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Terms in this set (25)

Topoisomerase: relieve torsional stress on chromosomes during replication. Ex: DNA gyrase in bacteria. They are important targets for some antibiotics

Helicase: unwinds DNA strand for replication


Promoter: region upstream of gene(s) where RNA polymerase binds to initiate transcription

Operator: segment of DNA that regulates transcriptional activity of gene(s) of an operon by interacting with specific repressor or activator. Lies in path between promoter and genes to be transcribed

Operon: one or more genes under the control of a promoter and an operator. Operons encoding many genes are called polycistronic


Sigma Factors: recognize the promoter (particular sequence of nucleotides in the DNA 0 to provide a docking site for RNA polymerase.
Σ70 activated in normal growing cells
RpoS activated when cell in stressed, enhances the binding of RNA polymerase to promoters for operons involved in stress response.

Repressors: bind to operator and prevent transcription


Silent mutation: at nucleotide level that does not change amino acid→ code degeneracy helps minimize effect of nucleotide mutation on protein function

Frameshift mutation: insertion or deletion that is not a multiple of 3, reading frame is shifted

Missense Mutation: nucleotide mutation results in different amino acid with a different property than the old amino acid→ protein function can be significantly impacted

Nonsense mutation: changes a codon to a stop codon. Prematurely ends peptide synthesis


Virulent phage: (AKA lytic phage) replicates to large numbers before lysing bacterial cell and releasing viral particles

Temperate phage: May carry "extra" genes that code for factors that can benefit bacterial cell. Can have a lytic cycle or lysogenic cycle: may become incorporated into the bacterial genome and replicate with the cell without causing cell death
Prophage: phage that have become incorporated into bacterial genome


Hfr strain: During bacterial conjugation, if the F plasmid sequence is integrated into the bacterial chromosome, then the cell is designated as a high-frequency recombination cell.
B-lactam antibiotics
Antibiotic exclusion: many gram - are intrinsically resistant to B-lactams because their outer membrane excludes entry
Drug Efflux: drug efflux pumps can actively pump toxic substances out of the cell. They are particularly useful for removal of antibiotics. They are only effective in gram - where they serve to pump the antibiotic out of the periplasmic space before it can interact with peptidoglycan. Would be ineffective for gram + because peptidoglycan is on outside of cell
Antibiotic inactivation: B-lactamase enzymes degrade B-lactam antibiotics before they can damage cell wall
Target alterations: Alteration of target so that it is no longer affected by B-lactams

Vancomycin
Antibiotic exclusion: Gram - are intrinsically resistant because Vancomycin antibiotic is too large to pass through outer membrane
Target Alteration:
D-ala-D-lactic acid synthesized instead of D-ala-D-ala
Plasmid mediated resistance has been observed in enterococci: where D-ala-D-lactic acid is synthesized instead of D-ala-Dala. Some bacteria are intrinsically resistant, such as Lactobacillus and Pediococcus, because they naturally produce D-ala-D-lactic acid

Aminoglycosides
Antibiotic Exclusion
Non-respiring bacteria are resistant
Aminoglycosides require the ETC to cross the cytoplasmic membrane. (fermentation does not use ETC)
Antibiotic inactivation- most common resistance to these
Enzyme modification of aminoglycoside
Modified aminoglycoside are inactive

Tetracyclines
Widespread resistance
Efflux pumps- most common type of resistance
Genes encoding for pumps can be plasmid mediated, therefore easily transferred between medically important bacteria

Macrolides
Antibiotic exclusion: outer membrane of most gram - is not permeable to macrolides
Target alteration: methylation of 23S rRNA
enzymes encoded by plasmid genes can methylate the 23S rRNA so that it is not recognized by macrolides
Commensalism: relationship where one organism benefits while the other remains unharmed

Mutualism: relationship where both organisms benefit

Pathogenicity: an organism that causes disease

Virulence: measure of degree of pathogenicity

Primary Pathogen: cause disease in an uncompromised host

Opportunistic pathogen: requires compromised host defence in order to cause disease

Adhesin: surface molecule that enables bacteria to bind to other surface (ex: pili)

Ligand: specific part of adhesin that binds to receptor

Receptor: molecule on the eukaryotic cell surface that binds to an adhesin

Hyaluronidase: enzyme secreted by bacteria invading by passing between cells that breaks down cement that holds cell together

Antigenic mimicry: bacterial surface components mimic those of the host

Endotoxin: only gram - produced. It is very effective at stimulating the innate immune response (fever, inflammation) by binding to macrophages and other cells causing the release of cytokines. Systemic infections (like sepsis) can result in endotoxins that cause a lot of damage that overwhelm the system and lead to shock.

Exotoxin: produced by gram + OR -. Is released during exponential growth. Ingestion of toxin alone can cause disease
Many have A and B subunits
A cause damage
B allow toxin to bind to target cells

Superantigens: specific exotoxin that activates T cell non-specifically. They bind simultaneously to T cells and MHC class II molecules causing the T cells to be activated without requiring antigen.
T cell activation can be massive, causing massive release of cytokines→ resulting in shock