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U4 prac exam > microbiology lab > Flashcards

microbiology lab Flashcards

1
Q

what bacteria is G+ spore former

A

Bacillus or Clostridium

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2
Q

how are bacteria classified?

A
  1. phonetic (phenotyoe)

2. phylogenetic (genotype)

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3
Q

what’s included in the phenetic classification

A
  1. gram reaction and morphology
  2. carbon sources, energy sources
  3. electron acceptors (e.g. aerobic/anaerobic)
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4
Q

what’s included in the phylogenetic classification

A
  1. ribosomal RNA sequence

2. other DNA, RNA, protein sequence

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5
Q

describe Vibrio.

A 
G morphology:G- CURVED rod 
motility: motile 
catalase: +
oxidase: +
O-F:A facultative anaerobe
others: curved rod
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6
Q

describe clostridium

A 
G morphology:G+ rod 
motility: -
catalase: -
oxidase: -
O-F:Fermentation (anaerobe)
others: drumstick endospores
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7
Q

describe arthrobacter

A 
G morphology:G+ coccus and rod 
motility: non-motile 
catalase: +
oxidase: -
O-F: O (obligate aerobes )
others: pleomorphism: can alter their shape/size in response to environmental conditions
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8
Q

describe micrococcus

A 
G morphology:G+ coccus in tetrades
motility: -
catalase: +
oxidase: +
O-F:O(aerobe)
others: tetrades
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9
Q

describe Corynebacterium

A 
G morphology:G+ rod 
motility: -
catalase: +
oxidase: -
O-F:O(aerobe)
others: L&V forms
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10
Q

describe Enterobacter

A 
G morphology:G+ coccus motility: +
catalase: +
oxidase: -
O-F:Fermentation (anaerobe)
others: N/A
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11
Q

describe Neisseria

A 
G morphology:G- diplococci
motility: -
catalase: +
oxidase: +
O-F: O (aerobe)
others: diplococci
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12
Q

describe streptococcus

A 
G morphology:G+ cocci in chains 
motility: -
catalase: -
oxidase: -
O-F:facultative anaerobic
others: chains
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13
Q

describe staphylococcus

A 
G morphology:G+ cocci in clumps
motility: -
catalase: +
oxidase: -
O-F:Facultative anaerobic
others: clumps maybe grape like
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14
Q

describe Bacillus

A 
G morphology:G+ rod 
motility: +
catalase: +
oxidase: -
O-F:facultative anaerobic
others: can form endospores
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15
Q

describe Proteus

A 
G morphology:G- rod 
motility: +
catalase: +
oxidase: -
O-F:Fermentation (anaerobe)
others: N/A
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16
Q

describe Pseudomonas

A 
G morphology:G- rod 
motility: +
catalase: +
oxidase: +
O-F: O (aerobe)
others: N/A
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17
Q

Briefly define the term “fermentation of carbohydrate”.

A

The anaerobic metabolic process utilised by some bacterium to fermentate glucose to produce energy, acid is produced as a waste product

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18
Q

Briefly define the term “oxidation of carbohydrate”.

A

The aerobic respiration utilise by some bacterium to produce energy, little acid is produce

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19
Q

Should we be cautious about interpreting catalase test results on growth taken from media containing blood? Please explain

A

Blood agar contains catalase, therefore it will show positive on catalase test. When taking the organism, any contamination from the blood agar will show as a false positive

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20
Q

What is the physiological significance (to the bacterium) of catalase production?

A

The organisms living under the aerobic condition will produce (H2O2) peroxide as the metabolite. The ability of producing catalase can break down the toxic peroxide into water and oxygen, protects the organism from accumulation of toxic waste

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21
Q

What does the oxidase test detect?

A

It detects the microrganisms that have cytochrome c oxidase. Cytochrome c oxidase is an enzyme used in the electron transport chain and able to reduce oxygen

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22
Q

What do you understand by the term “the electron transport chain”?

