Skin and Soft Tissue Infections Flashcards
Primary Pyoderma- Impetigo
Vesicular, later crusted, superficial infection of skin
Non-bullous impetigo
-Streptococcus pyogenes (20-30%)
-Staphylococcus aureus – now most common
-Mixed infection
Clinical findings
-Begin as erythematous papules that evolve into vesicles and pustules that rupture
-Dries to form honey-colored crusts on erythematous base
-Typically heals without scarring
Bullous Impetigo
Strain of S. aureus producing exfoliating toxin
Toxin cleaves dermal-epidermal junction
Ecthyma
Ulcerative pyoderma of skin – deeper form of impetigo
Follows insect bites or minor trauma
Etiology – S. aureus and/or S. pyogenes
Heals with scarring
Primary Pyoderma- Purulent
Cutaneous abscess
Collections of pus within dermis and deeper tissue
Etiology – typically S. aureus; can be polymicrobial
Folliculitis, carbuncles and furuncles
Folliculitis - pyoderma located within hair follicle
Furuncle (boil) – inflammatory nodule extending into subcutaneous tissue; follows folliculitis
Carbuncle – coalescent process involving multiple follicles
Etiology – S. aureus
Chancriform Lesions- Ulcerative lesions
Cutaneous anthrax
Direct inoculation with Bacillus anthracis
Begins as painless pruritic papule; enlarges, vesiculates (malignant pustule), becomes necrotic and covered by eschar
Local edema due to edema factor
Venereal infections - Treponema pallidum and Haemophilus ducreyi
Other infections – Francisella tularensis, Mycobacterium ulcerans, Mycobacterium marinum
Cellulitis
Infection involving upper dermis and subcutaneous fat
Follows previous trauma, often minor, or underlying skin lesion, e.g., furuncle or ecthyma
Pain, erythema, involved area very red, hot and swollen
Etiology: Streptococci – Group A and others; less often S. aureus
Rarely, other bacteria – clues include trauma, water contact or animal, insect or human bites
Erysipelas and Cellulitis
Diffuse, superficial, spreading skin infections
Not associated with collections of pus – clinically important
Purulent lesions (discharging pus) require drainage, e.g., abscess, furuncle or carbuncle
Cellulitis requires antimicrobial therapy
Erysipelas
Superficial cellulitis with prominent lymphatic involvement
Painful; sharp demarcation from adjacent normal skin
Etiology – almost entirely S. pyogenes
Necrotizing Fasciitis
Aggressive subcutaneous infection that tracks along the superficial fascia – all tissue between skin and underlying muscle
Most often an extension from a skin lesion
Systemic toxicity
Etiology – S. pyogenes, S. aureus, Vibrio vulnificus, Aeromonas hydrophila; often polymicrobic
Systemic bacterial infections producing rash or lesions
Bacteremia – S. aureus, group A Streptococcus, N. meningitidis
Leptospirosis (Weil’s disease) – Leptospira interrogans
Rat-bite fever – Streptobacillus moniliformis
Annular erythema – Lyme disease – Borrelia burgdorferi
Rocky mountain spotted fever – Rickettsia rickettsii
Toxin Induced Reactions
Scarlet fever
Scalded skin syndrome
Toxic shock syndrome
Scarlet Fever
Follows pharyngitis by group A streptococcus
Streptococcal pyogenic exotoxin A (SpeA)
Scaled Skin Syndrome
Follows local infection by Staphylococcus aureus
Staphylococcal exfoliating toxin
Toxic Shock Syndrome
Follows infection by Staphylococcus aureus
Staphylococcal TSST-1 - superantigen
Pyomyositis
Presence of pus within individual muscle groups
Usually S. aureus (90%)
Most cases in tropics
Myonecrosis/ Gas gangrene
Necrotic damage to muscle tissue
Occurs after muscle injury and contamination with soil or other material containing spores
Extreme pain, crepitus due to gas formation, yellowish/bronze discoloration
Etiology: Clostridium perfringens (most common) and other clostridial species
General features of streptococci
Gram-positive cocci in pairs or chains
Most are facultative anaerobes
Typically require complex media – blood or serum
Catalase-negative
CLASSIFICATION
Hemolytic patterns on blood agar
Antigenic – Lancefield grouping
Biochemical (physiological) properties
Complex classification – two general groups
β-hemolytic streptococci classified by Lancefield grouping
