A Test Result is Not a Diagnosis

Editorial (Rant?)

This is one of my own pet medical peeves, stimulated recently by a thread here on Lyme tests and what bands meet criteria, etc. It relates directly to the difficulties with negative tests for Chlamydia pneumoniae. Yes, I know it's a complex issue, but the basic rule is really a simple one:

A serologyi test, either negative or positive, does not a diagnosis make!

Medical diagnosis is a complex art which includes serologyi, clinical history, symptom patterns, treatment history, and other medical tests. True, some serology carries more weight in the clinical equation that others and may be taken almost defacto as diagnosis. For example, one is treated for many diseasesi on the basis of positive serology, such as for TB or STDi's, even if you are asymptomatic and have nothing obvious in your history.

But- the same does not hold true with negative tests, or with tests like Lyme's where the strict CDC criteria (specific bands must be positive) are not met. There are many reasons for negative tests and for missing criterian bands to occur even with the presence of the actual disease organism in the body. This is the complex part I won't go into here. It's really discussed more fully elsewhere on www.Cpnhelp.org<

With a negative serology test or lack of full criterian bands, other things are taken into account in good medical diagnosis: history, clinical picture, and even empirical response to an empirical treatment is legitimate diagnostic information. Criterian which designed to meet the needs of a research study, in order to weed out false positives and thus have a more homogeneous test group, are not the same requirements of a medical practice, where a doctor is obligated to make a best attempt to help the patient, even if not everything is crystal clear on serology tests.

Of course, we do sacrifice certainty when we receive treatment this way. Someone, for example, who has negative serology for Cpn, but suffers a Cpn related disease, and who uses a CAPi and has reactions or improvements, may have these from Cpn or from some other organisms (such as borrealis). And vice versa. Some people not meeting criteria for Lyme who treat with antibioticsi and flagyli anyway, could be treating Cpn. The famous Lyme herx/die-off is almost indistinguishable from the famous Cpn herx/die-off. It's likely that we are killing more than one organism off anyway, especially in diseases which produce immunocompromised individuals, like Cpn.

Now, there are other signs which tend to confirm one organism or the other. For example, as far as we know only Cpn creates secondary porphyriai because of it's stealing of host ATP. These porphyric symptoms are distinct in many ways from endotoxini or cytokinei symptoms, common when killing a number of organisms. So we can get empirical hints from empirical treatment, which may help clarify an empirical diagnosis.

What we may not have is certainty. But most of us can sacrifice a little certainty for getting better. I'd rather be well and uncertain, than still sick and looking for absolute guarantee!

 

Comments

Jim, fun rant! feeling your oats on day "x" of tinii pulse, hmm? I agree with you totally and it is time someone stepped up and said it outright as you did. Thanks
marie

On CAPi since Sept '05 for MSi, RAi, Asthmai, sciatica. EDSSi at start 5.5.
"Color out side the lines!"

On CAPi since Sept '05 for MSi, RAi, Asthmai, sciatica. EDSSi at start 5.5.(early cane) Now 6 (cane full time) Originally on: Doxyi 200, Azith 3x week, Tinii cont. over summer '07, Revamp of protocol in Summer '08 by Stratton due to functional loss; clarithro

Since I'm the one who blathered about the testing, I'll add a few things.

First, I thought I was pretty clear that the tests, although interesting, were not going to alter the course of anything we have been doing. I posted these results to let others know what possibly to expect from serologyi and to point out the nuances in some of the tests that people might miss. I kind of have been looking into this recently and I found it all to be interesting.

Given our limited technology in detection, clinical diagnosis and empirical treatment is often the only way to proceed and that is what we have done for 9 months.

Lastly, I do believe, however, it is possible to sacrifice more than just certainty if one treats just for Cpni with doxyi,zithi and flagyli. This is one of the biggest reasons I sought out a doctor. I wanted some latitude in possibly using other agents down the road. Ones that would target possible co-infectionsi of Lyme. Whereas this might be confusing to newcomers and I might be muddying the waters a bit, I think it is a legitimate to bring up.

I think this muddying actually illuminates the fact that this is all very trailblazing and is not static.

--------------- "Chance favors the prepared mind." --Louis Pasteur Husband treating MSi with CAPi

Killing two birds with one stone, I have moved over from here: http://www.cpnhelp.org/?q=the_husband_and_no_more_n< to save completely highjacking Kristen's blog. 

