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B2: microbiology > Microbiology 3: bacteria > Flashcards

Microbiology 3: bacteria Flashcards

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Biology 101 flashcards
1
Q

structural difference in organisation of cell contents between bacteria and eukaryotic cells

A

Bacteria do not have organelles (different to eukaryotes)

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2
Q

Outline the location of DNA in bacteria

A

hey just have their genetic material and ribosomes floating in the cytoplasm, as well as a cell wall

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3
Q

What kind of appendages coul dbacteria have? Does this affec virulence

A

Hypha/stalks Yes may do

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4
Q

Normal 3 tpes of naceria

A

Cocci, bacilli, spiral

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5
Q

List the common virulence features for bacteria

A

Diverse secretion systems, Flagella (movement, attachment), Pili (important adherence factors), Capsule (protect against phagocytosis) i.e. Streptococcus pneumoniae ,Endospores (metabolically dormant forms of bacteria) heat, cold, desiccation and chemical resistant i.e. Bacillus sp. and Clostridium sp. Biofilms Exotoxin Endotoxin

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6
Q

How does flagella and pili contribute to virulence

A

Flagella (movement, attachment) Pili (important adherence factors)

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7
Q

How does capsule contribute to virulence Example

A

Capsule (protect against phagocytosis) i.e. Streptococcus pneumoniae

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8
Q

How does endospores contribute to virulence Examle

A

Endospores (metabolically dormant forms of bacteria) heat, cold, desiccation and chemical resistant i.e. Bacillus sp. and Clostridium sp.

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9
Q

How does biofilms contribute to virulence. Examples

A

(organized agregrates of bacteria embedded in polysaccahride matricesi. e. Pseudomonas aeruginosa i.e. Staphylococcus epidermidis

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10
Q

3 types of exotoxin

A

Neurotoxin Enterotoxin Tissue invasive exotoxin Miscellaneous exotoxin Pyrogenic exotoxin

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11
Q

Outline neurotoxin wiht examples

A

act on nerves or motor endplate i.e. Tetanus or Botulinum toxins

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12
Q

Outline 2 types of enterotoxin withexamples

A
  1. Infectious diarrhea Vibrio cholera, Escherichia coli, Shigella dysenteriae and Campylobacter jejuni 2. Food poisoning Bacillus cereus or Staphylcoccus aureus

THEY ACT ON THE GI TRACT

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13
Q

Outline pyrogenic exotoxins

A

Stimulate cytokine release Staphylcoccus aureus or Streptococcus pyogenes

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14
Q

Outline Tissue invasive exotoxin

A

allow bacteria to destroy and tunnel through tissue i.e. Staphylococcus aureus, Streptococcus pyogenes Clostridium perfringens

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15
Q

Which enzymes might tissue invasive exotoxin involve

A

enzymes that destroy DNA, collagin, fibrin, NAD, red or white blood cells

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16
Q

Examples of miscellaneous exotoxin, and what is different about them

A

specific to a certain bacterium and/or function not well understood Bacillus anthracis and Corynebacterium diphtheriae

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17
Q

What is endotoxin released by

A

Only produced by Gram-negative bacteria

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18
Q

What is endotoxin

A

Not a protein but it’s the the lipid A moiety of LPS

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19
Q

Differentiate gram positive and gram negative

A

Gram +ve= big cell wall, 1 lipid bilayer Gram -ve= small cell wall, 2 lipid bilayers

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20
Q

What is seen on the lipid bilayer of

A

On the lipid bilayer of gram negative bacteria, we see LPS and sugars – these are endotoxins

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21
Q

What can happen if lots of the LPS is shed

A

Then it can cause endotoxic shock Normally shed in steady amounts

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22
Q

Why can giving antibiotics to gram neg bacteria be dangerous

A

when bacteria lyse they release large quantities of LPS/ Endotoxin Leads to septic shock

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23
Q

Define septic shock

A

Sepsis that results in dangerous drops in blood pressure and organ dysfunction is called septic shock. It is also referred to as endotoxin shock because endotoxin often triggers the immune response that results in sepsis and shock.

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24
Q

Differentiate endotoxin shock and septic shock

A

different effectors molecules in Gram-positive bacteria or even fungi can trigger this adverse immune response – so the term septic shock is inclusive (of endotoxin shock and other shocks too)

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25
Q

What is haemolytic-uraemic syndrome

A

triad of acute renal failure, hemolytic anemia and thrombocytopenia

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26
Q

What usually causes haemolytic-uraemic syndrome

A

Shiga toxin producing E. coli strain

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27
Q

Define outbreak

A

An outbreak is a greater-than-normal or greater-than-expected number of individuals infected or diagnosed with a particular infection in a given period of time, or a particular place, or both.

