Opportunistic infxns Flashcards

1
Q

How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
- Granulocytopenia (Low PMNs)

A

Chemotherapy or radiation therapy

GN and staphylococcus

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

How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
- Cellular immune dysfxn

A

AIDS, age, smoking, T cell defects

Intracellular pathogens (salmonella)
Mycobacterium tuberculosis
Listeria monocytogenes

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

How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Humoral immune dysfunction

A

Agammaglobulinemia
Splenectomy

Encapsulated pathogens
S. pneumoniae, meningococci

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

How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Foreign body

A

IV or urinary catheter, bone implant

GN, Staphylococci

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

How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Surgery

A

Staphylococci
Ecoli
Pseudomonas

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

Importance of iron in bacteria growth

A

almost all bacteria require iron for growth
- cept lactobacilli & treponema pallidum

Our bodies have most Fe2+ bound to transferrin or lactoferrin to keep iron levels down low
Our body also shunts income iron into storage (liver)

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

Host responses and defenses to prevent bacteria from taking up iron

A
  1. Iron binding proteins
    - Transferrin, lactoferrin
    - keep body’s levels low
  2. Shunt incoming iron into storage (liver)
  3. Decrease Iron adsorption (intestine)
  4. Decrease expression of microbial iron binding compounds (siderophores)
    - down reg. bacteria’s ability to make siderophores which compete and bind our Fe.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

FX of endotoxin on Hageman factor (XII)

A
activates Hageman factor (XII) -->
PLasminogen activator (fibrinolysis)
\+ 
Bradykinin 
(hypotension)

Can also activate complement activation and TNF
(good and bad FX depending on lvls)

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

Why is pseudomonas so highly resistant to treatment?

A

High innate resistance mech (many efflux pumps)

Propensity to form biofilms

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

Pathognomonic of P. aeruginosa septicemia

A

Ecthyma gangrenosum

  • gun metal gray infarcted lesion surrounding erythema
  • evolves into a necrotic black/gray eschar and surrounding erythema
  • one of phospholipases is highly cytotoxic to ENDOthelial cells and not epithelial cells –> vascular thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Most people with CF will die from what?

A

Lung infxn with Pseudomonas aeruginosa

  • settled in lung for life
  • forms a type of biofilm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CF pts cant make Cl- but they can make ___

A

Ca2+ gels the compounds that pseudomonas makes.
- macrophages cant get thru biofilm, get madder and madder –> inflammation and destroys the lungs.

*must shake/pound chest of pts with CF to clear their lungs

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

Small doses of endotoxin can stimulate the immune system, but at higher doses, it sets off a cascade that cannot be controlled, leading to severe shock.
What is the primary effector cell in the cascade?

A

The macrophage
- gets overstimulated by endotoxin –> releases TNF –>
tells macrophages to release more cytokines –>
targets endothelial cells

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

Nutritional immunity

A

ability of host to withhold trace nutrients from organisms

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

Pseudomonas is NOT the leading cause of nosocomial or opportinistic infxn, so why do we care?

A

It is number 1 in terms of mortality

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

Antibiotic resistance of pseudomonas is due to what?

A

Chromosomally mediated resistance associated with multiple efflux pumps

  • not via plasmids
17
Q

Virulence factor of pseudomonas

what bacteria toxin is it similar to?

A
  1. Exotoxin A
    - ADP ribosyl transferase: inhibits activity of EF-2 in mammalian cells
    - stops protein synthesis liek diphteria toxin
    - regulated by iron similarly
18
Q

Why is pseudomonas exotoxin A not have the same distal effects as diphtheria toxin when they both act the same?

A
  1. Cell receptors are different
    - target cells and tissues are different
  2. Diphtheriae only produces superficial infection
    (epidermal growth factor precursor)

*pseudomonas can invade tissue and blood stream

19
Q

WHy cant vaccination against diphtheria work against pseudomonas?

A

no immunological cross reactivity btwn their toxins and virtually no primary aa seq. similarity

20
Q

What allows pseudomonas to survive solely on the surfactant of the lung?

A

multiple phospholipases

21
Q

What compounds are critical for pseudomonas to form biofilms?

A

Homoserine lactones

in a process called quorum sensing

22
Q

Wound infxns in diabetics commonly contain what organisms?

A

pseudomonas and S. aureus

- very slow to heal and very diff to tx

23
Q

Alginate

A

mucoid substances prod by pseudomonas in CF pts
- a gluuronic mannuronic acid polymer

  • CF pts tend to select for pseudomonas strains that make alginate
  • due to high Ca2+ and osmolarity of CF lung