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Immuno mikro eng > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

1
Q

What is a macule?

A

Flat, red inflammatory response to a microbe or toxin

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2
Q

What is a papule?

A

Raised, red bump with more marked inflammation

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3
Q

What is a vesicle?

A

A blister

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4
Q

What is an ulcer? What is its developmental progression?

A

Rupture of epithelium

Macule -> Papule -> Vesicle -> Ulcer

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5
Q

What is impetigo?

A

A bullous, crusted, or pustular eruption.

Generally caused by S. pyogenes, called pyoderm, especially when honey-colored

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6
Q

What is a furuncle vs carbuncles?

A

Furuncle - boil

Carbuncle - collection of boils under the skin

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7
Q

What is erysipelas?

A

A well-defined, spreading inflammation of dermal lymphatics very diagnostic of S. pyogenes

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8
Q

What is cellulitis?

A

An acute, serious inflammation due to infection of subcutaneous fat

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9
Q

What is necrotizing fasciitis?

A

Inflammatory response in soft tissue below site of infection

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10
Q

Give the three virulence factors associated with S. aureus infection?

A
  1. Alpha-toxin
  2. Toxic shock syndrome toxin
  3. Exfoliative toxins
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11
Q

What is alpha toxin?

A

A pore-forming cytolysin which kills RBCs (hemolysin) and leukocytes
Works like complement

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12
Q

What is TSST?

A

Toxic shock syndrome toxin -> pyrogenic exotoxin which is a superantigen, crosslinking TCR to MHC2, causing cytokine release and shock

(rash, fever, hypotension, very similar to endotoxic shock from LPS)

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13
Q

How do exfoliative toxins work and what do they cause if all over the body or locally?

A

Induce intercellular splitting at desmosome, between stratum spinosum and granulosum

All over body: Staphylococcal Scalded Skin Syndrome, common on babies but gets better because it’s very superficial

Locally: Bullous impetigo

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14
Q

How is S. aureus generally transmitted?

A

Skin and nasal carriage, also fomites

No acquired immunity

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15
Q

What are the skin lesions which can be caused by S. aureus?

A

Furuncle -> folliculitis followed by coagulation of fibrin around lesion leads to boil

Carbuncle - focal abscess which can lead to entry of organism into blood via lymphatics

Scalded skin syndrome (bullous exfoliation) or bullous impetigo

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16
Q

Where are two places where TSS is caused?

A
  1. Vagina

2. Wound infection

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17
Q

What is the most common mechanism of S. aureus bacteremia and what are some clinical results of this?

A

Entry via wound contamination, spread to blood stream via lymphatics

Cause: Endocarditis, meningitis, pulmonary infection, osteomyelitis

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18
Q

What is the gram stain, catalase, and coagulase for Staphylococcus aureus?

A

Gram stain + clusters

Catalase positive (will cause O2 bubbles when H2O2 added to culture)

Coagulase positive (will cause coagulation when put in plasma, versus other staphylococcal infections which won’t)

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19
Q

How is antibiotic susceptibility testing done?

A

Spread the culture all the way across the agar with an Abx strip of descending concentration. The concentration where it starts growing is MIC

Need to be able to reasonably achieve MIC in vitro

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20
Q

What are four virulence factors for Streptococcus pyogenes?

A
  1. M protein
  2. Streptolysin O
  3. Streptococcal pyrogenic exotoxins (Spe A-C)
  4. Hydrolytic enzymes (Streptokinase)
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21
Q

What is the purpose of M protein? What is it responsible for?

A

Antiphagocytic, does molecular mimicry with antigen variation via N terminus (>80 serotypes)

Mediates binding to epidermis

Responsible for post-streptococcal sequelae, including acute glomerulonephritis, rheumatic heart disease

22
Q

What blood marker is very diagnostic of S. pyogenes infection?

A

Antibodies to SLO, which mediate self-attack and augment cell lysis by fixing complement

23
Q

What is the mechanism of action of Streptolysin O (SLO)?

A

Cytolysin, attacking cell membranes and forming large pores. It is oxygen-stable, and causes beta-hemolysis on blood agar plates

24
Q

What produces SpeA?

A

Lysogenized (bacteriophage-infected) Group A Strept.

25
Q

What are Spe’s?

A

Superantigens which are similar to TSST, inducing cytokine release causing shock and endotoxin sensitivity

26
Q

What do hydrolytic enzymes like streptokinase cause?

A

They dissolve fibrin to facilitate spread of bacteria, and are responsible for runny, thin pus.

