Bacterial Infections of Skin Flashcards by Elaina JoAnn

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

Staphylococcus aureus, Streptococcus pyogenes

How well did you know this?

Not at all

Perfectly

Skin Defense mechanisms

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.

How well did you know this?

Not at all

Perfectly

gram (+) rod, aerotolerant

propionibacterium acnes

How well did you know this?

Not at all

Perfectly

p. acnes

Gram (+) - rod, aerotolerant

Acne, folliculitis

present in follicle - releases lipases to digest trapped oil

Secretes: proteases, neuraminidase, hyaluronidase, WBC attractant

How well did you know this?

Not at all

Perfectly

p. acnes tx

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

How well did you know this?

Not at all

Perfectly

Impetigo

Superficial bacterial infection that causes skin to flake off

How well did you know this?

Not at all

Perfectly

Impetigo common causes

Staph aureus, strep pyogenes

How well did you know this?

Not at all

Perfectly

Tx impetigo

target both staph/strep - mupirocin or pleuromutilin or cephalexin

How well did you know this?

Not at all

Perfectly

How to differentiate strep p and staph a

Both Gram +

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

How well did you know this?

Not at all

Perfectly

Impetigo Hallmark

Honey-colored crusty flakes, usually around mouth/face

How well did you know this?

Not at all

Perfectly

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.

Staph aureus (also strep pyogenes)

How well did you know this?

Not at all

Perfectly

Clinical presentation: Staph aureus (localized, skin)

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

How well did you know this?

Not at all

Perfectly

Pathology staph aureus

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.

How well did you know this?

Not at all

Perfectly

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

S. aureus

How well did you know this?

Not at all

Perfectly

Staph aureus tree

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

S. aureus

How well did you know this?

Not at all

Perfectly

S. aureus Virulence factors for evading host defenses

protein A (binds Fc portion of IgG)

coagulase (forms fibrin coat around the organism)

hemolysins and leukocidins (destroy RBCs and WBCs)

How well did you know this?

Not at all

Perfectly

S. aureus virulence factors for deep tissue invasion

Hyaluronidase (breaks down connective tissue)

Staphylokinase (lyses formed clots)

Lipase (breaks down fat)

Toxin associated diseases of S. aureus

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)).

Pathology S. pyogenes

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.

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

S. pyogenes

S. pyogenes tree

Bacteria

Gram +

Cocci

Catalase -

b-Hemolytic

Bacitracin sensitive

S. pyogenes

Strep infections (localized, toxin)

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.

Virulence Factors Strep Pyogenes

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)

Strep Pyogenes Toxin-related pathology

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

Catalase Test

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

Coagulase Test

Differentiate between staph aureus (positive) and coagulase-negative staph Bound coagulase reacts directly w/ fibrinogen --\> precipitation when bacteria mixed w/ plasma

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

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

= 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.

Cellulitis

Cellulitis common causes

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.

Tx cellulitis

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.

Bacteria Gram + Bacilli Spore-forming Obligate anaerobe Non-motile

Bacteria Gram + Bacilli Spore-forming Obligate anaerobe Non-motile C. perfringens

Clostridium perfringens tree

Bacteria Gram + Bacilli Spore-forming Obligate anaerobe Non-motile C. perfringens

Cellulitis pathology (C. perfringens)

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).

Gas Gangrene pathology

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

C. perfringens tx

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

Bacteria Gram - Bacilli Lactose non-fermenter Oxidase + Glucose non-fermenter

Bacteria Gram - Bacilli Lactose non-fermenter Oxidase + Glucose non-fermenter P. aeruginosa

Pseudomonas aeruginosa tree

Bacteria Gram - Bacilli Lactose non-fermenter Oxidase + Glucose non-fermenter P. aeruginosa

P. aeruginosa causes

Hot tub folliculitis, burn wound infection (cellulitis)

Gas gangrene sxs

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

Tx for TSS w/o clostridium

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