Module 3 Flashcards
how do bacterial populations grow
binary fission
how can a bacterial cell grow and divide
by using osmotic pressure against its cell wall
describe causes of senescence in binary fission
one pole of the cell will always be made up of older material
can inherit damaged DNA
Inherit damaged proteins
Activation of damage defense systems (M) rather than growth systems (G)
difference between anabolism and catabolism
anabolism: the building of components such as DNA and protein
catabolism: the breakdown of molecules to obtain energy
physical requirements for growth of bacteria
temperature, water, pH, pressure all influence enzymatic activity and structure of proteins
oxygen levels differ per microbe
list the types of aerobes/anaerobes
Obligate aerobes
□ Aerobic respiration
□ Oxygen is the terminal electron acceptor in the ETC
Facultative anaerobe
□ Don’t need O2 for growth, but grow better in its presence
Aerotolerant anaerobe
Can tolerant O2 but do not use it
□ Fermentative process
Strict Anaerobe
□ Oxygen is toxic
□ Fermentation
□ Anaerobic respiration
Microaerophile
□ Damages by atmospheric levels of oxygen (20%) but still require 2-10% of atmosphere oxygen for growth
what are reactive oxygen species and why are they bad for cells
cellular proteins transfer electrons to O2 leaving extra paired or un[paired electrons forming reactive species that can damage proteins, lipids and nucleic acids in the cell
describe the metabolic groupings
energy source:
-chemotrophic
-phototrophic
carbon source
-autotrophic: CO2
-mixotrophic: CO2 and organic compounds
-heterotrophic: organic compounds
electron source
-lithotrophic: inorganic compounds
-organotrophic: organic compounds
how do bacteria establish infection
bacteria must constantly adapt their metabolic processes in order to balance biosynthesis with sufficient ATP biogenesis, using those nutrients available from the host environment
what are persister cells
Escape effects of antibiotics without genetic change
Phenotypic variants that occur in low numbers in a population
Dramatically shift metabolism to remain just viable, but not growing
-Not metabolically active so antibiotics cant target them
-Once antibiotic is gone shift back to a metabolic state
difference between persister and resistant cells
resistant cells include a genetic shift and do grow in the presence of antibiotics, persister cells do not do this
how do bacteria communicate
through quorum sensing: an accumulation of signalling molecules that enables a single cell to sense the number of bacteria and respond by changing metabolic activity
what are autoinducers and how do they work
signalling molecules in quorum sensing
small go back into bacterial cell to elicit response, large bind to receptors on cell surface to start a signalling cascade in the cytoplasm
gram + quorum sensing strategies vs gram -
+: autoinducer binds to outside of cell
-signal cascade
-changes in gene expression
-: autoinducer enters the cell
-changes in gene expression
describe quorum sensing and virulence
Bacteria are able to upregulate expression of virulence genes in the presence of high concentrations of autoinducers (which its concentration is dependent on the bacterial population density)
-genes that enhance survival (biofilm, toxins, motility)
using quorum sensing to make a biofilm
cells must coordinately upregulate expression of polysaccharide synthesis and down regulate genes involved in motility
phases of bacterial growth
lag phase
exponentiial phase
stationary phase
death phase
methods of controlling microbial growth
Antisepsis
○ The inhibition of microorganisms on, or in, living tissue
Sanitization
○ A reduction of total microbial population to levels considered safe by public health standards
Disinfection is a substantial reduction of total microbial population and destruction of pathogens (not including spores)
Sterilization
○ All living cells, spores, viruses, and prions are either destroyed or removed from the treatment environment
methods of sterilization and disinfection
physical: heat, radiation
mechanical: filtration
chemical: chemical agents
3 principles of antibiotics
antibiotics do not work on viruses
antibiotics may be bactericidal or bacteriostatic
an antibiotic must be selectively toxic
what do antibiotics target/what are some common processes targeted
metabolic pathways and cell growth mechanisms
folate synthesis and cell wall synthesis
tetrahydrofolic acid is essential for
synthesizing nucleotides and amino acids
what is opsonization and what are opsonins
the process of enhancing phagocytosis through the coating of a bacterium with opsonins
opsonins can be a antibodies or complements
structure of the innate immune system
barriers (physical, chemical, microbial)
cells (NK, dendritic, macrophage, neutrophils)
processes (phagocytosis, inflammation, opsonization)
what are the three C3 pathways that leads to increase inflammation and phagocytosis
○ Antibodies to the pathogen (classical pathway)
○ A host protein that binds to mannose on the pathogen’s surface (Lectin pathway)
○ Through direct interaction of C3 with repeating bacterial motifs on the pathogen surface that leads to cleavage generating C3b (alternative pathway)
what is the membrane attack complex (MAC)
The complement system can assemble into a membrane attack complex (MAC) in the cell membrane of pathogen cells, forming pores/holes that cause the cells to lyse
The MAC is particularly effective against Gram- pathogens because it can insert through the outer membrane and destabilize the cytoplasmic membrane
how do natural killer cells kill target cells
by secreting proteins that trigger target cells to commit suicide by apoptosis
innate to adaptive immune response
inflammation: infected area flooded with cytokines and chemokines that attract and activate phagocytic cells
cells devour and display aicrobial antigens so that lymphocytes can activate a specific response
