3. Community acquired and hospital acquired bacterial infections Flashcards
Do bacteria have organelles?
No (just genetic material, ribosomes and a cell wall)
What 6 common virulence factors are associated with bacterial infections?
- 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)
What are exotoxins?
Proteins produced by bacteria and secreted into the host
What do the following exotoxins do: • neurotoxins • enterotoxins • pyrogenic exotoxins • tissue invasive exotoxins • miscellaneous exotoxins
- 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
What are the endotoxins of bacteria?
- Only produced by gram negative bacteria
- Gram negative = 2 lipid bilayers
- Endotoxins = LPS and sugars on lipid bilayer (not protein)
Why can treating a person who has a gram negative infection with antibiotics worsen the condition?
When they lyse, they release large quantities of LPS/endotoxin => septic shock
What is an outbreak?
Greater than normal/expected number of individuals infected or diagnosed with a particular infection in a given period of time, particular place, or both
What is haemolytic-uraemic syndrome and how is it acquired?
- 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
In 2011, there was an outbreak of E. coli in Germany. How was this detected?
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)
What are the 2 virulence factors that the EHEC strain had?
- Shiga toxin
* ESBL plamids - genes for extended-spectrum β-lactamases
Did the EAEC strain originally produce the Shiga toxin?
- No, it was acquired
* Shiga toxin was introduced into the EAEC strain through a phage
What is the AB5 subunit of the Shiga toxin family useful for?
Helps the toxin bind to eukaryotic cells, so the toxin can be injected
What is StxA (subunit 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)
What is the StxB (subunit B) of the Shiga toxin responsible for?
StxB pentamer responsible for binding to host cell receptors
How is StxA and StxB linked together?
Non-covalent association
How can Shiga toxin transfer to another strain?
- 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
When which cycle of the phage is activated causing toxins to be highly expressed?
Lytic cycle
What does the EAEC and EHEC strain colonise?
EAEC - small and large bowels
EHEC - large bowel
What are the virulence factors of EAHEC and which strains are they aquired from?
- pAAF plasmid (fibres that assist with attachment) - EAEC
* Shiga toxin (prophage encoding) and ESBL resistance plasmid - EHEC
What response does aggregative adherence fimbriae (AAF) stimulate and what does it lead to?
- Strong IL-8 response
- Allows biofilm formation
- Disruption of actin cytoskeleton
Describe Legionella pneumophila (type, origin, infection route)
- 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
What is an important virulence factor for Legionella pneumophila?
Type IV secretion system
Can Legionella replicate in a Legionella containing vacuole (LCV)?
Yes - macrophages also take up these bacteria and they can replicate in macrophage vacuoles
Describe TB (type, treatment, state)
- 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