A

The proteins embedded in the mitochondria membrane takes the electron from the electron carriers (NADH, FADH2), the energy produced by this process is used for pumping of H ions into the intermembrane space, then produce ATP by pumping H ions into the mitochondrial matrix through ATP synthase

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23
Q

Define bacterial strains and species

A
  • species is used for taxonomy, it shows genetic similarity among species, a strain is a subset of species that is only show small variance

strains “a population of organisms that descend from a single organism or pure culture isolate”

species “ species of higher organisms are groups of interbreeding or potentially interbreeding natural populations that reproductively isolated. archael and bacterial species are often defined as collections of strains that have many stable properities in common and differ significantly from other strains

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24
Q

What is the function of the enzyme catalase in the aerobic cell?

A

catalase converts hydrogen peroxide into water and oxygen

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25
Q

How do catalase negative aerobic organisms tolerate hydrogen peroxide?

A

the enzyme Superoxide dismutase enzyme (SOD) is responsible for degradation of toxic superoxides (O2−) in catalase-negative aerobic organisms

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26
Q

Two precautions need to be observed when testing an organism for catalase:

           (i)      it is best to take the test culture from a solid medium rather than a broth;

            (ii)     the medium is free from blood why?
A

i> there is more bacterial can be tested on solid medium, the bacterial is much more diluted in liquid broth which may give false negative.
ii> the blood cells contain catalase, small of amount of carry over contamination could give false positive result

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27
Q

why use wooden stick in oxidase test

A

“Nickel, steel, and other wire loops may give false-positive results, so it is important to use only platinum or inert transfer loops, such as sterile wood sticks commonly used in teaching laboratories “

“false positive due to oxidation because iron contained in the loops and of the reagent

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28
Q

what is infection control, individually

A

measures taught to childer and adults to stop spread of an ailment that is transmissible:

  • coughing/Sneezing
  • physical contact
  • toilet hygiene
  • hand washing
  • segregation
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29
Q

what is infection control in community setting?

A 
neasures undertaken to limit public exposure to infectious agents:
1. safe water supply
2 effective sewerage removal
3. vaccination 
4. outbreak investigation
5. quarantine
6. public health awareness/education
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30
Q

what is infection control in hospital setting

A

measures taken to prevent acquisition of nosocomial infections

  1. identification
  2. isolation
  3. hand hygiene
  4. barrier nursing
  5. education
  6. surveillance
  7. review
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31
Q

what does nosomial mean

A

hospital acquired

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32
Q

what does moments for hand hygiene mean

A

is when there is perceived or actual risk of pathogen transmission from 1 surface to another via hand

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33
Q

what are the 5 moments of hand hygiene

A
  1. before touching a patient
  2. before a procedure
  3. after a procedure or body fluid exposure risk
  4. after touching a patient
  5. after touching a patient’s surroundings
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34
Q

what is the highest priority area to reduce the risk of healthcare-associated infection?

A

improved healthcare worker Hand hygiene

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35
Q

how many percent of patients worldwide develop a nosocomial infection

A

5 to 10%

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36
Q

what are the name of multi-drug reistant organisms

A 
MRSA
VRE
Acinetobacter baumannii
NDM-1 strains
Clostrium difficile
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37
Q

what are the common sources of infection in hospital

A
  1. surgical wound (most common)
  2. catheter associated urinary tract infections, nasocomial pneumonia, intravascular device-associated blood infections
  3. airborne respiratory pathogens such as TB, Legionella spp. are possible
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38
Q

what are the factors that predispose to hospital infections

A
  1. drug resistant microorganism more likely to exist in hospitals under antibiotic use pressure
  2. patients with lowered resistance due to age, immobility, underlying diseases, surgical/trauma wounds
  3. medical treatment e.g immunosuppresive drugs
  4. diagonostic and/ot therapeutic procedures involve skin and mucous membrane penetrance
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39
Q

how did EBOLA transmitted

A

via contact with infected human body fluids

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40
Q

what is the key driver of EBOLA outbreak

A

nosocomial transmission

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41
Q

what r the roles of microbiology lab

A
  1. accute + rapid identification of causative organism
  2. identity any antimicrobial resistance
  3. detect changes in susceptibility patterns.
  4. identification beyond genus level is critical so that outbreaks are not missed
  5. molecular techniques to link cause and results or for epidemiological tracing/fingerprinting
  6. storage of unusual organisms and sometimes sera for look back programmes
  7. selection pressure by continued or inappropriate use of antibiotics can lead to creation of multi-resistant flora in a particular establishment
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42
Q

what is current infection control focus on

A
  1. emphasis on breaking the cycle of transmission from patient to patient via HCW’s hands. education on hand washing
  2. education all HCW.
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43
Q

