*Updated March 2015
Dr Horowitz has released his new book in 2014 entitled Why Can’t I Get Better? A free chapter is available online including a symptom checklist that may be useful to some patients: http://us.macmillan.com/excerpt?isbn=9781250019400
Lyme Symptoms: This site contains an excellent breakdown of some of the common symptoms & complications such as eyes, bladder, heart, nervous system etc etc.
ILADS have released their latest set of guidelines in 2014 – this aims to place decision making between doctor & patient based on choice & risk analysis rather than the restrictive guide of the IDSA: https://ticktalkireland.files.wordpress.com/2014/08/ilads-2014.pdf
Also of interest may be the German Borreliose Society Guide (German equiv of ILADS): http://www.borreliose-gesellschaft.de/Texte/guidelines.pdf
For a comprehensive look at many ‘Non Antibiotic approaches to Lyme Disease‘ check out this excellent set of slides by Dr Steven Harris: http://www.acimconnect.com/Portals/0/Events/Dallas%202013/Presentations/Harris-%20DFW%20June%202013.pdf (PDF)
Lyme Treatment & Symptoms Guide – Burrascano
Dr Burrascano a leading pioneer in Lyme disease, treatments & diagnosis regularly publishes a useful guide. Take this to your doctor if you feel you may be affected. Don’t forget that Lyme testing in Ireland can be insensitive if you are not producing enough antibodies – (check out the blood tests section for more info!)
Also check out our newcomers guide, lots of useful tips in there 😉
CanLyme (Canadian Lyme Disease Foundation) have a good symptom check list (click on symptoms link on the site). They show 75 known symptoms of ‘chronic’ Lyme disease as well as the earlier signs! It also has various pictures of the erythema migrans rash. As you can see the rash is not always showing (between 30-50% people notice a rash) & also the rash may vary in shape, intensity & size depending on the body’s reactionto the bite & also depending on the type of co-infections that may have been transmitted! Well worth checking out by clicking on rash in the symptoms section.
Remember (fewer than 50% recall a tick bite or get/see the rash) – canlyme
“Clinical Pearls” in Lyme Borreliosis Complex
‘The sore throat that is not a sore throat’ – What is Carotidynia?
Frequently our patients describe sore throats as part of their recurring symptom complex. Often, when specifically asked, the patients note that ear pain accompanies the throat pain, but the patients often state that their primary physician can find no reason for their discomfort. In fact, on examination, there is no sign of inflammation of the throat or ear.
The condition ‘carotidynia’ is little known but is, in fact, common. On careful examination, one can easily detect swelling and pain at the carotid bulb, which is located just lateral to the top of the thyroid cartilage (Adam’s Apple) and is the location at which the internal and external carotid arteries separate, or bifurcate.
Our theory is that this is yet another sign of inflammatory neurological disease associated with LBC, since the carotid bulb is known to be a baroreceptor, which means it plays a prominent role in monitoring blood pressure. As such, it is loaded with nerve fibers, some of which mediate pain. Since the fibers at the bulb lie in proximity to the throat and may radiate to the ear area, our patients complain of ‘sore throat and earache’, when in fact the throat and ear pain arise from an inflamed carotid bulb. The mediation of this pain is most likely from the Nerve of Hering, a branch of the 9th cranial nerve (glossopharyngeal nerve), and/or a branch of the superior cervical sympathetic chain.
Health Protection Surveillance Centre
25-27 Middle Gardiner St
Dublin 1, Ireland.
Excerpts are below – full report or printable leaflet available in above link:
How do you come in contact with Lyme disease?
Lyme disease has been reported from North America, Europe, Australia, China and Japan. Infected ticks are most likely to be encountered in heathland and lightly forested areas of North America and Northern Europe. Ramblers, campers and those who work in such areas especially if they come into contact with large animals are at greatest risk of being bitten by ticks and of going on to develop disease. Cases of Lyme disease appear in Ireland every year.
What symptoms can it cause?
Many infected people have no symptoms at all. The commonest noticeable evidence of infection is a rash called erythema migrans that is seen in about three-quarters of infected people. *Tick talk note – remember that many Lyme sites indicate that 50% or less of sufferers experience a rash. The rash can be painless or painful but usually not itchy. It can be widespread or contained in small brown pigmentations. It can be in a bull’s eye ring or spread across the body. Check out Bing.com for rash pictures * This red, raised skin rash develops between 3 days and a month after a tick bite and spreads outwards from the initial bite site. This rash can last up to a month and be several inches in diameter. People can also complain of ‘flu-like symptoms such as headache, sore throat, neck stiffness, fever, muscle aches and general fatigue. Occasionally, there may be more serious symptoms involving the nervous system, joints, the heart or other tissues.
What complications can result from Lyme disease?
Complications following Lyme disease are not terribly common, and tend to occur less frequently in Europe than in North America. Complications tend to occur quite some time after initial infection and are common in people who did not realise they had been infected or who were not initially treated. Complications can affect different parts of the body including:
* Joints: swelling and pain in large joints (arthritis) which can recur over many years
* Heart: inflammation of heart muscle (myocarditis) with irregularities of heart rhythm
* Eye: conjunctivitis and eye pain.
* Nervous System: numbness and weakness, meningitis/encephalitis and Bell’s palsy (facial paralysis).