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28
Q

What are E.coli strains which release shiga toxin known as

A

EHEC enterohemorrhagic E. coli

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29
Q

Reservoirs for EHEC

A

reservoir are normally ruminants – mostly cattle

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30
Q

When does human infection with EHEC often occur

A

occurs through the inadvertent ingestion of fecal matter and secondary through contact with infected humans

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31
Q

Who does HUS affect more

A

usually the hemolytic-uremic syndrome is very rare in adults

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32
Q

What can be done with genetics in an outbreak

A

You can sequence the gene in the bacteria to find the virulent genes You can then do PCR on people to confirm this e.g on stool samples

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33
Q

Give an example of how bacteriophage transfer can cause increased virulence

A

E.g. EHEC contains shiga toxin causing HUS enteroaggregative E. coli (EAEC) contains 2 plasmids Baceriophage can infect the EHEC and transfer the shiga toxin genetic info to the EAEC

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34
Q

What 2 plasmids are contained in EAEC

A

pAA-type plasmids - contains the aggregative adhesion fimbrial operon ESBL plasmid - harbors the genes encoding for extended-spectrum b-lactamases (i.e. beta lactam resistant)

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35
Q

What is the result of transfer of EHEC to EAEC

A

EAHEC Now the bacteria which was aggregating and beta-lactam resistant (EAEC) also contains a shiga toxin

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36
Q

Composition of shiga toxin

A

have an AB5 subunit composition Subunit a (StxA) is non-covalently associated with a pentamer of protein B (StxB).

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37
Q

What is the function of subunit A and the B subunits in shiga toxin

A

StxA is enzymatically active domain. StxB pentamer is responsible for binding to host cell receptors.

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38
Q

Mechanism of subunit A action

A

enzyme that cleaves the 28S ribosomal RNA in eukaryotic cells ,,, inhbits protein synthesis

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39
Q

Why can a shiga toxin bacteria infection affect gut microbiota

A

Bacterial ribosomes are also a substrate for StxA and this will result in decreased proliferation of susceptible bacteria might affect the commensal microflora in the gut

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40
Q

Why is shiga toxin a mobile genetic element

A

Shiga toxins are encoded on a bacteriophage highly mobile genetic elements and contributes to horizontal gene transfer Toxins are highly expressed when the lytic cycle of the phage is activated (so that the gene can be taken up by lots of E coli)

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41
Q

When are shiga toxins highly expressed

A

Toxins are highly expressed when the lytic cycle of the phage is activated (so that the gene can be taken up by lots of E coli)

42
Q

Where is EHEC and EAEC found in the GI

A

EHEC= large bowel EAEC= large bowel and small bowel (the new virulence of the EAHEC may have been because there was now shiga toxin in the small bowel because of shiga in EAEC)

43
Q

Where is aggregative adherence fimbriae (AAF) located

A

genes encoding for AAF are on a plasmid mobilized between strains

44
Q

Funciton of AAF

A

Allows binding to enterocytes AND allows binding to eachother to make biofim

45
Q

What is the impact of AAF bunding to enterocytes with regard to human immune response

A

AAF stimulate a strong IL-8 response

46
Q

What happens to the cell when AFF binds

A

Lead to the disruption of actin cytoskeleton leading to exfoliations

47
Q

Communicable diseases occurring in Europe

A

1) Respiratory tract infections 2) Sexually transmitted infections, including HIV and blood-borne viruses 3) Food- and waterborne diseases and zoonoses 4) Emerging and vector-borne diseases 5) Vaccine-preventable diseases 6) Antimicrobial resistance and healthcare-associated infections

48
Q

Give example of BACTERIAL resp tract infections

A

Legionnaires’ disease (legionellosis) Legionella pneumophila (Gram -) Tuberculosis Mycobacterium tuberculosis (Gram +)

49
Q

What type of bacteria are TB and legionella pneumophilia

A

TB=gram +ve Legionella=gram -ve

50
Q

Where is legionella pneumophilia commonly found and what is the route of infection

A

 Lives in amoeba in ponds, lakes, air conditioning units  Infection route: inhalation of contaminated aerosols

51
Q

What cells are affected in humans by legionella pneumophilia

A

 In humans L. pneumophila will infect and grow in alveolar macrophages  Human infection is “dead end” for bacteria – the bacteria can’t survive here on

