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Micro 2024 > Week 1 - Staph > Flashcards

Week 1 - Staph Flashcards

1
Q

What does Staphyococci mean and what are the characteristics and look

A

-bunch of grapes
-found in clusters (singles, pairs or tetrad)
-catalase positive diff from strep
-coagulase positive - S aureus
-aerobic or facultative anaerobes
-not motile
-not spore forming
-small or medium size, smooth opaque domed
-white or gold
-BH or NH
-S.aureus is most clinically significant
-divide by binary fission

“coccus” related to Staphylococci
-can have catalase negative and Obligate ana = S.Saccharolyticus - rare
-can be catalase negative and ana or micro aero - S.aureus subsp anerobius - rare

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2
Q

Coagulase Negative Staphylococci

A

-coagulase positive would be a clot in plasma meaning the org produces staphylocoagulase
-FREE AND BOUND?

usually S.lugdunensis, S,epidermis, or S saprophyticus
- Lugdenensis can be seen an coag positive because it has a clumping factor causing bacterial cells to agglutinate in plasma on the slide- (tube negative)

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3
Q

where is staph found

A

-skin, nasopharynx, perineum and mucus membrane of humans and animals with warm blood
-on humans it is normal flora

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4
Q

what is the epidemiology of Staph and why is it significant

A
  • primary reservoir - nares
    -mainly transmitted through touch since its on skin, through mom +child, airborne or nose picking
  • nasal carriage (in patients)
    -colonization of axillae, nasopharynx, and skin surfaces
    -can be nosocomial infection SSIs in cardiovascular septicemia or orthopedic surgery, infection at catheter site
    -can be community acquired by furunculosis, or diabetic foot infection
    -staph is opportunistic and can be recovered from any specimen, can cause meningitis
    -issue with drug resistance - MSSA MRSA
  • can cause infections because of bacterial presence or toxins that can travel to other sites like scalded skin syndrome
    -severity varies from skin infections to osteomyelitis - toxic shock syndrome
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5
Q

S. aureas virulence factors
Secreted factors
Membrane bound factors
Enterotoxin
Exfoliative toxin

A

Secreted factors
-Toxins: TSST-1, Entrotoxins, alpha-hemolysin
-Invasins: Panton-Valentine, Leukocidin
-Enzymes : Coagulase, Staphylokinase

Membrane bound factors
-Adhesins- Collagen binding protein, Fibronectin Binding Protein, Elastin Binding Protein

Enterotoxin- heat stable, inhibit water adsorption in bowel causing vomiting and diarrhea - Food Poisoning (preformed toxin). Because cooking wont kill the toxin

Exfoliative Toxins - epidermolytic toxin which attacks the epithelium and causes skin to slough off

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6
Q

Scalded Skin Syndrome – exfoliative toxin

A

-known as extensive exfoliative dermatitis
-newborns and young children under 6
-in adults with chronic renal failure and failed immune system
-can be localized lesions like bullous impetigo or extensive like peeling skin

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7
Q

Toxic Shock Syndrome (TSS) -
enterotoxin B or TSST-1 -tampon

A

-DIC disseminated intravascular coagulation can be fatal
-fever, vomiting , sweaty palms, skin peeling, sunburn like rash on trunk that spreads, hypotension and shock
-after surgery, flu or through tampons , post flu or chickenpox
-high leuks and low platelets
-increased band and metamyelocytes early WBC

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8
Q

how does the tampon cause TSST -1

A

-production of superAG that produces T cell to make cytokines that causes the symptoms
-excessive activation of immune system with large activation of t cells
-multi system effects occur due to absorption through the vaginal mucosa

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9
Q

Cytolytic Toxins are what?

A

-Extracellular hemolysins and leucocidins affecting RBC and WBC

Hemolysins - degrade RBC
Alpha - pore forming causing damage to RBC
Beta- RBC hemolysis
Delta -RBC hemolysis, membrane disturbance
Gamma-Pore forming, hemolysis of RBC and WBC - this can be inhibited by agar

Leucocidins affect WBC - like the complement cascade they make pore in leukocytes examples are Panton-Valentine (PVL) which suppresses phagocytosis
-severe infection causing a more invasive disease with higher mortality rates

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10
Q

What are some virulence factors - Enzymes

A

Staphylocoagulase - virulence marker

Hyaluronidase - hydrolyzes the hyaluronic acid which makes it easier for bacteria to spread

