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101 Cards in this Set

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pathogenicity vs. virulence
Pathogenicity: ability to cause disease
Virulence: extent of pathogenicity
cell envelope
A multilayered structure that surrounds the bacteria, composed of the cytoplasmic mem., cell wall, outer mem. (gram neg) and capsule (if present)
bacterial cytoplasmic (cell) membrane
Lacks carbohydrates and sterols, unlike euks. Contains permeases (transporters) to bring in chopped up proteins.
Fxns: ox-phos, lipid/wall syn., mitotic apparatus, sensors.
bacterial cell wall
Provides rigidity, shape, protection from bile salts. Mycoplasma genus lack cell wall. Much thinner in gram-negs.
peptidoglycan
cross-linked polymeric mesh from which the cell wall is made. CHO-backbone is made of alternating NAM/NAG. Only NAM is cross-linked.
diaminopimelic acid (DAP)
An unusual AA cell wall component in gram-negs. It has direct bond with the terminal D-Ala on an adjacent strand NAM.
teichoic/lipoteichoic acid
Components of the gram+ cell wall that help link together the many layers of peptidoglycan. Some lipoteichoic acids can induce inflammatory response.
Outer Membrane
Unique to gram-negs, the outer leaflet contains LPS (lipopolysaccharide). Outer mem. confers antibiotic resistance to gram-negs.
Periplasmic Space/Periplasm
Found between the outer membrane and the inner mem. in gram-neg, where the cell wall and enzymes that break up antibiotics can often be found.
lipopolysaccharide (LPS)
An endotoxin in outer leaflet of outer mem. in gram negs. Produces fever, vasodilation, inflammation, shock, and release of cytokines (TNF-α, IL-1,6, PAF) LPS from all gram-negs have similar effects.
Lipid A
anchours LPS to the outer mem. of gram-neg, considered the toxic part.
Core polysaccharides
Middle component of LPS; short series of sugars, nearly invariant in most gram-negs. Includes KDO and a heptose.
O-Antigen
Terminal component of LPS; long CHO-chain of up to 40 sugars; hydrophilic, excludes hydrophoic compounds. Highly antigenic and defines a spp/strain of gram-neg.
Capsule (glycocalyx/slime layer)
A layer of sticky, viscous material (called slime layer if more loosely and amphorphously bound). Often associated with pathogenicity; sliminess protects bacterium from phagocytosis, or diffusion barrier against antibiotics. Non-encapsulated form usually avirulent.
flagellin
The protein subunit building block of bacterial flagella. H-Antigen of flagella highly antigenic. Flagella have a filament attached to the basal body by a hook.
pilin
Protein subunit of pili. Pili are shorter and thinner than flagella, not essential for normal growth, used for attachment.
Common Pili
Often related to pathogenicity; involved in adherence (tissue tropism); colonising factors that det. which tissue is infected. Can also be anti-phagocytic (like capusle), antigenic, and can be highly mutatable.
Sporulation
Certain genera transition from a dormant vegetative state during adverse conditions to the endospore. Endospores contain high conc. of Ca bound to dipicolinic acid.
exotoxin
bacterial toxic proteins released into the medium, unlike endotoxins which are part of the bacterial cell wall.
A/B Toxin
Contains a B (binding) part that binds to cell R, allowing the A (active) part to enter and damage the cell, usu. by ADP-ribosylation, which inactivates ribosylated enzymes. Exact result of toxin depends on enzyme ribosylated.
Toxoid
Attenuated toxins that have lost their toxicity but retain their immunogenicity for vaccine purposes.
Diptheria Toxin
An A/B exotoxin that blocks protein syn. with ADP-ribosylation.
Cholera Toxin
An A/B-5 exotoxin that causes ADP-ribosylation of G-proteins in the small intestines. Causes watery diarrhoea due to activation of AC and subsequent ↑cAMP, stimulating fluid secretion into lumen.
Botulinium Toxin
An A/B exotoxin with a metalloprotease as the active portion that blocks ACh vesicle fusion, creating progressive mm weakness and flaccid paralysis.
Tetanus Toxin
Very similar to botulinium toxin; also blocks ACh vesicle fusion, but causes spastic instead of flaccid paralysis.
Membrane Active Toxins
Exotoxins that disrupt host cell mems. Some are lipases, such as lecithinase (clostridia). Others are insertable channels that cause the cell to burst (α-toxin of S. aureus)
Colonisation Factors
Virulence factors such as pili and adhesins that foster attachment to host surfaces/cells, and establish the host range of a spp.
Pathway of Pathogenesis
1.) Attachment
2.) Growth and spread
3.) Evasion of host defences
4.) Shedding (exit from body)
5.) Damaging the host.
Obligate Intracellular Pathogens
These bacteria lack certain key metabolic pathways and depend on their host to supply a nutrient; will not grow on cell-free medium, only in tissue culture. Includes Chlamydia and Rickettsia.
Siderophores
Bacterial proteins that "steal" Fe bound to lactoferrin and transferrin from the host.
Minimal media
Glucose, ammonia, phosphate, and various ions. E. Coli can be cultured on minimal media.