How is Lyme disease diagnosed?
Lyme disease is diagnosed by medical history and physical examination. Diagnosis can be difficult if there has been no erythema migrans rash. The infection is confirmed by special blood tests. The tests used, look for antibodies to B. burgdorferi, which are produced by an infected person’s body in response to the infection. Antibodies will take several weeks to develop and may not be present in the early stages of the rash. They will usually be present in the later stages of the infection. More sophisticated tests can be used if the diagnosis is not clear.
How common is Lyme disease?
Lyme disease is not a notifiable infectious disease in Ireland. This means that there is no legal requirement on doctors to report cases to their local Director of Public Health. A number of cases are diagnosed each year, but the true figure is unknown. In the UK, about 300 laboratory-confirmed cases are reported to the Health Protection Agency annually; however, estimates suggest that the true figure could be between 1000 and 2000 cases annually. In the US, there are about 15,000-20,000 cases each year.
Who is at risk for Lyme disease?
Lyme disease can affect anyone but is commonest among ramblers, hill-walkers, hikers, campers and others whose leisure activities or work takes place in heathland or light woodland areas or brings them in contact with certain animals e.g. deer. Summer and autumn is the period when most cases occur.
Is there a treatment for Lyme disease?
Yes, common antibiotics such as doxycycline or amoxicillin are effective at clearing the rash and helping to prevent the development of complications. They are generally given for up to three weeks. If complications develop, intravenous antibiotics may need to be used. *Tick Talk’s note – stage 3 Lyme is where the early signs have not been caught or treated. In these cases antibiotics are needed for several months or even years. This is why it is VERY important to be treated as soon as possible*
This is a useful guide as explains very clearly the symptoms of Lyme from early to late stages, explains the various tests and traditional treatment as well as natural therapies and explains the problems of chronic Lyme for undiagnosed cases. The ILADS guidelines are mentioned too.
“Unfortunately, many Lyme patients go undiagnosed due to the similarity of the symptoms to other illnesses. The American Lyme Disease Alliance (ALDA) conducted a study in which 31 patients with Chronic Fatigue Syndrome. Lyme was the cause of the illness of 90.3% or 28 of 31 of these patients. ”
A very good guide by ILADS about ‘Chronic Lyme Disease’
Neurotoxins – Dr Shoemaker Protocol
This is a brilliant concept developed by Dr. Ritchie Shoemaker. He theorizes that many different infections can produce toxins. These are toxic chemicals that can persist in the body even after the infection is gone. Normally, the body is able to excrete toxins through the liver and kidneys and eliminate them from the body. What makes these toxins unique is that only the liver excretes them. The liver excretes the toxins into your bowel (via the bile) so that they can be eliminated from the body with your stool. Unfortunately, these toxins are able to be reabsorbed from the bowel and therefore cannot be eliminated (they continue to re-circulate to the liver and then back to the blood).
Dr. Shoemaker believes that one common situation where this occurs is in Lyme’s disease. The Lyme infection has often already been eliminated by using antibiotics but the toxins continues to persist in the body. Therefore people continue to be ill. He also believes that many other infections, including fungal infections that can be found in sick building syndromes and many waterborne infections can also produce similar toxins. It is possible that in the case of certain viral infections or after some traumatic injuries, the body’s own genes may even be able to be tricked into continually making the toxins.
In addition to getting rid of the neurotoxins, it is important to support the body in two other key ways. These were developed and popularized by Dr. Russel Jaffe Ph.D. and are called the Vitamin C flush and the “Alkaline Way Diet”. How to do these will be discussed below after we’ve discussed how to clear the neurotoxins.
For more information on the treatment, how to take and possible reactions go to http://www.ei-resource.org/articles/chronic-fatigue-syndrome-articles/neurotoxins-%11-treatment-information-sheet/
[Tick talk note – As well as constipation the patient may experience an exaggerated inflammatory response giving herx type symptoms. It is important to build up slowly if this is being considered.]
From a Eurolyme member Laurence Swift – an excellent read!
June 13 2009
In response to an article on Stella Huyshe-Shires of Lyme Disease Action:
Stella Huyshe-Shires is clearly suffering the effects of ongoing
Lyme (borrelia) infection. This is usually caught from infected ticks,
which by the way, are everywhere, as they are carried by birds and all
domestic animals and wildlife. The disease may be complicated by other
infections caught from the tick, such as Bartonella (we call it
“cat-scratch fever), Babesia (a malaria-like infection found in cattle
and dogs in parts of UK) and a whole list of sundry infections –
Erlichia, Tick-Borne Encephalitis – and others which may not yet be
recognised in the UK but which will become important with Global
Warming helping the vectors (insects) to survive.
Lyme Disease can also be transmitted by other biting insects like
stable-flies, fleas, lice, mites – and can also be transmitted from a
mother to her offspring, either via the placenta or through the milk.
Or like syphilis, by sexual contact. It appears to be a major cause,
if not the main cause, of autism in children.
The scary thing about Lyme (Borrelia) infection is its effects on
the body. It can mimic virtually every other disease. The bacterium
itself is the most sophisticated known to man. Being a corkscrew-shape
spirochaete it resembles its relatives like Leptospira (Weil’s
Disease) caught from rat’s urine, and Syphilis, but it has many more
genes and plasmids to generate its outer surface proteins (OSP’s) so
it can change its coat to avoid detection by the body’s immune system.
