People verus pathogens Flashcards
How bacteria can develop resistance to antibiotics
- random mutation resulting in resistance
- exposure to antibiotic (provides selection pressure) selects resistant mutants, natural selection
- more likely to survive and reproduce
- resistance gene passed on, descendants also have resistance
- transmission of plasmids
Why resistance to one antibiotic develops more slowly than other antibiotics
- antibiotic used less frequently
- fewer bacteria exposed
- less likely to select resistant mutant
Comparing sensitivity of bacteria to antibiotics
- bacteria X is sensitive to antibiotics A and B
- bacteria X is more sensitive to antibiotic A than bacteria Y
- neither bacteria are sensitive to antibiotic C
Penicillin
- works on gram-positive bacteria
- interferes with synthesis of cell wall
Why might viruses be resistant to interferon
- interferon does not prevent viral protein synthesis
- viruses able to reproduce
Why is it difficult for drug developers to treat HIV
- rapid reproduction
- many gene mutations (mutation more likely in a given time)
- variety of proteins and larger variation
- antigens on viral coat keep changing
- natural selection favours resistant gene
- drug development takes A long time, virus has changed by then
How bacteria become resistant to antibiotics
- mutation of resistance occurs
- increased use of antibiotics, more bacteria are exposed
- antibiotic provides selection pressure
- bacteria with resistant gene is selected for, reproduces and passes on resistant gene to offspring
- resistants organisms become more common
- horizontal gene transfer
- conjugation
- strand of plasmid carrying gene for resistance transfers between conjugating bacterium
Why are antibiotics not effective against viruses
- viruses have no cell wall or ribosomes
- no protein synthesis in viruses
- viruses use the host cell for protein synthesis
The effects of HIV on the ability of humans to combat TB
- HIV destroys T helper cells, numbers fall
- reduced immune response
- T cells cannot release cytokines to stimulate B cells to divide and produce antibodies
- less able to destroy TB, more like to show symptoms/develop TB
Effect of co-infection of HIV and M.TB on rate at which each disease develops
- HIV infects T helper cells which are destroyed by T killer cells
- less able to destroy M tuberculosis
- more phagocytosis occurs
- more infected macrophages
- positive feedback, both diseases progress more rapidly
Bactericidal
- cell wall destroyed
- lysis occurs
- decreases number of living bacteria
Bacteriostatic
- no reproduction
- same number of living bacteria
How do bacteriostatic antibiotics help overcome a bacterial infection
- slows growth (fewer cells)
- more time for the immune system to respond
- gives time for antigen to bind to B cell and stimulate specific immune response
- bacteria can be phagocytosed
How antibiotics affect bacteria
- gram positive have thick cell wall (peptioglycan layer)
- antibiotic affects cell wall synthesis
- inhibits formation of peptidoglycan bonds in cell wall
- weakening of cell walls
- cell lysis
How antibiotic resistant bacteria spread
- mutation causes resistant bacteria
- any resistant bacteria will multiply
- pass on resistant gene/plasmid