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advanced medical microbiology > week 4 > Flashcards

week 4 Flashcards

1
Q

Biomaterial associated infection (BAI) –

A

mostly by staphylococcus epidermidid and S. aureus

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2
Q

Race for the surface

A

the sooner the biomaterial gets coated by own cells, the lower the chance of bacteria colonizing the surface

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3
Q

biofilms

A
  • Quorum sensing – small molecules by bacteria can be recognized
  • Difficult to phagocytose
  • Not effectively reached by all antibiotics
  • In dormant state less susceptible to antibiotics
  • Persisters
  • A persisting inflammatory stimulus
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4
Q

Mouse soft tissue BAI model

A
  • Implantation
  • Challenge
  • Eplantation
  • Biopsy for quantitative culture (BM segment sonicated, homogenized tissue), histology, cytokines, mRNA
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5
Q

Localization of s epidermitidis

A

not on surface but in deep tissue. S epidermidis in tissue resist antibiotics. Stay in immune cells, are not killing.

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6
Q

In human catheter infections

A

high positive culture levels in skin, also in areas not in direct contact with biomaterial. 44% positive, mostly s epidermidis and e faecalis

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7
Q

Anti LTA staining

A

colors gram positive bacteria, test to esclude chance of contamination

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8
Q

S aureus in bone tissue

A
  • Intracellular; long term osteomyelitis patient
  • Canaliculi – can even deform to fit structure. Not only surface but also in bone holes
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9
Q

Biomaterial associated infection (BAI)

A
  • Mostly caused by staphylococci
  • Biofilm
  • Peri implant tissue colonization
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10
Q

Foreign body response –

A

from proinflammatory to anti inflammatory. In specific order immune cells accumulate, orchestrated by cytokines
* mononuclear leukocytes
* neutrophils
* macrophages
* foreign body giant cells (fused macrophages)

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11
Q

regulation foreign body response hindrance

A

by pram positive bacterial cell wall. strong inducer inflammation. Depends on combination of physical and chemical combination of material and bacteria, can lead to pro-inflammatory or anti inflammatory response.

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12
Q

SEpvp (coating)

A

too strong pro inflammatory result, protracted inflammatory phase (longer), strong delay in foreign body response

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13
Q

PApvp (coating)

A

giant cells visible after 14 days, but cultures grow and get incapsulated, dangerous with even systemic dissemination in murine models, sepsis. Localized in cluster like cells

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14
Q

low IFN

A

Spreading
Systemic disease
Sepsis

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15
Q

Orchestrate local immunity

A

develop materials which host proper response, resulting in infection free healing

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16
Q

Release systems antimicrobial coating

A

release antimicrobials
contact killing
anti adhesive
combinations

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17
Q

high IFN

A

Strong pro-inflammatory reaction
Protracted inflammatory phase
Strong delay in Foreign body response

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18
Q

Considerations for release

A
  • Railord to expected pathogen
  • Release profile tailored to desired protected area and required concentrations
  • Initial burst release, sustained release for sufficient period
  • Reservoir of antimicrobial sufficient to realise the above
  • Coating sufficiently attached
  • Active in vivo situation
  • Biocompatible
  • Mechanism of release; diffusion, controlled release, biodegradable (but what if antimicrobial is released and coating not yet degraded), triggered
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19
Q

Novel antimicrobial approaches

A
  • BALI – biofilm alliance
  • Superactive; supramolecular biomaterials with antimicrobial and regenerative activity
  • PRINT-AID – development of 3d printed devices with antimicrobial properties to prevent biomaterial infections
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20
Q

Synthetic antimicrobial and antibiofilm peptides (SAAP)

A
  • Derived from human cathelicidin LL37
  • OP145 is synthetic derived from P60 with impreoved helicity and amphipathicity; antimicrobial and antibiofilm. Plasma inhibits action of OP145
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21
Q

PLEX OP 145 controlled release coating

A

Combination lipids and polymers makes it stable, OP145 10%. In first 10 days 60% released, after that more slowly – burst first. Later improved activity SAAPS in presence of plasma due to optimization without resistance, prevents biofilm formation.