Which is why we get negative blood tests, as our current blood tests
are very primitive and only pick up antibodies generated by our immune
systems in response to OSP’s presented to it.
Simple bacteria often move around by being driven by a rotating
filament attached to one end, that acts just like an outboard motor,
spins and moves the bacterium. Borrelia has a bundle of flagellae
wrapped around its cellular contents, which act like an “inboard
motor” and drive the bacterium in a corkscrew manner which enables it
to penetrate every cell in the body.
Classically it penetrates the cartilage of joints and causes an
arthritis that appears to move from joint to joint, so-called
“migratory arthritis”, and which occurs even in young children. In
fact it was first characterised because of an outbreak of arthritis in
children. It also gets into nerve tissue and causes mayhem, known
technically as “neuro-borreliosis” . Facial nerves are attacked and you
get classic Bell’s Palsy with droopy eyelids, jaw, other facial
muscles. This can spread to the intestine and cause signs of
constipation and colic, known as Bell’s Palsy of the Gut. It can
affect nerves feeding glands so there are many glandular effects. A
big problem for some people is allergy. How Borrelia causes allergies,
is uncharted waters to me, but it does, as people often recover from
allergic situations when treated for Lyme.
If a suspected Lyme infection is treated within the first few (4
to 6) weeks of the actual infection, with reasonably high doses of
even simple penicillin, it may be killed off. But many people don’t
know even whether they’ve been bitten, let alone when, as they may not
have the classic tick-bite “bull’s eye” rash. Once the bacteria have
penetrated deep into the tissues – they prefer the low oxygen levels
found in cartilage, tendon, etc – they can be difficult, or often
impossible, to get at with antibiotics. High doses and long courses
are absolutely essential. Changing antibiotics can help. The bacterium
can also hide away in the form of cysts and coccal forms, where they
are neither recognised by the immune system nor touchable by
antibiotics – just the same as Syphilis and Tuberculosis. Special
drugs are used, in cycles, called “CystBusters” , to get them out, like
metronidazole. But once established, you may have the infection for
life, and you can only control, not completely cure, it, with constant
repeated courses of antibiotics.
One “inaccuracy” in your article is the mention by a
microbiologist that “all antibiotics have potentially serious side
effects”. OK, you may develop an allergy to penicillin. None of these
side effects are unconquerable and are often worth the risk
considering the life destroying effects of Lyme Disease. It is normal
to prescribe long-term antibiotics for certain well-known diseases
like TB, Brucellosis, and Syphilis – Lyme is actually at least as
important as these. The problem of resistant bacteria, like MRSA in
hospitals, has everything to do with the hospital environment and
hygiene and very very little to do with the use of antibiotics. In
fact, it is “under-treatment” of infections by doctors that has
allowed the resistant organisms to survive. If they used higher doses
and more prolonged courses in the first place, the organisms would not
have had a chance to develop resistance. By the way, drug resistance
in Lyme doesn’t seem to be a problem when antibiotics are rotated
properly – it’s the co-infections like Babesia that cause the
Very good article by Sam Donta –
Late and Chronic Lyme Disease: Symptom Overlap with Chronic Fatigue Syndrome & Fibromyalgia
May 15, 2002
By Sam Donta,M.D.
Following the introduction of Borrelia burgdorferi into the skin by an infected tick, the organisms begin to spread both locally and systemically. Several days typically elapse before the appearance of the first sign of infection, i.e., erythema chronicum migrans (ECM), or other less typical rashes (29).
The rash occurs in fewer than 50% of patients with Lyme Disease (8,10), but the true incidence of Lyme Disease in the absence of a rash is unknown.
The occurence of multiple rashes is indicative of systemic spread of the organisms. Multiple rashes usually do not occur until 2-4 weeks following the initial tick bite. This is the same time period during which the organisms are being disseminated to their target tissues and cells. The incidence of multiple rashes was initially reported to occur in as many as 50% of cases, but has been much less common in the last two decades, probably because of frequent use of antibiotics.
Approximately 4-6 weeks following the tick bite, the first systemic symptoms (other than multiple rashes) occur in some patients, usually in the form of “flu” (15). These symptoms include sore throat, severe headaches and neck aches, and severe fatigue. Rhinitis, sinusitis, and cough are not usually present, distinguishing this “flu” from other influenza-like illnesses. While the Lyme-flu symptoms can spontaneously resolve, patients can experience recurrent “flu”.
Soon after the onset of Lyme-flu, fatigue, arthralgias and/or myalgias may begin. The arthralgias appear to primarily involve the large joints (i.e., knees, elbows, hips, shoulders), although smaller joints (e.g., wrists, hands, fingers, toes) may be involved(29). Some patients may have actual arthritis, often oligoarticular, more frequently in men than in women. Earlier estimates were that 50-75% of patients who developed late Lyme Disease had arthritis, but more recent analyses suggest that the incidence of actual arthritis in patients with late or chronic disease is closer to 25% (33).
