What is the best way to remove a tick and what if I did not get the entire tick out?

The Centers for Disease Control provides this information about removing a tick: Remove a tick from your skin as soon as you notice it. Use fine-tipped tweezers to firmly grasp the tick very close to your skin. With a steady motion, pull the tick's body away from your skin. Then clean your skin with soap and warm water. Throw the dead tick away with your household trash. Avoid crushing the tick's body. Do not be alarmed if the tick's mouthparts remain in the skin. Once the mouthparts are removed from the rest of the tick, it can no longer transmit the Lyme disease bacteria. If you accidentally crush the tick, clean your skin with soap and warm water or alcohol. Don't use petroleum jelly, a hot match, nail polish, or other products to remove a tick. View a diagram of how to remove a tick.

How long does it typically take between the tick bite and Lyme symptoms to appear? Is it possible to test the tick to see if it is infected?

In most cases, it takes from three to 30 days after being bitten by a tick to develop the initial symptoms of Lyme disease. It is important to remove the tick as soon as possible after attachment, as rapid removal reduces the likelihood of transmission of a tick-borne microbe. Generally if a tick is removed within 24 hours, it is quite unlikely that a Borrelia burgdorferi spirochete will be transmitted. However, some microbes can be transmitted in less than an hour (e.g., Powassan Virus). It is possible that if you are bitten by a tick that had a partial blood meal prior to biting you, transmission of the Lyme disease microbe may occur even if the duration of attachment is less than 24 hours. Because the risk of infection transmission also depends on the infection rate in ticks in the area where the bite occurred, not all tick bites place a person at risk of getting Lyme or other tick-borne diseases. Testing ticks to see if they are infected is not routinely done but if you live in a Lyme endemic area, check with your local or state health departments to see if they conducted PCR testing on submitted ticks. The University of Rhode Island "TickEncounter" website has extensive information about tick identification as well as about labs that test ticks. Just as everyone who is bitten does not come down with Lyme disease, not everyone who has Lyme disease recalls being bitten by a tick. This is because the tick is small and can fall off without the person realizing they have been bitten or because the tick bite occurred in an area of the body that is not readily visible.

Lyme Signs, Symptoms, and Diagnosis

Does Lyme disease cause peripheral neuropathy?

Yes, patients with Lyme disease may develop "peripheral neuropathy" — a dysfunction of the nerves that transmit electrical signals between the body's periphery and the spinal cord and brain. Common symptoms of Lyme-related neuropathy include multi-site "neuropathic pain" (described as a "burning" or "stabbing" sensation), spinal or radicular pain, distal paresthesias (e.g., numbness, tingling), sensory loss, weakness and hyporeflexia. [Logigian et al, "Chronic Neurologic Manifestations of Lyme Disease," NEJM, 1990]. These symptoms are often caused by malfunctioning of small "A-delta fibers" and "C fibers" that carry pain and temperature signals. Pathology of the small nerve fibers can also disrupt autonomic functions such as heart rate, blood pressure, and gastrointestinal functions. Involvement of the cranial nerves can lead to blurry vision, double vision, facial droop, loss of balance, or tinnitus (ringing in the ears).

The precise mechanisms by which these nerve fibers are damaged in Lyme disease remains a subject of active investigation. Some possibilities include: direct assault on the nerve fibers by spirochetes during periods of active infection; immune-mediated damage to the nerve fibers or their protective myelin sheaths by the host's own innate (killer T-cell mediated) or adaptive (memory B- or T-cell mediated) immune system; or production of antibodies with accumulation of immune-complexes that disrupt the small vessels that supply oxygen and nutrients to the metabolically-active peripheral nerves.

The symptoms and immune-mediated mechanisms of peripheral neuropathy are not specific to Lyme disease, and must be understood within the broader clinical picture. Other disorders that might be considered, based on the history and presentation, may include: diabetes, vitamin deficiency, accumulation of endogenous toxins (e.g. uremia due to renal failure) or exogenous toxins (e.g. heavy metals such as lead, mercury or arsenic) or paraneoplastic disorders or Collagen Vascular diseases/autoimmune diseases (Sjogrens, Systemic Lupus), or other infectious or inflammatory processes such as HIV or hepatitis. Additional studies such as body fluid analysis, nerve conduction studies and peripheral nerve biopsy can be utilized to inform the diagnosis and treatment of a peripheral neuropathy. Additionally, neurocognitive testing may be ordered to help clarify the underlying diagnosis.

Can you get a new case of Lyme disease if you have been treated successfully once and how do you tell if the Lyme is a new case or just a second bout of a previous infection?