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22
Q

Novel ll37 derived SAAPs

A

broad spectrum, active in PBS and plasma AANVULLEN

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23
Q

Novel antimicrobial SuperActive (regenerative capacity biomaterial)

A

prevent infection and let tissue regenerate. Base polymer and stacking parts (SAAP). Materials can be dipcoated, effect was not complete elimination of the pathogens
Supramolecular UPy based materials
* Simple mix and match
* Retained activity SAAP148
* Incorporation into solid materials

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24
Q

3d printing antimicrobial devices

A

Antimicrobial agent and biomaterial can be made to fit the patient. Control of drug loading and release by adjusting layers. Advantage 10-100x higher concentration, minimal systemic effects. Disadvantage; not enough drug biomaterial options due to heat and sollluability, mixed on stage, antimicrobial resistance.
PRINT-AID Solutions:
 Local administration of gentamicin
sulphate (GS) in an 3D-printed PCL
coating
 Tailored polymer-SAAP release system by
Droplet-on-demand printing

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25
Q

Droplet on demand coat Ti bone plate SAAP148

A

active against MDR bacteria and biofilm formation. Droplet size controlled by pressure and nozzle opening. Release from one layer almost completed in first day, cumulative release only 13%

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26
Q

Coxiella burnettii

A
  • Obligatory intracellular = replicate inside cells
  • Enter via receptor mediated endocytosis
  • Come into Coxiella containing vacuole CCV
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27
Q

CCV coxiella containing vacuole

A
  • Small cell variants (SCVs) – metabolic inactive, resistant and extracellular
  • After invasion large cell variants (LCV) – metabolic active, intracellular, acidification triggers transcription
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28
Q

what does c burnetti infect

A

macrophages via actin-dependent phagocytosis

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29
Q

Alfavbeta3

A
  • Normally Involved in apoptotic cells via phagocytosis
  • C burnetti inhibits inflammation – silent infection
  • Adhesion of Coxiella is unknown protein
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30
Q

Host cell modulation

A
  • Binding receptor, uptake of c burnetti
  • Nasant CCV (coxiella containing vacuole) is formed, phagosome and lysosome interact (no fusion), vacuole becomes larger and bacteria replicate in this low pH
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31
Q

Mature CCV

A
  • Heavily loaded with bacteria – large will transform to small
  • Retains capacity to fuse and expand
  • Now also anti apoptotic markers
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32
Q

Coxiella has secretion apparatus

A
  • Needle like structure, injects effector proteins into host cells
  • Can manipulate host cells to not combat bacteria anymore
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33
Q

Defect in organelle traficing (Dot) intracellular multiplication (Icm)

A
  • Secretion system
  • Encoded on islands with relatively low CG contents
  • Eukaryotic protein motifs
  • Effector protein secreted
  • Polymorphic regions between pathotypes
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34
Q

How does it work (Dot and Icm)

A
  • Regulate transcription
  • Translocation efficiency
  • Protein stability
  • Expressed after 8h and require low pH
  • prmAB important for regulation transcription
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35
Q

functional assays used to test function prmAB

A

made a knock out of prmAB and placed cells in medium, no difference. Inside cells huge difference

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36
Q

how dows prmAB work

A
  • pmrA box like a fur box? To test first see if it binds to promotor region – fusion prm and lux (fluorescent). Knock out no translation so it binds there
  • regulates transcription
    (low pH stimulus)
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37
Q

Protein domains point to function

A
  • Anti apoptosis
  • Ubiquitylation
  • Lipid metabolism
  • Membrane trafficking
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38
Q

cell wall synthesis

A

penicillins, cephalosporins, bacitracin, vancomycin

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39
Q

Nucleic acid replication

A

quinolones, rifampin

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40
Q

Protein synthesis

A

chloramphenicol, erythromycin, tetracyclins, streptomycin

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41
Q

Plasma membrane

A

polymyxin B

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42
Q

Synthesis essential metabolites

A

sulfonamide, trimethoprim

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43
Q

Types of antibiotic resistance

A
  • Intrinsic resistance – vooral gram negatief difficult, has to go through pore in outer membrane or dissolve. Efflux pump is present and PBPs (penicillin binding protein)
  • Target site changes – AB targets protein, comes from gene. Mutation where AB cannot bind anymore, or if other compound binds enzyme.
  • Direct interactions with AB
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44
Q

PBPs

A

binds penicillin, those are peptidoglycan synthases and get inactivated by binding penicillin. PBP gets inactivated – destruction cell wall

