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(3002) Clinical Micro > Catalase Neg GPC > Flashcards

Catalase Neg GPC Flashcards

1
Q

What is the scientific name for Group A Streptococcus? Where is it found as normal flora?

A
  • Streptococcus pyogenes

- found in skin and mucous membranes of URT

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2
Q

What is the scientific name for Group B Streptococcus? Where is it found as normal flora?

A
  • Streptococcus agalactiae

- URT, GIT*, Genital tracts

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3
Q

What would be the minimum set of primary and secondary tests required to positively identify Group A and Group B Streptococcus without using grouping sera? (ensure you understand what is meant by primary and secondary).

A

A:
1º GPC, Catalase neg, Fermentative, Lrg B haem.
2º Bacitracin S

B:
1º GPC, Catalase neg, Fermentative, narrow a/g haem
2º Bacitracin R, Hippurate pos

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4
Q

a) What does VRE stand for?
b) How have these organisms thought to have become resistant?
c) How do these organisms get into the human GIT?

A

a) VRE: Vancomycin resistant Enterococcus
b) High use of vancomycin and cephlasporins; use of avoparcin (glycopept. too) as animal growth promoter
c) due to R enterococci in human food from encouraging R w/ use of growth promoters

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5
Q

If you identified an unknown organism as a GPC that was catalase negative and salt tolerant? What genera would most likely be implicated?

A

group D Enterococcus

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6
Q

If you identified a GPC that was catalase negative and was sensitive to Bacitracin what would the most likely identity be?

A

Streptococcus pyogenese

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7
Q

Features of Streptococci & Enterococci

A
  • GPC in chains/pairs (in clinical smear)
  • catalase neg
  • non-motile
  • Facultative anaerobe
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8
Q

Virulence factors of Strep. pyogenes (Group A) & brief explanation on how it cause disease

A
  1. M proteins: adhere to epithelial cells, resist phagocytosis, & cross reactive Aby resp.
  2. Haemolysin O & S: toxic to cells
  3. Streptococcal Pyrogenic exotoxins (SPE): toxic shock syndrome, hypotension and shock, scarlet fever
  4. Enzyme production: (Hyaluronidase) break down CT ground substance = spread
  5. Hyalorunic acid capsule: adherence & resist phogocytosis
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9
Q

Which virulence factor is thought to be responsible for causing rheumatic fever?

A

(following pharyngitis infection)

M protein = cross reaction of Aby produced against Strep. Ag that react to own tissue (similar Ag)

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10
Q

Differentiate between rheumatic fever and glomerular nephritis.

A
  • 1º: pharyngtitis -> 2º: Rhuematic fever

* 1º: URT infection/scarletfever OR skin/wound infection -> 2º: glomeruar nephritis

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11
Q

post streptococcal rheumatic fever. Discuss the clinical symptoms and lab. diagnosis.

A
  • S: sudden onset of fever & joint pain
  • congestive heart failure bc Abys produced for Ag cross react w/ tissue Ag
  • LD: Inc ESR, CRP, ASOT, aDNAseB
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12
Q

glomerular nephritis. Discuss the clinical symptoms and lab. diagnosis.

A
  • S: Onset after couple of weeks
  • S: malaise, weakness, anorexia, oedema, headache, hypertension
  • S: Aby/Ag complexes deposit in kidney => damage glomeruli
  • LD: Inc ESR, dec C3, haematuria, proteinuria, inc ASOT and aDNAseB
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13
Q

What is the significance of measuring ASOT and DNAse B?

A

Measures the titre of Aby made against O Ag (ASOT) and DNAse B

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14
Q

In the coroner’s report (slide 20), a) what claim was made regarding the blood cultures taken from the patient by PathWest? b) Later on during the afternoon of the 5th April, 2006 the doctors at the hospital were notified of a culture result, what was the culture result? c) What assumption was made by the doctor(s)? d) What did the evidence given to the inquest say about the significance of the culture result? e) Subject to the patient having any allergies to antibiotics, what antibiotic of choice could have been used to treat this infection?

A

a) Expired blood culture bottles
b) Positive blood culture
c) Dural tap for headache and involution pain for abdominal pain
d) Streptococcus or Enterococcus
e) erythromycin or 1GC

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15
Q

If GPC have been seen in the Gram smear from a clinical sample but the culture plates record no growth, what could this indicate? What action, if any, should be taken?

