Jackson: Skin and Soft Tissue Infections I

Question 1

Definitions:

Macule
Papule
Vesicle
Boils (Furuncle) and Carbuncles

Answer 1

Macule: flat, red inflammatory response to microbe or toxin

Papule: raised, red with more marked inflammation

Vesicle: blister

Boils (Furuncle) and Carbuncles: due to infection of hair follicle (folliculitis)

Question 2

Definitions

Ulcer: 
Impetigo: 
Erysipelas: 
Cellulitis:
Necrotizing Fascitis:

Answer 2

Ulcer: epithelium ruptures and microbe is discharged

Impetigo: bullous, crusted or pustular eruption

Erysipelas: well-defined spreading inflammation of dermal lymphatics

Cellulitis: acute inflammation due to infection of subcutaneous fat

Necrotizing Fascitis: inflammatory response in soft tissue below the site of infection

Question 3

Dermatophytic fungi

Infection site:
Disease:

Answer 3

Keratinized epithelium

Ringworm

Question 4

Impetigo

Infection site:
Microbe:

Answer 4

Epidermis

S.pyogenes and/or S.aureus

Question 5

Erysipelas

Infection site:
Microbe:

Answer 5

Dermis

S.pyogenes

Question 6

Folliculitis, boils (furuncles), carbuncles

Infection site:
Microbe:

Answer 6

Hair follicles

S.aureus

Question 7

Cellulitis

Infection site:
Microbe:

Answer 7

Subcutaneous fat

S.pyogenes or S.aureus

Question 8

Necrotizing faciitis

Infection site:
Microbe:

Answer 8

Fascia

Anaerobes

Question 9

Gas gangrene

Infection site:
Microbe:

Answer 9

Muscle

Clostridium perfringens

Question 10

Typhoid Fever

Pathogen:
Skin manifestation:

Answer 10

Salmonella typhi

Contaminated petechia

Question 11

What does Neisseria meningitidis cause?

Skin manifestation:

Answer 11

Septicemia, meningitis

Contaminated petechia

Question 12

What causes scarlet fever?

Answer 12

S. pyogenes

Question 13

What causes TSS?

Answer 13

S.aureus

Question 14

What causes Blastomycosis?

Skin manifestation:

Answer 14

Blastomyces dermatitidis

Granulomatous lesion

Question 15

Staphylococcus Aureus

Virulence Factors (Relevant to Skin/Soft Tissue Infections) (6):

Answer 15

Alpha toxin
Toxic Shock Syndrome Toxin (TSST-1)
Exfoliative Toxins
Exoproteins for spread
Antiphagocytic components
Quorum sensing

Question 16

Staphylococcus Aureus

Alpha toxin

Answer 16

o 7 subunit pore-forming cytolysin (complement-like MOA)

o Pore permits fluid loss from cell (kills erythrocytes, leukocytes)

Question 17

Staphylococcus Aureus

Toxic Shock Syndrome Toxin (TSST-1):

Answer 17

Pyrogenic exotoxin (related to those produced by Group A strep)

Superantigen that cross-links T cell receptor and MHC class II, resulting in cytokine release

Cytokines cause diverse effects, including endotoxic shock

Question 18

Staphylococcus Aureus
Exfoliative Toxins:
Two types:

Answer 18

Two types:

Chromosomal

Plasmid-encoded

Question 19

What causes scalded skin syndrome?

What layers are split?

Answer 19

Staph Aureus exfoliative toxins cause scalded skin syndrome by inducing intercellular splitting between straum spinosum and stratum granulosum (desquamation of upper layers of epidermis)

Question 20

Staphylococcus Aureus

Exoproteins for Spread (2):

Answer 20

Hyaluronidase (hydrolyzes connective tissue)

Staphylokinase (promotes fibrinolysis)

Question 21

Staphylococcus Aureus
Antiphagocytic Components (3):

Answer 21

Protein A: binds Fc portion of IgG (Ab binds upside down)

Coagulase: promotes surface polymerization of fibrin to resist phagocytosis

Catalase: neutralizes hydrogen peroxide (protective mechanism since it is an aerobe)

Question 22

Quorum sensing regulates:
Upregulates what at low density?
What at high density?

