In article <Pine.3.89.9410251235.A21882-0100000 at isnet.is.wfu.edu>,
bmorrell at ISNET.IS.WFU.EDU ("Robert Morrell Jr.") writes:
<This is yet another indication that the prostatitis was not the source of
the cloacae, for imipenem has good penetration in all tissues and should
have hit the organism there as well. E. cloacae is present in various
normal floras in the body. The dehibilitation of the patient by the
prostatitis might have enabled one of those sources to become
opportunistic.>
Wrong to assume patient is debilitated, he is not. As near as anyone can
tell he has an infected prostate and nothing else wrong. "Imipenem has
good penetration in all tissues and should have hit the organism" -- a
wild assumption. I challenge you to show me data directly measuring
imipenem in the prostatic fluid.
< What evidence do they have? You have cultures that are negative for an
organism that is easily recovered from such cultures. You also have a
differential response to therapy that should have cured both, were the
organism the causative agent in both. There is no rule that I know of that
says that we must have a clearly identifiable source of sepsis.>
Only the first rule of infectious disease: Find the organism and culture
it.
<It sounds like you and the consult team have labeled a source (the I
hate blank spaces on the chart approach) and are now unwilling to back
down in the face of considerable evidence to the contrary. This is the
"I've made up my mind, and if the lab doesn't confirm it, the lab is
wrong" mentality.>
More like we see these rods on microscopy, what are they?
<snip>< why CNS isolation indicates non-bacterial prostatitis is because
patients do not typically respond to treatment of the CNS, as I believe
you said that this patient did not. E cloacae was =not= found in the semen
or prostatic fluid, which proves my "bias".>
What treatment? What antibiotic has been proven to penetrate the prostate
and kill coagulase negative staff there?
<Why not indeed? The problem is you seem to have E cloacae on your mind.
Classical microbiology technique: rule out possibilities. Let us consider
E cloacae in this case:
1. It did not grow on culture, despite being a hardy organism routinely
isolated in other prostatitis patients =using identical techniques=.
2. It did not respond to therapy that would hit an E. cloacae.>
Number two assumes imipenem penetrate the prostate. Prove it.
<snip>,In my book the above points take together would be enough to rule
out E
cloacae as the rod supposedly being seen in the specimen. I would
certainly be interested in what that rod was, but I suspect it is in fact
a propionibacterium (if all the cocci you are seeing is normal skin
flora, then I would expect this organism) that will be hard to recover
apart from the staph, and then probably not be the pathogen.>
So why not prove what it is? Why not stop guessing?
< I would suggest that you are failing to go over a lot of microbiological
ground that has already been covered. The key to non-bacterial prostatitis
is probably related to what we are culturing for more than how we collect
the specimen. This is why you should turn your attention away from easily
recovered organisms and towards more unusual, seldom cultured for
pathogens, such as Mycobacteria or other difficult to grow, poorly
staining organisms.>
Your first first point is noted. But from my research and posts here, it
appears that PCR, Serial Dilution, Immumagnetic Enrichment, the Laser
Optical Trap, and Flow Cytometry, could all play a role in solving the
many controversies surrounding prostatitis and none of them have been
applied. Your last point is well taken and we are attempting to search
for unusual or difficult to grow organisms.