Neck stiffness is common. The pains are described as severe, jumping from joint to joint, and may be present for only short periods of time. Pain in the teeth or in the temporal-mandibular joints is not uncommon. Rib and
chest pains occur frequently, leading some patients to seek care in emergency rooms and urgent care centers for evaluation of possible cardiac disease. Frequently as well are paresthesias such as burning, numbness and tingling, and itching. Some patients experience crawling sensations, vibrations, or electric shock-like sensations. Rarely is there any actual palsy of the affected areas, making this much more of a neurosensory, rather than a motor, disease.
In addition to paresthesias, purely neurological symptoms and signs include headaches, an aseptic meningitis, facial nerve (Bell’s) palsy, and encephalitis or encephalopathy that may be manifested by cognitive dysfunction, especially short-term memory loss, and psychiatric symptoms such as panic, anxiety, or depression (14). The aseptic meningitis and Bell’s palsy tend to occur within the first few months following the tick bite, but may also occur as part of reactivation disease (9).
Other symptoms may include fevers (usually low grade, but may be high), sweats (which may be severe), visual dysfunction (described primarily as blurriness, but can include optic neuritis or uveitis), tinnitus, sensitivity to sounds, or hearing loss. Shortness of breath, palpitations and/or tachycardia, abdominal pains, diarrhea or irritable bowel, testicular or pelvic pain, urinary frequency or urgency, dysequilibrium, and tremors are also common symptoms. Some of the dysautonomia symptoms can be disabling.
Rarer symptoms may relate to panniculitis and hepatitis. Rarely as well are congenital and intrautero infection; when this occurs, it appears to be similar to toxoplasmosis and rubella, i.e., a primary infection during the first trimester. The occurrence of optic neuritis or uveitis raises other possibilities such as multiple sclerosis, but can be part of Lyme Disease.
The course of the disease can best be described as persistent, but with periods of worsening symptoms, often cyclical every few weeks or monthly. Especially disconcerting are persistent symptoms such as headaches and fatigue that can be exhausting. Some patients are more symptomatic than are others, which may reflect genetically- determined differences in responsiveness or extent of infection.
The disease does not appear to be progressive or destructive, as with cancer, nor is it fatal, but can be very debilitating.
The incidence of asymptomatic infection has not been adequately delineated. There appear to be substantial numbers of patients who remain asymptomatic, but reactivate their disease a number of months or years later, following trauma, pregnancy, a medical illness for which an antibiotic is prescribed, or other stresses, including psychological stresses (9). The Lyme OspA vaccine has appeared to reactivate Lyme Disease in a number of individuals who knew, but some who did not know, they had prior Lyme Disease (11). The mechanisms responsible for the reactivation of the disease have not been defined, but may include both molecular mimicry and underlying infection.
The pathogenesis of Lyme Disease remains to be defined. From the available studies, it would appear that the organisms are trophic for either the endothelial cells of the blood vessels that serve the nervous system or for the glial or neural cells themselves (4,24,26,31). Accumulating evidence supports the hypothesis of a persistent infection as the cause of the persisting or relapsing symptoms (26,31). Whether molecular mimicry is involved in the pathogenesis of some of the symptoms remains more speculative (18).
Although arthritis can occur in Lyme Disease, the organisms can only rarely be found in synovial tissue. And as many of the arthralgias that occur in the disease do not respond well to antiinflammatory agents, the disease is more of an infectious neuropathy than an actual invasion of synovial or bursal tissues.
The diagnosis rests heavily on the clinical symptomatology. When there are clinical signs, e.g., rash, aseptic meningitis, optic neuritis, arthritis, an appropriate differential diagnosis must be pursued. On a clinical basis, “chronic fatigue syndrome” or “fibromyalgia” cannot be readily distinguished from chronic Lyme Disease. Indeed, accumulating experience suggests that Lyme Disease may be a frequent cause of fibromyalgia or chronic fatigue (8,12).
Other microbes have been proposed as causative agents of multisymptom disorders that are being termed chronic fatigue and fibromyalgia, especially more recently recognized mycoplasma species such as M.fermentans and M.genitalium, but definitive proof of cause and effect has not yet been established (6, 23).
There has been an attempt to separate “late” Lyme Disease from “chronic” Lyme Disease, the former being manifested by objective signs of arthritis or neurological disease (32). Some have denied the existence of chronic disease, inferring that these patients suffer from psychiatric disorders; some have used the term “chronic” to mean post-treatment disease (“post-Lyme”), assuming that the infection has been treated, and the remaining symptoms are in the same realm as those patients who have “fibromyalgia” or “chronic fatigue” (27, 30).
These assertions are speculative and remain unproven. That chronic Lyme Disease actually exists, and is likely the most common form of the disease, is supported by epidemiologic studies demonstrating that 30-50-% of treated and untreated patients go on to develop a multisymptom disorder typical of, and indistinguishable from, fibromyalgia and chronic fatigue (1, 28). As with other multisymptom disorders, chronic Lyme Disease is a clinical syndrome consisting of fatigue, arthralgias and myalgias,and other nervous system dysfunction(7).
Furthermore, the results of treatment studies appear to support the hypothesis that persistent infection is responsible for the chronic symptoms. It is likely that Lyme Disease will serve as a useful model for other chronic multisymptom disorders. Whether the pathogenesis of “late” Lyme Disease differs from that of the chronic form of the disease remains to be established.
