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Microbiology > 3. Community acquired and hospital acquired bacterial infections > Flashcards

3. Community acquired and hospital acquired bacterial infections Flashcards

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Biology 101 flashcards
1
Q

Do bacteria have organelles?

A

No (just genetic material, ribosomes and a cell wall)

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2
Q

What 6 common virulence factors are associated with bacterial infections?

A
  • Diverse secretion systems
  • Flagella (movement and biofilm formation)
  • Pili (important adherence factors)
  • Capsule
  • Endospores (metabolically dormant forms of bacteria - head, cold, etc. resistant)
  • Biofilms (antibiotic resistant, organised aggregates of bacteria embedded in polysaccharide matrix)
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3
Q

What are exotoxins?

A

Proteins produced by bacteria and secreted into the host

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4
Q 
What do the following exotoxins do:
• neurotoxins
• enterotoxins
• pyrogenic exotoxins
• tissue invasive exotoxins
• miscellaneous exotoxins
A
  • Neurotoxins - act on nerves or motor endplate e.g. Botulinum toxins
  • Enterotoxins - act on the GIT e.g. in food poisoning
  • Pyrogenic exotoxins - stimulate release of cytokines
  • Tissue invasive exotoxins - enzymes that destroy DNA, collagen, fibrin, NAD, blood cells, allowing bacteria to tunnel through
  • Miscellaneous exotoxins - specific to a certain bacterium or function not well understood
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5
Q

What are the endotoxins of bacteria?

A
  • Only produced by gram negative bacteria
  • Gram negative = 2 lipid bilayers
  • Endotoxins = LPS and sugars on lipid bilayer (not protein)
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6
Q

Why can treating a person who has a gram negative infection with antibiotics worsen the condition?

A

When they lyse, they release large quantities of LPS/endotoxin => septic shock

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7
Q

What is an outbreak?

A

Greater than normal/expected number of individuals infected or diagnosed with a particular infection in a given period of time, particular place, or both

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8
Q

What is haemolytic-uraemic syndrome and how is it acquired?

A
  • Triad of acute renal failure, haemolytic anaemia and thrombocytopenia
  • Usually found in children and caused by the Shiga toxin producing E. coli strain - EHEC strains (enterohemorrhagic E. coli)
  • Reservoir normally ruminants (mostly cattle)
  • Human infection - inadvertent ingestion of fecal matter and secondary through contact with infected humans
  • Very rare in adults
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9
Q

In 2011, there was an outbreak of E. coli in Germany. How was this detected?

A

PCR
• Isolates screened by multiplex PCR for characteristic features of the outbreak strain
• Done on stool samples
• Outbreak found to be most similar to the EAEC (enteroaggregative) strain
• Main difference was the presence of a prophage encoding the Shiga toxin (characteristic for EHEC)

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10
Q

What are the 2 virulence factors that the EHEC strain had?

A
  • Shiga toxin

* ESBL plamids - genes for extended-spectrum β-lactamases

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11
Q

Did the EAEC strain originally produce the Shiga toxin?

A
  • No, it was acquired

* Shiga toxin was introduced into the EAEC strain through a phage

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12
Q

What is the AB5 subunit of the Shiga toxin family useful for?

A

Helps the toxin bind to eukaryotic cells, so the toxin can be injected

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13
Q

What is StxA (subunit A)?

A

Subunit of Shiga toxin
• Enzyme (active domain) that cleaves the 28S ribosomal RNA in eukaryotic cells
• This inhibits protein synthesis

(Bacterial ribosomes are also a substrate of the StxA
• decreases proliferation of susceptible bacteria
• affects commensal gut microflora)

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14
Q

What is the StxB (subunit B) of the Shiga toxin responsible for?

A

StxB pentamer responsible for binding to host cell receptors

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15
Q

How is StxA and StxB linked together?

A

Non-covalent association

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16
Q

How can Shiga toxin transfer to another strain?

A
  • Shiga toxins are encoded on a bacteriophage
  • Phage enters environment, and infects a closely related strain to produce the toxin
  • Highly mobile genetic elements - contributes to horizontal gene transfer
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17
Q

When which cycle of the phage is activated causing toxins to be highly expressed?