Answer 22

Quorum sensing regulates virulence factor expression in response to cell density

1. Upregulation of coagulase at low cell densities for colonization
2. Upregulation of staphylokinase at high densities for spread

Question 23

Staphylococcus Aureus

Transmission:

Answer 23

o High skin and nasal carriage rates in humans
o No acquired immunity
o Transmission occurs by fomites (inanimate objects)

Question 24

Staphylococcus Aureus

Pathogenesis:

Furuncle:
Carbuncle:
Scalded Skin Syndrome (Bullous Exfoliation):
Toxic Shock Syndrome:
Wound Contamination:

Answer 24

Furuncle:
Colonization of hair follicle (folliculitis)
Coagulation of fibrin around lesion

Carbuncle:
	Focal suppuration (abscess)
	May lead to entry of organism into bloodstream via lymphatics

Scalded Skin Syndrome (Bullous Exfoliation):
Common in neonates and children (often pick up from hospital workers)
Caused by exfoliative toxin
Bullous Impetigo

Toxic Shock Syndrome:
Caused by TSST-1
Results from vaginal colonizers (ie. tampons in too long) or wound infection

Wound Contamination:
Bacteremia and endocarditis

Question 25

What is bateremia? | What can it lead to? (4)

Answer 25

``` Bacteremia: spread to blood stream via lymphatics; can result in Endocarditis Osteomyelitis Meningitis Pulmonary infection ```

Question 26

What is Bullous Impetigo?

Answer 26

Localized scalded skin syndrome

Question 27

Staphylococcus Aureus Clinical Identification of Organism: ``` Collection G+ or G-? Catalase Coagulase Antimicrobial Susceptibility testing ```

Answer 27

Specimen Collection: surface swab, blood, pus (pyogenic) cultured on blood agar Gram positive cocci in clusters Catalase Positive: Coagulase Positive: Antimicrobial susceptibility testing allows you to determine the MIC of a particular antimicrobial against S.aureus

Question 28

Staphylococcus Aureus Antimicrobial Susceptibility Testing: Allows you to determine:

Answer 28

o Allows you to determine the MIC (minimum inhibitory concentration) of a particular antimicrobial against S.aureus o Once you determine MIC, can determine if that drug is a therapeutic option (ie. does MIC fall into proper dosing range)

Question 29

Staphylococcus Aureus Coagulase Positive: Differentiates from:

Answer 29

Coagulation of citrated plasma by culture Differentiates from other staphs (S.epidermis or S.saprphyticus, which are less virulent)

Question 30

Staphylococcus Aureus Catalase Positive: Produces: Differentiates from:

Answer 30

Produces O2 bubbles when hydrogen peroxide is added Differentiates from strep (catalase negative)

Question 31

Streptococcus Pyogenes Virulence Factors (Relevant to Skin/Wound Infections) (5):

Answer 31

M protein Protein F and Protein G Streptolysin O and Streptolysin S (cytolysins) Streptococcal Pyrogenic Exotoxins (SPE A-C) Hydrolytic Enzymes

Question 32

Streptococcus Pyogenes M Protein: Function Structure Molecular mimicry

Answer 32

Function: - Anti-phagocytic (subject to antigenic variation) - Mediates binding to epidermis Structure: - Fibrillar structure with C-terminus anchored in the peptidoglycan of the cell wall - Amino terminus variable due to genetic recombination (over 80 serotypes) Molecular Mimicry: - Believed to undergo in order to conceal itself during an infection (looks like our own cells) - Cross-reactive Abs contribute to acute glomerulonephritis

Question 33

Streptococcus Pyogenes | Protein F and Protein G:

Answer 33

Protein F: mediates fibronectin binding at wound sites Protein G: synonymous with protein A in S.aureus; binds the Fc portion of Abs

Question 34

Streptococcus Pyogenes Streptolysin O and Streptolysin S (Cytolysins): Cause of: Streptolysin O:

Answer 34

Cause of beta-hemolysis on blood agar plates SLO: - Oxygen labile (sulfhydryl-activated) - Cytolysin that attacks cell membranes and forms large pores - Abs to SLO can mediate self-attack and augment cell lysis

Question 35

Streptococcus Pyogenes | Streptococcal Pyrogenic Exotoxins (SPE A-C): (3)

Answer 35

SPE A: produced by lysogenized (bacteriophage-carrying) Group A strep Superantigens that have sequence homology with staphylococcal pyrogenic exotoxins Induce cytokine release (fever, rash, T-cell stimulation and endotoxin sensitivity)

Question 36

Streptococcus Pyogenes Hydrolytic Enzymes: Streptokinase:

Answer 36

Responsible for thin, runny pus found in streptococcal infections Streptokinase: dissolves fibrin and facilitates spread (used therapeutically to dissolve blood clots)

Question 37

Streptococcus Pyogenes Impetigo (Pyoderma) Transmission:

Answer 37

