DESCRIPTION

Lyme disease is an infection caused by the corkscrew-shaped bacteria Borrelia burgdorferi that are transmitted by the bite of deer ticks (Ixodes scapularis) and western black-legged ticks (Ixodes pacificus). The deer tick, which normally feeds on the white-footed mouse, the white-tailed deer, other mammals, and birds, is responsible for transmitting Lyme disease bacteria to humans in the northeastern and north-central United States. On the Pacific Coast, the bacteria are transmitted to humans by the western blacklegged tick.

Lyme disease most often presents with a characteristic "bull's-eye" rash, erythema migrans, accompanied by nonspecific symptoms such as fever, malaise, fatigue, headache, muscle aches (myalgia), and joint aches (arthlagia). The incubation period from infection to onset of erythema migrans is typically 7 to 14 days but may be as short as 3 days and as long as 30 days. Some infected individuals have no recognized illness (asymptomatic infection determined by serological testing), or manifest only non-specific symptoms such as fever, headache, fatigue, and myalgia.

It is thought that Lyme disease bacteria are NOT transmitted from person-to-person. However, some medical professionals are quite certain that Lyme disease IS transmitable from person to person, because they believe the infectious agent to be of a viral origin. This is not "proven public knowledge" as of yet, but here is enough information around to suggest that one should be careful.

CAUSE

Lyme disease was first recognized in 1975, when researchers investigated several cases of arthritis among children living in Lyme, Connecticut. The researchers suspected that an unidentified infectious microbe caused the illness, because the sick children lived near each other and became ill at the same time. Many of the children also recalled being bitten by a tick before becoming ill, and some developed a distinctive skin rash just before other symptoms appeared. From these clues, the researchers suspected that deer ticks, common arachnids the size of a pinhead, were involved in transmitting an unknown infectious microbe.

SYMPTOMS

Lyme disease spirochetes disseminate from the site of the tick bite by cutaneous, lymphatic and blood-borne routes. The signs of early disseminated infection usually occur days to weeks after the appearance of a solitary erythema migrans lesion.

For the red "bull's-eye" rash (erythema migrans), the incubation period is usually 7 to 14 days following tick exposure, though some patients present with later manifestations without having had early signs of disease. Within days to weeks following a tick bite, 80% of patients will have a red, slowly expanding bulls-eye” rash (called erythema migrans), accompanied by general tiredness, fever, headache, stiff neck, muscle aches, and joint pain.

In addition to multiple (secondary) erythema migrans lesions, early disseminated infection may be manifest as disease of the nervous system, the musculoskeletal system, or the heart. Early neurologic manifestations include lymphocytic meningitis, cranial neuropathy (especially facial nerve palsy), and radiculoneuritis.

Musculoskeletal manifestations may include migratory joint and muscle pains with or without objective signs of joint swelling.

Cardiac manifestations are rare but may include myocarditis and transient atrioventricular blocks of varying degree.

B. Burgdorferi infection in the untreated or inadequately treated patient may progress to late disseminated disease weeks to months after infection. If left untreated, weeks to months later some patients may develop arthritis, including intermittent episodes of swelling and pain in the large joints; neurologic abnormalities, such as aseptic meningitis, facial palsy, motor and sensory nerve inflammation (radiculoneuritis) and inflammation of the brain (encephalitis); and, rarely, cardiac problems, such as atrioventricular block, acute inflammation of the tissues surrounding the heart (myopericarditis) or enlarged heart (cardiomegaly). Some patients develop chronic axonal polyneuropathy, or encephalopathy, the latter usually manifested by cognitive disorders, sleep disturbance, fatigue, and personality changes. Infrequently, Lyme disease morbidity may be severe, chronic, and disabling. An ill-defined post-Lyme disease syndrome occurs in some persons following treatment for Lyme disease. Lyme disease is rarely, if ever, fatal.

DIAGNOSIS

The diagnosis of Lyme disease is based primarily on clinical findings, which can vary, and it is often appropriate to treat patients with early disease solely on the basis of objective signs and a known exposure. Serologic testing may, however, provide valuable supportive diagnostic information in patients with endemic exposure and objective clinical findings that suggest later stage disseminated Lyme disease.

When serologic testing is indicated, the Center for Disease Control (CDC) recommends testing initially with a sensitive first test, either an enzyme-linked immunosorbent assay (ELISA) or an indirect fluorescent antibody (IFA) test, followed by testing with the more specific Western immunoblot (WB) test to corroborate equivocal or positive results obtained with the first test.