A

Lytic cycle

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18
Q

What does the EAEC and EHEC strain colonise?

A

EAEC - small and large bowels

EHEC - large bowel

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19
Q

What are the virulence factors of EAHEC and which strains are they aquired from?

A
  • pAAF plasmid (fibres that assist with attachment) - EAEC

* Shiga toxin (prophage encoding) and ESBL resistance plasmid - EHEC

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20
Q

What response does aggregative adherence fimbriae (AAF) stimulate and what does it lead to?

A
  • Strong IL-8 response
  • Allows biofilm formation
  • Disruption of actin cytoskeleton
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21
Q

Describe Legionella pneumophila (type, origin, infection route)

A
  • Gram-negative bacterium
  • Lives in amoeba in ponds, lakes and air conditioning units
  • Route: inhalation of contaminated aerosols
  • Infects and grows in alveolar macrophages
  • Human infection is a dead end - bacteria can’t survive and be passed on
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22
Q

What is an important virulence factor for Legionella pneumophila?

A

Type IV secretion system

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23
Q

Can Legionella replicate in a Legionella containing vacuole (LCV)?

A

Yes - macrophages also take up these bacteria and they can replicate in macrophage vacuoles

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24
Q

Describe TB (type, treatment, state)

A
  • Gram-positive, with extra lipid layer
  • This layer and slow replication makes it more difficult to treat
  • Antibiotics needed for at least 6 months
  • TB can enter a dormant state
  • Latent TB: immunological tests can detect this but there are no symptoms
25
Q

What are the 3 main bacterial STIs and what type are they?

A
  • Chlamydia trachomatis
  • Neisseria gonorrhoeae
  • Syphilis (Treponema pallidum)

All gram negative

26
Q

Why can’t Chalmydia be cultured outside its host cells?

A

It is an obligate intracellular pathogen

27
Q

What is the most frequent STI in Europe?

A

Chlamydia

responsible for >3% world’s blindness

28
Q

Where does Gonorrhoeae establish infection and what are important virulence factors and traits?

A

• Urogential tract by interacting with non-ciliated epithelial cells

  • Pili and antigenic variation
  • Escape detection and clearance by the immune system
29
Q

What are 4 common food and waterborne diseases and zoonoses?

A
  • Campylobacteriosis
  • Salmonellosis
  • Cholera
  • Listeriosis
30
Q

What is the most commonly reported infectious GI disease in Europe?

A

Campylobacter SP. (mostly C. jejuni)

31
Q

What is the most likely cause of Campylobacter infection and what are its virulence factors?

A

• Undercooked poultry

  • Adhesion and invasion factors
  • Flagella motility
  • Type IV secretion system
  • Toxins
32
Q

What is the cause of Salmonella, who does it infect the most, and what are its virulence factors?

A
  • Undercooked poultry
  • Small children
  • Type III secretion systems encoded on pathogenicity islands

(Salmonella enterica: Type III secretion system - allows specific proteins to be injected
SPI1: for invasion
SPI2: intracellular accumulation)

33
Q

Are outbreaks of Campylobacter and Salmonella common?

A

Campylobacter - no, sporadic

Salmonella - outbreaks

34
Q

What is a pathogenicity island?

A

Series of genes in a pathogen, including one or more that determines virulence, acquired by horizontal gene transfer

35
Q

What is Vibrio cholerae, how can it kill someone, where was the last outbreak and what are its virulence factors?

A
  • Acute, severe diarrhoeal disease
  • Death within hours of onset of symptoms without prompt rehydration
  • Last outbreak in Haiti
  • Type IV fimbriae
  • Cholera toxin carried on phages
36
Q

Describe the cholera toxin and its effects

A
  • Similar structure to Shiga toxin
  • Makes eukaryotic cells produce high levels of cAMP
  • Activates transporter => chloride efflux
  • Water and sodium also leave the cell as a counter action
  • Results in diarrhoea
37
Q

What is the risk group for Listeria monocytogenes?

A
  • Immunocompromised
  • Elderly
  • Pregnant and their foetus
38
Q

How can you avoid Listeria monocytogenes?