Routine laboratory tests are usually normal in Lyme Disease. The ESR is most often normal, distinguishing it from some of the inflammatory disorders such as rheumatoid arthritis or lupus. Culture of the borrelia is possible early in the disease, usually from biopsies of the erythema migrans rash; however, most laboratories are not capable of culturing the organisms.
The only currently available useful laboratory tests are the immunologically-based ELISA and Western blot assays. The recommendation was made in 1994 to have a two-tiered testing system in which the Western Blot would only be done on ELISA- positive samples (5). The recommendation was based primarily on the results obtained from patients with arthritis (13), did not take into account the chronic form of the disease, and was made despite the lack of consistent reproducibility of results between various laboratories (2, 16).
The ELISA has been shown to be an unreliable test in many patients with Lyme Disease, both in early infection and later disease (8, 10). Part of the reason for the lack of sensitivity of the ELISA is the use of whole organisms, resulting in a high amount of background absorbance.
After correction for the high background, only a small percentage of positives can be detected. Because Western blots separate the proteins of the borrelia, specific reactions can be visualized, and more accurate interpretations of the results made. Over 75% of patients with chronic Lyme Disease are negative by ELISA, while positive by Western blot (8, 10). Patients with oligoarticular arthritis may be more likely to have robust IgG responses and positive ELISA tests and IgG Western Blots (13).
By Western blot analyses, the first immunologic reactions in Lyme Disease are to the 41kd flagellar protein, and the 23kd OspC protein. Typically, at the time of the ECM rash, there will be an IgM reaction against the 23kd and 41kd proteins, and no IgG reactions. Within the next few weeks, the IgM reactions persist, sometimes accompanied by less specific reactions against 60kd and 66kd proteins, and IgG reactions are now visible against the 23kd and 41kd proteins. Thus, in the presence of an appropriate clinical picture, the immunoreactivity against the 23kd and 41kd proteins appear to be diagnostic of Lyme Disease.
Whereas the 41kd protein is not unique to B. burgdorferi, the 23kd protein appears to be unique. Also apparently unique proteins of B.burgdorferi are the 31kd (Osp A) and 34kd (Osp B) outer membrane proteins, and the 35kd, 37kd, 39kd, and 83/93kd proteins. Reactions to the 31kd proteins are not usually seen until after a year or more following the onset of disease. Not all patients with symptoms for more than one year, however, display reactions to the outer membrane proteins.
Most symptomatic patients have specific reactions on IgM Western blots (8,10). With resolution of the symptoms, the IgM reactions disappear or attenuate. IgG reactivity may continue to be present with resolution of symptoms, but it typically also disappears or attenuates with successful therapy. There are some patients (20%) who have symptoms, but whose Western blots are negative (8,10). If the borrelial organisms remain intracellular, with no extracellular reemergence once established, this could explain the absence of additional or persistent immune responses.
PCR (Polymerase Chain Reaction) is a highly sensitive means to detect microbial DNA or RNA, and it was hoped that this technique would find an important role in the diagnosis of Lyme Disease. Thus far, however, despite the specificity of this method, borrelial DNA or RNA has not been reliably detected in the blood, urine, or spinal fluid of patients with early or later forms of Lyme Disease, findings again supportive of an intracellular
reservoir for the borrelia.
It should be possible to develop a better, highly specific ELISA for Lyme Disease, using recombinant 41kd, 23kd, 31kd and/or 34kd (and perhaps other B.burgdorferi-specific) proteins. Currently, however, the Western blot assay is the most reliable immunologic test.
In vitro, B. burgdorferi is sensitive to several antibiotics (20,25). This assumption is complicated, however, because of the long incubation times needed to determine minimum inhibitory concentrations (MIC), as the borrelia have doubling times of 20-24 hrs. With these limitations, the results of a few studies show minimum bactericidal concentrations (MBC) to penicillin of 8ug/ml, ampicillin: 2ug/ml, tetracycline: 1-2ug/ml, doxycycline: 2ug/ml, ceftriaxone: 0.5ug/ml, cefotaxime: 0.5ug/ml, cefuroxime: 1-2ug/ml, cefixime: 8ug/ml,erythromycin: 0.5ug/ml,
clarithromycin: 0.5ug/ml, azithromycin: 0.5ug/ml, and ciprofloxacin: 4ug/ml.
At the time of the first rash, any one of several antibiotics appear to be effective, if given for 2 weeks, according to several published studies. However, a number of patients so treated developed subsequent symptoms of arthralgias, fatigue, and paresthesias, with positive Western blots, who were then successfully treated with longer courses of antibiotics (8, 10). The recommendation at this time, therefore, is that tetracycline, doxycycline, or amoxicillin be used for 1 month if ECM is the only symptom of Lyme Disease.
Once any other symptoms appear, the treatment of Lyme Disease for only 2-4 weeks is associated with frequent failures and relapses (8, 10). Our initial experience suggested that a 3 month course of tetracycline was associated with a higher success rate(8).
In patients with symptoms present for more than six months, the treatment course may need to be more prolonged, or a retreatment course of varying length may be needed. In patients with symptoms for more than a year, 12-18 months may be needed for complete resolution of symptoms. The rationale for a longer treatment course is based on extensive observations (8,10), plus the analogy to the longer treatment courses required for tuberculosis, leprosy, Q fever, and certain fungal diseases.
