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Slide Show 

Lyme Disease Prevention 

 


USEFUL LINKS

 LymeMD Brochure

CDC Lyme Disease Information

Point: Antibiotic Therapy Is Not the Answer
for Patients with Persisting Symptoms Attributable
to Lyme Disease - Auwaerter

Counterpoint: Long-Term Antibiotic Therapy
Improves Persistent Symptoms Associated
with Lyme Disease - Stricker

Lyme Disease Controversy - Video by Jerry Paxman

 

 

EDUCATION

 [ Early Lyme Disease | Disseminated Infection | Late Manifestations | LymeMD Publications  

 

Lyme disease can be confusing and difficult to understand. The infection is more complicated than most bacterial infections because it has both an early and a late phase of disease. The early phase of the illness may remain localized to the immediate area surrounding the infecting tick bite or may result in signs of “disseminated” or blood-borne infection. Disseminated infection results when the bacteria enter the blood stream and infect other organs systems such as the joints, heart, and the nervous system. Late manifestations of infection may occur months to years after untreated early Lyme disease. Late Lyme disease results from bacteria that spread during the initial dissemination phase, only to result in symptoms months or even years later.

Perhaps the most difficult aspect of Lyme disease for both patients and physicians is recognizing and understanding the symptoms of Lyme disease that persist after standard courses of antibiotic therapy. This post treatment Lyme syndrome is a controversial topic where diverse opinions are the rule. Patients are often overwhelmed by the different sources of information that are found on the internet regarding Lyme disease because of this complexity. Post treatment Lyme Syndrome is often called chronic Lyme disease by the public. The name post Lyme disease syndrome is used in the recent Infectious Disease Society Guidelines [1] Much of the confusion may be clarified by understanding that many of the patients suffering from persistent symptoms of Lyme disease probably have post-treatment Lyme syndrome. Until we understand the origin and effective treatment of post treatment Lyme syndrome, the controversy and confusion will likely continue.

One paradigm of thinking about patients with Lyme disease separates the manifestation of untreated Lyme disease from symptoms that persist after treatment (whether intentional treatment for Lyme disease, or unintentional antibiotic treatment administered for an incorrect diagnosis). This way of thinking about pre and post treatment Lyme disease may help you to understand the various manifestations of Lyme disease including the newly defined syndrome of post treatment Lyme Syndrome. The following educational material and links will attempt to captures the complexity of Lyme disease and identifies those areas that a well understood while identifying those areas of uncertainty and confusion.

PART 1: Early Lyme Disease

In order to understand Lyme disease, it is very important to understand that the disease is a complicated illness that is manifested differently at different stages of the illness. This may be a new concept to many people who are used to the idea of simple infections like urinary tract infections or bronchitis that have a single phase and are treated and then go away. Unfortunately, Lyme disease is not like that. Lyme disease has three phases of illness that occur in a predictable order when a patient is not treated. The first early phase of Lyme disease is when the infection is localized to a single skin lesion. The second phase of Lyme disease occurs after the bacteria from the initial skin lesion spread in the blood stream throughout the system and are manifested in distant sites. Common sites of involvement include the joints, other areas of the skin, the nervous system and rarely the heart. The third phase is the late phase of Lyme disease that can occur months or even years after the initial infection. Late Lyme disease is manifested when the infection recurs at distant sites such as the joints or nervous system.

These three phases of Lyme disease follow in a natural progression which I will call the natural history of untreated Lyme disease. In order to understand the controversy of Lyme disease, however, it is also important to understand what happens to patients with Lyme disease after they are treated. Unlike many simple infections, many patients with Lyme disease have symptoms that persist even after what should be effective therapy. This concept may be familiar to people who know about the idea of fatigue that persists for many weeks or months after infectious mononucleosis. The same type of situation occurs after treatment of Lyme disease, although in this case symptoms can last for much longer periods of months or even years.

