Host Pathogen Interactions Flashcards

1
Q

What is the difference between a principal pathogen, an opportunistic pathogen and commensal organisms?

A

Principal pathogens: regularly cause disease in only a proportion of susceptible hosts with a normal immune system

Commensals: live on you and in you but don’t cause damage and actually maintain normal physiology

Opportunistic pathogen: don’t normally cause disease unless they have the “opportunity” to so, for example when you’re immune compromised

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2
Q

Koch’s postulates are to establish what?

A

Whether a specific organism causes disease

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3
Q

What are #Kochs_Postulates?

A

Koch’s postulates:

  1. Organism has to be in all cases of diseased folks (but not in healthy folks)
  2. Bug has to be isolated from the diseased folk and grown in culture
  3. Disease is reproduced in a new host when bug is inoculated in a susceptible host
  4. The bug has to be isolated from the newly infected host and cultured (and basically found to be the same one)
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4
Q

What are #Molecular_Koch’s_Postulates?

A

Factors to determine which specific factor contributes to a bug’s virulence

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5
Q

The 3 molecular Koch’s postulates are ___

A
  1. Gene encoding the phenotype should be ass’d with the pathogenic strain (and not in the non pathogenic strains)
  2. Inactivating the gene results in reduction of virulence
  3. Restoring the wildtype gene re-establishes virulence
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6
Q

The most common outcome of infection is ___

A

No #symptoms

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7
Q

Host factors that affect the emergence of new infections include changes in behavior, ___, ___, contamination of environment and food supply and ___

A

Host factors:

Changes in behavior: e.g. AC can lead to propagation of certain bugs as is the case of Legionella, or new eye infections with contact lenses

Expanding populations and increased travel: potential zoonotic transfer with folk going to new places and increasing travel allows for the easy propagation of these infections

Contamination of environment and food supply

Immunosuppression: one can be susceptible to infection if your immune system is dampened for whatever reason

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8
Q

What are some microbial factors that effect the emergence of new infections?

A

Short generation time: bacteria reproduce super quickly and new mutations produced with each generation can propagate quickly as well

Acquisition of new genetic material from other bacteria

Changes in vector distribution (like if you have a new vector for a particular bug, that might also affect the emergence of new infections)

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9
Q

The 3 ways bacteria can acquire new genetic material are by ___

A

Conjugation

Transformation

Transduction

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10
Q

Describe the 3 ways thru which bacteria can acquire new genetic material

A

Conjugation: exchange of dna between bacteria by direct contact (#bacteria_sex). Can also happen between unrelated bacteria

Transformation: transfer of “naked” dna >> basically one bacteria can release its dna into the cytosol and another bacterium can take that dna up

Transduction: transfer of dna mediated by a bacteriophage

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11
Q

What is the difference between commensals and pathogens if commensals follow the same steps as pathogens do in the infectious cycle?

A

Commensals do all of the steps in the infectious cycle EXCEPT cause damage (i.e. disease)

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12
Q

Two barriers for bugs to overcome as they try to enter the host are ___

What in the body serves as an ecological barrier to bug infection?

A

Entry into the host: barriers include the skin and mucosal surfaces

Overcoming barriers: overcoming anatomical barriers like the skin would normally require some kind of trauma to the barrier; ecological barrier = the host microbiome

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13
Q

The first step in establishment is ___

T/F: Bugs that don’t adhere are equally as virulent as those that do

A

The first step in establishment is adherence

Adherence is usually high avidity and over long distances to overcome electrostatic repulsion between the bug and the host cell surface

Adherence is also the result of adhesins on the surface of the bug, and receptors on the surface of the host cell

Mutants that aren’t adherent are typically avirulent

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14
Q

Describe the role of fimbriae/pili

A

Fimbriae/pili: rod like things that protrude from the bug’s cell surface. Proteins at the tip of these things actually mediate adherence

**note that the pilus rod provides the distance between the two negatively charged surfaces of the host cell and the bug cell to overcome electrostatic repulsion**

