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MICROBIOLOGY Flashcards

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1
Q

Advantages of exotoxins

A
  • May help transmission of disease – severe disease host may be an evolutionary dead end
  • However, with many toxins the disease causing activity may not be primary function
  • Allow colonisation, niche establishment and carriage – give evolutionary advantage
  • Evade immune response, phagosomes, enable attachment to host cells
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2
Q

What does Phenol soluble modulins do?

A
  • PSM and alpha toxins inhibit phagosome fusing with lysosome - bacteria escape into cytoplasm.
  • PSM target cohabiting bacterial species - competition.
  • PSM have surfactant proteins - allow sliding movement - ADV to colonise surfaces
  • Development of biofilm - alpha toxins establish cell to cell contacts - form secondary biofilm structures
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3
Q

Type I exotoxins

A 
Membrane acting toxin
Act without cell - inappropiate activation of host cell receptors interfering with signalling.
Target Guanyl cyclase = high cGMP
Target adenyl cyclase = high cAMP
Target Ras proteins
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4
Q

Describe the mechanism for E. coli heat stable toxin

A
  • Bind to GC-C receptor interfering with intracellular signalling.
  • cGMP interacts with cystic fibrosis transmembrane receptor - protein kinases controlling function of specific transporters
  • Affect equilibrium of ions = Cl-/HCO3- transporter and H+/Na+ co transporter affected
  • high conc. Na+ and Cl- = diarrhoea
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5
Q

Type 3 exotoxins

A

AB toxins
B = receptor binding and translocation
A = toxingenic

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6
Q

Types of enzymatic component A - in AB toxins

A

ADP - ribosyl transferases
Glucosyltransferases
Proteases
Adenylcyclases

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7
Q

Function ADP - ribosyl transferase

A

Modify activity of endogenous enzymes - covalent modification - + ribosyl groups

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8
Q

Function of glucosyltransferase

A

affect ribosome RNA - inhibit protein synthesis - transfer saccharide group

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9
Q

Function of Proteases

A

Destroy other proteins - affect pre-synaptic structure

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10
Q

Function of adenycyclase

A

affect production of cAMP

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11
Q

Mechanism of clostridium difficile

A
  1. Toxins binding to specific host cell receptors - toxin internalised = endosome
  2. endosome acidification - pore formation mediated by hydrophobic domain
  3. GTD release from endosome to host cell cytoplasm - interacts with Rho GTPases
  4. Rho GTPases inactivation by glycosylation
  5. Downstream effects within host cell - cytopathic effects or cytotoxic effects
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12
Q

Cytopathic effects

A

changing structure of cell
cytoskeleton break down.
decrease cell to cell contact

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13
Q

Cytotoxic effects

A

activating production of reacting reactive O2 species - toxic - apoptosis

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14
Q

Mechanism of VTEC disease

A
  1. Bind to receptor Gb3 or Gb4 on host cell membrane
  2. Bound toxin internalised by receptor mediated endocytosis
  3. carried by retrograde trafficiking via golgi apparatus to ER
  4. The A subunit is cleaved off by membrane bound proteases
  5. Once in cytoplasm A1 and A2 dissociate
  6. A1 binds to 28S RNA subunit - blocks protein synthesis
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15
Q

Pathogenesis of STEC

A

adhere to epithelial cell of gut mucosa.
Bind to glomerular endothelial cells of kidney, CVS, and CNS.
Cause damage to vasculature inducing thrombosis and blocking kidney function leading to uraemic syndrome.
GI to kidney - because kidney has most Gb3

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16
Q

VTEC disease symptoms

A

Abdominal cramps, watery or bloody diarrhoea - may not be present.
Haemolytic uraemic syndrome - anaemia, renal failure, thrombocytopenia
Neurological symptoms - lethargy, severe headache, convulsions

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17
Q

Structure of endotoxins

A

Only produced by gram negative bacteria.
Lipid A + long fatty acid chain = toxicity of molecule - diverse between bacterial species
Core of rare, uncommon saccharides - relatively stable not diverse
O side chain - interact with immune responses - antigenic highly variable

