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Skin MS: Week 1 > Bacterial Infections of Skin > Flashcards

Bacterial Infections of Skin Flashcards

1
Q

Most common pathogens for skin infections (except for childhood infections)

A

Staphylococcus aureus, Streptococcus pyogenes

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2
Q

Skin Defense mechanisms

A
  • Dry outermost layer comprised of continually regenerated, dead epithelial cells.
  • Covered with antimicrobial peptides produced by epithelial cells (defensins and cathelicidans) – disrupt bacterial membranes.
  • Low pH of sebum (produced by the sebaceous gland).
  • Low pH and high salt content of sweat.
  • Presence of lysozyme – breaks down peptidoglycan found in bacterial cell walls.
  • Resident phagocytes (like Langerhans cells) are present in the epidermis as a first line defense against colonization provided by the innate immune system.
  • Normal flora of the skin compete for colonization with potential pathogenic microorganisms.
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3
Q

gram (+) rod, aerotolerant

A

propionibacterium acnes

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4
Q

p. acnes

A

Gram (+) - rod, aerotolerant

Acne, folliculitis

present in follicle - releases lipases to digest trapped oil

Secretes: proteases, neuraminidase, hyaluronidase, WBC attractant

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5
Q

p. acnes tx

A

Treatment / prevention = topical agents to promote sloughing of skin cells and/or topical or oral antibiotics.

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6
Q

Impetigo

A

Superficial bacterial infection that causes skin to flake off

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7
Q

Impetigo common causes

A

Staph aureus, strep pyogenes

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8
Q

Tx impetigo

A

target both staph/strep - mupirocin or pleuromutilin or cephalexin

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9
Q

How to differentiate strep p and staph a

A

Both Gram +

Catalase test –> Strep negative, staph + (bubbles)

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10
Q

Impetigo Hallmark

A

Honey-colored crusty flakes, usually around mouth/face

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11
Q

Very common infectious agent of the skin. Can cause superficial infections like boils but it can also develop into deep tissue infections like carbuncles and abscesses. Also produces several toxins which can lead to serious toxin-mediated diseases.

A

Staph aureus (also strep pyogenes)

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12
Q

Clinical presentation: Staph aureus (localized, skin)

A

Localized skin/subcutaneous infection = impetigo, cellulitis, folliculitis, furuncles, carbuncles. Common infectious agent of surgical wounds.

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13
Q

Pathology staph aureus

A

Can colonize the skin (following breach) and evade the host defenses using:

protein A (binds Fc portion of IgG)

coagulase (forms fibrin coat around the organism)

hemolysins and leukocidins (destroy RBCs and WBCs)

Neutrophils localize to the infection site –> purulent abscesses form –> skin/subcutaneous infections may more deeply invade and reach the blood stream.

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14
Q

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

A

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

S. aureus

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15
Q

Staph aureus tree

A

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

S. aureus

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16
Q

S. aureus Virulence factors for evading host defenses

A

protein A (binds Fc portion of IgG)

coagulase (forms fibrin coat around the organism)

hemolysins and leukocidins (destroy RBCs and WBCs)

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17
Q

S. aureus virulence factors for deep tissue invasion

A

Hyaluronidase (breaks down connective tissue)

Staphylokinase (lyses formed clots)

Lipase (breaks down fat)

18
Q

Toxin associated diseases of S. aureus

A

Toxic shock syndrome = toxic shock syndrome toxin-1 (TSST-1), diffuses systemically, superantigen (promotes excessive cytokine release) –> acute fever, rash, desquamation on palms and soles, hypotensive shock, organ dysfunction, possible death.

Scalded skin syndrome = most often affects children, exfoliative toxins ET-A and ET-B, diffuse systemically, epidermis separates and skin sloughs off, fluid loss, secondary infection, possible death (50% mortality rate in adults, Ritter’s syndrome severe in neonates (umbilical cord infection)).

19
Q

Pathology S. pyogenes

A

May be normal flora of the skin.

Can colonize in the skin (following trauma) leads to colonization à inflammation à pustular lesions and honeycomb-like crusts (impetigo) at the site of inoculation. Deeper infections lead to erysipelas and cellulitis. Invasion from skin infections can lead to glomerulonephritis but not Rheumatic fever.

20
Q

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

A

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

S. pyogenes

21
Q

S. pyogenes tree

A

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

S. pyogenes

22
Q

Strep infections (localized, toxin)

A

Localized skin/subcutaneous infection = impetigo, erysipelas, cellulitis

Toxin-mediated = Toxic shock syndrome, necrotizing fasciitis

Also causes strep throat, scarlet fever, pneumonia, puerperal fever, nectrotizing faciitis, bloodstream infections, rheumatic fever, glomerulonephritis.

