Jackson: Skin and Soft Tissue Infections I Flashcards
Definitions:
Macule
Papule
Vesicle
Boils (Furuncle) and Carbuncles
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)
Definitions
Ulcer: Impetigo: Erysipelas: Cellulitis: Necrotizing Fascitis:
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
Dermatophytic fungi
Infection site:
Disease:
Keratinized epithelium
Ringworm
Impetigo
Infection site:
Microbe:
Epidermis
S.pyogenes and/or S.aureus
Erysipelas
Infection site:
Microbe:
Dermis
S.pyogenes
Folliculitis, boils (furuncles), carbuncles
Infection site:
Microbe:
Hair follicles
S.aureus
Cellulitis
Infection site:
Microbe:
Subcutaneous fat
S.pyogenes or S.aureus
Necrotizing faciitis
Infection site:
Microbe:
Fascia
Anaerobes
Gas gangrene
Infection site:
Microbe:
Muscle
Clostridium perfringens
Typhoid Fever
Pathogen:
Skin manifestation:
Salmonella typhi
Contaminated petechia
What does Neisseria meningitidis cause?
Skin manifestation:
Septicemia, meningitis
Contaminated petechia
What causes scarlet fever?
S. pyogenes
What causes TSS?
S.aureus
What causes Blastomycosis?
Skin manifestation:
Blastomyces dermatitidis
Granulomatous lesion
Staphylococcus Aureus
Virulence Factors (Relevant to Skin/Soft Tissue Infections) (6):
Alpha toxin Toxic Shock Syndrome Toxin (TSST-1) Exfoliative Toxins Exoproteins for spread Antiphagocytic components Quorum sensing
Staphylococcus Aureus
Alpha toxin
o 7 subunit pore-forming cytolysin (complement-like MOA)
o Pore permits fluid loss from cell (kills erythrocytes, leukocytes)
Staphylococcus Aureus
Toxic Shock Syndrome Toxin (TSST-1):
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
Staphylococcus Aureus
Exfoliative Toxins:
Two types:
Two types:
Chromosomal
Plasmid-encoded
What causes scalded skin syndrome?
What layers are split?
Staph Aureus exfoliative toxins cause scalded skin syndrome by inducing intercellular splitting between straum spinosum and stratum granulosum (desquamation of upper layers of epidermis)
Staphylococcus Aureus
Exoproteins for Spread (2):
Hyaluronidase (hydrolyzes connective tissue)
Staphylokinase (promotes fibrinolysis)
Staphylococcus Aureus Antiphagocytic Components (3):
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)
Quorum sensing regulates:
Upregulates what at low density?
What at high density?
Quorum sensing regulates virulence factor expression in response to cell density
- Upregulation of coagulase at low cell densities for colonization
- Upregulation of staphylokinase at high densities for spread
Staphylococcus Aureus
Transmission:
o High skin and nasal carriage rates in humans
o No acquired immunity
o Transmission occurs by fomites (inanimate objects)
Staphylococcus Aureus
Pathogenesis:
Furuncle: Carbuncle: Scalded Skin Syndrome (Bullous Exfoliation): Toxic Shock Syndrome: Wound Contamination:
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
What is bateremia?
What can it lead to? (4)
Bacteremia: spread to blood stream via lymphatics; can result in Endocarditis Osteomyelitis Meningitis Pulmonary infection
What is Bullous Impetigo?
