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Phase 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

commensal bacteria?

A

Organism which colonises the host but causes no disease in normal circumstances

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2
Q

opportunist pathogen?

A

Microbe that only causes disease if host defences are compromised

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3
Q

virulence/pathogenicity?

A

The degree to which a given organism is pathogenic/ any strategy to achieve this

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4
Q

how does gram staining work?

A
  • Apply a primary stain such as crystal violet (purple) to heat fixed bacteria
  • Add iodine which binds to crystal violet and helps fix it to the cell wall
  • Decolorise with ethanol or acetone
  • Counterstain with safranin (pink)
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5
Q

gram postive bacteria stain?

A

gram-positive bacteria, the decoloriser dehydrates the cell wall and the CV-I gets trapped in the multi-layered
peptidoglycan resulting in a purple appearance with counterstain

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6
Q

gram negative bacteria stain?

A

In gram-negative bacteria, the decoloriser interacts with the
lipids and cells lose their outer lipopolysaccharide membrane and the crystal violet-iodide (CV-I) complexes, thus they appear
pink with counterstain

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7
Q

Ziehl-Neelsen stain?

A

acid fast bacilli -> red eg, mycobacterium and non acid fast turn blue

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8
Q

what does catalase test differentiate between?

A

staphylococci and streptococci

gram pos

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9
Q

catalase test result for staphylococci?

A

catalase postive

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10
Q

catalase test result for streptococci?

A

catalase negative

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11
Q

coagulase test?

A

Coagulase is an enzyme produced by Staphylococcus. aureus that converts (soluble) fibrinogen in plasma to (insoluble) fibrin
*‘used to distinguish staph.A (coagulase positive) from other staphylococci

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12
Q

haemolysis test?

A

Haemolysis is the ability of bacteria to break down red blood cells inblood agar
• It requires the expression of haemolysin and useful in classifying streptococci

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13
Q

what type of lysis occurs in alpha haemolysis?

A

partial lysis -> partial destruction of RBCs that appears around the colony, often accompanied by a
greenish to brownish discolouration of the medium

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14
Q

eg of alpha haemolytic pathogens?

A

strep. pneuomaniea and strep.intermedius

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15
Q

what type of lysis occurs in beta haemolysis?

A

complete lysis so a clear and colourless zone appears around the colonies

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16
Q

eg of beta haemolytic pathogens?

A

strep. pyogenes also other non streptococci bacteria can be haemolytic eg, staph. aureus and listeria

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17
Q

lance field grouping?

A

A, C, G - tonsillitis and skin infections ( A - strep. pyogenes)
B - neonatal septic and meningitis
D - UTI

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18
Q

what type of lysis is gamma haemolysis?

A

no lysis occurs

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19
Q

optochin test?

A

Test to differentiate between streptococcus pneumoniae and virdins strep

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20
Q

sensitive optochin?

A

Streptococci pneumoniae - clear zone of no growth

around disc

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21
Q

resistant optochin?

A

Viridans streptococci and other alpha haemolytic

streptococci - there will be growth around the disc

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22
Q

macconkey agar?

A

Good at differentiating between lactose-
fermenting and non-lactose fermenting gram-
negative bacilli such as enterobacteria

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23
Q

lactose fermenting bacteria colour?

A

pink/red

eg, E-coli

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24
Q

non-lactose fermenting bacteria?

