Mechanisms of Pathogenicity Flashcards

1
Q

Pathogen

A

a pathogen is a microorganism that can cause a disease process

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

primary pathogen

A

always causes disease even in health immunocompetent individuals

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

Opportunistic pathogen

A

a microorganism that may cause disease if given the right circumstances

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

what are 3 examples of opportunistic pathogens and the circumstances in which they can infect?

A
  1. Candida albicans - immunosuppressed people (genetic problems or chemo therapy)
  2. Mucor species - diabetics [eye infection]
  3. Pseudomonas aeruginosa –> burn patients, Cystic fibrosis, HIV and neutropenic cancer patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pathogenicity

A

ability to cause disease by evading or overcoming the host defences

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

virulence

A

the extent to which the microorganism is pathogenic

its the measure of pathogenicity

i.e. C.albicans has low virulence

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

Virulence Factors

A

molecules/structures produced by pathogens that contribute to their “pathogenicity” or ability to cause disease (help the organism cause disease)

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

what is an example of virulence factor

A

the capsule of Streptococcus pneumoniae (s.pneumoniae is only a pathogen when it has the capsule)

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

4 portals of entry for pathogens to gain entry to the host?

A
  1. mucous membranes
  2. skin
  3. parenteral route via mouth (i.e. ingesting)
  4. surgical sites and implants (bacteria/micro-organisms can latch on to them and get into the body that way)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tropism

A

the cells and tissues of a host that support growth of a particular virus or bacterium.

Some bacteria and viruses have a broad tissue tropism and can infect many types of cells and tissues. Other viruses may infect primarily a single tissue.

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

6 determinants for tropism?

A
  1. Distribution of cell receptors for the microbes
  2. other competing microbes around
  3. accessibility of correct host cell types
  4. appropriate nutrients for growth
  5. physical and innate defences at the site of infection (the host’s age also plays into this)
  6. Permissive environmental condition i.e. pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are 4 examples of exotoxin producing bacteria?

A
  1. Corynebacterium diphtheriae (causes diphtheria) –> attaches to cells and produces exotoxins which moves through the blood and tissues
  2. Vibrio cholerae
  3. Clostridum tetani, botulinum, perfringens
  4. Bordetella pertussis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is different about exotoxin producing pathogens?

A

they remain at the site of infection and do not spread through the system to cause disease; instead their toxins are produced and it gets into cells and causes the diseases process

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

What is the first step to infection?

A

adherence

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

how do pathogens adhere to host cells?

A

pathogens have structures called adhesins or ligands which recognize and bind to receptors on host cells

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

what are most adhesins made of?

A

glycoproteins or lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are most receptors on host cells made of?

A

sugars like mannose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

adhesin possessed by N.gonorrhoeae bacteria

A

pili or fimbriae display adhesins (on tips of pili, helps bacterial attach to the surface of host)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

adhesin possessed by S.mutans

A

glycocalyx for adhesion (produces capsule to attach to surface [causes biofilms to be made and plaque]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

adhesins possessed by Enteropathogenic E.coli

A

specialized fimbriae that only bind to certain intestinal cells to cause diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

10 factors that help the bacteria evade or penetrate host defences

A
  1. capsules
  2. cell wall components
  3. biofilms
  4. enzymes
  5. invasins
  6. sueprantigens
  7. toxins
  8. secretion systems
  9. antigenic variation
  10. intra/extracellular growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do capsules help bacterial evade host cell defences?

A

glycocalyx layer

initially prevents the phagocyte from recognizing and ingesting the bacteria (inactivates opsonin)

many bacteria can produce capsules in the right environmental conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are three ways that cell wall components can help pathogens prevent opsonization?

A
  1. Fc Receptors on microorganisms prevent opsonization –> i.e. S.aureus has protein A on the cell wall which is a Fc receptor that binds to antibodies at the Fc end so phagocytes don’t find it and try to bind to it
  2. Streptococcus pyogenes –> has a protein “M” which is heat and acid-resistant protein in the cell wall that allows attachment of the bacteria to epithelial cells and inhibits phagocytosis
  3. Mycobacterium tuberculosis –> has mycolic acids which create waxy substances in cell walls make the bacterium resistant to digestion inside the phagocyte (makes it hard for the macrophage to break it down because its waxy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do biofilms help pathogens evade host cell defences?

