Med Micro 1.2 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Main mechanisms of pathogenesis

A

Invasion of tissue (entry!) and production of toxins. May be one or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is adhesion not mentioned in main mechanisms of pathogenesis?

A

It is a prerequisite for invasion. Goes without saying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Invasiveness factors

A

Intracellular and extracellular pathogens; capsules; adaptation; extracellular enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intracellular and extracellular pathogens

A

Few intra, cause chronic disease; extra- cause acute disease (needs to access nutrients - cause damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Endogenous and exogenous antigens and their result

A

Endogenous presented to cytotoxic T cells by MHC1: show viral infection, etc. Exogenous to T helper cells by MHC2: present results of phagocytosis; T helpers make cytokines, B cells make antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Capsules

A

hydrophilic gels that inhibit phagocytosis. Usually an essential virulence factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adaptation

A

microenvironments of host provide habitats for bacteria that are capable of selective tissue invasion. Not every pathogen in a region can cause an infection there.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Extracellular enzymes

A

Help degrade host tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Invasins

A

Basically a spreading factor, can’t stay in same place forever!; enzyme family, help get through tissue matrices and intercellular spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Quorum sensing

A

Need a certain number of microbes. Turns on many other genes. Others can bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Toxins

A

Exotoxins: toxic but heat labile; Good immunogens. Endotoxins: complex lipopolysaccharide from cell wall; poorly immunogenic; released when cells lyse; heat stable, mostly in gram negative.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is it important that LPS is a poor immunogen?

A

Immunogen = elicits immune response; most proteins are (except small ones). We don’t have a good response to LPS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Membrane-damaging exotoxins

A

Form pores in eukaryotic membranes; streptolysin from streptococcus lyse RBC, WBC, platelets; hemolysin lyses RBC (S. aureus) ; listeriolysin from Listeria helps it evade lysosomes when endocytosed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is hemolysin expression regulated?

A

In response to low iron levels so it can break open RBC and gain some

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Defining entry again

A

Portals of entry are the areas where the pathogen gains access to tissues. Actual entry is invading those tissues, actually getting into the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

A-B toxins

A

A chain inhibits some cell functions; B chain binds and helps A enter. In cholera

17
Q

Endotoxin (LPS)

A

Lipopolysaccharide or Lipid A in gram negative bacteria. Very variable in polysaccharide size even within one type of bac. Need to test for LPS even if bacteria don’t grow

18
Q

Virulence

A

combination of invasiveness and toxigenicity producing the ability to overcome host defenses and cause disease

19
Q

Testing Virulence

A

measured with LD50. lethal dose: the # of bacteria to kill half of a population

20
Q

What is the point of an LD50 study?

A

Gives level of virulence and we can look at virulence factors (mutate the bacteria and perform the test several times), which is needed for vaccine development

21
Q

Some host defences

A

Skin, mucous, innate immunity, inducible ; some are specific, others not; vary with alcohol, drugs, nutrition, genetics,

22
Q

Factors in innate immunity

A

Inflammatory response, phagocytes, antimicrobials, complement, other WBC (neutrophils), Natural killer cells

23
Q

Inducible/Adaptive response

A

Hemoral immunity (ABs from B cells), cell-mediated response

24
Q

Skin and mucous pupose

A

Mechanical factors, chemical (eg Lysosyme, sebum), microbial factors (normal microflora are competitive, release antibiotics to compete for resources)

25
Q

Phagocytic cells

A

Respond to and release cytokines when they consume pathogens. Cytokines turn on inflammation, neutrophils etc recruited. Monocytes in blood, macrophages/dendritic cells fixed in tissues.

26
Q

Responses to phagocytosis of a bacterial cell? (lots!)

A

Signal b/w 2nd and 3rd line of defense. Antigen presentation (humoral); inflammation (interstitial fluid leaks easier, enter lymph to present antigens or bacteria);

27
Q

Humoral factors - role of antibody mediated defense

A

Antitoxins. Bacteriolytic antibodies (AB plus complement - make hole in them). Opsonizing AB (coat cell surface and enhance phagocytosis - ie target for phagocytosis). Agglutinating ABs

28
Q

Cell-mediated factors

A

Cytotoxic T lymphocytes; NK cells; activate macrophages

29
Q

Communicability

A

Source (dormant or latent - carriers?); # infectious agents released from host; capability of surviving transit b/w hosts; Percent of host population susceptible

30
Q

Superinfector

A

Someone who doesn’t display symptoms but releases huge amounts of -particles

31
Q

Triangle of relationships

A

Humans, drugs, microbes. All interacting, all evolving.