Exam #1: Host Parasite Relationships Flashcards

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

Define commensalism.

A

Symbiotic relationship where microorganism benefits but the host is unaffected

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

Define mutualism.

A

Symbiotic relationship where both host & microorganism benefit.

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

Define parasitism.

A

Symbiotic relationship where microorganism benefits but host is harmed.

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

What are normal microbiota & how are they beneficial to the host?

A

Normal microbiota= commensal or mutual symbionts adapted to specific niches.

  • Beneficial to host because=
    1) Out-compete pathogenic microorganisms for niche
    2) Produce “bacteriocins” that are toxins that harm other pathogenic bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is the most dense grouping of the normal microbiota?

A

GI Tract

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

Describe the distribution of bacteria along the GI tract. Where is the highest density of normal flora in the body?

A
  • Esophagus & stomach= v. low density of bacteria
  • Small Intestine= low density
  • Large Intestine= high density
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are neonates colonized with bacteria? Is the fetus sterile?

A

Fetus is generally sterile & then with delivery the neonate is colonized with bacteria.

  • Vaginal delivery= skin colonized during birth
  • C-section= colonized shortly after birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What areas of an infant are normally colonized with bacteria?

A

Skin
Mucosa
Intestine
Urogenital Tract

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

What areas of an infant are normally sterile?

A

Internal organs
Cervix
Middle ear
Urinary bladder

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

How does the normal micobiota & its interaction with the immune system change throughout life?

A
  • Childhood= developing immunity as exposed to new microbes, shifting normal microbiota
  • Healthy adult= developed immunity & stable microbiota
  • Elderly= immune senescence & increased susceptibility to infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the difference between resident & transient microbiota?

A

Resident= long-term members of microbiota

Transient= organisms that attempt to colonize the body but are unable to remain because of:
1) Competition from resident
2) Elimination by immune system
3) Physical & chemical changes within the body
E.g. proton-pump inhibitors

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

Give an example of resident microbiota. Where is it found? List the characteristics of the bacteria. When is it associated with infection?

A

Staphyloccous epidermis is a resident bacterium of the skin, nose, & ears that is:

  • Gram +
  • Cocci in clusters

Infection associated w/ prosthetic device & intravenous catheters–also it is a common contaminant of blood cultures

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

Given an example of transient microbiota.

A

Group A Strep (GAS) or Streptococcus pyogens

  • Gram +
  • Cocci in chains

Transiently colonizes the oropharynx of children & young adults in the absence of clinical disease & causative agent of strep throat

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

What is a pathogen, & what is the difference between a strict pathogen & an opportunistic pathogen?

A

Pathogens= microorganisms that have the capability to cause disease i.e. almost anything

Strict= NOT associated w/ microbiota & always associated w/ disease
- E.g. mycobacterium tuberculosis (causitive agent of TB)

Opportunistic= part of the normal microbiota & take advantage of pre-existing conditions

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

Which type of pathogen more commonly causes disease?

A

Opportunistic

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

What is the difference between pathogeniticty, virulence, & virulence factor?

A

Pathogenicity= ability of organism to cause disease
Virulence= measure of pathogenicity
Virulence factors= factors produced by organisms that enable it to infect, cause disease, and/or kill host

17
Q

What is a carrier?

A

Carrier= harbor pathogens as part of their microbiota without showing signs of disease BUT they can transmit disease to others
- Can be transient of semi permanent e.g. “Typhoid Mary” & Salmonella Typhi

18
Q

What are the general steps of infection?

A

General steps of infection:

1) Entry into host
2) Adhesion, colonization, & pathogenic action of bacteria 
3) Mechanisms for escaping defense
19
Q

How is entry gained into the host?

A
  • Transplacental (mother to fetus)
  • Secretions (aerosol, mucosal)
  • Stool (fecal–>oral)
  • Skin (cuts, incisions, abrasions, burns)
  • Blood (STIs, IV drug use)
  • Zoonotic (animal to human)
  • Arthropod (insect to human)
20
Q

What are the barriers to protect from pathogen entry?