Can be used therapeutically to dissolve blood clots

27
Q

What is the pathogenesis / spread of pyoderma / impetigo?

A

Minor trauma such as insect bite on face or lower extremities causes a vesicle to rupture, leading to superficial spread especially between young children with poor hygiene.

Spread easily by fomites and exacerbated by staph aureus lesions (bullous impetigo)

28
Q

What do post-streptococcal sequelae typically cause?

A

Acute glomerulonephritis, especially following skin infection (rarely respiratory)

Hematuria, hypertension, proteinuria due to kidney damage. Rare in the US.

This is a type 3 hypersensitivity

29
Q

When does erysipelas occur and what does it progress to? What are the associated symptoms?

A

Occurs on face, especially following strept throat. Can rapidly spread infection to deeper layers and cause necrosis + septicemia.

Associated with edema, fever, and lymphadenopathy

30
Q

What causes cellulitis?

A

Deep skin infection or wound

Caused by Group A Strept / S. aureus

31
Q

What causes Toxic shock-like syndrome (TSLS)? Necrotizing fasciitis?

A

Highly invasive S. pyogenes strains producing SpeA, due to superantigen

Often caused by wound infection involving S. pyogenes

Same thing causes necrotizing fasciitis

32
Q

How is Streptococcus pyogenes indentified in the lab?

A 
Gram positive cocci in chains
Beta-hemolytic, pyogenic
Lancefield group A (carbohydrate antigen)
Catalase negative
Bacitracin sensitive
33
Q

What bacteria causes acne?

A

Propionibacterium acnes

34
Q

What does Clostridium perfringens cause?

A

Gram positive anaerobic rod causing Gas gangrene from wounds

35
Q

How does Candida albicans attach and invade?

A

Adheres vie fibronectin

Invades via pseudohyphae / germ tubes which extend across mucosal barriers, mediated by proteases / elastases

36
Q

How does our immune system protect us from yeast infection and what does Candida infection indicate?

A

Neutrophils are the first line of defense, Chronic candidiasis indicates T cell deficiency

37
Q

Where does Candida like to grow? Who does it affect most?

A 
Hair follicles (folliculitis)
Intertrigo (skin folds), especially wet skin folds. Thus, effects dishwashers on hands and infants (diaper rash)
38
Q

How is Candida identified?

A

Erythematous papules are scraped and seen under microscope with germ-tube pseudohyphae (they are unicellular)

39
Q

What causes Sporotrichosis?

A

Subcutaneous infection via thornprick and inoculation of conidia (spores) of Sporothrix schenckii

Affects gardeners and farmers the most

40
Q

When can Sporotrichosis get really bad?

A

The initial stage is a painless papule week post-inoculation. Can get really bad if it ulcerates and becomes chronic, draining lymph channels.

Can spread to CNS, bones, eyes, and lungs in rare cases

41
Q

What are the dimorphic growth phases of Sporothrix?

A

Yeast form - in humans at 37 degrees C

Mold form - with thin hyphae and conidial spores at 25 C, very ubiquitous

42
Q

How do the tinea infections live (virulence factors)?

A

They are adapted to living in keratinized tissue of nails, hair, and stratum corneum of skin

Arthroconidia will invade hair shafts plugging root, causing ring-shaped hair loss

43
Q

What organisms cause the Tinea infections?

A

Dermatophytes, like Epidermophyton, Tricophyton, and Microsporum

44
Q

What is ringworm?

A

Tinea infection, especially of the body (Tinea corporis, on nonhairy skin) or scalp (Tinea capitis)

45
Q

What is tinea pedis called? Where is it?

A

Athlete’s foot, interdigital spaces of feet

46
Q

What is tinea cruris called? Where is it?

A

Jock itch (groin area)

47
Q

What is tinea unguim? What does it cause?

A

Tinea of nails, causing discoloration and growth malformation

48
Q

What environments do tinea infections typically occur in?

A

Moist skin folds, and maceration promotes infection

49
Q

How is tinea passed?

A

They have low infectivity and virulence, typically passed via person-person transmission via very close contact with infected area, or infection from animal or soil.

50
Q

What limits the spread of tinea infections? What do chronic infections mean?

A

Rapid shedding of keratinized layers due to advanced skin growth which is induced by infection.

Cell mediated immunity is important and delayed-type (Type 4) hypersensitivity will result

Chronic infections: impaired T cell and lack of DTH reaction

51
Q

How is tinea identified in the lab?

A

Scraping from the edge of the lesion or infected hairs.

Some species fluoresce under UV light

Immuno mikro eng (56 decks)

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