Bali bug

A

majority of the patient has multi-resistant organisms from their wound within days of adminsion

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44
Q

what arethe problems for microbiology

A
  1. variety of organisms
  2. number of antibiotic involved
  3. number of patients involved
  4. prevent potential spread to other patient
  5. important to ensure patients treated whilst attempting to prevent nosocomial infections developing
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45
Q

why did other hospital have similar spectrum of organisms

A
  1. transport

2. swimming pool

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46
Q

what can you do in burns unit?

A

environmental cleaning

  1. identification of MRO patient
  2. cleaning of bay twice
  3. environmental broths sampled from bay
  4. Broths screened for MROs
  5. only after negative result is a new patient allowed to use that bay
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47
Q

what are the 3 infection control steps for C.difficile outbreak

A
  1. rapid diagnosis
  2. hand washing - failed due to spores EtOH res
  3. isolation +protective clothing + gloves
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48
Q

what r the therapy choice for C.difficile

A

VanC

MTZ

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49
Q

what are the different treatment s

A

VanC->kills C.D only, good Lacto+Bacteroides sp. not affected
MTZ->kills helpful bacteria allowing spores to germinate

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50
Q

in environment, how did C.difficile killed

A

by Cl2 or I2

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51
Q

what is spore resist to

A

EtOH reistant

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52
Q

how to overcome C.difficile outbreak overcome

A

by combination of antibiotic choice and environmental hygiene

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53
Q

what are the mode of action of antibiotics

A
  1. inhibition of cell wall synthesis
  2. alteration of cell membranes
  3. inhibition of protein synthesis
  4. inhibition of nucleic acid synthesis
  5. inhibition of meatbolic activity (folic acid biosynthesis)
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54
Q

what are the 3 antimicrobial testing standards

A
  1. antibody sysceptibility testing by CDS (disk diffusion test) method
  2. CLSI: clinical and laboratory standards institute
  3. eucast: european committe on antimicrobial susceptibility testing
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55
Q

what is intrinsic (natural) resistance

A

bacterial maybe inherently resistant to an antibiotic, without any modification to its genome

56
Q

give some example of intrinsic resistance

A
  1. outer membrane acts as a permeability barrier against an antibiotics (i.e. cant get through)
  2. organism lacks a transport system for the antibiotic (i.e. cant get in)
  3. organism lacks the specific target site of antibiotics (i.e can’t attach)
57
Q

what is acquired resistance

A
  1. where bacteria previously suscepitible to an antibiotic develop resistance to that antibiotics
  2. results from changes to the bacterial genome
58
Q

what are the driven for changing genome in acquired resistance

A
  1. mutation and selection (vertical evolution

2. exchange of genes (horizontal evolution)

59
Q

what antibiotics target cell wall synthesis?

A
  1. D-cycloserine
  2. Vancomycin
  3. Bacitracin
  4. Penicillins
  5. Cephalosporins
  6. Cephamycins
60
Q

what antibiotic target cell wall integrity

A

B-lactamases

61
Q

what antibiotics target replication?

