staphylococcus Flashcards
steps to identify staphylococci
- colony morphology/gram stain
- catalase test
- coagulase test
- biochemical/maldi-TOF analysis if results are inconclusive
list 4 laboratory tests used to distinguish staphylococcus from micrococcus
modified oxidase test
–> S (negative) M (positive)
lysostaphin
–> S (susceptible) M (resistant)
glucose
–> S(positive) M (negative)
bacitracin
–> S (resistant) M (susceptible)
most common laboratory test used to distinguish streptococci from staphylococci
catalase test
Staph = positive
Strep = negative
modes of transmission resulting in infections by gram + cocci
direct contact with infected person and respiratory droplets
modes of transmission of staphylococci
direct contact with contaminated person
bound coagulase test vs free coagulase (clumping factor test)
bound coagulase (slide) –> attached to wall of s. aureus
free coagulase (tube) –> released by wall of s. aureus
what is the use of coagulase tests in the identification of staphylococci
s. aureus is coagulase positive while other staphylococci species are negative (this differentiates between the different species)
describe the role of protein A in the virulence of s. aureus
binds human IgG on the Fc region to prevent it from binding to antigen
–> this protects s. aureus from. the immune system
activity of exotoxins produced by s. aureus
exotoxins (exofoliatin A and B) –> scalded skin syndrome
enterotoxins –> food poisoning
TSST-1 –> toxin shock syndrome
how do extracellular enzymes produced by staph can contribute to the severity of staph infections
coagulase which helps with the formation of blood clots contributes to the bacterias ability to evade the immune system
nuclease degrades nucleic acid
beta-lactamase breaks down penicillin
pathogenesis of impetigo
S. aureus or S. pyogenes colonizes damaged skin where it multiplies, produces toxins, blisters form and scab,
pathogenesis of carbuncles
S. aureus enters the hair follicle to form a furuncle (abscess within the follicle), degradation of connective tissue allows infection to spread and causes necrosis
–> pus filled
pathogenesis of furuncles
S. aureus enters the hair follicle to form a furuncle (abscess within the follicle)
–> pus filled
compare pathogenesis of toxic shock, staph scalded skin syndrome, and food poisoning
TSS: TSST-1 acts as superantigen causing a build up of toxin
Scalded skin: exfoliative toxins cause epidermal detachment and the skin peels
food poisoning: caused by intoxication of enterotoxins
differentiate staph food poisoning from other types of food poisoning
staph food poisoning has the fastest onset
activity of beta-lactamases and their clinical/diagnostic significance
beta-lactamases are enzymes produced by bacteria that break down the beta-lactam ring of penicillin based antibiotics
–> resistance to penicillin antibiotics
mechanisms of antibiotic resistance penicillinase producing s. aureus vs mrsa
PPSA –> penicillinase production destroys the beta-lactam structure of penicillin
MRSA –> presence of mecA gene which produces PBP2A protein that does not bind to beta-lactam antibiotics
significance of MRSA, VISA, and VRSA
MRSA is resistant to all beta-lactam antibiotics
VISA has intermediate resistance to vancomycin (reduced susceptibility)
VRSA complete resistant to vancomycin + penicillin
antimicrobial susceptibility of s. aureus and the coagulase negative staphylococci
colonization factors of staph and the role of foreign body implants
protein A –> prevents IgG from binding to antigen
capsule –> surrounds organisms to protect them from phagocytosis
biofilm –> coats and protects organisms from chemicals/environments
pathogenesis of s. saprohyticus and other coagulase negative staph
coagulase negative staph are non-pathogenic and typically opportunistic pathogens
what are the clinical situations where it is important to identify coagulase negative staphylococci to species level
endocarditis or device-related infections
biochemical reactions compare and contrast between s. aureus and s. lugdunensis
S. lugdunensis is positive for ODC
acute endocarditis vs subactute endocarditis
acute endocarditis begins more suddenly with more aggressive onset/symptoms