Microaerophilic organisms
Facultative anaerobes that grow best in reduced oxygen tension, such as Campylobacter (GI diseases).
Superoxide Dismutase (S.O.D.)
An enzyme in all aerobic organisms that takes oxygen radicals to H2O2. Obligate anaerobes lack this enzyme.
Peroxidase
An example is catalase; takes H2O2 to water and O2. Obligate anaerobes lack this enzyme.
Bacterial Growth Equation:
N_t=N_o x 2^(t/d)
N_t= # of bacteria after time (t)
N_o=initial # of bacteria
t=time of growth
d=doubling time
(t/d)=# of generations
Lag phase
Freshly inoculated bacteria are adapting to a new environment and grow slowly.
Log phase
Period of exponential bacterial growth after the lag phase. Many antibiotics are most effective in this state.
Stationary Phase
Following the log phase, nutrients have been delpleted, and some bacteria may undergo sporulation at this stage.
Death Phase
Following a period of stationary phase, cell viability will decline.
Multifork Replication
In bacteria, a new round of DNA replication begins before the previous round is completed. Synthesis is bi-directional. Daughter cells are "born pregnant".
Quorum sensing
Bacteria can monitor their own cell population density by producing diffusable autoinducers. When a threshold conc. of autoinducer is reached, transcription of certain virulence factors may be activated because critical density to establish an infection has been reached.
Temperate Phage
A phage which can integrate inot the host chromosome (becomes a prophage) at a non-random site. Repressor protein turns off lytic cycle genes until conditions deteriorate.
Lysogenic Bacteria
Bacteria that carry a temperate prophage, such as λ-phage. Diptheria toxin is encoded by a prophage.
Conjugative Plasmids
Plasmids with the ability to be transferred to another bacterium.
Episomes
Conjugative plasmids that can integrate into the host genome, cf. prophage. E. coli F-factor is an example.
Transposons
"Jumping genes" that mediate their own transfer from one locus to another, or even between the genome and plasmids. Flanked by inverted repeats on both ends.
Transformation
Direct uptake of naked DNA by a bacterium. Ability to do this is called competence. Certain genera are naturally competent.
Generalised Transduction
Occurs with lytic phage infection. Random section of host DNA is packaged into the virus when the phage excises itself, and is recombined into the next victim's genome.
Specialised Transduction
Occurs with prophages that excise themselves. Very specific, adjacent DNA are likely to be carried along, unlike in generalised transduction. (Integration site is specific)
High Frequency Recombination Cells (Hfr)
Cases in which an F plasmid becomes an episome and integrates into the bacterial genome. When the plasmid genes attempt to transfer themselves to a bitch, the entire genome gets transferred. Ironically, usu. not the entire genome gets transferred before the pilus breaks off, so the actual episome often remains un-transferred.
Pathogenicity Islands
Clusters of genes surrounded by transposon-like elements taht can confer pathogenicity to a formerly benign bacteria. Transposons usually carry a few virulent passenger genes.
True antibiotic
Of biological origin; penicillins.
True chemotherapeutics
Chemically synthesised antimicrobial agents; sulfonamides, trimethoprim.
Bactoprenol
A "conveyor belt" that takes pre-made subunits UDP-NAM to the outside, where they are attached to the pre-existing peptidoglycan mesh.
Penicillin Binding Protein (PBP)
A transpeptidase that catalyses cross-linking of adjacent glycan chains of NAM in the cell wall. β-lactam binding causes autolysin release.
β-lactam Resistance
1.) β-lactamase action
2.) ↓affinity of PBP (rare)
3.) Diffusion barriers (gram neg); altered porin polarity/size.
Cephalosporins
β-lactam; third-gen. broad spectrum antibiotic.
Carbapenems
β-lactam; actgive against virtually all groups of organisms. Ex. Imipenem, which is immune to most β-lactamases.
Monobactams
β-lactam; narrow-spectrum against aerobic gram negs. Like imipenem, also immune to most β-lactamases.
Bacitracin
Bactericidal; interferes with dephos'n of lipid carriers. Too toxic for systemic use, only topical.
Vancomycin
Glycopeptide; sterically interferes with formation of bridges btw peptidoglycan chains. Inactive against gram-negs; too big to cross outer mem.
Vancomycin resistance
VanS: senses Vancomycin
VanR: activates the resistance genes.
Van H: makes keto reductase that synthesises D-lactate.
VanA: depsipeptides that tacks D-lactate onto D-ala-D-lac, which has low affinity for vancomycin.
VanX: cleaves existing D-ala-D-ala
VanY: prevents internal D-ala-D-ala from reaching cell surface.
Isoniazid (INH)
Antibiotic for mycobacteria by inhibiting syn. of cell wall mycolic acid, making bacteria susceptible to reactive O2 free radicals. Activation of INH requires KatG and H2O2 as e- sink.
Polymyxins
Antibiotic class that act as pos.-charged detergent to fuck up bacterial cell mem. (euk mems neg- charged). Active against gram-neg. Nephrotoxic, limited to topical use.
Aminoglycosides
Antibiotic class that bind irreversibly to 30S subunit of bacterial ribosome, blocking initiation of protein syn. All are bactericidal, and use O2-dependent transport sys. making them useless against anaerobes.