A

DNA synethsis
- Metronidazole
DNA Gyrase
-Quinolones

62
Q

what antibiotics target transcription

A

Rifampicin target RNA polymerase

63
Q

what antibiotics target protein synthesis that involved in protein synthesis (50S inhibition )

A
  1. Erythromycin
  2. Choramphenicol
  3. Cindamycin
  4. Lincomycin
64
Q

what antibiotics target protein synthesis that involved in protein synthesis (30S inhibition )

A
  1. Tetracyclines
  2. Streptomycin
  3. Spectinomycin
  4. Kanamycin
65
Q

what antibiotics target cytoplasmic phospholipid membranes

A

polymyxins

66
Q

what antibiotic target G+ bacteria

A

Vancomycin

67
Q

what antibiotic target G-bacteria

A

polymyxin

68
Q

what antibiotics target Mycobacteria

A

Isoniazid

69
Q

what antibitotics target G+ &G- bacteria and Chlamydiae

A

Penicillins

70
Q

what antibitotics target G+ &G- bacteria and Chlamydiae and Rickettsiae

A

Tetracyclines

71
Q

what antibiotics target mycobacteria and G- bactiria

A

streptomycin and Aminoglycosides

72
Q

what antibiotics target G- and G+ bacteria

A

sulfonamides
cephalosporins
quinolones
carbapenems

73
Q

what is vertical evolution

A
  1. Darwinian-driven by natural selection
  2. spontaneous mutation in chromosome
  3. selective environment of the antibiotics selects out mutant strain, WT killed
74
Q

what is horizontal evolution

A
  1. Acquisition of resistance genes from another strains or species
    2, often follows the development of a resistance gene through process of mutation and selection
75
Q

what are the process for horizontal evolution

A
  1. conjugation
  2. transduction
  3. transformation
76
Q

what are the spread of resistance

A
  1. chromosome resistance (pt mutation), but extenuated when gene transfer happen
  2. common for DNA to be transferred as plasmids b/t mating bacteria
  3. bacteria usually develop their genes for drug resistance on extracellular DNA aka plasmids
77
Q

steps for evolution of Multi-resistance

A
  1. resistance genes cluster on chromosomes or more commonly R-plasmids
  2. Plasmids possess DNA elements that facilitate the capture of resistance genes and promoter sequences for their efficient expression
  3. this results in linkage of resistance genes to multiple antibiotics on 1 plasmids
  4. some acquire multiple plasmids
78
Q

what the bacterial resistance mechanism

A
  1. modification of outer membrane permeability. e.g. Ciprofloxacin resistance in Staph aureus
  2. active efflux (pumpting antibiotic out of cell)
    3.mutation in antibiotic target. e.g. Penicillin binding proteins
    Pen R strep pneumoniae (PRSP)
    Methiicillin resistance Staph aureus (MRSA)
  3. increased production of enzyme e.g. B-lactamases Pen R in S.aureus
  4. muation in existing enzymes e.g. ESBL’s in GNB
  5. Acquisition of new resistance enzymes e.g. amino glycoside resistance; vancomycin resistance in Enterococci
79
Q

what are the example of superbugs

A
  1. MRSA: methicillin resistant Staph aureus
  2. VRE: Vancomycin resistant enterococcus
  3. ESBL: extended spectrum B-lactamase
  4. MBL: Metallo- B- lactamase in G-bacilli
  5. CRE:Carbapenem resistant enterobacteriacae
  6. MRAB: multi-resistant Acinetobactor baumanii
80
Q

describe MRSA

A
  1. MRSA isolates produce an extra penicillin binding protein (PBP2a). PBP2a fails to bind most B-lactams (penicillins)
  2. this is encoded by an acquired chromosomal gene (mecA)
  3. MRSA can be multi drug resistant or non multi-resistant
  4. incidence of # MRSA increasing
81
Q

describe Vancomycin reistant enterococci (VRE)

A
  1. increasingly prevalent
  2. promoted by
    - 3rd generation cephalosporin use
    - vancomycin use in humans
    - animal supplement use
  3. VRE isolates multi-reistant and virtually untreatble
  4. significant screening now occurs
82
Q

who is at risk for VRE

A
  1. immunosuppressed, transplant, dialysis, prosthetic device patients most at risk
  2. risk of transmission to other species- MRSA
  3. risk of spread to other patients greg- especially in ICU, BU
  4. policies are instituted to curtail use of antibiotics that select for VRE
83
Q

describe entended spectrum B-lactamases (ESBL)

