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Derm, infectious disease, topical drugs, RBC disorders > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

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Dermatology Board Prep flashcards
1
Q

Primary Pyoderma- Impetigo

A

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

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2
Q

Bullous Impetigo

A

Strain of S. aureus producing exfoliating toxin

Toxin cleaves dermal-epidermal junction

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3
Q

Ecthyma

A

Ulcerative pyoderma of skin – deeper form of impetigo
Follows insect bites or minor trauma
Etiology – S. aureus and/or S. pyogenes
Heals with scarring

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4
Q

Primary Pyoderma- Purulent

A

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

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5
Q

Chancriform Lesions- Ulcerative lesions

A

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

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6
Q

Cellulitis

A

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

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7
Q

Erysipelas and Cellulitis

A

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

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8
Q

Erysipelas

A

Superficial cellulitis with prominent lymphatic involvement
Painful; sharp demarcation from adjacent normal skin
Etiology – almost entirely S. pyogenes

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9
Q

Necrotizing Fasciitis

A

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

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10
Q

Systemic bacterial infections producing rash or lesions

A

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

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11
Q

Toxin Induced Reactions

A

Scarlet fever
Scalded skin syndrome
Toxic shock syndrome

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12
Q

Scarlet Fever

A

Follows pharyngitis by group A streptococcus

Streptococcal pyogenic exotoxin A (SpeA)

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13
Q

Scaled Skin Syndrome

A

Follows local infection by Staphylococcus aureus

Staphylococcal exfoliating toxin

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14
Q

Toxic Shock Syndrome

A

Follows infection by Staphylococcus aureus

Staphylococcal TSST-1 - superantigen

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15
Q

Pyomyositis

A

Presence of pus within individual muscle groups
Usually S. aureus (90%)
Most cases in tropics

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16
Q

Myonecrosis/ Gas gangrene

A

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

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17
Q

General features of streptococci

A

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

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18
Q

Alpha hemolytic streptococci

A

Partial hemolysis - greening of agar
Numerous species: S. salivaris, S. mitis
Normal flora of mucous membranes

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19
Q

Beta Hemolytic streptococci

A

Complete hemolysis - clear zone

Streptolysins O and S

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20
Q

Gamma hemolytic or non hemolytic streptococci

A

No hemolysis

Misc. normal flora, opportunists and anaerobes

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21
Q

Streptococci Groups

A

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

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22
Q

Lancefield Carbohydrate (C carbohydrate)

A

Group specific - all S. pyogenes are group A
Polymer of rhamnose and N-acetyl-glucosamine
Located in matrix of cell wall

23
Q

M protein

A

Type specific
Subdivides group A into >100 types
Induces type-specific protective immunity

24
Q

Streptococci extracellular enzymes

A

streptolysin O, DNAse, hyaluronidase

25
Q

Group A strep skin and wound infections

A

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

26
Q

Group A strep Toxemia

A

Scarlet fever

Toxic shock-like syndrome (TSLS)

27
Q

Virulence Factors for streptococci- Adherence

A

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

28
Q

Virulence Factors for streptococci- avoiding phagocytosis

A 
Hyaluronic acid capsule
M protein
-Antiphagocytic
-Essential for virulence
-Induces solid type-specific immunity; > 100 types
-Candidate for vaccine development
29
Q

Virulence Factors for streptococci- toxins

A

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

30
Q

Virulence Factors for streptococci- tissue damage and spreading

A

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

31
Q

Serological tests for streptococci

A

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

32
Q

Treatment of streptococcal infections

A

Penicillin – unless there are other issues
All strains sensitive
Prompt use reduces antibody response – essential that infection be treated quickly and completely

33
Q

Other issues with treating streptococcal infections

A

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

34
Q

General feature of staph

A

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.

35
Q

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

A

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

36
Q

Staph aureus infections of skin and subcutaneous tissue

A

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

37
Q

S. aureus deep infections

A

Bacteremia
Osteomyelitis and septic arthritis
Pneumonia
Staphylococcal enterocolitis - follows upset of normal flora by broad spectrum antibiotics

38
Q

Diseases caused by staph toxins

A

Food poisoning
Scalded skin syndrome and bullous impetigo
Toxic shock syndrome

39
Q

Virulence factors of S. aureus- structural components

A

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

40
Q

Virulence factors of S. aureus- enzymes

A

Coagulase
-Converts fibrinogen to fibrin; helps localize lesions
-Marker for species
Catalase – facilitates intracellular survival
Penicillinase

41
Q

Staph Cytotoxins

A

Alpha, beta, delta and gamma toxins; P-V leukocidin

Toxic via various mechanisms for erythrocytes, leukocytes and platelets

42
Q

Exfoliating toxin (ETA and ETB)

A

scalded skin syndrome

43
Q

Pyrogenic exotoxins of staph

A

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)

44
Q

Staph food poisoning

A

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.

45
Q

Staphylococcal Scaled Skin Syndrome

A

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

46
Q

Staphylococcal Toxic Shock Syndrome

A

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

47
Q

Staph lab differential characteristics

A

Gram-positive coccus
Catalase positive - distinguishes Staphylococci from Streptococci
Coagulase positive - distinguishes S. aureus from other Staphylococci
Ferments mannitol

48
Q

Lab recognition of MRSA

A

Chromogenic media with disks of oxacillin or cefoxitin

PCR for mecA

49
Q

Staph treatment

A

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*

50
Q

Staph antibiotic resistance

A

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

51
Q

Antibiotic resistance- MRSA

A

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

52
Q

Health care-associated MRSA (HCA-MRSA)

A

Associated with risk factors, e.g., surgery, indwelling catheter, etc.
Multi-resistant

53
Q

Community-associated MRSA (CA-MRSA)

A

No/limited risk factors
Most common cause of skin and soft tissue infections in community
Usually carries the PV leukocidin
Pauci-resistant

54
Q

MRSA control

A

Control - decolonization of colonized patients or carriers – 1 week of body washing with chlorhexidine + nasal mupirocin

Derm, infectious disease, topical drugs, RBC disorders (8 decks)

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