You can get a new case of Lyme disease if you have had it previously and have been treated with antibiotics and recover. If you are exposed to the bacteria again through another tick bite you can become re-infected and require treatment. If you develop symptoms after initial treatment and recovery, you should see your doctor to determine if it is a new infection or a recurrence of symptoms from an earlier infection. It can be difficult to distinguish whether or not your symptoms are the result of a new infection or a previous infection. If you have not been exposed again to tick bites, then a symptom recurrence may be due to either another unrelated illness, a tick co-infection that was not previously identified, a Borrelia-triggered immune mediated symptom complex that now has its own time course for resolution, or a re-emergence of the initial infection that had been only partially treated. In most cases, a solo EM rash and fever would be a sign of a new acute infection. However, some patients do experience recurrent EM rashes known as satellite rashes that may occur later in the course of disease. Serologic testing carried out by your physician may help in the interpretation of your current symptoms. For example, if the quantity of antibodies in the serum as determined by a specific test such as the C6 ELISA shows a marked increased compared to what had been seen in a prior test after treatment, that would suggest a re-infection as the amount of spirochetal stimulus to the immune system is going to be vastly higher after a tick-bite than what might occur from a reactivated latent infection.

What percent of cases of reasonably proven Lyme disease present without erythema migrans?

According to the Centers for Disease Control (2008), erythema migrans occurs in 60-80% of Confirmed cases. Under careful monitoring of patients who develop new onset symptoms, about 20% have systemic symptoms (fatigue, muscle pain, headaches, joint aches) without a rash or other objective sign of Lyme disease (Steere 2003).

To be considered a confirmed case by CDC for epidemiologic surveillance in the absence of a rash, a person has to have laboratory evidence of infection and at least one late manifestation of Lyme disease. Late manifestations of Lyme disease considered diagnostic are: joint swelling, facial palsy or other specific signs of nervous system involvement, or specific cardiac conduction defects. The CDC also has criteria for a "probable case", defined as physician-diagnosed Lyme disease that has laboratory evidence of infection. Suspected cases without an EM are those with laboratory evidence of infection but no clinical information available.

At what point do I stop antibiotics for the psychological symptoms of Lyme disease and conclude that these symptoms will not go away?

The cause of the psychological symptoms in Lyme disease is unclear. It is clear that patients with acute Lyme disease who develop new onset depressive symptoms or irritability or cognitive disturbances often show a remarkable improvement when given antibiotic therapy. If the psychological symptoms persist or if the initial symptoms are severe, it is very important to consult with a psychiatrist to evaluate how best to treat these symptoms apart from the antibiotic therapy. When symptoms continue even after a repeated course of antibiotic therapy, this could be due to the fact that an activated immune system results in a change in neurotransmitter functioning. As a result, the altered neurotransmitter function may contribute to ongoing depressive symptoms, even after the immune system is no longer activated. Treatment of the psychiatric symptoms at that point would require anti-depressant or anti-anxiety medications or psychotherapy.

I was wondering if Lyme disease affects vision?

Lyme disease can affect eye sight in a number of ways. If the extraocular muscles are involved as in a cranial nerve palsy, then the muscle weakness may result in double vision. Patients may report that their visual acuity appears to be less or that they have lost color vision or can't see the full visual field. (Some patients mistakenly think that "floaters" seen on the surface of the eye are spirochetes — floaters are normal and are common in healthy people as well...and have nothing to do with Lyme disease.) If there is central involvement of the visual pathways, then some patients may experience a marked sensory hyperacusis such as prominent painful light sensitivity (requiring the wearing of sunglasses in normal daylight) or rarely visual trails. In very rare cases, an unattenuated increase of intracranial pressure (esp in children) from neurologic Lyme disease may result in blindness. Of course, any visual problems should be checked by an ophthalmologist or a neuro-ophthalmologist who can then perform a thorough differential diagnosis to rule out other conditions.

Overlap of Lyme Disease with Other Diseases

During the course of treatment for chronic fatigue it was discovered that I have chronic Lyme as well. Has there been a link between the two?

Chronic fatigue is a common problem after any infection. In many cases, the fatigue dissipates after the infection has resolved. In a subgroup of patients, the fatigue may persist for many months and sometimes longer. It is unknown why some patients go on to develop post-infectious fatigue and others do not. There is genetic evidence that some patients may carry genetic markers that may indicate their risk for post-infectious fatigue. At present, it appears that the problem of persistent fatigue is mediated by the autonomic nervous system, the hypothalamic-pituiatry-adrenal axis, and genetic vulnerability. Fatigue is a common problem in many disorders; before one attributes all to a post-infectious or persistent infectious state, one needs to make sure a thorough evaluation has been done to rule out other causes of fatigue, such as thyroid abnormalities, anemia, or cancer. Myalgic Encephalitis/Chronic Fatigue Syndrome has similar features to Lyme Disease, but the primary characteristic is "exercise intolerance"; patients with Lyme disease often can exercise and may experience more fatigue afterwards, but not usually to the same extent and duration as seen in ME/CFS. Studies conducted with our Columbia Lyme patients demonstrate that the spinal fluid profile of patients with post-treatment Lyme disease differs from that of patients with ME/CFS. In regards to Lyme disease, we assume that after treatment some patients have persistent fatigue as a result of the processes above, whereas others may still harbor a small amount of persistent infection that may require re-treatment. These are active areas of current research.