52
Q

What virulence factor is involved in L pneumophilia

A

Type IV secretion system There is a large protein spanning the 2 cell membranes and cell wall allows the bacteria to secrete effector proteins inside to out They are able to survive and replicate in macrophage vacuoles, because it can release special virulence factors due to the type IV system, and

53
Q

Why is TB difficult to treat

A

Because it is grouped with gram +ve bacteria, but it has a very different cell wall Lots of lipids attached to the cell wall

54
Q

What is latent TB

A

M. tuberculosis can enter a dormant state Latent TB - evidence of infection by immunological tests but no clinical signs and symptoms of active disease

55
Q

What is the treatment for TB

A

with antibiotics BUT TAKES at least 6 months

56
Q

Success rate of treatments for TB

A

72% success rate of treatment of new cases Treatment success rate for second infection is 54% Multi drug resistant (MDR) treatment success rate in is 32%

57
Q

List common bacterial STI

A

Chlamydia trachomatis infection Gonorrhoea Syphilis

58
Q

What bugs cause gonorrhoea and syphilis

A

(Neisseria gonorrhoeae) and (Treponema pallidum) for syph

59
Q

What type of bacteria is each of Chlamydia trachomatis Neisseria gonorrhoeae Treponema pallidum

A

Gram neg

60
Q

Outline the replication of Chlamydia trachomatis

A

Obligate intracellular pathogen Cannot culture outside of cell

61
Q

What is most common STI in europe

A

Chlamydia

62
Q

What other disease can Chlamydia trachomatis cause

A

Other parts of the world –> Eye infection Blindness

63
Q

What is the structure of Neisseria gonorrhoeae

A

Diplococcus (pairs of cocci, can remember as looks like two balls and gonorhea is an STI……)

64
Q

What cells does N gonorrhoeae interact with

A

Establishes infection in the urogenital tract by interacting with non-ciliated epithelical cells

65
Q

What is the important virulence of N gonorrhoeae

A

pili and antigenic variation escape detection and clearance by the immune system

66
Q

Most common food- and waterborne diseases

A

Campylobacteriosis (Campylobacter sp. mostely C. jejuni) Salmonellosis (- Salmonella sp.) Cholera (Vibrio cholerae) Listeriosis (Listeria monocytogenes)

67
Q

T/f shigella releases shiga toxin

A

Can do! Shigella dysenteriae

68
Q

T/F campylobacter sp. (mainly C jejuni) is usually a cause of epidemics What is the highest risk group

A

F Usually sporadic cases and not outbreaks Small children 0-4 years – highest risk group

69
Q

How can you acquire a Campylobacter sp. mostly C. jejuni infectin

A

Infection most likely through undercooked poultry

70
Q

Virulence factor of Campylobacter sp. mostly C. jejuni

A

Adhesion and Invasion factors, Flagella motility, Type IV Secretion system, Toxin

71
Q

T/f salmonella sp. is associated with outbreaks

A

T

72
Q

Where can salmonella sp. be acquired What is main risk group

A

Undercooked poltry Highest infection rate in small children (0-4 years)

73
Q

What is the virulence associated with salmonella sp

A

Type III secretion systems encoded on pathogenicity islands (SPI)

74
Q

Outline type III secretion system with the bug using it

A

Salmonella sp. uses it I think this is the injectisome, can inject proteins into the cell SPI1: is required for invasion SPI2: intracellular accumulation

75
Q

What disease does vibrio cholera cause

A

Cholera is an acute, severe diarrheal disease Without prompt rehydration, death can occur within hours of the onset of symptoms

76
Q

Important virulence factor with vibrio cholerae

A

type IV fimbria cholera toxin carried on a phages

77
Q

How did cholera acquire cholera toxin

A

It was infected with a first bacteriophage which gave it a gene to code for a receptor (type IV fimbria) The type IV fibria then allowed binding of a second bacteriophage The second bacteriopage gave the gene for the cholera toxin

78
Q

How does the cholera toxin work

A

Binds to enterocyte Through b pentamer to the GM1 ganglioside receptor on enterocyte A/B cholera toxins cleves A1 domain from A2 domain, activating A1. A1 faragment enters cytosol, activates Gsa, continually stimulating AC to produce cAMP. High cAMP activates CFTR… efflux of ions (esp chloride) and water from infected enterocytes Leads to diarrhoea

79
Q

How can cholera toxin be treated

A

Enkephalins bind to the opioid receptors on enterocytes, which act through G proteins to inhibit the stimulation of cAMP synthesis induced by cholera toxin, thereby directly controlling ion transport

80
Q

Risk group for listeria monocytogenes

A

Risk group immuno-compromised, elderly, pregnant and their fetus

81
Q

How does listeria infect

A

Listeria can enter non-phagocytic cells and cross three tight barriers Intestinal barrier, Blood / brain barrier and Materno / fetal barrier