23
Q

Virulence Factors Strep Pyogenes

A

Streptokinase (converts plasminogen to plasmin)

M protein (resists phagocytosis)

Hyaluronidase (breaks down connective tissue)

DNase (digests DNA)

Streptolysin O (destroys RBCs)

Streptolysin S (destroys WBCs)

24
Q

Strep Pyogenes Toxin-related pathology

A

Toxic shock syndrome = skin infection (cellulitis) –> systemic release of pyrogenic exotoxins A (superantigen) –> polyclonal activation of T cells –> acute fever, shock, multiorgan failure.

Necrotizing fasciitis = trauma allows for deep seated infection –> release of exotoxin B (protease) –> rapid necrosis along fascial planes with no damage to muscles

25
Q

Catalase Test

A

Aerobic and facultative anaerobic organisms - catalase capable of converting hydrogen peroxide to water and oxygen.

The presence of the catalase is possible by putting a small inoculum of bacteria into hydrogen peroxide. With catalase present there is a rapid release of oxygen bubbles. The lack of catalase is evident by a lack of or weak bubble production.

Strep - negative

Staph - positive

26
Q

Coagulase Test

A

Differentiate between staph aureus (positive) and coagulase-negative staph

Bound coagulase reacts directly w/ fibrinogen –> precipitation when bacteria mixed w/ plasma

27
Q

Used to differentiate between Staphylococcus saprophyticus (resistant) from Staphylococcus epidermidis (sensitive).

A

Novobiocin sensitivity - Novobiocin inhibits bacterial DNA gyrase in susceptible microorganisms.

28
Q

= fast-spreading infection in the dermis and in the subcutaneous tissues. It causes pain, tenderness, swelling, and warmth. Fever and swelling of the lymph nodes draining the area may also occur.

generally follows introduction of bacteria or fungi into the dermis. Symptoms take several days to develop.

A

Cellulitis

29
Q

Cellulitis common causes

A

The most common causes of the condition in healthy people are Staphylococcus aureus and Streptococcus pyogenes, although almost any bacterium and some fungi can cause this condition in an immunocompromised patient. In infants, group B streptococci are a frequent cause. Occasionally, cellulitis is a complication of varicella (chickenpox) infections.

30
Q

Tx cellulitis

A

Mild cellulitis responds well to oral antibiotics chosen to be effective against both S. aureus and S. pyogenes.

More involved infections and infections in immunocompromised people require intravenous antibiotics. If there are extensive areas of tissue damage, surgical debridement is warranted.

31
Q

Bacteria

Gram +

Bacilli

Spore-forming

Obligate anaerobe

Non-motile

A

Bacteria

Gram +

Bacilli

Spore-forming

Obligate anaerobe

Non-motile

C. perfringens

32
Q

Clostridium perfringens tree

A

Bacteria

Gram +

Bacilli

Spore-forming

Obligate anaerobe

Non-motile

C. perfringens

33
Q

Cellulitis pathology (C. perfringens)

A

pick up C. perfringens from the soil where the bacteria infect the anaerobic environment of a necrotic skin wound. The bacteria release degradative enzymes which results is a slow, painless infection with gas production. Forms collections of gas under the skin that crackle when touched (crepitus).

34
Q

Gas Gangrene pathology

A

pick up C. perfringens spores from the soil where they get introduced into deep muscle lacerations (military wounds, auto accidents, etc). Spores germinate and bacteria grow in the anaerobic environment releasing toxins (alpha toxin - hemolytic)and degradative enzymes that degrade muscle tissue and form gas. Black fluid may leak from the skin. Shock is possible.

*Toxins produced in large muscles and leak to nearby healthy tissue –> necrosis

35
Q

C. perfringens tx

A

Surgical removal of infected areas. Hyperbaric oxygen to kill anaerobic organisms. Penicillin or clindamycin (effective only in local, weak infections).

36
Q

Bacteria

Gram -

Bacilli

Lactose non-fermenter

Oxidase +

Glucose non-fermenter

A

Bacteria

Gram -

Bacilli

Lactose non-fermenter

Oxidase +

Glucose non-fermenter

P. aeruginosa

37
Q

Pseudomonas aeruginosa tree

A

Bacteria

Gram -

Bacilli

Lactose non-fermenter

Oxidase +

Glucose non-fermenter

P. aeruginosa

38
Q

P. aeruginosa causes

A

Hot tub folliculitis, burn wound infection (cellulitis)

39
Q

Gas gangrene sxs

A

Pain, edema, bloody exudate, fever, increased HR, black skin, crepitus

40
Q

Tx for TSS w/o clostridium

A

Linezolid + Meropenem + Piperacillin (started w/ empiric tx then dial back and focus in on definitive pathogen)

Skin MS: Week 1 (9 decks)

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