INF1 - E. BACTERIA AND PATHOGENICITY-COVERED Flashcards

1
Q

what are prokaryotes

A
  • no defined nucleus
  • smaller (<1-2 microns)
  • bacteria
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2
Q

what are eukaryotes

A
  • defined nucleus a
  • bigger (10-100+ microns)
  • animals, plants, fungi, protozoa, algae
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3
Q

what is unique to bacterial cells compared to ours

A

peptidoglycan cell wall

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4
Q

what is peptidoglycan made of

A
  • N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) pentapeptide (glycan monomer)
  • D-alanine in postions 4 and 5
  • additional pentaglycine sequence in some gram-+ve bacteria - attached to lysine at position 3
  • glycan monomers transported across cytoplasmic by bacteoprenol
  • monomers joined through glycosidic bonds by glycerotransferases to make polymer chains
  • polymer chains cross linked through peptide bonds between third positions on one polymer and D-alanine of another chain by transpeptidases
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5
Q

describe the gram-positive cell wall

A
  • 80-90% peptidoglycan
  • gram stain dyes cell blue/purple
  • teichoic acid embedded in wall which facilitates movement in to and out of bacterium (can stimulate inflammatory response)
  • proteins embedded in the wall: adhesins help with adhesion to host cells and surfaces
  • enzymes aid nutrient acquisition and can damage host cells and tissue
  • permeable to most antibiotics some species sporulate (bacilli)
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6
Q

examples of gram-positive bacteria

A
  • Staphylococcus aureus
  • Streptococcus pyogenes
  • Streptococcus pneumoniae
  • Clostridium difficile
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7
Q

describe the gram-negative wall

A
  • 10-20% peptidoglycan
  • gram dye stains cell pink
  • has an outer membrane which is linked to peptidoglycan by lipoprotein anchor
  • rich in lipopolysaccharide (endotoxin) which allows entry of molecules into cell (can stimulate strong inflammatory response)
  • proteins like enzymes and adhesions
  • impermeable to many antibiotics
  • no sporulating bacteria
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8
Q

examples of gram-negative bacteria

A
  • Escherichia coli
  • Salmonella enterica
  • Campylobacter jejuni
  • Vibrio cholera
  • Heliobacter pylori
  • Chlamydia trachomatis
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9
Q

what does lipopolysaccharide consist of

A

lipid A
core region oligosaccharide and other molecules
O-polysaccharide tail (O antigen)

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10
Q

describe the acid-fast cell wall (mycobacterium tuberculosis)

A
  • mostly made of mycolic acid (glycolipid) - Ziel-Neelson stain (red)
  • small amount of peptidoglycan
  • mycolic acids impede entry of molecules so slow growing bacteria but greater resistance to chemical agents and enzymes
  • this is why you need antibiotics for months due to hard access across cell wall
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11
Q

differences between prokaryotic and eukaryotic cells

A
  • fimbriae and pili in prokaryotic cells
  • capsules and slime layers in some bacteria
    (form biofilms: collection of micro-organisms surrounded by the slime they secrete and attached to an inert or living surface and hence antimicrobials can’t penetrate)
  • flagella in some bacteria
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12
Q

what are endospores

A
  • formed by some gram+ve bacteria due to ‘starvation’ or adverse environment, can cause infection
  • exist in state of dormancy, can persist for long periods
  • highly resistant to extreme of temp, pH, desiccation, radiation, chemical agents (ie - antibiotics, disinfectants)
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13
Q

what is the microbiome

A
  • bacteria in/on our body which don’t cause damage and can be beneficial or protective
  • unique in everyone
  • low virulence bacteria ie, low risk of causing disease
  • reduce risk of colonisation by pathogenic bacteria
  • disrupted by overuse/inappropriate use of antibiotics (we need antibiotic stewardship)
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14
Q

what is an infection

A
  • any microorganism or toxin (ie produced by bacteria and contaminating foodstuff) capable of entering human body and causing harm
  • via initial interaction/invasion of epithelial tissue (skin, eye, internal mucosa of airways, gut, genitourinary)
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15
Q

what is bacteraemia

A

presence of bacteria in blood

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16
Q

what is sepsis

A

systemic infection
host immune response to bacteria wall (LPS/teichoic acid)

