Staph Micro Lecture 1 Flashcards
Staphlococcus tend to form (clusters, chains)
clusters
Streptococci tend to form (clusters, chains)
chains
How to gram - and gram + stain with gram stain
gram + = blue
gram - = red
What are the structural differences between gram + and gram -? (cell membrane, walls, what is in the cell wall, perimplasmic space, etc)
gram - have 2 cell membranes
gram + have one cell membrane
gram + have a thick peptidoglycan cell wall and gram - have a thin peptidoglycan layer
gram - have a periplasmic space, gram + do not
gram - make lipoploysaccharide
gram + male liooteichoic acid
Why do gram ___ have a greater exposure to our immune system?
+
bc when they die, the cell wall fragments get everywhere (since they have bigger cell walls, they have more shit to activate immune cells)
gram + also has LPS which is a potent TLR agonist
Gram + cell wall must be very strong due to _______
high turgor pressure
Describe the structure of the peptidoglycan cell wall.
NAG and NAM polymers that are cross linked with peptide cross bridges
What is the basis of penicillin?
disrupt/inhibit formation of peptide cross bridges
What is the advantage to using phage lysins to kill bacteria
they do not have to be growing (i.e biofilms)
What is the MOA of phage lysins?
PlyC is a lysin derived from a bacteriophage that degrades the peptide cross bridge by chopping off
- the lactyl moitety from NAM and
- the L-Ala off of the pentapeptide
*target gram +, and are very specific to the genus they target
What are the 2 basic types of teichoic acids?
lipoteichoic acid (LTA) wall teichoic acid (WTA)
Describe the structures of LTA and WTA.
Similarities and differences
- Both have long poly-glycerolphosphate (PGP) chains that are very negatively charged (due to PO4)
- this is neutralized by the addition of D-ala (which has a + charge)
- LTA possesses a diglucosyldiacylgycerol moiety (2FA) on the end embedded in the cell wall then a couple of hexoses and then the long PGP backbone
- WTA is a PGP without the diaglycerol (no FA) and are attached to the wall at the ends of peptide crossbridges
If gram + bacteria are unable to add D-ala to LTA, then they are _______
much less virulent
What is a common target in teichoic acids for antimicrobials?
dec D-ala available to bacteria (no D-ala attached to PGP, the less virulent they are)
pus filled abcesses
S. aureus
indwelling medical devices
S. epidermis
UTIs
S. saprophyticus
What type of respiration do Staphlycocci use?
faculative aerobes (grow in O2, prefer low O2)
Where on our body does S. aureus tend to colonize?
nasal cavity, axilla, perineum
Where on our body does S. epidermis tend to colonize?
skin
Where on our body does S. saprophyticus tend to colonize?
GI, perineum
Is staph an extracellular or intracellular pathogen
mainly extracellular (i.e they do not invade other cells)
Why is a capsule considered a virulence factor?
it can sterically block phagocytosis by neutrophils and macrophages
*blocks access of FcR to complement or deposited Abs
Produces a capsule called “slime”
S. epi
Staph species that produces a variety of extracell toxins (as virulence factor)
S. aureus
T or F: S. aureus can produce a capsule, but it is minor
T
What does it mean for a bacteria to be pyrogenic?
pus forming
What test can be used to distinguish staph from strep and enterococci?
Catalase test
**ALL staph make catalase
Of the staphlococci, only S. ___ make coagulase.
What does coagulase do?
aureus
activates prothrombin in plasma (converted fibrin to fibinogen –> clotting)
What does catalase do? Why would a bacteria want to be able to make catalase?
breaks down H2O2 into H2O and O2
**degrades one of the enzymes phagocytes use to kill bacteria
What test can distinguish S. aureus from S. epi?
coagulase test
- S. aureus is coag +
- S. epi is coag -
T or F: S. aureus can spread to clothing and infect other individuals
T
What is a community acquired infection?
carriers of disease infecting people they come into contact with
***this is the most common way staph is spread
Who suffers from more severe infections: staph carriers or non-carriers
non-carriers
probably an adaptive immunity thing
Healthcare Acquired infections of staph usually follow _____
some sore of invasive procedure in which the skin was “breached”
What are the 3 exotoxins S aureus makes?
alpha toxin: cytolytic toxin = beta-barrel pore forming
Panton-Valentine Leukocdin (PVL): beta toxin that also forms pores
exfoliatin:
- epidermolytic exotoxin that causes scalded skin syndrome (SSS)
- protease that degrades desmoglein-1 (cadherin in desmosomes)
PVL gene was transferred to S. aureus from a phage, why is this important?
horizontal gene transfer = may virulence factors can be passed around = bacteria become more resistant to abx
Cause of enhanced virulence in CA-MRSA
PVL
*low prevalence in HA-MRSA and methicillin-sensitive S. aureus
seen in kids younger than 5 and is caused by extracellular toxin, _____, produced by S. aureus
exofoliatin
Scalded skin syndrome
Exfolative toxin A genes are found on _____
Exfolative toxin B genes are found on _____
A: on the chromosome
B: on a plasmid
In SSS, the skin separates at a relatively superficial layer, between _____ and _____. How can SSS lead to death?
