Microbiology of Pathogenic Factors Flashcards
Microbe?
-few are pathogenic
-bacteria
-many benefit the host without causing disease
-
Healthy biome=?
-how healthy we are
The Host?
-host factors influence the relationship b/w microbe and host
Commensalism?
-one organism benefits
-host is unaffected, we just provide shelter and nutrients for the microbe
mycobacteria of the ear and external genitalia
Mutualism?
- both benefit
- e-coli, vitamin K
- large intestine of the host can give nutrients to the bacteria that help use digest and metabolize our food.
Parasitism?
-microbe harms host from its ability to get nutrients and shelter, disease can follow
Amensalism?
-relationship where the host is harmed but the microbe doesn’t benefit nor is it harmed
Infection vs colonization?
Microbiome?
Infection= causes harm Colonization= Microbiomes, don't cause harm microbiome= portion is permanent (developed when baby is passed through birth canal), transient component that shifts when we are subject to new micro-organisms
Resident microbiota?
Transient microbiota?
Interaction b/w host cells and normal flora?
RM= permanently colonize the host
TM= temporarily colonize the host
-do not produce disease under normal conditions
Host cell and Normal Flora; distribution and composition determined by 1. Nutrients, 2. Physical and chemical factors
- Nutrients
- secretory and excretory products of cells
- bodily fluids
- food in the GI - Physical and Chemical Factors
- temperature
- pH
- O2
- CO2
- salt
- sunlight
Host cell and Normal Flora; distribution and composition determined by 3. mechanical factors, 4. other “host” factors
- Mechanical Factors
-chewing
flow of saliva and peristalsis of GI
mucous of respiratory system
-normal flora microbes must be able to hold on - Other “host” factors
-age (microbe weakens as it ages)
-nutritional status= healthy=healthier microbe
-disability= obese causes more skin folds and more places for microorganisms to grow
-stress=effects health of microbiome
-hygiene= different number of flora than someone who has access to a shower
-lifestyle= more exposed to fungi
-geography= depends on where we live
occupation= more contact with strangers/ travelling
Microbial Antagonism? (in relation to human and normal flora relationship)
- normal flora benefits the host by preventing growth of pathogenic microbes (make it hard for pathogenic microbes to grow/ cause infection
- colonizes the host without causing disease
What makes us less susceptible to acquiring infections?
- microbiome
- does not want to share us with the invading microbes
Normal Flora?
- competes with pathogen for nutrients
- makes substances that are harmful to the pathogen
- manipulate the hosts environment to make it hard for pathogenic microbes to survive (i.e: increase or decrease pH, increase or decrease O2 levels
Bacteriocins?
- proteins that inhibit growth of a particular species
- pathogenic microbe has to compete against our microbiome
Disruption of balance b/w normal flora and pathogenic microbes=?
- infection/ disease can result
- microbiome becomes overwhelmed, normal flora is damaged, disease occurs
4 factors that distrust the balance b/w normal flora and pathogenic microbes
- age
- antibiotic use (damage gut flora, makes them vulnerable to infection)
- nutritional status (not that good at protecting us)
- changes in hygeine
Microbial Antagonism?
-using established cultures of microorganisms to prevent the intrusion of foreign substances
Clostridium Difficile?
what happens if there is lots of normal flora in the gut?
-pathogen that causes a range of GO symptoms
9mild diarrhea to even fatal colitis
- lots of NF in gut prevents growth of C-difficile
Antibiotics and C-difficile?
- can destruct the GI NF, creating an environment suitable for C-difficile growth
- disease occurs
3 factors that can occur for opportunistic infections to occur?
- microbes from host NF move from normal habitat, which an cause disease
- hosts immune system is weakened or compromised
- composition of NF changes (antibiotic therapy), creates an opportunity for pathogenic microbes to grow and cause disease
Microbial mechanisms of pathogenesis?
- contact/exposure
- adherence (we cannot cough or pee it away)
- evasion of host defences and penetration
- damage to host cells (make us sneeze)
- transmission (cause infection in someone else)
Contact/exposure: 3 portals of entry?
- Mucous membranes
- upper respiratory tract
- GI
- GU
- Conjunctiva - Skin (barrier, but if broken pathogenic microbes can enter, can also enter through sweat glands and hair follicles)
- Direct deposition beneath mucous membranes or skin
- trauma, surgery, invasive procedures
Adherance?
- pathogen attaches to a host at a portal of entry
- accomplished by cell surface molecules (adhesions), binding to surface receptors on host cells
- adhesions are tissue and host specific
Adherence: Bacterial Structures
-adhesions are present on fibre and flagella on many bacterial pathogenic microbes
P-fimbriae on pyelonephritogenic E.coli
-adhere to a specific galactose disaccharide found on the surface of uro-epithelial cells (90% of UTI’s)
Adherence: Adherence Proteins?
- M-proteins produced by streptococcus progenies are hair like projections from cell surface
- mediates attachment of bacteria to epithelial cells of the host
Adherence: Glycocalyx?
- if well firmly attached to cell wall it is called a capsule
- binds to epithelial cells of the ventricles and vascular endothelium of the brain (meningitis)
Capsule? Slime layer?
Capsule= glycocalyx firmly attached to cell wall
Slime layer= glycocalyx loosely attached to cell wall
What facilitates to formation of biofilms?
-slime layer
Biofilm?
