Learn More About Lyme Disease

Borrelia burgdorferi (Bb) infection is commonly known as Lyme disease (Lyme borreliosis). It is a non-suppurative infection transmitted by the bite of an infected Ixodes scapularis tick, which feed on a wide variety of large and medium sized mammals including the white-tailed deer, cattle, dogs, and field mice. Lyme disease, the most prevalent vector-borne disease in the United States, is found predominantly in the northeastern states, the upper Midwest, and to a lesser degree in the upper northwest, and its incidence is increasing. The earliest cases were reported, in retrospect, in the 1970's, it was first recognized as a distinct disease entity in 1975, and the CDC initiated surveillance for this in 1982. Also in 1982, the spirochetal micro-organism 
causing Lyme disease was identified and named Borrelia burgdorferi, after its discoverer Dr. Willy Burgdorfer.

The early 1980's also saw the emergence of published information on treatment regimens for Lyme disease. Some of the early studies used oral penicillin, tetracycline, and erythromycin, followed by studies of intravenous penicillin. More recently, oral regimens using doxycycline or amoxicillin have been most often reported to be effective in various early and later manifestations of Lyme disease. Many physicians use intravenous ceftriaxone for late disease, especially neuroborreliosis. Ceftin has also been successfully used. 

An American College of Physicians publication (authored by Drs. DW Rahn and J Evans) in 1998 provides and excellent overview of clinical aspects of Lyme disease, and is highly recommended.

Clinical expression of Lyme disease relates to the stage of infection, and to the genospecies causing infection. Bb senso stricto is the most common species found in North American ticks, 
although genetic diversity is increasingly being recognized. Other species are often found in Europe. 

There are many controversial aspects of the clinical features of just what constitutes Lyme disease. This has led to considerable confusion among patients and healthcare providers. For the reader interested in pursuing this further, the following references are recommended:

Sigal LH. Pitfalls in the Diagnosis and Management of Lyme Disease. Arthrit Rheumat
1998;41:195-204

Reid MC, Schoen RT, Evans J, Rosenberg JC, Horwitz RI. The Consequences of the Overdiagnosis and Overtreatment of Lyme Disease. Ann Int Med 1998;128:354-362

Lyme Disease in Massachusetts, 1999 - an update for healthcare providers. April, 1999
By the Massachusetts Department of Public Health, Division of Epidemiology and Immunization. 

In general, Lyme disease is divided into the following stages:

Clinical Manifestations of Lyme disease*

EARLY, LOCALIZED

Erythema Migrans
Fatigue
Malaise
Lethargy
Headache
Regional of localized adenopathy
Myalgia
Arthralgia

EARLY, DISSEMINATED

- NEUROLOGIC -
Cranial Neuropathy (most commonly facial)
Lymphocytic meningitis
Peripheral neuropathy
Radiculitis
Encephalomyelitis
Myelitis

- CARDIAC -
Conduction defects
Mild cardiomyopathy

- OTHER -
Lymphodenosis benigna cutis (lymphocytoma)
Regional and/or generalized lymphodenopathy
Liver function test abnormalities
Hepatitis
Microhematuria
Proteinuria

LATE

- MUSCULOSKELETAL -
Polyarthritis
Chronic monoarthritis

- NEUROLOGIC -
Chronic; often subtle, encephalopathy
Chronic, often subtle, peripheral neuropathy

- CUTANEOUS -
Acrodermatitis chronica atrophicans
Mophea/localized scleroderma-like lesions

*Adapted and used with permission. Sigal, LH. The Specialist in Internal Medicine, 1992;13(6):24-34.


Lately, the emergence of other tick-borne infections is increasingly being recognized. Specifically, babesiosis and HGE have been shown to be transmitted by the same ixodes tick, and indeed co-infections with these agents have been reported in Lyme disease patients. In certain clinical situations, for example when Lyme disease patients are severely ill or have cytopenias or elevated liver function tests, the possibility of co-infection is often raised and appropriate testing is often indicated for these other tick-borne diseases. For more information on co-infections with multiple tick-borne pathogens, refer to our section on coinfections.

In addition to the coinfection issues, the story of Lyme disease continues to unfold. For example,
What is chronic Lyme disease? If it does exist, is it reflective of on-going active Bb infection, and will it respond to further or more prolonged courses of antibiotic therapy? Or is this predominantly a "post-Lyme syndrome" in a patient with no active infection? An important NIH study is in progress to address this.

Finally, the exact role of the Lyme disease vaccine is still unclear. Just how effective is it? Who should receive it? Are newer generations of this vaccine, expanding immunogens beyond a single OspA protein, likely to be necessary? How long is immunity and when are booster doses needed? What are the best laboratory tests to evaluate a vaccinated patient for possible Lyme disease? Are there any unforeseen or unexpected long term adverse consequences of vaccination in various patient groups? Continued surveillance and follow-up are needed to address these questions.


 


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