Only by understanding the progression and outcome of both untreated and treated Lyme disease will we be able to understand the controversies currently surrounding Lyme disease. As I will discuss later, this controversy really centers on understanding and explaining why patients who have been treated for Lyme disease often manifest persistent and often disabling symptoms.

Figure 1: The natural progression of untreated Lyme disease 

As this figure shows, Lyme disease has 3 distinct phases including an early skin lesion called erythema migrans, a second phase in the following 1-3 months which includes early involvement of the neurologic and other distant symptoms, and finally a third phase that is manifested months to years later involving the musculoskeletal and neurologic systems. There is a characteristic response of the human immune system manifested as antibody production that has a consistent relationship to this progression of Lyme disease. The figure shows that there are 2 types of antibodies, IgM and IgG antibodies, which form in a predictable time sequence in response to infection in Lyme disease.

The bacterial agent of Lyme disease is an unusual type of bacteria called a spirochete. The name of this spirochete bacterium is Borrelia burgdorferi, and as is shown in this figure the spirochete is found in the blood steam transiently in many patients early on in their infection. This accounts for the phenomenon of distant disease that spreads through the blood stream and appears at later periods of time in untreated patients.

Figure 1 shows the first phase of Lyme disease which is best known by the lesion or skin rash called erythema migrans (which may or may not be a classic bull’s eye rash, see below). The incubation period for early Lyme disease is anywhere between 3 and 30 days after the bite of the infected tick. There are three possible ways that infection with Lyme disease can manifest itself in this early phase. The first is asymptomatic infection where there actually is no evidence of infection in the person who was bitten. You may ask how we know the patient was infected if there are no symptoms, and the answer to that is that they develop antibodies that are characteristic and specific to exposure and infection with the bacteria. That is called asymptomatic seroconversion, and it occurs in about 11% of patients.

The second and most common way that a patient manifests infection is with the characteristic skin lesion called erythema migrans. Typically, this is seen about 7-10 days after the tick bite at a time in which the tick is no longer present. In addition, the majority of patients do not even recall a tick bite because of their small size and painless bite. Patients with the skin lesion may or may not be sick. Some of the patients have a flu-like illness and some do not. This flu-like illness can be present as the only manifestation of Lyme disease in approximately 16% of patients. The flu-like symptoms would include fever, achiness of the joints and muscles, headache, and tiredness. Patients may be mildly ill or may be sick enough that they are in bed and miss several days or even a week or two of work.   The classic skin lesion of Lyme disease is shown in figure 2.

Figure 2: “Classic” Lyme EM rashes: bulls eye and uniform lesion

People are usually aware that the classic skin lesion can have a “bull’s eye” appearance. What they are unaware of is that as many as 80% of skin lesions of Lyme disease are not bull’s eye in appearance but are uniformly red throughout. [2]   What is always characteristic, however, is that skin lesions of Lyme disease are round or oval and sharply demarcated. They are often warm, but they rarely are severely painful or itchy. The skin lesions last for weeks and expand at the rate of 1 or 2 cm a day reaching an average size of 15 cm, although they can be considerably larger. The skin lesion of Lyme disease may be missed or not diagnosed correctly. A patient may not see a skin lesion that is in an unapparent location because, again, they are often not painful. Sometimes, patients see skin lesions and misconstrue their cause and attribute them to spider bites or other types of injuries. [3]

Occasionally, the skin lesions of Lyme disease have different appearances that can be confusing to both patients and physicians. One or two percent of skin lesions have fluid-filled blisters or pustules at the center of the skin lesion.[4] Occasionally, the skin lesion has more of a bluish appearance and is misconstrued as a bruise. Examples of variations in the appearance of the skin lesion are shown in figure 3.