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45
Q

Multi drug resistance (MDR) efflux pumps gram negative bacteria; resistance nodulation division (RND) expression factors

A

Baseline of expression of proteins of the pump; Acr expression controlled by TetR repressor, can be overruled by AraC family transcription factor. araC is repressed by multi antibiotic resistance (MAR) protein MarR

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46
Q

Antibiotics effect on pump

A

usually bind to MarR protein, derepression, expression pump system

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47
Q

Highly resistant bacteria due to which mutation

A

TetR repressor mutation

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48
Q

MRSA expression PBP2a

A
  • Horizontal gene transfer from s epidermidis
  • PBP has different structure, but peptidoglycan synthesis not affected
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49
Q

Rifampicin resistance

A

RNA polymerase binding. High frequency rifampicin resistance, s epidermis. Not gradient loss of effect rifampicin, not functional at all anymore

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50
Q

Target site mutation rpoB

A

RNA polymerase of m tuberculosis causing rifampicin resistance

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51
Q

tetM

A

target site protection against tetracyclin. Normally binding to site in ribosome where translation normally starts, not with tetM, binding but function not affected

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52
Q

steric hindrance

A

binding without destroying

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53
Q

inactivation by hydrolysis

A

beta lactam and beta lactamases. Only carbapenem left

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54
Q

counteracting beta lactamase –

A

clavulanic acid. Blocks beta lactamases even in resistant bacteria (by inhibiting enzyme that gets produced by bacteria). In itself it is a beta lactam drug, not antibacterial so needs to be given together with AB
* with amoxicilline – augmentin
* with ticarcillin – co-ticarclav
* however, carbapenemases are still not susceptible to beta lactamase blockers

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55
Q

beta lactamases

A
  • ampC – inactivates 2/3 gen cephalosporin, Enterobacter and serratia, chromosomal inducible or constitutive
  • ESBL – also 2/3 gen cephalosporins, plasmid localized (can spread)
  • Inactivation by clavulanic acid variable
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56
Q

Resistance to beta lactam

A
  • Efflux
  • Direct interaction; ESBL, carbapenemases
  • Target site changes (MRSA)
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57
Q

Intrinsic resistance AB

A
  • Prevent influx
  • Efflux
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58
Q

Target site changes AB

A
  • Mutation
  • Protection
59
Q

Direct interactions AB

A

hydrolysis (enzymatic breakdown)
steric hindrance

60
Q

Antimicrobial peptides

A

amino acid chains with at least 2 positive charges. Amphipathic, broad spectrum gram pos, neg, fungi, parasite, cancer, virus, counteract sepsis, low MIC, synergy with AB and AMP

61
Q

Human antimicrobial peptides

A

epithelial, endothelial, leukocytes, platelets
* Rapid; stored and secreted, intracellular killing
* Inducible
* After tissue damage
* Inflammation
* Bacterial products

62
Q

Classes of antimicrobial peptides

A
  • Beta stranded; protegin, alpha/beta defensins
  • Alpha helical; ll37, cecropin
63
Q

Membrane disruption types after threshold passed

A
  • barrel stave
  • bending backward
  • carpet (micel) like soap like structure
64
Q

effects of thrombin on microbes -

A

thrombin activates thrombocidins (TCs), granules containing alpha granules get released

65
Q

membrane potential measure

A

DiSC3(5) assay. Higher fluorescence less potetntial, more disturbed

66
Q

TC84 actions

A
  • Membrane depolarization
  • Membrane permeabilization
  • Membrane invagination
  • Cytoplasmic content leakage, membrane disruption
  • Unmixes membrane
  • Colocalizes with fluid domains
  • Colocalizes with membrane invaginations
67
Q

Model of mode of action of TC19/AMP

A
  • Less organized, unmixing due to presence cationic peptides that form patches with membrane that is more liquid
    Mechanism of killing by Amp
  • Interaction membrane; disruption protein motive force, permeation, disruption, membrane passage (positively charged)
  • Interaction targets; nucleic acids, septum, heat shock proteins. The ones that don’t disrupt the membranes (negatively charged)
68
Q

Honey antimicrobial factors

A
  • Osmotic
  • Hydrogen peroxide due to glucose oxidase
  • Acidity
  • Methylglyoxal (manuka)
  • Bee defensin-1
69
Q

Biofilm formation

A

bacteria form extracellular matrix anker on surface, microcolonies, 3d structure

70
Q

Pellicle

A

protein layer on surface teeth. Bacteria can bind those proteins, other bacteria can bind those bacteria.