Localized scalded skin syndrome
Staphylococcus Aureus
Clinical Identification of Organism:
Collection G+ or G-? Catalase Coagulase Antimicrobial Susceptibility testing
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
Staphylococcus Aureus
Antimicrobial Susceptibility Testing:
Allows you to determine:
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)
Staphylococcus Aureus
Coagulase Positive:
Differentiates from:
Coagulation of citrated plasma by culture
Differentiates from other staphs (S.epidermis or S.saprphyticus, which are less virulent)
Staphylococcus Aureus
Catalase Positive:
Produces:
Differentiates from:
Produces O2 bubbles when hydrogen peroxide is added
Differentiates from strep (catalase negative)
Streptococcus Pyogenes
Virulence Factors (Relevant to Skin/Wound Infections) (5):
M protein
Protein F and Protein G
Streptolysin O and Streptolysin S (cytolysins)
Streptococcal Pyrogenic Exotoxins (SPE A-C)
Hydrolytic Enzymes
Streptococcus Pyogenes
M Protein:
Function
Structure
Molecular mimicry
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
Streptococcus Pyogenes
Protein F and Protein G:
Protein F: mediates fibronectin binding at wound sites
Protein G: synonymous with protein A in S.aureus; binds the Fc portion of Abs
Streptococcus Pyogenes
Streptolysin O and Streptolysin S (Cytolysins):
Cause of:
Streptolysin O:
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
Streptococcus Pyogenes
Streptococcal Pyrogenic Exotoxins (SPE A-C): (3)
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)
Streptococcus Pyogenes
Hydrolytic Enzymes:
Streptokinase:
Responsible for thin, runny pus found in streptococcal infections
Streptokinase: dissolves fibrin and facilitates spread (used therapeutically to dissolve blood clots)
Streptococcus Pyogenes
Impetigo (Pyoderma)
Transmission:
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
Streptococcus Pyogenes
Impetigo (Pyoderma)
Appearance:
Role of M proteins:
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)
Poststreptococcal Sequelae: Acute Glomerulonephritis
May follow:
Results in:
Cross-reactivity with:
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
Erysipelas:
Infection of:
Commonly seen where?
Associated symptoms:
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)
Cellulitis:
Extension of skin infection or wound
Caused by S.pyogenes or S.aureus
Streptococcus Pyogenes
Nosocomial Infections:
Rates decreasing due to better infection control (ie. in surgical wounds and burn patients)
Puerperal (Childbed) Fever: 19th century disease caused via physician transmission
Toxic Shock-Like Syndrome (TSLS):
Cause:
Symptoms: (6)
Compare to TSS:
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
Streptococcus Pyogenes
Clinical Identification of Organism:
Specimen collection
Classification
Biochemical Tests
Serologic Tests
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)
Propionibacterium spp.
Virulence Factors (Relative to Skin and Wound Infections):
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
Propionibacterium spp.
Etiology/Pathogenesis:
What is Acne vulgaris?
What is a blackhead?
When can normal flora cause infection?
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
Propionibacterium spp.
Clinical Identification of Organism:
Gram positive rods:
- Pleiomorphic (multiple shapes)
- Resemble Corynebacterium
Anaerobic or microaerophilic growth
Special Case Bacterial and Soft Tissue Infections:
Pasturella multocida:
Clostridium perfringens:
Clostridium tetani:
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
Candida Albicans
Virulence Factors (Relevant to Skin and Wound Infections):
Adhesion
Invasion
Immune system evasion
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
Candida Albicans
Etiology/Pathogenesis:
Folliculitis:
Intertrigo:
Occupational Hazards:
Chronic Mucocutaneous Candidiasis:
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
S.pyogenes
Hemolytic reaction
Lancefield group
Disease
Beta
A
Impetigo, Scarlet fever, Rheumatic fever
S.agalactiae
Hemolytic reaction
Lancefield group
Disease
Beta
B
Neonatal sepsis, meningitis
Candida Albicans
Clinical Identification of Organism:
Specimen Collection:
KOH/Gram Stain:
Germ Tube (Hyphae):
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
Sporothrix Schenckii:
Etiology/Pathogenesis:
Sporotrichosis:
Multiplication at site:
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)
Sporothrix Schenckii:
Clinical Identification of Organism:
Diagnosis:
Dimorphic Growth Phases:
• 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)
Dermatophytes: Epidermophyton, Trichophyton, Microsporum (Ringworm)
Virulence Factors (Relevant to Skin and Wound Infection):
Adaptation to:
Invasion of hair shaft by:
Adaptation to nonliving keratinized tissue of hair, nails, and stratum corneum of skin
Invasion of hair shaft by arthroconidia
Dermatophytes:
Genera (4):
What results in pityriasis/tinea versicolor?
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)
Dermatophytes: Epidermophyton, Trichophyton, Microsporum (Ringworm)
Cause what?
Common Names:
tinea corporis
tinea pedis
tinea cruris
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
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?
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
Dermatophytes
Clinical Identification of Organism: (3)
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)