A
  1. ESBLs are mutated enzymes which can breakdown 3rd and 4th generations cephalosporins, such as cefataxine and ceftazidime and cefepime
  2. present in G- bacilli e.g. Klebsiella, E.coli, Enterobacter etc
  3. cross- resistance to gentamicin, trimethoprim and ciprofloxacin
  4. as resistance is plasmid mediated there is a great risk of spread in hospital setting
84
Q

describe multi-reistant Acinetobacter baumanii

A
  1. hospital strain often multi-resistant;
  2. especially prevalent in burns units, ICUetc where antibiotic use at its greatest
  3. Bali disaster- patients brought back new strains of this organism
  4. has necessitated even more stringent ward cleaning, environmental practices etc
85
Q

why does antibiotic resistance occur

A
  1. capacity of bacteria to mutate and to transfer this genetic information to other strains/species
  2. excessive and/or inappropriate antibiotic use principal cause of emergence of resistance e.g. overuse of 3rd generation cephalosporins responsible for emergence of ESBL, VRE
  3. increasing # of severely ill and Immunocompromised patients surviving longer in hospital using ventilation, catheterisation etc
  4. medical tourism
  5. Veterinary FEED
  6. as resistnce more prevalently, increasing reliance on potent broad-spectrum drugs for treatment and prophylaxis- thereby maintaining the selection pressure
  7. over-interpretation of bacterial colonisation
  8. cross colonisation from patient to patient and from staff to patient
86
Q

what are the impact of antibiotic resistance

A
  1. increased morbidity/ mortality
  2. reduce therapy options
  3. increase cost of healthcare
    - prolonged length of stay due to nosocomial infections
    - treatment costs
    - infection control measures
  4. greater risk of empirical treatment failure
  5. Litigation
87
Q

what are the control measures for drug resistance

A
  1. surveillance
  2. infection control
  3. control of antibiotic use
    4 Government / media pressure
    - name and shame
88
Q

what can you do for surveillance

A
  1. surveillance
    - institution level
    - antimicrobial stewardship
    - state level (MRO funding)
    - national level (Australian group on antimicrobial resistance)
    - global level (sentry)
89
Q

what can you do for infection control

A
  1. infection control
    - screening patients and staff for resistant organisms
    - hand washing campaigns
    - isolation of infected colonised patients to prevent spread
    - single rooms/better designed wards
    - double cleaning esp in ICU, burns
90
Q

what can you do for control of antibiotic use

A
  1. control of antibiotic use
    - responsible reporting of susceptibilities
    - authorisation for using of high level AB
    - avoid inappropriate prescribing of AB
91
Q

what are the future for AB resistance

A
  1. greater reliance on DNA technology to identify resistance factors
  2. use of vaccination to reduce incidence of disease
  3. bigger and better antibiotics
  4. rapid ID testing e.g. Maldi-TOF
  5. improved education-prevention rather than cure
92
Q

why set a restrict time limit for observe colour change in oxidase test

A

within 10 seconds. reason: the paper can be oxidised by air as well as bacterial enzymes.too long will give false positive results

93
Q

what is alpha heamolysis

A

the reduction of haemoglobin to methaemoglobin in the medium surrounding the colony. This causes a greenish discolouration of the medium

94
Q

what is beta haemolysis

A

the lysis of red blood cells, resulting in a clear zonesurrounding the colony

95
Q

what is gamma haemolysis

A

Gamma (δ) haemolysis indicates nohaemolysis. No destruction of the red blood cells occurs and there is no change in the medium

96
Q

what colour is acid fast organism

A

acid fast red

other organisms are blue

97
Q

result for spore stain

A

bacterial bodies stain red

spores stain green

98
Q

result for O-F test

A

oxidation:yellow or turning yellow on top 1/2 to 1/4
fermentation: yellow or turning yellow throughout medium
no action on carbohydrate: blue or turning blue at top

99
Q

normal flora on skin

A
  1. coagulase-negative staphylococci
  2. Diphtheroids
  3. Staphlococcus spp.
100
Q

normal flora throat

A
  1. Viridans streptococci
  2. coagulase negative staphlococci
  3. veillonella
101
Q

normal flora nose

A
  1. coagulase negative staph
  2. viridans streptococci
  3. staph.aureus
102
Q

normal flora of FIT

A
  1. lactobacillus
  2. bacteroids
  3. clostridium
103
Q

Why is the flora of the nose relatively homogeneous and that of the throat so diverse?