A
  • Mechanical (skin & cilia)
  • Enzymatic (lysozome)
  • Chemical (acidic pH)
  • Immunity (complement & antibody)
  • Commensals
  • Physical (sheer forces & peristalsis)
21
Q

How do bacteria adhere to a host?

A

Binding of bacterial “adhesin” to host receptors

  • Note that “adhesins” or attachment proteins are often associated with pili
  • Specific adhesin & receptor combinations often define tropism
    i. e. where you have adhesin receptors defines where bacteria can adhere & infect
22
Q

What is a biofilm?

A

Biofilm= bacteria encased in exopolymeric substance , found throughout nature on surfaces that are commonly moist/wet e.g. shower, teeth…etc.

- Most bacteria don't live "planktonically," or freely moving in solution 
- Most are stationary
23
Q

How are bacteria in a biofilm different from planktonic cells?

A
  • Altered & generally slowed metabolism–>more difficult to treat
  • Increased resistance to abx
  • Increased genetic exchange
  • Resistant to disinfection b/c of decreased diffusion & increased organic matter
24
Q

How are biofilms related to disease?

A

Most chronic infections have a biofilm component

25
Q

What happens after adhesion?

A
  • Invasion into cell, often by hijacking host cell machinery to facilitate uptake
  • Dissemination
26
Q

How do bacteria destroy tissue?

A
  • Toxic byproducts of growth
  • Bacterial secretion of degradation enzymes

E.g. Clostidium perfingens (gas gangrene)

27
Q

What is endotoxin? What is the difference between endotoxin & exotoxins?

A

Endotoxin= lipid A portion of LPS which is very different from “exotoxin”

Exotoxin= bacterial products that directly harm tissue or lead to destruction
- Can be cytolytic or receptor binding

28
Q

What are AB toxins?

A

A class of exotoxins/ receptor binding proteins that contains A & B subunits with different functions (and initiate toxic reactions)

  • A= active
  • B= binding
29
Q

What are Non-AB toxins? Give examples of non-AB toxins.

A

Toxins that function without AB subunits. E.g:

  • Tetani that blocks the release of inhibitory neurotransmitter leading to excitation paralysis
  • Botulinism that blocks release of excitatory neurotransmitter leading to flaccid paralysis
30
Q

What is superantigen?

A

An exotoxin that binds both TCR & MHC Class II w/out requiring antigen
- Can cause life-threatening autoimmune-like responses

31
Q

What mechanisms do bacteria have for escaping host defenses?

A

1) Encapsulation= capsule masks more antigenic epitopes on surface to prevent binding of ab or complement
2) Antigenic Mimicry= bacteria produces compounds that host sees as self
- HA (hyaluronic acid)
- Fc
3) Antigenic Variation/ Shift= bacteria quickly change antigenic make-up of proteins on cell surface
4) Inactivation of ab= secretion of proteases that degrade specific antibody isotypes
5) Resistance to complement mediated killing=
- Limiting access to the membrane e.g. Long LPS O-antigen
- Degradation of complement proteins
6) Escaping phagocytic clearance

32
Q

What mechanisms do bacteria have for escaping host defenses?

A

1) Inhibit opsonization
2) Inhibit chemotaxis
3) Kill phagocyte
4) Inhibit lysosomal fusion
5) Escape from lysosome
6) Resist antibacterial lysosomal action

33
Q

How do bacteria regulate virulence factors?

A
  • Bacteria often do NOT constitutively express virulence factors; they sense their environment
34
Q

What is Quorum Sensing?

A

Quorum sensing= way for bacteria to sense the size of their population
- When the bacteria sense high population/ “critical mass” then they turn on virulence factor expression

35
Q

Where is normal human microbiota found?

A

GI Tract
Skin
Mouth
Upper respiratory tract (superior to trachea)

*Females, vagina as well

36
Q

What sites in the body are considered sterile i.e. do NOT contain microbiota?

A
Lower respiratory tract 
Upper urogenital tract (uterus & urinary bladder) 
Internal organs
Tissues 
Circulatory system