Principles of bacterial pathogenesis Flashcards
What are the key structural differences between Gram+ and Gram- Bacteria?
- Gram + structure consists of a thick peptidoglycan layer, no outer membrane, and teichoic acids.
- Gram- structure consists of a thin peptidoglycan layer, an outer membrane containing LPS (lipopolysaccharide), and a periplasmic space.
Name Five Bacterial shapes and provide an example for each:
1- Spherical (cocci) = Streptococcus.
2- Spiral (sprilla) = Heliobacter pylori.
3- Comma (vibrios) = Vibro chloerae.
4- Rod (bacilli) = E coli, salmonella.
5- Corkscrew (spirochaetes) = Troponema palldium.
What is the function of LPS in a Gram-bacteria?
- Acts as an endotoxin, which triggers immune responses (via TRL4)
- Can also cause septic shock at high concentrations.
What are the Koch postulates, and why are they important in medical microbiology?
- It helps establish causal relationship between a microbe and a disease.
What are the 4 creteria in Koch postulates that proves the relationship between a microbe and a disease?
1- Found in a diseased ( not healthy ) host.
2- Isolated and grown in cultures.
3- Causes disease when introduced to a new host.
4- Re-isolated from the new host.
- When it meets all this criteria, it is proven.
What is the difference between a strict and opportunistic pathogen? Give examples for each.
- Strict = Always pathogenic
( eg, Mycobacterium tuberculosis) - Opportunistic = Harmless unless the host is weakened
( eg Pseudomonas aeruginosa in cystic fibrosis )
How do asymptomatic carriers contain Koch’s postulates?
The carriers harbour the pathogen without the symptoms, violating Postulate 1 ( the microbe is not always linked to disease ).
What are virulence factors, and how do they contribute to bacterial pathogenesis?
Virulence factors are molecules such as toxins, adhesions, and invasions that help the bacteria invade, evade immunity, and cause damage.
What is a pathogenicity island (PAI), and how do bacteria acquire them?
- PAIs are clusters of virulence genes that are acquired via horizontal gene transfer (eg, plamids).
- Present in pathogenic strains but absent in non-pathogenic strains.
Name three bacterial adhesions and their role in infection:
Three adhesions:
- Pili/Fimbriae: Attach to host cells (eg, E.coli)
- Invasions: Promote cell entry (eg, Yersinia invasion )
- Capsules: Prevent phagocystis ( e,g Klebsiella)
Compare and contrast endotoxins and exotoxins:
- Endotoxins (LPS): Part of Gram- cell walls, released during lysis.
- Exotoxins: Secreted toxins ( eg AB toxins, pore-formers).
How does the AB toxin structure (e.g., clover toxin) function?
B-subunit: Binds host cell receptors.
A-subunit: Enters cytoplasm and disrupts function
(eg, cholera toxin ADP-ribtoslyates G proteins = watery diarrhea).
What is the mechanism of pore-forming toxins such as streptolysin O?
The mechanism consists of Oligomerization to form pores in host membranes = cell lysis.
How do botulinum and tetanus toxins affect the nervous system differently?
-Botulinum toxins: Blocks actylcholine release = flaccid paralysis.
- tetanus toxins: Inhibits Inhibitory neurons = spastic paralysis.
What is the role of T3SS in bacterial pathogenesis?
They are “molecular syrinage” injecting effectors into cells (Eg salmonella, shigella)
What is the role of T4SS in bacterial pathogenesis?
They are key virulence mechanisms for both antibiotic resistance and host cell manipulation.
- They inject virulence factors effectively into host cells (eg ,Legionella)
How does the Type VI secretion system (T6SS) differ from T3SS?
The T6SS systems attack other bacteria/host cells and are structurally similar to bacteriophage.
Which bacteria uses T4SS, and what can it transport?
Bacteria such as Legionella and Helicobacter use T4SS to transport DNA (antibiotic resistance genes) or proteins.
What are the main routes for bacterial transmission? Give an example for each.
Routes for transmission:
- Oral: Salmonella (food)
-Respiratory: M. tuberculosis (airborne)
- Cutaneous: Clostridium tetani (wounds) skin.
How does Salmonella use T3SS to invade host cells?
Salmonella uses T3SS (SPI-1) to trigger actin rearrangements leading to phagocytosis.
Why does shigella have such a low infectious dose (10-100 bacteria)?
- Shigella is highly invasive, and it evades stomach acid and immune defenses effectively.
How does Listeria monocytogenes spread from cell to cell?
It polymerises actin tails to propel into neigbouring cells.
What are the “attaching and effacing” A/E lesions, and what bacteria causes them?
A/E lesions are caused by EPEC/EHEC bacteria that attach tightly, efface microvilli, and form actin pedestals.
Why is LPS (endotoxin) a major concern in septic shock?
LPS overactivates immune responses, which causes a cytokine storm and leads to organ failure.
