1/103
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Bacteria Overview
Unicellular, ubiquitous, mostly beneficial in normal microbiota
Most bacteria are not…
Pathogenic (causing disease)
Are bacterial small or large?
Small (they are smaller than eukaryotic cells)
Bacterial Morphology
Small
Shapes and arrangements
Surface Area-to-Volume
Smaller size = higher ratio
Why is higher surface area-to-volume important?
More nutrients and waste can diffuse out of bacteria
What does bacterial shape influence?
Obtaining nutrients
Attachment
Movement
Invasion
Monomorphic
Bacteria that have one shape
Pleomorphic
Bacteria that have multiple shapes dependent on environment
Cocci
Ball-shape
Bacilli
Rod-shaped
Coccobacillus
Intermediate between cocci and bacilli
Strep
Chain
Staph
Cluster of cocci
Streptobacilli
Strips of bacilli
Streptococci
Strips of cocci
Palisades
Cluster of bacilli
Staphylococci
Clusters of cocci
Vibio
Comma-shaped
Spiralla
Spiral-shaped
Spirochetes
Corkscrew-shaped
Filamentous
Long, thread-like
Internal Bacterial Structures
Cytoplasm
Nucleoid
Ribosomes
Inclusion bodies
Cytoskeleton
Which internal structure do bacteria lack?
Membrane-bound organellessuch as a nucleus and mitochondria.
Cytoplasm
Aqueous solution for all cellular functions/structures
Nucleoid
Region of bacterial genome (1 circular chromosome)
No nuclear envelope (nucleus)
Ribosome
RNA and Protein (70S)
vs. 80S in Eukarya
Site of translation (RNA → Protein)
Densely dispersed
Inclusion Bodies
Aggregates for storage of nutrients
Viral replication
Insoluble, recombinant proteins
Cytoskeleton
Structure and support body
Plasma Membrane
Boundary separating intra vs. extracellular spaces
Function of Plasma Membrane
Response to environment (fluid, gas, waste levels)
ATP generation, electron transport, transport
Passive or active diffusion
Structure of Plasma Membrane
Fluid Mosaic lipid bilayer
Allows protein movement trans or surface
Selective permeability
Selective Permeability
Small molecules, gases, and water allowed
Charged, bound, large molecules require help
How does temperature affect the plasma membrane?
Colder temp = harder to move around
Passive Transport
No energy
Concentration gradient: High → Low
Osmosis and solute diffusion
Osmosis
Movement of water to equalize solute
Water moves to higher solute concentration
Isotonic, hypertonic, hypotonic
Isotonic
Equal solute inside and outside cell = no water gain/loss
Hypertonic
Higher solute outside cell = water out of cell = cell shrinkage
Hypotonic
Higher solute inside cell = water into cell = cell lysis/swelling
Simple Diffusion
Molecules pass freely through membrane (high → low)
Facilitated Diffusion
Molecules require transporter (High → Low)
Active Transport
Movement against gradient (Low → High)
Energy required to open/close protein pump
Faster
External Bacterial Structures
Cell wall
Glycocalyx
Pili
Flagella
Capsule
Slime Layer
Peptidoglycan
Protein and sugar mesh cross-linked with amino acids
How are bacteria classified based on cell wall?
Gram Stain
Graim Stain
Differentiates bacteria as Gram+, Gram-, Gram Indeterminant
Which bacteria are gram-indeterminant?
Spirochetes, Mycobacteria, Mycoplasmas
Gram-negative Bacteria
Contain lipid-rich outer-membrane (2nd)
Thin layer of peptidoglycan
Periplasmic Space - OM & PG
Stain pink
Outer Membrane
Contain LPS (Lipid A/Endotoxin)
Causes inflammation if lysed
Outer-membrane proteins (porins)
Porins
Gram-negative OMPs from the outer membrane
Form channels for transport that excludes large/harmful molecules
Which gram-bacteria is more resistant?
