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Microbial Pathogens > Bacterial Pathogens (1-3) > Flashcards

Bacterial Pathogens (1-3) Flashcards

1
Q

What is a pathogen?

A

A microbe roar is able to cause disease in a plant, animal or insect

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2
Q

What is pathogenicity?

A

The ability to produce disease in a host organism
→ expressed through their virulence
→ determinants of virulence: genetic, biochemical or structural features that enable it to produce a disease

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3
Q

What are the underlying mechanisms of bacterial pathogenicity?

A

Ability to invade → colonisation (adherence and multiplication), ability to overcome host defence, extracellular substances that facilitate entry
→ e.g. adhesins like fimbiae

Ability to produce toxins → exotoxins: released from bacteria e.g. Cholera toxin
→ endotoxins: cell-associated e.g. LPS, capsule

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4
Q

How can pathogens enter the human body?

A

Respiratory → inhalation
Gastro-intestinal → ingest
Urinary/genital tracts

via insect bites or accidental/surgical trauma to skin

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5
Q

What are some examples of human primary pathogen transmission?

A

Bordetella pertussis → whooping cough, requires contact with infectious material

Neisseria gonorrhoeae → sexually transmitted, requires direct person-to-person mucosal contact - man only natural host so dies in environment

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6
Q

What does the environment that a pathogen can colonise effect?

A

The environments that can be colonised by a pathogen are critical in determining its reservoirs and potential modes of transmission

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7
Q

What is a psychrophile, psycotroph, mesophile and thermophile?

A

Psychrophile → microbes that grow best at low temps (optimum 10-15C)
Psychotroph → able to grow at low temps, but prefer moderate (optimum 15-30C)
Mesophile → most bacteria (optimum 30-40C)
Thermophile → optimum 45-70C

(phile = loves)

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8
Q

Are bacterial growth curves symmetrical?

A

No → steady increase to optimum then crash after

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9
Q

What is the acclimation phase in cold shock?

A

A downshift in temp causes inhibition of most protein synthesis - has to produce new machinery (ribosomes)
→ causes a growth lag - acclimation phase
→ a group of cold shock proteins (Csp) are dramatically induced - essential for cell growth to resume at the low temp

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10
Q

What are E. coli cold shock proteins?

A

Involved in ensuring ribosome function and DNA/RNA synthesis

Class I → >10-fold induction
→ e.g. CspA family: CspA RNA chaperones, CspB/CspC RNA&DNA chaperone, RNP ribonuclease
Class II → <10-fold induction
→ e.g. RecA: recombination factor, H-NS: nucleoid-assocaited DNA-binding protein

→ conditioning ribosome for cold temps.

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11
Q

What is Listeria?

A

Non-spore forming Gram +ve bacilli
→ causes listeriosis
→ serious for pregnant women and immunocompromised people
→ widespread in environment, vegetation, water4, soil, wild/domestic animals, fish

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12
Q

What is unique about Listeria bacterial growth?

A

Capable of growth over a wide range of temperatures (4-40C)
→ e.g. can survive in fridge

→ can be spread through contaminated food: meats, unpasteurised milk, vegetables (coleslaw) - foods that require no further heat treatment

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13
Q

What virulence factors of Listeria is involved in the invasion of mammalian cells?

A

Internalin A and B

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14
Q

What virulence factors of Listeria are required for its escape from membrane vacuole?

A

LLO (listeriolysin) → pore-forming cytotoxin punches holes in membrane - surrounded by vacuole upon entry so must degrade

PI-PLC (PlcA) → an enzyme that removes charged head groups from phospholipids

double membrane vacuole:
PC-PLC (PlcB) → a phospholipase that cleaves the head group from many kinds of lipids

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15
Q

What virulence factors of Listeria are required for movement through the cytoplasm (cell-cell spread)?

A

ActA → stimulates host cell actin polymerisation (in wrong place ie. surface of bacterium), actin tail forms and propels bacterium through cytoplasm
→ causes projections from the host cell enter adjacent cells

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16
Q

How are Listeria virulence factors regulated?

A

PrfA → positive regulator of virulence genes
→ may repose to temp
→ DNA binding protein

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17
Q

How is Listeria controlled in food?

A

Can grow and multiply at normal refrigeration temps, freezing, and relatively high cooking temps - also can grow in other food preservatives

→ controlled by: heating at 70C for 2 mins, avoiding unpasteurised milk, avoid coleslaw and deli meats, cook meat thoroughly and reheat after refrigeration

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18
Q

What is Legionella pneumophila?

A

Motile, aerobic Gram -ve rod
→ cause Legionnaire’s disease - a form of bacterial pneumonia
→ normal environment: biofilm (in air con) or inside protozoa - humans accidental host

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19
Q

How does pH affect growth rate?

A

Growth rate curve symmetrical around the optimum pH

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20
Q

What are the terms used in relation to pH and growth?

