Bacterial Microbiology Flashcards

1
Q

Give a few important characteristics of bacteria.

A

Small and unicellular, no intracellular organelles, haploid round chromosome, some have flagella, different cell wall

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2
Q

Explain gram staining and identifying bacteria-with a few exemples of shape and genus

A

Gram staining was developed in the 1800 and it distinguished between types of cell wall-pink is gram-negative and purple-gram-positive
gram negative-2 cell lipid wall, seperated by peptidoglycan-and Lipopolysacharides achored at the exterior eg: e.coli, salmonella, shigella
Gram positive-1 cell wall covered in large peptidoglycan exterior layer-and no LPS eg: Staph aureus, step pneumonia, step pyogenes
Bacterias can take many shapes, but main ones are cocci, bacilli and spirilli

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3
Q

Describe the 5 goals of a bacteria in its host

A

colonize (find a niche), persist (avoid, subject and escape immune system), replicate (aquire nutrients such as iron, energy and grow), disseminate (in cell or tissue-move around to grow more), cause disease (produce toxins that kills hosts, induce diarhea, dysregulate immune system)

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4
Q

Can bacteria be extra cellular? Intracellular? Both? Explain mechanisms if needed and give exemples of any
What does salmonella use for mobility and invasion?
Give another exemple of actin manipulation by bacteria?

A

They can be both-some extracellular are Staph, Strep, Neisseria
Intracellular pathogens aim to be uptaken into a vacuole-then want to escape the vacuole (Shigella, Listeria), survive in the phagolysosome (coxiella) or prevent fusion with lysosome (Salmonella, Chlamydia)
Salmonella moves around to find cells with a flagellae (motility), but also uses an injectisome to inject virulence proteins into the host-and cause actin polymerisation that forces uptake by membrane
Listeria also acts on actin-gets inside cell and use it to move around and go from cell to cell

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5
Q

What is horizontal gene transfer? Explain the 3 mechanisms. And what is a pathogenecity island

A

Transformation-DNA uptake. DNA in the solution is stipped into ssDNA and uptaken by the bacteriam then integrated into the bacteria chr
Conjugation-Replication of plasmid from one cell to another. Mating bridge form between bacteria, and some plasmids have gene allowing transfer-rolling replication through the bridge into new cell-each have the plasmid
Transduction-bacteriophages infest bacteria-and when they package, can inadventerly pack up host DNA-then when integrate into genome of other bacteria, gene added
A pathogenecity island in horizontally acquires DNA that contribute to virulance-packaged and expressed together and can usually be the cause of illness

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6
Q

List the 6 main portals of entry for pathogens in the body, give an example of each and explain possible sources. Quickly explain expected and unexpected pathogens

A

Upper respiratory tract -S.pneumoniae, Stomach-Heliobacter pylori, Skin-Staph epidermis, Mouth-Strep spp, Small Intestine-E.coli, Lower genital tract (Lactobacillius)
Bacteria usually come from 2 sources-extrinsic (environement) or Intrinsic (from own body)
Expected bacteria/entry are bacterias that usually live in the body, like small intestine of vagina (harmless)
Unexpected pathogens are those tnetering

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7
Q

Describe the URT as a portal of entry for bacteria. Give exemples of pathogens, disease and dangers

A

URT-usually extrinsic bacteria acquired from other URT-airborne on droplets, airborne or hand as intermediates
Exemples of bacteria: Step spp (dental), Step pneumoniae, step pyogenes, strep pneumo, neisserisa meningitis
If it reached throat-tonsilitis, parynghytis
From there, can either stay around and replicate (middle ear infection) and in some cases, reach trough the bone into brain-brain abcesse or meningitis (Neisserissa particularly good at that)
Or can go down to Lower RT (lungs), causing bronchitis, pneumonia (Step pneumoniae good at that)
All of these routes, if left too long can reach the bloodstream-bacteraemia-systemic damages can causes spesis-immune response usually the danger

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8
Q

Describe the Urogenital tract as a portal of entry for bacteria. Give exemples of pathogens, disease and dangers

A

Urogenital (vagina, urthra, penis, bladder) can be extrinsic (catheter) or intrinsic (large intestine/colon or surgery)
Usually URINARY intrinsic-exemples are (E.Coli, Klebstriella, Enterobacter, candida) but can be exterinsic (catheters mostly E.Coli and Klebstriella)
Usual genital tract are- Extrinsic-stepp group B (pregnancy), candida or extrinsic (STD’s-Neisserissa gonorrhoae, chalmydia, syphilis)
Consequences of genital (gonnococal urethritis, pelvic inflamation disease, tubo ovarian abscesses), pregnancy (neonatal step group B, neonatal gonococcal), or Urinary (cystitis, pyelonephritis (spread to kidney)
all these can spead to the blood again-cause dangerous bacteremia

