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VETM 423 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

list 6 modifying factors that would cause the development of a clinical disease in an infected animal

A
  1. stress
  2. poor nutrition
  3. tissue damage
  4. immunosuppression
  5. metabolic dysfunction
  6. intercurrent disease
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2
Q

define the following:
- pathogen
- pathogenicity
- virulence
- opportunistic pathogens
- obligate pathogens

A

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

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3
Q

the host contains mucosal defenses. list some examples

A

in the mucus: lyzozyme, antibodies, peptides, complement factors
tight junctions between cells, peristalsis clearance, commensal flora competition, and glycoproteins

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4
Q

what are virulence factors?

A

mechanisms to circumvent host defenses and multiply

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5
Q

adherence to a eukaryotic cell or tissue surface requires a _____ and a _____

A

receptor, ligans

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6
Q

the receptor is specific _____ or ______ residues on the eukaryotic host surface

A

carbohydrate, peptide

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7
Q

the bacterial ligand, called an _____ is typically a ______ component of the bacterial cell surface

A

adhesion
macromolecular

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8
Q

what is tissue tropism?

A

particular bacteria are known to have an apparent prefrence for certain tissues over others

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9
Q

what is an invasin?

A

virulence factors that enable internalization of the bacteria, lets the bacteria IN

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10
Q

what is a “type III secretion system”?

A

machinery possessed by many gram neg bacteria to delivery effector ptoteins and hijack the host cell signaling pathways

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11
Q

what is the difference between secretion and translocation?

A

secretion: into extracellular environment
translocation: directly into a host cell

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12
Q

what are two examples of type III secretion systems, one for E coli and one for salmonella?

A
  • 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
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13
Q

salmonella typhimurium can release invasins into host cells but can also release a protein called SopB. Exaplin what this does

A

SopB induced enterocytes to transform into M cells to promote host colonization and invasion (M cells are the preferred entry cell)

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14
Q

what are spreading factors?

A

bacterial enzymes that affect the physical properties oftissue matrices and intercellular spaces, thereby promoting the entry/spread of the pathogen

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15
Q

birefly explain what each of these spreading factors do/how they work:
- hyaluronidase
- collagenase
- neuraminidase
- streptokinase

A

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

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16
Q

what are the 3 main roles of the complement system?

A
  1. tag microbes for destruction by phagocytic cells
  2. microbial lysis
  3. generate proinflammatory response
17
Q

what are the 3 ways in which bacteria can evade complement?

A
  1. capsules: polysaccharide capsules can hide bacterial components, some can even inhibit formation of complement
  2. LPS modification by attachment of sialic acid residues to the LPS antigen prevents membrane attack complex killing
  3. destruction of complement component: extracellular elastase enzyme
18
Q

some bacteria can overcome host phagocytic defenses. what are the 5 “steps” that the bacteria can eliminate/manipulate?

A
  1. contact between phagocyte and microbial cell
  2. engulfment
  3. phagosome formation
  4. phagolysosome fusion
  5. killing and digestion
19
Q

what are the 3 processes by which bacteria can avoid contact with phagocytes?

A
  • 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!)
20
Q

what is the main way in which bacteria inhibit phagocytic engulfment?

A

via antiphagocytic substances on the bacterial surface

21
Q

what are the 3 main processes that bacterial can survive inside of phagocytes?

A
  • they can inhibit phagosome-lysosome fusion
  • they can survive in the phagolysosome
  • they can escape the phagosome
22
Q

what are the two broad ways in which bacteria can kill or damage phagocytes?

A
  • kill the phagocytes before ingestion
  • kill the phagocytes after ingestion
23
Q

what are hemolysins and streptolysins? what do they do?

A

hemolysins: extracellular enzymes secreted by many gram pos bacteria that can kill/damage phagocytes

streptolysin: secreted by pathogenic streptococci, it an kill neutrophils

24
Q

many intracellular pathogens can destroy macrophages after theyve been phagocytized. how does this happen?

A

we don’t know!

25
Q

there are several ways in which bacteria can resist the adaptive immune response. list some examples

A
  • 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
26
Q

two broad qualities of pathogenic bacteria underlie the means by hich they cause disease which are:

A

invasiveness (ability to invade tissues)
toxigenesis (ability to produce toxins)

27
Q

what is the difference between exotoxins and endotoxins?

A

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

28
Q

many protein toxins are basically enzymes, which means:

A
  • they are denatured by heat, have high biological activity, and exhibit specificity of action
29
Q

what do E coli enterotoxins do?

A

activate ion and water pumps causing loss of fluid and electrolytes from cells

30
Q

when are endotoxins released?

A

when the bacteria dies

31
Q

what part of LPS is toxic?

A

lipid A

32
Q

endotoxin release results in wide spectrum of :

A

nonspecific pathophysiological reactions related to inflammation such as fever, changes in WBCs, DIC, hypotension, shock, death

33
Q

toxin induced damage and include what 7 things?

A
  • CV disturbance
  • destruction of blood vessels
  • diarrhea
  • disruption of the nervous system
  • plasma membrane disruption
  • inhibition of protein synthesis
  • shock
34
Q

what are 3 host responses to bacterial infection that can cause host damage?

A
  1. reactive oxygen species and nitrogen species
  2. inflammation
  3. septic shock

VETM 423 (9 decks)

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