ONE Identifying Lyme Disease The History of Medicine: 2000 BCE: Here, eat this root. It will make you strong. 1080 BCE: Throw out that root and drink this potion; it is better for you. 250 AD: Get rid of that potion; it is bad for you. Take this herb instead. 1910: Get rid of this herb and take this potion; it is more effective. 1950: That potion is bad for you; here, take this drug. 2000: That drug is no longer effective; here, eat this root.
How is it possible that an epidemic of tick-borne diseases could be spreading without getting the proper attention? How could patients throughout the United States continue to be desperate for help? To understand the answer to this dilemma, you need to understand the intricacies of Lyme disease and the constructs of the medical paradigm that doctors and health authorities work under. First of all, we must look at the history of medicine. Medicine is a continuously changing and expanding field, and it is said that almost half of everything that we learn in medical school will usually be proven to be wrong every five to ten years. There are numerous examples of the undeniable blessings of modern medicine: antibiotics and other pharmaceuticals; new high-tech diagnostic machines and tests; groundbreaking surgeries; and public health initiatives have extended human life (most especially in infancy) and increased well-being in the general population. But along the way to modern medicine, some medical pioneers have been dismissed or even attacked for what others believed were their heretical ideas. For example, consider Dr. Ignaz Philipp Semmelweis, a nineteenth-century Hungarian physician, who is now known as an early pioneer of antiseptic procedures described as the "savior of mothers." Semmelweis made an important scientific observation: When he washed his hands before delivering babies, the women in his clinic did not die as often from puerperal sepsis (a bacterial infection that kills women shortly after giving birth) as those in another clinic in the same hospital, which had a death rate of 10 percent.
When he shared this important observation with his colleagues, he was ridiculed. As patients abandoned his colleagues and begged to deliver in his clinic, he was ostracized by his medical society and driven out of medicine. He was committed to an asylum, where ironically, he died of septicemia only fourteen days later, possibly the result of being severely beaten by his guards. Dr. Louis Pasteur was another example of a scientist who was ridiculed. It was years before his theory of the germ origins of illness was proven to be correct. Helicobacter pylori were first discovered in the stomachs of patients with gastritis and stomach ulcers in 1982 by Australian doctors Barry Marshall and Robin Warren. The conventional thinking at the time of their research was that no bacterium could live in the strong acid environment of the human stomach.
They also proposed that treatment with antibiotics rather than the practices then in use, which included stomach removal, were best for ulcer patients. Their discovery was ignored for almost twenty years, while patients had their stomachs removed because of bleeding ulcers, or were told to drink large quantities of milk, or were cautioned that their ulcers were due to stress alone. There is a long list of other examples available for anyone who wants to explore the history of medicine. Many of these pioneers pushed the boundaries until the paradigm of that specific disease process was transformed. Are things different today? Have we learned to listen to those challenging the medical establishment? Certainly not with respect to Lyme disease and associated tick-borne disorders. To understand Lyme disease, we need to go back to the mid 1970s, when portrait painter Polly Murray first noticed an outbreak of what had been called "juvenile rheumatoid arthritis" in the town of Lyme, Connecticut, that had affected her and her children from decades earlier. Dr. Alan Steere, a rheumatologist at Yale University, was called in to investigate the epidemic, as were researchers from the National Institutes of Health (NIH) and Rocky Mountain Labs.
Dr. Willy Burgdorfer, a researcher at Rocky Mountain Labs, identified a microscopic spirochete, a spiral-shaped bacteria that resembles the one that causes syphilis. This was eventually identified as the causative agent of the newly identified disease, and the spirochete was named Borrelia burgdorferi (Bb) after Dr. Burgdofer's discovery, and the related disease was called Lyme, after its initial outbreak in the town of Lyme, Connecticut. Although patients may have had other manifestations of the disease, Dr. Allan Steere primarily investigated patients with rashes and rheumatologic manifestations, including hot, swollen joints, for the Connecticut Department of Public Health. He was instrumental in determining that many became ill in summer or early fall and lived in geographic clusters in mostly rural areas. He did recognize that patients were very ill and not just psychologically disturbed.