A

the nose is relatively homogenous with S.aureus, because S.epidermidis and Corynebacterium have negative symbiosis relationship with S.aureus.

the throat have ideal habitat for microbes. real supply of water and nutrients, neutral pH and moderate temperature

104
Q

What factors determine the indigenous flora of a particular body site?

A

Nutritional and environmental factors:

  • nutritients avalability at a particular site and types of nutrients.
    e. g. moist area dominated by diphtheroids, Propionibacterium spp. colonise in the duct of the hair follicle due to their ability to break down the skin lipids into fatty acids.
  • pH at the site

the colonisation of indigenous flora also dependent on the the ability of the microorganism to attatch on a particular site, that is be able to resist on antibacterial effect of molecules such as lysozyme, bile.

105
Q

What role does the normal flora at a particular body site play in protecting the host from infection?

A
  • the development of immunologic competence
  • the normal flora occupy the space such that the exogenous pathogens will be blocked and prevent colonisation, and they compete nutrients with pathogens, and creating a hostile environment for other microorganism.
106
Q

Why are more organisms, both in number and type, usually found on the finger print on the culture plate after washing with soap than before?

A

the transient and oil in unwashed. soap move the transient, and oil. washing doesnt kill what he resident microbes

107
Q

What is a carrier state?

A

it is a condition such that the host is capable of transmitting the infection without showing any symptoms after pathogenic organism invasion.

108
Q

What is the difference between carrier states and reservoirs of infection?

A

reservoirs of infectious: “places where the pathogen can grow and accumulate” such that human, animals and non living reservoirs. carrier state belongs under the reservoir of infection. human reservoir can be sick (show symptoms) or carrier (no symptoms)

109
Q

define symbiosis

A

living together of organisms

110
Q

commensalism

A

1 benefits, 1 not affected

111
Q

mutualism

A

both benefit

112
Q

parasitism

A

1 benefit 1 harmed

113
Q

what does normal flora do

A
  1. compete with pathogens for attachment sites, nutrients
  2. produce anti-microbial compounds
  3. aid digestion
  4. supply essential growth requirements
  5. stimulate immune system, aid resistance to infection
114
Q

Micrococcus luteus belongs to normal flora on skin where as Serratia marcescens is pathogenic microbe. The salty, dry and acidic environment promote the growth of Micrococcus luteus to grow on skin over time and compete the attachment site with Serratia marcescens. Overtime, the large amount of Micrococcus luteus inhibit the pathogenic species Serratia marcescens. The skin act as a very useful barrier and have distinctive environment which create a particular niche for the normal flora, which decrease the change of pathogenic species invasion

A

t

115
Q

M.luteus is normal flora on skin, however it could get to the mucous membrane of the eye. The lysosome contain the enzyme that destroy the peptidoglycan layer of bacteria. The majority of the G+ cell wall is made of PG, once disrupted by lysozyme, the bacteria will be very sensitive to environment which cause the bacteria to die. This is show in the M.luteus plate with clearing zone.

S.marscens is G- bacteria, it has thin layer of PG and outer membrane wall which act as a protective layer, the lysozyme cannot effectively act on PG due to the outer membrane layer. Therefor no clearing zone. This could explain most of the eye infection is caused by G- bacteria because lysozyme cannot kill them.

A

t

116
Q

lysosome is effective against G+

A

t

117
Q

Describe the mechanisms whereby bacteria evade phagocytosis.

A

“RESISTING PHAGOCYTOSIS:

  • slippery mucoid capsule that prevents the phagocyte from effectively contacting the bacterium. e.g. Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae
  • producing specialized surface proteins. These proteins interfere with adherence between a phagocytic cell and the bacterium like the capsules.e.g. the M protein on S.pyogenes.

