Bacterial Structure & Function Flashcards
Characteristics of G+ or G- cell wall
G+: very thick PG layer, +/- capsule
G-: thin PG layer between inner and outer membrane, +/- capsule
Gram positive envelope components
No true periplasmic space; IM, OM, and TM proteins; have teichoic and lipoteichoic acid
Significance of teichoic and lipoteichoic acid
Specific for G+
TA: cross-links PGs, not embedded in membrane
LA: cross-links PGs, also embedded in outer membrane; a pyrogen (not as bad as LPS)
Gram negative envelope components
True periplasm between membranes with thin PG layer
OM: unique to G-
LPS on OM: lipid A (strong pyrogen), O-antigen (polysach)
K-antigen: specific to G-
G-: smooth vs. rough appearance on agar plate
Smooth: long PS surface molecules
Rough: lipid A and short PS -> matte on plate
Significance of O-antigen
Immunogenic because on outside, strains can be serotyped, specific strains important in different conditions
Key features of O-antigen
Lipid A: an endotoxin with many FA chains, highly conserved, G- specific
Core PS: highly conserved, contains KDO acid (G- specific)
O side chain: types strain, very non-conserved
Peptidoglycan synthesis
MurA-F makes UDP-MurNAc
MurY transfers it to undecaprenyl-P = lipid 1
MuG adds GlcNAc (from UDP-GlcNAc) = lipid 2
Translocated by flippase to periplasm, where PGTs & TPs elongate PG chain
Energy for transpeptidation
Second D-Ala (of D-ala, D-ala) reacts with free AA = energy (no ATP used), lose D-ala
Same for G- & G+, but G+ adds AA in between linkages
Gram stain method & outcome
Fixation to slide, crystal violet, iodine (helps CV hold on), decolorization, counter stain safranin
*Blue stain remains in G+ bc think PG layer, but released from G-
Differences in H antigen between G+ & G-
H antigen = flagellin
G+: shorter TM portion
G-: longer TM portion (to span both membranes)
Bacterial growth phases
Lag phase
Log phase (exponential growth in optimized conditions)
Stationary phase (nutrients exhausted or waste products build up)
Death (decline) phase (never reaches zero)
Bacterial replication in G- bacteria
After chromosome replication & polarization, Z-ring forms into noose and pinches off/degrades PG, which is resynthesizes after separation
Bacterial replication in G+ bacteria
After chromosome replication & polarization, Z-ring forms into a noose, GP septum forms and remodels into 2 cells
Endospore formation
In some G+
Chromosome replication & septum formation in forespore
Engulfment of forespore by cell
Cortex (PG) and keratin-like coat synthesized
Maturation (replace water with DPA or Ca2+ dipicolinate)
Mother cell lysis
DAP vs. DPA
DAP: diaminopimelic acid, 3rd AA in E. coli PG synthesis
DPA: dipicolinic acid, can replace water in endospore maturation
Virulence factors
Adherence, persistence, invasion, toxigenicity
Bacterial adherence
Pills with adhesin to recognize host protein
Afimbrial adhesion: adhesin on organism itself, no pilli
Bacterial persistence
Attachment to surface, production of EPS (exo-PS) = irreversible attachment, dev & maturation of biofilm, dispersion of single cells from biofilm
Bacterial invasion
Paracellular, translocate through M cell, trans-epithelial migration, luminal capture by dendritic cells, growth inside MF, entry through epithelial cells, hijack actin to rocket from cell to cell
Bacterial toxins
Released exotoxin can cause pore formation, cleave surface molecules, bind receptor to enter cell or cause activation of target, modulate activation
Hypodermic: a pillus-like structure inserts into cell
Thanatomicrobiome
Post-mortem microbiome that may help find COD, TOD