Presentation on theme: "MANAGEMENT OF SKIN AND SOFT TISSUE INFECTIONS Jose A. Vazquez, M.D. Senior Staff Division of Infectious Disease Henry Ford Hospital Professor of Medicine."— Presentation transcript:
MANAGEMENT OF SKIN AND SOFT TISSUE INFECTIONS Jose A. Vazquez, M.D. Senior Staff Division of Infectious Disease Henry Ford Hospital Professor of Medicine Wayne State University
Skin and Soft Tissue Infections General Considerations n Primary vs. Secondary infections n Portal of entry n Status of host defenses n Associated manifestations u Toxicity, severity of illness n Localization and morphology of lesions n Environmental exposure
PRIMARY PYODERMAS u u Impetigo u u Bullous impetigo u u Staphylococcal Scalded Skin Syndrome u u Folliculitis u u Furuncles and Carbuncles u u Erysipelas u u Cellulitis
PRIMARY PYODERMAS Impetigo >90% due to group A Streptococcus u u Most occur in children u u <10% mixture of Staph with Strep u u Manifestations - small vesicles with erythematous halo - pustulates - ruptures - characteristic golden-yellow thick stuck-on crusts - painless - minimal constitutional symptoms
PRIMARY PYODERMAS Impetigo Therapy u u Penicillin still drug of choice u u Alternatives: -1st generation cephalosporin (Duricef, Keflex) -If Pen allergic: Erythromycin or Azithromycin u u Local wound care wet-to-dry dressings u u Topical antimicrobials far inferior
PRIMARY PYODERMAS Bullous Impetigo u u Primarily in kids u u Due to Staphylococcus group II (Type 71) u u Manifestations: - Begin as vesicles that turn into bullae - Bullae rupture and leave moist red surface - No Nikolsky sign - Finally form a thin “varnish”-like” light brown crust u u Therapy - Dicloxacillin - 1st generation ceph - Erythromycin or Azithromycin
PRIMARY PYODERMAS Erysipelas u u A superficial cellulitis of the skin with prominent lymphatic involvement u u Generally due to group A Strep (rarely group C or G) u u Most common in: - infants - young kids - older adults - immunocompromised (diabetics, alcoholic, nephrotic syndrome, venous statsis, paraparesis) u u Portal of entry - skin ulcers, local trauma, abrasions, primary dermatologic conditions, Tineas
PRIMARY PYODERMAS Erysipelas - Manifestations u u 70-80% of lesions are on the lower extremity 5-20% are on the fact u u A painful lesion with a bright red edematous indurated appearance and an advancing raised border-sharply demarcated u u Fever u u Bacteremia ~ 5% u u Occasional spread to deeper structures u u Leukocytosis very common
PRIMARY PYODERMAS Erysipelas - Manifestations u u Penicillin oral vs parenteral u u Alternatives - 1st generation ceph. - Erythromycin or Azithromycin
PRIMARY PYODERMAS Cellulitis u u Acute spreading infection of the skin extending into the subcutaneous tissue u u Etiology: - Staph and Strep most common - Erysipeloid- E. rhusiopathiae - salt water fish, poultry - Anthrax - Bacillus - raw wool - Pseudomonas - spas, heel tennis shoe puncture wounds - Aeromonas - lesions in water - Sporotrichosis - Blastomycosis
PRIMARY PYODERMAS Cellulitis u u Generally due to: - Previous trauma - Underlying skin condition u u Skin lesion: borders are not sharply demarcated with erythema, tenderness, warmth, edema u u Fever - malaise - chills u u Regional adenopathy u u Bacteremia ~ 20%
PRIMARY PYODERMAS Cellulitis u u If strong suspicion of etiologic agent treat with specific antimicrobial. u u If etiologic agent unknown: - No underlying risk factors 1st generation ceph (cover Staph and Strep) Alternative: if Pen allergic - Erythromycin or Azithromycin (Zithromax)
Staphylococcus aureus u Frequent cause of cellulitis, especially in diabetic patients u 2 nd – 3 rd most common cause of BSIs in hospitalized patients. u Etiology: > 80 % line infections: u Susceptibility has evolved dramatically over the past few year
What about resistant S. aureus ??
