Culture shows Staph Infection
AllwithHIM
anitbiotics worked fine. For the last 3 years the've not worked. Neither my uro
or gp ever did a culture to see what kind of bacteria they were dealing with at
least not like my new uro did (swab attached to wire, stick in penis. Ooouch!).
They just found bacteria in my urine and gave me Cipro, etc.. I decided to
change uros and this guy did the above culture. I went back to him a few days
ago and he said he found a weird type of staph bacteria in my prostate. He told
me the other antibiotics the other uro and gp were using wouldn't kill this
type of bug. He even let me see the chart and sure enough the bug is resistant
to Cipro, Noroxin, etc.. As he handed me the new antibiotic perscription he
said, "Ok, here is your wonder drug". Could it be so. Could this staph bacteria
have been the problem all along, or at least the last few years? If this drug
kills this staph bacteria could I be back to normal? I just started the new
antibiotic. Starts with an R but I can't remember what it is. I'll let everyone
know. TICKS me off that none of my old doctors cultured my prostatic fluid.
Jeff
Anonymous
This is only relevant if the new drug cures you. If not, as usually
happens, why get upset?
Andy Domonkos
GP's/URO's have done or were willing to do a culture.
Andy
AhandleBT
That's really shocking. Not one Dr. did a culture?
ABT
AllwithHIM
>
Nope, not one. Thats what bothers me. They knew the antibiotics weren't working
so you would think that they would have done a culture to find out what they
were dealing with.
Jeff
Andy Domonkos
do was stay on the latest AB, Cipro, for 6 weeks.
Andy
AhandleBT wrote:
> Andy,
>
> That's really shocking. Not one Dr. did a culture?
>
AllwithHIM
all the drugs others have put me on to get rid of this thing would in know way
work on this bug. I am not expecting a total cure but if it would get me back
like I used to be (On antibiotics for a month and off of them for 8 or 9) then
I could live with that.
Jeff
Anonymous
AhandleBT wrote:
>
> OKAY, let's be cautious here. As I understand it, Staph is "everywhere" it is
> necessary to be quite careful in obtaining samples that aren't contaminated.
>
> My Dr thoroughly cleaned the head of my penis with providine swabs etc. THEN
> collected fresh EPS (I partially voided ahead of time as well). I'm convinced
> that the staph was "from within" and not from the skin. (Could it have been
> urinary? I had no symptoms.) Anyway, staph grew (as well as a couple others),
> the microbilogist then tested the bacteria for sensitivity to different drugs.
> Interestingly, more than one bacteria grew, and each were resistant to some of the
> abx I have taken for years (there's a real surprise!).
>
> Point: *insist* on culturing. I just don't think it is as useless as some
> claim. Follow through and find out if this stuff is resistant.
>
> ABT
Staph exists happily and harmlessly in the distal urethra (in your
penis, basically). That's why it is largely disregarded. See:
Carson: What pathogens generally do not
cause prostatitis?
Childs: Many of us who conduct extensive
clinical research have cultured out certain
gram-positive organisms, for example,
streptococci, in addition to coagulase-
negative staphylococci. But are these true
pathogens? Many patients get better
following 30 days of treatment, which leads
some clinicians to believe that if these men
have Staphylococcus epidermidis in their
expressed prostatic secretions [EPS], these
organisms must be deep inside the
prostate. I bought into that philosophy for
awhile, considering the efficacy results of
these studies. One study did an excellent
job of showing the normal flora in the
urethra of 30 patients (6). The researcher
cultured the urine of healthy males for
everything from Garduerella, Neisseria
gonorrhoeae, and U urealyticum to
Mycoplasma, C trachomatis, and
Trichomonas in search of true gram-
positives and gram-negatives. Essentially,
no gram-negatives were found in normal
asymptomatic flora. As part of this research,
each patient's fossa navicularis was cultured
meticulously, along with the external orifice
and about 3 to 4 cm of the mid-penile shaft.
Again and again, Streptococci viridans,
coagulase-negative staphylococci, and a few
enterococci were found. Interesting to note
is that the farther the researcher got, the
lower the colony count became, with few
exceptions.