stratum granulosum and stratum spinosum
large amts of fluid can be lost –> dehydration
SSS reaction in older children is usually less severe and may only cause _____
bullous impetigo
toxin than separates desmosomes
exfolatin
2 ways the skin be breached
- disruption in skin layer (burns, bites, cuts)
2. shit gets in thru ducts and pores of sweat glands
What are SAg toxins? How are they bad? Who makes them?
made by some S. aureus strains (10%)
they are superantigens that have specificity for both MHC II and TCR and will bind both to cause a polyclonal expansion of up to 20% of T cell population –> cytokine storm = bad
What enterotoxins does S. aureus make?
SEA, SEB
causes food poisoning (most commonly)
SEB
MOA and effects that enterotoxins have on body
very stable proteins (can hand around even after bacteria dies) that act like SAgs –> stimulates a GI reflex transmitted to medullary emetic centers via vagus N
a few hrs after exposure –> vomiting and intestinal cramping
Surface bound S. aureus virulence factor
adhesins
MSCRAMM , what is it?
microbial surface components recognizing adhesive matrix molecule
~ to adhesin, general term for things on microbial surface that binds host cell receptors
Sortase
enzyme that anchors MSCRAMMs to cell wall
Describe sortase mechanism of anchoring MSCRAMMS
- protein to be anchored has signal sequence that gets protein to PM
- if protein has LPXTG aa moteif at C term, the sortase will clip between the T and G
- sortase then covalently anchors the T of the protein to a G of a peptidoglycan peptide crossbridge
aids in the spread of infection within tissues be degrading hyaluronic acid
hyaluronidase
cell wall components that are potent stimulators of TLRs (on monocytes and machrophages/innate immune system) –> excessive cytokine secretion
PAMPs
_____ is very important for the development and dispersal of biofilms
quorum sensing
Describe the regulation of virulence factor expression
TIGHTLY REGULATED via QUORUM SENSING:
Big colony –>inc AIPs –> AIPs bind AgrC and activate it –> AgrA is P and activated –> AgrA + SarA activate RNA III promoter –> more AIPs, toxins, adhsins, and polysaccharide matrix made
Order these VF in the sequence they would be made
polysaccharide matrix
adheins
cytolysins
adhesins –> cytolysins –> polysaccharide matrix
Why are biofilms difficult to eradicate?
they are less susceptible to abx
- abc cannot penetrate the extracellular polysaccharide matrix around the colonies
- bacteria are not growing so cell wall abx dont work
What are the phases of biofilm development?
- adhesion
- colonization
- microcolony formation
- quorum sensing at work
- begin to make polysacchride matrix - maturation
- dispersal (–> nidus)
**this happens with catheters and other indwelling devices
Folliculitis
S. aureus infection of skin (specifically hair follicles which serve as the point of entry)
usually does not leave skin/not systemic
another term for boils
furuncles
*pus just beneath the epidermis
bunches of boils
carbuncle
**start to have systemic symptoms!
symp assc with carbuncle
fever, chills
What is infected with external styes?
sebaceous glands or sweat glands
What is infected with internal styes?
Meibomian (or tarsal) glands
blistering vesicles that crust over
What S. aureus toxin causes these?
bullous impetigo
exfoliatin
T or F: pneumonia caused by Strep pneumoniae has a worse prognosis than pneumonia caused by staph aureus
F: staph aureus worse than strep bc staph forms necrotizing abscesses!
S. aureus pneumonia is freqently secondary to ______
influenza infections
What are risk factors for pneumonia?
CF, alcoholism, and DM
Staphylacoccal TSS is caused by _____
TSST-1
Where is the gene for TSST-1 found?
within a pathpgenicity island in S. aureus chromosome
**mobile genetic element
Signs and symptoms of Staphylacoccal TSS is caused by TSST-1
high fever, vomiting, diarrhea, sore throat, and erythematous skin rash that blanches when pressure is applied, hypotension (<90), multisystem involvement (hepatic, renal, CNS)
Does strep or staph TSS have a worse prognosis?
strep is worse than staph TSS
A pt has symptoms and Hx consistent with TSS, would you expect blood culture to be positive for S. aureus?
not necessarily
A pt has symptoms and Hx consistent with TSS, would you expect a serology test for TSST-1 to be positive?
yes
T or F: Staphyloccocal food poisoning is intoxication not infection
true (is self-limiting)
What lab findings are consistent with Dx of S. aureus infection
- Gram + bacteria in clusters (blue)
- Beta-hemolysis on BAP (agar clears completely around coloies)
- golden appearence of colonies due to carotenoid pigment
- Catalase +/coagulase +
infections with ___ became a problem with the rise in use of indwelling devices
S. epi
What are the 2 major virulence factors of S. epi?
- colonize forgein bodies
2 form bioflims
What are the coag negative staph?
S. epi and S. saprophyticus
