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Medische Microbiologie > Bacteriologie > Flashcards

Bacteriologie Flashcards

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1
Q

Virulence factors S. aureus

A

Toxins: cytolytic, enterotoxins, exfoliative toxins
Enzymes: coagulase, hyaluronidaselipase, fibrinolysis, catalase

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2
Q

bad bacteria in microbiome

A

Neisseria meningitidis
streptococcus pneumoniae
s. aureus

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3
Q

virulence definition

A

degree of pathogenicity (ability to produce disease) of the microbe

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4
Q

virulence factors, examples

A

adhesins, invasins, capsule, toxins, enzymes, pili

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5
Q

gram+ bacteria divided into 2 subgroups

A

cocci

bacilli

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6
Q

what type of bacterium is N. meningitidis

A

gram negative diplococcus

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7
Q

what does bromelia burgdorferi cause?

A

lyme disease

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8
Q

wat is serologie?

A

het aantonen van immunoglobulinen tegen agens

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9
Q

welke vormen hebben deze soorten respectievelijk: coccus, baccillus, spirochetes

A

sphere, rod, spiral

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10
Q

what is MIC?

A

minimal inhibitory concentration –> sterkste verdunning waarbij bacterie niet meer groeit

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11
Q

voorbeelden moeilijk kwetsbare bacteriën

A

mycobacterium, mycoplasma, chlamydia, legionella

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12
Q

what kind of bacterium is N. meningitidis

A

gram negative diplococcus (meningococcus)

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13
Q

4 steps of invasive meningococcal disease (IMD):

A
  1. colonization
  2. invasion epithelium
  3. invasion blood (septicaemia)
  4. dissemination (to CSF)
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14
Q

4 results meningococcemia (meningococci in bloodstream)

A
  1. sepsis
  2. rash
  3. disseminated intravascular coagulation (DIC); abnormal blood clotting
  4. meningitis
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15
Q

what determines meningococcal serogroup, and how many are there?

A

polysaccharide capsule

13

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16
Q

2 typing methods for N. meningitidis

A

phenotype and genotype

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17
Q

annotation for N. meningitidis

A

Example: Nm: B:P1.7,4:F5-1

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18
Q

what methods can be used in genotype typing for N. meningitidis, and what do they do?

A
  1. multi locus sequence typing (MLST), sequencing of 7 loci
  2. ribosomal MLST, sequencing of 53 loci

these methods assign numbers to alleles

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19
Q

what does the sequence type (ST) of N. meningitidis say?

A

the combination of allele numbers, assigned by MLST

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20
Q

what is a singleton?

A

a strain that doesn’t belong to a certain clonal complex (CC, a complex matching the central genotype)

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21
Q

what clonal complexes (CC) overrepresented in patients with IMD

A

CC41/44 & CC32

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22
Q

What clonal complexes are overrepresented in carriers

A

CC53 & CC35 (no capsules, important virulence factor)

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23
Q

why is there no MenB vaccine?

A

CPS of B is poorly immunogenic; it is identical to sialic acid in nerve tissue

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24
Q

what does Factor H binding protein (FHbp) do?

A

enables microbe to bind factor H (from complement) enabling bacterial survival in blood