Krieger: The counterpoint to this story is
from Tanner and colleagues from UCLA,
who diagnosed and treated chronic bacterial
prostatitis with those same organisms based
on culture criteria (7). They found a tenfold
increase in Cornyebacterium species, but
that does not really meet the Meares-
Stamey definition. This definition refers to
recurrent infections caused by the same
organism localized to the prostate. That's
quite different from getting a set of cultures
that reveal a tenfold increase of any
organism.
Childs: Certainly, you can't just take a
person who has a history of prostate pain
and who's been treated repeatedly with
trimethoprim-sulfamethoxazole [TMP/SMX]
or ciprofloxacin [Cipro, Bayer
Pharmaceuticals], massage his prostate,
and establish an accurate diagnosis. You
need to see that patient for months to
document exactly what is going on.
Carson: During that time, the patient should
be antibiotic free. If you influence a
patient's bacteria-laden flora with
medication, making a correct diagnosis
won't be easy.
Childs: Do normal bacteria such as
coagulase-negative staphylococci ever
cause bacterial prostatitis?
Krieger: Most of the men whom we see in
our practice harbor standard gram-negative
bacteria. Some clinicians believe patients
who have these bacteria demonstrated by
culture must be treated. A big problem with
this issue is the absence of a control group.
Another problem is accuracy of culture
methods.
----
6. Spaine DM, Mamizuka EM, Cedenho AP,
et al. Microbiological aerobic studies of
normal male urethra. J Urol. 1999;161 (4
suppl):33. Abstract 117.
7. Tanner MA, Shoskes D, Shahed A, et al..
Prevalence of corynebacterial 16S rRNA
sequences in patients with bacterial and
nonbacterial prostatitis. J Clin Microbiol.
1999;37(6):1863-1870.
------
AhandleBT
necessary to be quite careful in obtaining samples that aren't contaminated.
My Dr thoroughly cleaned the head of my penis with providine swabs etc. THEN
collected fresh EPS (I partially voided ahead of time as well). I'm convinced
that the staph was "from within" and not from the skin. (Could it have been
urinary? I had no symptoms.) Anyway, staph grew (as well as a couple others),
the microbilogist then tested the bacteria for sensitivity to different drugs.
Interestingly, more than one bacteria grew, and each were resistant to some of the
abx I have taken for years (there's a real surprise!).
Point: *insist* on culturing. I just don't think it is as useless as some
claim. Follow through and find out if this stuff is resistant.
ABT
thread
Anonymous <nob...@noisebox.dhs.org> wrote:
>
> Staph exists happily and harmlessly in the distal urethra (in
> your penis, basically). That's why it is largely disregarded.
I've heard many a doctor repeat this logic, but I've never agreed
with it. Just because a microbe is part of the normal flora does
*not* necessarily mean that it is harmless. All you have to do is
look to the field of dermatology to know that this is simply not
true.
For example, virutally all humans have P. Acnes and Malassezia
furfur on their skin (i.e. it's part of their normal skin flora),
but not all humans suffer from inflammatory acne or seborrheic
dermatitis, respectively (both of which are chronic inflammatory
diseases, but are not considered to be 'infections'). Given the
right set of circumstances, members of the 'normal' skin flora
can generate heavy inflammation. Why is this the case? In
inflammatory acne, for example, some researchers have suggested
that host response is the key. The following paper discusses
this:
"Inflammatory acne represents hypersensitivity to
Propionibacterium acnes." - by Guy F. Webster, MD, PhD, published
in Dermatology 1998;196(1):80-1.
I can post excerpts later, but the basic concept is that factors
like the absolute number of P. Acnes, etc. do not correlate to
the inflammatory reaction seen in acne. Rather it appears that
affected hosts produce an exaggerated and prolonged immune
response to P. Acnes (or its products), while 'normal' hosts
produce no response.
I then have to ask myself, why would this phenomenon be limited
to the skin? Something along these lines could explain why some
people with chronic prostatitis, who are negative for infection,
are sometimes helped by antibiotics (i.e. the antibiotics alter
the normal flora). When antibiotics are discontinued (and when
the normal flora re-asserts itself), the symptoms reappear.
And yes, Anonymous, I agree antibiotics have anti-inflammatory
properties (and that they are likely of benefit in treating CP,
as well as some other diseases), but I don't believe this
explains entirely why they are sometimes effective in
'non-bacterial' CP. E.g. recent evidence (Shoskes study?) shows
that antibiotic effectiveness in CP discriminates based on
certain factors, something I wouldn't expect if its actions were
solely anti-inflammatory.
