Saturday, January 17, 2009

Lyme dieases for dummies: Part two

Lyme disease is so named because the current epidemic was first noticed in the town of Lyme Connecticut in the mid 1970's. A group of children developed an unusual form of arthritis which resembled rheumatoid arthritis. Researchers discovered that it seemed to be a vector(tick borne) illness. It is a zoonosis because it is known to be transferred from infected animals to humans with the aid of a vector. The famous microbiologist, Willie Burdorfer examined the Ixodes ticks which were the suspected vector. He identified small spirochetes- spiral shaped bacteria. These were found to be the cause of the illness. All living organisms in the world are identified by a term which describes features shared by a particular cohort of organisms, and a second term, which designates the species. A species is consider a distinct subset of life which reproduces and maintains its own unique features. Species may mutate-change to some degree, but basic unique features do not change. This spirochete was of the genus- Borrelia. There were other well known spirochetes of this genus. This specific Borrelia was a new species. It should be noted that in biology new species are identified on a regular basis. This species was named after the scientist who discovered it. The new spirochete associated with Lyme disease was named Borrelia(genus) burdoferi(species). The nomenclature has changed over the years, but this remains the primary microbe responsible for Lyme disease. It is likely that the germ has existed for hundreds, if not thousands of years. In the past it probably only rarely caused human disease. Microbes can mutate and become more pathogenic- develop a greater potential to cause a severe disease state. Certainly this can be seen with certain strains of influenza. (Differing strains can exist within a given species- with different biological properties). The standard Influenza A is nasty but not deadly. There are mutated strains which are extremely deadly- this is why there has much concern about "bird flu."

There are perhaps many reasons why the disease spread quickly into the human environment. There has been a loss of habitat for a major host of the adult ticks, the deer. Deer have moved into closer proximity to human habitation. The ticks have rapidly proliferated. Changes in the environment, including global warming, have been considered factors. At any rate, the disease has spread rapidly over the past 30 years. Cases have now been reported in 49/50 states. The disease has also jumped the Atlantic Ocean and is rapidly spreading throughout Europe and many other areas in the world.

Early on scientist performed tests to see which antibiotics worked well against the germ. Test tube tests showed that many antibiotics were active against the germ. Rocephin, Doxycycline, Amoxicillin and others were found to be effective. Treatment recommendations were developed which were based on this early work. It was a new disease. Physicians turned to their experience with other tick borne illnesses when they made initial recommendations about the duration of treatment. For example, experience with diseases such as Rocky Mountain Spotted Fever was drawn upon. Other information about the treatment of spirochetes was drawn from the well known therapy for syphilis. My sense is that the early researchers were thinking about early, stage I syphilis when treatment guidelines were drawn up. It was certainly known that the treatment for stage 2 and stage 3 syphilis is more complex.

Initially it was thought that Lyme was primarily transmitted by the bite of the adult deer tick (Ixodes scapularis). It was thought that the tick bites could generally be observed. It was felt that the ticks needed to be attached to the
host- humans for a prolonged period of time, perhaps 48 hours or more, for the spirochetes to be transmitted. It was also believed that early Lyme infection would be evident because infected individuals would developed the tell tale rash- Erythem chronicum migrams, or just erythema migrans, frequently referred to as EM. The public knows this as the bulls eye rash. It was believed that early treatment would prevent significant complications such as arthritis. Even when these secondary complications occurred, it was still believed that short courses of antibiotics would kill the spirochetes.

Early on it became clear that testing for the illness was problematic. Initially an ELISA test was used. This is a commonly used technology which detects human antibodies to a particular microbe. The test results were surprising. Many blood samples from the control group, not infected with Lyme, also developed antibody reactions in the test. These were considered false positives. The test did not work, it picked up patients who were not Lyme infected. Because of this a second tier test of greater accuracy, the Western Blot was added. The issues surrounding the use of these tests remains the focus of heated controversy.

In 1994 the CDC developed a standard test for surveillance of Lyme cases. The test was not developed as a diagnostic assay. Unfortunately this research tool morphed into something which it was never intended to be: a diagnostic test. This too remains an area of heated controversy.

Since the 1980s and 1990s much has been learned about Lyme disease. I am of the opinion that much of this information has not filtered down to practicing physicians. I am also bewildered as to why the IDSA seems to be ignoring most of this information as well.

It is known that most infections are conferred by the nymph form of the tick, not the adult form. Deer ticks have a two year life cycle and go through three stages: larvae, nymph and adult. The nymphs are about the size of a poppy seed. They are rarely observed when they are attached to human victims. It is not really known how long the ticks need to be attached before the disease is transmitted. The nymph Ixodes ticks are frequently called stealth vectors. It is known that many persons infected with Lyme do not develop the bulls eye rash. It also known that a wide array of rashes can occur which bare little resemblance to the classic EM rash.
These factors make it clear that early detection and treatment if usually not an option.

It is well known that Lyme disease is not just a rash and joint pain illness. The spirochetes can widely disseminate throughout the body causing protean manifestations. For example, their is no dispute that it can cause brain disease and heart disease.

The heated fight over the duration of treatment and the sorts of antibiotics has been protracted. On one side it is argued that the germ is relatively easy to kill and that short courses of antibiotics are all that is needed. The proponents of this approach claim that residual symptoms are due to "Post-Lyme" syndrome. The germs have been eliminated, but an inflammatory or autoimmune response continues. This is the basis of the guidelines which have been promulgated by the Infectious Disease
Society of America.

The other group of physicians with whom I am affiliated, advocate an entirely different position. The term Post-Lyme is not used. Rather the term chronic Lyme is used. This implies that ongoing symptoms are due to persistent infection.

Scientists have demonstrated numerous mechanisms by which the Lyme organism can resist both the immune system and antibiotics. This discussion is beyond the scope of this entry, but some information can be found in other places in this blog.
Perhaps the most important reason for the persistence of Lyme in the body is that it has the ability to become intracellular, live inside our cells. Recent research with regard to Lyme and other intracellular germs like Mycoplasmas and Chlamydia pneumonia, as well as a better understanding of how the immune system responds to these infections, has established that it is impossible to completely eradicate these organisms from our bodies. I do not believe this is conjecture on my part. I believe this assertion is completely supported by current science.

Academic physicians are frequently out of touch with "bench top" science, which characterizes aspects of micro-organisms in the lab setting not in humans.

However, there is a body of clinical evidence, studies on infected humans, which demonstrate the benefits of extended antibiotic therapy, well beyond that recommended by the Infectious Disease Society.

Doctors who treat chronic Lyme patients and their patient are astounded by the lack of acceptance of the existence of chronic Lyme disease by "mainstream" medicine. It is even more astounding that medical boards have systematically attacked the treatments proffered by such physicians and in many cases suspended their licenses to practice medicine.

This is a brief overview which I hope will provide some basic information about terms and concepts frequently seen in Lyme. It also briefly touches upon the professional disputes which have termed a paradigm war or the "Lyme Wars."
This topic is worthy of further discussion.
Future entries will continue to explain Lyme issues in an easy to understand format.

Note: Many of us have forgotten high school biology. All living things are organized in orders/classes, which go from general(more shared features) to specific(more unique features). The categories are: Domain- Kingdom- Phylum- Class- Family-
Genus- Species- and subspecies or strains. Many factors are used in categorizing living things. Frequently, scientists change their minds and re-categorize various organisms. Bacteria species are particularly difficult to classify for various reasons. The Genus is Capitalized and the species is lower case.

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