gram positives Flashcards

1
Q

pathogenesis of toxic shock syndrome

A
  • usually antigen presented via MHCII to specific T cell
  • in toxic shock: no APC needed
  • toxin allows MHCII to bind to T cell > polyclonal T cell activation
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2
Q

Rx for toxic shock

A

empirical:
fluclox (strep/staph)/ vanc (MRSA) > switch to 3rd gen cef (staph) or penicillin (strep) if identify

+ clinda to cover the eagle effect

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3
Q

staph vs strep TSS

A
staph: 
younger, females
generalised erythroderma and rash more likely to desquamate
N/V/D common
bacteraemia uncommon
TSST1 toxin
mortality low 
strep: 
older, M=F
uncommon n/v/d, no erythroderma 
bacteraemia commmon
strep pyogenic exotoxin A and B
mortality high 30%
coagulopathy + ARDS
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4
Q

when are the coagulase negative staphs more pathogenic

A

when foreign material present e.g. central line

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5
Q

examples of coagulase negative staph

A

staph epi, staph saprophyticus, staph hominis, staph haemolyticus

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6
Q

what feature of CoNS is important in how bad the are?

A

Exopolysaccharide protective biofilm

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7
Q

empiric Rx for CoNS

A

vancomycin! (think about patient Ila)

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8
Q

staph aureus exotoxins can cause what 3 clinical pictures

A

1) SSSS - exfoliatin
2) food poisoning - enterotoxins (A/ B/C1/C2/ D/E)
3) toxic shock - Toxic shock syndrome toxin (TSST-1) - the only superantigen

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9
Q

what microbiological makes MRSA different from MSSA

A

Altered penicillin-binding protein (PBP) - MecA encoding PBP2a

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10
Q

what does alpha vs beta haemolytic actually mean for strep? give examples for each.

A

alpha = partially haemolyses surrounding RBC
- pneumoniae, viridans

beta = fully haemolyses RBC
- pyogenes, agalactiae

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11
Q

Lancefield antigen classification: GAS vs GBS vs GDS example each

A
GAS = strep pyogenes
GBS = strep agalactiae
GDS = enterococcus
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12
Q

invasive disease most commonly follows what kind of strep disease?

A

skin not pharyngitis

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13
Q

all the manifestations of GAS!

A

skin: follicles, cellulitis, erysipelas, nec fasc, impetigo
scarlet fever
tss
pharyngitis

immune: RF, PSGN, ps arthritis, PANDAS

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14
Q

GAS tonsillitis vs viral tonsillitis - how to tell?

A

more likely GAS if:
>4yo
tender tonsillar LN
scarlet fever - blanching, sandpaper-like rash, usually more prominent in skin creases, flushed face/cheeks with peri-oral pallor

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15
Q

rheumatic fever tends to occur when post GAS

A

2-6 weeks (average 3) post GAS pharyngitis

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16
Q

transmission rate of maternal GBS

A

50%

17
Q

early onset vs late onset sepsis GBS

A

early: <7 days, pneumonia/septicaemia, maternal chemoprophylaxis helps
late: 7-30 days, bacteraemia/meningitis, chemoprophylaxis doesn’t help

18
Q

Rx for the different enterococci

A
Ampicillin = most active beta lactam 
Vancomycin = ampicillin resistant enterococci 
Teicoplanin = VRE
19
Q

VRE - what makes it resistant?

A

Alteration of binding site D-alanyl-D-alanine terminus of peptidoglycan precursors

VanA = most common phenotype, higher level resistance, cross-resistance to teicoplannin

VanB = 2nd most common, usually teicoplanin susceptible

20
Q

strep pneumoniae - what protects it from phagocytosis?

A

polysaccharide encapsulated diplococcus

21
Q

3 very specific immunocompromised states a/w strep pneumoniae

A

asplenia
sickle cell
nephrotic syndrome

22
Q

compare the two types of strep pneumo vaccines available

A

Prevenar 13 = CONJUGATE vaccine: Provides T cell immunity, reduces nasopharyngeal colonization by up to 60-70%

Pneumovax 23 = POLYSACCHARIDE vaccine: more capsular types of strep pneumoniae. if higher risk.

23
Q

pathophysiology of clostridium tetani infection

A

tetanospasmin toxin binds at NMJ > via motor nerve to spinal cord > blocks normal inhibition of antagonistic muscles by cleaving SNARE proteins > contraction and unable to relax!

24
Q

clinical features of tetanus

A

classic triad:

1) trismus
2) opisthotonus= abnormal posturing with arched back caused by strong muscle spasms
3) risus sardonicus, or “Sardinian grin”: abnormal looking, sustained grin, caused by facial muscle spasm

Laryngeal and respiratory muscle spasm can cause airway obstruction and asphyxiation

sympathetic overactivity

25
Q

Rx for tetanus

A

if had 3 doses of the vax: give booster if due or if bad wound, >5y since last one (exposure to toxin alone doesn’t give immunity!)

If not/uncertain: vax if clean minor wound; vax + tetanus IG if bad wound

26
Q

what is the new recommendation for boosters for tetanus

A

10-yearly tetanus boosters are no longer required up until the age of 50, provided that the primary series of 3 vaccinations plus 2 boosters have been given

27
Q

how does clostridium botulinum work?

A

botulinum toxin inhibits ACh release > blocks neuromuscular transmission

28
Q

classic botulism symptoms vs infant botulism

A

Classic triad:

i. Symmetrical flaccid ascending paralysis
ii. Clear sensorium
iii. No fever, no paraesthesias

infant:
constipation, poor feeding then the above with resp failure

29
Q

classic risk factor for infant botulism

A

HONEY

30
Q

which abx in particular are associated with clostridium difficile infection

A

fluoroquinolones, cephalasporins, clindamycin (lincosamide)

31
Q

treatment of c.diff

A

metro tds 7-10 days

severe disease vancomycin

32
Q

clinical manifestations of c.diphtheria

A
  1. pharyngeal - bull neck swelling!!
  2. cutaneous - gross ulcers
  3. neuropathy
  4. cardiomyopathy
33
Q

albert stain =

A

c.diptheria!

34
Q

diphtheria neuropathy - describe

A

10 days – 3 months: symmetric polyneuropathy with motor deficits with ↓ reflexes, distal to proximal

35
Q

what is the only gram positive bacteria with an ENDO toxin

A

listeria monocytogenes!

36
Q

Rx for listeria

A

penicilin - the reason penicillin is included in empiric neonatal sepsis!