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MS Week 1 > Bacterial Skin Infections > Flashcards

Bacterial Skin Infections Flashcards

1
Q

What are the 3 ways that bacteria may initiated infection?

A
  1. Breach the skin (wound etc)
  2. Systemic disease (virus- whole body response)
  3. Toxin-mediated damage
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2
Q

Describe the skin’s defenses

A

Outer layer of continually regenerated dead cells, antimicrobial peptides (defensins and cathelicidans), low pH of sebum, low pH and high salt content of sweat, lysozymes of urine tears and sweat, resident phagocytes and normal flora compete for colonization.

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3
Q

What causes acne/folliculitis?

A

Inflammation of the hair follicle, due to oil and the anaerobic environment. Bacteria like to feed on the oil in this area. Immune response –> neutrophils aka pus.

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4
Q

What is a comedo?

A

A clogged pore. Whitehead is closed, blackhead is open (oxidized).

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5
Q

What agent commonly causes acne? How does it work?

A

Propionibacterium acnes is an aerotolerant bacteria that is present in the follicle and releases lipases to digest oil –> acne

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6
Q

What is impetigo? Which agents may cause it?

A

Impetigo is a superficial bacterial infection causing skin to flake/peel. Typically found around mouth/face or extremities. Highly contagious, especially common in children!
Caused by staphylococcus aureus or streptococcus pyogenes

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7
Q

How do folliculitis and impetigo vary?

A

Folliculitis is NOT contagious whereas impetigo is HIGHLY contagious.

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8
Q

Describe the clinical presentation of staphylococcus aureus?

A

Localized skin/subcut infection, may be superficial or deep –> impetigo, cellulitis, folliculitis, furnucles and carbuncles.
* Common surgical would agent (MRSA) takes a few days to present

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9
Q

Virulence factors of staphylococcus aureus?

A

Protein A- binds Fc portion of IgG (antibody cannot be recognized by macrophages to destroy pathogen)
Coagulase- forms fibrin coat around organism
Hemolysins and leukocidins- destroy RBC and WBCs

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10
Q

Differentiating factors of staphylococcus aureus

A

Gram + cocci bacteria
Catalase +
Coagulase +
Beta hemolytic

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11
Q

Virulence factors of staphylococcus aureus for deep tissue infection

A

Hyaluronidase- breaks down connective tissue
Staphylokinase- lyses formed clots
Lipase- breaks down fat

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12
Q

Toxins produced by staphylococcus aureus

A

Toxic shock syndrom toxin 1 (TSST-1) (menstrual or non-mestrual) is a superantigen leading to excessive cytokine release (TNF and IL1) leading to acute fever, rash, hypotensive shock, organ dysfunction and possible death!

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13
Q

What is scalded skin syndrome? Which pathogen causes it? What toxins?

A

SSS is caused by exfoliative toxins ET-A and ET-B of Staphylococcus aureus! They diffuse systemically and the epidermis separates and skin sloughs off –> fluid loss, secondary infection and possible death

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14
Q

Describe the clinical presentation of streptococcus pyogenes

A

Localized skin/subQ infection –> impetigo, erysipelas, cellulitis
Toxin mediated= toxic shock syndrome (STSS), necrotizing fasciitis!!!

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15
Q

Differentiating factors for streptococcus pyogenes

A

Gram + cocci bacteria,
catalase -
beta hemolytic
bacitracin sensitive

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16
Q

What lab test differentiates between strep and staph infections???

A

CATALASE! Staph is catalase +, strep is catalase -

17
Q

Which microbe may be pathogenic or part of normal flora?

A

Strep pyogenes

18
Q

How does strep pyogenes colonize to become an infection?

A

Following trauma, colonization occurs –> inflammation –> impetigo. Deeper infections include erysipelas and cellulitis. Invasion from skin infections can lead to glomerulonephritis but not rheumatic fever!

19
Q

Which pathogen may cause endocarditis in IV drug users? May also be due to secondary infection of varicella-zoster.

A

Staph aureus

20
Q

What causes strep throat? What happens if its untreated? What happens if its an infection of the skin?

A

Strep pyogenes causes strep throat and if left untreated it can leave to glomerulonephritis AND rheumatic fever. Infections of the skin can cause glomerulonephritis BUT NOT rheumatic fever!

21
Q

Describe the virulence factors of strep pyogenes. What is important about the encoding of some?