A

white/transparent eg, salmonella

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25
what is a gram positive chain bacteria?
streptococcus
26
what is a gram positive cluster?
staphylococcus
27
gram positive bacteria cell envelope>
- single cytoplasmic membrane - large amount of peptidoglycan - no endotoxin
28
gram negative bacteria cell envelope?
- two membranes - small amount of peptidoglycan - outer membrane has lipopolysaccharide (endotoxin)
29
endotoxin?
- Action is non-specific • Stable on exposure to heat • Produced by mostly gram NEGATIVE bacteria • Cannot be converted to a toxoid (a non-active toxin)
30
exotoxin?
- action specific; can inhibit and stimulate NS - unstable on exposure to heat - produced mostly by gram pos bacteria - can be converted to toxoid
31
types of gene transfer?
transformation, transduction, conjugation
32
transformation?
The genetic alteration of a bacterial cell via the uptake of a exogenous substance e.g. via plasmid
33
transduction?
Process by which foreign DNA is introduced into a bacteria via vector or virus e.g. via a bacteriophage (virus)
34
conjugation?
The transfer of genetic material between bacterial cells by direct cell-cell contact e.g. via sex pilus
35
clinical presentation of staph. aureus?
Pain in shoulder - Elevated temperature - MRI scan - disc injection & OSTEOMYELITIS (bone infection) C6 & C7 - Blood cultures show staphylococcus aureus
36
treatment for staph.aureus?
flucoxacillin for 3 months
37
what antibiotics are MRSA resistant to?
B-lactams antibiotics • Gentamicin • Erythromycin • Tetracycline
38
eg, coagulase negative staphylococci?
staph. epidermis; opportunistic infection in protest limbs and catheters
39
complications with strep.pyogenes?
Some strains produce erythrogenic toxin which is responsible for scarlet fever, this toxin is a super-antigen meaning it gives rise to an exaggerated immunological response and increased circulating cytokine levels
40
lipopolysaccharide comprises of?
- lipid A - the toxic portion of LPS that is anchored in the outer leaflet of the outer membrane - core (R) antigen - short chain of sugars - Somatic (O) antigen - highly antigenic repeating chain of oligosaccharides
41
e-coli anaerobic or aerobic?
facultative anaerobe
42
fungi cell wall?
chitinous | contains mannoproteins, B1,3 and B1,6 gluten
43
drug targeting final nucleus?
Flucytosine
44
drug targeting cell wall of fungi?
Echinocandins - inhibit 1,3 B gluten synthase
45
drug targeting plasma membrane of fungi?
plasma membrane contains ergosterol | Amphotericin, Terbinafine and Azoles
46
treatment for TB
Isoniazid (INH), Rifampicin (RIF), Pyrazinamide (PZA),Ethambutol (ETH) for two months
47
primary TB?
Bacilli settle in apex (top part near shoulders) and granuloma forms • Bacilli taken in lymphatics to hilar lymph nodes • In apex of lungs there is more air and less blood supply thus fewer defending white cells to fight off infection • Granuloma + Lymphatics + Lymph nodes = Primary complex
48
latent TB?
Cell mediated immune (CMI) response from T-cells • Primary infection is contained but CMI persists • No clinical disease (normal chest x-ray) • Detectable CMI to TB on tuberculin skin test of IGRA
49
pulmonary TB?
Could occur immediately following primary disease (post-primary) or after latent reactivation • Cell mediated immune (CMI) response from T-cells • Necrosis in lesion • Caseous material coughed up leaving cavity • TB may spread in lung causing other lesions • CMI and caseation in lesion results in cavity
50
groups of worms?
nematodes, trematodes and cestodes
51
nematodes
round worms
52
trematodes
flatworms and flukes | *blood*
53
cestodes
tapeworms
54
protozoa?
Single-celled eukaryotic organisms with a definitive nucleus
55
flagellates?
- protozoa | - intestinal -> giardia
56
malaria?
Protozoan infection causes by Plasmodia spp.
57
types of malaria?
P. falciparum (most common) • P. ovale • P. vivax • P. malariae
58
stages of viral replication; attachment
Viral and cell receptors e.g. HIV (gp120 on HIV and CD4 on T cell)
59
stages of viral replication; cell entry
