Jackson: Skin and Soft Tissue Infections I Flashcards Preview

Micro Exam 1 > Jackson: Skin and Soft Tissue Infections I > Flashcards

Flashcards in Jackson: Skin and Soft Tissue Infections I Deck (60):
1

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)

2

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

3

Dermatophytic fungi

Infection site:
Disease:

Keratinized epithelium

Ringworm

4

Impetigo

Infection site:
Microbe:

Epidermis

S.pyogenes and/or S.aureus

5

Erysipelas

Infection site:
Microbe:

Dermis
S.pyogenes

6

Folliculitis, boils (furuncles), carbuncles

Infection site:
Microbe:

Hair follicles
S.aureus

7

Cellulitis

Infection site:
Microbe:

Subcutaneous fat
S.pyogenes or S.aureus

8

Necrotizing faciitis

Infection site:
Microbe:

Fascia
Anaerobes

9

Gas gangrene

Infection site:
Microbe:

Muscle
Clostridium perfringens

10

Typhoid Fever

Pathogen:
Skin manifestation:

Salmonella typhi
Contaminated petechia

11

What does Neisseria meningitidis cause?

Skin manifestation:

Septicemia, meningitis
Contaminated petechia

12

What causes scarlet fever?

S. pyogenes

13

What causes TSS?

S.aureus

14

What causes Blastomycosis?
Skin manifestation:

Blastomyces dermatitidis

Granulomatous lesion

15

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

16

Staphylococcus Aureus
Alpha toxin

o 7 subunit pore-forming cytolysin (complement-like MOA)
o Pore permits fluid loss from cell (kills erythrocytes, leukocytes)

17

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

18

Staphylococcus Aureus
Exfoliative Toxins:
Two types:

Two types:

Chromosomal

Plasmid-encoded

19

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)

20

Staphylococcus Aureus
Exoproteins for Spread (2):

Hyaluronidase (hydrolyzes connective tissue)

Staphylokinase (promotes fibrinolysis)

21

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)

22

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

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

23

Staphylococcus Aureus

Transmission:

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

24

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

25

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

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

26

What is Bullous Impetigo?

Localized scalded skin syndrome

27

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

28

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)

29

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)

30

Staphylococcus Aureus

Catalase Positive:
Produces:
Differentiates from:

Produces O2 bubbles when hydrogen peroxide is added

Differentiates from strep (catalase negative)

31

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

32

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

33

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

34

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

35

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)

36

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)

37

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

38

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)

39

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

40

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)

41

Cellulitis:

Extension of skin infection or wound

Caused by S.pyogenes or S.aureus

42

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

43

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

44

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)

45

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

46

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

47

Propionibacterium spp.

Clinical Identification of Organism:

Gram positive rods:
- Pleiomorphic (multiple shapes)
- Resemble Corynebacterium

Anaerobic or microaerophilic growth

48

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

49

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

50

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

51

S.pyogenes

Hemolytic reaction
Lancefield group
Disease

Beta

A

Impetigo, Scarlet fever, Rheumatic fever

52

S.agalactiae

Hemolytic reaction
Lancefield group
Disease

Beta

B

Neonatal sepsis, meningitis

53

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

54

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)

55

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)

56

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

57

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)

58

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

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?

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

60

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)