Opportunistic infxns Flashcards
How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
- Granulocytopenia (Low PMNs)
Chemotherapy or radiation therapy
GN and staphylococcus
How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
- Cellular immune dysfxn
AIDS, age, smoking, T cell defects
Intracellular pathogens (salmonella)
Mycobacterium tuberculosis
Listeria monocytogenes
How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Humoral immune dysfunction
Agammaglobulinemia
Splenectomy
Encapsulated pathogens
S. pneumoniae, meningococci
How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Foreign body
IV or urinary catheter, bone implant
GN, Staphylococci
How does this factor arise?
This factor predisposes indivs to which opportunistic infxns?
Surgery
Staphylococci
Ecoli
Pseudomonas
Importance of iron in bacteria growth
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)
Host responses and defenses to prevent bacteria from taking up iron
- Iron binding proteins
- Transferrin, lactoferrin
- keep body’s levels low - Shunt incoming iron into storage (liver)
- Decrease Iron adsorption (intestine)
- Decrease expression of microbial iron binding compounds (siderophores)
- down reg. bacteria’s ability to make siderophores which compete and bind our Fe.
FX of endotoxin on Hageman factor (XII)
activates Hageman factor (XII) --> PLasminogen activator (fibrinolysis) \+ Bradykinin (hypotension)
Can also activate complement activation and TNF
(good and bad FX depending on lvls)
Why is pseudomonas so highly resistant to treatment?
High innate resistance mech (many efflux pumps)
Propensity to form biofilms
Pathognomonic of P. aeruginosa septicemia
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
Most people with CF will die from what?
Lung infxn with Pseudomonas aeruginosa
- settled in lung for life
- forms a type of biofilm
CF pts cant make Cl- but they can make ___
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
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?
The macrophage
- gets overstimulated by endotoxin –> releases TNF –>
tells macrophages to release more cytokines –>
targets endothelial cells
Nutritional immunity
ability of host to withhold trace nutrients from organisms
Pseudomonas is NOT the leading cause of nosocomial or opportinistic infxn, so why do we care?
It is number 1 in terms of mortality