Lecture 3 Flashcards
list 6 modifying factors that would cause the development of a clinical disease in an infected animal
- stress
- poor nutrition
- tissue damage
- immunosuppression
- metabolic dysfunction
- intercurrent disease
define the following:
- pathogen
- pathogenicity
- virulence
- opportunistic pathogens
- obligate pathogens
pathogen: microorganism that is able to produce disease
pathogenicity: ability of a microorganism to cause disease in another organism, namely the host
virulence: degree of pathogenicty
opportunistic: bacteria that do not need to cause disease to facilitate their own transmission
obligate pathogens: require a host for survival and transmission, infection with these usually results in disease
the host contains mucosal defenses. list some examples
in the mucus: lyzozyme, antibodies, peptides, complement factors
tight junctions between cells, peristalsis clearance, commensal flora competition, and glycoproteins
what are virulence factors?
mechanisms to circumvent host defenses and multiply
adherence to a eukaryotic cell or tissue surface requires a _____ and a _____
receptor, ligans
the receptor is specific _____ or ______ residues on the eukaryotic host surface
carbohydrate, peptide
the bacterial ligand, called an _____ is typically a ______ component of the bacterial cell surface
adhesion
macromolecular
what is tissue tropism?
particular bacteria are known to have an apparent prefrence for certain tissues over others
what is an invasin?
virulence factors that enable internalization of the bacteria, lets the bacteria IN
what is a “type III secretion system”?
machinery possessed by many gram neg bacteria to delivery effector ptoteins and hijack the host cell signaling pathways
what is the difference between secretion and translocation?
secretion: into extracellular environment
translocation: directly into a host cell
what are two examples of type III secretion systems, one for E coli and one for salmonella?
- enteropathogenic E coli (EPEC) delivers a receptor for one of its own adhesions into a host cell membrane which allows binding of E coli to the cell
- salmonella typhimurium delivers effectors called invasins that manipulate the hosts actin cytoskeleton and uptake into membrane vacuoles which allows hiding from the immune system
salmonella typhimurium can release invasins into host cells but can also release a protein called SopB. Exaplin what this does
SopB induced enterocytes to transform into M cells to promote host colonization and invasion (M cells are the preferred entry cell)
what are spreading factors?
bacterial enzymes that affect the physical properties oftissue matrices and intercellular spaces, thereby promoting the entry/spread of the pathogen
birefly explain what each of these spreading factors do/how they work:
- hyaluronidase
- collagenase
- neuraminidase
- streptokinase
hyaluronidase: attacks the intracellular matric of connective tissues by depolymerizing hyaluronic acid (aka it dissolves the cement holding the cells together)
collagenase: breaks down collagen, the framework of muscles, which facilitates gas gangrene, AND it triggers blood plasma clotting, allowing bacteria protection from immune defenses
neuraminidase: degrades neuramic acid which is the residue in mucin in the intestinal tract
streptokinase: converts inactive plasminogen to plasmin which digests fibrin and prevents clotting of the blood
what are the 3 main roles of the complement system?
- tag microbes for destruction by phagocytic cells
- microbial lysis
- generate proinflammatory response
what are the 3 ways in which bacteria can evade complement?
- capsules: polysaccharide capsules can hide bacterial components, some can even inhibit formation of complement
- LPS modification by attachment of sialic acid residues to the LPS antigen prevents membrane attack complex killing
- destruction of complement component: extracellular elastase enzyme
some bacteria can overcome host phagocytic defenses. what are the 5 “steps” that the bacteria can eliminate/manipulate?
- contact between phagocyte and microbial cell
- engulfment
- phagosome formation
- phagolysosome fusion
- killing and digestion
what are the 3 processes by which bacteria can avoid contact with phagocytes?
- remain confined to regions inaccessible to phagocytes like the lumen of the GI tract, oral cavity, urinary tract, mammary gland, kidney tubule
- hide the antigenic surface of the bacterial cell (like a capsule or being surrounded by fibrin)
- inhibit the phagocyte chemotaxis (so the phagocytes din’t sniff you out!)
what is the main way in which bacteria inhibit phagocytic engulfment?
via antiphagocytic substances on the bacterial surface
what are the 3 main processes that bacterial can survive inside of phagocytes?
- they can inhibit phagosome-lysosome fusion
- they can survive in the phagolysosome
- they can escape the phagosome
what are the two broad ways in which bacteria can kill or damage phagocytes?
- kill the phagocytes before ingestion
- kill the phagocytes after ingestion
what are hemolysins and streptolysins? what do they do?
hemolysins: extracellular enzymes secreted by many gram pos bacteria that can kill/damage phagocytes
streptolysin: secreted by pathogenic streptococci, it an kill neutrophils
many intracellular pathogens can destroy macrophages after theyve been phagocytized. how does this happen?
we don’t know!
there are several ways in which bacteria can resist the adaptive immune response. list some examples
- if its an aggressive and acute attack, antibodies wont be made in time to get ya!
- proteinases degrade antibodies
- cell wall can protect the bacteria like LPS or peptidoglycans
- they can hide inside cells
- they can do antigenic mimicry to appear like the host cells
- they can make superantigens to divert the T and B cells, like a fake antibody, putting the adaptive immune system on the “wrong trail” and they waste their time on making useless antibodies instead of the correct one
two broad qualities of pathogenic bacteria underlie the means by hich they cause disease which are:
invasiveness (ability to invade tissues)
toxigenesis (ability to produce toxins)
what is the difference between exotoxins and endotoxins?
exotoxins: released from bacteria and may act at tissue sites removed from the site of bacterial growth
endotoxins: bacterial cell associated supstances and when released from cells they may be transported by blood or lymph and cause cytotoxic effects at tissue sites remote from the original point of invasion or growth
many protein toxins are basically enzymes, which means:
- they are denatured by heat, have high biological activity, and exhibit specificity of action
what do E coli enterotoxins do?
activate ion and water pumps causing loss of fluid and electrolytes from cells
when are endotoxins released?
when the bacteria dies
what part of LPS is toxic?
lipid A
endotoxin release results in wide spectrum of :
nonspecific pathophysiological reactions related to inflammation such as fever, changes in WBCs, DIC, hypotension, shock, death
toxin induced damage and include what 7 things?
- CV disturbance
- destruction of blood vessels
- diarrhea
- disruption of the nervous system
- plasma membrane disruption
- inhibition of protein synthesis
- shock
what are 3 host responses to bacterial infection that can cause host damage?
- reactive oxygen species and nitrogen species
- inflammation
- septic shock
