Download Skin Infections I

Microbiology: Skin and Soft Tissue Infections I (Jackson)
DEFINITIONS:

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)
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Ulcer: epithelium ruptures and microbe is discharged

Impetigo: bullous, crusted or pustular eruption
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Erysipelas: well-defined spreading inflammation of dermal lymphatics
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Cellulitis: acute inflammation due to infection of subcutaneous fat
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Necrotizing Fascitis: inflammatory response in soft tissue below the site of infection
SKIN INFECTIONS VIA DIRECT INOCULATION:
Infection Site
Keratinized epithelium
Epidermis
Dermis
Hair follicles
Subcutaneous fat
Fascia
Muscle
Microbe
Dermatophytic fungi
S.pyogenes and/or S.aureus
S.pyogenes
S.aureus
S.pyogenes or S.aureus
Anaerobes
Clostridium perfringens
Disease
Ringworm
Impetigo
Erysipelas
Folliculitis, boils (furuncles), carbuncles
Cellulitis
Necrotizing faciitis
Gas gangrene
BACTERIA CAUSING SKIN INFECTIONS:
Staphylococcus Aureus:

Virulence Factors (Relevant to Skin/Soft Tissue Infections):
Alpha Toxin:
o 7 subunit pore-forming cytolysin (complement-like MOA)
o Pore permits fluid loss from cell (kills erythrocytes, leukocytes)
Toxic Shock Syndrome Toxin (TSST-1):
o Pyrogenic exotoxin (related to those produced by Group A strep)
o Superantigen that cross-links T cell receptor and MHC class II, resulting in cytokine release
o Cytokines cause diverse effects, including endotoxic shock
Exfoliative Toxins:
o Two types:

Chromosomal

Plasmid-encoded
o Cause scalded skin syndrome by inducing intercellular splitting between straum spinosum and stratum
granulosum (desquamation of upper layers of epidermis)
Exoproteins for Spread:
o Hyaluronidase (hydrolyzes connective tissue)
o Staphylokinase (promotes fibrinolysis)
Antiphagocytic Components:
o Protein A: binds Fc portion of IgG (Ab binds upside down)
o Coagulase: promotes surface polymerization of fibrin to resist phagocytosis
o Catalase: neutralizes hydrogen peroxide (protective mechanism since it is an aerobe)

Etiology/Pathogenesis:
Transmission:
o High skin and nasal carriage rates in humans
o No acquired immunity
o Transmission occurs by fomites (inanimate objects)
Pathogenesis:
o Furuncle:

Colonization of hair follicle (folliculitis)

Coagulation of fibrin around lesion
o Carbuncle:

Focal suppuration (abscess)

May lead to entry of organism into bloodstream via lymphatics
o

Scalded Skin Syndrome (Bullous Exfoliation):

Common in neonates and children (often pick up from hospital workers)

Caused by exfoliative toxin

Bullous Impetigo: localized scalded skin syndrome
o Toxic Shock Syndrome:

Caused by TSST-1

Results from vaginal colonizers (ie. tampons in too long) or wound infection
o Wound Contamination:

Bacteremia: spread to blood stream via lymphatics; can result in
 Endocarditis
 Osteomyelitis
 Meningitis
 Pulmonary infection
Clinical Identification of Organism:
Specimen Collection: surface swab, blood, pus (pyogenic) cultured on blood agar
Gram positive cocci in clusters
Catalase Positive:
o Produces O2 bubbles when hydrogen peroxide is added
o Differentiates from strep (catalase negative)
Coagulase Positive:
o Coagulation of citrated plasma by culture
o Differentiates from other staphs (S.epidermis or S.saprphyticus, which are less virulent)
Antimicrobial Susceptibility Testing:
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)
Streptococcus Pyogenes:

Virulence Factors (Relevant to Skin/Wound Infections):
M Protein:
o Function:

Anti-phagocytic (subject to antigenic variation)

Mediates binding to epidermis
o Structure:

Fibrillar structure with C-terminus anchored in the peptidoglycan of the cell wall

Amino terminus variable due to genetic recombination (over 80 serotypes)
o 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
Protein F and Protein G:
o Protein F: mediates fibronectin binding at wound sites
o Protein G: synonymous with protein A in S.aureus; binds the Fc portion of Abs
Streptolysin O and Streptolysin S (Cytolysins):
o Cause of beta-hemolysis on blood agar plates
o 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
Streptococcal Pyrogenic Exotoxins (SPE A-C):
o SPE A: produced by lysogenized (bacteriophage-carrying) Group A strep
o Superantigens that have sequence homology with staphylococcal pyrogenic exotoxins
o Induce cytokine release (fever, rash, T-cell stimulation and endotoxin sensitivity)
Hydrolytic Enzymes:
o Responsible for thin, runny pus found in streptococcal infections
o Streptokinase: dissolves fibrin and facilitates spread (used therapeutically to dissolve blood clots)


Etiology/Pathogenesis:
Impetigo (Pyoderma):
o 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
o 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
o 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
 Can follow impetigo (rarely follows respiratory strep infections)
 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:
o Rapidly spreading infection of deeper layers (can progress to necrosis and septicemia)
o Commonly seen on the face following streptococcal throat infection
o Symptoms Associated:

Edema

Fever

Lymphadenopathy (swollen/enlarged LNs)
Cellulitis:
o Extension of skin infection or wound
o Caused by S.pyogenes or S.aureus
Nosocomial Infections:
o Rates decreasing due to better infection control (ie. in surgical wounds and burn patients)
o Puerperal (Childbed) Fever: 19th century disease caused via physician transmission
Toxic Shock-Like Syndrome (TSLS):
o Cause: highly invasive “flesh-eating” strains that produce SPE A (superantigen)
o Symptoms:

Shock

Renal impairement

Rash

Respiratory failure

Diarrhea

Rapid death
o Up to 30% mortality rate: as compared to 3% for TSS caused by S.aureus
Clinical Identification of Organism:
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

Etiology/Pathogenesis:
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
o As normal flora, can cause infections:

In immunocompromised

Endocarditis, contamination of prosthetic heart valves, cerebrospinal shunts

Clinical Identification of Organism:
Gram positive rods:
o Pleiomorphic (multiple shapes)
o Resemble Corynebacterium
Anaerobic or microaerophilic growth
Special Case Bacterial and Soft Tissue Infections:

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
FUNGI CAUSING SKIN INFECTIONS
Candida Albicans:

Virulence Factors (Relevant to Skin and Wound Infections):
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

Etiology/Pathogenesis:
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

Clinical Identification of Organism:
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: subcutaneous infection caused by this fungi
o Ubiquitous saprophyte in the soil
o Inoculation of conidia (spores) by trauma, usually in the extremities of gardeners and farmers
o 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)
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 nonliving keratinized tissue of hair, nails, and stratum corneum of skin
Invasion of hair shaft by arthroconidia

Etiology/Pathogenesis:
Genera:
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)
Cause superficial infections of the skin (usually the extremeties);
o Common Names:

Ringworm: tinea corporis

Athlete’s Foot: tinea pedis

Jock Itch: tinea cruris
o 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
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

Clinical Identification of Organism:
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)