Gram+ Cocci Flashcards
what are the 3 major genera of Gram+ Cocci?
- staphylococci
- streptococci
- enterococci
in what formation (clusters or chains) do staphylococci and streptococci grow in, respectively, and why is this?
staphylococci: clusters, because they divide in random planes
streptococci: chains, because they divide in a single plane (same direction)
both appear blue/purple, because they are Gram+
what kind of bacteria family does this describe?
- Gram+ cocci
- grow in clusters
- resistant to heat and drying, persist on fomites
- normal skin or nasal flora
- common wound and nosocomial infections
staphylocci
*note that fomites are simply objects or materials that can carry infection
which of these is Catalase positive, streptococci or staphylococci?
(remember that these are both families of Gram+ cocci)
all pathogenic STAPHylococci are CATALASE POSITIVE
how are staphylococci divided?
(2 categories, hint - a major and then sort of everything else)
- coagulase positive: Staph. aureus
- coagulase negative (CoNS/CNS): all other pathogenic strains (S. epidermidis, S. saprophyticus)
*note that coagulase clots plasma
what species of bacteria does this describe?
- appear as golden colonies on agar
- coagulase positive
- normal flora of anterior nares (1/3 people)
- considered most common bacterial human pathogen
staphylococcus aureus !
describe the function of the following virulence factors of Staph. aureus:
a. Protein A
b. invasins (staphylokinase, collagenase, lipase)
c. cytotoxins (hemolysins, PVL/Leukocidin)
d. superantigen exotoxins (TSST-1, enterotoxin, exfoliatin)
a. Protein A: binds Fc portion of antibodies, escapes immune response (Fc receptors on phagocytes cannot bind)
b. invasins: for invading deep tissue
c. cytotoxins: lyse human cells
d. superantigen exotoxins: cause polyclonal T cell activation (lots of cytokines released, inflammation)
this surface protein of Staph. aureus binds the Fc portion of antibodies to evade the immune system. what is?
Protein A: anti-opsonization effect
*remember that Fc receptors are present on phagocytes, and thus their action will be blocked by Protein A
what are 4 important invasins that may be present in Staph. aureus? (Gram+ cocci)
invasins: for invading deep tissue
- staphylokinase
- collagenase
- lipase
- hyaluronidase
what are 2 important cytotoxins that may be present in Staph. aureus? (Gram+ cocci)
cytotoxins: lyse human cells
- hemolysins: lyse erythrocytes (example: alpha-toxin)
- PVL (Panton-Valentine Leukocidin): lyse PMNs, produced predominantly by CA-MRSA
*CA-MRSA = community-acquired MRSA
what are 3 important cell surface virulence factors of Staph. aureus? (Gram+ cocci)
- Protein A: anti-opsonin effect by binding Fc portion of antibodies
- capsule: antiphagocytic polysaccharide
- adhesins: facilitate attachment to host cells/tissue
what are 3 important superantigen toxins that may be present in Staph. aureus? (Gram+ cocci)
superantigen exotoxins: cause non-specific polyclonal T cell activation via cross-linking MHC to TCR
- TSST-1 (toxic shock syndrome toxin)
- enterotoxins (food poisoning)
- exfoliatin (“scalded skin syndrome”)
what are the SSTI clinical manifestations of Staph. aureus infection (4)? (Gram+ cocci)
SSTIs: Skin and Soft Tissue Infections; usually require surgical debridement with antibiotics, most common presentation of staphylococcal infections
- furuncles: small pus-filled local infections
- carbuncles: larger skin abscesses
- impetigo: spreading, crusted skin infection
- cellulitis: deep skin infection
FUR and CARs for UNCLES is IMPEritive to buy with your CELL
most common cause of bone infections in children (osteomyelitis)
staph. aureus infection (Gram+ cocci)
S. aureus metastasis of superficial infections may cause:
- osteomyelitis
- septic joint/ septic arthritis (esp. children)
- pneumonia (often follows viral influenza, esp. hospitalized patients)
- endocarditis (associated with IV drug use, rapid onset of vegetation on valve - usually tricsupid)
- bacteremia and septicemia
what are the 3 most common toxinoses of staph. aureus infection (Gram+ cocci)?
- Toxic Shock Syndrome: TSST-1 exotoxin —> high fever, hypotension, rash, multi-organ failure, desquamation (palms, soles)
- food poisoning (Gastroenteritis): heat stable enterotoxins on food —> acute onset of GI distress
- Scalded Skin Syndrome (neonates, children): exfoliatin —> red flush, bullae (blisters), bulbous impetigo, desquamation
note that toxinoses may be associated with “negative cultures” because it is released exotoxin causing symptoms
what type of bacteria have endotoxins?
Gram- (typically LPS)
[Gram+ have exotoxins]
generally speaking, what are the 3 categories of clinical manifestations of Staph. aureus? (Gram+ cocci)
- SSTIs: skin and soft tissue infections
- infections of other tissues (osteomyelitis, septic joint, endocarditis, pneumonia, septicemia)
- toxinoses (superantigens): toxic shock, food poisoning, scalded skin syndrome
what kind of drugs are methicillin, oxacillin, and nafcillin?
methicillin, oxacillin, and nafcillin are “anti-staphylococcal penicillins”
contain bulky side groups that prevent binding of penicillinase/ beta-lactamase by staphylococcus
[of course remember that there is now MRSA - methicillin resistant S. aureus]
what are the 3 important penicillinase-resistant penicillins, which were developed after almost all clinical strains of staphylococcus developed penicillin resistance (via penicillinase/ beta-lactamase)?
nom nom nom bacteria yum
- nafcillin
- oxacillin
- methicillin (watch out for MRSA!)
[note that MRSA resistance protein PBP2a is encoded by the mec A gene]
what confers methicillin resistance in MRSA?
MRSA = methicillin resistant Staph. aureus
PBP2a (penicillin binding protein), encoded by mec A gene
HA-MRSA vs CA-MRSA
hospital-acquired MRSA: tend to be resistant to additional antibiotics (tetracycline and clindamycin), but less virulent
community acquired MRSA: susceptible to broader range of antibiotics, but more virulent (PVL/Panton-Valentine Leukocidin gene present)
how are we treating Staph. aureus infections these days?
if MSSA (methicillin-sensitive SA) —> treat with oxacillin or nafcillin (methicillin not used clinically anymore)
but… most clinical isolates are MRSA
so…
vancomycin is first line of treatment for MRSA
[note that VISA and VRSA are on the rise]
vancomycin is the first line of treatment for _____ infections
MRSA
where are the 2 important coagulase negative staphylococci found? (must be able to name them first!)
- Staph. epidermidis: normal skin flora
- Staph. saprophyticus: normal vaginal flora
which bacteria does this describe?
- produces cell surface polysaccharide “slime” that adheres to bioprosthetics
- frequently involved in nosocomial and opportunistic infections (catheters, medical devices, IV lines)
- most are highly resistant to penicillins and methicillins
staph. epidermis (Gram+ cocci, coagulase negative): major component of normal skin flora, causes wound infections through broken skin, relatively less virulent
which bacteria does this describe?
- causes UTI and cystitis in females
- natural resistance to novobiocin
- sensitive to penicillin/oxacillin
Staph. saprophyticus (Gram+ cocci, coagulase negative): normal vaginal flora
what kind of infections does Staph. saprophyticus cause, and what distinguishes it from other coagulase negative staphylocci and staph. aureus?
Staph. saprophyticus (Gram+ cocci, coagulase negative): normal vaginal flora
causes UTI and cystitis in females
has natural resistance to novobiocin
(but sensitive to penicillin/oxacillin)