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18
Q

Effects of pro-inflammatory cytokines

A
  1. increase number and lifespan and activation state of innate immune cells
  2. increase adhesion molecule and chemokine expression by endothelial cells
  3. increase acute phase protein - complements, fibrinogen
  4. cause fever
  5. cause neutrophils to release NETs made of DNA and antimicrobial proteins - form scaffold for platelet activation.
  6. cause release of microparticles by activated platelets
  7. increase tissue factor expression by blood monocytes
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19
Q

Sepsis dysregulation

A

Produce ROS - NO and hydroxyl - damage cellular protein, DNA, and impair mitochondria = decrease ATP, cell hibernation = organ dysfunction

Complement activation - change tissue factor expression - increase ROS, enzyme release
Wide spread immunothrombosis - disseminated intravascular coagulation

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20
Q

Sepsis resolution

A

Production IL-10 at end of acute inflammatory response = decrease IL-6 interferon and increase receptors that remove inflammatory cytokine
Remove PAMP and DAMP
Damaged cells = apoptosis and engulfment by macrophages

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21
Q

Meningococcal sepsis

A

Caused by Neisserio meningitis
LOS instead of LPS - activate and dysregulate immune response
Produce blebs - secreted capsules of the membrane - help hyperactivate immune response - induce sepsis

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22
Q

Definition of a virus

A

An infective agent that consists of nucleic molecule in a protein coat.
Is too small to be seen my light microscopy, and is able to multiply only within the living cells of a host.

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23
Q

Bacteria

A

Contain nucleic acid covered in protein, have a polysaccharide cell wall and can replicate outside of the cell

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24
Q

Prions

A

Are proteins, do not contain nucleic acid and replicate inside the cell

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25
Q

Structure of mature HIV-1 particle

A

Outer envelope consists of lipid bilayer - protruding env spikes.
Inside envelope = Gag proteins
2 genomic RNA strands

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26
Q

Virus entry mechanism

A

Engagement of viral envelope proteins with cell receptors - attach and fuse to the cytoplasm.
CD4 recognises sequence of surface subunit - GP120 of HIV envelope.
Native trimer - CD4 binding - CoR binding, open/uncover transmembrane sub-unit = 6 helix bundle formation - fusion
Helix bundle = push membrane apart so virus can get into cells

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27
Q

Early phase of HIV-1 infection

A

Utilise cells microtubule network - move core containing genome into nuclear membrane.
Viral core has capside modifications - determine it gets to the core
Once it gets to the nucleus = reverse transcription

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28
Q

Integration of HIV-1

A

End of viral linear DNA = specific sequences
Integrase enzyme recognises the sequence
Bind viral DNA and cellular DNA - cut cellular DNA and paste the viral DNA into cellular DNA
PRE-INTEGRATION COMPLEX - cellular proteins - LEDGF and TRN-SR2 - recognise cellular DNA and guide viral DNA to it

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29
Q

Gene expression HIV-1

A
  • Recruit cellular proteins required for mRNA transcription to viral genome.
  • Lef and Nf-kb = promote binding on promoter enhancing region - increase transcription of viral genome.
  • 1st thing produced = viral Tat protein - bind to specific viral RNA - increase RNA - preferential treatment.
  • Rev produced from viral RNA = + feedback loop = binds to RRE region - increase movement of viral NRA out of nucleus
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30
Q

Assembly and release of HIV-1

A

HIV coordinates production of viral proteins towards the cell surface.
Unspliced viral genomic RNA - dimerises - increase movement to plasma membrane and capsid

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31
Q

Myristoylation

A

Myristoylation of glycines in the matrix domain of Gag mediates association with the plasma membrane.
Polyprotein made - myristoylated - transferred using TG101 to cell surface and myrisolation stick it to the cell surface of plasma membrane

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32
Q

ESCRT machinery

A

Hijacked by HIV to perform abscission before viral release.
During abscission - viral proteins pushed out - cut up into individual proteins - protein can reorganise forming capsid structure
Capsid pushed out - extracellular space taking envelope proteins with it

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33
Q

Abscission

A

Organisation of proteins and RNA together in new capsid

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34
Q

Virus pathogenesis - Immunodeficiency

A

Viruses must evade immune responses - replicate in immune cells so can hide - inhibit immune cell function.

