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Multisystems > Micro- Staphylococci & Staphylococcal Disease > Flashcards

Micro- Staphylococci & Staphylococcal Disease Flashcards

1
Q

Where is the most common reservoir for staph aureus?
What is overall carriage rate? Prolonged? Intermittent?
How does it get introduced to the body?

A

It commonly is in the anterior nasal vestibule of healthy people. Overall carriage rate is about 30% [2% for MRSA]

  • 60% intermittent
  • 20% prolonged [nasopharynx and on the skin]

When there is trauma or another penetrating event, it can be introduced into the body

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2
Q

What is a carbuncle?

A

Lesion resulting from the lateral and deeper extension of S. aureus from the skin. It has multiple openings with pus discharge.

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3
Q

What is exfoliatin?

A

Extracellular product of some strains of S. aureus that is responsible for the intraepidermal splitting of tissues and necrosis seen in Staph Scalded Skin Syndrome

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4
Q

What are the 3 most medically important species of staphylococci?
How are they differentiated in a lab?

A

All staph strains are G+ cocci in clusters that are catalase+.

  1. S. aureus = coagulase +
  2. S. epidermidis = coagulase -
  3. S. saprophyticus = coagulase -, novobiocin resistant
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5
Q

What are the 8 main diseases that can be caused by S. aureus?

A
  1. localized skin infection
  2. localized skin infections with diffuse rash
  3. septicemia
  4. endocarditis, pericarditis
  5. pulmonary infections
  6. osteomyelitis
  7. septic arthritis
  8. food-borne disease [toxin-mediated]
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6
Q

In patients particularly prone to colonization by S. aureus in the anterior nares, what can be done?

A

Mupirocin [topical antimicrobial agent] can be applied to the anterior nares

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7
Q

What genetic system controls the expression of many of the virulence factors of S. aureus?

A

Global regulatory proteint: SarA

Global regulatory system : agr

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8
Q

How does agr [global regulatory system] control the expression of virulence factors for S. aureus?

A

It is a two-component sensory transduction system that responds to the bacterial density [#bac/volume]

If bacterial density is LOW the system expresses surface proteins like adhesins.
If bacterial density is HIGH, the system expresses exoproteins/toxins

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9
Q

What are the 4 surface factors involved in S. aureus pathogenesis?

A
  1. polysaccharide capsule - antiphagocytic
  2. MSCRAMM [microbial surface component reacting with adherence matrix molecule] - bind to human proteins like IgG, fibrinogen and collagen
  3. Lipoteichoic acids - bound to bacterial cytoplasmic membrane and are inflammatory factors
  4. Peptidoglycan - anchors MSCRAMMs, inflammatory
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10
Q

What are MSCRAMMs?

A

S. aureus bacterial surface adhesins that bind to a number of different human host proteins like IgG, fibrinogen, collagen.

They use LPXTG anchoring domain

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11
Q

What are the 3 main secreted proteins/toxins that give S. aureus virulence?

A
  1. exoenzymes like:
    - protease, lipase, hyaluronidase that can help infection spread in tissue
    - a-helical peptides [PSMa] that kills neutrophils
  2. hemolysins [a,b,d,g] - form lytic pores in eukaryotic cells
    - a kills macrophages and lymphocytes [MRSA pneumonia]
  3. S. aureus superantigen family - exfoliative toxin, TSST-1, staphylococcal enterotoxin = bypass normal immune system activation
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12
Q

What exoenzyme does S. aureus use to kill neutrophils?

What strain has particularly high levels of this exoenzyme?

A

PSM-a [a-helical peptides]

In high levels in community MRSA

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13
Q

What S. aureus secreted protein kills macrophages and lymphocytes and is the major virulence factor for producing pneumonia in community-associated MRSA?

A

a-hemolysin

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14
Q

What are the 3 major S. aureus superantigens?

What do superantigens do?

A
  1. TSST-1
  2. exfoliative toxin
  3. staphylococcal enterotoxin

They bypass the normal interaction between immune cells and antigens causing non-specific activation of 20% of the total T cells in the body causing massive cytokine release leading to:

  • hypotension
  • fever
  • shock
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15
Q

What 2 S. aureus virulence factors are necessary for colonization of the host?
What is necessary for invasion?