A

Acidophiles → grow at an optimum below neutrality (>7pH)
Neutrophiles → grow best at neutral pH
Alkaliphiles → grow best under alkali conditions

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21
Q

What is an obligate acidophile?

A

Require a low pH for growth
→ their membranes dissolve and cells lyse at neutrality
→ several genera of archaea

22
Q

What are obligate alkaliphiles?

A

Can grow around pH 10
→ Na+ gradient (instead of pmf = proton motive force = pH gradient and electrochemical gradient) supplies the energy

23
Q

What does the intracellular pH for most organisms need to be?

A

Intracellular pH mostly needs to stay around neutrality
→ to prevent destruction of acid or alkali labile macromolecules

anomalies: extreme acidophiles and alkaliphiles
→ their internal pH can very by several units from neutrality

24
Q

What are the problems posed by acidic conditions?

A

3 major aspects of cell function cane affected by acidic conditions
1. the capacity for nutrient acquisition and energy generation
2. cytoplasmic pH homeostasis
3. protection of proteins and DNA → critical for cell survival

25
Q

How can proteins and DNA be protected in acidic conditions?

A

Chaperone proteins and alkalisation of the periplasm

(periplasm in Gram -ve cell walls, between outer and cytoplasmic membrane)

26
Q

What is Helicobacter pylori?

A

Gram -ve curved rod, highly motile 4-7 polar flagella
Cause gastric and duodenal ulcers (associated with development of gastric cancer)
Reservoir: lining of the stomach
Main virulence factors: flagella, urease, adhesions,

27
Q

How do we know Helicobacter pylori causes ulcers?

A

Known to be associated but there was no animal model so couldn’t follow usual method to confirm Koch’s postulates
→ Barry Marshall drank culture of H. pylori - 2 weeks later had inflamed stomach

28
Q

How does H. pylori survive in the acidic pH of the stomach?

A

Organism doesn’t colonies the lumen but the mucin layer that covers the stomach
→ mucus resists diffusion of protons from stomach acid due to -ve sulphated polysaccharides

However must reach the mucin layer so needs:
→ motility
→ short term pH protection using enzyme urease

29
Q

What does the enzyme urease do?

A

Urease takes up urea (waste product) and hydrolyses it producing ammonia and CO2
→ ammonia neutralises stomach acid in its immediate vicinity
→ urease is intraceullular so exports ammonia to periplasm where pH can rise ~ pH 6

30
Q

How does Helicobacter pylori give rise to ulcers?

A

Uses urease to protect it from stomach acid during transit
→ colonises mucin layer

Products provoke inflammatory response that ultimately damage the mucosa

BabA: adhesin that recognises Lewis b antigen which binds sulphated mucin sugars on epithelial cells
NAP: neutrophil activation protein - activates neutrophils, leads to inflammation
VacA: vacuolating cytotoxin - produces large vacuoles in mammalian cells

31
Q

What is Salmonella typhimurium?

A

Characteristics: Gram-negative rod, motile
Disease: gastroenteritis, diarrhoea
Reservoir: human carriers, livestock animals, reptiles
Transmission: contaminated food
Main virulence factors: acid tolerance response, adhesins, invasion of mucosal cells, type III secretion system
Prevention: proper food handling
Treatment: antibiotics

32
Q

What is the Salmonella typhimurium acid tolerance response?

A

Allows S. typhimurium to survive in the acid environment of the stomach

Rapid exposure to low pH → rapid die-off

More gradual exposure to low pH (i.e. adapted to pH6 first) → cells can survive down to pH 3

33
Q

What cells regulate acid shock proteins?

A

Fur = the regulator of iron acquisition genes
→ Fur senses pH and iron separately
→ iron is an essential micro-nutrient

34
Q

How can pH tolerance in Gram + bacteria affect human health?

A

mutans Streptococci → causes dental caries - organisms produce acid and can survive at low pH

Listeria → causes listeriosis - drop in pH activates haemolysin permitting its escape from the phagosome, capable of surviving acid stress in food like cottage cheese, yoghurts and orange juice

Rhodococcus equi → causes broncopneumonia in horses - encounters low pH in alveolar macrophages - acid resistant

35
Q

What are the mechanisms of acid resistance in Gram positive bacteria?

A

Proton pumps → F1F2-ATP ases, GAD
Protein/DNA repair → some chaperones
Regulators → e.g. several 2 component systems (sensor + response) in Listeria
Altered metabolism → e.g. a quorum sensing system & biofilm - acid tolerance in S. mutans
Envelope alterations → e.g. S. mutans increased levels of mono-saturated and longer chain fatty acids at pH5 than pH7
Production of alkali → e.g. urease production (increased pH)

36
Q

What are obligate aerobes and anaerobes?