Is it possible for Lyme disease to be misdiagnosed as amyotrophic lateral sclerosis (ALS)? Are there similarities in symptoms between these two diseases?

The question of a relationship between Lyme Disease and ALS first received significant academic attention when Dr. John Halperin who was then a neurologist at Stony Brook conducted a study in which he compared the frequency of blood test positivity to the agent of Lyme disease among patients with ALS to community controls. The results indicated a higher percentage of the ALS patients were seropositive for Lyme Disease. Since then, there have been isolated case reports both in the media and one or two in the academic literature indicating that a patient had been misdiagnosed with an ALS-like illness only later to be re-diagnosed and treated for Lyme disease with good clinical response. Although we suspect that there may be rare individuals who have symptoms similar to ALS but actually have proximal motor neuropathy caused by Lyme disease, the vast majority of patients with ALS are not thought to have Lyme disease as the cause of their serious disease. Clinical trials have been underway using antibiotics for ALS (such as minocycline or ceftriaxone) not because there is belief that ALS is caused by a microbe but because these antimicrobial agents have other properties as well, such as decreasing inflammation or decreasing glutamatergic excitotoxicity. The studies examining intravenous ceftriaxone as a treatment for ALS were not successful.

Are there any diseases that can be misdiagnosed as Lyme disease?

Lots of diseases could be misdiagnosed as Lyme disease. This of course makes sense when you know that Lyme disease itself may manifest as a multisystemic disorder that can mimic other diseases. This means that just as the Lyme disease might be "missed" in some cases, some individuals may be misdiagnosed as having Lyme disease when in fact they have another disease. Erring on either side of this diagnostic divide can be dangerous. Given that the main symptoms that afflict patients with Lyme disease are fatigue and pain and given that these are non-specific symptoms seen in a wide ranges of diseases, including cancer, hematologic, and endocrine disorders, one has to make sure to rule out other reasonable causes of fatigue and pain before making the diagnosis of Lyme disease. It is also important to realize that a patient can have two independent diseases - Lyme disease and another emergent condition. For example, concurrent depression,sleep apnea or hypothyroidism may exacerbate fatigue in a patient with actual Lyme disease.

Can autism be misdiagnosed as Lyme disease? What research is there to prove this? Can a child with autism be successfully treated for Lyme disease?

It would be extremely unusual to misdiagnose a child with autism as having Lyme disease. Lyme disease typically gets diagnosed when a child has joint and muscle pains, along with fatigue, positive blood tests, and central or peripheral nervous system involvement. Certainly a child with autism may also get Lyme disease and thus have two disorders. In that situation, treatment of Lyme disease should result in a resolution of the Lyme disease but it would not likely result in a change in the autism symptoms. The question of interest to us is whether there are cases of "regressive autism" that occur in older pre-school age children (4-5 years olds) for example that has been induced by a central nervous system infection, such as with Borrelia burgdorferi. In such a situation, treatment with antibiotics may well result in an improvement in the developmental regression. This area however has not been adequately studied.

My child had Lyme disease, got treated, and is now depressed. Could this be a sign of a relapse?

Depression is a word that encompasses physical, cognitive, and emotional components. The physical would be poor sleep, fatigue, low energy, lack of sex drive. The cognitive would include poor concentration and trouble making decisions. The emotional would include feeling guilty, hopeless, suicidal, and being unable to enjoy life in any aspect. Chronic symptoms triggered by Lyme disease are most often associated with insomnia or hypersomnia, fatigue, headaches, pain, and, not uncommonly, problems with cognition as well. In other words, chronic Lyme symptoms are most often associated with the physical and cognitive parts of the depressive picture and less often with the emotionally despairing part. When a person presents with the emotional part that is sustained for at least 2 weeks, it may be that a full syndrome depression has emerged related to the Lyme disease or that it is a concurrent but unrelated illness. The emotional aspects of depression might occur secondarily to being sick with a physical illness or directly from an infection affecting the brain or from chemicals affecting the brain that were released by infection outside of the brain. When a person has Lyme encephalitis (ie, infection in the brain causing inflammation), the emotional part of depression can be very dramatic. The person might be suddenly tearful for no apparent reason, have very poor frustration tolerance, become paranoid or angered at the least provocation, and appear to have a personality change.

One should wonder about an underlying medical illness when there are: a) atypical features to the depression; b) an atypical response to good psychiatric treatments; or c) when the physical symptoms are more predominant. It should be noted that the elderly often present with primarily physical complaints — not emotional ones — as their manifestation of primary depression.