Lipase and Protease- destroy tissue and help infection spread

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11
Q

What are some virulence factors - Protein A - Structural

A
  • found in staph cell wall
    -binds to fc region of IgG which blocks IgG phagocytosis
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12
Q

how is the severity of an infection determined

A

-by virulence of the strain, status of host and site of inoculum
-normal vs impaired immune system
-disease occur because of the infection, or because of the toxin the org releases

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13
Q

Skin and wound infections -what happens

A

-causes abscess and pus
-tissue get necrotic and leukocytes are damaged
-usually happen through previous skin injuries which is how the staph gets in and or secondary its hygiene
-people at most risk are those with invasive devices or are immunocompromised

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14
Q

what are furuncles and carbuncles - skin infections

A

furuncles- boils
-raised superficial abscess
-can spread deeper to become a carbuncle

carbuncles- invasive due to multiple furuncles
-can go deeper and become systemic- fever

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15
Q

what is folliculitis , impetigo,

A

folliculitis- raised infection in follicles

impetigo - common child skin infection with pus and yellow crust around lesions. They go away with antibiotic no complicatons

Non bullous impetigo- 2ndary to bite, eczema, or herptic lesions caused by S aureus, S pyogenes

Bullous impetigo- S.aureus , very contagious (direct contact, autoinoculation, formites), cause larges blisters with pus and erythema when skin rubs together

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16
Q

Toxic Epidermal Necrolysis (TEN)

A
  • drug induced from infections and vaccines
    -hypersensitivity reactions with erythema, necrosis, skin detachment and fever
    -solved by steroids
    -can cause sepsis and death
    -issues with keratinocytes in the basal layer that causes the skin to detach
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17
Q

what can occur in wound and surgical infections

A

-pulmonary abscess
-endocarditis - IV drug users
-bacteremia (via needle, focal lesions from skin, respiratory, genitorinary
-osteomyelitis (2ndry to bacteremia, infection in long bone)
-septic arthritis in kids
-nail bed infection -paronychia

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18
Q

what are penicillin and what is its resistance like

A
  • bind to PBPs
    -natural
    -should not be taken orally as it be inactivated by the acids in the stomach better when inject intramusc.
    -excreted in urine quickly
    -gram pos Cocci

the semi synthetic penics (ampi or carben)
-modified for better absorption and resistance to acids in stomach and they last longer

-resistance occurs because the Staph starts making Beta lactamase enzymes which hydrolyze and inactivate penicillin before it binds to the cell wall to stop cell wall synthesis
-current penicillinase resistant penicillin - OXACILLIN

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19
Q

what is Methicillin Resistance ***

A

-occurred through natural selection
-new protein was acquired to avoid methicillin PBP2a

-the PBP2a gene is encoded by mecA
-all Beta lactam drugs like ‘cillins cannot bind to altered PBP2a meaning all beta lactam drugs are resistant
-PBP2A doesnt let any of the PBP binding proteins in the cell
-because cell wall synthesis is not disturbed bacteria survives

beta lactamase developed by penicillin which breaks down beta lactam which is in penicillin so there are all resistant to penecillin
so stronger cillins -oxa and meth were developed resistant to beta lactamase
-then resistant to cillins occurred naturally by staph by changing PBP to PBP2A so cillins can no longer bind therefore cannot destroy the antibiotic

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20
Q

what is MRSA

A
  • when S aureus is resistant to oxacillin treatment
    -clue to resistance comes from Vitek -MIC
    -can cause Pneumonia, surgical site infections, blood stream infections, CNS infections
    -reservoirs are pt who are already infected with MRSA, carriers who are asymptomatic
    -can be transmitted through hands, hcw, contaminated equipment and open wounds
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21
Q

why is MRSA such a concern?

A

-pathogenicity and small treatment options
-current treatment would be vancomycin
-rifampin can be used however it must be paired with other drug
-this condition is resistant to all B lactam drugs including cephalosporins and carbapenems, erythromycin, tetracycline
-all these resistances cause longer hospital stays with higher mortality rate
-usually pts are screened and segregated so immunocompromised are not effected
-dialysis units or nursing homes - healthcare acquired

22
Q

what is community acquired MRSA

A

-MRSA taken from people who have 1 year history without any hospital procedures; and get a positive MRS culture <48 hours after hospital admission . Thats how you know they got it elsewhere
-able to spread very quickly
-starts as skin and tissue infections like pimples or boils that are painful, swollen and drain
-from military , contact sports, illegal tattoo parlors
-PVL are mostly found in CA-MRSA

