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Microm 442 > Lecture 11 Staphylcocci > Flashcards

Lecture 11 Staphylcocci Flashcards

1
Q

What are the features of staphylcocci?

A
  • G positive cocci in clusters.
  • Staphylos: grape like clusters.
  • Facultative anaerobes
  • aerobic and anaerobic respiration.
  • catalase positive
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2
Q

How is S aureus differentiated from other staphylcocci?

A

-Coagulase test: allows to differentiate S aureus from other staph
CoNS (coagulase Negative staphylococci).
-golden orange pigment

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3
Q

What are some key features of S. aureus?

A
  • colonizes nasopharynx (30 percent people)
  • ß-hemolytic, Coagulase +
  • golden orange pigment
  • ferments mannitol
  • not dangerous until penetrates into skin.
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4
Q

What are some key indicators of S. eperdermidis?

A
  • colonizes skin
  • Υ-hemolytic, Coagulase -
  • does not ferment mannitol.
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5
Q

What are some indicators of S. saphrophyticus?

A
  • Colonizes the gastrointestinal tract
  • Urinary tract infections – SexuallyAactive women
  • Υ-hemolytic, Coagulase-
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6
Q

What is the toxin made by S. Aureus that causes skin disease?

A
  • Protein A

- Exfolitin (scalded skin)

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7
Q

What is the effect of Protein A?

A

Binds to Fc portion of antibody, inhibiting phagocytosis (block attachment to Fc receptors on whit blood cells)

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8
Q

what is the purpose of capsules?

A

inhibits phagocytosis

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9
Q

what is the effect of coagulase?

A

Impede progress of leukocytes into infected area by producing clots int the surrounding capillaries.

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10
Q

What is the effect of exfoliatin?

A

Separates layers of epidermis, causing scalded skin syndrome.

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11
Q

What is the effects of Hyaluronidase?

A

-Breaks down hyaluronic acid component of tissue, there by promoting extension of infection.

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12
Q

What is the purpose of Leukocidin?

A

Kills white blood cells by producing holes in their cytoplasmic membrane.

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13
Q

What is the purpose of Lipase?

A

Breaks down fats by hydrolyzing the bond between glycerol and fatty acids.

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14
Q

What is the purpose of proteases?

A

Degrade collagen and other tissue proteins.

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15
Q

What are sx of Toxic shock syndrome toxin?

A

Causes rash, diarrhea, and shock.

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16
Q

What are some diseases caused by S. aureus?

A
  • Skin infections
  • bacteremia
  • pneuomonia
  • Toxin-mediated
  • Endocarditis
  • Osteomyelitis
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17
Q

What are some skin infections that S. aureus causes?

A
  • Folliculitis, impetigo
  • boils, abscess, furuncles
  • Cellulitis
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18
Q

What are some toxin-mediated disease caused by S. Aureus?

A
  • Gastro-intestinal intoxication
  • scalded skin syndrome
  • toxic shock syndrome
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19
Q

How does S. aureus cause folliculitis and abscess?

A

The organism enters through a hair follicle causing Folliculitis, but once it gets to the subcutaneous tissue, it causes and infection attracting white blood cells.

20
Q

What causes Staphylococcus to change from a commensal organism to a pathogen?

A

-Quorom sensing causes toxins to be produced. Staph has a lot of different toxins that can vary between species, 25-30.

21
Q

What is the the process of Quorom sensing in Staphylcocci?

A

-AIP (sensing peptide) will bind to receptor once a high enough concentration is met, causing the phosphorylation of Agr A, up regulating the agr operon that contains all the virulance factors.

22
Q

What are the cytolytic toxins made by S. Aureus?

A
  • alpha (RBCs, leukocytes, excluding neutrophils), beta, delta gamma.
  • PVL, PSM
23
Q

What are the two types of cytolytic toxins made by S. aureus?

A
  • Receptor mediated (Alpha, PVL, gamma) Bi-component. Formation of a defined pore(hexamer to octamer)
  • Receptor independent (alpha type PSM) forms short-lived pores.
24
Q

What are the the general effect of Superantigens?

A

Causes systemic diseases, not specific to local site.

25
Q

What are the effects of superantigens created by S. Aureus?

A
  • Exfoliative toxin (scalded skind syndrome)
  • Enterotoxins- (food poisoning)
  • Toxic shock syndrome (TSST-1)
26
Q

What major abx have Staphylcocci developed resistance to?