With Lyme Disease, the slow growth rate and metabolic activity of the borrelia would seem to correlate with the need for longer treatment periods.
Once treatment is initiated for patients beyond the earliest signs of infection, their symptoms frequently increase during the first several days, or even for the first several weeks of therapy. For patients with preexisting symptoms of more than a few months, relief of any of their symptoms may not occur until after 4-6 weeks of therapy (8, 10). Typically, there are short periods of relief, followed by relapsing or migrating symptoms; with continued therapy there are longer symptom-free periods. Some arthralgias may require 3 months or more to resolve, and fatigue may be the last symptom to disappear.
The preference for tetracycline evolved because of the large number of failures that were noted in patients who had been on ampicillin and doxycycline. Patients generally had some response to doxycycline, but it was uaually not complete, nor long-lasting. Tetracycline may be more effective than doxycycline simply because of the greater dose, i.e., 100mg of doxycycline twice daily is not equivalent to 500mg of tetracycline three times daily; also, doxycycline is highly protein-bound, compared to tetracycline, which could limit the availability of free drug to diffuse into tissues and cells.
Some physicians use doxycycline at doses of 300-400mg daily to try to achieve a successful result. A strict comparison between doxycycline and tetracycline has not yet been made. Minocycline has also been used by some physicians, with varying success, but faces the same issues of dosage and protein binding.
Of the beta lactams used for the treatment of Lyme Disease, the most efficacious appears to be ceftriaxone. In limited comparitive trials, cefotaxime appears to be equally efficacious, and high-dose IV penicillin may also be effective.
In early Lyme Disease, oral amoxicillin is as effective as doxycycline. In later disease, many failures are noted, despite the use of up to 3 grams of amoxicillin daily, with probenicid. Cefixime would also not appear to be
effective therapy. Cefuroxime axetil has been evaluated only in the treatment of early Lyme Disease, and appears comparable to doxycycline. Limited reports of its use in later Lyme Disease have not shown it to be efficacious.
The role of the newer macrolides in the treatment of Lyme Disease needs further assessment. Erythromycin has been regarded as ineffective, despite its good in vitro sensitivities. Azithromycin has been reported to be less effective in the treatment of early Lyme Disease than amoxicillin (21). Some physicians use clarithromycin and azithromycin in higher dosages and for longer periods of time, but there have been no reports of greater success with these drugs than with the tetracyclines or beta-lactams. In our experience, all macrolides are effective
when combined with a lysosomotropic agent, especially hydroxychloroquine(see below)(10).
In evaluating the possible factors, it would appear that antibiotics that can achieve intracellular concentrations and activity are the most efficacious drugs. The results of studies in Klempner’s laboratory using a tissue culture model of borrelia infection demonstrated that ceftriaxone was incapable of eradicating intracellular organisms (17); similar experiments in Raoult’s laboratory using an endothelial cell model demonstrated that tetracycline and erythromycin were effective, but beta lactam antibiotics were not (3). These results are in line with our experience that the tetracyclines and macrolides achieve the greatest success.
In contrast to beta lactams, antibiotics of the tetracycline and macrolide classes are capable of good intracellular penetration. Experience with the macrolide antibiotics has been disappointing, however, when compared with
its in vitro activities against the Lyme borreliae, and with the established efficacy of macrolides against other intracellular parasites such as chlamydia, legionella, mycobacterium-avium intracellulare, and toxoplasma. If, though, the Lyme borreliae reside in intracellular vesicles that are acidic, the macrolides’ activity would be sharply decreased at the lower pH.
This is in contrast to the tetracyclines, which are active at acid pH; even so, the activity of doxycycline was shown to be further increased by increasing the pH. In a tissue culture model of ehrlichia infection, the use of lysosomotropic agents such as amantidine, NH4Cl, and chloroquine increased the killing of intracellular organisms by doxycycline (22).
Based on those studies, and the hypothesis that late Lyme Disease symptoms are due to persisting intracellular infection, we have been successfully treating patients using the combination of a macrolide and hydroxychloroquine (10).
As regards “CNS” disease, there is no evidence that ceftriaxone is more successful than either the tetracyclines or the combination of macrolide and hydroxychloroquine; if our presumption that the pathogenesis of the disease involves the localization of the borrelia to the endothelial cells of the blood vessels serving the nervous system or to glial or neural cells is correct, then one would not need to have a drug that can cross the blood-brain barrier to be effective. Indeed, the tetracyclines can cross the blood-brain barrier to some extent, and were used when initially introduced into clinical medicine for the treatment of meningitis, with some success.
Macrolide antibiotics do not cross the blood-brain barrier, but have been effective in treating other CNS infections (e.g., toxoplasmosis), and in our experience have been effective in reversing the neuropsychiatric symptoms and signs (eg SPECT scans) of Lyme Disease (10). With regard to the issue of bactericidal vs bacteristatic effects, any such effect in vivo has not been demonstrated.
Finally, there have been no reports showing any change in antibiotic resistance patterns during the course of treatment. Ultimately, the determination of efficacy of therapy depends on the clinical response.