Kevin Davis
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Anonymous
> Anonymous <nob...@noisebox.dhs.org> wrote:
> >
> > Staph exists happily and harmlessly in the distal urethra (in
> > your penis, basically). That's why it is largely disregarded.
>
> I've heard many a doctor repeat this logic, but I've never agreed
> with it. Just because a microbe is part of the normal flora does
> *not* necessarily mean that it is harmless. All you have to do is
> look to the field of dermatology to know that this is simply not
> true.
>
> For example, virutally all humans have P. Acnes and Malassezia
> furfur on their skin (i.e. it's part of their normal skin flora),
> but not all humans suffer from inflammatory acne or seborrheic
> dermatitis, respectively (both of which are chronic inflammatory
> diseases, but are not considered to be 'infections'). Given the
> right set of circumstances, members of the 'normal' skin flora
> can generate heavy inflammation. Why is this the case? In
> inflammatory acne, for example, some researchers have suggested
> that host response is the key. The following paper discusses
> this:
>
> "Inflammatory acne represents hypersensitivity to
> Propionibacterium acnes." - by Guy F. Webster, MD, PhD, published
> in Dermatology 1998;196(1):80-1.
>
> I can post excerpts later
Here's all I could find in Medline:
Dermatology 1998;196(1):80-1
Inflammatory acne represents hypersensitivity to Propionibacterium
acnes.
Webster GF
Jefferson Medical College, Philadelphia, Pa., USA.
Hypersensitivity to P. acnes may account for the great variation in acne
severity. Alternative explanations such as hyperandrogenism fail to
account for disease severity in large numbers of patients.
PMID: 9557234, UI: 98217987
> but the basic concept is that factors
> like the absolute number of P. Acnes, etc. do not correlate to
> the inflammatory reaction seen in acne. Rather it appears that
> affected hosts produce an exaggerated and prolonged immune
> response to P. Acnes (or its products), while 'normal' hosts
> produce no response.
This is very interesting.
> I then have to ask myself, why would this phenomenon be limited
> to the skin?
Good point.
> Something along these lines could explain why some
> people with chronic prostatitis, who are negative for infection,
> are sometimes helped by antibiotics (i.e. the antibiotics alter
> the normal flora). When antibiotics are discontinued (and when
> the normal flora re-asserts itself), the symptoms reappear.
This seems entirely logical.
> And yes, Anonymous, I agree antibiotics have anti-inflammatory
> properties (and that they are likely of benefit in treating CP,
> as well as some other diseases), but I don't believe this
> explains entirely why they are sometimes effective in
> 'non-bacterial' CP. E.g. recent evidence (Shoskes study?) shows
> that antibiotic effectiveness in CP discriminates based on
> certain factors, something I wouldn't expect if its actions were
> solely anti-inflammatory.
Yes, that study was a shot across my bows. Any more studies like that
and I may have to eat humble pie on my theory of why antibiotics help
some of us for some of the time.
> Kevin Davis
You make a very good, thoughtful point here. I think this theory (of
bacterial "sensitivity" and disordered immune response) has been voiced
before, by Dr Shoskes in particular, but not with such a good analogy
and study attached. Ken should make sure this appears in the website on
the bacterial page. Are you listening, Ken? This is a "sub theory" which
falls within the bacterial theory ("Active Infection" page, I'd say).
Anonymous
> thread wrote:
>
> > Something along these lines could explain why some
> > people with chronic prostatitis, who are negative for infection,
> > are sometimes helped by antibiotics (i.e. the antibiotics alter
> > the normal flora). When antibiotics are discontinued (and when
> > the normal flora re-asserts itself), the symptoms reappear.
>
> This seems entirely logical.
Let me add: this is in line with the studies of rodents who are bred in
completely germ-free environments (no bugs anywhere, not even in their
bowels). When normal flora are added to their bowels they develop a
variety of inflammatory reactions, even within their prostates and
urogenital tracts, where no bugs have colonized. So it's conceivable
that the CPPS symptoms reappear after antimicrobial discontinuance not
because of flora re-establishment in the prostate, but merely because of
flora rebound in the gut. This would also explain all the many pts who
have CPPS/CP and IBS too.