Regarding your question about your child, we can not give specific advice regarding a specific person we have not seen. However, in general, if the child does not have other features of Lyme disease present, such as marked fatigue, headaches, joint pain, muscle pain, then it is less likely that the depression is a sign of a relapse. Remember that Lyme disease is most often a multi-systemic illness with multi-systemic problems. It may be helpful to refer to a child psychiatrist. If the child is not improved within several months, then consider a more thorough work-up. The work-up might include repeat blood tests, neuropsychological tests, MRI, SPECT. A spinal tap can be helpful — although not always abnormal in neurologic Lyme disease, when it is abnormal that is a helpful sign of brain involvement currently. When a brain SPECT scan is moderately-severely abnormal in a person under age 25, one needs to pay attention; if the pattern is one of heterogenous hypoperfusion, that would raise concern about a variety of causes, including autoimmune disease, infection, or substance abuse (stimulants/cocaine).

Is there any relationship between sleep apnea and Lyme disease?

We do not know of any evidence that Lyme disease causes sleep apnea, although sleep apnea has been associated with other encephalitic disorders. Sleep apnea may look like Lyme disease. For example, patients with sleep apnea may be difficult to arouse when asleep, will have excessive daytime sleepiness, and may complain of insomnia. They may have morning headaches, inattentiveness, and a decline in school or work performance. Hypertension may also occur. One can have sleep apnea without being obese. The problem can occur in children as well as adults. The diagnosis is made at a sleep lab after special tests of respiratory function and all-night polygraphic sleep monitoring. Patients with central sleep apnea may have lesions in the medulla with ninth and 10th cranial nerve palsies with trouble swallowing or speaking. Patients with obstructive sleep apnea tend to be overweight and to have large tonsils. These patients may snore and then have 10-30 second periods at night when breathing appears to stop. Patients will then take a deep snorting breath and then return to sleep, unaware of what just happened. Treatment is determined by the severity of the symptoms and the type. In central apnea, medroxyprogesterone and protriptyline can be helpful. Weight loss and surgical correction are the treatments for the obstructive type. Patients may experience enormous relief after the surgery. Symptoms previously incorrectly attributed to Lyme disease may now resolve completely.

​How does one distinguish between multiple sclerosis (MS) and neurologic Lyme disease?

Multiple sclerosis and Lyme disease may have similar clinical and neuroimaging manifestations. Further, MS patients can get superimposed Lyme disease — a concomitant infection which might make the MS worse by triggering an exacerbation. Similar to MS, infection with the agent of Lyme disease can cause a progressive encephalomyelitis characterized by para- or tetraspastic pareses with gait difficulties, ataxia, bladder dysfunction, visual disorders, impaired hearing. Other manifestations of encephalomyelitis might include lateral nystagmus, intention tremors, dysarthric speech, seizures, facial palsies, retrobulbar neuritis, mild cognitive disorders (though rare dementia-like manifestations may occur). MS and Lyme disease may cause brain and spinal MRI hyperintense lesions. Lyme disease however more often causes a CSF pleocytosis and elevated protein. In Lyme disease, evoked potential studies are generally but not always normal. MS patients do not have extra-neural features, as one may often find in patients with neurologic Lyme disease (arthralgias, arthritis, myalgias, erythema migrans, carditis). Generally with MS, the laboratory studies reveal "abnormal evoked potentials (50%), CSF oligoclonal bands (90-95%), intrathecal IgG production (70-90%), and CSF myelin basic protein." (Coyle, 1992, Seminars in Neurology). If one finds intrathecal production of antibodies against Borrelia burgdorferi in the CSF, then the diagnosis of Lyme encephalomyelitis is confirmed. If one finds elevated myelin basic protein and oligoclonal bands and no signs of intrathecal Lyme antibody production, then the diagnosis of MS is much more likely. A case of a man with an MS-like illness that ultimately proved to be Lyme disease responsive to antibiotics is described in the following citation: Psychiatric Clinics of North America, v21: 693-703, 1998.

I would like to know if morphea is common with Lyme disease. Is it even connected?

Dr. Andrew Frank of NYU has investigated this question and reports having identified a strain of Borrelia burdorferi by PCR in biopsy specimens. For futher information, you may wish to consult with Dr. Frank.

What is the relationship between Obsessive Compulsive Disorder (OCD) and Lyme disease?

OCD is a neuropsychiatric illness that is quite common, occuring in 1 in 40 individuals. Typically it starts in either childhood or young adulthood. The cause is undoubtedly multifactorial, but there is a strong genetic contribution. The neural circuity underlying OCD connects the orbital frontal brain area with the basal ganglia. If there is injury to this circuitry in a healthy person, OCD may result. This has been reported for example with wasp stings to the caudate. The important point regarding infections and OCD relates to the observation that certain infectious illnesses have resulted in a higher than expected incidence of OCD. This was reported after the Von Economo's viral epidemic in the 1920s and again more recently among children after strep infection. We have seen children and young adults develop new onset OCD after getting neurologic Lyme disease. There was improvement after IV antibiotic treatment in some of these cases, raising the issue of whether Lyme disease causes OCD in some situations. Given that the individuals we've observed this in did not have a family history of OCD or other predisposing features (such as trauma or other OC spectrum disorders), it seems reasonable to suspect that Bb may affect a portion of the brain in some individuals and trigger OCD. This is speculative at this point and requires further study.