17
Q

what is a disease

A

recognisable systems/illness often with defined damage of injury to host tissues

18
Q

what is pathogenicity

A

ability to cause disease

19
Q

what are pathogenicity/virulence factors

A

features that enable attachment, colonisation, tissue invasion, production of toxins or enzymes etc

20
Q

examples of pathogenicity factors

A

Enzymes
Adherence - pili/fimbriae, M protein, lipoteichoic acids
Toxins - exotoxins and endotoxins (released by damaged bacteria)
Resistance to antibiotics - prevent entry, degradation, modification/increased expression, efflux
Invasion of sterile body sites - invasions, enzymes, toxins or opportunistic wounds
Circulation - systemic infection, spread through host
Evasion of immune responses - capsule, enzymes, toxins

21
Q

what is virulence

A

measure of ability to cause disease

22
Q

what is infectiousness

A

ease of spread in a population, linked to pathogenicity and virulence

23
Q

what is intoxication/food poisoning

A

ingestion of bacterial-derived toxin or in absence of infection (toxin contaminating food)

24
Q

what do bacteria need apart from ability to cause infection

A

opportunity
- can minimise this by hygiene, social distancing, wound care, PPE etc

25
Q

what is epidemiology

A

monitoring and studying of incidence disease eg - tracing and controlling epidemics etc

26
Q

what are exotoxins

A
  • made by the bacteria and excreted (true toxins as actively made by bacteria)
  • produce local/systemic actions and symptoms
  • pyogenic effects (local)
  • pyrogenic effects (local but can spread)
  • emesis/diarrhoea (food poisoning)
27
Q

what are the different types of exotoxins

A
  • cytolytic toxins (damage cell membranes)
  • A-B toxins (disrupt protein synthesis or intracellular signalling)
  • ‘superantigen’ toxins (non-specific activation of our immune system)
28
Q

what happens when bacteria secretes collagenase

A

breaks up collagen which holds our cells and tissues together

29
Q

what happens when bacteria secretes streptokinase

A

breaks up blood clots

30
Q

what are endotoxins

A
  • not true toxins, parts of the bacterial cell wall that induce a toxic response
  • accidental toxins
  • cause immune system to become over-activated, resulting in excessive production of cytokines so get symptoms of inflammation and fever
  • LPS can get into bloodstream (sepsis)
  • teichoic acids produce similar response as LPS
31
Q

how do bacterial infections arise

A
  • invasion of wound (Staphylococcus aureus - boils)
  • antibiotic therapy as disrupt natural flora (Clostridium difficile - HCAI)
  • nosocomial infections
  • latrogenic infections
    (wounds, catheters, antibiotics, asymptomatic carriers, poor disinfection policies)
32
Q

examples of bacteria associated with hospital-acquired infections

A
  • MRSA
  • Clostridium difficile (GI infection, spore-forming)
  • Streptococcus pneumoniae (intubation/air support)
  • Acinetobacter baumannii (wound infections)
33
Q

examples of bacteria which cause GI infections by faecal-oral route due to poor hygiene standards

A
  • Escherichia coli
  • Campylobacter and salmonella (chicken is source)
  • Vibrio cholera (water - sewage)
34
Q

examples of bacteria which cause person-person infections

A
  • Neisseria meningitidis (bacterial meningitis)
  • Staphylococcus aureus
  • Streptococcus pyogenes
  • Mycobacterium tuberculosis
  • Chlamydia trachomatis
  • Neisseria gonorrhoeae
35
Q

examples of environmental bacteria which cause infections

A
  • Clostridium tetani (muscle cramps - lives in soil)
  • Legionella (pneumonia - failure to maintain air conditioning units)
36
Q

what are biofilms

A
  • collection of microorganisms surrounded by the slime they secrete, attached to an inert or living surface
  • ie: plaque on teeth
  • can exist wherever surfaces contact water (catheters)
  • altered phenotype so resistance to antibiotics