1/2 bacterial structure and pathogenesis Flashcards
what organelle do prokaryotes have
- ribosome, just free in cytoplasm
- no other organelle
- nothing membrane bound except cell itself
cocci
round
ex: streptococci
diplococci
two round cells
ex: Neisseria
Baccili
rod shape
ex: bacillus
spirilla
spiral
ex: campylobacter
**spirochetes = true spiral, corkscrew, oral treponemes
pleomorphic
morphology can vary depending on environment (fusobacteria)
Gram stain - 3 groups
G pos = purple
G neg = pink
acid fast = myobacteria (tuberculosis) – MYCOLIC ACID
why do acid fast not stain?
mycolic acid
cell envelope
multiple functionally adn chemically distinct layers
describe G neg
(stains pink)
- inner membrane
- periplasmic space with peptidoglycan
- outer membrane with LPS outer leaflet
describe G pos
(stains purple)
- thick peptidoglycan layer
- *peptidoglycan later gas teichoic acid and lipoteichoic acid
- over membrane
what is only found in G pos adn only in G neg
G pos - only cells with teichoic adn lipoteichoic acids
G neg - only cells with LPS (outer leaflet of outer membrane)
spetic shock cause
LPS, Lipid A (G neg)
teichoic/lipoteichoic acids (G pos)
variable components = flagella, pilus, capsule
- flagella, G neg its anchored in many places
- pilus = fimbria
- capsule = optional; also can be induced in some when env conditions call for it
LPS components
(LPS is outer leaflet of G neg and renders outer membrane)
- O antigen: external, highly variable, connects to core
- core region: inner core (heptose sugars adn KDO0 and outer core (hexose sugars)
- lipid A: membrane anchoring, toxic component
LPS can cause what and how
septic shock, MSOF – Lipid A is released when cells are lysed. normally lipid A buried deep
lipid A: fatty acid attached to sugar component - when this is altered slightly, you affect the potentcy. **AA in D configuration
teichoic and lipoteichoic acids
- only in G pos
- polymer of modified ribose phosphate or glycerol phosphate
- lipoteichoic acids are anchored to cell membrane by FA
- Teichoic acids are covalentyly linked to peptidoglycan
- can trigger septic shock adn MSOF
peptidoglycan (murein)
- in G pos (very thick) and G neg (thin, periplasmic space)
- alternating units of NAM and NAG
- strands linked by peptides of D and L-aa’s
- forms rigid mesh that maintains cell rigidity
- can be cleaved by lysozyme
what can tear peptidoglycan apart
lysozyme
bacterial capsule aka glycocalyx aka slime layer
- polysaccharide or AA network
- made by some G pos and some G neg
- promotes adherence (to teeth)
- protect from our immune system: anti-phagocytic (harder to engulf) and inhibits complement
- production is regulated, many only produce when needed
- increase virulence
how does capsule protect & how is it functional
- anti phagocytic (harder to engulf)
- inhibits complement
-helps bacteria adhere to teeth
^^increaes virulence
pathogenic
yes or no question. does it cause diseae? yes or no.
pili and fimbrae
- hollow protein cylinders
- in most G NEG adn only a few G pos
- overcome electrostatic repulsion adn help with cell to cell contact adn adhesion
- pili can do DNA transfer
- fimbreae shorter adn more numerous
pili in fimbrae found more in which bacteria
G neg
pili vs fimbrae
- fimbrae are shorter and more numerous
- pili can fxn in DNA trasnfer
- BOTH are hollow protein cylinders that play a role in adherence and cell to cell contact (overcome electrostatic repulsion)
afimbrial adhesins
clusters of protein that are not organized in a defined structure that mediate cell to cell binding
- do not form hollow tube
- just embedded in membrane
- lock and key interaction, like pili, but stronger
what proteins are located at pilus tip?
adhesin proteins that mediate initial binding are at tip of pilus….lock adn key receptor (explains why E coli causes UTI)
what does pili mediated adherence have to do with location of germ
- adhesin protein at tip of pilus = lock adn key type combo with host cell
- so where you find bacteria is determined by env.condiitions AND where there are cells it can interact with, adhere to
specialized pili
fxns: adherence, DNA uptake and exchange, important role in motility
**type 4: extend and attach to surface and then retract to pull bacteria forward, allows for movement along surface
**F pili = sex pili = conjugation, DNA transfer
type 4 pili
F pili
type 4 - movement along surface (extend to surface and then retract to pull bacteria to surface)
F pili = sex pili = conjugation = DNA transfer
(general fxn = adherence, DNA uptake, motility)
flagella
- monotrichious = single flagella at one end
- lophotrichois = many flagella, all at same end
- amphutrichous = bundles at both ends, one set for one way and one for another
- peritrichous = extend all directions
**spirochetes – endoflagella
monotrichous
1 flagella frmo 1 end
lophotrichous
multiple flagella, from one end
amphithrichous
bundles of flagella at each end
peritrichous
flagella extend all directions
spirochete flagella type
endoflagella – use like cork to drill in tissue, (perio disease!), periplasmic flagellum on inside of cell, localized between inner and outer membranes, many from each end, can reverse direction
what do we need to know about flagella structure?
