Infectious Diseases & Pathogenicity Flashcards

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1
Q

What are the 2 shapes/morphologies of bacteria - single-celled?

A

-Cocci (round cells)
-Rod-shaped cells (bacilli)

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2
Q

How are cocci named alone & multiple?

A

single = monococcus
paired = diplococcus
grouped = staphylococcus
chained = streptococcus

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3
Q

What rod-shaped bacteria do you get?

A

single rod = bacillus
grouped/clustered
chains

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4
Q

Label this prok cell.

A

-Outer memb = (some)
-Cell wall = (most)
-Inner memb
–> ALL 3 = cell wall complex
Mebs used to create potential = ATP
-Fimbriae/Pili = (some)help w/ adhesion & sometimes motility
-Flagella = motility - spin
-Capsule = sticky - prevents phagocytosis
-Ribosomes = 70s
-Plasmids = extra chromosomal DNA - antibiotic resistance genes, can move between bacteria
-Nucleoid = nuc acid & histone-like prots - folds
-Cytoplasm = contains inclusion bodies e.g.,
Ca2+

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5
Q

What are the 2 types of bacteria shown from gram staining?

A

-Gram -ve
-Gram +ve

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6
Q

What are gram -ve bacteria?

A

-Small amount of peptidoglycan
-Has 2 membs - inner & outer
–> so has x2 periplasmic spaces
–> so is more selective
-Have bulk transporters on OM - move groups of things in (little selectivity)
-OM transports stuff into periplasmic space - enzymes degrade polymers = monomers - taken up by IM
-Greater time for enz to act on material as are x2

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7
Q

What are gram +ve bacteria?

A

-Have lots of cell wall material - peptidoglycan
-Has inner memb only
–> so has x1 periplasmic space - enzymes here = break down material before get into cell & capture enzs

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8
Q

What is peptidoglycan?

A

-Cross-linked chain of carbs (hexose sugars) w/ peptides (AAs)
–> gives rigidity to cell wall (due to cross-linking)
-Mesh-like structure

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9
Q

What is periplasmic space?

A

-Gaps in bacteria cell wall complex - where enzymes are secreted by bacteria
-These enzymes degrade polymers & antibiotics

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10
Q

What are spores?

A

-Produced by some bacteria
-Dormant form of bacteria
-Lacks water
-Stain bacteria - spore positioning = help identify bacteria species
-Can survive in extreme envs
-Able to germinate to = new bacterial cell
-Removes water from its components - DNA & RNA - so spores can survive for long time
-Dehydrate spore - where is lots of water & nutrients - rehydrate so spore can germinate

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11
Q

What are some positionings of spores of bacteria - used to identify bacteria species?

A
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12
Q

Why are spores an issue for infection control?

A

-Responsible for transmission
-Effect treatment - drugs only kill viable things - not spores
-Difficult to kill - no water (often target water to kill things)
-Small = easily spread - infection control = hard

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13
Q

Example of spore forming bacteria & description of it?

A

Clostridium difficile
= gram +ve
= rod shaped
-Link to elderly & antibiotic use
-Sub type - makes toxin = diarrhoea & organ failure
-Spore production - effects management - isolation, barrier nursing, inc cleaning of rooms (Cl based disinfectants)

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14
Q

What to do with patient if think has infection - Infectious Disease Diagnosis & Control?

A

Sequence of treatment
* Observation of patient - symptoms
* Sampling
* Laboratory observation & culture
* Identification tests
* Treatment - e.g. antibiotic therapy
* Observation of population (epidemiology)
* Prevention of transmission

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15
Q

What is empirical prescribing?

A

-Prescribing based on symptoms (prescribe before diagnose)
-Bets guess
-Don’t know exactly what is but know symptoms indicate sometime a specific antibiotic will treat

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16
Q

Why are hospital acquired infections & community acquired infections different?

A

In hospital = more likely to be antibiotic resistance (more likely to diagnose) & closed env

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17
Q

What does disease mean?

A

A disturbance in the state of health where the body cannot carry out all its normal functions

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18
Q

What does infectious disease mean?

A

Due to infection by pathogenic microorganisms

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19
Q

What does infection mean?

A

Invasion by and multiplication of a pathogenic microbe within or on a host

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20
Q

What does contamination mean?

A

The presence of microbes in a location/env

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21
Q

What are Koch’s Postulates?

A

-To link presence of pathogens in someone w/ a disease to that disease
-Concept of linking an organism to a disease

  1. Causative agent must be observed in every case of the disease
  2. The agent must be isolated from a diseased host & grown in pure culture
  3. When the agent from the pure culture is
    inoculated into healthy, but susceptible, hosts the agent must cause the same disease
  4. The agent must be re-isolated from the inoculated, diseased host & identified as identical to the original specific causative agent
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22
Q

Why are Koch’s postulates less useful now?