A

Could indicate culture not incubated at ideal media and conditions (O2/AnO2/CO2). Try to re culture but best to take another sample

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16
Q

Explain why the Beta haemolysin from a Group B streptococcus could potentiate neonatal infection?

A

As the baby takes a gasp of air it could inhale the Group B strep in mum’s genital tract => goes to baby’s lungs => active against lung tissue and endothelial cells

17
Q

What does vertical transmission of infection mean?

A

Mother to foetus transmission

18
Q

How would you identify two non-haemolytic streptococci, “A” and “B”, given that organism A did not grow on CLED but organism B did grow on CLED and was a Non Lactose Fermenter (NLF)? i.e. name the tests performed and the possible identities of the organisms that could be involved.

A

S. equinus (Gp D Strept) vs S.agalactiae (Gp B Strept)
Hippurate test: Pos = Group B, Neg = Group D
*Viridance Strept. could be an organism (Hippurate v)

19
Q

If you had a GPC that was catalase negative and it grew very well on CLED with a yellow colony, describe how you would identify this to species level without using a commercial ID system? i.e. name the tests performed, the expected results (pos and neg) and the possible identities of the organisms that could be involved.

A

6.5% salt tolerance test or PYR:
Pos = Enterococcus sp.
Neg: Group D Strept. (S. bovis or S.equinus)

20
Q

How would you identify an alpha-haemolytic streptococci that did not grow on CLED? i.e. name the tests performed and the possible identities of the organisms that could be involved.

A

Bile solubility: Soluble (S. pneumo)
Optochin (BA in CO2): Sensitive (S. peumo)
*Viridans Strep. not bile soluble & R to Optochin

21
Q

Virulence factors of Strep. agalactiae (Group B) & brief explanation on how it cause disease

A
  1. Capsular polysaccharide Ag: Type III cause sepsis
  2. Enzymes: Hyalurodinase = break down CT
  3. Beta Haemolysin: active against lung tiss & endothelial cells in RT & CNS
  4. Lipoteichoic acid= adherance
22
Q

a) Location of Group C, F, G Strep (NF) in body b) and features

A

a) GIT, Vagina, Skin, Oropharynx

b) b haem, Similar colony morph as Group A, bacitracin R

23
Q

How do you differentiate the 2 common Group D Strep.: S. bovis and S. equinus

A

S. bovis: LF on Mac

S. equinus: NLF on MAC

24
Q

In what type of infection(s) and under what circumstances would an isolate of the viridans group be considered to be clinically significant? What infection are they most noted to be associated with?

A

Bacterermia (get in blood via mucous membranes)
=> Septicemia
=> endocarditis (esp. sub-acute bacterial endocarditis)
=> meningitis

25
Q

Where is S.pneumoniae found as normal flora?

A

URT

26
Q

Name the 2 most common species of Enterococcus. Which one is most often associated with VRE?

A
  • Enterococcus faecium (>90% associated w/ VRE)

* Enterococcus faecialis

27
Q

Which organism in this lecture has an association with gastrointestinal neoplasia?

A

Streptococcus gallolyticus associated w/ colorectal malignancies

28
Q

What is the clinical significance of isolating a member of the genus Leuconostoc from an infection in a long term hospital patient?

A

Significant bc intrinsically R to vancomycin

29
Q

If a patient or staff member of a health care facility is found to harbor a VRE, how many screening tests do they need to pass before being considered to be clear?

A

need to pass 4 consecutive screening samples

30
Q

How do glycopeptides prevent bacterial growth? i.e. how do they affect susceptible bacteria/what is their mode of action?

A

Glycopeptides bind to terminal D-alanyl-D-alanine residue in cell wall = disrupt lipid outer membrane= leakage= kills

31
Q

The enterococci that have the vanC1-3 genotype express the VanC1-3 phenotype of resistance to glycopeptides. What level of expression does this result in?

A

D-alanyl-D-alanine replaced by D-alanyl-D-serine

32
Q

In the flow diagram on slide 75, why is there a question mark associated with the measurement of a 14mm diameter around an optochin disc?*

A

bc the diameter might vary based on the density of growth?* OR diameter has changed? OR indicates any zone present is S?

33
Q

If an isolate of S.pneumoniae appears susceptible to penicillin on an agar plate, why is it necessary to determine the MIC of the strain to
penicillin (usually using an E-test) before the laboratory issues a sensitivity result?

A

Bc there’s an increase in Penicillin R S.pneumoniae

(3002) Clinical Micro (19 decks)

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