Gram negative is more resistant
Gram-positive Bacteria
Thick PG layer
High sensitivity to penicillin and lysozyme
Contains teichoic acids
Stains purple
Teichoic Acids
Found in Gram-positive Bacteria
Glycopolymers attached to PG or membrane to stabilize, maintain, and divide
Mycoplasma
Lack a cell wall or PG
Resistant to PG-targeting therapy
Pleomorphic
Mycobacteria
Thick, mycolic acid-rich CW
Waxy, lipid coat
Identified with acid-fast stain (red)
Glycocalyx
Carbohydrate mucoid layer
Adherence, protection
Slime or capsule
Capsule
Organized polysaccharide/protein coat acting as a virulence factor
Groups species into serogroups
Used for vaccines (targeting capsules)
Pili
Hair-like projections with adhesin tips
Common in Gram(-)
Virulence factor for adherence
Conjugation (F Pili) and twitching motility
Flagella Overview
Long rotary propellors in bacilli
Infection and invasion
Taxis to or away from chemicals, light, osmotic pressure, oxygen, temperature
Extracellular flagella
Monotricious (1)
Amphitricious (1 on each end)
Lophotricious (tuft on 1 end)
Peritrichous (all over)
Intracellular flagella (endo)
Periplasmic space of spirochetes for corkscrew motion
Endospores
Made by gram-positive bacilli
Allow for dormant state for resistance
Become vegetative as conditions improve
Steps to Infection
Enter
Adhere
Invade and obtain nutrient
Replicate and defend
Transmit to new host
Adherence
Colonization of host tissues and multiply
Depends on adhesin binding to receptors
Surface or pili (or both) adhesins
Tropism - specificity for adhesin binding
Which adhesin would attach first?
Pili pull to host, surface create stronger adhesion
Tropism
Preference for a host, cell, or tissue based on host factors
Planktonic
Unicellular, free-floating phase
Sessile
Multicellular, biofilm phase
Biofilms
Microbial communities encased in EPS with multiple protective layers
Which layers of biofilm are most protected?
The inner layers
Exopolymeric Matrix (EPS)
Protective, slimy layer of biofilm allowing for nutrient sharing and protection
Quorum Sensing
Cell-to-cell communication system of biofilm for coordination and gene expression (multicellular-like)
Common Sources of Biofilms
Implanted devices, inert objects, natural sources, etc.
Why are biofilms resistant to immune system and antibiotics?
Phagocytes and antibiotics can only reach top layer and there is no active metabolism
Biofilm and Sequelae
Linked to recurring, chronic infections due to release of planktonic bacteria after phagocytosis
Invasion
Use of invasins to invade, obtain nutrients, and damage host cells
Do pathogens always invade?
No, they may stay on the surface of hosts
Invasins
Virulence factors assisting invasion locally/immediately
Uptake induction
Motility
Toxin release
Protection
Break down of tissues (collagenases, etc.)
Iron-binding Proteins
Bind to host proteins to internalize iron inside of host protein
Siderophores
High affinity for iron to take to bacteria
Exoenzymes
Break down nutrients or spread
Lipase
Protease
Nuclease
Hyaluronidase
Cytopathic Effects
Direct damage or induction of autoimmune byproducts
Chronic Inflammation
Disruption by taking nutrients, exoenzymes, toxins
What are a major virulence factor?
Exotoxins…
Exotoxins
Proteins produced by both gram bacteria in low concentrations to aid, disrupt, alter, aid
Potent
Immunogenic - anti-toxin antibodies, toxoids
Endotoxins
Lipid A of LPS in Gram-Negative ONLY, released from lysis
Which gram-bacteria produces Lipid A endotoxin?
Gram-negative produce Lipid A
Which toxins are responsible for symptoms?
Exotoxins
Toxoid
Toxin deactivated by heat or chemical for vaccines
Lipid A Endotoxin
Gram-negative ONLY
Release via lysis results in endotoxemia, systemic inflammation, sepsis
Lipid-based, no vaccine, wrong antibody can cause sepsis
Septic Shock
Life-threatening hypotension and multi-organ failure
Which toxin is more toxic?
Exotoxins because they require lower concentrations (potent)
Evasion of defenses
Escape host defenses by either hiding or undermining immunity
Hiding
Antigen Masking
Antigen Mimicry
Antigen Variation
Intracellular
Latency
Antigen Masking
Covered in host factors to hide pathogen itself
Antigen Mimicry
Antigen production similar to host so host doesn’t attack ‘itself’
Antigen Variation
Once recognized, bacteria changes its antigens
Intracellular Pathogen
Hiding by living inside host
Latency
Remaining dormant in biofilm or endospore, protects from drugs and immunity
Undermining
Immune suppression
Phagocytosis interference
Immune Suppression
Kill immune cells with cytolysins, exoenzymes
Break down antibodies with proteases
Cytokine signal interference