Lyme Testing

What is the significance of band 41 on the IgM and IgG Western blot? It is not Lyme specific and the CDC requires more bands to be present before a diagnosis. However, it is a band for bacteria so what else could cause that to be positive if not Lyme?

The 41 kd band is often found on the Western blot. We did a study where we looked at the banding patterns of patients with chronic Lyme disease and healthy controls from the inner city of NY who have never had Lyme disease. We found that a large percentage of the healthy controls tested positive on the 41kd band. For that reason, we don't feel the 41kd band has much clinical signfiicance in guiding us as to whether a person has been exposed to the agent of Lyme disease. One reason a positive 41 kd band might emerge is that our mouths contain non-pathogenic spirochetes; it is conceivable that some may seed the blood stream periodically and lead to the positive 41kd immune responses.

Can you have Lyme disease without any symptoms? I had blood work that showed I have Lyme but I don't have any symptoms.

If a person doesn't have signs or symptoms of Lyme disease, then the person does not have Lyme disease as the definition of disease requires symptoms. A blood test may be positive for several reasons. First, the positive test may indicate that the person was infected previously by the agent of Lyme disease and the immune system mounted a successful attack which resulted in the long-term production of antibodies against the agent of Lyme disease. That's why tests can stay positive for months to years, even when active infection is no longer present. We expect, however, that over time the ELISA titer should decrease in magnitude. Second, a positive test may also indicate that there is a small amount of persistent infection that is continuing to partially stimulate the immune system. The residual organism may not be biologically active; i.e., it might be in a latent or dormant state and thus not causing any disease symptoms. In this case, the ELISA titer may stay elevated for long periods without a gradual decline. Third, a positive test may be a false positive, especially if the positive test is only an ELISA. It is well known for example that concurrent viral infections (such as Epstein-Barr) may result in a false positive Lyme ELISA. If the positive test is an IgG Western blot or a C6 Lyme ELISA, it is very unlikely that either test would be falsely positive. Fourth, a positive test may indicate that you did have some of the signs or symptoms of Lyme disease in the past but didn't recognize the problem as Lyme disease. You may have then been treated with antibiotics for another reason and this may have led to a resolution of the Lyme disease without your awareness of ever having had Lyme disease.

Can you have Lyme disease without any symptoms? I had blood work that showed I have Lyme but I don't have any symptoms.

If a person doesn't have signs or symptoms of Lyme disease, then the person does not have Lyme disease as the definition of disease requires symptoms. A blood test may be positive for several reasons. First, the positive test may indicate that the person was infected previously by the agent of Lyme disease and the immune system mounted a successful attack which resulted in the long-term production of antibodies against the agent of Lyme disease. That's why tests can stay positive for months to years, even when active infection is no longer present. We expect, however, that over time the ELISA titer should decrease in magnitude. Second, a positive test may also indicate that there is a small amount of persistent infection that is continuing to partially stimulate the immune system. The residual organism may not be biologically active; i.e., it might be in a latent or dormant state and thus not causing any disease symptoms. In this case, the ELISA titer may stay elevated for long periods without a gradual decline. Third, a positive test may be a false positive, especially if the positive test is only an ELISA. It is well known for example that concurrent viral infections (such as Epstein-Barr) may result in a false positive Lyme ELISA. If the positive test is an IgG Western blot or a C6 Lyme ELISA, it is very unlikely that either test would be falsely positive. Fourth, a positive test may indicate that you did have some of the signs or symptoms of Lyme disease in the past but didn't recognize the problem as Lyme disease. You may have then been treated with antibiotics for another reason and this may have led to a resolution of the Lyme disease without your awareness of ever having had Lyme disease.

If a second Western blot is still positive for IgG and IgM, months after treatment, does that mean the Lyme disease is still active and further treatment is necessary?

The positive IgM or IgG Western blot indicates that your immune system is generating antibodies against some of the surface proteins that are carried by the organism that causes Lyme disease. Your immune system however may continue to generate these antibodies long after the infection has left your body. It is not clear at this point how long the "immunologic memory" of prior infection stays active. There are very healthy people who live in Lyme endemic areas who have fully positive Western blot test results but who do not have sickness with Lyme disease. There are also very sick people with active Lyme disease whose Western blot test results are not positive. This may sound confusing. The problem is that the Western blot does not tell you about the presence of the spirochete itself — all it tells you is indirect information about the immune system's response to the spirochete (either present or past). Some doctors believe that the IgM Western blot, if positive, is indicative of current infection. Others believe that the IgM later in the course of illness is sometimes falsely positive and is not a good marker of active current infection. The best marker of current active infection is culture — but culture is rarely achievable in later phases of Lyme disease. The second best marker is presence of the DNA of the organism detectable by PCR — but this is also not often found. Unfortunately, we do not have definitive fully reliable and sensitive laboratory markers of when the infection is no longer present and when treatment should be stopped.

