1 Bacteria (Host Pathogen Interactions) Flashcards
What organisms make up the normal flora (microbiome) of the human body?
Fungi, Viruses, Bacteria, Helminths/Protozoans
prevent pathogen infections, stimulate immune system, provide nutrients
Bacteria classification
- Shape: Coccus (round), bacillus (rod), coccobacillus (oval), fusiform bacillus (stretched oval), vibrio (boomerang), spirrillum, spirochete
- Gram staining: Gram positive, Gram negative
- Metabolic requirements: Aerobic vs anaerobic, fermenters vs non-fermenters
Gram Stain
Differentiating step is ACETONE/ALCOHOL
Metabolic Pathways
- Aerobic respiration: oxygen is final electron acceptor
- Anaerobic respiration: inorganic compounds are electron acceptor
- Facultative anaerobe: respire aerobically until oxygen depleted, then ferment
Metabolic products and enzymes
-Coagulase (staphylococcus), Catalase (staph vs strep), Oxidase (cytochrome c oxidase), Hemolysis (alpha, beta, gamma)
Bacterial Cell Wall Structure/Components
- Gram (+) cell wall: teichoic/teichuronic acids –> Major surface antigen, influences virulence, helps in attachment
- Gram (-) cell wall: lipopolysaccharide (endotoxin) –> shock due to LPS and Lipid A cause systemic effects
- Flagella, Fimbriae (Pili), Cell membrane
Bacterial Cell Wall
- Alt molecules of NAG and NAM joined by Beta 1-4 link
- NAM PEPs are crosslinked: DAP at 3rd/D-Ala at 4th spot
- Beta lactam antibiotics prevent crosslinking
Gram positive bacteria use a _____ bridge to crosslink N-acetylmuramic acid units
PENTAGLYCINE
Glycocalyx
- Made of polysaccarides
- Mediates adherence
- Protects from phagocytosis and antibodies
Appendages
- Pili (Fimbriae): mediate attachment
- Flagella: mediated motility/highly antigenic
Ribosomes
Prokaryotic ribosomal differences allow for antibiotic targeting
Bacterial Pathogenesis
- Entry (air, food, water, damage to skin)
- Adhesion (fimbriae, pili, glycocalyx, biofilm)
- Invasion (degradative enzymes, inflammation, tissue cell penetration, intracellular growth)
- Propagation (bacterial replication)
- Damage to host (toxin/immune-mediated)
- Progression, resolution or chronic
Toxins
- Endotoxin: LPS triggers potent inflammatory response
- AB toxins: toxin binds (B) to membrane –> The A subunit “actively” cleaves/modifies target (ie diptheria, cholera)
- Superantigens: induce inflammation by binding MHC molecules and T-cell receptors (TCR)
Bacterial Host Evasion Mechanisms
Phagosome evasion; Antigenic mimicry; Intracellular growth; Inactivation of complement or antibody; Destruction of phagocytes; Resisitance to lysozyme enzymes; Antigenic switching
Antibiotic Resistance
Enzymes destroy antibiotics; Change in permeability to antibiotic; Altered metabolic pathway; Altered enzymes; Efflux pumps