Aminoglycoside Resistance
1.) Most use inactivating enzymes to acetylate, phos', or adenylate critical groups.
2.) Less common mechanisms include mutations of ribosome binding site and (-)'d transport.
Chloramphenicol
Bacteriostatic (bactericidal against intracellular); acts on 50S subunit, broad spectrum against gram +/-. Can cause aplastic anaemia (rare).
Chloramphenicol Acetyltransferase (CAT)
Enzyme behind chloramphenicol resistance; acetylates the antibiotic and deactivates it.
Tetracyclines
Bacteriostatic; bind reversibly to 30S. Broad-spec against gram+/-, bactericidal against obligate intracellular bacteria.
Tetracyline Resistance
1.) Efflux-based (tet protein); most common
2.) AA sxr change or post-translational modification of 30S.
Macrolides
Bacteriostatic against 50S Broad-spec. Ex.: erythromycin, azithromycin.
Lincosamides
Bacteriostatic against 50S Broad-spec. Ex.: Clindamycin (inactive against aerobic gram negs)
Macrolide Resistance
1.) Methylation of rRNA to prevent binding of antibiotic.
2.) Hydrolysis
3.) Efflux
4.) Barrier
Quinolones
Bactericidal agent that inhibits DNA gyrase or topoisomerase IV.
Ex.: nalidixic acid, ciprofloxacin
quinolone resistance
1.) ↓'d permeability
2.) Mutations in gyr gene for DNA gyrase.
Rifampin
Bactericidal; Binds to and inhibits RNA polymerase, blocking RNA syn. in aerobic gram + cocci and mycobacteria. Effective against intracellular pathogens and TB due to high penetration.
Rifampin Resistance
Mutation in RNA poly.
Sulfonamides
Bacteriostatic antimetabolites that compete with PABA for DHF-synthase, inhibiting folic acid syn. in bacteria. Can be overcome by excess PABA. Effective against gram+/-.
Trimethoprim
Bacteriostatic antimetabolite that inhibits DHF reductase; higher affinity for prok. form. Synergises with sulfonamide.
Antimetabolite Resistance
1.) Perm. barrier
2.) ↓affinity for DHF reductase
3.) Start using exogenous thymidine
4.) Int gene that codes integrase, creating sulfonamide resis.
Platensimycin (PM)
Broad-spec gram+ that inhibits lipid syn. pathway essential to virtually all pathogenic bacteria. Currently shows no cross-resistance.
Events of Acute Inflammation
1.) Tissue injury
2.) Vasodilation
3.) ↑perm
4.) Leukocyte entry
5.) Chemotaxis of macs and neutrophils
6.) Phagocytosis
Lactobacilli
Colonise the vagina and produce lactic acid to lower the pH, also produce biofilm to protect mucosal surface from pathogens.
Stages of phagocytosis
1.) Attachment
2.) Ingestion
3.) Destruction
Pathogen-associated Microbial Patterns (PAMPS)
Highly conserved common molecular patterns on the surface of pathogens that are recognised by the innate immune system, allowing self-nonself differentiation. Ex: LPS, lipoteichoic acid, cell wall, dssRNA.
Pattern Recognition Receptors (PRRs)
Recognise PAMPs and have a wide range of specificity. 3 types: secreted, endocytic, and signaling. Endocytic and secreted promote opsonisation.
Toll-like Receptor
Subset of PRRs.
Some TLRs are in the nuclear mem. and recognise pathogen breakdown remnants/viral particles. TLRs trigger cytokine release.

TLR5 recognises flagellin
TLR-4 recogises LPS
TLR2 recognises peptidoglycan, lipoteichoic acid.
Respiratory Burst
NADPH-oxidase reduces O2 to superoxide, which is then converted to H2O2 by SOD. H2O2 then reduced to hydroxyl radical.
Myeloperoxidase
Converts Cl- into hypochlorite, which disrupt bacterial cell walls by halogenation, and also reacts with H2O2 to form singlet oxygen.
Chronic Granulomatous Disease (CGD)
Hereditary immunodeficiency
Defect: NADPH oxidase; phagocytes can't kill the bacteria they engulf.
Cationic Proteins
An oxygen-independent killing mechanism discharged by Azurophil granules into phagosomes that affect gram neg more than pos.
Chédiak Higashi Syndrome
Neutrophil disease in which they have inability to fuse endosome with lysosome, can't kill engulfed bacteria. Recurrent pyogenic infections.
Resident Member
Normal flora that are always present at a particular site.
Transient Member
Flora that are normal for certain parts of the population. Pneumococcus found in 10% of people's throats normally.
coagulase-neg Staphylococcus
Normal flora of moist skin (groin, btw toes)
Staphlyococcus
Normal flora of resp. tract.
Streptococcus mutans
Normal flora on teeth
Bacteroides
Normal flora in large intestines; an obligate anaerobe.
E. coli
Normal flora of large intestines; a facultative anaerobe.
Enterococcus
Normal flora of large intestines; a facultative anaerobe.
Sterile Body Sites
blood, CSF, synovial fluid, deep tissues.