82
Q

What is special about listeria

A

Can infect cell to cell without exiting and then re-entering It polyermises actin using profilin *see tutorial* Important for immunology and for research

83
Q

What are the bacterial emerging and vector borne diseases and hat are they caused by

A

Plague (Yersinia pestis; Gram-) Q fever (Coxiella burnetti; Gram –)

84
Q

Which vaccine preventable diseases are bacteria

A

Invasive Haemophilus influenzae disease Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus

85
Q

What are these vaccine preventable disease cause by and what gram type: Invasive Haemophilus influenzae disease Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus

A

Haemophilus influenzae (-ve) Clostridium diphtheriae (Gram +) Neisseria meningitidis (gram -ve) Streptococcus pneumoniae Gram + (Bordetella pertussis Gram -) (Clostridium tetani Gram +)

86
Q

Define Antimicrobial Antibacterial Antibiotic

A

Antimicrobial interferes with growth & reproduction of a ‘microbe’ Antibacterial commonly used to describe agents to reduce or eliminate harmful bacteria Antibiotic is a type of antimicrobial used as medicine for humans, animals originally referred to naturally occurring compounds

87
Q

What are the most frequent types of HAI

A

surgical site infections, urinary tract infections, pneumonia, bloodstream infections and gastrointestinal infections.

88
Q

What about a hospital can cause infection

A

Interventions Dissemination Concentration

89
Q

Outline intervention as a hospital source of infection

A

LINES (iv, central, arterial, CVP) CHEMO CATHETERS INTUBATIN PROSTHETICS Prophylactic antibiotics Inappropriate prescribing

90
Q

Outline dissemination for Hospitals as a source of infection

A

hospital personnel can spread infection from one patient to another

91
Q

Outline concentation for Hospitals as a source of infection

A

there are more people with infection in the environment, increasing risk

92
Q

Which pathogens ar ea major problem in hospitals Gram neg or pos

A

Enterococcus faecium (+ve) Staphylococcus aureus (+ve) Clostridium difficle (+ve) Acinetobacter baumanii (-ve_ Pseudomonas aeruginosa (-ve) Enterobacteriaceae (-ve)

93
Q

Give examples of Enterobacteriaceae

A

E.coli, Klebsiella pneumoniae, Enterobacter sp.

94
Q

State the drug resistance of the following Enterococcus faecium (+ve) Staphylococcus aureus (+ve) Clostridium difficle (+ve) Acinetobacter baumanii (-ve_ Pseudomonas aeruginosa (-ve) Enterobacteriaceae (-ve): -E.coli, Klebsiella pneumoniae, Enterobacter sp.

A

Enterococcus faecium (vancomycin resistance) Staphylococcus aureus (methicillin resistant - MRSA) Clostridium difficile (can establish infection because of previous antibiotic treatment) Acinetobacter baumanii (highly drug resistant) Pseudomonas aeruginosa (multi drug resistant i.e fluoroquinolone-resistant) Enterobacteriaceae pathogenic E. coli (multi drug resistant) Klebsiella pneumoniae (multi drug resistant) Enterobacter species (multi drug resistant)

95
Q

What happens as more bacteria become drug resistant

A

Clinicians are forced to use older, previously discarded drugs, such as colistin, that are associated with significant toxicity and for which there is a lack of robust data to guide selection of dosage regimen or duration of therapy

96
Q

Outline pathogenic e. coli

A

Most frequent cause of bacteraemia by a Gram-negative bacterium Most frequent cause of community and hospital acquired UTI

97
Q

What is the main problem with the escape pathogens?

A

They are antibiotic resistant

98
Q

Which antibiotics is E. coli resistant to in many countries?

A

Cephalosporins

99
Q

Which antibiotics is E. coli still sensitive to?

A

Carbapenems

100
Q

State the target proteins and the method of resistance to the following classes of antibiotics:

a. Cephalosporins
b. Carbapenems
c. Methicillin
d. Vancomycin

A

a. Cephalosporins
Target: Penicillin binding proteins (PBP)
Resistance: Extended-Spectrum Beta-Lactamase (ESBL)
b. Carbapenems
Target: PBP
Resistance: Carbapenemase enzymes
c. Methicillin
Target: PBP
Resistance: alternative target (PBP2A), which has low affinity for methicillin and can function in its presence
d. Vancomycin
Target: peptidoglycan precursor
Resistance: synthesis of a different peptidoglycan precursor

B2: microbiology (35 decks)

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