Only the viral ‘core’ which carries the nucleic acid and some associated proteins acting as enzymes for replication and negation of intracellular host defence factors are freed into the host cell cytoplasm - Outer protein coat does not enter
60
stages of viral replication; interaction with host cell
Virus uses cell materials (enzymes, amino acids, nucleotides) for their own replication - Also needs to subvert host cell defences
61
stages of viral replication; assembly
Can occur in nucleus e.g. herpesvirus - Can occur in cytoplasm e.g. polio virus - Can occur in cell membrane e.g. influenza virus
62
stages of viral replication; release
By bursting open (lysis) of cell e.g. rhinovirus - By ‘leaking’ (exocytosis) from the cell overtime e.g. HIV & influenza virus (2-3 days from upper respiratory tract) - Only a few virus particles will enter the host but millions will exit due to replication
63
Carbapenemase producing Enterobacteriaceae
E.coli • Klebsiella • Serratia • Enterobacter
64
carbapenems?
These are the broadest spectrum beta-lactam antibiotics available Carbapenemases HYDROLYSE carbapenems but also other beta- lactams effectively conferring resistance to the entire class of antibiotic
65
beta lactams targets?
These bind to bacterial cell wall and result in the inhibition of cell wall synthesis e.g. penicillin binding proteins on bacteria surface
66
Metronidazole and Rifampicin targets?
Interfere with nucleic acid synthesis or function
67
quinolones targets?
Inhibit DNA gyrase (essential for bacterial DNA replication)
68
Aminoglycosides, Tetracyclines, Macrolides & Chloramphenicol targets?
Inhibit ribosomal activity and protein synthesis
69
Sulphonamides and Trimethoprim targets?
Inhibit folate synthesis - required for bacteria to grow since folic acid cannot cross the bacteria cell wall
70
conc. dependent killing antibiotics?
The ‘knockout punch’ • Key parameter is how high the concentration is above the MIC eg, aminoglycosides and quinolones
71
time dependent killing antibiotics?
• Sustained killing • Key parameter is the time that serum concentrations remain above the MIC during the dosing interval eg, beta lactams
72
c. diff antibiotics?
any antibiotic that begins with a C
73
how bacteria can resist antibiotics
target site mutation, destruction of antibiotic, prevention of antibiotic entry, remove antibiotic from bacterium
74
eg of intrinsic natural resistance
Vancomycin is not taken up by gram negative bacteria - it | cannot penetrate their outer membrane since its too large
75
how can acquired resistance occur?
spontaneous gene mutation, horizontal gene transfer
76
VRE?
Vancomycin-resistant enterococci • Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding • Promoted by cephalosporin use *gram pos*
77
beta-lactamases
Enzymes that hydrolyse penicillins • TEM-1 in E.coli, H. influenzae and N. gonorrhoea • SHV-1 in K. pneumoniae • But such strain typically remain sensitive to beta-lactamase inhibitors
78
ESBL
Extended spectrum B-lactamases • Have further mutation at active site means it can destroy more than just penicillin or amoxycillin • Typically they can also inactivate: - Cephalosporins e.g. cefuroxime, cefalexin, cefotaxime - Combination antibiotics such as co-amoxiclav & tazocin
79
glycopepides target?
cell wall | vancomycin and teicoplanin
80
aminoglycosides, which bacteria do they target and eg.
gram negative and gram + eg, gentamicin inhibit protein synthesis UTI, skin infections
81
cephalosporins, which bacteria?
gram - and gram +
82
tetracylcines, which bacteria?
gram + and gram - eg, doxycline inhibit protein synthesis
83
quinolones, which bacteria?
gram + and gram - | inhibit DNA replication
84
macrolides, which bacteria?
gram + eg, erythromycin, clarithomycin inhibit protein synthesis STI, sinus and skin infections
85
sulphonamides, which bacteria
gram + and gram - inhibit folate sythesis eg, trimethoprim
86
glycopeptides, which bacteria
gram + vancomycin used in MRSA and c.diff
87
what would you use for chronic bronchitis?
amoxicillin
88
what to use in staph.pneumonia?
flucoxacillin
89
what antibiotic for uncomplicated lower UTI?
trimethoprim

Phase 2a (12 decks)

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