Micro: Staph Flashcards Preview

Block 11 - Multisystems > Micro: Staph > Flashcards

Flashcards in Micro: Staph Deck (26):
1

What are the three medically important species of staph?

all are catalase positive
s. aureus - coagulase postivie
s. epidermidis - coagulase negative
s. saprophyticus - coagulase negative, novobiocin resistant

2

What is the epidemiology of s. aureus?

leading cause of CA inf
anterior nasal vestibule is most common reservoir
carriage rates: MRSA 2%, vaginal 10%, prolonged 20%, intermittent 60%
most bacteremia caused by strain colonizing anterior nares

3

Who can be more prone to colonization w s. aureus and what can be done in the situation?

hospital personnel
apply mupirocin (topical antimicrobial) to ant nares

4

How does s. aureus control its own virulence factors?*

global regulatory protein SarA and agr global regulatory system
agr = two component sensory transduction system that responds to bacterial density - makes s. aureus express adhesins when density low and toxins when density high

5

What are the surface factors involved in the pathogenesis of s. aureus?

polysaccharide capsule
MSCRAMM - surface adhesins that bind human proteins
lipoteichoic acids = inflammatory factors
peptidoglycan - anchor MSCRAMMS and is inflammatory

6

What are the secreted proteins and toxins of s. aureus?

exoenzymes: (proteases, lipases, a hyaluronidase), alpha helical peptides that kill neutrophils by MRSA
hemolysins - 4 different (alpha by MRSA kills lymphocytes and can cause pneumonia)
superantigen family - exfoliative toxins, TSST-1, enterotoxins

7

How does the superantigen family of s. aureus toxins work?

directly link T cells to MHC class II outside binding groove
not processed, cause nonspecific activation of 20% of total T cells and massive cytokine release --> fever, hypotension, shock

8

What does invasion of s. aureus normally require?

break in skin integrity or mucosa
adherence via teichoic acids and MSCRAMMs

9

What are local infections of the skin caused by s. aureus?

folliculitis, furuncules, impetigo, mastitis (breast inf in nursing mothers), post surgical wound inf
erysipleas, cellulitis, fasciitis - all have severe pain

10

What are localized infections with diffuse skin rashes caused by s. aureus?

staph scalded skin syndrome (SSSS)
toxic shock syndrome: menstrual by TSST-1 --> fever, hypotension, edema, diffuse macular rash, desquamation, nonmenstrual by TSST-1 or enterotoxins frequently involves wounds

11

What is SSSS?

= Ritter's dz: caused by exfoliative toxin A (phage encoded) or B (plasmid encoded), usually infants in umbilical stump or wound site, toxin binds GM4 ganglioside in skin
generalized and localized (also called bullous impetigo) - spread may be limited by pre-existing antibodies

12

What are other diseases caused by s. aureus?

bacteremia: community onset from health care efforts or predisposing med condition, nosocomial from catheters
endocarditis (native or prosthetic valve, IVDA)
meningitis
pneumonia (nosocomial >> CAP)
osteomyelitis, septic arthritis, septic bursitis
food poisoning - heat stable toxins not inactivated by cooking or heating = intoxication not infection

13

How is s. aureus resistant to penicillin?

plasmid encoded
in 95% of isolates

14

How is s. aureus resistant to methicillin (a beta lactam)?

methicillin and cephalosporin resistance by expressing penicillin binding protein (PBP2A) that has low affinity for methicillin and other beta lactams, encoded on SCCmec
beta lactams normally bind to transpeptidase domains of PBPs and inhibit transpeptidase activity which inhibits cell wall synthesis

15

What are the two different types of MRSA?

hospital acquired or healthcare associated (HA)-MRSA: tends to be resistant to other antimicrobials, make up 85%, multiple SCCmec
community acquired (CA)-MRSA: tend not to be resistant to other antimicrobials, smallest SCCmec that can be spread by transduction, more resistant the HA-MRSA to killing by PMNs (up-regulation of virulence factors?)

16

What is supremely important with MRSA strains?

antimicrobial testing to determine what might be active against a particular isolate

17

What are the statistics on HA-MRSA and CA-MRSA?*

HA declined from 2005-2011, CA remained constant

18

How are life-threatening MRSA inf treated?

vanc - blocks transpeptidation by binding to D-ala-D-ala
VISA/GISA = intermediate resistance to vanc, susceptible to other abx
full resistance can happen (VRSA): susceptible to other abx, expression of vanA --> D-ala-D-lactate

19

What are newer antimicrobials for treating MRSA?

linezolid - binds ribosome and inhibits protein synthesis
daptomycin - affects membrane causing leaking of K
tigecycline - binds 30S ribosomal subunit

20

How can s. aureus be diagnosed?

gram stain
grows readily on ordinary lab media, tolerant of high salt conditions
positive coagulase test

21

Where is s. epidermidis usually found?

skin and mucous membranes
inf involves indwelling foreign bodies

22

What is the epidemiology of s. epidermidis?

almost always HA except natural valve endocarditis

23

What are the virulence factors of s. epidermidis?

*biofilm formation and production of exopolysaccharides

24

What is the antibiotic resistance of s. epidermidis?

similar to s. aureus except 80% strains resistant to methicillin

25

What are some types of inf caused by s. epidermidis?

endocarditis of native and prosthetic valves
IV catheters
CSF shunt infections
UTIs
Bacteremia in immunocompromised
Prosthetic joint infections

26

What is s. saprophyticus?

common cause of UTI in young sexually active women
essentially indistinguishable from UTI by E. Coli
contrast to s. epidermidis - inf responds well to antimicrobials used to treat UTIs