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9
Q

Describe Broken Skin as a portal of entry for bacteria. Give exemples of pathogens, disease and dangers

A

Many sources: Surgery/wounds, skin diseases, synringes (drugs), Insect bites, animal/human bites, IV
Usually skin pathogens are opportunistic-those not are Staph aureus, strep pyogens , in hospital MRSA, or after surgery of gut-exposure. Unusual bacteria can come in-Pasteurella from dogs, Aeromonas Hydrophilia from leeches, Clostridium Perfingens from soil
Consequences can be superficial infection, cellulitis, abcesses, fascilits, myosisys, grangrene, and ofc bacterimia

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10
Q

Describe the feaco-oral route as a portal of entry for bacteria. Give exemples of pathogens, disease and dangers

A

Also called gastrointestinal-bacteria that target stomach
Exemples: E.Coli, Shigella, Cholerae, Salmonella, listeria, Clostridium difficiles
Usually cause diarhoeal illnesses-Vomiting, D&V, diarhoae, dystentry (bloody stool). Toxins can spread and cause diarhoae or neurological damage (botulism)
Can also spread to be systemic after a while (typhoid (s.tyohi), listeriosis (listeria), salmonella and sceptic arthiritis and aortitis

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11
Q

Define pathogens, commensals, pathogencity factors affecting pathogencity, infectious dose and factors affecting it, virulance and exemples of virulence

A

Pathogens are bacteria that cause diseas (true-always and can infect healthy being, opportunistic-take advantage of weakness/other illness)
Commensals are bacteria that do not cause disease
pathogenicity is the ability to cause disease
Its affected by infectivity (features favoring infection)- such as transmission, ability to colonise, tropism, replication, immune evasion
and its affected by virulence (features that cause disease) such as toxin production, enzyme that degrade host molecules, interuption of host processes and complete immune evasion
Infectious dose is the number of bacteria required to cause an infection-affected by route (stomach-acid requires high numbers), ability to colonise host (adherence, etc), Tropism and motility (where they want to live, how easy is it to get there-cholerae has flagella), replication speed (faster usually better-but TB is so slow it evades immune system), and immune evasion
Virulence can be caused by toxins (pneumolysin made by S pneumoniae makes a pore in cells-affect lung architecture), Degradation of host molecules (eg Hyaluronan lyase-degrades host EC for nutrition and spead), Interference with host function (Superantigens by S.Aureus interfere with T cell activation) and immune evasion (S aureus leukocidins killd neutrophils, causing absesses)

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12
Q

What are Beta lactams? Give a few exemples

A

Beta lactams are a type of anti-biotics that interfere with peptigoglycan cell wall synthesis-kills bacteria
penicillin, methicilin, imipenem

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13
Q

What is an antibiotic? Where do they come from? What are different terms to describe their function?

A

Antibiotics describe any form of antomicrobial agent produced by a microorganism or inhibits microorganism
Classically, most Abx come from soil dwelling fungi (Penicillium) or bacteria
But today, Use range of natural, semi-synthetic or synthetic chemicals
Antimicrobial-chemical that selectively kills miccrobes
Bacteriocidal (kills bacteria), Bacteriostatic (stops bacteria from growing), Antispetic-chemical killing microbes to stop infection

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14
Q

What is meant by Abx resistance? Why does it arise?

A

It describes the ability for a bacteria to grow above the breakpoint (maximum clinically achievable concentration)
Minimal inhibitory concentration-lowest conc of Abx required to inhibit growth
Abx resistance exist naturally (and always has), but Abx use provides selective pressure-only those with resistance survive and proliferate, and if they do, take over-so survivors are Abx resistant

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15
Q

Give exemples of the main Gram negative and gram positive Abx resistant bacteria?

A

Gram - : Pseudomonas aeruginosa, E.Coli, Klebstriella, Salmonella, Neisserissa ghonorrhoae
Gram +: Staph aureus (MRSA), Strep pneumoniae, clostrum difficile, enterococcus, mycobacterium

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16
Q

Explain the mechanism of action and characteristics of Aminoglycosides, Rifampicin, Vancomycin, Linezolid, Daptomycin, macrolides and quinolones

A

Aminoglycosides: Bacteriocidal-targets 30S ribosome, RNA synthesis and cell wall-limited toxicity but not much resistance
Rifampicin: Bacteriocidal, targets RNA polymerase-spontaneous resistance frequent, and makes patient secretion orange (compliance problem)
Vancomycin-Bactericidal-targets wall integrity and biosynthesis-limited toxicity but not much resistance
Linezolid-Bacteriostatic, Inhibits protein synthesis (50S) rRNA)-mostly vs gram +
Daptomycin-bactericidal-targets cell membrane, gram+ mostly, toxicity limits usage/dose
Macrolides-Target 50S, stops aminoacyl transfer-mostly gram + but some gram -
Quinolones-synthetic broad spectrum bacteriocidal-target DNA gyrase in gram - and topoisomerase in gram +

17
Q

What is Abx selective toxicity? How is that achieved?