Infection through minor trauma (ie. insect bite) typically on face and lower extremeties; usually auto-inoculation (scratching) Can also be person-to-person and by fomites Epidemics occur in children, especially in hot, humid climates, and due to poor hygiene/crowding

Question 38

Streptococcus Pyogenes Impetigo (Pyoderma) Appearance: Role of M proteins:

Answer 38

Appearance: - Small vesicle ruptures, resulting in serous exudates, superficial spread and honey-colored crust - S.aureus can also cause bullous (blister) impetigo or cause secondary super infection of streptococcal lesions Role of M Proteins: - Causative M protein serotypes in impetigo differ from the respiratory serotypes (ie. those seen in strep throat)

Question 39

Poststreptococcal Sequelae: Acute Glomerulonephritis May follow: Results in: Cross-reactivity with:

Answer 39

Can follow impetigo (rarely follows respiratory strep infections in children) Results in edema, HTN, hematuria and proteinuria (kidney dysfunction) 3 weeks following skin infection Cross-reactivity with nephritogenic M serotypes results in deposition of immune complexes in the glomerulus

Question 40

Erysipelas: Infection of: Commonly seen where? Associated symptoms:

Answer 40

Rapidly spreading infection of deeper layers (can progress to necrosis and septicemia) Commonly seen on the face following streptococcal throat infection Symptoms Associated: Edema Fever Lymphadenopathy (swollen/enlarged LNs)

Question 41

Cellulitis:

Answer 41

Extension of skin infection or wound Caused by S.pyogenes or S.aureus

Question 42

Streptococcus Pyogenes Nosocomial Infections:

Answer 42

Rates decreasing due to better infection control (ie. in surgical wounds and burn patients) Puerperal (Childbed) Fever: 19th century disease caused via physician transmission

Question 43

Toxic Shock-Like Syndrome (TSLS): Cause: Symptoms: (6) Compare to TSS:

Answer 43

Streptococcus Pyogenes Cause: highly invasive “flesh-eating” strains that produce SPE A (superantigen) ``` Symptoms:  Shock  Renal impairement  Rash  Respiratory failure  Diarrhea  Rapid death ``` Up to 30% mortality rate: as compared to 3% for TSS caused by S.aureus

Question 44

Streptococcus Pyogenes Clinical Identification of Organism: Specimen collection Classification Biochemical Tests Serologic Tests

Answer 44

Specimen Collection: surface swab, blood, pus (pyogenic) cultured on BAP with 10% CO2 Classification: o Gram (+) cocci in chains o B-hemolytic on blood agar plates (due to SLO and SLS) o Pyogenic (pus forming) o Group A Lancefield Classification (carbohydrate Ag in cell wall) Biochemical Tests: o Catalase negative (differentiate from staph) o Serotyping for Lancefield Group A (cell wall) o Bacitracin sensitivity assay on agar plate (differntiate from other beta-hemolytic streptococci) Serologic Tests: o Rise in Ab titers to S.pyogenes Ags (SLO, M protein)

Question 45

Propionibacterium spp. Virulence Factors (Relative to Skin and Wound Infections):

Answer 45

These are skin flora that break down sebum lipids to fatty acids Organic propionic acid produced by organism contributes to inflammatory process Hormone production at puberty alters sebum secretion and enhances the growth of P.acnes

Question 46

Propionibacterium spp. Etiology/Pathogenesis: What is Acne vulgaris? What is a blackhead? When can normal flora cause infection?

Answer 46

P.acnes: predominant anaerobe of normal skin flora o Can contribute to acne: Increased sebum production at puberty (due to hormones) High cell numbers in hair follicles and associated sebaceous glands Acne vulgaris: inflammation of hair follicle and associated sebaceous glands Blackhead: keratin, sebum and bacteria As normal flora, can cause infections: - In immunocompromised - Endocarditis, contamination of prosthetic heart valves, cerebrospinal shunts

Question 47

Propionibacterium spp. Clinical Identification of Organism:

Answer 47

Gram positive rods: - Pleiomorphic (multiple shapes) - Resemble Corynebacterium Anaerobic or microaerophilic growth

Question 48

Special Case Bacterial and Soft Tissue Infections: Pasturella multocida: Clostridium perfringens: Clostridium tetani:

Answer 48

Pasturella multocida: Gram (-) rods; animal bites Clostridium perfringens: Gram (+) rod, anaerobic, spores; gas gangrene after wound Clostridium tetani: Gram (+) rod, anaerobic, spores; tetanus after wound

Question 49

Candida Albicans Virulence Factors (Relevant to Skin and Wound Infections): Adhesion Invasion Immune system evasion

Answer 49