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35
Q

Direct killing of T cell

A

Infection of T cells - not all T cells are permissive to HIV replication - 5% permissive
Production of new viruses in permissive cells = activate apoptosis

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36
Q

Indirect killing of T cell

A

Non permissive cells
Do not allow virus to replicate
Seen by innate system so does not replicate - pyroptosis
Pyroptosis - inflammation - recruitment of more T cell to site of infection = + feedback.
Uninfected cell undergoing cell death = inflammation lead to cell death

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37
Q

Oppourtunistic infections of HIV associated pathogens

A

Inhibition of function - pathogens replicate in virus infected hosts leading to disease

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38
Q

2 possible routes of infection in HIV associated pathogens

A

Primary infection

Reactivation from latency

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39
Q

Viral latency - Herpes simplex

A

Virus encounter epithelial cells and replicates - move to dendrites of PNS and CNS - virus can move up and down axon
Virus stay in axon - does not replicate = virus latency
Stimulated to reactivate - virus move down axon and replicate out of productive infection and move into epithelial cells

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40
Q

Primary infection

A

HIV infected individual does not have either virus - encounters virus 1st time = infected.

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41
Q

Reactivation from latency

A

Primary infection resolved , Infection moves to sites in the host the immune system does not access - virus resides without replicating = latency.
Decrease T cells = reactivation

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42
Q

Protozoa transmission

A

Protozoa in human intestine transmitted by faecal oral route

Protozoa in blood/tissues transmitter by arthropod vector

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43
Q

Entamoeba histolytica

A

Amoebic dysentry

Cause ulcers in large instestine - epithelium

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44
Q

Giardia lamblia

A

Diarrhoea with blood

Common cause in areas with poor hygeine

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45
Q

Trichomonas vaginalis

A

Cause infection in genital tracts

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46
Q

Soil transmitted helminths

A

Ascaris lumbricodes
Trichuris trichiuria
hookworm - hold onto intestinal mucosa
Enterobius vermicularis - itchy bum in infants

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47
Q

Filarial parasites

A

Wuchereria bancrofti - lymphatic filariasis - damage lymphatic system
Loa loa - scleral surface of eye
Onchocerca volvulus - blindness - transmitted by black flies
Drancunculus medinensis - common in africa - contaminate H2O - intestine = ulcers in lower limb - could lead to disability

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48
Q

Schistoma

A

Cause disease in intestinal tract, liver and urinary system

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49
Q

Clonorchis sinensis

A

Ingestion of contaminated crustaceans - hepatic system = chronic infections

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50
Q

Fasciola hepatica

A

Liver and hepatic system - ingest contaminated cloves/vegetation

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51
Q

Paragonimus

A

Lung worm infection - ingestion of crustaceans poorly cooked - cough blood

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52
Q

Tapeworms

A

Taenia saginata

Taenia solium

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53
Q

How is trypanosoma cruzi / chagas disease transmitted

A

Leads to chagas disease
Bite - feeds and defecates - itch and scratch through the skin and allow access or bug to feed through mucosal membrane - invade cells and asexual reproduction

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54
Q

Acute chagas

A

Tissue damage caused by inflammatory response to parasite in nest of amastigotes in cardiac, skeletal and smooth muscle.
Parasite killing by antibodies leading to innate immune response and Th1 pro-inflammatory cytokines

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55
Q

Indeterminate chagas

A

Regulatory immune response characterised by IL-10 and IL-17

Life long infection - trypanosomes not detectable but + for parasite DNA

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56
Q

Chronic chagas

A

Damage to conduction system of heart or damage to myocardial muscle
Arrhythmia or sudden tachycardia.
Long term damage to muscle leading to heart failure, enlargement of the heart and thin muscular wall.
Chronic inflammatory response to persisistent parasites in muscle and nerve cells
Predominance of Th1 cytokines and CD8+ T cells.