Resistance in S. aureus u HA-MRSA u CA-MRSA u VISA or GISA F MIC 8-16 to vancomycin u VRSA F MIC > 32 to vancomycin u HR-SA F MIC < 4 (susceptible) to vancomycin F subpopulations that are VISA Cosgrove SE. et al CID;39:
Community-Associated MRSA u Prevalence ~ 36 % u Risk Factors: F Recent hospitalization F Recent antimicrobials F Surgery F Exposure to MRSA colonized person F Athletes (wrestlers, football players) F Chronic illness F Nursing home, jails, IVDU Eguia JM, Chambers HF. Hosp Epidemiol 5:2003
Community-Associated MRSA u Most common infections are SSTI and Resp. tract u Many remain susceptible to: clindamycin (89 v 21%); genta (94 v 80%);rifampin (96 v94%); TCN (92%); Bactrim (95v90%) u ~ 60 % probably originate from hospitals or long-term care facilities u Risk Factors: F Recent hospitalization`OR 0-6 months months months months2.2 F Nursing home2.1 Charlebois ED. Et al. CID 2004;39:47-54: Naimi TS. Et al. JAMA;290:
Community-Associated MRSA Management u Outpatient F Mild Infection Clindamycin 450mg q8 hrsClindamycin 450mg q8 hrs Doxycycline 100mg BIDDoxycycline 100mg BID Bactrim DS 2 tabs po BIDBactrim DS 2 tabs po BID F Moderate to severe Zyvox 600mg BIDZyvox 600mg BID u Inpatient F Vancomycin 15mg/kg q12 hrs F Zyvox (linezolid) 600mg IV/PO BID F Daptomycin (Cubicin) 4mg/kg Charlebois ED. Et al. CID 2004;39:47-54
Management of Gram Positives n MSSA u Nafcillin 2 gm q4 h u Cefazolin (ancef) 2gm q 8 h IV u PCN allergy (vanco or linezolid) IV u Linezolid oral n MRSA u Vancomycin u Linezolid u Daptomycin
VRSA – Its All About Sex Michigan Case 1 Michigan Case 1 n Gangrenous foot – VRE, MRSA, multiple courses of vanco n VRE + MRSA = VRSA ( van A ) PA Case 2 n Foot ulcer, VRE in the past. Allergic to Vanco n MRSA 1:132 ( van A)
Vancomycin-Resistant Staphylococcus aureus n The isolate was resistant to: – Oxacillin (MIC>16 μ g/mL) – Vancomycin (MIC>128 μ g/mL) n The isolate contained: – The oxacillin resistance gene mecA – The vanA vancomycin resistance gene from enterococci MIC = minimal inhibitory concentration. CDC. MMWR. 2002;51: June 2002: First case of vancomycin-resistant S aureus (VRSA) isolated from a swab obtained from a catheter exit site.
