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  #1  
Old 09-02-2011
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Question most important factor causing increasing frequency and severity of his Pseudomonas infection

29-year-old gentleman has had a fever and productive cough for the past 10 days. He was born at term, but developed abdominal distention in the first week of life from meconium ileus. He has had persistent steatorrhea with passage of foul-smelling stools for the past 10 years. He has had frequent bouts of pneumonia with cough productive of thick mucoid sputum for 2.5 years. Sputum cultures have consistently grown Pseudomonas aeruginosa. Each new bout of pneumonia is longer and increasingly non-responsive to antibiotics. On physical examination, his temperature is now 38.2C. Genetic testing reveals homozygosity for the ΔF508 mutation of the cystic fibrosis transmembrane conductance regulator ( CFTR ) gene. Which of the following is the most important factor causing increasing frequency and severity of his Pseudomonas infections?


(A) Abnormal folding of CFTR protein
(B) Coexistent mutations in the TGFβ1 gene
(C) Defect in ciliary action from dynein arm malfunction
(D) Formation of respiratory epithelial biofilms
(E) Loss of bicarbonate secretion into bronchioles


plz explain ur choices too
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  #2  
Old 09-02-2011
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ans is A, this is the case of CF, and the most common cause of death in CF is P. auroginosa leading to respiratory failure...
in CF, ALPHA 1 ANTITRYPSIN DEF there is abnormal protein folding.
there is loss of Na and Cl in CF, causing dehydration and also inc of Na, H20, n Cl in epithelium!
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  #3  
Old 09-03-2011
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i'm thinking a too.
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Old 09-14-2011
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(C) Defect in ciliary action from dynein arm malfunction

Well this is my explanation:

we know that in kartagener there is increase risk of pseudomonas infections, so this malformation should rise the risk of infection in CF.
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Old 09-14-2011
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A.abn folding of cftr protein.
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Old 09-15-2011
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I think answer is C because even though in cystic fibrosis there is unfolding of CFTR protien but the main cause of recurrent resp. infection is decreased cilliary activity which results in increase mucoid obstruction and increase in resp. infesction.
so I will go with C

Last edited by mohitkmc; 09-15-2011 at 05:01 AM.
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Old 09-15-2011
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(A) Abnormal folding of CFTR protein
in cf
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Old 09-15-2011
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(D) Formation of respiratory epithelial biofilms
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  #9  
Old 10-08-2011
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Warning! A or D ?

----
To initiate infection, P. aeruginosa usually requires a substantial break in first-line defenses. Such a break can result from alteration of the immunologic defense mechanisms (e.g., in chemotherapy-induced neutropenia, mucosal clearance defects from cystic fibrosis, AIDS, and diabetes mellitus).

Reference: http://www.drlera.com/bacterial_dise...aeruginosa.htm

----
Once pseudomonas are established as biofilms, even the most potent antibiotics have little effect on their viability, especially during late-stage chronic infections.


Read More: http://informahealthcare.com/doi/abs...28220903454988


So, either of A and D are possible . I think that C is not correct, because the dynein malfunction is pathological aspect of Kartagener syndrome not CF.
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Old 10-09-2011
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I ll go with a
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Old 10-09-2011
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(D) Formation of respiratory epithelial biofilms
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Old 10-11-2011
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i think it is D
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Old 10-12-2011
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once the mucosal clearance mechanisms are gone in CF the biofilm of P.aerigunosa attach to the respiratory mucosal surface very easily.So, the defect in CFTR caused the CF and clearance problem i will go with A
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Old 10-15-2011
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very good question. cant decide whats the answer
a or d?
help


Quote:
Originally Posted by aungawa View Post
29-year-old gentleman has had a fever and productive cough for the past 10 days. He was born at term, but developed abdominal distention in the first week of life from meconium ileus. He has had persistent steatorrhea with passage of foul-smelling stools for the past 10 years. He has had frequent bouts of pneumonia with cough productive of thick mucoid sputum for 2.5 years. Sputum cultures have consistently grown Pseudomonas aeruginosa. Each new bout of pneumonia is longer and increasingly non-responsive to antibiotics. On physical examination, his temperature is now 38.2C. Genetic testing reveals homozygosity for the ΔF508 mutation of the cystic fibrosis transmembrane conductance regulator ( CFTR ) gene. Which of the following is the most important factor causing increasing frequency and severity of his Pseudomonas infections?


(A) Abnormal folding of CFTR protein
(B) Coexistent mutations in the TGFβ1 gene
(C) Defect in ciliary action from dynein arm malfunction
(D) Formation of respiratory epithelial biofilms
(E) Loss of bicarbonate secretion into bronchioles


plz explain ur choices too
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  #15  
Old 10-15-2011
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I'll go with 'A'.
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  #16  
Old 10-15-2011
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Surprised to see this Q under Step1, but the answer is (D). The hint is increasing severity/frequency, which discredits answers (A) & (C) (static mutations). Specifically, prolonged Pseudo infection leads to selective pressure that ultimately induces exopolysaccharide production (alginate, maybe others). Once this phenotypic conversion occurs, the infection is nearly intractable, and morbidity/mortality increase. Studied this in grad school.
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