The research of Dr. John Martin at the Centrer For Complex infectious Disease (CCID) suggests that "stealth virus infected patients are being inadvertently diagnosed as having chronic Lyme disease. With only a few exceptions, blood samples from patients being treated for chronic Lyme disease have tested positive in an assay designed to detect stealth-adapted cytopathic viruses. CCID has been successful in demonstrating positive stealth virus cultures in blood samples from over 90% of patients referred with a diagnosis of chronic Lyme disease. By comparison, the incidence of a positive stealth virus culture among healthy blood donors and healthy non-medical personnel is less than 15%. The high prevalence of stealth virus infections in patients with chronic Lyme diseases matches well with similar high prevalence rates in CFS patients and patients with other forms of stealth virus associated illnesses. It is known that a stealth virus has assimilated bacterial sequences, some of which are related to genes of Borrelia burgdorferi, the causative agent of classical acute Lyme disease. The presence of bacteria-derived sequences, rather than actual Borrelia bacteria, may account for the positive serological and molecular based assays that are often, but not always, seen in patients labeled as having chronic Lyme disease. The partial clinical response seen in response to antibiotic therapy may reflect the known capacity of certain antibiotics to suppress the production of virus-growth-enhancing chemokines. If the hypothesis of this paper is correct, then many patients currently being classified as having chronic Lyme disease, may respond to therapies being developed for stealth virus infections."

Dr.Martin writes that "laboratory support for a clinical diagnosis of chronic Lyme disease is currently provided by positive results in various antigen, antibody and/or molecular based assays for Borrelia burgdorferi. Inter-laboratory variability in the performance, reading and interpretation of Lyme disease testing has thrown into question the reliability of such assays, even to the extent that the clinical diagnosis is not infrequently sustained even in the face of negative or inconsistent laboratory findings. Conversely, over time, many patients already diagnosed as having Lyme disease on the basis of positive serological tests are now revealing additional positive assays to such diverse infectious agents as Babesia, Ehrlichiosis, Mycoplasma, Chlamydia, human herpesvirus-6, parvo virus, etc.The clinical manifestations of patients currently labeled as having chronic Lyme disease are essentially indistinguishable from those exhibited by patients categorized as having chronic fatigue syndrome (CFS). In turn, a CFS diagnosis merges with vaguely defined conditions such as fibromyalgia, Gulf War syndrome and depression. Relevant to the present discussion, several CFS patients from non-Lyme disease endemic regions, such as Los Angeles, are showing positive serological test for Borrelia. Centers for treating Lyme disease are springing up with no basis beyond a positive Borrelia antigen and/or antibody test." For more detailed information go to www.ccid.org

TREATMENT

Current treatment is with antibiotics for 3-4 weeks with doxycycline or amoxicillin being generally effective some of the time in early disease. However, even after symtoms subside, there is still a tendency for symtoms to return. Later disease, particularly with objective neurologic manifestations, may require treatment with intravenous ceftriaxone or penicillin for 4 weeks or more, depending on disease severity. In later disease, treatment failures may occur and retreatment is often necessary.

Although antibiotic treatment in early localized disease may blunt or abrogate the antibody response, patients with early disseminated or late-stage disease usually have strong serological reactivity and demonstrate expanded WB immunoglobulin G (IgG) banding patterns to diagnostic B. Burgdorferi antigens. Antibodies often persist for months or years following successfully treated or untreated infection. Thus, seroeactivity alone cannot be used as a marker of active disease. Neither positive serological test results nor a history of previous Lyme disease assures that an individual has protective immunity. Repeated infection with B. burgdorferi has been documented. B. burgdorferi can be cultured from 80% or more of biopsy specimens taken from early erythema migrans lesions. However, the diagnostic usefulness of this procedure is limited because of the need for a special bacteriologic medium (modified Barbour-Stoenner-Kelly medium) and protracted observation of cultures.

The FDA has since approved a vaccine against Lyme disease, LYMErix, produced by SmithKline Beecham.

The Center For Complex Infectious Disease is developing a viral inhibitor that will treat Lyme Disease (and other chronic illnessess) on the basis that those suffering from Lyme Disease improve when treated for stealth viruses. Dr. John Martin explains, "An argument advanced for Borrelia infection is that many patients show a partial clinical response following the administration of certain antibiotics. This conclusion discounts the various cellular activities mediated by antibiotics outside of their direct effect on bacteria. For example, erythromycin and clarithromycin (Biaxin) are known to suppress the cellular synthesis of chemokines. This observation is relevant, since at least some stealth viruses have multiple genes encoding both chemokine and chemokine receptors." If Dr.Martin's hypothesis is correct, then "patients mistakenly being diagnosed as having chronic Lyme disease should benefit from courses of therapy designed to suppress stealth viruses. Ongoing studies are evaluating the use of a combination of anti-oxidant, anti-rheumatic, antibiotics, and other drugs known to down regulate chemokine production." Patients may have their clinicians contact CCID for additional information. These and other investigations will ultimately contribute to a greater understanding of Lyme disease and the development of ways to prevent and treat this emerging infectious disease.

PREVENTION

Having had Lyme disease doesn't protect against reinfection. Some persons have had Lyme disease more than once after re-exposure to infective tick bites. This stresses the need for continued tick bite prevention activities such as wearing appropriate clothing when in tick-infested areas, daily tick checks, and quick removal of attached ticks. It would also be wise to look into some of the newer theories about the transmission of Lyme Disease from person to person to prevent infection and re-ifection.

CONDITION & SUPPORT SITES

Center for Disease Control: http://www.cdc.gov/ncidod/dvbid/Lymeinfo.htm