SECONDARY PYODERMAS u u Bite wounds u u Infections of burns, wounds, or underlying dematitis u u Diabetic wound infections u u Decubitus ulcers u u Surgical wound infections
BITE WOUNDS AND INFECTIONS u u ANIMAL - Dog - Cat - Snake ~ 8,000/year - few get infected - venom is sterile - Exotic animals - monkey tend to be the most serious - organisms will reflect habitat of animals u u HUMAN - Occlusional bites - Clenched-fist injuries
CAT BITES Epidemiology u u ~ 400,000/year u u Primarily in women u u Infection rates > 50%/bite - Teeth slender, sharp, closer together - High colony counts - Teeth penetrate into bones, capsules, and bones easier
CAT BITES MICROBIOLOGY u u Pasturella multocida isolated > 50% of bites u u Otherwise same isolates as dog u u Rochalimea spp. - R. hensenulae May cause Cat Scratch Disease May produce disseminated disease in immunocompromised host Tx. Erythromycin
BITE WOUNDS AND INFECTIONS Dog Bites u u ~ 80% of all animal bites u u ~ 15-20% become infected u u Generally a polymicrobial infection u u Role of prophylactic antimicrobial therapy ??? - No good prospective studies u u Probably prudent to provide antimicrobial coverage for at least 3-5 days after the bite
DOG BITES Microbiology u u Gram positive cocci - alpha hemolytic streptococci ~ 30% - S. aureus ~ 15% - S. intermedium ~ 27% - generally in dogs < 40 lbs. - Beta-hemolytic streptococci - Enterococci - Micrococcus
DOG BITES Microbiology u u Gram negative rods - Haemophilus - Proteus - E. coli - Enterobacter cloacae
HUMAN BITES/CLENCHED FIST INJURIES Epidemiology u u Like monkey bites, generally more serious and more prone to develop infection and complications than are animal bites u u Most tend to occur during fights u u ~ 20% of injuries are “love nips” and are related to sexual activity
HUMAN BITES/CLENCHED-FIST INJURIES u u Unfortunately most patients tend to wait until the infection has set in before seeking medical attention u u Generally results in cellulitis u u Frequently however, it produces: - deep-space infection - septic arthritis - osteomyelitis u u ~ 20% of injuries require amputation if no antibiotic is provided
HUMAN BITES Microbiology u u ~ 55% are mixed polymicrobial infections with anaerobes u u E. corrodens ~ 25% u u S. aureus u u Streptococci u u Hemophilus influenzae
BITE WOUND AND INFECTION MANAGEMENT u u Tetanus immunization u u Rabies vaccintion/Rabies immune globulin - if indicated u u Incision/Drainage/Debridement - if indicated u u Gram stain and culture of all material u u Elevation of injured area - frequent cause of failure u u Follow-up - preferably within hours
BITE WOUNDS AND INFECTIONS Antimicrobial Therapy - Outpatient u u Amoxicillin-clavulanate (Augmentin) mg TID oral u u Doxycycline 100 mg BID oral u u Tetracycline 500 mg QID oral
BITE WOUNDS AND INFECTIONS Antimicrobial Therapy - Inpatient u u Ampicillin-sulbactam (Unasyn) 3.0 gm IVPB Q 6 hrs. u u Cefoxitin or cefotetan 2 gm Q 8-12 hrs. IVPB (No enterococcal coverage) u u Imipenem/cilastin (Primaxin) mg IVPB QID u u Piperacillin/tazobactam (Zosyn) 3.75 gm Q 8 hrs.
Building a better mouse trap ?
Zyvox (Linezolid) n 1 st oxazolidinone – inhibits protein synthesis at the initiation of 50S ribosome n Spectrum: gram positive pathogens: u Staph aureus (MSSA or MRSA) u Enterococcus F E. fecalis or E. faecium and VRE u Streptococcus Group A u S. pneumonia including (PCN-Resistant SP) u Nocardia spp.
Zyvox (Linezolid) n Dose : 600mg BID n Oral and IV n Bioavailability ~ 100% n Metabolism: u ~ 65 % non-renal n AE: diarrhea ~ 8-10 % thrombocytopenia ~ 2.5% thrombocytopenia ~ 2.5%
CUBICIN ™ (daptomycin) Overview n Lipopeptide natural product n Activity in Gram-positive organisms only n Bactericidal in vitro and in vivo n Safety profile similar to vancomycin n Long T1/2 (once-daily IV dosing) n No oral formulation n FDA approved for SSTI only.
Future Antimicrobial Agents For Gram Positives Organisms n Glycopeptides u Telavancin u Oritavancin u Dalbavancin n Tetracyclines u Tigecycline (broad spectrum activity) n Cephalosporins u Ceftibiprole (5 th generation) F Excellent gram positive activity (MRSA & Enterococcus)
Conclusions u Recent data has shown us: u Emerging resistance u CA-MRSA greatest concen ?? u MRSA, GISA, VRSA n Better understanding of mechanisms of antimicrobial resistance - e.g., selective pressure n Better understanding of risk factors predisposing to CA-MRSA infection u Future u Molecular testing for resistance organisms u Newer antimicrobials