This also leads me to remind you of the research going on around
Crohn's, where patients experience relief when deliberately infected
with parasitic worms. I'll repost the article today ("Get rid of germs?
Not so fast"). Could it be that by overusing antibiotics, for example
for treating acne long-term, we have set the stage for these problems?
We thereby "prime" the immune system to overreact by suppressing
bacteria in our bodies for periods, then when they come flooding back
it's an invitation, to some of us with specific genetic makeups, to
overreact and start up this cycle.
Here's some background reading from Dr Dimitrakov:
thread
Anonymous <nob...@noisebox.dhs.org> wrote:
> Here's all I could find in Medline:
>
> Dermatology 1998;196(1):80-1
>
> Inflammatory acne represents hypersensitivity to
> Propionibacterium acnes.
I actually bought the entire issue of Dermatology that this study
appeared in. I can post a few paragraphs from the study when I
have it in front of me. The issue was a special on acne, but it
also contained some interesting studies on anitbiotics and their
potential to reduce inflammation.
thread
Anonymous <nob...@noisebox.dhs.org> wrote:
>Anonymous wrote:
> Let me add: this is in line with the studies of rodents who are
> bred in completely germ-free environments (no bugs anywhere,
> not even in their bowels). When normal flora are added to their
> bowels they develop a variety of inflammatory reactions, even
> within their prostates and urogenital tracts, where no bugs
> have colonized. So it's conceivable that the CPPS symptoms
> reappear after antimicrobial discontinuance not because of
> flora re-establishment in the prostate, but merely because of
> flora rebound in the gut. This would also explain all the many
> pts who have CPPS/CP and IBS too.
I wouldn't be shocked if this turned about to be the case. And
ironically, my doctor thinks I may have Crohn's disease. I have
to get a colonoscopy this Thursday. I have had chronic
prostatitis for about the last 6 or 7 years, and I also have
chronic epididymitis. I've lost faith in doctors to treat the
prostatitis and epididymitis. They don't take it seriously, the
antibiotics they prescribe help while I am on them, but the
symptoms recur when I stop. Quercetin has helped the prostatitis
a lot...
I'll look into the other information you posted. Thanks.
Anonymous
> Anonymous <nob...@noisebox.dhs.org> wrote:
>
> > Let me add: this is in line with the studies of rodents who are
> > bred in completely germ-free environments (no bugs anywhere,
> > not even in their bowels). When normal flora are added to their
> > bowels they develop a variety of inflammatory reactions, even
> > within their prostates and urogenital tracts, where no bugs
> > have colonized. So it's conceivable that the CPPS symptoms
> > reappear after antimicrobial discontinuance not because of
> > flora re-establishment in the prostate, but merely because of
> > flora rebound in the gut. This would also explain all the many
> > pts who have CPPS/CP and IBS too.
>
> I wouldn't be shocked if this turned about to be the case. And
> ironically, my doctor thinks I may have Crohn's disease.
This is indeed amazing! But I'm sorry to hear about this, Kevin. I hope
the colonoscopy only shows vague inflammation, as it did in my case, My
doctor also thought I had Crohn's and put me through all the tests... it
could be we are similar sorts of patients, suffering similar symptoms. I
see you too were helped by quercetin. If there are subcategories of
CPPS, looks like the two of us fall under the same subheading :-)
> I have
> to get a colonoscopy this Thursday. I have had chronic
> prostatitis for about the last 6 or 7 years, and I also have
> chronic epididymitis.
I've had sore balls on and off too. My testicles are sensitive to any
sort of rough contact. I usually can't walk around without underpants
because the swinging of the testicles and knocking against legs etc. is
uncomfortable, if not quite painful. Usually I'm unaware of the
testicles though.
> I've lost faith in doctors to treat the
> prostatitis and epididymitis. They don't take it seriously, the
> antibiotics they prescribe help while I am on them, but the
> symptoms recur when I stop.
Alas, I've never been helped by antibiotics.
> Quercetin has helped the prostatitis
> a lot...
Same here.
thread
<threadN...@servtech.com.invalid> wrote:
> Dermatology 1998;196(1):80-1
>
> Inflammatory acne represents hypersensitivity to
> Propionibacterium acnes.
