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Micro Quiz 3 > 22: staphylococci - jonathan > Flashcards

22: staphylococci - jonathan Flashcards

1
Q

What bacteria is the major cause of hospital bacteremias?

A

Staphylococcus aureus and Staph Epidermis

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2
Q

What are the major causes and concerns with hospital Staph infections?

A

IV catheters or other implanted devices
Resistance to Methicillin and even Vancomycin
High mortality and high costs

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3
Q

What are the lab Dx features that S. aureus, S. epidermis, and S. saprophyticus share?

A 
All...
G+ grape clusters
Catalase
Faculative anaerobes, although S. saprophyticus is slow anaerobic growth
Teichoic acid
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4
Q

What color are the colonies for S. aureus, S. epidermis, and S. saprophyticus?

A

S. aureus is yellow

S. epidermis and S. saprophyticus is white

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5
Q

In terms of catalase, compare Staph from Strep.

A 
Staph = catalase
Strep = NO catalase
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6
Q

Which Staph is resistant to novobiocin?

A

S. saprophyticus

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7
Q

List the many positive tests for S. aureus that are not positive for S. epidermis and S. saprophyticus.

A 
Coagulase
Mannitol
DNase
hymolysis
Protein A
Phage receptor
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8
Q

Staph aureus epidemiology…
On what tissues is it normally found?
What patients are more susceptible?

A

Skin, mucous membranes, and nose

Diabetics, drug addicts, immunocompromised patients, and those with implanted devices.

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9
Q

How is S. aureus strains determined during outbreaks?

Doubtful we need to know the details

A 
Serology
Phage sensitivity/Phage typing
DNA fingerprinting
Ribotyping (rRNA)
DNA of Protein A and Coagulase
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10
Q

T/F Staph aureus is pathogenic because it is an INVASIVE disease, rather than an exotoxin producing bacteria.

A

False.

S. aureus produces toxin-mediated diseases and invasive diseases.

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11
Q

What is the pathogenesis of S. aureus as a toxin-mediating bacteria.

A 
bacterial colonization (food, tampons, vasculature, skin) and production of the toxin.
Toxin can affect areas anywhere in the body, not just at the site of colonization
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12
Q

How does S. aureus contribute to colonization of vasculature and/or skin?
What is the tampon-related infection called?

A

Vasculature: S. aureus contains fibrinogen and fibrinogen receptors
Skin: S. aureus contains exfoliatins that bind to damaged skin (wound sites)
Tampon: Toxic Shock Syndrome toxin

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13
Q

As an invasive bacteria, what is the method of adhesion and invasion?

A

Lots of adhesive molecules that bind to host membranes (fibrinogen, fibronectin, collagen, platelets)
Bind to membranes, colonize, secrete toxins, and evade host defenses.

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14
Q

What are the notable toxins and enzymes through which S. aureus causes damage.

A

1) Alpha toxin: lyses host cell membrans
2) Coagulase: forms clot in human plasma

These were also mentioned…
Leukocidins: lyse leukocytes
Proteases
Staphylokinase: lysis of blood clot or fibrin
Hyaluronidase: disovles hyaluronic acid
Lipase: dissolves lipids and lipoproteins

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15
Q

What are the methods that S. aureus uses to evade host defenses?

A

1) Protein A: binds the “wrong end” of IgG
2) enterotoxins A-E, G, H, I
Protein A is a B-cell superantigen
The enterotoxins are T-cell superantigens

Also mentioned…
Capsule is antiphagocytic
Eap (Map) is a surface protein that impairs neutrophils

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16
Q

Note: S. aureus can be contained or become systemic. If it is systemic, it can affect any organ system.

A

Note: S. aureus can be contained or become systemic. If it is systemic, it can affect any organ system.

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17
Q

What are the three toxin-mediated diseases caused by S. aureus?

A

1) Food poisoning
2) Toxic Shock Syndrome (TSS)
3) Staphylococcal Scalded Skin Syndrome (SSSS)

18
Q

What are the three toxin-mediated diseases caused by S. aureus?
What are the toxins in general?
For which is colonization necessary?

A

1) Food poisoning (by enterotoxin some are superantigens) colonization is NOT required. Toxin can cause illness.
2) Toxic Shock Syndrome (TSS) (TSST-1 supersuperantigen) Colonization REQUIRED
3) Staphylococcal Scalded Skin Syndrome (SSSS) by exfoliatins A and B. Infection site does not have to be the site of toxin action

19
Q

Are food-poisoning enterotoxins secreted by S. aureus heat stable? To what temperature?

A

Heat stable.

Resists boiling.

20
Q

What do the cytokines do the superantigens of the enterotoxin or TSST-1 elicit?

A

IL-1
IL-2
TNF

21
Q

Yada Yada What are the clinical syndromes of food poisoning by S. aureus?

A

Nausea, vomiting, non-bloody diarrhea

Note: these are specifically caused by the T-cell superantigen.