71
Q

Ecological succession

A

change in species in ecological community. Succession occurs when we disturb colonized or after initial colonization. Competitive, more complex over time

72
Q

Biofilm

A
  • Healthy – in slightly higher CO2 concentration, streptococci etc
  • Biofilms become thicker – oxygen lower and anaerobic bacteria can grow
  • Periodontitis – accumulation dysbiotic bacteria (gum disease)
73
Q

Why buccal cells divide so fast

A

Buccal cells also get colonized with bacteria, both inside and outside. Possible start for dental plaque. Important in recolonization, early colonizers and in fact early proliferators

74
Q

Oral biofilm from ecological perspective

A
  • Daily removal
  • Many environmental changes hourly
  • Mostly healthy, yet caries and gingivitis most common worldwide
  • Spatio temporal heterogeneity
75
Q

Multi kingdom biofilms

A
  • More complex in vivo
  • Fungi, archaea and amoeba
76
Q

Aerobic vs anaerobic biofilms bacteria

A
  • C albicans alters bacterial microbiome, as shown by sequencing; with candida anaerobes, without aerobes
  • Antimycin A inhibits oxygen removal, aerobes can grow
77
Q

Caries;

A

stress (sugar intake and acid production), environmental shift to low pH, ecological shift (strep and a naeslundii to mutants streptococci and lactobacilli), disease enamel and caries

78
Q

Fluoride

A

prevents caries by preventing low pH to affect teeth, only reduces symptoms

79
Q

Gingivitis

A

redness of gums, bleed easily. Untreated can lead to periodontitis (bone absorption due to inflammation) and can lead to teeth loss

oral hygiene drops, gingival inflammation, more leakage GCF, protein and iron, more bacteria

80
Q

Root surface bacteria on border enamel and teeth

A

live of off proteins that are available in high concentrations there

81
Q

Oral microbiome

A

total of all micro-organisms in a specific location.

82
Q

Holobiont

A

host/microbiota coevolution. assemblage of a host and the many other species living in or around it, which together form a discrete ecological unit through symbiosis

83
Q

Why rather target tick itself instead of lyme

A

there are other tick born diseases (1/3 other tick born diseases, 1/5 lyme).

84
Q

Tick saliva

A

proteins that inhibit coagulation, inhibits inflammatory/immune response.

85
Q

Salp15

A

in tick saliva inhibits DC and T cells proliferation

86
Q

Tick immunity

A

less susceptible to tick born diseases by investing animals with ticks multiple times, possibility for vaccine?

87
Q

Cycle of borrelia

A

Blood enters gut tick (outer surface protein A OspA associated), migrates hemolymph to saliva (OspC expression, which is bound by Selp15 which functions as invisibility cloak), transmitted to host unrecognisable

88
Q

Tick vaccine by targeting salivary proteins

A
  • Identify tick proteins to use; by feeding (not at all, 24h, fully) dissecting, making cDNA libraries of salivary glands, grouping. Most is happening in early tick feeding phase (24h), might be better to target this with vaccine. Narrowing down proteins; expression 5x higher vs uninfected, significant, remove biological replicates, Q RT PCR validate compounds
  • Infected ticks injected with RNAi knocking down those transcripts, mice infected, tick weight after feeding stayed the same. Also unfortunately no differences in loads of bacteria in heart and ear compared to normal tick
89
Q

Tick vaccine by targeting salivary gland antigens

A
  • Focusing on tick salivary gland antigens; feeding uninfected ticks, cDNA library, next gen seq, feeding induced tick proteins discovered. Narrowing down; high log2, significantly upregulated etc. 20 validated.
  • With antigen 11 present; higher levels of borrelia after infection, phagocytosis reduction
  • Without antigen 11 (p19) ticks could feed perfectly normal, borrelia levels significantly lower (culture protected)
90
Q

what provides protection tick borne encephalitis

A

antigen 22 and antigen 16 provide moderate protection in lethal model against tick borne encephalitis. Combining provides more protection

