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Microm 442 > Lecture 11 Staphylcocci > Flashcards

Lecture 11 Staphylcocci Flashcards

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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?

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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?

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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?

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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?

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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?

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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?

Study These Flashcards
A

Causes systemic diseases, not specific to local site.

25
What are the effects of superantigens created by S. Aureus?
- Exfoliative toxin (scalded skind syndrome) - Enterotoxins- (food poisoning) - Toxic shock syndrome (TSST-1)
26
What major abx have Staphylcocci developed resistance to?
-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
What is the difference from Hospital MRSA to Community MRSA?
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
What are the respiratory diseases caused by S. Aureus?
- Pneumonia - Cystic fibrosis - Community acquired Pneumonia
29
How was S. Aureus Pneumonia occurring?
- Hospital acquired - 20-40 percent - intubation/ ventilator - Stay at long-term facility - IV treatment for wounds - Elderly, Immunocompromised
30
What is known about Community acquired S. Aureus Pneumonia?
- Necrotizing lung tissue - younger pts - preceding influenza like illness - 30 percent mortality rate
31
What is known about S. Aureus caused Cystic fibrosis?
- Early association in young children - Bacterial infection hard to treat because of biofilm - Increasing MRSA - Typically replaced by other pathogens
32
What are the specifics of Exfoliative toxin-mediated skin disease?
- 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
What are the specifics of Toxic shock syndrome?
-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
How is Toxic shock syndrome treated?
Rapid treatment with abx | -Methicillin, vancomycin, clindamycin
35
What are some severe outcomes of Toxic shock syndrome?
-organ failure, death
36
What is the unique about S. Aureus (picnic pathogen)?
- Enterotoxin mediated - 20 different toxins - Staphylococcal enterotoxin B (SEB) is a biological warfare weapon. - Does not need live bacteria to cause disease
37
What are some sx of the picnic pathogen.
- 30 min- 6 hr onset - Violent vomiting - stomach cramping - Nausea - Possible Diarrhea - Rexolve withing 24-48 hours
38
What are some ways to treat/ prevent the picnic pathogen?
- 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
What are the steps to forming a biolfilm?
1. Pre-conditioning of surface 2. Attachment 3. Cell-to-cell adhesion 4. proliferation 5. maturation 6. dispersion
40
What are some key features of biofilms?
-partially anaerobic -slow growing -cycle of cell dying and replacement -difficult to treat: Abx do not penetrate wall different than planktonic bact
41
What is endocarditis?
- 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
How do you treat Endocarditis?
- Prolonged abx therapy | - removal of infected heart valves
43
What is osteomylitis?
- 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
What are some treatments of Osteomylitis?
- Prolonged IV abx | - For severe can amputate or debridement.
45
What is S. epidermidis Disease?
- Biofilm growth requires capsule (polysaccharide intercellular adhesin) - Hospital acquired infection (Cathether, shunts, heart valves)
46
How do you treat S. Epidermidis disease?
Remove contaminated device.

Microm 442 (16 decks)

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