Figure 3: Lyme EM Rashes can be mistaken for spider bites or other skin infections

It is important to understand that only a minority of tick bites actually transmit Lyme disease. On average, approximately 2% of tick bites result in Lyme disease. Tick bites that do not cause Lyme disease still may leave a small dime-sized or less lesion where the tick was attached to the skin. These small tick bite skin lesions can last for weeks but do not expand and enlarge the way the Lyme disease skin lesion does.

Figure 4: Tick bite reaction without rash of Lyme disease

The diagnosis of early Lyme disease is what is called in the medical field a “clinical diagnosis.” This means that the diagnosis of early Lyme disease is based on the physician’s recognition of the characteristic erythema migrans skin lesion. Blood tests should not be counted on for diagnosis of early Lyme disease and, in fact, can be quite misleading. Blood tests are misleading in early Lyme disease because there are a high percentage of falsely negative Lyme blood tests in the first 2-4 weeks of infection. [5] If the characteristic skin lesion of Lyme disease is not present in the early illness the diagnosis is much more difficult to make. The most appropriate course of action may be to draw blood tests, realizing that they may be negative, and observe the patient without beginning antibiotic treatment. The test can then be repeated in 2-4 weeks’ time. After this 2-4 week time period, the human immune system should have had time to make the characteristic antibodies and the follow-up blood test should be positive. There may be cases where the clinical situation calls for antibiotic treatment in the absence of a skin lesion, however in this situation, the treatment must be an individual decision made by the physician and patient without the benefit of a definitive diagnosis.

The treatment of early Lyme disease with a skin lesion and no other manifestations of spread of infection is with oral antibiotics. [6] In adults, oral doxycycline is the treatment of choice. In children under the age of 12, amoxicillin is the preferred antibiotic because of the side effects of doxycycline. An important point to make, however, is that many commonly used antibiotics for other infections such as quinolone antibiotics (the most well known being ciprofloxacin), as well as other commonly used antibiotics such as a Z-Pak or antibiotics called first generation cephalosporins do not effectively treat Lyme disease. [7,8] As we all know, these other antibiotics are used for other types of infections such as sinusitis and urinary tract infections commonly treated in primary care medicine. Because these antibiotics are not effective against Lyme disease, it is very important that physicians be certain of the diagnosis and that they are aware that they should not prescribe antibiotics without activity against Lyme disease in situations where the diagnosis of Lyme disease is a possibility.

PART 2: Disseminated infection and late manifestations of Lyme disease

The second phase of untreated Lyme disease occurs between 1-3 months after the tick bite and is called early disseminated infection. In some of these instances the rash of early Lyme disease will still be present; however, in a significant number of patients, the early rash cannot be identified (see figure 1). This second phase of disseminated or distant Lyme disease occurs because the blood stream is invaded by the bacteria of Lyme disease. In studies done at Johns Hopkins Hospital, we showed that many patients with the early rash of Lyme disease already had bacteria spread through the blood stream despite the absence of any symptoms or manifestations. [9] This is consistent with the fact that untreated patients often go on to develop distant manifestations of the disease. These typically involve other areas of the skin, the nervous system, the heart, or the joints.

When the bacteria of Lyme disease spread through the blood stream to other areas of skin, they can cause multiple skin rashes called disseminated cutaneous Lyme disease (figure 5). Although disseminated cutaneous Lyme disease may resemble multiple tick bites, it is actually due to spread of the infection from a single tick bite through the blood stream. Because of this, the distant rashes do not have the classic characteristic appearance of erythema migrans and are often much more variable in their shape, size, and other characteristics.

Figure 5: Disseminated cutaneous lesions of Lyme disease

The next manifestation of disseminated Lyme disease is involvement of the nervous system, often in the nerves outside of the brain. The most common manifestation is 7th nerve palsy, often called Bell’s palsy, in which the nerve is transiently damaged, producing a droopy face that resembles a stroke (figure 6). Other nerves throughout the body can also less commonly be infected, which can cause pain that mimics other conditions such as sciatica. Lyme disease can also manifest as a viral-like meningitis syndrome.  Very rare manifestations of disseminated Lyme disease include cardiac involvement that may cause damage to the electrical system of the heart and may require temporary hospitalization and pacemaker placement.