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25
what is an important AMP and what does it do
Lactoferin; pulls away iron from pathogens
26
what is GAS
Group A Streptococcus (Streptococcus pyogenes)
27
what causes impetigo?
S. aureus: exfoliated toxin | GAS
28
major component of cell wall S. aureus
protein A
29
what does S. aureus toxin panton valentine do, and what kind of toxin is it?
destroys leukocytes, exotoxin
30
what kind of bacterium is S. pyogenes (GAS)
gram positive, from chain structures
31
exotoxins secreted by GAS
SPE: A, B and C
32
3 examples of invasins and adhesins from GAS
Invasins: 1. streptolysins 2. streptokinases 3. proteases adhesins: 1. M protein (in fimbriae) 2. lipoteichoic acid (LTA) 3. protein F and Sfb
33
what is a BAI?
biomaterial associated infection: e.g. breast implants, CSF shunts, pacemaker often caused by staph epidermis
34
through which 3 mechanisms can staphylococci form biofilms
1. through exopolysaccharide production 2. through release of DNA 3. through factors of proteic nature
35
how does a s. aureus biofilm detach
via phenol soluble modulins (PSM)
36
describe biofilm process
1. biofilm formation (through 3 mechanisms) 2. primary attachment phase (MSCRAMM & Aap) 3. accumulation phase 4. detachment (PSMs)
37
rifampicine mechanism
inhibits RNA synthesis by inhibiting RNA pol
38
tetracycline mechanism
inhibits protein synthesis by inhibiting ribosomes
39
kanamycin mechanism
inhibits protein synthesis by binding to bacterial 30S ribosomal subunit, causing misreading of tRNA
40
penicillin mechanism
inhibits cell wall synthesis by blocking peptidoglycan production
41
3 virulence factors Proteus mirabilis
1. urease 2. flagella 3. fimbriae
42
what is a McConkey plate
selective plate for Gram neg bacteria
43
difference S. aureus and proteus mirabilis?
s. aureus is non motile, p. mirabilis is motile
44
what kind of bacterium is p. mirabilis
gram neg bacilli, with flagella to move
45
true or false: more fimbriae = more bacteria colonizing
true
46
3 point hierarchy of fimbriae regulatory mechanisms
1. DNA structure 2. transcriptional regulation 3. post transcriptional regulation (sRNA)
47
mrp fimbriae gene cluster expression in high and low oxygen
high oxygen: phase off; flagellum expression by not expressing mrpJ low oxygen: phase on; flagellum inhibition by expressing mrpJ
48
what does mrpJ do
block flhD/C, which code for flagella
49
is chlamydia trachomatis gram neg or pos
gram neg
50
what kind of bacterium is neisseria gonorrhoea
gram neg diplococci
51
what does Treponema palladium (a spirochete) cause
syphilis
52
which 2 bacteria in the family of Neisseriaceae are the only pathogens in this family
N. gonorrhoeae and N. meningitidis
53
4 antibiotic resistance mechanisms is N. gonorrhoeae
1. plasmid mediated 2. mutations in antibiotic binding site 3. mutations in topo-isomerase 4. overexpression of efflux pumps
54
how does N. gonorrhoeae acquire tetracyclin resistance
through tetM sequence on conjugative plasmid. It protects the ribosome from binding the antibiotic
55
2 toxins attracting and killing neutrophils
S. aureus: PVL, PSM
56
3 mechanisms of defense on neutrophils
1. block of chemotaxis (CHIPS) 2. toxins 3. biofilm formation
57
4 complement evasion mechanisms by microorganisms
1. capsule prevents complement activation 2. LPS prevents C3b contact 3. LPS prevents C3 and MAC 4. factor H binding molecules; degrading C3b
58
5 mechanisms for antibody evasion
1. phase variation 2. antigenic variation 3. decoy: capture/block antibody 4. Ig-proteases 5. Fc receptors
59
how do salmonella, proteus and s. aureus evade AMPs?
salmonella: phoP/Q pmrA/B: inducible aminoarabinose proteus: aminoarabinose on LPS s. aureus: via dlt operon; D-alanine in LTA. and QacA exporters
60
name 2 microorganisms that can cause endocarditis and if they can infect WITH or WITHOUT pre existing heart vegetation
s. aureus; without | viridans streptococcus; with
61
4 s. aureus virulence factors in endocarditis
1. capsule 2. adhesins (FnBP, CflA, Protein A) 3. toxins 4. exoenzymes
62
3 viridans streptococci virulence factors
1. exopolysaccharides (glucans, fructans) 2. MSCRAMM 3. PAAP
63
what are thrombocidins (TC) and what do they do
- compound preventing endocarditis | - C terminally truncated derivatives of CXC chemokines
64
what is a potential role for platelets in endocarditis
formation of vegetation; susceptible to endocarditis
65
what do activated platelets secrete
Platelet Basic Protein (PBP)
66
what results from N terminal truncations of PBP, and in turn C terminal truncation of these products?
- CTAP-III and CXC-L7; fibroblast activation and neutrophil chemotaxis - C terminal truncation of these results in TC-1 and 2 --> highly potent AMPs
67
which 2 receptors do platelets have for IgA and IgE and what do they induce
- MHC-I and Fc | - activate complement
68
what 4 antigens do TLR receptors on macrophages and monocytes bind
1. LPS 2. peptidoglycan 3. LTA 4. flagellin
69
which 3 pathogens cause sinusitis
1. S. pneumoniae 2. Moraxella catharallis 3. H. influenzae
70
name virulence factors for GAS (6)
exotoxins (SPE A, B and C), M protein, LTA, capsule, adhesins, invasins
71
which 3 mechanisms do the large aiways have to defend against airway infections
1. mucus and coughing 2. IgA secretion 3. cilia
72
which 3 mechanisms do small aiways have to defend against airway infections
1. dendritic cells (produce AMPs) 2. epithelial cells (produce cytokines) 3. presence of lymphocytes and macrophages
73
how do the alveoli defend against infections
type 2 cells which produce type 1 cells
74
what kind of bacterium is Bordatella pertussis and what does it cause
- gram neg coccoide rod | - lower airway infection; whooping cough (kinkhoest)
75
what specific toxin does Bortadella pertussis secrete to kill host epithelial cells
adenylate cyclase toxin; increases host cell cAMP
76
what is the role for the S1 subunit in pertussis toxins
ADP-ribosylating (adding ADP to target molecules)
77
explain in 6 steps how diphteria toxins works
1. contains A and B part 2. B attaches to cell 3. toxin cleaved by protease 4. A contains ribosylating enzyme and binds NAD 5. it couples NAD to EF-2 (ADP ribosylated EF-2) 6. protein synthesis is ceased
78
what is S. pneumoniae for bacterium and what does it cause
- gram pos diplococcus | - abnormal liquid levels in alveoli; inflammation
79
what is special about m. tuberculosis?
it is not gram pos or neg, it is Ziehl-Neelsen stained (required for mycobacteria)

Medische Microbiologie (3 decks)

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