Staphylococci Flashcards

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1
Q

General Staph Facts

A

Major cause of nosocomial bacteremia

Foreign bodies help colonization

Lots of resistance out there

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2
Q

General Staph Characteristics

A

Gram + cocci

GRAPE CLUSTERS

Facultative

Catalase positive

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3
Q

What is Coagulase?

A

Enzyme that clots plasma by activating fibrinogen

S. Aureus POSITIVE

Other staph NEGATIVE

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4
Q

Staph Aureus Epi

A

Found on skin, mucous membranes, nares

Colonizes diabetics, drug addicts, and hospitalized diabetics more

FOREIGN BODIES are often colonized

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5
Q

How do you take Staph outbreaks?

A
  1. DNA fingerprinting
  2. Ribotyping (ribosomal RNA)
  3. DNA sequencing of genes
    - SPA
    - MLST
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6
Q

How does Staph A. Toxin produce disease?

A
  1. Toxin Contamination
    - enterotoxins -> food poisoning
  2. Bacterial colonization
    - toxin produced in host
    a. TOXIC SHOCK SYNDROME TOXIN
    b. Exfoliatins- scalded skin
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7
Q

How does Staph A cause invasive disease?

A

Damaged skin has lots of exposed matrix proteins

Easy for colonization through adhesive molecules

Can invade into tissue and blood

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8
Q

What Staph A toxins cause direct damage?

A

ALPHA TOXIN - lyse host cell membrane

Leukocidins - lyse leukocyte so

Proteases, COAGULASE, hyaluronidase, lipase

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9
Q

What toxins allow Staph A to evade our immune response?

A

PROTEIN A

  • cell wall protein
  • binds IgG
  • less complement
  • B-cell super antigen

ENTEROTOXINS

  • many types
  • T-cell super antigen

CAPSULAR POLYSACCHARIDE
-stops phagocytosis

EAP
-helps neutrophil evasion

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10
Q

What are the three toxin mediated SA diseases?

A

Food poisoning

Toxic Shock Syndrome (TSS)

Staphylococcal Scalded Skin Syndrome (SSSS)

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11
Q

What causes SA food poisoning and what does it look like?

A

Enterotoxins A-I except F

  • HEAT STABLE
  • A and C are Super antigens

Nausea

Vomiting

Non-bloody diarrhea

Does not require colonization

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12
Q

How does SA cause TSS and what does it look like?

A

Requires prior colonization

EXOTOXIN F / TSST-1

  • super antigen
  • IL-1/2 and TNF

Fever
Rash
Desquamation

HYPOTENSION AND SHOCK

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13
Q

What’s SSSS?

A

Caused by EXFOLIATINS A and B

encoded by eta genes

Superantigens

Usually infants

SUPERFICIAL LAYER OF EPIDERMIS DETACHES

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14
Q

What does superficial SA invasion look like?

A

Impetigo (red, vesicular lesions of the skin)

Folliculitis (follicle infection)

Furuncles and Carbuncles (skin boils)

Cellulitis

CATHETER SITE INFECTION

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15
Q

What are the deep seated SA infections?

A

Pneumonia (usually postoperative/hospitalized pts)

Endocarditis

Arthritis

Abscess

Sepsis

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16
Q

How do you treat SA?

A

Abscesses are surgically drained or removed

Semisynthetic penicillin
-dicloxacillin or oxtail in

VANCO last resort
-be judicious

17
Q

How can we prevent SA infections?

A

WASHING HANDS

No ties?

Judicious use of antibiotics to curb resistance

Fight nasal infections with mupirocin

18
Q

Staphylococcus Epidermidis distinguishing characteristics

A

Gram + cocci

WHITE colonies

COAGULASE NEGATIVE

CATALSE POSTIVE

Does not ferment mannitol

Sensitive to Novobiocin

19
Q

S. Epiderm Epi

A

Skin colonizer, there normally

Very opportunistic

Loves FOREIGN BODIES (who doesn’t)

20
Q

How does S. Epiderm infect?

A

Normally found on skin

indwelling device or immunosuppression makes it easy to colonize

Create biofilm

Can invade skin

21
Q

How does S. Epiderm manifest?

A

Low fever

Pain

Discomfort

22
Q

Diagnosing S. Epidermidis

A

TREAT PATIENT AND NOT THE CULTURE

Found normally on skin
-> common culture contaminant

23
Q

How would you treat S. Epiderm?

A

Remove indwelling device

Treat with VANCO

If TSS use combination, rifampin or gentamicin

24
Q

S. Saprophyticus distinguishing features

A

COAGULASE NEGATIVE

Catalase positive

Does NOT ferment mannitol

RESISTANT TO NOVOBIOCIN

25
Q

S.S. Epi

A

Skin commensal

Common cause of UTI

26
Q

Treating SS

A

Trimethoprim sulfamethoxazole (BACTRIM)

NORFLOXACIN (quinolone)