Is it possible to have negative Western blot test and have Lyme disease?

Yes, it is possible to have a negative Western blot and have Lyme disease. The Western blot is a test that tells you what antibodies exist in the blood serum against proteins of a certain molecular weight. A Western blot report will usually tell you which bands or antibodies were identified. The Western blot test is a better test than the ELISA because it is more specific. For example, at a good lab, a positive IgG Western blot is 100% specific for exposure to the agent of Lyme disease. A positive ELISA howvever is much less specific, because it does not separate out the Lyme-specific bands from bands that arise from "cross-reactive" antibodies as one might see among patients with other diseases such as lupus or rheumatoid arthritis. The IgM Western blot is well recognized as having insufficient sensitivity in early Lyme disease. The IgG Western blot may not become positive until six or more weeks later. So, the staging of the infection is important. In addition, if a person has received antibiotics, this may suppress or abrograte the immune response so that a person may test negative on the ELISA or Western blot even though a definite Lyme infection occurred. The FDA recommendation is that the diagnosis of Lyme disease be made on clinical grounds rather than relying only on blood testing for the diagnosis.

Lyme Treatment

For chronic cases of Lyme does IV IgG hold hope for remitting symptoms and improving the quality of life?

To our knowledge, IV Ig has never been studied in a controlled fashion as a treatment for chronic Lyme disease, although some physicians are using this treatment for patients who are thought to have autoimmune-mediated neurologic sequelae from Lyme disease that persist after antibiotic treatment. There is insufficient data at this point to say whether IVIg treatment will have acute or sustained benefit for patients with persistent symptoms after being treated with antibiotics for Lyme disease. This is an area of research which is worth pursuing. Certainly, given that there is evidence that IV Ig may be beneficial for a variety of inflammatory and autoimmune diseases such as relapsing and remitting multiple sclerosis (MS), myasthenia gravis, pemphigus, polymyositis (PM), dermatomyositis (DM), Wegener's granulomatosis (WG), and chronic inflammatory demyelinating polyneuropathy, it is reasonable to consider that this treatment may also be beneficial for patients with post-treatment Lyme disease if there is evidence of immunologic dysfunction. This treatment may be especially helpful if there is evidence of autoimmune-mediated neuropathic pain. IV Ig treatment is expensive and not without risks, so such treatment should only be initiated if the potential for benefits significantly outweigh the risks.


What can patients with chronic neuropsychiatric symptoms from Lyme disease do to get proper treatment if we are in a so called non-endemic area?

Chronic neuropsychiatric Lyme disease is a confusing entity to treat. That is why it is best to consult with someone who has had considerable experience evaluating these patients. That specialist may then be able to guide you and your doctor regarding the next phase of treatment. For example, while one patient may need additional antibiotics, another may need symptomatic therapies focused more on the residual symptoms. If one lives in an area in which Lyme disease is not common, it can be helpful to ask your doctor whether he or she would consider it useful for you to consult with a doctor from another state who might be more familiar with the latest treatment strategies. Most doctors would appreciate the recommendation of a colleague with more extensive expertise. It helps both the treating doctor and the patient. Your doctor may also wish to call a specialist in another state who has more experience; often informal professional to professional consultation is quite helpful. We wish to add however that we have seen many patients who have avoided going to regular doctors or regular psychiatrists because of a fear of being misunderstood. This can be risky because it delays help which that particular doctor may be able to provide. One does not necessarily need to be an expert on neuropsychiatric Lyme disease to treat depression or irritability related to Lyme disease.


​What criteria do doctors use to choose different antibiotics?

Partly, doctors rely on what medicines have been shown in published studies to be effective for Lyme disease. For neurologic Lyme disease, the best tested antibiotic is IV ceftriaxone ("Rocephin"). For early Lyme disease, the best tested antibiotics include oral doxycycline, cefuroxime (ceftin) and amoxacillin. Physicians however often use other antibiotics well. For example, because one mouse study and several in vitro studies indicate that the agent of Lyme disease can penetrate and lodge inside cells, some doctors prefer to use medications that have good intracellular penetration (such as clarithromycin (Biaxin)). Other factors that go into the decision include whether the patient is allergic to a particular family of antibiotics or whether the patient can tolerate oral medications; intolerance might suggest the use of intramuscular penicillin whereas if a person is allergic to penicillins or cephalosporins a doctor would want to avoid long-acting intramuscular penicillin-family medicines.


Lyme Transmission and Prevention

How can/will chronic Lyme symptoms impact getting pregnant/being pregnant?

To our knowledge, having had a Lyme disease infection that has been treated does not have a negative impact on the ability to become pregnant.


Can Lyme disease (Western blot positive) be sexually transmitted?

