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48 Cards in this Set

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General info about skin and soft tissue infection + epidemiology:
*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
What is the simple classification for skin and soft tissue infections?
What skin layers do various bugs infect?
Most common bugs in skin and tissue infections:
*Staphylococcus aureus
*Streptococcus pyogenes and others
*GNRs: Enterobacteriaeciae, Pasteurella multocida, Vibrio, etc
*Anaerobes: Clostridia, anaerobic cocci
*Polymicrobial
*Fungi, viruses
How does the host encounter a microbe?
*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
How do microbes enter the skin?
*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
What microbial factors affect pathogenesis?
*“Virulence factors”
*Toxins: TSST, enterotoxins, endotoxin
*Enzymes: coagulase, hyaluronidase, DNAse
*Structural components: cell wall, capsule
What key enzymes does s. aureus have?
*Catalase: converts toxic oxygen radicals from peripheral mononuclear cells (PMN) to non-toxic forms, deactivating them
*Hyaluronidase: hydrolyzes mucopolysaccharides in the extracellular matrix of connective tissue
*Beta-lactamases: mediate drug resistance
*Lipases, nuclease
What toxins does s. aureus have?
*Alpha-toxin: membrane-damaging (hemolysin), dermonecrotic
*Beta-toxin: membrane damaging, sphingomyelinase
*Leukocidin: forms pores in phagocyte membranes
*Epidermolytic toxins: exfoliatins (SSSS)
*TSST-1: related enterotoxins, causes TSS
*Enterotoxins: heat-stable causes of food poisoning
*ET, TSST, SE are superantigens: directly activate T cells to induce cytokines
Streptococcal Toxins and Enzymes:
*Pyrogenic exotoxin: scarlet fever
*Hemolysins: affect PMNs also
*Dnases, hyaluronidase, streptokinase, NADases, proteinases, etc: may help bug spread through tissue planes
What host factors affect pathogenesis?
*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
Impetigo:
*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
Folliculitis:
*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
*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
Furuncles, carbuncles:
*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
*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
Cellulitis: what does it look like?
*cardinal signs of inflammation
*Rubor (redness), dolor (pain), calor (heat), tumor (swelling)
Uncomplicated cellulitis
Uncomplicated cellulitis
Bullous disease due to exfoliative toxin-producing S aureus
Bullous disease due to exfoliative toxin-producing S aureus
Erysipelas:
*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
*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
Describe cellulitis:
*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
Ascending Lymphangitis; part of advanced cellulitis.
Ascending Lymphangitis; part of advanced cellulitis.
Staphylococcal scalded skin syndrome:
*SSSS due to exfoliative toxin
*Fever, scarlatiniform eruption
*Flaccid bullae, denudation, desquamation, recovery
*∆: TSS or a drug rxn
*SSSS due to exfoliative toxin
*Fever, scarlatiniform eruption
*Flaccid bullae, denudation, desquamation, recovery
*∆: TSS or a drug rxn
Toxic shock syndrome:
*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)
*TSS skin manifestations.
*TSS skin manifestations.
Bite-Associated Cellulitis: Pasteurella multocida
Bite-Associated Cellulitis: Pasteurella multocida
Bite Wound Cellulitis:
*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
Cutaneous Anthrax
Cutaneous Anthrax
Cutaneous Anthrax
Cutaneous Anthrax
Cutaneous Anthrax: Differential Diagnosis:
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)
Loxosceles Spider Bites
Loxosceles Spider Bites
Loxosceles Spider Bites:
*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
This causes a lesion in a bite from a goat or sheep:
orf virus
Ecthyma Gangrenosum from pseudomonas.
Ecthyma Gangrenosum from pseudomonas.
Cutaneous Manifestation of Systemic Infection: Meningococcemia
Cutaneous Manifestation of Systemic Infection: Meningococcemia
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
rash in Lyme disease
rash in Lyme disease
monkeypox
monkeypox
Clinical features of necrotizing fasciitis:
strep vs. mixed infection
Clinical Clues to Diagnosis of Necrotizing SSTI:
*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
Synergistic (Necrotizing) Cellulitis/Gangrene
Synergistic (Necrotizing) Cellulitis/Gangrene
Necrotizing Fasciitis: Abdominal Wall
Necrotizing Fasciitis: Abdominal Wall
Gas Gangrene: Clostridial Myonecrosis
Gas Gangrene: Clostridial Myonecrosis
*Vibrio vulnificus necrotizing cellulitis
*Bacteremia, metastatic cutaneous lesions in compromised host (cirrhosis), exposure to seawater
*Vibrio vulnificus necrotizing cellulitis
*Bacteremia, metastatic cutaneous lesions in compromised host (cirrhosis), exposure to seawater
Concepts in Therapy for SSTIs; group one and group two infections:
*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
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
Community-acquired MRSA:
*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
Epidemiology of CA-MRSA:
*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
Management of SSTIs in the Era of CA-MRSA:
*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
How do you limit the spread of MRSA?