culture results - anyone treat?

angelsmom

New member
Is it possitble to know whether staph causes less damage than PA? Or at least at a slower pace than PA? Would it maybe be better to treat staph, at least sometimes? Our doc doesn't typically treat it but if my daughter were showing signs of an exacerbation, we would treat it. I just worry what the damage will be from NOT treating it!

Thanks for the explanations though!
 

point

New member
Amy - Can you post links to these studies? I asked my dr. about this theory (S aureus keeps PA at bay or even away) and she said it wasn't true.

I wouldn't mind looking at the papers and then forwarding them to my dr. Thanks -
 

point

New member
Amy - Can you post links to these studies? I asked my dr. about this theory (S aureus keeps PA at bay or even away) and she said it wasn't true.

I wouldn't mind looking at the papers and then forwarding them to my dr. Thanks -
 

point

New member
Amy - Can you post links to these studies? I asked my dr. about this theory (S aureus keeps PA at bay or even away) and she said it wasn't true.

I wouldn't mind looking at the papers and then forwarding them to my dr. Thanks -
 

Chaggie

New member
It hasn't been proven and still isn't an accepted theory yet but here's an <a target=_blank class=ftalternatingbarlinklarge href="http://thorax.bmj.com/cgi/content/full/56/10/819b">article</a> on it.

"AUTHOR'S REPLY I thank Drs Smyth and Walters for their comments concerning the issue of whether antistaphylococcal prophylaxis leads to a higher risk of colonisation with Pseudomonas aeruginosa in patients with cystic fibrosis. I share their concern as to the lack of definitive data supporting this notion and, indeed, tried to illustrate this in my article by stating "There is some evidence that it may be associated . . .".1 I would suggest, however, that the authors' evidence of a lack of association is equally thinto quote a multicentre trial whose methodology was presented as an abstract some 9 years ago but whose results do not appear to have ever been published in a peer reviewed journal is certainly not basing one's evidence on hard evidence based facts. I did not mention the review by Smyth and Walters2 in my own paper as I submitted my review some 18 months before theirs had been published; however, the authors did not include in their own letter discussion of the recent paper by Ratjen et al3 using data from the German CF database which included 639 patients, all under 18 years of age and P aeruginosa negative prior to entry in the study. 48.2% of the patients received continuous antistaphylococcal treatment, 40.4% received intermittent antibiotic treatment, and 11.4% received no antibiotic treatment. While the rate at which patients acquired positive respiratory cultures for Staphylococcus aureus was significantly lower in the group receiving continuous antistaphyloccocal antibiotic treatment than in those receiving no such treatment, patients receiving continuous antistaphyloccocal antibiotic treatment had a significantly higher rate of P aeruginosa acquisition than patients receiving only intermittent or no antibiotic treatment. This difference was especially apparent for children under the age of 6 years. The authors concluded that "continuous therapy with antistaphyloccocal antibiotics directed against Staph aureus increases the risk of colonisation with P aeruginosa".

This interesting study I believe again supports my original statement that "there is some evidence that it (continuous antistaphyloccocal antibiotic therapy) may be associated with earlier acquisition of P aeruginosa". "



It also references other studies and papers. Here's the <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11180669&dopt=Abstract">German study </a> the Author mentions.
 

Chaggie

New member
It hasn't been proven and still isn't an accepted theory yet but here's an <a target=_blank class=ftalternatingbarlinklarge href="http://thorax.bmj.com/cgi/content/full/56/10/819b">article</a> on it.