A
  • community for bacteria (same or different species), often surrounded by a shared glycocalyx layer (capsule) –> there is communication between bacteria in biofilm
    (bacteria with capsules cause biofilm formations more)
  • biofilms educe antibiotic penetration and increases resistance [reduces antibiotic penetration because they are not actively metabolizing]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are two examples of biofilms in the human body?

A
  1. Porphyromonas gingivalis in oral cavity

2. Pseudomonas aeruginosa in lungs, on medical implants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are 7 exoenzymes (enzymes released from bacterial cells) that help bacteria evade host cell?

A
  1. Leucocidin –> destroys WBC
  2. Kinase –> breaks down fibrin and dissolves clots formed by the body to isolate the infection (important for the spread of the infection)
  3. Hemolysin –> breaks down red blood cells
  4. coagulase –> clots; converts fibrinogen to fibrin (protein strands) to form clots; the clot can wall the bacteria off from host defences
  5. Collagenase: breast down collagen
  6. lecithinase: destroys plasma membranes
  7. proteases: inactivate antibodies and other body proteins like IgA protease [breaks down IgA and allows the bacteria to attach to mucosal membrane]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is an example of a bacteria that has Leucocidin exoenzyme?

A

S. aureus

Actinobacillus species

28
Q

what is an example of a bacteria that has kinase exoenzyme?

A

Streptococcus pyogenes

29
Q

what is an example of a bacteria that has Hemolysin exoenzyme?

A

staph, strep, listeria, clostridium

30
Q

what is an example of a bacteria that has Coagulase exoenzyme?

A

Staphylococcus aureus

31
Q

what is an example of a bacteria that has Collagenase exoenzyme?

A

Clostridium perfringens

32
Q

what is an example of a bacteria that has Lecithinase exoenzyme?

A

Clostridium perfringens

33
Q

what is an example of a bacteria that has proteases exoenzyme?

A

Neisseria gonorrhoeae

34
Q

How do we do a coagulase test?

A

You take a test tube of rabbit plasma plus bacteria [fibrinogen is present in the plasma] and then you incubate it for 4-24 hours, then you check if a clot has formed or not by the presence of fibrin (insoluble). If coagulase is present, then you will get a positive result of clotting and if its not present, you get a negative result of no clot with no fibrin

35
Q

How do invasins help pathogens evade host cells?

A
  • invasins are surface proteins on some bacteria which activate actin, the cytoskeleton of eukaryotic cells
  • rearranges and facilitates bacterial engulfment into the host cells
  • they use the host cell cytoskeleton to get into the host cell
36
Q

what are two examples of bacteria that use invasins to penetrate host cell wall?

A

Salmonella and E.coli –> use pedestal formation

Listeria monocytogenes uses re-arrangement of actin as a propellent

Shigella and Listeria –> use invasins to move from one host cell to another laterally by activating cytoskeleton. They infect intestinal epithelial cells laterally as well as from outside in, to avoid going detected by WBCs

37
Q

What are super-antigens / Type 1 exotoxins?

A

aka Type 1 exotoxins

  • they are protein antigens that stimulate a very large immune response
  • less than 1% of t-helper cells are activated by an infection NORMALLY but with a superantigen as an activator, the response can be 20% T-helper cells activated (20X more cytokines)
38
Q

How do super antigens (aka type 1 exotoxins) help pathogens evade host cells?

A

They unspecifically bind to MHC 2 and TCR around the binding groove
this results in excessive release of cytokines which results in nausea, fever, diarrhea, shock and death

39
Q

what is an example of super-antigen bacteria?

A

Staphyloccocus aureus TSST-1 toxin which causes toxic shock syndrome

40
Q

What are toxins?

A

toxins are virulence factors and are usually proteins that can produce fever, heart failure, diarrhea, deem and shock

they can destroy cells as well as inhibit protein synthesis, leading to cell death

41
Q

What are two major types of Toxins?

A
  1. Endotoxin like lipopolysaccharide (Lipid A) [structural part of the bacteria]
  2. Exotoxin like super antigens (made by the ribosomes; and is an extra protein that the bacterial cell makes to affect cells other than itself)
42
Q

what are endotoxins?

A

outer cell wall of gram negative bacteria (LPS)

LPS is made out of a polysaccharide and lipid A portion

the lipid A is the endotoxin and it is HEAT STABLE

causes chills, fever, weakness, aches, shock and death

activates the blood clotting system (DIC)

causes SHOCK (LOSS OF BLOOD PRESSURE) CALLED ENDOTOXIC SHOCK

43
Q

What are exotoxins?