The first part of the paper analyzes the various factors involved
in acne, and concludes that none of these factors explain the
severity of inflammation in acne.
The second half of the study starts with the following
hypothesis:
"A potential explanation for the variability of acne consistent
with all of these observations is that the patients' reactivity
to P. Acnes determines the severity of their acne. In other
words, inflammatory acne is due to hypersensitivity to P. Acnes.
The oversensitive individual would mount a vigorous response to
the organism, while the nonreactive one would form no lesion at
all."
The rest of the paper presents evidence to support the above
hypotheseis. Genetic factors are also mentioned in this paper.
It's worth noting that almost 100% of humans have P. Acnes on
their skin. There is little to no difference in the numbers of P.
Acnes in controls and acne sufferers. No correlation exists
between P. Acnes populations and severity of inflammation,
despite the fact P. Acnes is the key factor responsible for the
inflammatory reaction.
The paper concludes with the following statement (prostatitis and
hypersensitivity could be substituted here):
"The question that logically follows - 'which came first, the
acne or the hypersensitivity?' - is hard to answer with current
technology since no animal models exist for the disease."
The point of mentioning this paper is to provide an example that
shows that a microbe that is part of the normal flora is capable
of generating a significant, chronic inflammatory reaction. There
are other examples as well. Whether something similar to this
takes place in chronic prostatitis isn't known, but I would
imagine that it is at least a possibility. Other factors beside
bacteria undoubtedly (in my mind, at least) contribute to chronic
prostatitis.
On a somewhat related note, this issue of Dermatology has several
papers on antibiotics. I'm sure the following two studies have
been posted here at one time or another, but here are a couple of
papers on antibiotics and inflammation:
"The possible role of reactive oxygen species generated by
neutrophils in mediating acne inflammation." - published in
Dermatology 1998;196:82-85.
and
"An overview of topical antibiotics for acne treatment." -
published in Dermatology 1998;196:130-134.
The latter paper states (in the abstract, as well as the full
text):
"The main mechanism of action in topical antibiotics for acne
treatment is inhibition of inflammation caused by bacteria rather
than a direct bactericidal effect."
and
"... Thus, the therapeutic effect of these topical antibiotics
for acne may be due to their antiinflammatory action rather than
a direct bactericidal action."
I don't think that's the prevailing wisdom in acne research (yet,
anyhow), but these researchers apparently believe it.
Anonymous
> Anonymous <nob...@noisebox.dhs.org> wrote:
>
> > thread wrote:
>
> > > I have
> > > to get a colonoscopy this Thursday. I have had chronic
> > > prostatitis for about the last 6 or 7 years, and I also have
> > > chronic epididymitis.
> >
> > I've had sore balls on and off too. My testicles are sensitive to any
> > sort of rough contact. I usually can't walk around without underpants
> > because the swinging of the testicles and knocking against legs etc.
>
> markedly improved in the last few weeks, this exact type of mild
> soreness and discomfort is still present.
>
> I'm taking quercetin now - and I'll post more on this later - but in
> the meantime, a question for both Anonymous and Kevin: have you noticed
> whether Q has improves the particular symptom of epididymitis/testicle
> soreness in your cases?
To be honest the testicle discomfort is not something I notice often, so
I can't say.
> Also, what role did colonoscopy play in determining/treating your
> conditions?
None. It just ruled things out (Crohn's, gluten intolerance/celiac
disease)
Bangkok Dave
Anonymous <nob...@noisebox.dhs.org> wrote:
> thread wrote:
> > I have
> > to get a colonoscopy this Thursday. I have had chronic
> > prostatitis for about the last 6 or 7 years, and I also have
> > chronic epididymitis.
>
> I've had sore balls on and off too. My testicles are sensitive to any
> sort of rough contact. I usually can't walk around without underpants
> because the swinging of the testicles and knocking against legs etc.
Same for me on both counts. Although my epididymitis appears to have
markedly improved in the last few weeks, this exact type of mild
soreness and discomfort is still present.
I'm taking quercetin now - and I'll post more on this later - but in
the meantime, a question for both Anonymous and Kevin: have you noticed
whether Q has improves the particular symptom of epididymitis/testicle
soreness in your cases?
Also, what role did colonoscopy play in determining/treating your
conditions?
Thanks,
BKK Dave
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