Figure 6: VII Nerve Palsy in Lyme Disease

The diagnosis, treatment, and prognosis of early disseminated infection with Lyme disease are well known. The diagnosis is based on finding the characteristic illness in conjunction with either the rash of early Lyme disease or a positive serologic blood test for Lyme disease. Serologic blood tests are based on the finding of the human antibodies that are made in response to the infection. By the time of early disseminated infection, these antibodies are almost always present in the blood stream and can be identified with simple blood tests. Occasionally, patients with early disseminated Lyme disease need a test called a spinal tap to exclude infection of the nervous system. This is an important finding because involvement of the nervous system is one of the indications for treatment with intravenous therapy.

Fortunately,the prognosis for the early disseminated manifestations of Lyme disease is good. Patients with 7th nerve palsy almost always recover function of their nerve, and their facial muscles return to normal. Permanent cardiac damage is extraordinarily rare, and the overall outcome from this group of patients is very good when they are appropriately diagnosed and treated.

The third manifestation of untreated Lyme disease is late Lyme disease, which manifests months to years after the initial tick bite and untreated early infection.  As a result, the rash is never present at the time that late Lyme disease is diagnosed. Diagnosed patients have had infection for many months and thus should universally have a positive IgG western blot for these Lyme antibodies.  The most common manifestation of late Lyme disease is swollen joints, especially the knee joint (figure 7). This was the initial manifestation that led to the discovery of Lyme disease in Connecticut, when an observant mother noticed that many children were developing swollen knees months after they had had a rash. This connection between a previous rash and a swollen knee was one of the first clues to the discovery of Lyme disease in the United States. Patients with swollen knees often go first to orthopedic surgeons because of the pain and swelling. Swollen joints eventually occur in up to 60% of individuals who were untreated at the time of their initial Lyme infection.

Figure 7: Swollen knee joint in Lyme Disease

 

You may ask how the patients were not initially diagnosed and treated, allowing the infection to go on to develop late complications. This may occur because initial illness was simply misdiagnosed or because patients often have no recollection of their primary infection. In some cases, patients never notice or even develop a rash, and the early symptoms alone are not always recognized as being compatible with Lyme disease. It should be recalled that without treatment those initial manifestations resolve on their own and may not recur until the patient notes the swollen knee months or even years later. Occasionally, other joints besides the knee, such as smaller joints of the hands or feet, can be involved with late Lyme arthritis.

The neurologic system may again be involved in the late phases of Lyme disease. Rarely, the central nervous system is infected with syndromes that mimic strokes or multiple sclerosis. More commonly, the peripheral nervous system is involved with damage to the nerves resulting in pain, numbness, and abnormal sensations in the skin.

The diagnosis of late manifestations of Lyme disease is based on the objective findings of the damage done by the disease process. By objective findings, we mean abnormalities that can be seen by an experienced physician on the physical examination of the patient. In the instance of arthritis, this would mean that the joints are visibly swollen and inflamed. In the manifestations of neurologic involvement, this would mean that there are visible findings of nerve damage that can be objectively quantified by a physician. All patients with late Lyme disease who have not previously been treated should have positive blood tests for the antibodies to Lyme disease. In the case of joint involvement, fluid may be obtained from the joint by an orthopedic surgeon. If this is done, there are characteristic findings of the cells that are removed, allowing the opportunity to verify the diagnosis with what is called a PCR test on the joint fluid.

In the case of neurologic involvement, the diagnosis is confirmed with imaging tests such as MRIs that would show damage to the nervous system. Spinal tap or lumbar puncture is also an important test in neurologic disease to confirm that there is, in fact, evidence of inflammation in the cerebrospinal fluid which would be expected with active infection. An additional test that is used in patients with nerve damage in the extremities is called a nerve conduction study where a series of needle tests is used to demonstrate that there is damage to the functioning of the nerves in the extremities or face.

