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48 Cards in this Set
- Front
- Back
General info about skin and soft tissue infection + epidemiology:
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*Common cause of outpatient and inpatient presentations to clinical care
*>$350 million cost per year for uncomplicated SSTI alone *Broad clinical spectrum of diseases *Multiple approaches to categorize illness: e.g. by lesion type, pathogen, or anatomically |
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What is the simple classification for skin and soft tissue infections?
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What skin layers do various bugs infect?
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Most common bugs in skin and tissue infections:
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*Staphylococcus aureus
*Streptococcus pyogenes and others *GNRs: Enterobacteriaeciae, Pasteurella multocida, Vibrio, etc *Anaerobes: Clostridia, anaerobic cocci *Polymicrobial *Fungi, viruses |
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How does the host encounter a microbe?
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*Microbes can be endogenous, systemic or introduced exogenously
*Colonization: affected by local (e.g. pH, moisture) and systemic factors (e.g. immune status, co-morbidities) *S. aureus, GNR can be colonizers *Resident microflora can be pathogens under certain conditions *Pathogen determined by internal and external environment and source of infection: consider these as a part of possible etiologies of infection *Examples: consider resident mouth flora in animal or human bite wound infections; marine environments in cellulitides; unusual pathogens in bioterrorism |
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How do microbes enter the skin?
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*Stratum corneum as primary mechanical barrier: disrupted by trauma, surgery, underlying exfoliative disease, etc.
*Microbes enter via macro- or microscopic breaches or metastatically (i.e. systemic) *Skin as portal-of-entry for local (e.g. wound, superficial or deep soft tissue) or systemic (e.g. rabies, tularemia, WNV) infections |
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What microbial factors affect pathogenesis?
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*“Virulence factors”
*Toxins: TSST, enterotoxins, endotoxin *Enzymes: coagulase, hyaluronidase, DNAse *Structural components: cell wall, capsule |
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What key enzymes does s. aureus have?
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*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 |
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What toxins does s. aureus have?
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*Alpha-toxin: membrane-damaging (hemolysin), dermonecrotic
*Beta-toxin: membrane damaging, sphingomyelinase *Leukocidin: forms pores in phagocyte membranes *Epidermolytic toxins: exfoliatins (SSSS) *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 |
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Streptococcal Toxins and Enzymes:
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*Pyrogenic exotoxin: scarlet fever
*Hemolysins: affect PMNs also *Dnases, hyaluronidase, streptokinase, NADases, proteinases, etc: may help bug spread through tissue planes |
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What host factors affect pathogenesis?
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*Host status determines colonization risk: resident microflora differ in different scenarios
*Colonization risk factors: IDU, frequent hospitalizations, DM, hemodialysis, etc. *Disruption of anatomic barriers: foreign bodies, bites, burns, trauma, skin disease *Alterations in micro-anatomy: previous cellulitis, post-CABG, vascular disease *Underlying immunologic status: HIV, leukemia, chemotherapy, primary immunodeficiencies |
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Impetigo:
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*Primarily young children
*Two forms: nonbullous and bullous *Multiple vesicular lesions progress to pustules then plaques with dried honey-colored crust *Systemic signs or symptoms uncommon; pruritus common *S. pyogenes and S. aureus (alone or in combination) *Bullous disease caused by S. aureus strains producing exfoliative toxin *Strains transmissible within families *Oral antimicrobials or topical |
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Folliculitis:
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*Benign infection of hair follicle
*Raised, painful, erythematous lesions *Central pustule; org can be cultured *Absent constitutional symptoms *S. aureus; Pseudomonas in hot tubs *Rx: topical/systemic + hygiene |
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Furuncles, carbuncles:
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*Deep-seated, extension of hair follicle infection to dermis; S. aureus
*Painful nodules, fluctuant *Rx: antimicrobials *Carbuncles are larger and deeper with central necrosis, pain and “B” symptoms *Rx: I&D + antimicrobials |
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Cellulitis: what does it look like?
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*cardinal signs of inflammation
*Rubor (redness), dolor (pain), calor (heat), tumor (swelling) |
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Uncomplicated cellulitis
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Bullous disease due to exfoliative toxin-producing S aureus
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Erysipelas:
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*Superficial, involves cutaneous lymphatics (dermis)
*Areas of preexisting lymphatic obstruction/edema *Extremities>>face *Constitutional symptoms *S. pyogenes >>other strep and S. aureus *Margins are raised and well-demarcated *Rx: antimicrobials |
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Describe cellulitis:
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*Infection of dermis and subcutaneous fat (deeper than erysipelas)
*Preferentially affects extremities *Warmth, erythema, tenderness, edematous, poorly demarcated +/- systemic symptoms *Predispositions: trauma of any kind, primary skin dis, vasc or lymphatic alterations *Pyogenic streptococci, S. aureus most common but many organisms can cause cellulitis in specific scenarios *Bacteremia in minority of patients (<5%) *Rx: Antimicrobials, elevation, treat underlying problem |
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Ascending Lymphangitis; part of advanced cellulitis.
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Staphylococcal scalded skin syndrome:
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*SSSS due to exfoliative toxin
*Fever, scarlatiniform eruption *Flaccid bullae, denudation, desquamation, recovery *∆: TSS or a drug rxn |
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Toxic shock syndrome:
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*S. aureus (TSST-1 producing strains) or streptococci
*More common in non-menstrual setting now (e.g. post-op, traumatic, foreign body) *Fever, hypotension, rash with desquamation *Case definition REQUIRES multi-system involvement: vascular, GI, CNS, renal, heme, hepatic *Rx: supportive care, antistaphylococcal rx, debridement, foreign body removal, ?IVIG *Mortality: 5% (Staph) vs. 50% (strep) |
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*TSS skin manifestations.
