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MSK I > Microbiology: Skin Infection Staph and Strep > Flashcards

Microbiology: Skin Infection Staph and Strep Flashcards

1
Q

Why do gram positive bacteria stain blue?

A

Thick murein layers (peptidoglycan)

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2
Q

A teenager comes to see you with acne. Where is the most likely source of bacteria that caused her acne?

A

Resident skin flora. Staph epidermidis to be exact.

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3
Q

Who are the transient bacterial bums of our skin?

A

Staph aureus and staph pyogenes

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4
Q

A child comes to see you with a bacterial infection around their mouth confined to the epidermis. What spreading infection may the child have?

A

Impetigo from strep or staph

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5
Q

Lab results indicate your patient has a spreading bacterial infection of the dermal lymphatics. What might your patient have?

A

Erysipelas from strep

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6
Q

Your cousin cuts his leg and gets a spreading bacterial infection in the subcutaneous fat layer. What would you call this infection?

A

Cellulitis from strep or staph

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7
Q

After shaving you notice razor burn bumps that form little abscesses across your face. What do you call this?

A

Folliculitis from staph

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8
Q

What bacteria do you suspect when you see pus and pyogenic skin infections?

A

Staph and strep

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9
Q

Characteristics of pyogenic cocci

A

Invasive, pus-filled lesions, obligate extracellular bacteria, anti-phagocytic mechanisms

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10
Q

Can strep and staph be lysed by antibody and complement?

A

No, only gram negative bacteria can be lysed. Antibody and complement aid in phagocytosis of gram positive bacteria.

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11
Q

Characteristics of streptococci

A

Gram +, come in pairs or chains, and are catalase negative (can’t make water from a dilute solution of hydrogen peroxide)

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12
Q

Bacteria is placed in a dilute solution of hydrogen peroxide. Bubbles are observed, what is the likely bacteria?

A

Staph. It is a catalase positive bacteria.

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13
Q

What helps the clinical laboratory determine what type of strep has been isolated?

A

Beta-hemolytic pattern around the colony on blood agar. Antigenic composition. Also using physiological traits (can the organism grow in salt).

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14
Q

What type of strep is always beta hemolytic?

A

Group A strep

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15
Q

What are rapid group A strep tests looking for?

A

Group A carbohydrate antigen on cell wall. All group A strep have this antigen.

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16
Q

How can you test for group A strep with antibiotics?

A

Apply bacitracin to a plate of the bacteria and incubate over night

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17
Q

Lab tests come back for gram-positive, chain forming, catalase negative, bacitracin/PYR sensitive, beta hemolytic bacteria. What is the likely bacteria?

A

Group A streptococcus

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18
Q

Why does our body have a hard time recognizing strep capsules?

A

It is made of hyaluronic acid, which we also have in our body.

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19
Q

What is the major anti-phagocytitic component of group A strep?

A

M protein extending out of the bacterial capsule

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20
Q

Why do some people get endocarditis after a group A strep infection?

A

The M protein of group A strep is similar to the cells in the heart

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21
Q

What regulates production of bacterial pyrogenic exotoxins?

A

Transduction of a bacterial phage and expression of toxin gene. These toxins can produce super antigens

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22
Q

How do super toxins work?

A

Super activation of T cells.

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23
Q

What effects stem from a bacteria that produces toxic shock-like symptoms?

A

The bacteria also becomes systemic and symptoms are systemic.

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24
Q

This bacterial product causes RBC lysis on blood plates and we make antibodies against it.

A

Streptolysin O

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25
Q

How does strep escape destruction by PMNs?

A

DNAses chop up the DNA that entangles them from the PMNs

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26
Q

What strep product is useful during surgery?

A

Streptokinase. It lyses blood clots which can help bacteria spread but can also be used in surgery.

27
Q

What strep product helps it escape complement opsinization?

A

C5a peptidase. It degrades C5a so PMNs are not attracted.

28
Q

What are the suppurative strep diseases?

A

Pharyngitis, Pyoderma and TSS

29
Q

What sub diseases are pyodermas?

A

Impetigo, Erysepelas, Cellulitis and Necrotizing fasciitis

30
Q

What are examples of non-suppurative strep diseases?

A

Acute glomerular nephritis and rheumatic fever due to antibody production for M protein

31
Q

A patient presents with strawberry tongue, rash and desquamation of the skin. What might this patient have and how are these symptoms being produced?

A

Scarlet fever. It is a staph infection that causes systemic symptoms but the bacteria stays in the same place.

32
Q

A patient comes to your clinic with symptoms of rheumatic fever following a sore throat. Why should the sore throat have been treated more seriously in the first place?

A

Group A strep infections have the M protein which mimics heart tissue. If not treated quickly, the body will develop anti-M antibodies and these antibodies will attack the heart.