91
Q

Species complexity higher in Europe

A

B afzelii, garinii, burgdorferi and bavariensis, need vaccine that targets all 4

92
Q

ospA (expessed by borrelia) downregulation

A

borrelia migration from gut to salivary gland and host

93
Q

mechanism of ospA based vaccine

A

antibody goes into tick, binds borrelia in tick, prevents borrelia transfer from gut to saliva

94
Q

first generation LB vaccine (ospA)

A
  • lymerix; whole ospA used, only burgdorferi targeting, 76% efficacy
  • imulyme; whole ospA used, phase 3, only burgdorferi, 92% efficacy
  • hypothetical vaccine induced adverse effects, mimicry with hLFA1 T cell epitope. Has been disproven, but still discontinued due to lack of demand leading to poor sales. Not licenced
95
Q

second generation ospA vaccine

A
  • VLA15; combination of 3 proteins
  • Broad protection to 4 genospecies representing 6 serotypes
  • Phase 3 started
96
Q

Experimental LB chimeric ospA

A

truncated stabilized c terminal fragment to investigate protection by multivalent ospA. Surface shaping approach – multiple epitopes on one protein
* CHECK STEP 1
* Homology modelling/structural scaffold = combining 2 proteins and see if they fold in the way you predicted
* Surface partitioning – see if you can make or keep the patches where Ab can bind
* Patch layout – devide surface in different patches and take patches that bind to create different layouts by differently linking the parts together
* Serotype distribution – serotypes bind different patches, algorithm decides what is the best combination to protect against different serotypes, not always covered all serotypes by one protein. using different disulfide bonds to stabilize
* Immunized mice; ELISA, flow cytometry, bactericidal assay (bind and neutralize borrelia in vivo possible?), collect final sera, organs, serology, another ELISA
* V3 and V5 combination chosen for creation of fusion protein

97
Q

V3-V5 and L2 single antigen ospA vaccine, produced as one protein

A
  • Could induce immune response against all serotypes
  • Tested for serotype 1 and 2 especially because those are most prevalent in NL and ENG. Provided 100% protection against tick challenge
98
Q

Destinguish between different malaria species

A

using microscope based on morphology

99
Q

Genetic variation between plasmodium species measurements

A

PCR

100
Q

Plasmodium malariae

A

difficult to see under microscope, when PCR was done, it revealed another species; plasmodium knowlesi.

101
Q

Plasmodium knowlesi

A

zoonosis

102
Q

Why plasmodium falciparum causes more serious anemia

A

Multiply inside red blood cell, ruptures. Is worse in falciparum, might be because of the quicker development, higher parasitaemia, blocking blood vessels

103
Q

Temperature chart different plasmodium species

A
  • Vivax/ovale - Ring stage gives fever, rupture also causes fever
  • Malariae – slower development.
  • Falciparum – patterns more spiked, more quick so quicker development
104
Q

Why quicker development, higher parasitaemia in falciparum why

A

because preverance of parasite to type of blood cell (infects all), whereas malariae invades old, vivax/ovale invades young, hemoglobin is used, change in surface (knob formation)

105
Q

Overview pathogenesis of malaira

A
  • Change surface
  • Lysis
  • Use of food source – hemoglobin
  • Can all lead to tissue damage
106
Q

Why certain groups are more vulnerable

A
  • Children- no immunity
  • Non-immune (travelers)
  • Pregnant – harmful for patient and child. Effect depends on age, gravidity, endemicity, HIV status. Parasite can target placenta specifically (not found in non pregnant), also immunostatus decreases
107
Q

difference pregnancy associated and placental malaria

A

Pregnancy associated malaria – not involve placenta
Placental malaria – infection including placenta

108
Q

Immunity against malaria

A

only partial, due to different variants, takes many rounds of infections to gain immunity

109
Q

Consequences malaria during pregnancy

A
  • Growth restriction
  • Anemia
  • Preterm delivery
  • abortion
110
Q

microbiome

A

aggregate of all microbioata (microorganisms in specific environment). Mostly commensial/symbiotic

111
Q

role gut microbiota

A
  • digest fiber
  • produce viamins
  • synthesize amino acids
  • produce short chain fatty acids
  • interaction with immune
  • protect against pathogens
112
Q

habitats within human gut

A

lumen mucin and food particles.