A

produced by certain types of bacteria and released into tissues (can be g+ or g-)

genes for these exotoxins can be carried by bacteriophages or plasmids

potent proteins and are heat sensitive (can get rid of it if u boil it)

our body has antitoxins to neutralize exotoxins

44
Q

two common bacteria with exotoxins?

A
Colostridium botulinum (botox)
flaccid paralysis due to botulism toxin
Clostridium tetani 
spastic paralysis (lock jaw) due to tetanus toxin
45
Q

Common exotoxin structure

A

A-B toxin

A is toxic part
B binds to cells

46
Q

How do secretion systems allow bacteria to get into host cells?

A

G- genes have a chromosome that codes for type 3 secretion apparatus; the chromosomal region where these genes are clustered is called Pathogenicity Island

it forms an apparatus that can shoot the baccterial secretions into the host cell like a needle

47
Q

Type 3 secretion apparatus

A

enables G- bacteria to inject proteins into host cell, killing or altering it

the needle can puncture holes into host cells and the secretions it releases into host can kill it

48
Q

How does antigenic variation allow bacteria to evade host cells?

A

it fools the immune system

pathogens have antigens on their surface where the host B-cells will form antibodies to
- some pathogens change the make up of their antigens as they replicate (called mutation)

immune system sees those mutated antigens on the same pathogen as NEW PATHOGEN and the previous antibodies do not work

49
Q

what are two bacteria that use antigenic variation

A

neisseria gonorrhoeae and trypanosome species

50
Q

Obligate intracellular bacteria

A

can only grow inside of host cells in a protected vacuole and cant make their own ATP

51
Q

two examples of obligate intracellular bacteria

A

chlamydia and rickettsia

52
Q

facultative intracellular bacteria

A

bacteria that can multiply outside of host cells, but often use intracellular growth as a means of evading the host defences

53
Q

3 examples of facultative intracellular bacteria

A
  1. bordatella
  2. mycobacterium
  3. salmonella
54
Q

Three methods of horizontal gene transmission

A
  1. conjugation: transfer of plasmids containing genes for virulence or antibiotic resistance
  2. Transduction: acquisition of genes for toxin production (c. diphtheria bacteria by transfer of bacteriophage)
  3. Transformation: acquiring a new gene for toxin, capsule production etc.. but absorbing naked DNA in the environment around the bacteria
55
Q

plasmids

A

small circular DNA molecules that are seperated from the main bacterial chromosome

  • encode for antimicrobial resistance or virulence factors
56
Q

Bacteriophages

A

viruses which infect specific bacteria and transfer these genes to another bacteria via transduction

57
Q

example of bacteriophage infecting a bacteria

A

Corynebacterium diphtheriae

not pathogenic unless its lysogenized by a phage and then produces the toxin

58
Q

How are the pathogenic effects of viruses different from bacteria?

A

different from bacteria because of the nature of the virus, which invades the host cells and resides intracellular (in the cell) and is protected from the immune cells

59
Q

what do most viral pathogenesis cause?

A

inflammation and activation of immune system which produces disease

60
Q

Two forms of viral pathogenesis?

A
  1. Cytopathic effects (CPE)

2. Syncytium formation

61
Q

cytopathic effects (CPE)

A

killing or damaging of the host cell by the virus
causes host cells to become round

different strains of virus cause different CPE

62
Q

Syncytium formation

A

this occurs when virally infected cells fuse together to form a giant multi-nucleated cell

this cell eventually dies when the viruses use up all the building material and cause tissue necrosis

this permits viral multiplication without exposing the virus to antibodies (blocks it off)

63
Q

which viruses cause syncytium formation?

A

RSV and measles

64
Q

what are two ways viral cells can evade immunity?

A
  1. downregualte MHC1 (prevent it from being produced by the cell)
  2. Syncytium formation
65
Q

what are three ways viruses can disrupt cellular life cycle and activity?

A
  1. inhibit macromolecular synthesis of host proteins/ mitosis
  2. cause host cell to release enzyme in lysosomes resulting in cell death
  3. deregulate cell function like affecting hormone production
66
Q

what are two ways viruses can cause cancer?

A
  1. induce chromosomal changes in cells i.e. oncoviruses
  2. deregulate contact inhibition –> when one cell bumps into another cell, it usually bounces off, but if thats deregulated then it will attach to it and keep growing (uninhibited cell growth)