A

Aerobes: require O2 for growth
→ they use O2 as a final electron acceptor in aerobic respiration

Anaerobes: don’t need O2 as a nutrients (O2 is toxic - kills or inhibits growth)
→ may live by fermentation, aerobic respiration, bacterial photosynthesis or methanogensis

37
Q

What are facultative anaerobes?

A

Organisms that can switch between aerobic and anaerobic metabolism
→ no O2 - fermentation, anaerobic respiration
→ O2 - aerobic respiration

38
Q

What are aerotolerant anaerobes?

A

Bacteria with an exclusively anaerobic (fermentative) type of metabolism but are insensitive to presence of O2
→ live by fermentation alone whether of not O2 is present

39
Q

How do flavoproteins react with O2?

A

Oxidation of flavoproteins results in the formation of H2O2 (peroxide) and small quantities of O2- superoxide (an even more toxic free radical)
→ ROS can damage cells - will kill the cell if nothing is done about them

40
Q

How is the potential for lethal accumulation of superoxide prevented in aerobes?

A

The enzyme superoxide dismutase
→ all organisms which can live in the presence of O2 contain superoxide dismutase

41
Q

How is peroxide decomposed?

A

By the enzyme catalase
→ certain aerotolerant bacteria lack catalase so they use peroxidase enzymes (derive e- from NADH2 producing water)

42
Q

Why do obligate anaerobes undergo lethal oxidations by various oxygen radicals when exposed to O2?

A

They lack superoxide dismutase and catalase
→ can’t protect against ROS

43
Q

What is the action of superoxide dismutase, catalase and peroxidase?

A

Detoxify oxygen radicals

Superoxide dismutase: [O₂-] + [O₂-] (+2H+) → O₂ + H₂O₂

Peroxidase: H₂O₂ + O₂ (+ NADH + H+ → NAD+) → 2H₂O

Catalase: 2H₂O₂ → 2H₂O + O₂

44
Q

How does Clostridium spp. obtain ATP?

A

Substrate-level phosphorylation
→ most lack respiratory chain cytochromes, catalase, peroxidase and superoxide dismutase

45
Q

What is Clostridium botulinum?

A

Commonly found in soil samples and aquatic sediments
→ causative agent of botulinum food poisoning
→ releases exotoxin bolutlinum - extremely potent + can form spores
→ poorly canned foods create anaerobic environment - unskilled spores germinate and produce toxin

46
Q

What is botulism?

A

Result of ingesting bacterially produced neurotoxins
→ the toxins block the release of neurotransmitter acetylcholine
→ resulting in double vision, slurred speech, decreased saliva, general weakness
→ paralysis with accompanying respiratory failure can be fatal

47
Q

What are the types of exotoxin produced by Clostridium botulinum?

A

7 - A, B, C1, D, E, F, G
→ A, B, E, and F are the most toxic to humans (often released in inactive form, proteolytic cleavage activates them)
→ A is the most potent exotoxin known

48
Q

What is the mode of action of botulinum toxin?

A

Botulinum toxin has heavy chain (HC) and light chain (LC)
→ HC binds toxin to the presynaptic receptor - toxin enters the cell
→ disulphide bond cleaved - liberates the LC into cytoplasm and endosomal compartment
→ cleaves the SNARE proteins (involved in vesicle docking)
→ prevents fusion of acetylcholine vesicles at the cell membrane

Prevents the release of Act → no stimulus → can’t contract → flaccid paralysis

49
Q

What is Clostridium tetani?

A

Causative agent of tetanus (lockjaw)
→ result of trauma/puncture wound leading to tissue contamination
→ caused by release of single antigenic type endotoxin by C. tetani - circulates in blood and adheres to neuronal receptors
→ fixes to gangliosides - blocking release of the neurotransmitters glycine and y-amino butyric acid (GABA)
→ muscles permanently contracted

50
Q

How does the tetanus toxin work?

A

Tetanus toxin made up of a heavy chain (HC) required for cell entry and a light chain (LC) which causes disease
→ C-terminal domain of the HC binds to gangliosides, N-terminal domain allows LC to cross into cell cytoplasm
→ LC interrupts the release of neurotransmitters
→ cleaves SNARE proteins - GABA and glycine containing vesicles can’t dock thus no neurotransmitter released

Glycine usually induces muscle relaxation - constant release of Act - muscles permanently contracted

51
Q

How are hosts affected by Clostridium tetani?

A

Toxin causes tetanus
→ host usually dies from respiratory paralysis

heroin addicts are particularly susceptible

52
Q

What is Clostridium difficile?

A

Gram positive, obligately anaerobic, spore forming

Antibiotic use reduces normal microbiota → C. diff overgrows produces toxins A and B
→ A and B - large exotoxins that modify host cell membrane G proteins

Toxins cause: diarrhoea and lesions on colon surface
→ coalesce forming tissue damage - pseudomembranous colitis
→ can be rapidly fatal

Microbial Pathogens (6 decks)

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