Three years ago, I was David's first Chlamydia pneumoniae patient, yet when I started we had no idea whether I was positive for the pathogen.  David went totally on instinct and was proved correct (despite the fact that he doesn't like me using the word "proof".)   I showed signs of responding to the antibioticsi very quickly, whereas if I had no infection, there would have been no response.  Obviously at that point, it might not have been CPn which was causing this, but any other pathogen which would have responded to doxycycline.  A few weeks later I was tested for CPn by serologyi.  I had a reading of 1:64, which is very low.  Many doctors on seeing this would not have treated me.  David would have written on the report: 1:64, treat if there is evidence of infection."  Multiple sclerosis would not have been considered as evidence of infection, but luckily I was already being treated by David so was not reliant on making a GP see reason for treatment.  
I started on doxycycline then added roxithromycin a few weeks later.  Metronidazolei was added in pulses after about three months.  I never took NACi or amoxicillini then.  After about six or seven months I changed doxycycline for rifampicin, so I can't say how much I was helped by this, except that reactions to metronidazole had petered out to nearly nothing by then.  Rifampicin is totally non immunomodulatory and it really threw my walking for a while, but I am only assuming it was the lack of immunomodulation which caused this, rather than deeper tissue penetration.I moved onto intermittent treatment after a year, with the aim, because of the slow growing nature of the organism, of doing two months off, two weeks on.  I restarted after only a month, not because I felt a return of symptoms, but cause I panicked: I didn't know anyone else who was doing this, nor even anyone else locally with MS  -  I didn't want to.  The one certain thing in all this is that I was getting better.  I even now have had no adverse MS events.  I still have certain deficits, but these are due to demyelinationi and axonal damage.  They are gradually improving with either finding new pathways or remyelinationi.  This would not be speeded up by still taking antibiotics full-time.  I do now take NAC every day, to guard against reinfection, which kind of goes along with Stratton's current experiments.

 

I think there is no such thing as absolute certainty in life, except in retrospect, so as Jim says, "I'd rather be well and uncertain, than still sick and looking for absolute guarantee!".......Sarah

 

An Itinerary in Light and Shadow  Berger.

Started the Wheldon regime in August 2003, due to very aggressive SPMSi.  Moved to intermittent therapy after one year.  In 2006 still take this, two weeks every two months.  EDSSi was about 7, now less than 2

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Sarah, I think I would have said: 'Microimmunofluorescence titres against Chl. pneumoniae 1:64. A low value. This does not exclude chronic active infection.' [Hides rolling-pin.]

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

Hide the rolling pin?  I don't care what you do with the rolling pin  -  I'm a mallet person myself, and I know where that is.......Sarah

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Sarah, isn't a mallet a kind of duck? Oh no, that's a mallard. Well the image was quite amusing, you chasing David about the kitchen flailing a duck at him. He probably would have cried foul.

Must be the Tinii that's doin' it to me.

Sojourner, I don't think your approach to cover Lymes as well as Cpni is muddying up the waters, even though it' broader than most of us here need. It underscores the whole point-- that protocolsi are shaped around individual patients by knowledgeable doc's and educated patients. Why we are here. We can present the "typical" approaches worked out over time, which as Sarah has pointed out is has evolved even in her own pioneering case, and our full-on discussion here at cpnhelp will hopefully broaden our thinking as we get more educated in the core ideas and treatments. We are already discovering some differences in the needs of CFSi patients and MSi patients, and Red has helped us understand the particular sensitivities of rosaceai patients. Lyme, mycoplasm and other co-infectionsi with Cpn will probably require different needs as well.

We are just damned lucky to have a starting point in the Vanderbilt work, as it's a lot easier to figure out how to modify something to fit particular needs if you are getting better while you figure it out! 

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei &amp; Fibromyalgiai- Currently: 150mg INHi, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

[quote=Jim K]

We are just damned lucky to have a starting point in the Vanderbilt work, as it's a lot easier to figure out how to modify something to fit particular needs if you are getting better while you figure it out! 

[/quote]

I just could not agree with you more,---and I literally do thank goodness almost every day for Stratton, Wheldon and for this site, tooSmile.

 

--------------- "Chance favors the prepared mind." --Louis Pasteur Husband treating MSi with CAPi

Jim, is that a dead duck, or a live one?

 

I think that my treatment for someone not overly sensitive to various drugs, was the best way to start, since I had very rapidly evolving MSi, so there was no time to be lost.  I didn't mess around with building up to full doses and so got rid of the main bulk of the infection by month six or seven.  I never took amoxicillini but now take MAC.  Other people have a harder time of building up, but I think that apart from the MS, now obviously a Can infection in my case, I was very fit and healthy.  I held the MS in reasonable check from the age of 24, but was gradually getting more frequent relapses, then a new infection threw me over the edge.  Many people on these regimens for MS take other things, such as statins and LDNi, in order to cover as many possibilities as possible.  Lexy's approach with Jim, seems very sensible, bearing in mind his history, although I do wince at the thought of taking even tinidazole for a fortnight, having personally evolved my treatment in the intermittent courses to taking all the doxycycline and roxithromycin in the morning, then the two lots of tinidazole with dinner.......Sarah

 

An Itinerary in Light and Shadow  Berger.

Started the Wheldon regime in August 2003, due to very aggressive SPMSi.  Moved to intermittent therapy after one year.  In 2006 still take this, two weeks every two months.  EDSSi was about 7, now less than 2

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Comment viewing options

Select your preferred way to display the comments and click "Save settings" to activate your changes.