The diagnosis and treatment of Lyme Disease have been hampered by less than adequate diagnostic tests and inadequate comparisons of antibiotic regimens. Specific antigen-based ELISA tests should result in greater specificity, but sensitivity of any tests based on measurements of the host immune response might still be of limited value if the borrelia remain intracellular. Most useful would be the development of
tests that can determine the presence and extent of any residual borreliosis. In the therapy of Lyme Disease, double-blind, placebo-controlled and comparitive trials are needed to answer the questions relating to duration and class of antibiotic therapy.
The apparent failure of a regimen of one month of IV ceftriaxone, followed by two months or oral doxycyline,
to improve the outcomes of patients with chronic Lyme Disease (19) was not surprising, based on prior observations that neither regimen used for a limited duration was capable of yielding patient improvement (8,10,33). Additional trials are needed to evaluate whether longer durations of treatment, using tetracycline
itself, or the novel combination of macrolide and lysosomotropic agent, would be proven effective treatments.
(For list of cross references refer to http://www.prohealth.com//library/showArticle.cfm?libid=8441)
LYME DISEASE (Borreliosis)
A Plague of Ignorance Regarding the Ignorance of a Plague
© Copyright 2004, Dr Scott Taylor, DVM, All rights Reserved
NB link now broken but have kept on file for information..
Contained lots of info. on symptoms, history of Lyme, problems with testing, persistence of infection, EM rash pictures, treatments and alternative meds and some studies on Lyme.
An extract of some of the text is below:
Borrelia lack the microbial toxins called lipopolysaccharides (LPS) however, they have over 150 genes that encode for the BLPs that are the key to their pathogenicity. This is over 50 times greater than other pathogenic bacteria. That is, other bacteria usually only have 3 genes for lipoproteins, while borrelia have 150!
With this many BLPs triggering an imbalance of the immune system and other innate responses in the body, it’s not hard to see how a cascade of chronic problems can arise from this.
For example, when we look at psychological problems of neuroborreliosis, it’s clear that the cause of these symptoms arise from BLPs triggering encephalitis and that this inflammation not only causes imbalances in numerous neurotransmitters, it also causes vasculitis which leads to hypoperfusion and hypoxia of the brain.
These toxins also cause a channelopathy, which lead to a dysfunction of signals along neurons, muscles and cells making them easily excitable, but not able to discharge correctly…since the electrical potential across the cell membranes don’t function normally.
This can attribute to numerous symptoms such as anxiety, paresthesias, hyperacusis, tremors and even susceptibility to static shock that many LD patients have.
Thus, the evidence is pretty clear that BLPs plays a large role in the pathogenesis of borreliosis and is a key to understanding this disease.
IMO, without BLPs, borrelia would not be virulent.
Some questions I’ve received regarding the pathogenesis of borreliosis:
Q: I don’t see anything so far that would describe why these inflammatory mediators, which would be activating the T-cells, would not be phagocytized by these and other macrophages.
A: Initially it does. The initial infection of borrelia can be acute and flu-like or it may not even be noticable. Unfortunately, this initial immune response doesn’t completely rid the body of borrelia.
I don’t think we have the complete answer to why this happens. But there are probably several factors involved. Borrelia can adapt and be very stealthy. Another reasonable theory is that apoptosis of monocytes, macrophages, neutrophils and other immune cells triggered by TLR-2 stimulation may account for immune dysfunction and supression.
This makes a lot of sense to me since we see immune dysfunction & suppression in chronic LD and in CFIDS, which I believe have a very similar pathogenesis.
Q: Also, if it’s somehow a more severe activation of these mediators, especially if caspase and IL-12 are involved, why is there not more obvious toxic shock-like symptoms apparent early on?
A: I wouldn’t say that it’s a more severe activation of these mediators, but more of a long term chronic/relapsing imbalance of them.
It may also have to do with borrelia’s ability to grow slowly and not trigger an acute toxic shock.
It also may have something to do with borrelia’s ability to hold on to it’s BLPs and not release them into the surrounding tissue until they are killed.
We know that when we kill borrelia (such as with abx tx) the BLPs are released from them and we experience a herx reaction. In severe cases this response can be quite acute.
There are probably several other factors such as lipid depot effect and slow release.
The immune supressing effect of BLPs likely plays a role here too.
Q: It seems that many people are not even symptomatic until years after the original tick exposure.
A: This is true with borreliosis…(this happened in my case). It’s also true with syphilis.
This may be due to borrelia’s ability to code for so many different BLPs. They have the genetic code for over 150 different BLPs.
Depending on which ones and how strong the expression of these BLPs genes are may determine how virulent the borrelia is at different times.
We know that borrelia change the expression of these genes when exposed to different environmental factors such as temperature.
They express different BLPs in ticks since they are in ambient temperature, but once inside a mammal, they begin to change the BLPs that they express.
They also have an effective ability to accept plasmids and pick up other pathogenic genes in this way.
Work has shown that removing certain BLPs from virulent strains makes the borrelia avirulent.
The evidence is very suggestive that BLPs determines the pathogenesis of borrelia.
When to suspect Lyme Disease – a very comprehensive report by Dr Bleiweiss MD
Lyme disease factsheet by European Centre for Disease Control & Prevention:
Lyme disease factsheet by Health Service Executive, Ireland:
Jemsek’s Detailed Overview of Lyme Disease & its Co-infections
A symptoms list for Lyme & Co-infections by Joseph Burrascano:
Lyme Disease: A Diagnostic Dilemma By VirginiaSavely,DNP,MEd,MSN,RN,FNP-C
In the July 2010 The Nurse Practitioner
Welcome to the Lyme Log. This tool helps those with Lyme Disease to log their feelings, thoughts and symptoms each day as well as excercise or activities completed and medication taken during that day.
