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
Q

what is a gram positive chain bacteria?

A

streptococcus

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26
Q

what is a gram positive cluster?

A

staphylococcus

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27
Q

gram positive bacteria cell envelope>

A
  • single cytoplasmic membrane
  • large amount of peptidoglycan
  • no endotoxin
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28
Q

gram negative bacteria cell envelope?

A
  • two membranes
  • small amount of peptidoglycan
  • outer membrane has lipopolysaccharide (endotoxin)
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29
Q

endotoxin?

A
  • 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)
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30
Q

exotoxin?

A
  • action specific; can inhibit and stimulate NS
  • unstable on exposure to heat
  • produced mostly by gram pos bacteria
  • can be converted to toxoid
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31
Q

types of gene transfer?

A

transformation, transduction, conjugation

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32
Q

transformation?

A

The genetic alteration of a bacterial cell via the uptake of a exogenous substance e.g. via plasmid

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33
Q

transduction?

A

Process by which foreign DNA is introduced into a bacteria via vector or virus e.g. via a bacteriophage (virus)

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34
Q

conjugation?

A

The transfer of genetic material between bacterial cells by direct cell-cell contact e.g. via sex pilus

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35
Q

clinical presentation of staph. aureus?

A

Pain in shoulder
- Elevated temperature
- MRI scan - disc injection & OSTEOMYELITIS (bone infection) C6
& C7
- Blood cultures show staphylococcus aureus

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36
Q

treatment for staph.aureus?

A

flucoxacillin for 3 months

37
Q

what antibiotics are MRSA resistant to?

A

B-lactams antibiotics
• Gentamicin
• Erythromycin
• Tetracycline

38
Q

eg, coagulase negative staphylococci?

A

staph. epidermis; opportunistic infection in protest limbs and catheters

39
Q

complications with strep.pyogenes?

A

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
Q

lipopolysaccharide comprises of?

A
  • 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
Q

e-coli anaerobic or aerobic?

A

facultative anaerobe

42
Q

fungi cell wall?

A

chitinous

contains mannoproteins, B1,3 and B1,6 gluten

43
Q

drug targeting final nucleus?

A

Flucytosine

44
Q

drug targeting cell wall of fungi?

A

Echinocandins - inhibit 1,3 B gluten synthase

45
Q

drug targeting plasma membrane of fungi?

A

plasma membrane contains ergosterol

Amphotericin, Terbinafine and Azoles

46
Q

treatment for TB

A

Isoniazid (INH), Rifampicin (RIF), Pyrazinamide (PZA),Ethambutol (ETH)
for two months

47
Q

primary TB?

A

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
Q

latent TB?

A

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
Q

pulmonary TB?

A

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
Q

groups of worms?

A

nematodes, trematodes and cestodes

51
Q

nematodes

A

round worms

52
Q

trematodes

A

flatworms and flukes

blood

53
Q

cestodes

A

tapeworms

54
Q

protozoa?

A

Single-celled eukaryotic organisms with a definitive nucleus

55
Q

flagellates?

A
  • protozoa

- intestinal -> giardia

56
Q

malaria?

A

Protozoan infection causes by Plasmodia spp.

57
Q

types of malaria?

A

P. falciparum (most common)
• P. ovale
• P. vivax
• P. malariae

58
Q

stages of viral replication; attachment

A

Viral and cell receptors e.g. HIV (gp120 on HIV and CD4 on T cell)

59
Q

stages of viral replication; cell entry

A

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
Q

stages of viral replication; interaction with host cell

A

Virus uses cell materials (enzymes, amino acids, nucleotides) for their
own replication
- Also needs to subvert host cell defences

61
Q

stages of viral replication; assembly

A

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
Q

stages of viral replication; release

A

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
Q

Carbapenemase producing Enterobacteriaceae

A

E.coli
• Klebsiella
• Serratia
• Enterobacter

64
Q

carbapenems?

A

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
Q

beta lactams targets?

A

These bind to bacterial cell wall and result in the inhibition of cell wall
synthesis e.g. penicillin binding proteins on bacteria surface

66
Q

Metronidazole and Rifampicin targets?

A

Interfere with nucleic acid synthesis or function

67
Q

quinolones targets?

A

Inhibit DNA gyrase (essential for bacterial DNA replication)

68
Q

Aminoglycosides, Tetracyclines, Macrolides & Chloramphenicol targets?

A

Inhibit ribosomal activity and protein synthesis

69
Q

Sulphonamides and Trimethoprim targets?

A

Inhibit folate synthesis - required for bacteria to grow since folic acid
cannot cross the bacteria cell wall

70
Q

conc. dependent killing antibiotics?

A

The ‘knockout punch’
• Key parameter is how high the concentration is above the MIC
eg, aminoglycosides and quinolones

71
Q

time dependent killing antibiotics?

A

• Sustained killing
• Key parameter is the time that serum concentrations remain above
the MIC during the dosing interval
eg, beta lactams

72
Q

c. diff antibiotics?

A

any antibiotic that begins with a C

73
Q

how bacteria can resist antibiotics

A

target site mutation, destruction of antibiotic, prevention of antibiotic entry, remove antibiotic from bacterium

74
Q

eg of intrinsic natural resistance

A

Vancomycin is not taken up by gram negative bacteria - it

cannot penetrate their outer membrane since its too large

75
Q

how can acquired resistance occur?

A

spontaneous gene mutation, horizontal gene transfer

76
Q

VRE?

A

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
Q

beta-lactamases

A

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
Q

ESBL

A

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
Q

glycopepides target?

A

cell wall

vancomycin and teicoplanin

80
Q

aminoglycosides, which bacteria do they target and eg.

A

gram negative and gram +
eg, gentamicin
inhibit protein synthesis
UTI, skin infections

81
Q

cephalosporins, which bacteria?

A

gram - and gram +

82
Q

tetracylcines, which bacteria?

A

gram + and gram -
eg, doxycline
inhibit protein synthesis

83
Q

quinolones, which bacteria?

A

gram + and gram -

inhibit DNA replication

84
Q

macrolides, which bacteria?

A

gram +
eg, erythromycin, clarithomycin
inhibit protein synthesis
STI, sinus and skin infections

85
Q

sulphonamides, which bacteria

A

gram + and gram -
inhibit folate sythesis
eg, trimethoprim

86
Q

glycopeptides, which bacteria

A

gram +
vancomycin
used in MRSA and c.diff

87
Q

what would you use for chronic bronchitis?

A

amoxicillin

88
Q

what to use in staph.pneumonia?

A

flucoxacillin

89
Q

what antibiotic for uncomplicated lower UTI?

A

trimethoprim