By Tom Grier M.S.
Three Main Categories of Lyme Disease Tests:
1. Indirect Tests (serum antibody tests):
ELISA; Western Blot; IFA; Borreliacidal Antibody Assay (Gunderson test);T-cell Activation Test
2. Direct detection tests:
PCR (DNA amplification); Lyme Urine Antigen Test (LUAT); Antigen Capture Test; culturing of skin, blood, CSF, urine, or tissue; immune complex / antigen-antibody test
3. Tissue Biopsy and Staining:
Silver Stain; Gold Stain; Fluorescent Tagged Monoclonal Antibody Stains; Acrodine Orange; Gram Stain; Muramidase; etc.
There is a great deal of confusion and controversy surrounding Lyme disease testing. The first problem is that most of the manufacturers of these tests want you to believe that their tests are the best. At every medical convention, I listen to sales pitch after sales pitch from sales people making their product sound infallible. Often the terminology is confusing and the customer frequently misinterprets what is really being said.
For example, a salesman may say the rate of false positive or false negative is less than one percent. This sounds like the test is more than 99% accurate. In reality, what it is saying is if you have 1000 test samples from the same known laboratory sample, then in less than ten samples will there be a result that differs significantly from the other 990.
In any of this, did you hear the words: "percent reliability" or "percent accuracy" in diagnosing Lyme disease in humans? No! People often mistake "false positive rate" for accuracy. The truth is that no Lyme disease test to date is close to 100% accurate, because each test has its own particular set of shortcomings. So, while the first problem with Lyme disease tests is in the way they are promoted, the second problem is the way the tests are primed to recognize laboratory strains of Bb, rather than wild types. Third, the Lyme spirochete can hide in the human body, and fool the immune system into thinking it isn't there. So, no antibodies are produced, resulting in negative tests. Stealth technology isn't new, it evolved millions of years ago by the first bacteria that evaded its host's defenses.
Immune Responses
The first antibody our body makes in response to a foreign invader is usually immunoglobulin type M, abbreviated as IgM. This large antibody takes two to four weeks to be made in quantities large enough to be consistently measured. It is at its peak of production four weeks after exposure to an antigen. The IgM antibody will only stay in circulation for about six months, and then levels are usually too low to detect. If infection persists, this antibody may also persist. In general, a Lyme patient who consistently has detectable IgM levels is usually chronically ill, but its absence is not a reliable indicator of cure.
The second antibody we make after the IgM is the IgG antibody. This antibody takes four to eight weeks to form, and is gone in less than twelve months. It peaks at about six weeks. This antibody crosses the placenta, so an infected mother can pass this antibody to her child. An IgG antibody titer in a newborn does not have to mean active infection. It does mean the mother has had exposure, and the child must be carefully monitored for signs of the disease.
Because of the difference in the two antibodies, two separate tests are available to test for their presence. Therefore, a physician must specify whether or not a patient should have an IgM or IgG Western Blot, or an IgM or IgG ELISA test.
IgM:
This is the earliest of the antibodies to appear in response to an infection. It is produced in quantity. It is six times larger than the IgG antibody. Because of its size, this immunoglobulin does not cross the placenta. Since it cannot enter the fetus from the mother, any newborn that starts to make IgM antibodies against Lyme disease must be infected. However, a fetus exposed to Borrelia burgdorferi early in the pregnancy may never make an antibody response to the Lyme bacteria because the baby's immune system doesn't recognize it as foreign.
IgG:
This antibody remains the longest and is the foot soldier of the immune system. It attacks viruses, bacteria, yeast, toxins, and transplants. The IgG antibody can kill bacteria indirectly by tagging or marking the foreign invaders for destruction by the killer cells (T-cells, macrophage). Or, it can kill the bacteria directly by evoking compliment, a series of enzymes and proteins that will dissolve the intruder.
Note: It was once thought that plasma cells could produce antibodies that could conform to any shape necessary to attack foreign intruders. If this were true, we would have almost unlimited immunity. It is now thought that each person has a finite collection of specialized lymphocytes that are able to create a finite number of antibodies. Each antibody shape is predetermined, and can be produced by only one type of lymphocyte. When the body is invaded by a foreign antigen, it will stimulate one of these cells, and only that cell will begin to clone itself. This process takes several weeks. If we lack the right cell type to do the job, we are left with a gap in our immunity. This might account for why some Lyme patients with certain tissue types have greater morbidity, while others have relatively mild symptoms.
Dr. Alan Steere, M.D., observed that Lyme arthritis patients with tissue type HLA-DR2 and HLA-DR4 had more severe arthritis and chronic disease. Other tissue types have been associated with an increased incidence of multiple sclerosis and other neurological diseases. It might be that different patient tissue types might account for a difference in patient's symptoms to a greater degree than different strains of the bacteria.
It is known that this bacteria has an affinity for specific tissues. If you have a specific lack of immunity, this may cause the disease to manifest differently in those tissues. For example, let's say hypothetically that your heart is infected with Borrelia burgdorferi bacteria. Perhaps most people make an antibody that suppresses attachment of Bb to certain fibers in the heart. If you lack that antibody, the infection may continue more aggressively and manifest differently - for instance, causing an enlargement of the muscle fibers or destruction of the conduction pathways.
Instead of lacking a specific antibody, perhaps some individuals make a different kind of antibody, an antibody that not only attacks the bacteria - but may attack the heart as well! It is well known and documented that some patients produce auto-antibodies, which are antibodies that our own body produces that attack our own tissues. This is the basis of autoimmune disease. In some Lyme disease patients, an auto-antibody against cardiolipin has been clearly established in Lyme patients with Lyme carditis.
Perhaps, in addition to other Lyme tests, we should also be tissue typing patients and searching for auto-antibodies? Tissue typing requires a small blood sample, and costs about $200.