57
Q

Chronic chagas - digestive

A

Develop in 10-15% of patients
Chronic infections - oesophagus, rectum and sigmoid colon
Damage to PNS - uncoordinated peristalsis - faeces build up in colon = enlargement megacolon
Can lead to ulceration, perforation, obstruction or twisting

58
Q

Transmission of Leishmaniasis

A

Transmit through vector - transmit a pro amastigote - invade immune cells - develop into amastigote, multiply sexually and burst - increase number.
Cutaneous leishmaniasis - ulcers - present for 3-6 months - scarring

59
Q

Mucocutaneous leishmaniasis

A

damage to nose tissues - progressive necrotising tissues lesion of nasal tissues = destruction of nose
Mucocutaneous disease associated with strong but inadequate inflammatory response to parasites that have metastasized to mucosa

60
Q

Leishmaniasis latency

A

parasites present long term - regulatory immune response characterised by balance of Th1 and anti-inflammatory response

61
Q

Diffuse cutaneous leishmaniasis

A

Nodular skin

Diffuse cutaneous leishmaniasis associated with uncontrolled replication

62
Q

Cercarial dermatitis

A

Exposure to cercariae - allergic type reaction.
Feature of immune response = granuloma formation - Th2 granuloma - IL4 and IL13
Eggs become organised in granuloma = repairs with scar formation - repeated damage = fibrosis and organ damage

63
Q

Hepato-intestinal schistomiasis

A

Mansoni and jponicum
Egg released into capillaries - push through capillaries into submucosa by immune response - and pushed into lumen of intestine
Long term damage = cirrhosis, damage to liver and splenomegaly

64
Q

Urinary schistomiasis

A

Bladder - strong immune response to eggs pushed through mucosa
Eosinophils surround - strong allergic response - haematuria
Changes in bladder - pre-cancer changes - nodular carcinoma of bladder.
Infections and fibrosis - calcified bladder wall

65
Q

Onchocerciasis transmission and effect

A

Blinding disease
Black fly bites - transmit L3 larvae - migrate to skin - females live in nodules in skin and males go from nodule to nodule fertilising females.
Repeated inflammation to prescence of microflaria = permanent damage in skin and eyes

66
Q

Microfilaria in skin

A

Free of inflammatory infiltrates – strong immune modulation of host – allow parasite to live
Immune regulation delicate – breaks down leading to strong inflammatory response – damages urticaria – bad reaction to microfilaria

67
Q

Acute papular onchodermatitis

A

Papular onchodermatitis = individuals who are chronic infected get periods when immune regulation breaks down leading to microfilaria

68
Q

Chronic onchodermatitis

A

Long term damage to collagen and elastin leading to premature ageing of skin (presbydermia)

69
Q

Sclerosing keratitis

A

Long term damage to cornea from puntate capacities

Microfilaria in cornea leading to fibrovascular pannus

70
Q

Chorioretinopathy

A

Microfilaria can invade back of eye - affect retinal pigment epithelium - layer of cells needed for metabolic need of neuroretina.
Advanced scar can lead to seeing underlying choroid vessels

71
Q

How do Ticks cause paralysis

A

Progressive flacidity due to failure of ACh liberation in NMJ.
Ticks produce toxin that blocks the motor nerve fibres

72
Q

Why do some viruses not infect us

A

They are adapted to non-human hosts
Excluded by surface barriers – innate immunity prevents them from establishing
Adaptive immune response has seen something similar

73
Q

Acute infection

A

Limiting life span - disease symptoms correlate to peak virus load
Huge spectrum of disease and range of outcomes

74
Q

Latent infection

A

Reactivating infection - infection longer and for life - waves of viral activation
Life long infection, controlled by immunity

75
Q

Herpes simplex and VZX latency

A

Virus migrate into sensory neurons - in dorsal root ganglion - IMMUNO PRIVILEGED SITE - establish latent infection in those cells
Viruses move out of transient state - travel back down neuron to specific tissue and eruption of virus

76
Q

2 types of persistent infection

A

Viral levels constantly controlled by active host immunity - occasional change in viral protein = eruption of virus
End of life = immune system can no longer control virus

77
Q

Congenital rubella

A

Virus levels stay up - not controlled by immune system
If infected in utero - baby is immunotolerant and virus continues to replicate = damage neonatal tissue - continues for 2 years after birth

78
Q

cytopathic damage of EBOLA

A

Targets vascular endothelial cells

Endothelial rupture and release its content

79
Q

Cytopathic damage of Influenza A

A

Targets lung epithelia - destroy ability of cilia to stand/beat to expel lung fluid