A

-Organism = diff types of disease in diff people - due to genetics
-Some infectious agents - can’t isolate & grow (worked well for most bacteria but not for viruses)

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23
Q

Do organisms only affect 1 site?

A

No - some can affect many across body - e.g., staphylococcus aureus
-Some sites can be affected by many types of organisms

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24
Q

What is the iceberg concept of infectious diseases?

A

-Severe = symptoms are impacting greatly on you - more likely to go to GP
-Mild = less likely to go to GP

(not all infected show symptoms!)
-Only people presenting to clinicians = at top of iceberg - at bottom don’t see - these spread disease

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25
Q

Describe how a disease progresses?

A

-Microbe encounters host (human)
-Encounter
-Transition - between contact & impact (stages which lead to entry/estab - most pathogens don’t get through as we manage them beforehand)
-Entry/establishment - adheres to cells
-Colonise - pathogen now on tissues & SOME pathogens spread from initial site to other organs via bloodstream:
.Spread
.Multiply
.Damage
.Outcome of infection (spread to others & impact on us - our recovery)
-Commensals (normal flora - on body surfaces) - produce antimicrobial peptides - to stop colonisation by pathogens - as stop establishment. In return these ‘want’ nutrients
-OR CAN BE ASYMPTOMATIC

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26
Q

What influences successful transmission & exposure?

A

-No. microbes - more = more chance (infectious dose needed for infection - CAN be low though for some pathogens!)
-Airborne - size, density, surface features (how pathogen interacts) - thicker pathos when sneeze - surrounded by mucus - bact don’t desiccate
(so these 3 factors necessary for being airborne - must have right ones of each)
-Waterbourne - correct density, surface features, hydrophobicity - density as if floats on water - more likely to drink & infect - so low density - & hydrophobic so stay on surface
-How do we contact them? - spores?, adhesion to surfaces?, resist dessication?
-How do they get in? - cuts?, dig syst?, GU syst?, lungs?
-Any vectors that can transmit the pathogen (e.g., insects)

27
Q

How do pathogens adhere & invade (attach to surface)?

A

-Adhesion - of host & microbe - is it specific to what binds to?, or bind to spec cell type (part of tropism = meaning infect a specific location)
-Damage/break in normal microbial floral on surface - for adhesion
-To invade - chemotaxis, motility
-Attach to pili/non-fimbril adhesins
-To invade - penetrate ep/cells (use proteases?)
-Capsules - let pathos survive on phagocyte

28
Q

Name a virulence factor?

A

When a pathogen adheres/attaches to cell - can alter protein expression on surface - so more pathogens can bind
-Because the virulent bact inject ep cells w/ molecules to do this

29
Q

How do pathogens colonise & cause tissue damage?

A

-To grow - must resist host immune resp
-Neutralising ability (stop being killed ) - enzy/capsules
-Growth - nutrients needed e.g., iron (micronutrient - need as grow v. fast - need lots of energy - energy generating prots = iron requiring)
-Damage cells - released nutrients into env
-Toxins released due to growth - damages cells - exposes tissues to continued colonisation
-Tissue damage = as host cells die, toxins build up, tissues digested (enzy)

30
Q

What is normal/commensal?

A

-Natural organisms that live symbiotically w/ host (can contain pathogen - which can become pathogenic in certain circumstances)

31
Q

What changes normal flora?

A

-Time
-What eat
-Stress
-Heath state

32
Q

Examples of normal flora?

A

Staphylococcus aureus
E. coli (non-toxigenic)
Lactic acid bact
Candida yeast…

33
Q

Role of normal/commensal flora?

A

Part of body’s defence system

34
Q

Why do we not cause immune resp to normal flora?

A

Imm system adapted so won’t respond to (kill the lymphocytes w/ comp recs)

35
Q

What condition changes can alter normal flora?

A

-Stress
-Antibiotic treatment
-Hormonal changes
-Climatic/env stress

36
Q

What happens if normal flora is altered under certain conditions?

A

Interaction of these organisms w/ host changes:
-Microbes grow more - cause infection

37
Q

How can the impact of antibiotics cause infection?

A

Can target other macrobacteria not just pathogen - if is antibact drug e.g., - has more chance of affecting flora if is wide-spect ant
-Altering flora = more susceptible to infection
-Some microbial flora can be caused to grow - & infect

38
Q

What does the host do to prevent infection - disease resistance?

A

-Surface defences (skin, acid) - tears, mucus
-Cellular defences (phagocytes, killer cells)
-Inflammation
-Cytokines (e.g. interferons)
-Complement system
-Immunity - memory cells, antibodies

PHYSICAL DEF & IMM RESP

39
Q

What does a pathogen do to resist being killed (mostly links to bacteria)?

A

-Pathogenicity
-Virulence
-Virulence/pathogenicity factor

40
Q

What is pathogenicity?

A

Ability of organism to produce infectious disease in an organism
-Primary factor of this = toxins

41
Q

What is virulence?

