gram positives Flashcards
(36 cards)
pathogenesis of toxic shock syndrome
- 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
Rx for toxic shock
empirical:
fluclox (strep/staph)/ vanc (MRSA) > switch to 3rd gen cef (staph) or penicillin (strep) if identify
+ clinda to cover the eagle effect
staph vs strep TSS
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
when are the coagulase negative staphs more pathogenic
when foreign material present e.g. central line
examples of coagulase negative staph
staph epi, staph saprophyticus, staph hominis, staph haemolyticus
what feature of CoNS is important in how bad the are?
Exopolysaccharide protective biofilm
empiric Rx for CoNS
vancomycin! (think about patient Ila)
staph aureus exotoxins can cause what 3 clinical pictures
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
what microbiological makes MRSA different from MSSA
Altered penicillin-binding protein (PBP) - MecA encoding PBP2a
what does alpha vs beta haemolytic actually mean for strep? give examples for each.
alpha = partially haemolyses surrounding RBC
- pneumoniae, viridans
beta = fully haemolyses RBC
- pyogenes, agalactiae
Lancefield antigen classification: GAS vs GBS vs GDS example each
GAS = strep pyogenes GBS = strep agalactiae GDS = enterococcus
invasive disease most commonly follows what kind of strep disease?
skin not pharyngitis
all the manifestations of GAS!
skin: follicles, cellulitis, erysipelas, nec fasc, impetigo
scarlet fever
tss
pharyngitis
immune: RF, PSGN, ps arthritis, PANDAS
GAS tonsillitis vs viral tonsillitis - how to tell?
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
rheumatic fever tends to occur when post GAS
2-6 weeks (average 3) post GAS pharyngitis
transmission rate of maternal GBS
50%
early onset vs late onset sepsis GBS
early: <7 days, pneumonia/septicaemia, maternal chemoprophylaxis helps
late: 7-30 days, bacteraemia/meningitis, chemoprophylaxis doesn’t help
Rx for the different enterococci
Ampicillin = most active beta lactam Vancomycin = ampicillin resistant enterococci Teicoplanin = VRE
VRE - what makes it resistant?
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
strep pneumoniae - what protects it from phagocytosis?
polysaccharide encapsulated diplococcus
3 very specific immunocompromised states a/w strep pneumoniae
asplenia
sickle cell
nephrotic syndrome
compare the two types of strep pneumo vaccines available
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.
pathophysiology of clostridium tetani infection
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!
clinical features of tetanus
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
