreillon P. Staphylococcus aureus. ln: Bennett JE, Dolin R, Blaser MJ, eds. Principles and practice of infectious disease. Bth ed. Philadelphia, PA: Elsevier Saunders; 2015:2250. Copyright 2015, Elsevier.

bA definite case is defined by the isolation of GABHS from a sterile site; hypotension with systolic blood pressure <90 mm Hg; plus the presence of two or more of the clinical findings listed. Reprinted with permission from Oue YA, Moreillon P. Staphylococcus aureus. ln: Bennett JE, Dolin R, Blaser MJ, eds. Principles and practice of infectious disease. Bth ed. Philadelphia, PA: Elsevier Saunders; 2015:2250. Copyright 2015, Elsevier. setting, to fatal infections. Rates of infection, hospitalization, specific pathogens are listed in Table 8. Severity of illness, and death increase with advanced age; the incidence of hospi- which influences site of care, is used to guide empiric antibi- talization for CAP among adults 80 years or older is 25 times otic therapy (Table 9). higher than in adults younger than 50 years. Streptococcus pneumoniae, the leading bacterial cause of Health care-associated pneumonia (HCAP), previously CAB has decreased in incidence and accounts for only 5% to 15% considered a distinct entity, has been recategorized as CAP of hospitalized cases in recent studies. This at least partially after studies confirmed that patients residing in long-term results from the success of vaccination strategies. Rates of CAP care facilities or who were hospitalized in the preceding caused by Staphylococcus eureus (including methicillin resist- 3 months do not differ substantially from community- ant strains), Pseudomonas aeruginose, and Enterobacteriaceae, dwelling patients with similar comorbidities. In contrast, hos- however, are rising, even among patients without identifiable pital-acquired pneumonia (HAP) remains a distinct syndrome, health care exposure. The CDC-EPIC trial, a multicenter study with unique microbiologr, antibiotic treatments, and outcomes that performed prospective microbiologic and molecular testing (see Health Care-Associated Infections for HAP discussion). on patients hospitalized with CAB more frequently identified a viral rather than a bacterial pathogen in this population (Figure 9, on page 18). S. pneumonioe was the most common Microbiology bacterial cause, although rhinovirus (97,) and influenza virus CAP is usually caused by infection with a viral or bacterial (O%) were higher in incidence. The significance of viral detec- pathogen; fungal or mycobacterial infections occur much less tion in CAP is unclear; an antecedent mild upper respiratory frequently. The probability of infection with a specific organ- viral infection may increase the risk for a secondary bacterial ism varies based on age, comorbidities, seasonality, and geog- pneumonia. This phenomenon is well documented for post raphy. Epidemiologic risk factors or conditions associated with influenza CAP caused by S. oureus, S. pneumoniae, and

setting, to fatal infections. Rates of infection, hospitalization, specific pathogens are listed in Table 8. Severity of illness, and death increase with advanced age; the incidence of hospi- which influences site of care, is used to guide empiric antibi- talization for CAP among adults 80 years or older is 25 times otic therapy (Table 9). higher than in adults younger than 50 years. Streptococcus pneumoniae, the leading bacterial cause of Health care-associated pneumonia (HCAP), previously CAB has decreased in incidence and accounts for only 5% to 15% considered a distinct entity, has been recategorized as CAP of hospitalized cases in recent studies. This at least partially after studies confirmed that patients residing in long-term results from the success of vaccination strategies. Rates of CAP care facilities or who were hospitalized in the preceding caused by Staphylococcus eureus (including methicillin resist- 3 months do not differ substantially from community- ant strains), Pseudomonas aeruginose, and Enterobacteriaceae, dwelling patients with similar comorbidities. In contrast, hos- however, are rising, even among patients without identifiable pital-acquired pneumonia (HAP) remains a distinct syndrome, health care exposure. The CDC-EPIC trial, a multicenter study with unique microbiologr, antibiotic treatments, and outcomes that performed prospective microbiologic and molecular testing (see Health Care-Associated Infections for HAP discussion). on patients hospitalized with CAB more frequently identified a viral rather than a bacterial pathogen in this population (Figure 9, on page 18). S. pneumonioe was the most common Microbiology bacterial cause, although rhinovirus (97,) and influenza virus CAP is usually caused by infection with a viral or bacterial (O%) were higher in incidence. The significance of viral detec- pathogen; fungal or mycobacterial infections occur much less tion in CAP is unclear; an antecedent mild upper respiratory frequently. The probability of infection with a specific organ- viral infection may increase the risk for a secondary bacterial ism varies based on age, comorbidities, seasonality, and geog- pneumonia. This phenomenon is well documented for post raphy. Epidemiologic risk factors or conditions associated with influenza CAP caused by S. oureus, S. pneumoniae, and 15