80
Q

Cytopathic damage of RSV

A

Induce syncytia in lung epithelia - cell fusion

81
Q

Immunopathology - Hepatitis C

A

Non-cytopathic

Associated with extensive liver infiltration of leukocytes - CD8+ cells attach infected cells and destroy them

82
Q

Immunopathology - Dengue fever

A

Most common mosquito borne infection
Increase risk is previous infection with different serotypes.
Antibodies formed in response to infection - not protective against other serotypes can lead to severe diseases due to antibody dependent enhancement

83
Q

Antibody dependent enhancement

A

Antibody bind to virus and phagocytes see virus but does not neutralise - take up virus with Fc receptors = virus get into cells and replicates elsewhere
Get secondary response - complement binding = cell destroyed - increase vascular permeability

84
Q

RSV infections in early life

A

Unbalanced Th1/Th2 responses - Increase Th2 response and decrease inflammatory cytokine production - Increase IgE production

85
Q

Virus isolation in cell culture

A

Use different cell lines - cells are specialised - slow
Different viruses may give different appearances
Different cell lines may support growth of different viruses
Identify virus using antigen detection techniques or neutralisation of growth
Cell culture + antiviral - look for inhibition of cytopathic effect

86
Q

Direct immunofluorescence

A

Cell associated antigens
Antigen from infected host bound to slide - specific antibody to antigen is tagged to fluorochrome - viewed with microscope with ultraviolet

87
Q

Enzyme immunoassay

A

Free soluble antigens or whole virus
Component reaction is adhered to solid - 3 formats - indirect, direct, and sandwich
Antibody adsorbed to well - antigen binds to antibody - 2nd antibody with enzyme added - chromogenic substrate added - colour change = antigen present

88
Q

Immunochromotographic methods

A

Lateral flow tests - blood or saliva

89
Q

Antibody detection by serology - what can serology be used for

A

Detect antibody response in symptomatic patients

Determine if vaccination has been successful.

90
Q

How is serum produced

A

produced from processing blood – coagulated with silica and gel trap cellular components
Contains proteins, antigens, antibodies, drugs, and electrolytes

91
Q

Diagnosis by antibody detection - serology

A

Infected by virus - humoral immune response = production of immunoglobulins
Diagnosis made by detection of IgM or by demonstration of seroconversion - switch of IgM to IgG

92
Q

Stages of NAAT

A
  1. specimen collection
  2. extraction of nucleic acid
  3. DNA transcription for RNA viruses
  4. Cycles of amplification of DNA target - requires polymerase, dNTPs
  5. Detection of amplicons
93
Q

Commensal non pathogen

A

In host - present but not capable of causing disease - E. coli

94
Q

Zoonotic non pathogen

A

In carrier - present but only capable of causing disease in another host

95
Q

Commensal opportunist

A

In host - present and capable of causing disease in host but certain circumstances

96
Q

Non selective media

A

Blood agar - blood help organisms grow because can release cofactors - like haem or iron

97
Q

Semi selective media

A

DCA, CLED - selection of things that will grow certain things
CLED AND DCA - non lactose fermenting bactera
CLED = red = uses lactose

98
Q

Selective atmosphere

A

Aerobic culture - cell that are non-aerobe will not grown

Microaerophilic culture - respiratory pathogens - cell adapted to living in low CO2 - 5% CO2 and can grow

99
Q

Phage type

A

Small virus like particles - attach to certain type orf bacteria - receptors on surface add phage to organism. Phage grows and lysis

100
Q

Virology detecting steps

A
  1. Culture and microscopy
    will not grow on plate - intracellular organism - need permissive cell lines.
    Will cause a cytopathoc effect when there is a permissive cell line
  2. Direct antigen detection
    ELISA will look for organism or antibodies against organism - can do dilution series and dilute samples - see how much antibody/virus is present
101
Q

Selective toxicity

A

Differences between structure and metabolic pathways between host and pathogen
Harm microorganism, not host - usually target microbe - difficult to target viruses as they are intracellular.
Variation between viruses - antivirals work sometimes depending on strain of virus