A

Selective toxicity is the ability to only target bacteria-which is usually achieved by targetting processes/proteins/enzymes that are specific to them (such as ribosome, polymerase, replication, mRNA, walls and much more)

18
Q

What are the 4 molecular mechanisms of Abx resistance?

A

Altered target site-The site where the Abx binds changes-making it innefective. Can arise via aquisition of alternative gene, or mutation of gene eg: MRSA has PBP with low B-lactam affinity
Inactivation of the Abx-Enzymatic degradation or alteration, rendering it ineffective. Eg: B-lactamase (degrades middle ring), can now be broad-spectrum B lactamase (vs nearly all of them)
Altered metabolism-Increased production of enzyme (target) which outcompete Abx inhibitor-too much enzyme for Abx, OR reducing reliance of the enzyme
Decreased drug accumulation-Reduced Abx penetration, or increases efflux of Abx-cannot reach high conc enough to be effective

19
Q

What are the main sources of Abx resistant genes? How are Abx resistance genes transfered?

A

Main sources-plasmids (can carry multiple-worth as long as it doesnt cost too much to replicate it-can be transfered), Transposons-‘Jumping’ DNA, can integrate into host genome, and allow transfer from plsamid to chr, Naked DNA-DNA from dead bacteria in the environement can be uptaken
Abx genes can come vertically (parents) or horizontally (how they spread)-Transformation, tranduction and conjugation

20
Q

What are non genetic mechanism for resistance/treatment failure?

A

Biofilm formation, Intracellular location, slow growth, spores, persisters, innapropriate Abx, poor penetration of Abx to target site, inapropriate dose (half life), inapropriate administation (oral vs IV), Abx resistance in commensal (secrete B lactamase)

21
Q

Why do hospitals have high levels of resistance? Why is there hospital acquires infection? Give an exemple

A

Hosptials provide a strong selective pressure for Abx resistance-because so much are used. Furthermore, more infections arise because-high number of ill people, crowded wards, pathogens present, broken skins, indwelling devices, Abx can supress normal flora, transmission by staff (contact with many patients)
C.Difficiles takes advantage of Abx supression of gut bacteria to spread and overtake the rest-then spread

22
Q

What are methods to adress/limit resistance? How about to overcome it? And what is the future?

A

Adress: Prescribing startegies-tighter contol, temporary withdrawals to lower resistance, reduce broad spectrum Abx, Quicker identifications of resistante disease, Combination therapy (if more than one Abx-wont be able to resist one without being killed by other-go to the end of course and no resistant left), knowledge of mechanism
Overcoming-Modification of existing medication (methilin is enhances), Combination of Abx and inhibitor of abx resistance enzymes-however thats reactive
The future are new Abx, vaccines, but aslo siRNA, phage lysins, and more

23
Q

What are the 4 main type of bacterial vaccines? give a fast overview of host defence and its relation to vaccines. What are the ideal properties of a vaccine?

A

bacterial vaccines can be toxoids, conjugates, live attenuated, killed whole cells
Innate: first line, fast, doesnt require previous exposure, mediated by monocytes and creates inflam reaction and not precise
Adaptive-better after first exposure due to memory. takes time to develop, highly specific-mediated by lymphocyte (Cell mediated or humoral) in combination with most immune cells-memory cells connect to vaccines
Ideally, a vaccine stimulate an effective immune response, safe and no adverse reaction, cheap to make and distrubute (no chain of cold for stability), stable, easy to give (oral), easy to control

24
Q

Explain direct protection and herd immunity

A

Direct protection is a vaccine-the individual is protected from infection/symptoms by having a reacting immunity
Herd immunity is the concept that the more a population is vaccinated, the less the pathogen will spread-and there is indirect protection becaue the pathogen wont be able to move around/spread because of immunity-for babies that cant be vaccinated, vaccine parents-only people baby touches so cannot get it from them
Herd immunity also quickly dampens infectious outbreaks-if one person can infect 3, then no vaccine-1,3,9,27, etc v fast. With herd-if 2/3 are vaccinated-1,1,1,1,1,1 etc

25
Q

How is the safety of vaccines assessed? How is it calculated/expressed?

