Lyme disease antibody tests (western blot) have a low level of sensitivity compared to some other antibody tests. This leads to some Lyme disease victims being told they do not have Lyme disease, because of a negative or equivocal result, when in fact they do have the disease.
The following explanation of the diagnostic significance of antibodies against Borrelia species is taken from the instructions for interpreting test results published by ViraMed, the manufacturer of the Western blot test kit used by RIPL.
The full instruction document is available here.
Please note that this test kit uses antigens from Borrelia afzelii and Borrelia Burgdorferi sensu stricto but no native antigens from Borrelia Garinii, which is the commonest genome of Borrelia found in the UK. Further information on European genomic groups of Borrelia can be found in “Distribution of Borrelia burgdorferi sensu lato genomic groups in Europe, a review” Habálek, Z.; Halouzka, J. (1997-12-01), European Journal of Epidemiology 13 (8): 951–957).
DIAGNOSTIC SIGNIFICANCE OF ANTIBODIES AGAINST BORRELIA SPECIES
1. IgG antibodies are produced for the first time several weeks to months after infection and are often not detectable in early stages of infection (22). In suspicion of a recent infection, IgM antibodies should be checked and a second sample should be analysed later. Patients in the 2nd or 3rd stage of the disease are usually positive for IgG antibodies. Antibody titers decrease gradually during convalescence (22).
2. IgM antibodies usually appear 2-3 weeks after onset of the disease for the first time (22). Antibody titers often decline several weeks to months after convalescence. But they may also persist up to several years (7,11,20).
3. IgA antibodies are detectable at an early stage of borreliosis in many patients, in some cases earlier than IgM antibodies.
4. The immune response and consequently the band pattern differs from patient to patient. As a general rule: The number of antibody types and therefore the number of specific bands is increasing with progression of the disease (1).
5. An early antibiotic therapy can suppress the development of antibodies (17).
6. Medication and immunoglobulin therapy can cause unspecific antibody reactions (24).
7. Cross reactivities to Borrelia antigens are described for infections with Treponema, Leptospira and other bacteria with flagella (2,15,22). An acute EBV infection can cause a polyclonal stimulation of Borrelia antibodies (22). If IgM antibodies against OspC or p41 are detected without clinical symptoms for borreliosis an EBV infection needs to be tested for. Cross reactivities in cases of autoimmune diseases, MS, ALS, Influenza and Syphilis are described as well.