102
Q

Why is it difficult to develop effective non-toxic anti-viral drugs

A

Viruses enter cell using cellular receptors - IF try inhibiting cellular receptors there would be downstream effect on the cell
Viruses replicate inside cells
Some viruses have a high mutation rate esp. RNA viruses
Anti-virals must be selective toxicity - effect only host cells

103
Q

Amantidine function

A

Used for influenza - inhibit uncoating of virus by blocking M2 protein needed to uncoat virus - no longer used - was toxic and not very effective

104
Q

Acyclovir mechanism/function

A

IV/ORAL/TOPICAL - HSV, VZV or prophylaxis - doesn’t work well in CMV
Viral thymidine kinase activate drug - phosphorylate ACV - triphosphorylated by cellular guamylate = activated form
Inhibit viral DNA polymerase - chain termination

105
Q

Acyclovir selective toxicity

A

ACV triphosphate = 30x affinity for HSV DNA polymerase than cellular DNA polymerase
ACV triphosphate - increase polarity = difficult to leave/enter cells - enter cells prior phosphorylation

106
Q

Drugs that can be used for herpes virus

A

ACYCLOVIR
GANCICLOVIR
FOSCARNET
CIDOFOVIR

107
Q

Ganciclovir function

A

IV/ORAL for CMV
CMV does not encode thymidine kinase but has UL97
UL97 - inhibit DNA polymerase

108
Q

Foscarnet function

A

IV/LOCAL APPLICATION for CMV
Selectively inhibit viral DNA/RNA - bind to pyrophosphate binding site - allosteric
non-competitive inhibitor
Used because of ganciclovir resistance - mutation in UL97

109
Q

Cidofovir function

A

IV for CMV
chain terminator - compete with dCTP - target DNA polymerase
Phosphorylated by cellular kinase - diphosphate - active against CMV but toxic - nephorotoxic

110
Q

Thymidine kinase mutants

A

Drugs not needing phosphorylation are still effective

111
Q

DNA polymerase mutants

A

All drugs less effective

112
Q

Anti HIV drugs

A

Used in combination - HAART - avoid resistance

  1. Anti-reverse transcriptase inhibitors
    - Nukes – nucleotide RT inhibitors OR non nukes – allosteric
  2. Protease inhibitors – multiple types
  3. Integrase inhibitors – POL gene – 3’ encoding for IN allow pro-viral DNA to integrate – block it
  4. Fusion inhibitors – block ability of virus to fuse with surface of cell
113
Q

AZT - nuke

A

Synthetic analogue for thymidine - converted to tri-nucleotide = block RT by:
Compete for dTTP and incorporate into DNA causing chain termination

114
Q

Nevirapine - non nuke

A

Non competitive inhibitor of HIV-1 RT - synergistic with AZT

115
Q

PEP

A

Post exposure prophylaxis and preventing infection - HIV
Within 72 hours post exposure
take 28 days - 2xNRTIs + integrase inhibitor

116
Q

PrEP

A

Pre-exposure prophylaxis - HIV

Block transmission - 2xNRTIs

117
Q

Consequences of

Resistance to antivirals

A

Use single agent leading to rapid development of resistance

Increase viral load = increase mutation rate = resistance

118
Q

Neuraminidase inhibitors

A

ZANAMIVIR OR OSELTAMIVIR
Virus budding - attached to receptor containing sialic acid - neuraminidase cleave receptor = release virus
Inhibitor - prevent release of sialic acid residues from cell receptor - prevent virus budding

119
Q

Treating Hepatitis B

A

Immunoglobulin - passive immunity and vaccination - treatment = anti-virals NRTIs
DNA virus - but must copy RNA component into DNA component - inhibited by NRTI

120
Q

Treating Hep C

A

Interferon + Ribavirin for 6 months within 1st 2 month exposure
RIBAVIRIN - block RNA synthesis by inhibiting GTP synthesis block IMP to XMP

121
Q

Direct acting anti-virals and hep C

A

Shorten length of therapy decrease side effects and target virus itself, improve sustained virologic response.
• NS ¾ protease inhibitors – inhibit processing of polyproteins into active proteins – translation
• NS5B polymerase inhibitors – inhibit polymerase
• NS5A inhibitors – block replication, complex formation, and assembly – block viral release