23
Q

What is BORSA Border line Oxacillin Resistant S. aures

A

-mostly intermediate to oxacillin on plate and barely on MIC
-not related to mec A
-superproduction of beta lactamase
-it has an altered penicillin binding protein that is not PBP2A
-MIC break above that oxacillin but dont grow on the ox plates

24
Q

Vancomycin and S aureas - relation

A

-Vancomycin MIC needed to inhibit S aures is 0.5 and 2 ug/ml
-need to check on VISA and VRSA
- check GISA - which is staph with resistance to glycopeptide antibiotic - vanco and teichoplanin
-VISA occurs because the cell wall thickens and traps the vancomycin, blocking it from acting on the cell membrane
-VRSA occurs because vanA resistence is acquired via plasmids or transposons from Vanc resistance Enterococci - happens through conjugation and transposition

25
Q

Clinical signifinance of CoNS

A

-usually considered normal flora
-mostly nosocomial infections in pt after surgery bone and joint infections, endocarditis, septicemia, UTSI, catheter,
-Staphylococcus epidermis
-Staphylococcus saprophyticus
-Staphylococcus lugdunensis

26
Q

S.epidermidis -

A

-normal flora on skin
-when it causes infections it will be healthcare acquired- UTI
-most common cause of prosthetic valve endocarditis
-predisposed due to instrumentation like catheterizaton, medical implantation, taking immunosuppressive drugs

Virulence factor
-can produce a bioflim on implants and catheter, dialysis, shunt
-adherence factor

27
Q

S saprophyticus - women of child bearing age
where is it found , how it transmits, and its virulence, symptoms, and Epidemiology

A

found
-on epithelial cell lining of urogenital tract; GI

transmits
-by introducing endogenous flora into urinary tract
-A CA-UTI rather then HA-UTI

Virulence Factor
-adherence factor to uroepithelial cells
-Urease: helps with growth and pathogenicity in urinary bladder

Symptoms
-pyuria, frequent urination with burning , dysuria, hematuria

Epidemiology
-causes cystitis in young women
-found in urine of menstruating women

28
Q

Staphylococcus lugdunensis
need sterile site
where is it found
and its characteristics

A
  • found as both a CA and HA infection
    -catheter related bacteremia and septicema
    -aggressive endocarditis which leads to valve replacement - high mortality rate
    -meningitis, tissue infections, UTI
    -abscesses; joint infections and pacemaker

-copies S Aures but is more virulent and can be mistaken for S aures
-has the mecA for oxacillin resistance
-has esterase, hemolysins, lipase
-it is tube coagulase negative but gives false pos because it has clumping factor

29
Q

micrococcus what is it

A
  • non pathogenic
    -found mostly in tetrads instead of S aureas clusters
    -different in glucose fermentation
    -catalase positive
    -coagulase negative
    -bright yellow
30
Q

rothia mucilaginosa
where is it found and what are its characteristics

A

-normal flora in mouth and UPT
-low virulence
-causes septicimia, endocarditis, catheter
-GPC in clusters; facultative anaerobe
-grey-white wet sticky NH

31
Q

Atmospheric Requirements of Staph

A

Primary - Facul Anaerobe
-grows on BA, CHOC, CNA, BA (AnCO2) at 35C after 24hours

saccharolyticuc - obligate anaerobe
micrococcus - strict aerobe

32
Q

What is the Rapid Slide Agglutination Test

A

Staphaurex - reverse indirect
-detect protein A and clumping factor as well as capsular antigens
-confirm with tube coagulase

33
Q

what is tube coagulase

A

-Detects found and free coagulase
-confirmatory
-incubated 4 hours and then RT overnight because it auto agglutinates in the oven
-S.aures post

34
Q

Flow of work to detect if Staph

A

Colonial morphology -> gram -> catalase -> staphaurex -> tube coagulase

35
Q

what would you do next if the coagulase was negative

A
  • can be lugdunensis or saprophyticus
    -if neither then just CoNS
36
Q

what are the identifiers of Lugdunensis

A

-need to rule out if you have a sterile sample aka blood, fluid or CSF
* Catalase positive
* Staphaurex negative (But maybe look slight positive)
* Tube coagulase NEG
* PYR positive
* ORN positive
* (Novobiocin susceptible)

Colonial morphology -> gram -> catalase -> staphaurex -> tube coagulase ->PYR -> ornithine

The overnight tests are the tube coagulase and Ornithine

37
Q

what are the identifiers of S. saprophyticus
what special test would you do with this ID

