bacteria growth rates Flashcards
(43 cards)
1
Q
bacterial growth rates
A
- can take under an hour to many days
- at every division populations could double, this leads to large numbers very quickly
2
Q
logarithmic growth
A
- the eponential growth of bacteria requires us to think and graph using a logarithmic scale instead of a linear and arithmetic scale
- one log10 increase of E Coli in just over an hour
3
Q
lag phase
A
- new environment - bacteria will not grow as quickly
- tailoring gene expression
4
Q
growth phase
A
- once gene expression is lined up = large growth rate
5
Q
stationary phase
A
- colony is full, nutrients run out, numbers dont change
- cells dividing = cells dying
6
Q
death
A
- eventually the nutrients is gone and metabolic waste increases = death
7
Q
counting bacteria
A
- it can be important ti know how many bacteria are present in a sample
- samples may require dilution or concentration
- may require viable counts or whole cell counts
- counts are often expressed as cfg = colony forming units
8
Q
working backwards through serial dilution
A
- start with colony count
- divide by the volume plated
- multiply by volume of tube
- divide by volme placed in that rube from the previous
9
Q
antibiotic
A
-kills bacteria when applied to the host, without harming the host
10
Q
bactericidal
A
kills bacteria
11
Q
bacteriolytic
A
kills bacteria by bursting cell open
12
Q
bacteriostatic
A
the population number is not going up
13
Q
mechanism of action
A
target/ the way it kills
14
Q
spectrum of activity
A
- broad: targets lots and sometimes unrelated bacteria
narrow: goes for specific bacteria
15
Q
effective dose
A
kills bacteria concentration needs to be above effective line
16
Q
toxic dose
A
kills bacteria and damages host
17
Q
therapeutic index (T/E)
A
-taking toxic/effective
- to make the right dosage
18
Q
natural
A
made by living thing
19
Q
semi synthetic
A
- natural changed by chemistry to be more effective but cannot synthesize from scratch
20
Q
synthetic
A
- fully made from chemistry
21
Q
antibiotic sources
A
- since the 1940s antimicrobial compounds have been utilized from various bacteria and fungi
- best sources are soil dwellers due to their evolution in competitive and nutrient - poor enviroments
22
Q
spectrum of activity = range of killing
A
- activity spectrum can be broad or narrow
- the closer an organism is to us, the harder it is to treat as drugs must be more specific
23
Q
cell wall inhibitors
A
- natural and semi synthetic forms
- all contains a B lactam ring
- natural penicillin works only ahainst gram +
- semisynthetic modification
1. makes it more resistant to acid break down
2. makes it more stable (body and bacteria )
3. broaden the activity spectrum
24
Q
protein synthesis inhibitors (static)
A
- many different classes that affect protein synthesis by interfering with the ribosome/mRNA/tRNA complex
25
chloramphenicol
- broad spec, can cause anemia (poison mitochondria)
26
streptomycin
- gram - can cause deafness during pregnancy
27
neomyocin
- topical streptomycin variant
28
tetracycline
broad spectrum, yeast over proliferation, also discolors developing teeth as it chelates calcium
29
plasma membrane damaging
- polymyxins: damage gram - membranes
- porly absorbed and toxic to neurons and kidneys
- daptomycin : depolarizes gram + membranes
- polymyxin b and bactracin (a gram + wall inhibator that also causes kidney damage) make a valuable topical antibiotic despite low usefulness as systemic drugs
30
nucleic acid synthesis inhibitors
- rifamycin/rifampin: most useful against mycobacteria (TB leprosy), inhibits mRNA synthesis, highly permeable into cells and through cell walls
- quinilones: ciprofloxin, inhibit DNA gyrase - DNA replication, undo extra chains or seperate to allow others to pass through, broad spectrum
31
metabolic inhibitors
- sulfonamides (sulfa drugs)
- completely synthetic, originally used in dye making
- first antimicrobial tests in 1932, in mass production before penicillin
- WWII soldiers got sulfa packets to spread on wounds to prevent gangrene
- competitively inhibits an enzyme needed to generate folate (folic acid)
- folic acid is used to produce thymine and uracil
- humans are unable to synthesize folate
32
sensitivity testing
- disk diffusion assays can determine what drugs are useful against a bacteria
- non quantitative
- distance ranges for resistance and sensitivty
-
33
epsilometer tests
- use a strip of antibiotic to determine a therapeutic dose
34
MIC
- minimal inhibitory concentration
35
antibiotic resistance
- even with proper use, bacteria will eventually become resistant to any antibiotic
- misuse of antibiotics accelerates the development od resistance
- discontinuing antibiotics before the pathogen is readicated
- using a poorly chosen antibiotic
- use of antibiotics against viral infections
- preventative use of antibiotics in animal feed
36
modes of resistance
- any possible way to survive an antibiotic is passed to the next generation
1. drug modification/ destruction (B-lactamases for penicillin)
2. pathway protection ( overexpression of GTPases create false targets for tetracycline, diverting it from the true targets)
3. target alteration ( a single ribosomal protein alteration of rRNA methylation can obscure a target)
4. rapid efflux ( actively pumping out the antibiotic (heavy metal efflux pumps acquired by s.aureus also pump out ciprofloxacin and some disinfectants)
5. alternative pathways ( folate scavening gives resistance to sulfonamides
37
spread of antibiotic resistance
- many species are naturally ressistant or less sensitive
- some species will become resistant and this genetic change will (at random) become part of a plasmid
- a plasmid is a small extra-chromosomal ring of DNA that can be transferred to other individuals or species (or virus or free DNA)
- natural selection
38
resisting resistance
- use a combination of drugs greatly decreases the chance of developing drug resistance (not all combinations will be synergistic)
- directly combating resistance : B-lactamase inhibitor, efflux pump inhibitor
- withholding newer/better antibiotics to reduce bacterial exposure when unecessary
39
antibiotic resistance
- even with proper use, bacteria will eventually become resistant to any antibiotic
40
misuse of antibiotics accelerates the development of resistance
- discontinouing antibiotics before pathogen is eradicated ( any surviving bacteria will create resistance)
- using a poorly chosen antibiotic (wont fit in the scope of change
- use of antibiotics in viral infections ( resistance can transfer casuing a placebo effect and not actually fix problem)
- preventatice use of antibiotics in animal feed ( a bit of antibiotic will continue to breed resistant populations
41
modes of resistance
- drug modification/ destuction ( bacteria requires an enzyme - antibiotic doesnt fit into the target)
- pathway protection ( overexpression of GTPase creates false targets for tetracycline, diverting it from the true targets, not stopping bacteria from growing)
- target alteration (a single ribosomal protein alteration or rRNA methylation can obscure a target )
- rapid efflux ( actively pumping out the antibiotic (heavy metal efflux pump aquired by s.aureus also pump out ciprofloxacin and some disinfectatns)
- alternative pathways ( folate scavenging gives resistance to sulfonamides)
42
spread of antibiotic resistance
- many species are naturally resistant or less sensitive
- some species will become resistant and this genetic change will (at random) become part of a plasmid
- a plasmid is a small extra chromosomal ring of DNA that can be transferred to other individuals or species (or viruse or free DNA)
- natural selection will promote these rare occurances
43
resisting resistance
- using a combination of drugs greatly decreases the chance of developing drug resistance (making sure is doesnt aquire rapidly)
- not all combinations will be synerhistic
- directly combating resistance: B lactamase inhibitor, efflux pump inhibitor
- withhold newer better antibiotics to reduce bacterial exposure when unnecessary
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