A

Streptokinase- converts plasminogen to plasmin
M protein- resists phagocytosis
Hyaluronidase- breaks down connective tissue
DNase- degrades DNA
streptolysin O- destroys RBC
strepolysin S- destroys WBCs
*Streptokinase and hyaluronidase are encoded by a lysogenized prophage! These bacteria are themselves suffering from a viral infection!

22
Q

Toxins produced by streptococcus pyogenes

A

Toxic shock syndrome begins as a skin infection (cellulitis) leading to a release of pyrogenic exotoxin A a SUPERANTIGEN –> polylclonal activation of T cells –> acute fever, shock, multiorgan failure

Necrotizing fasciitis= TRAUMA allows for deep seated infection leading to release of exotoxin B a protease –> rapid necrosis along fascial planes with no damage to muscles.

23
Q

How does necrotizing fasciitis proceed? Which pathogen?

A

A trauma leads to deep seated infection of strep pyogenes –> exotoxin B protease –> fever, necrosis along fascial planes

24
Q

How is impetigo diagnosed and treated?

A

Diagnosed by observation.
Treated by topical antibiotics or oral cephalexin.
Only distinguish between strep or staph if the rash does not respond to empiric treatment!

25
Q

Why do we do a catalase test? What principle is it based on?

A

Catalase test to differentiate between staph (+) and strep (-). Aerobic organisms produce ROS during metabolism including hydrogen peroxide and superoxideradical. These bacteria have enzymes to detoxify the products of their metabolism, including catalase. If you inoculate bacteria with hydrogen peroxide you would see a rapid release of O2 bubbles (and water) if catalase enzyme is present. Without catalase, there would be weak or no O2 bubbles.

26
Q

Why do we do a coagulase test? What principle is it based on?

A

Coagulase test to differentiate between staphyloccous species, aureus (+) and epidermitis (-). Coagulase reacts with fibrinogen which results in precipitation of fibrinogen on staph cells leading to a clump when in a bacterial suspension with blood plasma.

27
Q

Why do we do a novobiocin sensitivity test? What principle is it based on?

A

Novobiocin sensitivity test to differentiate between staph saprohyticus (resistant- may cause UTI) and staph epidermidis (sensitive). Do this AFTER a coagulase negative test.

If a staph strain is sensitive the antibiotic disc will not have a complete lawn of growth- it will be unable to grow near the antibiotic disc.

28
Q

Describe cellulitis infection. Symptoms, onset, causative agent/s.

A

A fast spreading infection of the DERMIS and subQ tissues- causes pain, redness, tenderness, swelling and warmth. Takes a few days to develop symptoms. Caused by either staph aureus or strep pyogenes, though almost any bacterium can cause. May be a complication of varicella (breaks in the skin).

29
Q

Describe gas gangrene. Which pathogen causes it? Symptoms? onset?

A

Gas gangrene is caused by clostridium perfingens, spores are found in soil. Bacteria are ANAEROBIC and require release of exotoxins to mediate damage in disease. Require deep muscle lacerations! Symptoms include, gas formation, black fluid, shock.

30
Q

What is the most important exotoxin of clostridium perfingens? What does it do?

A

Alpha toxin, common to gas gangrene. Causes red blood cell rupture, edema and tissue destruction!

31
Q

Describe a cellulitis infection caused by c. perfingens. How does it differ from staph or strep?

A

Bacteria is picked up from soil and infect a necrotic skin wound. Release enzyme leading to slow, painless infection with GAS production. Forms collections of gas under the skin that crackle when touched aka crepitus!

32
Q

How do you treat a clostridium perfingens infection?

A

Surgical removal of infected areas, hyperbaric oxygen to kill anaerobic organisms. If a weak, local infection could try penicillin or clindamycin.

33
Q

What agent causes hot tub folliculitis? How does it present? What is the more common and more severe infection?

A

Pseudomonas aeruginosa, infection arises by breach in host defense barriers. Able to grow and divide in a hot tub leading to folliculitis anywhere you were in water.

May cause more common and more severe infection of cellulitis.

34
Q

Key characteristics of c. perfingens

A

Gram + BACILLI bacteria
Spore forming
Obligate ANEROBE (deep seated infections!)
Non-motile

35
Q

Key characteristics of pseudomonas aeruginosa

A 
Normal flora- 
Gram NEG Bacilli bacteria
Lactose non-fermenter
oxidase +
Glucose non-fermenter

MS Week 1 (11 decks)

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