very defined portions of the motor
G neg has more anchor sites since more layers
bacterial injectisome
- type 3 secretion system
- structural similarity to flagella
- directly injects effector protein into host cell
**important in pathogenesis for many G neg cells!
what is important to the pathogenesis of many G neg cells
injectisome, type 3 secretion system – like a flagella that injects effector protein into host cell
bacterial spores
- produced by some G pos
- resistant to heat/desication
- have a chromosome copy
- metabolicaly inactive
- can persist for YEARS
- germinate to form a new vegetative cell
- anthrax
what happens to inactive spore when conditions are right
it GERMINATES to form a new vegetative cell that can thrive
infection
signs and symptoms of disease occur
pathogenic
can cause disease
virulence
quantitative term for disease causing capacity
ID 50
dose required to INFECT 50% test population
LD 50
lethal dose required for killing 50% test population
opportunistic pathogen
usually not a problem, buut under certain conditions causes disease
LD 50 vs ID 50
lethal vs infect
-minimum dose to either kill (LD) or infet (ID)
gnotobiotic
animals devoid of microflora (survive, but do not thrive)
- less healthy
- less developed lymphoid tisues & low Ab titers
- thin intestinal walls
- low metabolism rate
- prone to infections
- require dietary supplements
benefits of normal flora
- food metabolism (proteolytic enzymes facilitate absorption –> malabsorption)
- vitamin production: biotin, panthotenic acid, pyridoxine, riboflavin, vitamin K
- protective effects: competition, antibacterial production, immune stimulation
vitamins produced by normal flora
biotin, panthothenic acid, pyridoxine, riboflavin, vitamin K
protective effects of normal flora
- competetion for nutrients/space
- production of antibacterials: metabloic by products are non specific, bacteriocins are specific
- immune response stimulation (example of M cell, bacterial antigen stimulates IgA antibody production)
study of M cells that showed immune stimulation by normal flora
- bacteria taken up by M cell and pass through
- presented to macrophage that takes it up adn degrades it
- macrophage presents to cells that make Ag’s which then interact with T cells adn B cells to make ANTIBODIES
- IgA = antibody in lumen that protects mucosa
IgA
antibody that protects mucosa of lumen of GI tract, protects against establishment of salmonella and shigella and otehr mucosal pathogens
IgA production is due to normal flora
number bacteria in large intestine vs oral mucosa
lg intestine- 10^14 per gram tissue
oral mucos- 10^10
oxygen levels in air, mouth, subgingiva
21%
12% mouth
2% subgingiva
what enzymes to anaerobic bacteria lack?
catalase and superoxide dismutase
environmental variables that affect flora
- oxygen
- Temp
- pH
- diet
- age
- hormonal state
how are normal floar harmful?
-leading cause of infection in…
dental caries, perio disease, UTI
-bacteria capitalize on trauma, weak immune systems, or altered health – and then cause disease
5 steps to infection
- relocation of normal flora or entry of pathogens
- adherence and colonization
- establishment of porductive population
- dissemination (NOT ALL SPREAD)
- outcome = disease and host damage
what constitutes infection
host damage adn disease
how can pathogens be transmitted
- aerosols (whooping cough)
- fecal/oral (cholera)
- contact (conjunctiva): pink eye
- arthropods/insect (lymes)
- transplacental (gonorhea)
- blood (Hep)
arthropod vectors
mosquito = west nile, malaria, yellow fever
ticks = lyme, relasping fever, CO tick feevr
assasin bug = chagas disease (trypanosomiasis)
adherence and colonization - point adn example
ACTIVE, not passive process
ex: E.coli induces cytoskeleton rearrangement in the host, resulting in pedestal formaation (EFFACING)
- -germ can bind pedestal v tightly
capsules and host defense evasion
- anti phagocytic: cells hard to engulf, capsule pulls away when grabbed
- capsule binds protein that inhibits Ab binding and complement
- molecular mimicry: capsules sometimes made of material that resembles the host
host evasion bia antigenic variation
- switch surface antigens
- ex: relapsing fever–borrelia hermsii–high density in blood, 40vmp genes but only 1 expressed so when host makes Ab to 1, just switch to another
- -cyclic fevers
borrelia hermsii
- relapsing fever
- 40 vmp genes but only 1 expressed
- example of antigenic variation in bacteria to evade host defense
evasion of host via intracellular localization
- some intracellular pathogens are obligate while others are facultative
- nutrient rich environment
- protection from Ab adn complement
direct pathogen induced damage
- destructuve enzymes (proteases, callagenases) = PERIPATHOGENS
- toxic metabolic by products
- exotoxins – cholera, tetanus
- release cellular components
LPS has host dirven damage
- LPS has separable toxic and immunostimulatory activities
- endotoxin = lipid A
- endotoxic effects only occur upon cell lysis bc lipid A normally buried in membrane
physio response to LPS –> all leads to septic short (vascular collapse) and MOSF (multi system organ failure)
- Fever – cytokines
- neutropenia – neutrophils sequestered in organs, transient decrease in circulating n.phils results
- DIC = disseminated intravascular coagulation: platelets adhere to and occlude small blood vessels (form clots)
- hypotension: vacular leakage causes low BP
- lysozymal enyzmes relaesed, damage endothelium
DIC (LPS respons)
disseminated intravascular coagulation = platelets adhere to and occlude small vessels (form clots)
LPS response - hypotension
- low BP bc of vascular leakage
- complement proteins C3a adn C5a attract PMNs (polymorphonuclear leukocytes) which adhere to endothelial cells
LPS response - neutropenia
neutrophils get sequested in organs causing a transient decrease in circulating neutrophil count
