Staph Micro Lecture 1 Flashcards by Jennifer Watson

Staphlococcus tend to form (clusters, chains)

clusters

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Streptococci tend to form (clusters, chains)

chains

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How to gram - and gram + stain with gram stain

gram + = blue

gram - = red

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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

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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

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Gram + cell wall must be very strong due to _______

high turgor pressure

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Describe the structure of the peptidoglycan cell wall.

NAG and NAM polymers that are cross linked with peptide cross bridges

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What is the basis of penicillin?

disrupt/inhibit formation of peptide cross bridges

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What is the advantage to using phage lysins to kill bacteria

they do not have to be growing (i.e biofilms)

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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

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What are the 2 basic types of teichoic acids?

lipoteichoic acid (LTA)
wall teichoic acid (WTA)

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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

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If gram + bacteria are unable to add D-ala to LTA, then they are _______

much less virulent

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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)

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pus filled abcesses

S. aureus

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indwelling medical devices

S. epidermis

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UTIs

S. saprophyticus

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What type of respiration do Staphlycocci use?

faculative aerobes (grow in O2, prefer low O2)

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Where on our body does S. aureus tend to colonize?

nasal cavity, axilla, perineum

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Where on our body does S. epidermis tend to colonize?

skin

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Where on our body does S. saprophyticus tend to colonize?

GI, perineum

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Is staph an extracellular or intracellular pathogen

mainly extracellular (i.e they do not invade other cells)

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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

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Produces a capsule called “slime”

S. epi

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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

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

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

1. 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

1. protein to be anchored has signal sequence that gets protein to PM 2. if protein has LPXTG aa moteif at C term, the sortase will clip between the T and G 3. 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?

1. adhesion 2. colonization 3. microcolony formation - quorum sensing at work - begin to make polysacchride matrix 4. maturation 5. 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?

1. colonize forgein bodies | 2 form bioflims

What are the coag negative staph?

S. epi and S. saprophyticus