A

Relative degree of damage done by pathogen or degree of pathogenicity (producing infectious disease in organism) of a pathogen
-Signif tissue damage

42
Q

What is virulence/pathogenicity factor?

A

Microbial product or strategy contributing to virulence or pathogenicity
-Strategy can modify protein expression - to make pathogen more virulent

43
Q

Molecular determinants/what causes pathogenicity?

A

-Attach to host
-Produce & deliver factors that influence cells bind to (secretion system into host cell) - materials into host
-Rep & evade imm resp
-Damage tissues - by toxin release

44
Q

What are bacterial secretion systems?

A

-Prot complexes on cell memb of bact for secretion of substances
-Are the cellular devices used by pathogenic bacteria to secrete virulence factors (mainly of proteins) to invade host cells

45
Q

What is LD50?

A

Lethal dose of microbes toxin that will kill 50% of experimentally inoculated test animal

46
Q

What is ID50?

A

Infectious dose needed to cause disease in 50% of inoculated test animals
e.g., for vibrio cholerae = 100,000,000 cells to get infection - but will package large amounts on protozoa
-no need for spore as is water borne - transmit as viable organism
e.g., for inhalation anthrax = 5-10,000 spores
- spores = dehydrated so not affected by dehydration in env

47
Q

How can bacteria attach to host cells?

A

-Adhesins on tip of pili or fimbriae = interact w/ glycoprots recs on host cell memb

-Alternatively on bact cell memb can have adhesins containing glycocalyx
(Glycocalyx = outer viscous covering of fibers extending from bact)

-More pili = more adhesive

-Capsules - sticky - carb based - viscous (polymeric) - so adhere to host too

48
Q

What else can capsules do (except adhere)?

A

Prevent (not fully stop) bacteria being phagocytosed
-Increases size & stops inducing phagocytosis - as recs of pathogen hidden by capsule - polymeric matrix

-Prevent dehydration of bacteria in env

49
Q

Name some bacteria that have capsules

A

-Streptococcus pneumoniae
-Klebsiella pneumoniae
-Haemophilus influenzae
-Bacillus anthracis
-Streptococcus mutans

–> all affect resp syst - airborne

50
Q

What are released by bact?

A

-Enzymes
-Toxins

–> toxigenic materials/ toxic products released by microbes

51
Q

Mechanism of action of collagenase (of clostridium spp.) toxinigenic enzyme?

A

-Gets cells to disperse (if they are tightly packed) - by breaking down collagen making up CT
-So bacteria get through tissue more effectively - & spread - more mobility
–> BUT affects cell viability too

52
Q

Mechanism of action of leukocidins & porins - as toxins, released by bacteria?

A

Protein based
-Make pores in euk cells
-Causes change to euk cells - releases ions into env - cell loses viability

53
Q

What do alpha haemolytic streptococci release (toxin) - what does this cause?

A

-Haemolysins
–> causes incomplete lysis (haemolysis) - targeted to RBCs - releases haemoglobin i.e., iron (source of iron, once remove AAs)
- leaky RBCs - not fully
-Can’t read though these RBCs (paper underneath)

54
Q

What do beta haemolytic streptococci release (toxin) - what does this cause?

A

-Haemolysins
–> causes complete lysis (haemolysis) of RBCs - haemoglobin released - obtain iron from AAs
-Can read through these RBCs (paper underneath)

55
Q

What does C. Coagulase (toxin) do, & what may be coagulase +ve?

A

-Cause blood to coagulase (clot) - protects bact from phagocytosis from WBCs & other host defences (stops migration of imm cells & inflamm cells - only tissues cells in - minimises impact of blood borne & inflamm cells & stops material leaving)
-Staphylococcus aureus

56
Q

How do clots form?

A

Thrombin enzyme converts fibrinogen –> fibrin (clot)

57
Q

What does F. Collagenase (toxin) do, & what uses this?

A

-Breaks down collagen (in many CTs)
-Clostridium perfrinogens - uses to spread through muscle tissue (gas gangrene)

58
Q

What are toxins?

A

Poisonous substances microorganisms produce

59
Q

How do the majority of toxins affect euk cells?

A

Damage cell memb

60
Q

What is toxemia?

A

-Toxins get into bloodtsream

61
Q

What is toxigenicity?

A

Capacity of microorganisms to produce toxins - i.e., whether a microorganism can produce toxins

62
Q

What are exotoxins?

A

-Produced inside mostly gram +ve bact
-Involved in growth & metabolism of bact
-Then release into env
-Produced by viable (growing) cells

63
Q

What are endotoxins?

A

-Part of outer cell wall of bact
-In gram -ve bact
-Break off when bact dies or is killed (as cell wall breaks up)
-Not a toxin but has toxic effects e.g., lipopolysaccharide - causes blood vs dilation & causes reduced blood flow & BP drop
-can cause signif toxaemia - when give antibiotics