A

Clinical trials are the main method
Phase I: Primarly testing safety in small number of adults
Phase II: assess for immune response and expand safety database-includes target group
Phase III-protection studies, placebo controlled-statistically conclusive, good disease surveillance-endpoint defined
Vaccine efficacy is determined in phase 3: Vax efficacy= 1-Attackrate with vaccine/attack rate without vaccine
Herd effect can also be calculated, as vac coveraged needed to acheieve immunity- 1-1/R0 /effectiveness, and heard effect is =1-attack rate in unvax post vax/att rate un unvax pre vax

26
Q

What are the main constituents of vaccines, giving their use and exemples

A

AG-stimulate the immune response
Can be live attenuated organisms, killed whole organisms, purified components, toxoids or polysach conjugates
Adjuvant-enhance and modulate immune response
Excipients-Buffer, salts, sacharrides, protein, preservatives, etc

27
Q

List the main UK paediatric vaccines, explain their components and possible short comings

A

Pre-primary: DTaP-IPV, MMR, influenza
Girls 12/12-HPV, later: dT-IPV booster, MenACYM
DT-Tetanus and diptheteria, aP-whooping cough, Hib-Influenza, IPV-Poliovirus
DT-Chemically inactivated exotoxins-simple to produce, safe, pure and very good efficacy
aP-whooping cough-caused by Bordetella pertussis toxins-convulsive cough. Whole cell vaccine was good (>90%), but had adverse reactions (anaphylaxis, seizures, encephalopathy-development of acellular vaccine-using proteins that bacteria use to attatch to epithelum )FHA, etc), aherence prots, toxins (PT, etc)-make them multicomponent (bi, tri, penta)-good efficacy and SAFE
Problem is that not complete after a few years-boosters? Improved vaccines? It might be because it might not provide herd immunity-aP vaccinees were not protected from transmission and colonisation-convalescent were much better
HiB-Influenza type B-meningitis and speticimia in the young-conjugate vaccine made of polysachs and more
overall packaged together-Pediacel/Infantrix

28
Q

What are conjugate vaccines? Describe their reason for existing, their efficacy and 2 big sucess strories

A

Polysacchs can lead to t cell independent activation-AG is usually large and linear, non degradable, repetitive-and response is mainly IgM, poor memory and bad AB avidity
Conjugate vaccines aim to make carbohydrates linked by immunogenic protein-expensive, but very pure and effective-long lived boostable immunity, offers herd immunity
So the polysacchs can be packaged in many ways with proteins-randomly. or linking back to one another, or several per protein
Licensed Conjugates are-Hib vaccinesm pneumococcal, MenC, and more (group B strepp)
Very common and good with MenC-93% efficacy, good herd immunity BUT preferable to have a later MenC booster around 20s
Pneumoccal disease-strep pneumoniae is a major cause of meningitis and mucosal infection-more than 90 serotypes with different capsules-Abx resistance associated with some-vaccine has to have a lot of serotypes-usually the most comment (Pneumovax II has 24 valent polysacchs-good efficacy for the target serotypes and good effects regardless of serotypes (89% efficacy) BUT has caused the ones that arent vaccinated against to rise in numbers and become more populat

29
Q

Describe the new vaccine being developped agaisnt group B meningococcal disease

A

group B men produced outer membrane vesicle (secreted) which have a lot of toxins, but also AG for the bacteria-the vaccines are produced by extracting by detergent which reduces the toxin content (have even now made hyper producing mutants)
Clinical trials starts around 1987-efficacy from 80% to 50%-good protection mainly against homologous strain

30
Q

Explain the reverse vaccinology approach to designing and creating vaccines

A

Instead of randomly testing types of AG, or different AGs, can try and use a computer to predict which proteins are the best AG to use, then express the proteins in e.coli and use them to prepare a vaccine. Thats because the calssic isolate, inactivate inject doesnt always work (aP)
MenB OMV vaccine have newly been enhances to contain AGs that were identified using reverse genomics-a large increase of effectiveness

31
Q

What are other exemples of bacterial vaccines that are not paediatric ones?

A

The main 3 exemples of weird vaccines are BCG, Typhoid and Cholera
BCG-TB vaccine-attenuated strain of Myco Bovis-ancient passed 231 times-lead to to loss of RD1 coding 9 prots
When it first got created, it couldnt be for everyone, and its effectiveness is unsure (was instored at a time of great health improvement in general), there were no trials-nowadays, new candidates for vaccines are in the work (recombinant vaccines AG 85A)
Typhoid: Vivotif live attenuated vaccine, Or Typhim VI polysacchs-only suitable for adults and if travelling
Cholera-killed whole cell vaccines-poor efficacry
Whole cell oral vaccine-good efficacy, safe and easy to give
Dukoral-killed cell+oral live-drinkable (3weeks + boosters)-may also protect vs ETEC

32
Q

Explain the role of adjuvants, giving exemples and mechanisms

A

Adjuvants are key to the response-can be either delivery systems (Sats, surface active agetns, liposomes or immune potentiators (Toxins, lipids, nucleic acids, Peptides, cytokines)-activate PAMPS which leads to faster immune response in general