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15
Q

What is the significance of a #biofilm to bug adherence

A

Staph epidermidis can adhere to catheters via formation of a biofilm

Many bugs form biofilms on foreign surfaces

The biofilms are typically composed of polysaccharides and other things that not only help with adherence but are also resistant to anti-microbial treatment

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16
Q

3 ways thru which bugs can evade killing by the host immune system are complement evasion, ___ and ___

A

Complement evasion

Invasion and alteration of cell biology

Avoidance of phagocytosis

17
Q

Other ways bugs can evade killing by the host immune system include ___

A

Survival in the phagocyte

Antigenic variation

Inactivation of antibodies

18
Q

An example of bacteria escaping complement activation is #Neisseria infection

How does Neisseria evade killing by the complement system? How does this cause pathology in the host?

A

Neisseria meningitidis can bind Factor H on its surface (recall that Factor H is a complement inhibitor)

Binding factor H will allow the bacteria to inactivate complement on their surface.

Because there are many bacteria, the bacteria’s binding to Factor H reduced the functional level of Factor H for the host so the host actually has complement constantly activated which can lead to vascular damage

There’s also a polymorphism affecting expression of factor H that is ass’d with increased risk of N. meningitidis infection

19
Q

Another way for a bug to evade killing by complement and antibodies is __

What are two example systems thru which a bug can achieve this?

A

Surviving inside the host cell is another way of getting inside the cell

On the slide: trigger mechanism = using the type 3 secretion system, and the zipper mechanism = using cellular receptors

20
Q

What is a type III/IV secretion system?

A

One way that bugs alter host cell biology is through Type III secretion systems that can deliver virulence factors into the host cell cytoplasm and the factors cause changes that effect the host cell

(think of it like a delivery system except the package that the host cell is receiving is #virulence instead)

21
Q

One way that bugs evade phagocytosis is by expressing what?

A

A #polysaccharide capsule

22
Q

An example of a bug surviving killing by phagocytosis is Listeria monocytogenes. Explain how this bug does this

A

Listeria monocytogenes escapes from the phagosome and goes into the cytosol as a way to evade killing by the host. It can also move around inside the cell and once it pops out of one cell, it can go right into another one (so it won’t be sensed by the host environment)

Listeria’s that ho that just keeps dude hopping

23
Q

Some bugs evade phagocytic killing by inhibiting fusion of the phagolysosome. Who are these dudes?

A

Legionella pneumophila

Toxoplasma gondii

Histoplasma capsulatum

**borrowed from Yas

Ghandi didn’t believe that just coz you were a toxic (toxoplasma) person that you deserved to fry. He was all about keeping the lysosomes + phagosomes #separate to avoid the violence against toxoplasma that would happen

Something about him going down in HISTory (histoplasma capsulatum) not just in this legion of pneumophila (Legionella pneumophila) but around the world as well :/

24
Q

In other cases, phagolysosomal fusion happens but the bug survives still. Who all are these folks that do this?

A

Leishmania

Coxiella burnetii

**this girl Coxie (lla) got some burns all over herself and then she went somewhere and got Leishmaniasis. How unfortunate**

25
Q

What is antigenic variation and how does that help pathogens evade the host immune system?

A

Antigenic variation: changing the targets of antibodies

Neisseria gonorrheae expresses pili that are targets for antibodies. Problem is these bugs can actually change the targets of the antibodies, making the antibodies #useless

26
Q

How does Staph inactivate antobodies?

What’s another example of antibody inactivation?