α- and γ-hemolytic streptococci classified by biochemical testing
Alpha hemolytic streptococci
Partial hemolysis - greening of agar
Numerous species: S. salivaris, S. mitis
Normal flora of mucous membranes
Beta Hemolytic streptococci
Complete hemolysis - clear zone
Streptolysins O and S
Gamma hemolytic or non hemolytic streptococci
No hemolysis
Misc. normal flora, opportunists and anaerobes
Streptococci Groups
Carbohydrate antigen in cell wall (C-carbohydrate); primarily beta hemolytic streptococci. method to differentiate beta hemolytic streptococci
Group A - S. pyogenes; most human pathogens
Groups B, C, F, G, H, K, L - normal flora of mucous membranes, occasional pathogens
Groups E, M, N - lower animals
Group D – enterococcus; now Enterococcus faecalis
Lancefield Carbohydrate (C carbohydrate)
Group specific - all S. pyogenes are group A
Polymer of rhamnose and N-acetyl-glucosamine
Located in matrix of cell wall
M protein
Type specific
Subdivides group A into >100 types
Induces type-specific protective immunity
Streptococci extracellular enzymes
streptolysin O, DNAse, hyaluronidase
Group A strep skin and wound infections
Impetigo – colonization of healthy skin; infection via minor trauma
Erysipelas - dermal infection with spreading erythema and edema
Cellulitis – subcutaneous tissues
Myositis and necrotizing fasciitis – deep subcutaneous tissues; destruction of muscle and fat
Group A strep Toxemia
Scarlet fever
Toxic shock-like syndrome (TSLS)
Virulence Factors for streptococci- Adherence
Lipoteichoic acid – adhesion to epithelial cells
F protein (SfbI – streptococcal fibronectin binding protein I)
-Binds fibronectin
-Adhesion to nasopharyngeal epithelial cells
M protein – binding to epithelial cells
Hyaluronic acid capsule
-Facilitates adhesion to nasal mucosa
-Essential for early colonization
Virulence Factors for streptococci- avoiding phagocytosis
Hyaluronic acid capsule M protein -Antiphagocytic -Essential for virulence -Induces solid type-specific immunity; > 100 types -Candidate for vaccine development
Virulence Factors for streptococci- toxins
Streptococcal pyrogenic exotoxins (Spe)
-Synonyms: Erythrogenic toxin, scarlet fever -toxin
-Rash of scarlet fever
-Role in toxic shock-like syndrome (TSLS)
-Superantigens - Stimulate release of IL-1, IL-2, -IL-6, TNF-a and IFN-g
-Coded by lysogenic bacteriophage
Lipoteichoic acid
-Activates steps in inflammation and septic shock, e.g., complement cascade, cytokine secretion, coagulation cascade
Virulence Factors for streptococci- tissue damage and spreading
Hemolysins, enzymes, etc.
Streptolysin O - porin; oxygen labile; antigenic - anti-streptolysin O (ASO)
Streptolysin S - oxygen stable; non-antigenic
Streptokinase - converts plasminogen to plasmin; lyses blood clots
Streptodornase – DNase; reduces viscosity of abscess material
Hyaluronidase
Serological tests for streptococci
Anti-streptolysin O:
Typically negative in patients with skin infection
Useful for diagnosis of rheumatic fever
Not helpful with glomerulonephritis
Anti-DNase:
Antibodies produced after skin infection
Particularly useful if glomerulonephritis is suspected
Treatment of streptococcal infections
Penicillin – unless there are other issues
All strains sensitive
Prompt use reduces antibody response – essential that infection be treated quickly and completely
Other issues with treating streptococcal infections
Possible mixed infection, e.g., S. aureus – oxacillin or vancomycin
Necrotizing fasciitis:
High dose penicillin + clindamycin
Need for drainage and surgical debridement
Allergy – clindamycin or a narrow spectrum cephalosporin; perhaps a macrolide – check current AHA recommendations
Antibiotic prophylaxis for patients at risk for rheumatic fever
General feature of staph
Gram positive cocci in grape-like clusters; aerobic
Catalase positive
May have golden pigment
Beta- or non-hemolytic; depends on hemolysins
Relatively resistant to physical and chemical agents
Carry multiple plasmids and bacteriophage
Penicillinase (beta lactamase)
Toxin production, e.g., enterotoxin, toxic shock, etc.
