Thursday, 10 December 2009


I am still trying to get hold of the original paper of Wilske quoted by HPA on >95% in late stage Lyme testing

Wilske B. Diagnosis of Lyme borreliosis in Europe. Vector-Borne Zoonotic Dis 2003;3:215-27.So far I have only seen the abstract.

However I have been looking at this Wilske

There is much here that doesn't support HPA stance. Just a few extracts.

6.4. Sources of error in serodiagnosis False negative results. False negative results can be caused both by the test itself or biologically. Thus the high background reactivity of first-generation tests may lead to a lack of specificity, with sensitivity being comparable to that of second or third-generation tests. Differences between the test antigen and the strain causing infection in the patient may occasionally play a role, but also expression of diagnostically relevant proteins in the strains used for antigen production may be lacking(cf. Chapters 5.3.10 and 5.3.4.). Of utmost importance, however, are thediagnostic gaps due to the localisation and stage of the clinical manifestations (detailed in Table 7).
However, these criteria cannot be adopted for diagnostics in Germany or Europe because they were developed using B. burgdorferi s.s. and American sera only. Dressler et al. have shown in an immunoblot study that the immune response of European patients is obviously restricted to a narrower spectrum of Borrelia proteins [8], compared with that shown by American patients. Using different serum panels (first serum panel from Germany, second serum panel from various European countries) Hauser et al. demonstrated in two studies that interpretation rules must be defined strain-specific [22, 24]. Thus different interpretation rules are required in order to achieve equal sensitivity and identical specificity values, resp., when different strains are used. The criteria established by Hauser have been re-evaluated by Kaiser and Brauer [31a], who also believe that they are more suitable for application to the European situation than the American rules [13].
Therefore, the rules for the whole-cell lysate immunoblot established by Hauser et al. are cited here as reliable interpretation criteria [22, 24].

5.4 Fig 10
Step 2 confirmatory assay Igg immunoblot and Igm immunnoblot
Report as a negative serologic result
If short duration Lyme Borreliosis is suspected clinically serological follow up control
If a long course Lyme Borreliosis is still suspected clinically
Check special indications for
1 for serological follow up control
2 use of additional serological methods (eg use of another Borrelia species as a blotting antigen)
III 90-100% Usually solely IgG sensitivity (WHAT OF THE POSSIBLE 10% THEN!)

Extensive interlaboratory tests conducted in the United States reveal that the average specificity of commercial tests has even diminished over the past decade. Use of the immunoblot not only lacks standardisation in the form of established minimum requirements, but also goes without thoroughly evaluated interpretation rules. This deficiency results in diagnostic uncertainty and lack of comparability of results obtained by different laboratories.

During my search I came across this hypothesis

The 100% figure we all dispute. My understanding is that the US CDC produces panels of blood that are 'known to have Lyme disease' mixed with 'false positives' such as lupus and people who had Lyme but are now 'cured'. All serological tests are tested against these panels. Of course, I wish life were so simple as to say that the 'false positives' are truly false positives and people are definitely cured.
If a researcher requests a panel of blood (often they come in groups of 40) somewhere in the neighbourhood of 30 would be 'true positives' and the remaining 10 would be a mix of true negatives and false positives. Of course the exact mix has been double blinded and the 'key' is only released after the experiment is run. This allows the researcher to give percentages of 'my test gives 100% accuracy for Lyme arthritis'. Of course, I doubt that it's as simple as that. Lyme is truly a 'shape shifting superbug' and has more plasmids than any other bacterium yet described, so it defies easy answers.

I would really appreciate comments and thoughts on both the Wilske and the hypothesis.

One other interesting extract from Wilske is
4. Clinical Picture of Lyme Borreliosis
In the majority of cases the infection is self-limiting. However, even after antibiotic treatment, B. burgdorferi may persist in the tissue [39]. Persistence of the pathogen may be associated with clinical symptoms

39. Preac-Mursic V, Weber K, Pfister H-W, Wilske B, Gross B, Baumann A, Prokop J (1989) Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis. Infection 17:355-359

Seems to me yet more examples of our Health Authorities cherry picking research to support their opinions.

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