A

Some bugs also have ways to inactivate antibodies

Staph aureus expresses Protein A, which binds antibodies at the Fc region and not the Fab region, thereby rendering the antibody unable to perform its antibacterial function

Protein A can also cause B cell apoptosis, which further reduces the level of functional antibodies

Some mucosal pathogens secrete an IgA protease that degrades IgA (recall that IgA is your major antibody for mucosal defense)

27
Q

A direct way that pathogens can cause damage to the host is thru secretion of (exotoxins/endotoxins)

A

Direct:

Exotoxins – proteins secreted by growing bacteria that cause damage to the host cell (the 1st ones discovered where tetanus and botulinim toxins)

28
Q

Indirect ways that bugs can cause damage to the host include ___

A

Superantigens and endotoxin

29
Q

Diptheria is an upper respiratory infection caused by ___ and is characterized by a ___

A

Upper respiratory infection by Corynebacterium diphtheriae

Dense white-grey pseudomembrane in swollen posterior pharynx

Listen , Cory’s bacteria causes diptheriae. The thing makes a fake blanket (membrane) over the back of the throat and makes it so big (swollen)

30
Q

The pathogenesis of Diptheria is mediated by ___

How does this work?

A

Diptheria toxin

Diphtheria toxin is an A/B toxin

It has an active domain and a binding domain

The toxin enters the cell via receptor mediated endocytosis thru the B subunit

After acidification of the endosome, the B subunit changes conformation and forms a pore in the endosomal membrane

The A subunit (at this point has been clipped by the Furin host protease) then translocates across the pore of the B subunit and binds to ADP which ribosylates Elongation Factor 2, thereby inhibiting the cell’s protein synthesis and killing the cell

31
Q

How does Shiga toxin cause damage to the host cell?

Name 2 organisms that make Shiga toxin

A

Shiga toxin is another A/B toxin that has one A subunit and 5 B subunits that are noncovalently attached

The subunits bind a cell surface receptor, are endocytosed and the A subunit ends up in the cytosol where it disrupts protein synthesis by depurinating the 28S ribosomal RNA

Shigella dysenteriae and some E. coli

32
Q

How does Shiga toxin cause Hemolytic Uremia syndrome (typical)?

A

Shiga toxin is also important in kidney cells

Shiga toxin causes typical hemolytic uremic syndrome. The toxin can bind to microvessels in the kidney which leads to tissue and organ damage

33
Q

2 examples of membrane damaging toxins include ___

A

Other toxins damage the membrane directly by forming elaborate pores in the host cell membrane thru multimerization

Other bacteria secrete phospholipases that digest the phospholipid bilayer

34
Q

Explain how superantigens and LPS binding can cause damage to the host cell/are involved in damage mediated by host responses

A

Recall that superantigens damage the host cell by skipping binding to MHC and instead binds to the side and causes cytokine storms >> shock

Recall also that TLR4 binding causes inflammatory responses which can cause damage if there’s too much stimulation (this is a host cell indirect kind of disease)

35
Q

Which of these features best distinguishes pathogens from commensals?

A.Ability to overcome anatomical barriers

B.Adherence to host cells

C.Damage to the host

D.Evasion of host immune responses

E.Transmission to susceptible hosts

A

C

36
Q

Molecular Koch’s postulates can be used to determine

A.how a pathogen evades host immunity

B.how to isolate a pathogen from an infected animal

C.that a specific organism is the cause of a disease

D.whether a specific factor contributes to infection

A

D

37
Q

Which of the following is not a mechanism used by pathogens to evade host immunity?

A.Binding of complement regulatory factors

B.Cleavage of MHC and TCR molecules

C.Production of a polysaccharide capsule

D.Survival inside host cells

E.Variation of surface antigens

A

B

38
Q

Which of the following is a factor in the emergence of new infections?

A.Decontamination of the environment

B.Exchange of genetic material between bacteria

C.Long generation time of bacteria

D.Stability of human populations

A

B

39
Q

•A 20-year-old admitted the day prior for fever and confusion and is now improving after prompt initiation of antimicrobial therapy. Neisseria meningitidis was cultured from his cerebral spinal fluid. The physician recommends that all members of his family receive prophylactic treatment with an antimicrobial. In the absence of such treatment, which of the following is the most likely outcome in the family members after household exposure to N. meningitidis from this patient?

A.Death

B.Meningitis

C.Mild headache

D.No symptoms

A

D