A

-rule out if you have a urine sample from woman 12-65 years old

  • Catalase positive
  • Staphaurex negative
  • Tube coagulase NEG
  • Novobiocin resistant
  • (PYR negative)

Colonial morphology -> gram -> catalase -> staphaurex -> tube coagulase->novobiocin

The overnight tests are the tube coagulase and novobiocin

38
Q

Novobiocin

A

-sensitivity on MHA with 0.5 McFarland Standard
-read ZOI of novobiocin disk after 18-20 in O2
-resistant <16mm
-not in CLSI guidelines
-MAKE PURITY PLATE since a suspension is being made

39
Q

Other Coagulase negative Staphylococci
sp. - Identification workflow

A

Colonial morphology -> gram -> catalase -> staphaurex -> tube coagulase

if PYR is neg - stop
if novobiocin is sensitive -stop

40
Q

Mannitol Salt Agar

A

-selective and diff
-isolates Staph in contaminated specimen
-7.5 % salt concentration
-S aureus and S saprophyticus are yellow on the agar because they ferment the mannitol all other staph is pink or neg

41
Q

DNase Agar

A

-enzyme that cleaves DNA
-inoculate directly on DNA agar plates
-SA- clearing seen - all others neg

42
Q

how do we know which antibiotics to screen for in Staph, MRSA, LUG, SAP CoNS

A

S. aureus:
* AST testing with Kirby or Vitek
* then Oxacillin screen to screen for MRSA

MRSA:
* If OX and Vitek suggest MRSA, perform PBP2a test to confirm presence of the altered penicillin binding protein
* Perform Vancomycin screen to screen for VISA/VRSA

S. lugdunensis:
* AST testing with Kirby or Vitek

S. saprophyticus:
* Add a comment since there is little resistance to UTI-specific antibiotics. No need to test.

Other Coagulase Negative Staphylococci sp.
* No AST testing since these are considered normal flora!

43
Q

Screening for MRSA

A

-patients coming to the hospital are screened for MRSA colonization not infections to prevent the spread of drug resistant org
-nasal or rectal swab but any site will do since Staph lives on the skin

44
Q

MRSA chromogenic agar

A
  • high salt concentration
    -antibiotic and antifungal which inhibits yeast, GN, GP except methicillin resistant Staph

-inoculate directly and streak with 0.5McF
-24 hours, 35C O2

45
Q

Denim Blue Agar

A

-color change is denim blue due to phosphatase activity which is found in MRSA
-has antibiotics

-inoculate directly and streak with 0.5McF
-24 hours, 35C O2

46
Q

Detection of MRSA on oxacillin screen

A

-wont degrade and more likely to detect heteroresistant strains - all cells have mecA but only some have resistance phenotype
-35C max 24hours

-use MH with 4%NaCl as control and MH with 4%NaCl and 6ug/mL oxacillin
-0.5mcF
-run QC with each test
-everything will grow on control , G on test MRSA and NG on test MSSA

47
Q

Cefoxitin Testing

A

-Cefoxitin acts in place of oxacillin when you do KB
-it induces PBP2A in strains with mecA
-oxacillin read on cefoxitin result
-dont need a confirmatory test
-tests CoNs like lug
-on Vitek cefoxitin will say if you have MRSA or MSSA

48
Q

MRSA – Latex agglutination kit what is it

A

-tests for mecA
-or for PBP2A
-predicts oxacillin resistance -Denka Alere

49
Q

how to enhance detection of oxacillin resistance

A

-direct inoculum
-grow at neutral pH
supplement the agar/broth with 2-4% NaCl
-incubate at 35C
-read under transmitted light looking at media side after 24 hours to allow slower strains to grow

50
Q

To Identify a MRSA

A

*Oxacillin screen = resistant
* Oxacillin MIC (Vitek) = resistant
* Cefoxitin Screen (Vitek) = resistant
* PBP2a = positive

then once MRSA is confirmed do VISA/VRSA since vacomycin is used to treat MRSA
-use vancomycin screen (brain heart infusion with vaco even 1 colony is positive) and Vitek2 NOT DISC DIFFUSION

51
Q

S. lugdunensis - AST what happens

A

-AST with vitek
or can do KB with cefoxitin disc for oxacillin

52
Q

S. sappy - AST what happens

A

No AST dont
add comment sensitive to urinary concentrations of nitrofurantoin, SXT and fluoroquinolones

Micro 2024 (13 decks)

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