Adhesion: through mannoproten complexes extending from cell wall; receptor site in humans is fibronectin Invasion: o Hyphae bind fibronectin, collagen and laminin to extend across mucosal barriers o Proteases and elastases may also be involved Immune system evasion: neutrophils are first line of defense; chronic candida infections indicate T cell problem

Question 50

Candida Albicans Etiology/Pathogenesis: Folliculitis: Intertrigo: Occupational Hazards: Chronic Mucocutaneous Candidiasis:

Answer 50

Folliculitis: infection of hair follicle Intertrigo: infection in folds of skin (crural folds) o Wet, macerated surfaces are chronically exposed o Erythematous papules and tender cracked areas associated with chronic irritation Occupational Hazards: o Dishwashers: infection on hands o Diaper rash Chronic Mucocutaneous Candidiasis: o Localized to skin, hair or mucocutaneous junctions o Indicates T cell deficiency

Question 51

S.pyogenes Hemolytic reaction Lancefield group Disease

Answer 51

Beta A Impetigo, Scarlet fever, Rheumatic fever

Question 52

S.agalactiae Hemolytic reaction Lancefield group Disease

Answer 52

Beta B Neonatal sepsis, meningitis

Question 53

Candida Albicans Clinical Identification of Organism: Specimen Collection: KOH/Gram Stain: Germ Tube (Hyphae):

Answer 53

Specimen Collection: exudates or epithelial scrapings KOH/Gram Stain: budding round/oval yeast cells with hyphae (unicellular in the body) Germ Tube (Hyphae): outgrowth released by spores of spore-releasing fungi during germination; indicative that it is C.albicans

Question 54

Sporothrix Schenckii: Etiology/Pathogenesis: Sporotrichosis: Multiplication at site:

Answer 54

Sporotrichosis: subcutaneous infection caused by this fungi - Ubiquitous saprophyte in the soil - Inoculation of conidia (spores) by trauma, usually in the extremities of gardeners and farmers Multiplication at Site: local pyogenic/granulomatous inflammatory reactions - Initial stage painless papule (weeks to months after inoculation) - Papule can ulcerate/become chronic and drain into lymph channels - In worst cases, can spread to bone, eyes, lungs and CNS (less than 1% of cases)

Question 55

Sporothrix Schenckii: Clinical Identification of Organism: Diagnosis: Dimorphic Growth Phases:

Answer 55

• Clinical Identification of Organism: - Diagnosis: requires culturing of infected pus or tissue - Dimorphic Growth Phases: o Cigar shaped yeast in tissue/culture at 37 degrees (body temperature) o Mold with thin, septate hyphae and terminal conidia (spores) at 25 degrees (room temperature)

Question 56

Dermatophytes: Epidermophyton, Trichophyton, Microsporum (Ringworm) Virulence Factors (Relevant to Skin and Wound Infection): Adaptation to: Invasion of hair shaft by:

Answer 56

Adaptation to nonliving keratinized tissue of hair, nails, and stratum corneum of skin Invasion of hair shaft by arthroconidia

Question 57

Dermatophytes: Genera (4): What results in pityriasis/tinea versicolor?

Answer 57

o Tricophyton o Epidermophton: never infects hair o Microsporum: rarely infects nails o Malassezia furfur: commensal that can cause superficial mycoses - Results in pityriasis/tinea versicolor (a patchy discoloration)

Question 58

Dermatophytes: Epidermophyton, Trichophyton, Microsporum (Ringworm) Cause what? Common Names: tinea corporis tinea pedis tinea cruris

Answer 58

Cause superficial infections of the skin (usually the extremeties); Common Names: Ringworm: tinea corporis Athlete’s Foot: tinea pedis Jock Itch: tinea cruris Lesions occur most often in moist skin folds (maceration/softening promotes infection) o Arthroconidia can invade outside/within hair root, plugging the root and causing ring-shaped hair loss o Invasion of nail bed causes malformed growth

Question 59

Dermatophytes: Epidermophyton, Trichophyton, Microsporum (Ringworm) Source of Infection: The infection induces advanced skin growth, limiting its spread: Infection normally induces: Immunosuppressive agents do what to infection?

Answer 59

Source of Infection: o Domestic/wild animals or soil o Have low infectivity and virulence; person to person transmission requires close contact with infected skin or hair The infection induces advanced skin growth, limiting its spread o Infection normally induces DTH reaction; because of cell-mediated response, immunity can be acquired o Immunosuppressive agents prolong infection (decreased shedding of keratinized layers); chronic infections associated with impaired T cell function

Question 60

Dermatophytes Clinical Identification of Organism: (3)

Answer 60

Sampling: scrapings from edge of lesion or infected hairs Stained with KOH or Calcifor: culture and microscopy used for identification Microsporum spp: fluoresce under UV light (Wood’s lamp)