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Bite-Associated Cellulitis: Pasteurella multocida
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Bite Wound Cellulitis:
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*Dog bites most prevalent (~20% become infected)
*Micro: S. aureus, Pasteurella, Eikenella, Capnocytophaga (GNR can cause sepsis in asplenic), anaerobes *Cat bites: 28-80% infection rate; P. multocida most common *Human bites most susceptible; S. aureus, Eikenella, strep, oral anaerobes *Surgical consult generally needed *Remember tetanus and ?rabies |
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Cutaneous Anthrax
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Cutaneous Anthrax
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Cutaneous Anthrax: Differential Diagnosis:
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Orf (Parapoxvirus)
Glanders (B. mallei) Tularemia Rat-bite fever Ecthyma gangrenosum Rickettsialpox Plague Staphylococcus Tuberculosis Leprosy M. ulcerans Diphtheria Lyme disease (atypical) Spider bite (Loxosceles reclusa) |
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Loxosceles Spider Bites
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Loxosceles Spider Bites:
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*brown recluse
*Painful from outset *Begin as pale ecchymotic lesions that rapidly turn purple. *May ulcerate and develop necrotic centers *Unlike anthrax, borders are irregular, ill-defined and without significant surrounding edema |
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This causes a lesion in a bite from a goat or sheep:
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orf virus
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Ecthyma Gangrenosum from pseudomonas.
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Cutaneous Manifestation of Systemic Infection: Meningococcemia
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Cutaneous Manifestations of Systemic Disease:
what diseases cause skin lesions? |
*Infective Endocarditis: Janeway lesions, splinter hemorrhages, etc.
*Viral exanthems: varicella, variola, parvovirus, rubella, measles, erythema infectiosum, roseola, coxsackievirus, etc. *RMSF (Rocky Mountain Spotted Fever) *Disseminated gonococcal infection *Fungemia *Drug reactions *Lyme disease *meningococcemia |
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rash in Lyme disease
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monkeypox
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Clinical features of necrotizing fasciitis:
strep vs. mixed infection |
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Clinical Clues to Diagnosis of Necrotizing SSTI:
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*Cutaneous: erythema, tense edema, gray or “dishwater” drainage, bullae, necrosis, crepitus
***Pain out of proportion to physical findings*** *Local hypesthesia or anesthesia *Fever *Tachycardia, tachypnea *Mental status changes |
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Synergistic (Necrotizing) Cellulitis/Gangrene
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Necrotizing Fasciitis: Abdominal Wall
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Gas Gangrene: Clostridial Myonecrosis
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*Vibrio vulnificus necrotizing cellulitis
*Bacteremia, metastatic cutaneous lesions in compromised host (cirrhosis), exposure to seawater |
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Concepts in Therapy for SSTIs; group one and group two infections:
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*Group one infections: oral antimicrobials targeted against gram positives in mildly ill outpatients
*Parenteral treatment in hospitalized: use antipenicillinase beta lactam to cover S. aureus (and strep) in most cases, unless MRSA suspected (see next slide) *Topicals may help in certain scenarios *Some require drainage: bite infections, abscesses *Group two infections: surgery as primary mode, antimicrobials necessary adjunct |
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Methicillin-resistant Staph. aureus (MRSA):
oral and parenteral treatment: |
*Responsible for majority of S. aureus skin and soft tissues in some areas; rates on the rise
*Beta-lactam agents no longer reliable empiric Rx *Differences between hospital-acquired and community-acquired MRSA strains re: antibiotic susceptibility profiles *I&D w/culture and susc testing when possible (debridement may be sufficient with small lesions) *Outpatient oral Rx: clindamycin (not as reliable vs. CA-MRSA), TMP-SMZ, doxy >> linezolid *Parenteral Rx: vanco >> linezolid, daptomycin |
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Community-acquired MRSA:
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*Less likely to be multiresistant to non-beta lactams
*Susceptible to clindamycin *High prevalence of PVL toxin genes (associated with abscesses and necrosis) *Genetic elements easily transferrable *Cannot distinguish CA-MRSA based solely on clinical features |
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Epidemiology of CA-MRSA:
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*2 >Age >65
*Athletes (contact) *IDU, MSM *Persons living in institutional settings: military, corrections, shelters *Known colonization or intimate contact with colonized person *Recent ILI +/- CAP *Pets/vets/farmers *CA-MRSA is major cause of skin/soft tissue infections in previously healthy persons |
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Management of SSTIs in the Era of CA-MRSA:
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*Incision and drainage +/- ABs for purulent lesions; consider systemic signs, lesion size, severity of syndrome
*Obtain material for culture *Antibiotics a must if systemic signs, cellulitis, high-risk site, compromised host; empirically cover CA-MRSA if >10% prevalence *Older drugs (clinda, tetracyclines, TMP-SMZ) useful—beware of ↑clinda resistance and false neg. susc. tests (i.e. inducible resistance) and possible GAS resistance to TMP-SMZ and tetracyclines *Newer agents: high cost, side effects, resistance (no FQ due to resistance) *Outcome studies with different agents lacking *Invasive disease: vanco (beware of MIC “creep”), tigecycline, *Preventive measures to reduce further transmission |
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How do you limit the spread of MRSA?
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