A

-Penicillin (Used in 1940, resistance rose to 80 percent by 1960, Penicillinase presence).

-Methicillin 
Beta lactam used to combat resistance
Mec A gene regulates resistance.
Resistance developed in 1970.
At 60 percent resistance.
27
Q

What is the difference from Hospital MRSA to Community MRSA?

A

Hospital:

  • Abx resistance developed first to many different drugs
  • Found in Elderly, immunocompromised, and diabetics

Community:

  • abx spreads to community
  • Genetically distinct strains
  • Generally simple skin infections
  • Necrotizing Pneumonia
  • In Prisons, Athletes, soldiers, obtained from environmental factors.
28
Q

What are the respiratory diseases caused by S. Aureus?

A
  • Pneumonia
  • Cystic fibrosis
  • Community acquired Pneumonia
29
Q

How was S. Aureus Pneumonia occurring?

A
  • Hospital acquired
  • 20-40 percent
  • intubation/ ventilator
  • Stay at long-term facility
  • IV treatment for wounds
  • Elderly, Immunocompromised
30
Q

What is known about Community acquired S. Aureus Pneumonia?

A
  • Necrotizing lung tissue
  • younger pts
  • preceding influenza like illness
  • 30 percent mortality rate
31
Q

What is known about S. Aureus caused Cystic fibrosis?

A
  • Early association in young children
  • Bacterial infection hard to treat because of biofilm
  • Increasing MRSA
  • Typically replaced by other pathogens
32
Q

What are the specifics of Exfoliative toxin-mediated skin disease?

A
  • 2 toxins, exfoliatin A and B
  • Causes separation of the skin (desquamation)
  • Most common in children under 6 (Newborn-Ritter’s syndrome)
  • Treatment . (methicillin, Vancomycin, Clindamycin)
33
Q

What are the specifics of Toxic shock syndrome?

A

-1980’s
-Extended use of tampons (overnight 8 hr)
-Toxin (TSST-1 strains) causes sytemic infection
-Symptoms:
High fever
Sunburn rash
rapid drop in BP
flu-like sx

34
Q

How is Toxic shock syndrome treated?

A

Rapid treatment with abx

-Methicillin, vancomycin, clindamycin

35
Q

What are some severe outcomes of Toxic shock syndrome?

A

-organ failure, death

36
Q

What is the unique about S. Aureus (picnic pathogen)?

A
  • Enterotoxin mediated
  • 20 different toxins
  • Staphylococcal enterotoxin B (SEB) is a biological warfare weapon.
  • Does not need live bacteria to cause disease
37
Q

What are some sx of the picnic pathogen.

A
  • 30 min- 6 hr onset
  • Violent vomiting
  • stomach cramping
  • Nausea
  • Possible Diarrhea
  • Rexolve withing 24-48 hours
38
Q

What are some ways to treat/ prevent the picnic pathogen?

A
  • Fluids (toxin-mediated hard to treat)
  • Wash hands prior to food prep
  • don’t leave food at room temp
  • Use caution with foods at picnics
39
Q

What are the steps to forming a biolfilm?

A
  1. Pre-conditioning of surface
  2. Attachment
  3. Cell-to-cell adhesion
  4. proliferation
  5. maturation
  6. dispersion
40
Q

What are some key features of biofilms?

A

-partially anaerobic
-slow growing
-cycle of cell dying and replacement
-difficult to treat:
Abx do not penetrate wall
different than planktonic bact

41
Q

What is endocarditis?

A
  • biofilm infection of the hear tissues
  • Both S. aureus and CoNS, faster onset than other bacterial organism
  • Due to prior damage to heart
  • Common in IV drug users (right side)
42
Q

How do you treat Endocarditis?

A
  • Prolonged abx therapy

- removal of infected heart valves

43
Q

What is osteomylitis?

A
  • Biofilm infection of the bone
  • most common in children
  • Usually found in adults due to IV drug abuse or exposure of bone (severe cellulitis, joint replacement surgery)
44
Q

What are some treatments of Osteomylitis?

A
  • Prolonged IV abx

- For severe can amputate or debridement.

45
Q

What is S. epidermidis Disease?

A
  • Biofilm growth requires capsule (polysaccharide intercellular adhesin)
  • Hospital acquired infection (Cathether, shunts, heart valves)
46
Q

How do you treat S. Epidermidis disease?

A

Remove contaminated device.

Microm 442 (16 decks)

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