"AUTHOR'S REPLY I thank Drs Smyth and Walters for their comments concerning the issue of whether antistaphylococcal prophylaxis leads to a higher risk of colonisation with Pseudomonas aeruginosa in patients with cystic fibrosis. I share their concern as to the lack of definitive data supporting this notion and, indeed, tried to illustrate this in my article by stating "There is some evidence that it may be associated . . .".1 I would suggest, however, that the authors' evidence of a lack of association is equally thinto quote a multicentre trial whose methodology was presented as an abstract some 9 years ago but whose results do not appear to have ever been published in a peer reviewed journal is certainly not basing one's evidence on hard evidence based facts. I did not mention the review by Smyth and Walters2 in my own paper as I submitted my review some 18 months before theirs had been published; however, the authors did not include in their own letter discussion of the recent paper by Ratjen et al3 using data from the German CF database which included 639 patients, all under 18 years of age and P aeruginosa negative prior to entry in the study. 48.2% of the patients received continuous antistaphylococcal treatment, 40.4% received intermittent antibiotic treatment, and 11.4% received no antibiotic treatment. While the rate at which patients acquired positive respiratory cultures for Staphylococcus aureus was significantly lower in the group receiving continuous antistaphyloccocal antibiotic treatment than in those receiving no such treatment, patients receiving continuous antistaphyloccocal antibiotic treatment had a significantly higher rate of P aeruginosa acquisition than patients receiving only intermittent or no antibiotic treatment. This difference was especially apparent for children under the age of 6 years. The authors concluded that "continuous therapy with antistaphyloccocal antibiotics directed against Staph aureus increases the risk of colonisation with P aeruginosa".

This interesting study I believe again supports my original statement that "there is some evidence that it (continuous antistaphyloccocal antibiotic therapy) may be associated with earlier acquisition of P aeruginosa". "



It also references other studies and papers. Here's the <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11180669&dopt=Abstract">German study </a> the Author mentions.
 

Chaggie

New member
It hasn't been proven and still isn't an accepted theory yet but here's an <a target=_blank class=ftalternatingbarlinklarge href="http://thorax.bmj.com/cgi/content/full/56/10/819b">article</a> on it.

"AUTHOR'S REPLY I thank Drs Smyth and Walters for their comments concerning the issue of whether antistaphylococcal prophylaxis leads to a higher risk of colonisation with Pseudomonas aeruginosa in patients with cystic fibrosis. I share their concern as to the lack of definitive data supporting this notion and, indeed, tried to illustrate this in my article by stating "There is some evidence that it may be associated . . .".1 I would suggest, however, that the authors' evidence of a lack of association is equally thinto quote a multicentre trial whose methodology was presented as an abstract some 9 years ago but whose results do not appear to have ever been published in a peer reviewed journal is certainly not basing one's evidence on hard evidence based facts. I did not mention the review by Smyth and Walters2 in my own paper as I submitted my review some 18 months before theirs had been published; however, the authors did not include in their own letter discussion of the recent paper by Ratjen et al3 using data from the German CF database which included 639 patients, all under 18 years of age and P aeruginosa negative prior to entry in the study. 48.2% of the patients received continuous antistaphylococcal treatment, 40.4% received intermittent antibiotic treatment, and 11.4% received no antibiotic treatment. While the rate at which patients acquired positive respiratory cultures for Staphylococcus aureus was significantly lower in the group receiving continuous antistaphyloccocal antibiotic treatment than in those receiving no such treatment, patients receiving continuous antistaphyloccocal antibiotic treatment had a significantly higher rate of P aeruginosa acquisition than patients receiving only intermittent or no antibiotic treatment. This difference was especially apparent for children under the age of 6 years. The authors concluded that "continuous therapy with antistaphyloccocal antibiotics directed against Staph aureus increases the risk of colonisation with P aeruginosa".

This interesting study I believe again supports my original statement that "there is some evidence that it (continuous antistaphyloccocal antibiotic therapy) may be associated with earlier acquisition of P aeruginosa". "



It also references other studies and papers. Here's the <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11180669&dopt=Abstract">German study </a> the Author mentions.
 

JoAnn

New member
Hi - My original question was in regard to the other things listed in the culture:



ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS
ASPERGILLUS

Anyone have any feedback on these?
Thanks!
 

JoAnn

New member
Hi - My original question was in regard to the other things listed in the culture:



ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS
ASPERGILLUS

Anyone have any feedback on these?
Thanks!
 

JoAnn

New member
Hi - My original question was in regard to the other things listed in the culture:



ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS
ASPERGILLUS

Anyone have any feedback on these?
Thanks!
 