First of all, if you have been treated for Lyme disease, even if your Western blot is positive, it is very unlikely that there are any spirochetes still circulating in your bodily fluids. Second, there is no good documentation that Lyme disease can be contracted by sexual contact. Given the number of cases of Lyme disease that have been diagnosed over the last 20 years and the fact that there are have been instances where people with active infection are having sexual intercourse but have not yet been treated, one would expect there to be many well documented cases of suspect partner to partner transmission; this is not the case. Therefore, for all these reasons, it is highly unlikely that a person could acquire Lyme disease through unprotected intercourse or other sexual contact.


Is there a cure or a drug prescribed for people who have not had Lyme disease but are suffering from the LYMErix vaccination?

The issue of adverse events from the LYMErix vaccine has been under active investigation. If you are suffering from neuropathic pains or arthritic problems after the vaccine, you might consider contacting the Lyme Disease Association for a referral to a physician with a particular clinical and research interest in this question.


How safe is the Lyme vaccine?

The simplest answer to this question is that we do not know for certain. When the LymeRix vaccine produce by Glaxo Smith/Kline was first considered for approval by the FDA, there was considerable concern about the safety of the vaccine among patients who carry the HLA-DR4 genetic marker because past research had indicated that patients who carry this marker are at increased risk of developing a chronic treatment-refractory arthritis after infection with Borrelia burgdorferi. The fear was that the vaccine itself could cause symptoms in a genetically vulnerable population. Since approval in 1998, the FDA has received reports of cases of patients who developed arthritis after the vaccine. According to the FDA, the frequency of this occurrence has not been greater than one would expect for the development of arthritis in the community at large. Nevertheless, because of the increasing concern generated by these cases, the FDA convened a special committee hearing in Jan 2001. The conclusion of this committee reportedly was that the data did not yet indicate that the vaccine caused an increased risk of arthritis, however concern was great enough to warrant recommendation of a change in the package insert and the aggressive pursuit of more safety data from a larger sample of patients. It was not clear at that time what the long-term safety of the vaccine would be, given that patients would need to be re-vaccinated on an ongoing basis in order to keep the protective antibody levels elevated. The Lyme vaccine was withdrawn from the U.S. market in 2002; the exact reason for withdrawal remains unclear.

Should I be concerned about Lyme disease if I am pregnant?

The simplest answer to this question is that a woman who contracts Lyme disease during her pregnancy is at risk of transferring infection to her fetus. These women should receive antibiotic treatment as soon as possible; it might also be wise after childbirth to have the placenta examined histologically and for spirochetes. Antibiotics that may be used include amoxicillin or penicillin. Pregnant women in Lyme endemic areas should be particularly vigilant about avoiding areas with high tick exposure. Less clear is what to recommend to women who contracted Lyme disease prior to pregnancy and who have been treated adequately. Research suggests that these women appear to be at no increased risk of adverse fetal outcomes than women who did not have Lyme disease. That is good news, of course. This question needs to be studied more carefully with larger sample sizes. Research reports indicate the following: a. Transplacental transmission of Bb (the agent of Lyme Disease) has been documented in a woman who did not receive antibiotic therapy. The mother developed Lyme disease during the first trimester of pregnancy and her infant died of congenital heart disease during the first week of life. Histologic examination of autopsy material showed the Lyme disease spirochete in the spleen, kidneys, and bone marrow. b. Dr. Alan MacDonald in 1986 reported on 4 cases of aborted fetuses in which Borrelia spirochetes were cultured from fetal liver. In one case, there was evidence of positive fluorescence after a monoclonal mouse antibody specific for Bb was applied to the tissue. c. In 1986, Drs. Markowitz, Steere, Benach, Slade and Broome reported on 19 cases of Lyme disease during pregnancy in which 13 received antibiotic therapy. Adverse outcomes occurred in 5 of the 19 pregnancies; the varied outcomes could not be definitely linked to Lyme disease. d. In 1989, Dr Olesk and others reported that of 143 pregnant women who had been serum tested for Lyme disease, only one of the 12 patients who miscarried had tested positive -- this was consistent with the conclusion that a positive serum Lyme test does not increase risk of miscarriage. e. In 1993, Drs. Strobino, Williams, and others reported on a study of prenatal exposure to Lyme Disease in which seroconversion was assessed at the time of the first visit to delivery. Of 1,290 women tested twice, only one seroconverted and this woman had a healthy child. This study found that neither the diagnosis of Lyme disease in the past nor living in a highly endemic area were associated with fetal death, low birth weight, or congenital malformations. f. In 1995, Dr. Williams, Strobino and others reported on an umbilical cord serologic study of 5,000 babies: one cohort from an endemic area and one from a non-endemic area. Infants were followed up to 6 months of age. Mothers of infants in the endemic area were 5-20 times more likely to have been exposed to B.Burgdorferi in the past compared to mothers of infants in the non-endemic area. Within the endemic cohort, there were no differences in the rate of major or minor malformations or birth weight by maternal LD history or cord blood serology. g. In 1999, Drs. Strobino, Abid and Gewitz reported on a case-control study in a Lyme endemic area designed to specifically address the risks of congenital heart disease and maternal Lyme disease. Cases were comprised of children with congenital heart defects and controls were selected from among children seen at the same pediatric cardiology service with no abnormalities. There was no association between congenital heart disease and maternal tick bite, or maternal Lyme disease within 3 months of conception or during pregnancy.