122
Q

COVID-19 antivirals

A

REMDESIVIR
Prodrug that is metabolised in cells = active nucleotide analogue
Active = inhibit RNA dependent RNA polymerase - incorporate RdRp into growing RNA chain = delayed chain terminator

123
Q

What are antibiotics

A

Natural products of fungi and bacteria - natural antagonism and selective advantage
Most derived from natural products by fermentation then modified to increase pharmacological properties and increase antimicrobial effect

124
Q

Antibiotic associated colitis

A

Broad spectrum antibiotics damage normal flora = overgrowth of organisms - disrupt the microbiome of gut = ulceration, inflammation, diarrhoea

125
Q

Bactericidal class of antibiotics

A

Kill bacteria
Used when host defence mechanism are impaired - immunosuppressed
Requried in endocarditis, kidney infection

126
Q

Bacteriostatic class of antibiotics

A

Inhibit bacteria
Used when host defence mechanisms are in tact
Used in many infectious diseases

127
Q

Beta lactam antibiotics

A

Base on molecular structure of penicillin and cephalosporins
Structure contain beta lactam ring - active structure in penicillin.
Pass through porin to penicillin binding protein - inhibit peptidoglycan synthesis - structure disrupted - produce autolytic enzyme = bacteria lysis

128
Q

Bacterial targets for common antibiotics

A

Cell wall synthesis inhibitors
Protein synthesis - prokaryotic ribosomes are different to eukaryotic
DNA and RNA processing - inhibit unwinding
Folic acid synthesis inhibitors
Cell membrane inhibitors - bacteria and norm cell membrane similar = so can be toxic
Antibiotics that produce free radicals

129
Q

Examples of cell wall synthesis inhibitors

A

Penicillin
cephalosporins
vancomycin

130
Q

Examples of protein synthesis

A

Different ribosomes - good selective toxicity
50S inhibitor = erythromycin, chloramphenicol
30S inhibitor = tetracycline, gentamicin

131
Q

Examples of DNA and RNA processing

A

Inhibit DNA gyrase - prevent DNA unwinding
Quinolones - inhibit DNA gyrase - drug selectively inhibits this - prevent replication
Rifampicin - used to treat TB - block DNA directed RNA polymerase - can’t make mRNA

132
Q

Examples of folic acid synthesis inhibitors

A

Block pathways that make tetrahydrofolic acid
Sulphonamids, trimethoprim - 2 enzymes involved in making THFA
Block THFA = block metabolic activity = death

133
Q

Examples of antibiotics that produce free radicals

A

Metronidazole - work well against anaerobic organisms

Nitrofurantoin - produce free radicals - used to treat UTI

134
Q

Mechanism of cell wall synthesis inhibition

A

Vancomycin - recognise 2 alanine at the end of peptide chain - inhibit cross linking
Penicilin and cephalosporin - inhibti enzyme cross linking peptides - act as competitive inhibitors that cross link

135
Q

Mechanism of folic acid synthesis

A

Humans can’t produce own folic acid
Prokaryotic and eukaryotic dihydrofolate reductase are different = selective toxicity
Eukaryotes do not have dihydropteroate synthetase - prokaryotes produce THFA from substrates - so antibiotics inhibit the enzyme = no THFA

136
Q

Methods of antibiotic resistance

A 
Drug inactivation
Altered or new target
Efflux pump
Overproduction of target
Metabolic bypass
Intrinsic impermeability
137
Q

Non genetic mechanism of growth phase - tolerance

A

Bacteria rapidly replicate - stop growing and form biofilms (ENDOCARDITIS) - stop growing and compromise the function of the organ = tolerance

138
Q

Augmentin/co-amoxiclav

A

Drug combination - clavulanic acid - bind to and inactivates beta lactamase - allow amoxicillin to work - no anti bacterial activity of its own

139
Q

Vancomycin resistance

A

Makes D-ala D-lactate - prevent vancomycin from binding because there are missing cross linking reactions.
Acquires genes that encode new metabolic pathway - allow bacteria to make D-ala D-lactate

MICROBIOLOGY AND IMMUNOLOGY (3 decks)

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