A

Colonization of the anterior nares:

  1. teichoic acid of the cell wall
  2. MSCRAMMs

Invasion requires a break in the integrity of the skin/mucosa

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16
Q

What is the host response to infection by S. aureus?

A

After the bacteria breaches the epithelium or mucosa:

  1. chemotactic response occurs as a result of staph factors [esp. lipoteichoic acid] triggering complement activation.
  2. host factors opsonize staph and they are ingested by phagocytes where the bacteria is killed
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17
Q

What are the 6 “localized infections of the skin” caused by S. aureus?

A
  1. folliculitis
  2. furuncles
  3. impetigo
  4. mastitis - nursing mothers
  5. wound infection -post surgical
  6. erysipelas, cellulitis, fasciitis
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18
Q

What is folliculitis? Furuncles? Carbuncle?

A

Folliculitis - infection of the hair follicle
Furuncle- boils–more extensive infection involving hair follicles.
Carbuncle - coalesced furuncles that extend into subcutaneous tissue

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19
Q

What is impetigo?
What age group is affected?
What areas of the body?
What is the microbiological cause of 20% of cases ?

A

Superficial infection in children that involves the face and legs and is erythematous with yellow/brown crust due to the purulence.

Most are S. aureus, but 20% are caused by strep pyogenes or a mixed infection.

20
Q

What is a common feature of erysipelas, cellulitis and fasciitis?
What is the most common cause?

A

SEVERE pain.

The most common cause is strep pyogenes, but s. aureus can do it to

21
Q

What are the 2 “localized infections, with diffuse skin rash” associated with s. aureus?

A
  1. Staph Scalded Skin Syndrome

2. TSS

22
Q

Describe the pathogenesis of SSSS [Ritter’s disease].
What % of s. aureus strains have the capability to cause this?
What age is most commonly affected?
What is the primary site of infection frequently?

A

S. aureus produces exfoliative toxin A [phage encoded] and exfoliative toxin B [plasmid encoded]

—fewer than 2% of strains carry these genes—-

Occurs in children less than 5 but usually infants where the primary site of infection is the umbilical stump.

Bacteria grows and secretes the toxin which binds GM4 ganglioside in skin [present only in young children] and is internalized by keratinocytes.

23
Q

What are the 2 forms of Staph Scalded skin Syndrome?

A
  1. Localized - AKA bullous impetigo

2. Generalized

24
Q

What are the 2 forms of TSS?

Which has a higher case-fatality rate?

A
  1. Menstrual TSS caused by TSST1 from a high absorbency tampon
  2. Non-menstrual - TSST1 or another enterotoxin anywhere in the body but frequently involving wounds.

Fatality is higher or non-menstrual form

25
Q

A patient presents with fever, hypotension, edema, diffuse macular rash and desquamation. What % of s. aureus isolates produce the toxin that can cause this reaction?

A

20% of S. aureus strains make TSST1 which causes this

26
Q

What are the 2 kinds of bacteremia associated with S. aureus?
What is each most frequently associated with?

A
  1. Community-onset bacteremia- usually associated with health care efforts [indwelling devices or predisposed medical conditions]
  2. nosocomial - catheters [IV or urinary]
27
Q

The majority of S. aureus caused endocarditis occur in _______________ but about 1/5 of cases are due to ______________________.

A 
MOST = IV drug users
1/5 = prosthetic valve endocarditis
28
Q

How does S. aureus cause food poisoning?

A

It has enterotoxins that are produced and growing in food.
When people eat the food, there is a 2-6 hour incubation and then they have acute vomit and diarrhea.

The heat-stable enterotoxin CANNOT be inactivated by cooking or heating. Intoxication NOT infection.

29
Q

Timmy eats some cold pizza. 2-6 hours later he has acute vomiting and diarrhea. His mom yells at him and tells him he should have heat the pizza up to kill all the bacteria. Would heating the pizza up have helped?

A

No because enterotoxin from s. aureus is heat-stable

30
Q

What percent of S. aureus isolates are resistant to penicillin?
How is resistance achieved?

A

95% are resistant to penecillin.