How do I know whether I have received a sufficiently long course of antibiotic therapy?

Obviously if a person is no longer having symptoms, that is a good sign that the duration of treatment was adequate. However a large number of patients continue to have symptoms after a course of antibiotic therapy, particularly in the later stages of Lyme disease. Some doctors believe that the symptoms will clear up over time without antibiotics or that the residual symptoms reflect residual damage or an autoimmune response that would no longer respond to antibiotic therapy. Other doctors believe that persistent symptoms require longer courses of antibiotic therapy and that the antibiotics themselves should not be stopped until the signs and symptoms of disease are gone. A middle-of-the-road approach might be to advocate a repeated course of antibiotic therapy if the symptoms haven't cleared up after 3-4 months. Most valuable would be to use objective markers to measure change in response to treatment, such as neuropsychological testing or neuroimaging before and after the repeated course of treatment. The use of these objective tests allows the clinician to determine whether physiological and cognitive changes occurred, and it allows insurance companies who pay for the treatment to see that their investment was worthwhile. Neuropsychological testing before and after re-treatment was reported in a pilot study at Columbia (see Fallon et al, Journal of Spirochetal Diseases, v 6: 94-102, 1999. This article is available on Medscape); the results indicated that patients given a repeated course of IV antibiotic therapy showed considerable cognitive improvement. This however was an uncontrolled study. There have now been 4 controlled studies of chronic Lyme disease. Two studies (Klempner et al) using the same treatment approach (1 month of IV and 2 months of Doxy) showed no benefit with repeated treatment. One study (Krupp et al) using one month of IV ceftriaxone showed improvement in fatigue at 6 months to a greater extent in the drug treated group than in the placebo treated group; this finding was replicated in a later study by Fallon et al. Finally, the fourth study (Fallon et al, 2008) found a temporary benefit in overall cognition after 10 weeks of IV ceftriaxone but this improvement was lost when patients were off antibiotics for another 14 weeks; this study also reported that patients who had more pain or physical dysfunction at the start of the study were more likely to show improvement in these domains if given IV ceftriaxone compared to IV placebo and that this improvement was sustained even after being off of antibiotics for 14 weeks.


Taken together, these study results suggest that repeated antibiotic therapy may be beneficial for a subgroup of patients. However all of these studies also reported troubling adverse effects associated with the IV antibiotic therapy. Given these potentially dangerous risks, it is clear that other safer and more durable treatments are needed for patients with persistent symptoms.

Can Lyme disease be transmitted between humans via bodily fluids such as blood, semen, saliva, etc.?

We know that the spirochetes that cause Lyme disease disseminate through the blood stream after the tick bite and then lodge in various tissues of the body, such as the brain, joints, heart. So can Lyme disease be transmitted via blood transfusions, for example? The answer is most likely "yes" given what we know about dissemination. For this reason, the American Red Cross does not accept blood donations from patients with Lyme disease. Regarding other bodily fluids, I know of no evidence finding borrelia burgdorferi spirochetes in saliva. I also know of no published evidence to indicate that viable Lyme spirochetes can be found in semen. Hence, at this point, it is reasonable to assume that Lyme disease cannot be sexually transmitted.

Lyme Research and Outreach

I am wondering if Columbia University uses xenodiagnosis for detection of infectious diseases?

This is an interesting question. Xenodiagnosis in this case refers to allowing an uninfected tick to feed on an individual with suspected infection to see whether the tick is able to suck up spirochetes when the spirochetes might not have been detectable otherwise. As strange as this concept appears, it has been used successfully recently by Dr. Steven Barthold at UC Davis. After being unable to identify persistent infection in a treated infected mouse using the standard PCR and culture techniques, he was then able to identify the spirochetes in these mice after treatment using the xenodiagnosis method. We at Columbia are not using this method on humans. This is a very intriguing scientific question that should be studied in humans.


​Where can I get geographical statistics on areas with high rates of Lyme disease?

The Centers for Disease Control publishes national statistics and identifies those counties with the highest rates of Lyme disease in the United States. The web sites of many state health departments provide data on Lyme disease by town of residence.


I would like to find a support group (online or other) specifically for people diagnosed with chronic neuropsychiatric Lyme disease. Can you make some recommendations?

Support groups can be found by calling the Lyme clinics or Lyme disease organizations in your state. You might also call a national organization, such as the Lyme Disease Association for the names of support groups in your area.