The prognosis of patients with late Lyme disease after appropriate treatment is a mixed picture. This is a theme in Lyme disease that is important to understand. It was known very early on that some patients with late Lyme arthritis did not always recover completely after appropriate treatment. Even patients who received intravenous therapy occasionally had persistent evidence of joint inflammation. Dr. Alan Steere at Yale University has spent his career studying patients with persistent joint disease after treatment for Lyme disease. Approximately 10% of patients who are treated have persistent symptoms, and these patients are called antibiotic refractory late Lyme arthritis patients. Of note, persistent infection cannot be demonstrated in patients after treatment. When fluid from their joints is examined, bacteria are not able to be recovered, raising questions about why patients continue to have ongoing symptoms.

Some patients with late neurologic disease may not recover completely after treatment. This may be due to the fact that the neurologic system does not heal easily after it has been damaged for a long period of time.  We are all well aware that other neurologic diseases such as stroke may result in permanent damage that is not able to be repaired by the body. This is the case in Lyme disease as well and accounts for the fact that recovery from neurologic symptoms may be partial or very slow and may not occur for a period of months or even years after treatment.

Patients with late Lyme disease who are treated may also have persistent subjective symptoms after treatment. The term “subjective symptoms” refers to symptoms that are readily apparent to the patient but do not result in quantifiable or visible damage to the patients body that can be seen and objectively described by the physician. An example of this would be a painful joint that is disabling to the patient but does not exhibit any signs of inflammation or infection to the examining physician. Other subjective symptoms would be symptoms such as fatigue or memory problems that again cannot be quantified in a typical clinical examination but can be completely disabling to the patient. What is apparent in Lyme disease is that subjective symptoms after treatment are common. In late Lyme disease after treatment, anywhere from 13% to 30% of patients have persistent post treatment symptoms such as joint achiness, weariness, and memory problems.

Reference:

  1. Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS, Krause PJ, Bakken JS, Strle F, Stanek G, Bockenstedt L, Fish D, Dumler S & Nadelman RB. The clinical assessment, treatment and prevention of Lyme disease, Human Granulocytic Analplasmosis and Babesiosis: Clinical Practice Guidelines by the Infections Diseases Society of America. Clin Infec Dis 2006;43: 1089-1134Early Lyme Wormser
  2. Tibbles CD & Edlow JA. Does this patient have erythema migrans? JAMA 2007;23:2617-2627.
  3. Osterhoudt KC, Zaoutis T, Zorc JJ. Lyme Disease Masquerading as Brown Recluse Spider Bite. Annals of Emerg Med 2002;39(5):558-61.spider bite reference
  4. Goldberg NS, Forseter G, Nadelman RB, et al. Vesicular erythema migrans. Arch Dermatol 1992 Nov;128(11):1495-8.
  5. Wormser GP. Early Lyme disease. N Engl J Med 2006; 354:2794-2801
  6. Treatment of Lyme Disease. The Medical letter on Drugs and Theraputics. 2007; v49 (issue 1263) 49-51
  7. Failure of treatment with cephalexin for Lyme disease. Arch Fam Med 2000; 9:563–7
  8. Luft BJ, Dattwyler RJ, Johnson RC, et al. Azithromycin compared with amoxicillin in the treatment of erythema migrans: a double blind, randomized, controlled trial. Ann Intern Med 1996; 124:785–91.
  9. Coulter P, Lema C, Flayhart D, Linhardt AS, Aucott JN, Auwaeter PG & Dumler JS.  Two-year evaluation of Borrelia burgdorferi culture and supplemental tests for definitive diagnosis of Lyme disease:  J of Clin Micro 2005;43(10: 5080-5084.

PART 3: Late manifestations -- Coming Soon

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