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58 Cards in this Set

  • Front
  • Back
4 distinguishing characteristics of Staphylococci
can grow in high salt
facultative anaerobe
catalase+
Gram+ in grape-like clusters
hemolysis: can see thru
3 most common Staph
S. Aureus
epidermidis
saprophyticus
where does staph colonize?
nasopharyngeal area mostly (30% of population)
role of peptidoglycan?
antigenic, attracts PMN, stimulates IL-1 from monocytes
(damange from immune response)
role of techoid acid
binds to fibronectin and mucosal sufraces to colonize
role of Protein A
binds Fc on IgG=>evade complement
, VWf; binds TNFR recruiting leukocytes
Hyaluronidase
hydrolyzes HA
What are 3 secreted staph virulence factors?
Catalase
coagulase (binds fibrinogen)
staphylokinase (digest fibrin)
Penicillilnase
blocks transport of drug
Lipaase
invade into cutaneous and subQtissue
a hemolysin
permeabilizes cell membranes
B toxin (sphingomyelinase C)
degrades sphingomyelin
delta toxin
small pores in membranes
Leukocidin
permeabilizes PMN mac membranes
exfolitin
staphyococcal scalded skin syndrome
may target Desmoglein 1
T cell mitogen
Hallmarks of Staph food poisoning
Rapid onset 4-6 hours
pre-formed
amount ingested
quick resolution
resistant to boiling (30min)
resistant to GI enzymes
mayo salads, processed meat, baked foods
food associated with staph poisoning
processed meat
mayo salads
baked goods
waht do these staph toxins cause:
A
B
C,D
A- food poisoning
B- pseudomembranous colitis
C,D- contaminated milk products
TSST
staph aureus
multiple organ failure
induces TNFa, TNFB, interferon
cutaneous skin manifestations of staph
furuncle, folliculitis
carbuncle
bullous impetigo
impetigo
what causes Endocarditis
S. epidermidis
staphylococcus saprophyticus
UTI only
how can you distinguish from epidermidis
resistance to novobiocin
staph virulence factors
capsule
peptidoglycan
techoic acid
protein A
Clumping factor (binds fibrinogen)
altered penicillin binding protein
enzymes secreted by staph
staphylokinase
coagulase
catalase
hyaluroidase
staphylokinase
lipase
nclease
penicillinase
toxins secreted by staph
a toxin (a hemolysin)
B toxin (sphingomylinase)
Delta (detergent)
Leukocidin (perm. PMN)
Exfoliative (SSSS)
Enterotoxins A-E
TSST
Syndrome from S. Aureus
cutaneous infections
SSSS
TSS
food poisoning
wound infections
bacteremia (endocarditis, pneumonia, osteomyelitis, septic arthritis)
Syndroms of S. epidermidis
endocarditis
prostethics/shunt infectiosn
syndrome of s. saprophyticus
UTI
RESISTANT TO NOVOBIOCIN
syndrome of S. Lugnunesis
native valve endocarditis
4 characteristics of S. pyogenes (group A)
Gram+ cocci in chains or pairs
B hemolytic
catalse -
BACITRACIN SENSITIVE
4 cellular components of S. Pyogenes
Cell wall: peptidoglycan
capsule: hyaluronic acid
Mprotein: antiphagocytic
lipoteichoic acid: binds to host
7 extracellular products of S. pyogenes
C5a peptidase
streptolysin O: RBC/WBC
streptokinase: fibrin
streptodornase: DNA
hyaluronidase: spread thru CT
pyrogenic exotoxins ABC
protease: augment invasion
superficial disease caused by Group A strep
Pharyngitis (+rash= scarlet fever)

Impetigo
invasive diseases caused by Group A strep
Puerperal sepsis
Erysipelas and necrotising fasciitis
Lymphangitis/adenitis
streptococcal sepsis and STSS
2 post-infectious sequelae of Group A strep
Acute post-streptococcal glomerulonephritis

acute rheumatic fever: arthritis, carditis, chorea
growth characterisitcs of streptococci
complex medium
Lactic acid producers
sugar Fermentation pattern can be used for ID
Hemolytic activity of Strep
a- incomeplete (green)
B- complete
G- none
Group B strep ID
most B hemolytic
CAMP test
Blood, CSF, genital cultures used most
Group B strep pathogenesis and Rx
overwhelm immature immune system of newborn

penicillin
Strep B diseases
most important cause of:
neonatal sepsis
meningitis

maternal obstetric infection
Where is group D strep found normally

what does it cause
normal intestinal flora

UTI
peritonitis
subacute bacterial endocarditis
lab ID of gropu D strep

2 organisms of group D
enterococcus and strep bovis

gamma hemolytic
grows in bile esculin
6.5%NaCl
Tx for group D
ampicillin and gentamicin


there is vancomycin resistant enterococci- VRE needs newer antibiotics
where is viridians strep normally found

what does it cause?
upper respiratory tract

SBE, dental caries
Lab ID of viridians
a-hemolytic that is not strep pneumoniae
pathogenesis of Viridians diseases

Rx
SBE: bacteremia (from dental work) leading to inoculation of damaged heart valve

Dental caries: found in plaque-> lactic acid->

Penicillin
strep pneumoniae virulence mechansim
capsule

R (rough) mutants are avirulent
Lab ID and diffrerentiation of strep pneumoniae from other apha stre
Optochin test
mouse virulence
inulin fermentation
bile solubility

all these are pneumo +, a strep -
Diseases caused by S. Pneumoniae
Lobar pneumonia
otitis media
sepsis
meningitis (now most important cause)
Rx of pneumococci
penicillin
but now resistance is up (20%)

Polysaccharide vaccine or new heptavalent conjugate vaccine (for peds)
Neisseria
general bio

staining/ growth
G- cocci
aerobic, non-motile,
non-spore forming
oxidase positive: purprle tatramethyl-p-phenylenediamine
difficult to grow-autolyze easy
how are 4 neisseria differentiated?
gonorroea- no fermentation from M/L/S->lactic acid

Meningitidis-> no L/S
lactamica-> no S
Sicca-> fermentation from all sugars
what are non capsular cell wall antigen and structer that helps meningococci attaach to human cells
Lipooligosaccharide- endotoxin like

pili
where do carriers carry meningococci

and how is it transferred?
nasopharynx

respiratory route
what are 4 clinical manfestations of neisseria
Bactermia w/o sepsis
meningococcemia (septicemia) w/o meningitis
meningitis
meningococemia with meningitis
pathogenesis of meningitis and sepsis
organisms reach blood stream from nasopharynx=> high fever and hemorrhagic rash develops, may reach CNS to cause meningitis.

may be fulminant sepsis, DIC, and circulatory collapse
Dx of neisseria
Blood and CSF culture
gram - diplococci in wbc CSF
Ag detection techniques