113
Q

Challenges studying microbiome

A
  • Hard to culture
  • Ecology and community composition important
  • Genomic markers important for identification
114
Q

Solutions to challenges studying microbiome

A
  • DNA based
  • Metagenomic seq
  • DNA probe bases microscopy
115
Q

SSU rRNA vs metagenomics

A

specific gene used, meta is also for functionality. Gives amount in percentage

116
Q

Recovering genomes from metagenomes –

A

extract DNA, shotgun metagenomics gives reads. Reads can be assembled into contigs. Map reads to contigs, table to display sequence characteristics and combine both to bin contigs to reconstruct genomes (MAG – metabolic assembled genome)

117
Q

MAGs

A

give insight into unsequenced organisms. Applicable to every dataset with little bias, incomplete and contamination tho

118
Q

Proximity ligation sequencing (Hi-C)

A

crosslinker on top of bacteria, connect to different materials and put in different organisms

119
Q

Culturomics

A

cheap and allows for follow up, but culturing bias and work intensive

120
Q

Combining isolates and metagenomics

A

combining isoates and metagenomics can help understand strain dynamics and in person evolution

121
Q

Obtain DNA of microbiome

A
  • metagenomics
  • Hi-C
  • Culturomics
122
Q

What influences our own microbiome

A
  • Relatively stable over time, strain composition even more stable
  • Animal based diet increased harmful bacteria, effects of vegan diet were very small
123
Q

Diseases and microbiome

A
  • Dysbiosis
  • Single causative agent – C difficile, EHEC etc
124
Q

C difficile

A
  • Can be resistant to AB, makes it worse
  • Better to give fecal matter transplantations (after AB)
125
Q

Streptococcus suis

A
  • Pigs
  • zoonotic
  • Gram positive
  • Capsule polysaccharides – multiple serotypes
  • Risk of disease increases after viral infection
  • Mainly serotype 2 in humans
  • meningitis
126
Q

Disease s suis

A
  • Meningitis – irreversible hearing loss in 60%
  • Sepsis with high mortality – skin bleeding
  • Endocarditis, peritonitis, arthritis
127
Q

Risk factors s suis

A
  • Raw pork consumption
  • Exposure to pigs
  • Male sex
  • Pig related occupation
128
Q

Core genome

A

pool of genes shared by all members of bacterial species

129
Q

Pangenome

A

core and accessory genome

130
Q

Accessory genome (dispensable)

A

pool of genes present in some species

131
Q

Metagenome

A

gene repertoire of mixed microbial population

132
Q

Whole genome seq with illumina

A

contigs produced using overlap sequencing reads.

133
Q

Serotype differences s suis

A

Loss and acquisition of genes may lead to increased virulence and zoonotic potential by polysaccharide capsule switch. However, humans only get infected with 2, known by serotype antibodies measurements
Reinfection s suis is possible

134
Q

Restriction modification system functions

A
  • Restriction function - endonuclease
  • Methylation function
  • S unit can vary with phase variation mechanism, different phases means different DNA motifs recognized, different gene expression
135
Q

Knocking out xerD in s suis

A

prevents recombination as seen in FAM assay. Cannot adapt to certain conditions
Order genes s suis - does not affect growth, but does affect pathogenicity

136
Q

Pathogenicity island –

A

adapt to circumstances, obtained by horizontal gene transfer

137
Q

ICE

A

Streptococci contain Integrative and Conjugative Elements (ICE) in their accessory genome. Combine features of phages, transposons and plasmids. Integration in genome of ICEs

138
Q

The tragedy of the commons

A

benefit for individual is enormous, but burden to all

139
Q

Cause of AMR pathogens

A

Socio economic (availability of AB), environmental (more infections) and ecological changes (use of AB, settings animals)

140
Q

Colistin

A

last resort AB, but used in large volumes in food animals

141
Q

Colistin resistance

A

create surface defect, effect against gram negative

142
Q

Anthropogenic and environmental factors associated with high incidence of mcr1 carriage in humans

A

link between agriculture and mcr1
Mcr1 transposon jumps over time, loss of insertion sequence

143
Q

After banning using colistin in animals

A

drop in prevalence mcr and resistant e coli

144
Q

PCI

A

Photochemical
internalization of
gentamicin
mediated cytosolic release of gentamicin

advanced medical microbiology (4 decks)

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