SpinyChaff

New member
The idea that staph can keep pseudomona's at bay is an interesting one, but I do suspect that it is completely wrong.

In the UK, which has one of the lowest rates for pseudomona colonization (less that 4% of CF children under 12 are chronically infected with pseudo), anti-staph prophylaxis is pretty much the norm:

Here's what a recent article from the cf trust has to say, and its based on the recent copenhagen conference:

'Routine anti-staphylococcal antibiotic treatment (flucloxacillin) from diagnosis was recommended as the presence of Staphylococcus aureus has been significantly associated with earlier PA acquisition and may predispose the airways to PA infection'

See <a target=_blank class=ftalternatingbarlinklarge href="http://www.cftrust.org.uk/scope/documentlibrary/Publications/CFToday-Autumn06.pdf">http://www.cftrust.org.uk/scop...s/CFToday-Autumn06.pdf</a> on page 7
 

SpinyChaff

New member
The idea that staph can keep pseudomona's at bay is an interesting one, but I do suspect that it is completely wrong.

In the UK, which has one of the lowest rates for pseudomona colonization (less that 4% of CF children under 12 are chronically infected with pseudo), anti-staph prophylaxis is pretty much the norm:

Here's what a recent article from the cf trust has to say, and its based on the recent copenhagen conference:

'Routine anti-staphylococcal antibiotic treatment (flucloxacillin) from diagnosis was recommended as the presence of Staphylococcus aureus has been significantly associated with earlier PA acquisition and may predispose the airways to PA infection'

See <a target=_blank class=ftalternatingbarlinklarge href="http://www.cftrust.org.uk/scope/documentlibrary/Publications/CFToday-Autumn06.pdf">http://www.cftrust.org.uk/scop...s/CFToday-Autumn06.pdf</a> on page 7
 

SpinyChaff

New member
The idea that staph can keep pseudomona's at bay is an interesting one, but I do suspect that it is completely wrong.

In the UK, which has one of the lowest rates for pseudomona colonization (less that 4% of CF children under 12 are chronically infected with pseudo), anti-staph prophylaxis is pretty much the norm:

Here's what a recent article from the cf trust has to say, and its based on the recent copenhagen conference:

'Routine anti-staphylococcal antibiotic treatment (flucloxacillin) from diagnosis was recommended as the presence of Staphylococcus aureus has been significantly associated with earlier PA acquisition and may predispose the airways to PA infection'

See <a target=_blank class=ftalternatingbarlinklarge href="http://www.cftrust.org.uk/scope/documentlibrary/Publications/CFToday-Autumn06.pdf">http://www.cftrust.org.uk/scop...s/CFToday-Autumn06.pdf</a> on page 7
 
2

2perfectboys

Guest
YES AMY- Tell us where the support for your statement it and post links to these studiesthat show S aureus keeps PA at bay or even away
 
2

2perfectboys

Guest
YES AMY- Tell us where the support for your statement it and post links to these studiesthat show S aureus keeps PA at bay or even away
 
2

2perfectboys

Guest
YES AMY- Tell us where the support for your statement it and post links to these studiesthat show S aureus keeps PA at bay or even away
 

Allisa35

Member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>JoAnn</b></i>

Hi - My original question was in regard to the other things listed in the culture:







ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS

ASPERGILLUS



Anyone have any feedback on these?

Thanks!</end quote></div>


I have never heard of these before. Sorry I can't help you. It will be interesting to see if anybody else cultures these. Mine are usually either Staph, normal flora, or PA. Hope you get some answers.
 

Allisa35

Member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>JoAnn</b></i>

Hi - My original question was in regard to the other things listed in the culture:







ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS

ASPERGILLUS



Anyone have any feedback on these?

Thanks!</end quote></div>


I have never heard of these before. Sorry I can't help you. It will be interesting to see if anybody else cultures these. Mine are usually either Staph, normal flora, or PA. Hope you get some answers.
 