22
Q

What are the clincial syndromes associated with toxic shock syndrome TSS?

A

Fever, rash, desquamation of palms and soles.

Hypotension and shock.

23
Q

What are the toxins that produce Staph Scalded Skin Syndrome?
Are they in the main genome or a plasmid?

A

Exfoliatins A and B

Plasmid

24
Q

Detail: What strain of S. aureus contain exfoliatins A and B?

A

phage group I

25
Q

What patient population does S. aureus SSSS usually affect?

What are the symptoms

A

infants.

Erythematous skin followed by exfoliation

26
Q

Why are antibiotics not always helpful with S. aureus toxin-mediated diseases?

A

Immunological effects due to the superantigen are already in effect before symptoms develop.

27
Q

What distinguishes S. aureus “invasive disease” from an toxin-mediated disease in terms of localization and presentation.

A

Suppuration and abscess formation according to anatomic locations

28
Q

There is a huge list of invasive disease examples by S. aureus on page R-4 and R-5. There is only one example that is in bold. What is it?

A

Catheter site infections

29
Q

What is the Tx for S. aureus abscesses…
Name 1 physical treatment
Name 3-4 antibiotics
Name antibiotic combo for tolerant S. aureus

A

Abscesses need to be drained
Semisynthetic penicillin: Dicloxacillin (oral) or Oxacillin (IV)
Vancomycin is a last resort (methicillin resistance)
Combo with Rifampin and/or Gentamicin

30
Q

Prevention of S. aureus (Just general stuff. Nothing noteworthy)

A

handwashing
judicious use of antibiotics
intranasal mupirocin, when necessary

31
Q

What do you need to know about the bacteriology of S. epidermidis?
Gram stain and other distinctive features…

A

Coagulase negative (S. epidermidis and S. saprophyticus only)
Gram +
Staphylococci with white colonies
Catalase + (distinguishes staph from strep)
Sensitive to NOVOBIOCIN

32
Q

Detail: S. epidermidis and …
blood agar?
Mannitol?

A

Little hemolysis on blood agar

Does NOT ferment mannitol

33
Q 
Epidemiology of S. epidermidis...
Colonizes on what tissue?
How opportunistic?
Adheres to what?
Who is susceptible?
A

Normal skin flora
Very oppotunistic that adheres to medical implants very efficiently
Neonates, patients in renal failure, immunocompromised patients

34
Q

Pathogenesis of Staphylococcus epidermidis…

Nothing exciting here. Just wing it.

A

colonizes prosthetics, produces biofilms, there is a carbohydrate that mediates biofilm
poorly misunderstood

35
Q

What are the clinical syndromes of Staphylococcus…
How does it compare in intensity with S. aureus?
What should you suspect if the patient is symptom free but is blood positive for S. epidermidis?

A

Low grade fever, pain, and discomfort.
Less severe than S. aureus
If symptom negative, but blood positive, suspect skin flora contamination

36
Q

What is Tx for Staphylococcus epidermidis?

A

1) remove implant
2) Vancomycin
3) possible combo with Rifampin and/or Gentamicin

Interesting. Infection seems more mild, but we whip out the big guns for antibiotics.

37
Q

Bacteriology of Staphylococcus saprophyticus…

gram stain and distinctive features.

A

G +
Coagulase negative (S. epidermidis and saprophyticus are neg. S. aureus is positive)
Catalase + (distinguishes from Strep)
Resistant to novobiocin

38
Q

Epidemiology of Staphylococcus saprophyticus
What is normal tissue?
What illness is it a common cause of?

A

skin commensal

2nd leading cause of UTI in women

39
Q

What are symptoms of S. saprophyticus UTI?

A

UTI with poluria and dysuria

40
Q

What is Tx for S. saprophyticus?

Why are these the drugs of choice?

A 
Trimethoprim sulfamethoxazol (Bactrim)
Norfloxacin (quinolone)
excellent penetration into urinary bladder.
41
Q 
Why are the following used?
On which staph?
VANCOMYCIN
RIFAMPIN
GENTAMYCIN
BACITRIM + Sulfonamide + Trimethoprim
NORFLOXACIN (a Quinolone)
A

S. aureus and S. epidimidis use VANCO, RIFAMPIN, AND GENTAMYCIN
S. saprophyticus uses BACTRIM AND NORFLOXACIN

Vanco: Cidal, G+ multi resistannt enterococcus and MRSA, cell wall inhibitor
Rifampin: Cidal broad spectrum RNA synthesis inhibitor, often used in TB
Genta: Cidal, 30s aminoglycoside protein synth inhibitor
Bacitrim: static antimetabolite inhibits folic acid via DHF reductase and PABA
Quinolone: Cidal, G- and G+ DNA inhibitor (DNA gyrase). Note MRSA is resistant. Used for UTI and P. aeruginosa

Micro Quiz 3 (12 decks)

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