SURVIVAL INSIDE THE PHAGOCYTIC CELLS

escape from the phagosome before it merge with lysosome as seen with Listeria monocytogenes, Shigella and Rickettsia

  • use actin-based motility to move with mammalian host cells and spread betwen them. Upon lysing the phagosome, they gain access to the cytoplasm. Each bacterium then recruits to its surface host cell actin and other cytoskeletal proteins and activates the assembly of an actin tail. the actin tails propel the bacteria through the cytoplasm of the infected cell to its surface where they push out against the plasma membrane and form protrusions.the protrusions are engulfed by adjacent cells, and the bacteria once again eneter phagosomes and escape into the cytoplasm. In this way, the infection spreads to adjacent cells. the lysosomes never have a chance to merge with phagosomes.
  • resist the toxic products released into phagolysosome after fusion occurs. e.g. bacterium that resistant to the lysosomal enzyme is Mycobacterium tuberculosis, because of its waxy external layer.
118
Q

Give examples of organisms that employ each mechanism to prevent recognition, ingestion and destruction by phagocytic cells.

A

Bacterial pathogens use other mechanisms to resist phagocytosis. e.g. Staphylococcus produces leukocidins that destroy phagocytes before phagocytosis can occur. S. pyogenes releases a protease that cleaves the C5a complement factor and thus inhibits complement’s ability to attract phagocytes to the infected area.”

119
Q
  1. What virulence mechanisms are possessed by some micro-organisms that allow them to evade phagocytosis?
A

E.g. the Staphylococcus aureus have coagulase which clotes the fibrinogen in plasma, the clots mark the antigen present on the membrane surface, thus protect the pathogen from phagocytosis, and prevent isolation which can detect by other host defence mechanisms.

Another example is that the Salmonella enterica have porins, “which inhibit leukocyte phagocytosis by activating adenylate cyclase system.

“RESISTING PHAGOCYTOSIS:

  • slippery mucoid capsule that prevents the phagocyte from effectively contacting the bacterium. e.g. Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae
  • producing specialized surface proteins. These proteins interfere with adherence between a phagocytic cell and the bacterium like the capsules.e.g. the M protein on S.pyogenes.

SURVIVAL INSIDE THE PHAGOCYTIC CELLS

escape from the phagosome before it merge with lysosome as seen with Listeria monocytogenes, Shigella and Rickettsia

  • use actin-based motility to move with mammalian host cells and spread betwen them. Upon lysing the phagosome, they gain access to the cytoplasm. Each bacterium then recruits to its surface host cell actin and other cytoskeletal proteins and activates the assembly of an actin tail. the actin tails propel the bacteria through the cytoplasm of the infected cell to its surface where they push out against the plasma membrane and form protrusions.the protrusions are engulfed by adjacent cells, and the bacteria once again eneter phagosomes and escape into the cytoplasm. In this way, the infection spreads to adjacent cells. the lysosomes never have a chance to merge with phagosomes.
  • resist the toxic products released into phagolysosome after fusion occurs. e.g. bacterium that resistant to the lysosomal enzyme is Mycobacterium tuberculosis, because of its waxy external layer.
  • producing specialized surface proteins. These proteins interfere with adherence between a phagocytic cell and the bacterium like the capsules.e.g. the M protein on S.pyogenes.” - microbiology textbook
120
Q

coagulase test medium

A

for coagulase, it has pathogenicity to allow the break of tissue and live on it.

there are 3 types of medium of the culture can be sued for tesing coagulase,

  • for solid culture, it indicate the surface present coagulase
  • liquid culture, the cell excrete the coagulase into the medium
  • staphorex, coagulase on surface and Protein A.
121
Q

what is unique to Klebsiell pneumonia

A

positive on Voges proskauer test

122
Q

what is unique to e.coli

A

citrate utilization shows -

123
Q

what is unique to proteus mirabilis

A

methyl red test: weakly positive

positive to urease prodction

124
Q

what is unique to salmonella typhimurium

A

methy red weakly positive, negative for urease production

125
Q
  1. What tests distinguish:

a) Escherichia from Klebsiella?