A

Don’t drink unpasteurised milk

39
Q

How does Listeria infect people?

A

• Enters non-phagocytic cells and crosses 3 tight barriers due to motility
- intestinal barrier
- BBB
- materno/foetal barrier
• Can spread from cell to cell without leaving the cell

40
Q

Give 2 examples of emerging and vector-borne bacterial diseases

A
  • Plague - Yersinia pestis (Gram negative)

* Q fever - Coxiella burnetti (Gram negative)

41
Q

What important bacterial diseases have mass vaccinations eliminated?

A

Smallpox and Poliomyelitis

42
Q

What does antimicrobial and antibacterial mean?

A
  • Antimicrobial - interferes with growth and reproduction of a microbe e.g. antibiotics
  • Antibacterial - agents that reduce or eliminate harmful bacteria
43
Q

What are Healthcare-associated infections (HAIs)?

A

Infections that occur after exposure to healthcare (start >48hrs after admission)

e.g. surgical site infections, pneumonia, UTI etc.

44
Q

What 3 factors cause or increase the risk of HAIs?

A
  • Intervention - lines, catheters, chemotherapy, prosthetics etc.
  • Dissemination - hospital personnel spreading infections
  • Concentration - more people with an infection in the environment increase the risk
45
Q

Why are escape pathogens e.g. Clostridium difficile (G+) or Enterobacteriaceae (G-) major problems in hospitals?

A
  • Show drug resistance
  • Forced to use older, previously discarded drugs associated with significant toxicity
  • Lack of robust data to guide selection of dosage regiment or duration
46
Q

Which common bacteria is vancomycin resistant?

A

Enterococcus faecium

47
Q

Which bacteria commonly establishes infection due to previous ABx treatment?

A

Clostridium difficile

48
Q

What does Enterobacteriaceae include?

A
  • Pathogenic E. coli
  • Klebsiella pneumoniae
  • Enterobacter species

All gram negative, and multi-drug resistant

49
Q

What is the most frequent cause of community and hospital acquired UTI?

A

Pathogenic E. coli

50
Q

What do the pathogenic E. coli isolates that are resistant to cephalosporin express (for resistance), and what are they still sensitive to?

A
  • Express extended spectrum beta lactamase - causes resistance to cephalosporins
  • Still sensitive to carbapenems
51
Q

How does methicillin cephalosporins and carbapenems work?

A
  • Beta-lactam antibiotics
  • Target peptidoglycan synthesis
  • Do this by inhibiting the activity of penicillin binding proteins
52
Q

Where does resistance to cephalosporins carbapenems arise from?

A

Cephalosporins
• Extended spectrum beta lactamases encoded on a plasmid
• Cleave this antibiotic

Carbapenems
• Carbapenemase enzyme encoded on a transposon
• Cleaves this antibiotic

53
Q

What is a risk group for Klebsiella pneumoniae, what is it an important cause of and what is it resistant to?

A

Immunocompromised patients
• UTIs
• Respiratory tract infections
• Restance to cephalosporins, fluroquinolones and aminoglycosides

54
Q

What is the most important cause of antimicrobial resistance infection worldwide?

A

MRSA

55
Q

How does resistance against methicillin arise?

A
  • Expression of additional penicillin binding protein PBP2A
  • This protein has a low affinity for methicillin and can still function in the presence of the antibiotic
  • MRSA strains can synthesise peptidoglycan and survive in the presence of methicillin
56
Q

How does Vancomycin work?

A
  • Beta-lactam antibiotic
  • Binds to a precursor for peptidoglycan synthesis
  • Therefore, inhibits peptidoglycan synthesis
57
Q

How does resistance against Vancomyocin arise?

A

• Vancomycin normally binds to a precursor for peptidoglycan synthesis

  • Mutation arises from multiple proteins (genes encoded on a plasmid or transposon)
  • Results in the synthesis of a different peptidoglycan precursor
58
Q

What are the ESCAPE pathogens?

A
  • Enterococcus faecium
  • S. aureus
  • C. difficile
  • Acinetobacter baumanii
  • Pseudomonas aeruginosa
  • Enterobacteriaceae

Microbiology (6 decks)

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