33
Q

A patient comes to your clinic with symptoms of acute glomerulonephritis after a sore throat. Why should the sore throat have been treated more seriously in the first place?

A

The body made anti-M antibodies and the antigen-antibody complex has deposited in the kidney.

34
Q

What syndrome follows a strep A infection that affects neurological function in pediatrics?

A

PANDAS

35
Q

What must people with rheumatic fever be treated with for the rest of their lives?

A

Penicillin G. This is so they don’t have another autoimmune response against the heart.

36
Q

How does s. aureus differ from a strep?

A

They form clusters instead of pairs and lines. It is still hemolytic but catalase it positive (makes H2O2 bubble).

37
Q

Which type of staph is not beta-hemolytic?

A

S. epidermidis

38
Q

How would an agar plate of s. aureus and s. epidermidis differ?

A

S. aureus is yellow and hemolytic. S. epidermidis is white an non hemolytic

39
Q

How does s. aureus differ from s. epidermidis in coagulase tests?

A

S. aureus is positive and s. epidermidis is negative

40
Q

What happens if you mix S. aureus with mammalian plasma?

A

You get a fibrin clot. This is the coagulase test used to test for S. aureus which turns fibrinogen to fibrin.

41
Q

A patient presents with a sty on the eye. How would you classify this subcutaneous skin infection?

A

Furuncle

42
Q

A patient with a furuncle loses the medication for it and the sty gets worse and begins to produce pus. What is it classified as now?

A

Carbuncle. The furuncles coalesce and begin producing pus as they recruit neutrophils.

43
Q

A breast feeding mother gets mastitis. What are possible sources of infection?

A

Her normal flora staph or the hospital

44
Q

Where does all of this patient’s acne come from?

A

Staph in his nose. It is a chronic furuncluosis

45
Q

What does a staph infection progress to after a carbuncle?

A

Cellulitis or impetigo

46
Q

What are possible consequences of staph infections going deep?

A

Osteomyelitis, septic arthritis, meningitis or pneumonia.

47
Q

What are possible consequences of staph getting into the blood stream (bacteremia)?

A

Endocarditis, meningitis, pneumonia, pyelonephritis and septic shock

48
Q

Why are diabetics at higher risk for staph aureus infections?

A

They have poor circulation and decreased neutrophil response to bacteria.

49
Q

What is the body’s #1 defense against gram positive bacteria?

A

Neutrophils. This is why complement C3b is crucial.

50
Q

How does staph aureus defend itself against phagocytes?

A

Capsule, Protein A (binds Fc end of antibodies to decrease specific antibody opsinization), Catalase breaks down toxic by products from O2 burst, Leukocidin pokes holes inside neutrophils.

51
Q

How are staph aureus infections so good at making abscesses?

A

Initiates conversion of fibrinogen to fibrin and surrounds the infection site with fibrin.

52
Q

How does staph aureus induce toxic shock?

A

Techoic acid induces TLR2 action

53
Q

How does staph aureus make it easier for itself as far as moving through subcutaneous tissue?

A

They produce hyaluronidase, which breaks down ECM hyaluronic acids.

54
Q

What cytotoxins are produced by staph aureus and what do they do?

A

Alpha hemolysin: pore-former, Beta and Delta Toxin: disrupts cell membranes, Gamma toxin and leukocidins put holes in neutrophils and macrophages

55
Q

What are the toxin-mediated diseases caused by staph aureus?

A

Bullous impetigo, scaled skin syndrome, staphylococcal scarlet fever, TSS and food poisoning

56
Q

*

A

Bullous impetigo caused by exfoliatin toxin from staph

57
Q

*

A

Scaled skin syndrome. Caused by exfoliatin toxin from staph.

58
Q

How do exfoliatins work?

A

They split desmosomes in the stratum granulosum

59
Q

What causes toxic shock syndrome?

A

TSST-1. Nonspecifically binds T cells with APCs.

60
Q

How can you confirm what strain of bacteria someone has?

A

Pulsed Field Gel Electrophoresis (PFGE) chops up chromosomes into fragments with restriction enzymes. The fragments are run on a gel and compared. Bacteria is also immune to its own phages and phage typing can be used.

61
Q

How are MRSA bacteria resistant to antibiotics?

A

It has a mecA gene which codes for an altered PCN binding protein that won’t bind antibiotics.

62
Q

How are VRSA bacteria resistant to vancomycin?

A

They have the vanA gene changes the peptidoglycan terminus to D-ala-D-lactate instead of D-ala-D-ala which is what vancomycin acts on and inhibits peptidoglycan chain production.

63
Q

Why do you wipe someone’s arm with alcohol before a shot?

A

To prevent s. epidermidis infection

64
Q

Why is s. epidermidis particularly good at nosocomial infections?

A

They form biofilms that can mix with other bacteria.

MSK I (37 decks)

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