- colony of bacteria that adheres to surfaces (teeth, contacts, heart valves, hip replacement, catheters, industrial food equipment
- embedded in extracellular slime layer
- can consist of bacteria cells as well
- involved in many infections
- resistant to infection and antibiotics
- few treatments available, surgical intervention is often required
Enzymatic Bacteriophage?
-virus that eat bacteria, digest the biofilm which kills the slime layer
clears the infection
Evasion of host defences: Capsule
-impairs phagocytosis by host cell, so that phagocytic cells can’t adhere to the bacterial/pathogenic microbe
reproduce quickly, doesn’t take long to evade
Evasion of host defences: Cell wall
-M-proteins help bacteria resist phagocytosis
Evasion of host defences: Coagulase
-enzyme
coagulate fibrinogen in blood to form fibrin
fibrin clots protect the bacteria from phagocytosis
-“hide” from the body
Evasion of host defences: Kinase
- enzyme
- degrades fibrin
- digests clots in the body meant to hide the bacteria for protection from phagocytosis
- can also break up clots that our body has formed and get into deeper more nutrient rich tissue
4 ways how intracellular bacteria can survive in immune cells?
- escape phagosome before fusing with host cell lysosome
- preventing phagosome lysosome fusion
- reducing the toxic components inside a lysosome
- making cell walls resistant to proteases from lysosomes
- body cannot recognize this
Penetration of host tissues: Hyaluronidase
- enzyme
- degrades hyaluronic acid (polysaccharide that holds cells tight junctions together)
Penetration of host tissues: Collagenase
- degrades collagen fibres
- allows bacteria to move deeper into host tissue
Penetration of host tissue: entering non-phagocytic cells
-penetrate without destroying acid
-enter cells that can’t phagocytose
-propel invasions inside non-phagocytic cells, this causes actin filaments to rearrange
cell membrane looses integrity, bacterial cell can sink inside form vesicles and cause the inflammatory response to set off, inducing the symptoms
Membrane ruffling?
-disruption of cytoplasm causes the tight junctions to open and the bacterial microbe can sink in
Advantages of entering non-phagocytic cells?
-lots of nutrients
-protected from immune system
protected from antibiotics
Damage to host cells?
-disease/ cell damage occurs if evading the host cell is effective
4 ways to cause host cell damage?
- taking nutrients from host
- physical damage to tissues surrounding site of invasion (parasitic relationship
- producing toxins
- hypersensitivity runs
4 ways to cause host cell damage: taking host nutrients
- What are siderophores?
- Toxins used?
- Bind directly to host cells?
-taking nutrients harms us and our growth ability
-iron is needed for growth of pathogenic bacteria; they can only get it from us
-iron deficiency in bacterial cell drives it to take it from host cells
siderophores= bind to iron more tightly than host iron-transport proteins (made from bacteria)
-bind directly to host iron-binding proteins
-some produce toxins that kill host cell, release of iron pathogen can acquire the iron
Siderophores?
-bind to iron more tightly than host iron-transport proteins (made from bacteria)
4 ways to cause host cell damage: Direct damage to tissues surrounding site of invasion
- Bacteria grow and multiply inside host cells, they aggressively rip open and get out
- once released they are spread to other tissues
- damage from ripping open yields the signs of infection/ disease
4 ways to cause host cell damage: Toxins
-toxins alter normal metabolism of host cells
used in the pursuit of iron
create opportunities to gain nutrients as well as facilitating transmission
2 broad toxins: Exotoxins
-actively produced by bacteria and are actively released to cause their cellular damage
-secreted into surrounding environment
water and fat soluble, can move all throughout the body
can be fatal
-exposure to the toxin can cause disease or sickness
2 broad toxins: Endotoxins
- lipid A that is in the outermsmbrane of gram-negative bacteria
- one and only endotoxin
- when bacteria dies lipid A is released into our blood stream
- if we target and destroy gram negative bacteria lipid A can be released making the client worse
- try to choose antibiotics that target ribosomes weather than the entire cell
- cause macrophages to release large amounts of IL-1
A-B Exotoxins?
A-B toxins
A= active enzymatic component
B=Binding component
B binds to host cell then A changes the host cell function
Bordetella Pertussis?
-release AB exotoxins, get inside, increase cAMP levels, cause cell to make more mucous=causes coughing “whooping”
Exotoxins: membrane disrupting toxins?
- induces cell lysis
- rip apart RBC and WBC
- destroys lipid membrane bilayer
Exotoxins: superantigens?
- produce intense immune response
- bind on MHC class II on macrophage surface (not produced by macrophages)
- causes excessive TNF-a, IL-2, TF production
- fever, nausea, vomiting, diarrhea, can sometimes lead to septic shock
Signs and symptoms of endotoxin (lipid A) toxicity?
- chills, fever, weakness, generalized aches
- can cause clots to form in intravascular
How do Endotoxins produce fever?
- macrophage ingests gram-negative bacteria
- bacterium is degraded, releasing endotoxins (Lipid A), induce macrophage to make IL-1
- IL-1 released into blood stream, travels to hypothalamus of brain
- IL-1 induces hypothalamus to produce prostaglandin to increase bodies temperature
Are exotoxins associated with fever?
when do exotoxins produce a fever?
-No, only if they are a super-antigen
Transmission? portals of exit?
-leave body through portals of exit in secretions, excretions, discharges
respiratory tract, GI, GU, skin, conjunctiva, blood
