Below are extracts from an article written by Dr Bransfield the preseident of ILADS. For the full article click here.
Lyme Disease, Comorbid Tick-Borne Diseases, and Neuropsychiatric Disorders
By Robert C. Bransfield, MD 01 December 2007
Many recall the phrase "To know syphilis is to know medicine." Now Lyme disease (Lyme borreliosis), the new "great imitator," is the ultimate challenge to the breadth and depth of our knowledge. In psychiatry, we generally treat mental symptoms or syndromes rather than the underlying cause of a disorder. A greater awareness of immune reactions to infections and other contributors to mental illness enhances our psychiatric capabilities. Lyme disease, like syphilis, is caused by a spirochete with a multitude of possible manifestations and 3 stages: early with dermatological symptoms, disseminated, and late stage.
Unlike Treponema pallidum, the cause of syphilis, the causative agent of Lyme disease, Borrelia burgdorferi, can be much more difficult to eliminate, diagnostic testing is less reliable, and interactive copathogens are major contributors in the pathophysiology. B burgdorferi is highly adaptable with 6 times as many genes as T pallidum and 3 times as many plasmids as any other bacteria that allow rapid genetic adaptations. It is a stealth pathogen that can evade the immune system and pathophysiological mechanisms. Knowingly or not, most psychiatrists have at some point been perplexed by patients with late-stage psychiatric manifestations of Lyme borreliosis. Several factors are associated with the risk of infection as well as the different manifestations of Lyme borreliosis
The following composite case illustrates a number of problems that may make diagnosis and treatment of Lyme borreliosis anything but straightforward. The patient is in good health and enjoys outdoor activities. Often this person has the HLA DR4 genotype. He or she may acquire a small tick bite that goes unnoticed because the subsequent rash may not be of the classic bull's-eye type, may be easily overlooked in dark-skinned individuals, may be misdiagnosed, or may occur only with a second or subsequent infection. There may be flu-like symptoms with migratory musculoskeletal aches and pains. If a diagnosis of Lyme disease is made, the initial course of antibiotic treatment may not have been sufficient to eliminate the infection. (Although standardized by 1 set of guidelines, psychiatrists often see the failures of some of the "standard" treatments.) Low-grade symptoms may remit and periodically relapse over time. An accident, emotional stress, vaccination, or childbirth can trigger an exacerbation of symptoms.
The patient, who did not have psychosomatic symptoms and was not hypochondriacal in the past, now complains of an increasing number of somatic, cognitive, neurological, and psychiatric symptoms. Although Lyme disease may be suspected, the laboratory tests available to most clinicians often lack sensitivity and thus are read as negative for Lyme disease. Fibromyalgia, chronic fatigue syndrome, or multiple sclerosis (MS) may be erroneously diagnosed.
Treatment of some symptoms with corticosteroids may initially provide relief, but a more rapid decline often follows. The patient sees multiple specialists, each of whom restricts the examination to his area of expertise. Nothing is resolved, and the patient is frustrated that his symptoms cannot be explained. In view of the growing list of unexplained symptoms, including psychiatric symptoms, the patient is treated with tranquilizers and antidepressants with some benefit, but gradual decline persists.
The major complaints include fatigue, multiple cognitive impairments, depression, anxiety, irritability, head-aches, and a multitude of other symptoms. When general medical treatment fails, the patient may be referred to a psychiatrist for 3 reasons: the unexplained medical symptoms give the appearance of a psychosomatic or somatoform condition; complex mental symptoms are thought to require psychiatric assessment; and a psychiatrist is thought to be needed to more effectively manage psychiatric treatments.
General theoretical issues
The causes of most psychiatric illnesses are unknown. The catecholamine hypothesis does not adequately explain the cause of abnormal neurotransmitter functioning. Mendel stated that human traits are determined by individual genes that function independently of other genes and environmental influences. Koch believed that many human diseases are caused by microbes that exert their effect independently of other microbes, environmental factors, and genes. The cause of most mental illnesses cannot be explained by neurotransmitters, genes, or infections alone. Instead, as stated by Yolken,
most common human diseases are caused by the interaction of environmental insults and susceptibility genes.Many of the susceptibility genes are diverse determinants of human response to environmental factors, including infections, and prevention or treatment of the infections may result in the effective treatment of complex disorders.
Tick-borne diseases and chronic infectious diseases
B burgdorferi, the principal organism associated with Lyme borreliosis, is one of the most complex bacteria known to man. In addition, a tick bite can presumably transmit more than 1 disease-causing organism. Thus, 2 major clinical hurdles in diagnosis and management are the absence of a clear therapeutic end point in treating Lyme borreliosis and the potential presence of tick-borne coinfections that may complicate the course of the illness. The more common interactive coinfections may be caused by M fermentans, Mycoplasma pneumoniae, B microti, Ba- besia WA-1, Chlamydia pneumoniae, Ehrlichia, Anaplasma, and B henselae, and multiple viruses and fungi. When multiple microbes grow together, they can promote immunosuppressive effects and cause marked symbiotic changes that alter their functioning.
Neuroborreliosis is an infection within the brain; however, infections in the body that do not pass through the blood-brain barrier may also impact the brain indirectly via immune effects. All the clinical manifestations, acute or chronic, of infection with B burgdorferi are characterized by strong inflammation with the production of several proinflammatory and anti-inflammatory cytokineswith an aberrant innate proinflammatory response and inflammatory brain changes. Most of the dysfunction caused by these infections is associated with immune reactions.
All involved with late state Lyme disease agree there is a large amount of inaccurate information on this subject. This disagreement exists at every level – journals, scientific meetings, clinical practice, media outlets,etc. Some of this disagreement can best be viewed as the normal difference of opinion seen when scientists approach a very complex problem from a very different perspective. To fuel the intensity of these disputes, some approach these issues with a significant bias. The full recognition of this illness has implications, which could effect tourism, real estate values, disability, insurance company/managed care liability, workman’s compensation cases, motor vehicle issues, some criminal cases, and political issues. Bias issues can adversely effect patient care, research funding, and medical regulatory issues. Some of those previously impacted by bias now have difficulty approaching this disease with full-unhampered objectivity.
Lyme disease is clearly a very complex disease. When considering a similar spirochete disease, syphilis, it has been said, “To know syphilis is to know medicine.” However, to know Lyme disease is not only to know medicine but also neurology, psychiatry, politics, economics, and law.
Another interesting article by Dr Bransfield here
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