A

indole + to ecoli, - for citrate and urease

126
Q

Salmonella from Proteus?

A

urease present in prpteus, absent in salm

127
Q

Explain why changes in rRNA can be used to distinguish between distantly related organisms.

A

rRNA does not evolve very fast, it retain the function over time, whole genera have similar rRNA. The PCR reaction allow to test hypervariable reigion within the rRNA.

128
Q

Why would examination of rRNA of closely related organisms be useless?

A

since rRNA does not evolve quicky, the rRNA of closely related organisms will be useless.,

129
Q

penicillin

A 
primary effect: Cidal
mechanism of action:
-Inhibit transpeptidation enzymes involved in cross-linking the polysaccharide chains of the bacterial cell wall peptidoglycan.
-Activate cell wall lytic enzyme
specturm narrow (G+)
130
Q

Vancomycin (30µg) VA 30

A

primary effect:CIDAL
mechanism:-prevent transpeptidation of peptidoglycan subunits by bind to D-Ala-D-Ala aino acids at the end of peptide cross-bridges. Thus it has a different binding site than that of the penicillins.
narrow (G+)

131
Q

rifampicin

A

primary effect cidal
mechanism -inhibit bacterial DNA dependent RNA polymerase.
spectrum: Mycobacterium infections and some G- such as Neisseria meningitides and Haemophilus.

132
Q

What is the relationship between susceptibility to the disc content and the actual therapeutic level required?

A

“conditions may be strandardised so that susceptibility to the antibiotic can be determined by comparing the diameter of the zone of clearing with standard tables of velues. From this , a suitable concentration for therapeutic use can be detrmined.”

133
Q

Discuss the concept of ‘high and low level’ resistance of micro-organisms to antibiotics with your demonstrators.

A

STAMP OF ANTIBIOTICS METHOD

there are some colony grows within the centre, where the antibiotic is most concentrated, creating a zone of inhibition.

This is due to mutation that originated naturally in nature.

the colony present at the centre, and have a bigger colony. the strain shows high degree of resistance of the strain.

whereas smaller colony in the zone of inhibition shows lower degree of resistance.

STREPTOMYCIN PLATE

the streptomycin binds to rRNA, inhibit the ribosomal RNA to function.

resistance can be developed by 3 mechanisms:

  1. develop of different ribosomal structure, THIS IS AN EFFECTIVE STRATEGY. this is happen to the high resistance strains present in the centre and have bigger colonies. THE MUTATION IS DUE TO CHROMOSOMAL MUTATION.
  2. produce digestive enzyme which break the bond between streptomycin and the rRNA. THIS MUTATION IS FROM THE PLASMID, WHICH CAN BE FORMED BY RECOMBINATION FROM OTHER MUTATED STRAINS.” Through hydrolysis, the lactamase enzyme breaks the β-lactam ring open, deactivating the molecule’s antibacterial properties.”
  3. changing the receptor that binds to the antibiotic, this prevent the entry of antibiotic into the bacterial cells. THIS IS LESS EFFECTIVE COMPARE TO THE CHANGE IN CHROMOSOMAL STRUCTURE.. this explains the smaller colony in the zone of inhibition, they produce lower level of degree of resistance.
134
Q

Is there any relationship between the relative resistance of the mutant strains and their original position on the initial gradient plate?

A

the mutant strains have more resistance will grow close to the original position, since the original place have the highest conc. of the antibiotics. The absent of growth in the furthest is the most susceptible strains as no growth at the most diluted part of the antibiotics

135
Q

What is the currently accepted mechanism of the antimicrobial action of streptomycin?

A

the streptomycin bind to 30S subunit of the rRNA, which stop the initiation of proetin synthesis.

136
Q

How do you think development of resistance to antibiotics could be minimised within a community.

A

The static antibiotics cannot be used in the intact immunity population such as immunocompromised AIDs

it is better to use narrow spectrum antibiotics to avoid damage to the normal flora

the antibiotics gradient method can be used for:

  • dosage
  • side effect

resistant/susceptible

  • site of target and absorption

U4 prac exam (4 decks)

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