Penicillin is plasmid-encoded resistance .

31
Q

What is the MOA of methicillin?

How did bacteria confer resistance?

A

methicillin is a penicillinase-stable B-lactam.

B-lactams bind to the transpeptidase domain of the bacterial penicillin binding protein [PBP] and inhibit transpeptidase activity so the bacteria cannot finish cell wall synthesis.

MRSA express penicillin binding protein 2A [PBP2A] which has low affinity for methicillin and B-lactams. Because the B-lactam doesn’t bind PBP, cell wall synthesis can continue.

32
Q

What gene encodes PBP2A [the protein that confers methicillin resistance]?

A

mecA gene on a a mobile chromosome designated SCCmec [staph cassette chromosome]

33
Q

What is the difference between HA and CA MRSA in terms of what else the strains will be resistant to?
In terms of who they infect?
Is HA or CA more resistant to killing by PMNs?

A

HA-MRSA tend to be resistant to MANY other antimicrobials and are associated with risk factors.

CA-MRSA tends to NOT be resistant to multiple other antimicrobials but can cause pneumonia and skin infections in otherwise healthy people. CA is more resistant than HA to killing by PMNs

34
Q

What percent of invasive MRSA infections involved healthcare in some form?

A

85%

35
Q

What are the 2 most serious sequelae of CA-MRSA?

A
  1. furunculosis

2. severe hemorrhagic pneumonia [high fatality]

36
Q

CA-MRSA contains the __________SCCmec which is spread among S. aureus strains by _______________/

A

Smallest SCCmec which is spread by transduction

37
Q

What accounts for the increased virulence of CA-MRSA?

A

Upregulation of certain virulence factors like:

  1. a-hemolysin [kill lymphocytes, macrophages]
  2. PSMa [kill neutrophils]
38
Q

Because many MRSA are multiply resistant to commonly used antimicrobials, what it is important to do?

A

Test each MRSA isolate to determine which antimicrobials might be active against the specific MRSA.

39
Q

What are life-threatening MRSA infections treated with?

What is the MOA?

A

Vancomycin which blocks transpeptidase in cell wall synthesis but NOT by binding PBP but rather by binding to the D-ala-D-ala terminus of cell wall precursor.

40
Q

Full Vanc resistance [32mg/ml] has occurred in 11 cases [VRSA].
Intermediate resistance [8-16mg/ml] has also occurred [VISA].
What is the good news so far?
What is the mechanism of resistance?

A

These resistant strains have been susceptible to other antimicrobials.

vanA resistance gene modified d-ala-d-ala to d-ala-d-lactate so the vancomycin cannot bind and halt cell wall synthesis.

41
Q

What is the MOA of:

  1. linezolid
  2. daptomycin
  3. tigecycline
A
  1. binds ribosome and inhibits protein synthesis of s. aureus
  2. affects cell membrane causing K leakage
  3. inhibits protein synthesis by binding 30S
42
Q

How is the lab diagnosis of S. aureus made?

A
  1. Gran stain
  2. grows on ordinary media and is tolerant to high salt conditions
    • coagulase test
43
Q

What is the microbiology of S. epidermidis?
Where is S. epidermidis commonly found?

What do infections caused by this organism usually involve?

A

S. epidermidis = G+, catalase +, coagulase neg

Found on human skin and mucous membranes.
Infections usually involve indwelling foreign bodies

44
Q

Almost all s. epidermidis infections are ______-acquired.

What are the 6 major types of infections?

A

Hospital -acquired

  1. endocarditis
  2. IV catheter
  3. CSF shunt
  4. UTI
  5. bacteremia in immunocompromised
  6. prosthetic joint infection
45
Q

What % of s. epidermidis strains are resistant to methicillin?

A

80%

46
Q

What are the 2 main virulence factors of s. epidermidis?

A
  1. biofilm formation

2. production of exopolysaccharides

47
Q

What is the micro of S. saprophyticus?

What is it the most common cause of?

A

G+, catalase +, coagulase -, novobiocin resistant

It is a cause of UTI in young, sexually active females
It responds well to antimicrobials [unlike s. aureus and s. epidermidis which have resistance]

Multisystems (29 decks)

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