80% of the S. aureus genome is a core genome conserved among all Staphylococcus species and strains
Remainder of genome is mobile DNA (mobile genome). what is the composition, function and regulation of the mobile DNA
Composition
- Bacteriophage
- Plasmids
- Transposons
- -Staphylococcal chromosomal cassette – much like a transposon
Function
- Virulence factors
- Antibiotic resistance
- Regulation
Operon-like
Example - accessory gene regulator (agr) – quorum sensing
Staph aureus infections of skin and subcutaneous tissue
Impetigo – bullous and pustular; S. aureus accounts for ~80%; S. pyogenes alone or in combination with S. aureus is the remainder
Abscesses, folliculitis, furuncles and carbuncles
S. aureus deep infections
Bacteremia
Osteomyelitis and septic arthritis
Pneumonia
Staphylococcal enterocolitis - follows upset of normal flora by broad spectrum antibiotics
Diseases caused by staph toxins
Food poisoning
Scalded skin syndrome and bullous impetigo
Toxic shock syndrome
Virulence factors of S. aureus- structural components
Capsule – antiphagocytic; 75% of clinical isolates are type 5 or 8
Peptidoglycan and lipoteichoic acids – contributes to inflammation
Protein A – high affinity for IgG Fc fragment
Virulence factors of S. aureus- enzymes
Coagulase
-Converts fibrinogen to fibrin; helps localize lesions
-Marker for species
Catalase – facilitates intracellular survival
Penicillinase
Staph Cytotoxins
Alpha, beta, delta and gamma toxins; P-V leukocidin
Toxic via various mechanisms for erythrocytes, leukocytes and platelets
Exfoliating toxin (ETA and ETB)
scalded skin syndrome
Pyrogenic exotoxins of staph
Encoded by plasmids (enterotoxins) or bacteriophage (TSST)
Superantigens
- Induce release of IL-1, TNF-a, and other toxins
- Related to Streptococcal pyrogenic exotoxins
- Have specific toxic activities distinct from superantigen effects
Staphylococcal enterotoxin (SEA, SEB, SEC, SED, SEE)
Toxic shock syndrome toxin (TSST-1)
Staph food poisoning
Ingestion of preformed staphylococcal enterotoxin
Resistant to heat (boiling for 30 min) and gastric enzymes
1-6 hr. incubation
Targets sensory nerve endings in smooth muscle of intestine
Nausea, cramps, vomiting, diarrhea
Recovery in 24 hr.
Staphylococcal Scaled Skin Syndrome
Syn., exfoliative skin disease
Toxemia - infection at distant site; release of exfoliating toxin
Bullous impetigo is local form
Toxin is a serine protease
Cleaves dermal-epidermal junction to form fragile, thin-roofed vesicopustules
Usually in children
Staphylococcal Toxic Shock Syndrome
Toxemia producing fever, vomiting, diarrhea, rash, shock
Possible mechanisms
-Induction of cytokine release, e.g., IL-1 and TNFa
-Increased susceptibility to endogenous endotoxin
-Direct effects on vascular endothelial cells
TSST-1 production stimulated by poor growth conditions
Blood cultures usually negative
Staph lab differential characteristics
Gram-positive coccus
Catalase positive - distinguishes Staphylococci from Streptococci
Coagulase positive - distinguishes S. aureus from other Staphylococci
Ferments mannitol
Lab recognition of MRSA
Chromogenic media with disks of oxacillin or cefoxitin
PCR for mecA
Staph treatment
Drain lesion; remove foreign body if present
Control underlying disease
Antibiotics – in the era of MRSA, this is a complete lecture in itself
Weapons in the arsenal – in no particular order
-Penicillinase-resistant penicillins, e.g., oxacillin
-Clindamycin
-TMP-SMX
-Doxycycline
-Linezolid
-Vancomycin
-Daptomycin
Recommendations vary with clinical disease*
Staph antibiotic resistance
Penicillinase producing S. aureus - very common
Resistance to intermediate levels of vancomycin (VISA)
Thicker, more disorganized cell wall with free ala-ala groups
Acts as a decoy for vancomycin
Vancomycin resistant S. aureus (VRSA)
Due to vanA gene operon – encodes ala-lactate production
Requires rigorous susceptibility testing
Still relatively rare
Antibiotic resistance- MRSA
Lies on a mobile genetic element – staphylococcal chromosome cassette – SCCmec
SCCmec
Includes regulator genes – negative repressor operon
mecA – encodes PBP 2a with low affinity for beta lactam antibiotics
Health care-associated MRSA (HCA-MRSA)
Associated with risk factors, e.g., surgery, indwelling catheter, etc.
Multi-resistant
Community-associated MRSA (CA-MRSA)
No/limited risk factors
Most common cause of skin and soft tissue infections in community
Usually carries the PV leukocidin
Pauci-resistant
MRSA control
Control - decolonization of colonized patients or carriers – 1 week of body washing with chlorhexidine + nasal mupirocin