Allisa35

Member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>JoAnn</b></i>

Hi - My original question was in regard to the other things listed in the culture:







ACHROMOBACTER XYLOSOXIDANS SS. XYLOSOXIDANS

ASPERGILLUS



Anyone have any feedback on these?

Thanks!</end quote></div>


I have never heard of these before. Sorry I can't help you. It will be interesting to see if anybody else cultures these. Mine are usually either Staph, normal flora, or PA. Hope you get some answers.
 

point

New member
Hello JoAnn - -
I can reply with very little info. It is known to colonize CF patients. It is a pretty "strong" bacteria, similar to Psuedomonas in that sense. It can actually live in alcohol.

I will post some things from the internet.
You may want to search not under achromobacter, but under alcaligenes xylosoxidans. It was historically under alcaligenes and you will probably find more information using that search info.

Here is the full link to some info listed below... <a target=_blank class=ftalternatingbarlinklarge href="http://www.cdc.gov/ncidod/eid/vol12no11/06-0143.htm
">http://www.cdc.gov/ncidod/eid/vol12no11/06-0143.htm
</a>
Achromobacter (formerly Alcaligenes) xylosoxidans is a newly emerging microorganism isolated with increased frequency from the lungs of patients with cystic fibrosis (CF), but information about its clinical relevance is limited (1). A. xylosoxidans is innately resistant to many antimicrobial drugs (2), except piperacillin, piperacillin-tazobactam, and imipenem, and moderately susceptible to ceftazidime (45% of susceptible isolates), which is widely used to treat infection due to Pseudomonas aeruginosa (3,4). The mechanisms involved in cases of high-level resistance to ceftazidime have not been described for A. xylosoxidans. Possible mechanisms for ceftazidime resistance among gram-negative bacilli are alterations in outer membrane proteins, overproduction of cephalosporinase, or production of an extended-spectrum ?-lactamase (ESBL). ESBLs are enzymes distributed worldwide (5) that hydrolyze oxyimino-cephalosporins and monobactams and are susceptible to ?-lactamase inhibitors such as clavulanic acid and tazobactam. We report on the isolation from a CF patient of A. xylosoxidans that produced the VEB-1 ESBL. This is the first report of ESBL production in A. xylosoxidans and the first report of a VEB-1 - producing isolate from a CF patient.

<b>Conclusions</b>
This finding of a VEB-1 - producing A. xylosoxidans from a CF patient enhances the scant information available to laboratorians and clinicians about ESBL production by isolates from CF patients. A very recent study reports 3 ESBL-positive isolates of P. aeruginosa from CF patients in New Delhi, but the ESBL has not been characterized (14). Resistance to expanded-spectrum cephalosporins mediated by ESBLs has never been described in A. xylosoxidans. The detection of the ESBL production was difficult in AX476; therefore, the frequency of A. xylosoxidans isolates that produce an ESBL might be underestimated. We recommend the use of BioRad combination disks, especially for isolates that are highly resistant to ceftazidime and susceptible to piperacillin or when synergy exists between ticarcillin and ticarcillin plus clavulanic acid.

The origin of the strain remains unclear. Because A. xylosoxidans is widely encountered in the environment, acquisition of AX476 by our patient may have resulted from poor adherence to handwashing, contamination of respiratory therapy equipment (nebulizer), or contaminated water. We can exclude nosocomial acquisition because our patient had never been hospitalized.

The location of blaVEB-1 on an easily transferable plasmid might represent a clinical threat if spread among other species widely encountered among CF patients, especially P. aeruginosa. Such a transfer would create serious therapeutic problems. Therefore, to prevent person-to-person transmission, our patient visits the physician on different days than the other CF patients. If he needs to be hospitalized, our patient may not share a room with immunocompromised patients or with other CF patients anywhere in the hospital, which is the recommendation for patients with other multidrug-resistant pathogens (15). In conclusion, this first finding of a VEB-1 - producing A. xylosoxidans from a CF patient emphasizes the need to study the mechanism(s) of resistance to ceftazidime among a wide collection of isolates originated from different centers. The sequence of the class 1 integron reported in this paper has been assigned GenBank accession no. DQ393569.
 
Top