But what caused this mysterious illness? This mysterious illness was actually not a new discovery at all. Lyme disease had already been reported in Europe in the late 1800s, as a rash of the hands: Dr. Alfred Buchwald described a skin lesion; others in Europe and the United States reported the same lesion as part of a condition called Bannwarth syndrome, a triad of radiculitis (a pain radiating along a nerve), with Bell's palsy (the sudden onset of facial paralysis), and meningitis (an inflammation occurring in the membranes covering the brain and spinal cord). In 1909, Dr. Arvid Afzelius described an expanding ring-like skin rash, later named erythema chronicum migrans, or ECM (in 1990, dermatologist Dr. Bernard Berger recognized that the rash was not chronic in all cases and renamed it Erythema Migrans or, simply, EM). Ten years later, Afzelius connected the disease with joint problems and speculated that they are somehow related to the bite of a tick. In 1922 the disease was found to be associated with neurological problems, and in 1930 the diagnosis further included psychiatric disturbances.
A few years later, arthritic problems were added. In 1965 Dr. Sidney Robbin, a semiretired internist living in Montauk, New York, described expanding circular rashes that responded to penicillin treatment that appeared in conjunction with a peculiar type of arthritis that he named Montauk knee. Five years later, Dr. Rudolph Scrimenti, a Wisconsin dermatologist, published the first report of an ECM rash in the United States. As Dr. Robbin had observed, he too reported that the rash responded to penicillin. No one, however, had put all the pieces together.
And no one yet connected these symptoms to the patients who were so ill in rural Connecticut. Was this a new illness, and, if so, where did it come from and how should we treat it? By 1977, Dr. Steere was reporting a whole host of specific and often bizarre signs of this new disease, including fever, fatigue, headache, migratory joint pains, as well as multiple cardiovascular and neurological abnormalities. As the result of treating patients with antibiotics for (only) seven to ten days, many patients went on to develop other symptoms. It appeared that antibiotics just wouldn't help Lyme patients. Perhaps Lyme was caused by a virus, or was an autoimmune disorder. When you have been trained in a particular medical specialty, you see the world through certain lenses and diagnostic paradigms. A gastroenterologist, for example, sees the world through the lens of the gastrointestinal (GI) tract and tries to link up a patient's symptoms to diseases known in their specialty.
This is the same for neurology or infectious disease or, in the case of Dr. Steere, a rheumatologist, for diseases of the joints, which include autoimmune diseases. It is not that the thinking of these doctors and subspecialists is necessarily wrong, but it may be that their worldview only includes part of the whole picture. There is relative truth, and then there is absolute truth. When the three blind men are feeling the elephant, they each describe a different part. One describes the elephant as having a long, movable nose, another tough skin with thick legs and big nails, and the third might just describe a thin, coarse tail. Each has described a certain relative truth, and none is incorrect, but none of them have seen the big picture: It's an elephant! So it is with Lyme disease. The initial paradigm created for diagnosis and treatment of these patients was through a rheumatologist's narrowly focused eyes.
Soon the infectious disease doctors claimed Lyme disease as part of their turf. I was trained as an internist to be a medical detective, with a wide diagnostic perspective: We have to know something about all of the medical subspecialties. The vision of an internist must be broad and inclusive of all possibilities, since his or her job is to diagnose patients to effectively determine who needs to be referred to subspecialists. An internist, therefore, will not necessarily have some of the inherent biases or diagnostic schema associated with subspecialists. As Lyme diagnosis and treatment fell into the domains of the rheumatologists and infectious disease doctors early on, a paradigm was forming based on the way these subspecialists viewed the world. In addition, traditional medical education has always taught doctors to find one cause for all of the patient's symptoms. This is deeply ingrained in every physician's education. We generally are not taught to look for multifa.