‘A useful tool for plotting your daily symptoms & medication. Compare from day to day or monthly charts. A space is available for making notes on how you feel.’
Lyme Symptoms Charts:
Many doctors treating Lyme and tick-borne diseases suggest their patients keep track of their symptoms on a monthly calendar chart. This allows one to show a reliable history of symptoms without resorting to memory at the time of the office visit. It also allows someone to track progress over several months or longer by laying out the charts side-by-side.
Monthly chart with pre-printed symptoms: PDF format
Monthly chart without symptoms (spaces to fill in your own): PDF format
Month Calendar format – blank PDF format
Check out Tick Talk’s own Lyme symptom chart:
The Need for Clinical Judgment in the Diagnosis and Treatment of Lyme Disease
by Elizabeth Moloney, MD
Clinical practice guidelines are increasing in number. Unfortunately, when scientific evidence is uncertain, limited, or evolving, as is often the case, conflict often arises between guideline committees and practicing physicians, who bear the direct responsibility for the care of individual patients. The 2006 Infectious Diseases Society of America guidelines for Lyme disease, which have limited scientific support, could, if implemented, limit the clinical discretion of treating physicians and the treatment options available to patients.
A snippet as follows:
Consider the situation in which 100 patients with undiagnosed Lyme disease seek medical attention for evaluation of fever, headache, fatigue, and body aches occurring at the end of June. Recall that CDC data indicate that erythema migrans (EM) rashes are reported in 68% of patients meeting the surveillance case definition, and that the guidelines recommend two-tier serologic testing of patients lacking the diagnostic rash. In the two-tier scheme, patients are first tested with an enzyme-linked immunoabsorbant assay (ELISA) or indirect fluorescent antibody (IFA) test, and those with positive or equivocal
results are then tested withWestern blotting; patients who are negative on ELISA are not tested further. Trevejo et al. found the sensitivity of two-tier testing in early Lyme disease to be 29%-32%; Bacon et al. found it to be 38%. As Table 1 demonstrates, the laboratory confirmation requirement is problematic; as many as 22% of early Lyme disease patients would go untreated.
Clearly, this is unacceptable; patients would be left untreated at the stage when therapy is most efficacious. Owing to the potential for false negative results in these circumstances, Steere et al. suggested that physicians consider treating patients with “summertime flu” symptoms. The need for such a suggestion emphasizes the principal reason for this challenge—laboratory confirmation requirements undermine the value and primacy of clinical data andmay impede care, as would be the case in this very common clinical scenario.
The same problem with laboratory confirmation holds true for late neurologic Lyme disease. Starting again with 100 patients who have undiagnosed Lyme disease and objective, non-EM findings, 43%-56% would be misdiagnosed because of deficits in laboratory capabilities, as shown in Table 2. In late Lyme, sensitivity of the testing procedure was found to be 44% by Ledue et al. , and 57% by Dressler et al. The low sensitivity of two-tier testing in late neurologic Lyme disease can be traced back to the original paper by Dressler et al.,10..
Lyme Disease: The Great Imitator
Describes all three stages of Lyme in great detail:
Comparison of Findings for Patients with Borrelia garinii and Borrelia afzelii Isolated from Cerebrospinal Fluid
F. Strle,1 E. Ruzˇic´ -Sabljic´ ,2 J. Cimperman,1 S. Lotricˇ -Furlan,1 and V. Maraspin1
1Department of Infectious Diseases, University Medical Centre Ljubljana, and 2Institute of Microbiology and Immunology, University of Ljubljana, Slovenia
Lyme borreliosis is the most common tick-transmitted illness in the Northern Hemisphere [1, 2]. It is caused by Borrelia burgdorferi sensu lato . Human disease is associated with at least 3 Borrelia species: B. burgdorferi sensu stricto (B. burgdorferi), Borrelia afzelii, and Borrelia garinii. All isolates from North American patients have been members of the genomic group B. burgdorferi, whereas European isolates have included at least 2 additional genospecies: B. afzelii and B. garinii . Although probably all 3 genospecies can cause all major manifestations, there are indications that infection with different B. burgdorferi sensu lato genospecies results in distinct clinical manifestations of Lyme borreliosis, most probably as a consequence of their distinct organotropism. For example, in Europe, B. afzelii is mostly associated with skin manifestations, such as erythema migrans (EM) and acrodermatitis chronica atrophicans, whereas B. garinii is the main cause of Lyme neuroborreliosis [1, 5–8]. Differences in geographical distribution of genospecies may explain the distinctions between the clinical picture of Lyme borreliosis in Europe and in North America [1, 2, 9]. Although data indicating the association of different B. burgdorferi sensu lato genospecies with distinct clinical manifestations of Lyme borreliosis are relatively abundant and obvious [1, 2, 7–9], comparisons of the characteristics of individual clinical manifestations caused by different Borrelia genospecies are quite scarce. In fact, information is limited to the reports concerning patients with EM [10–12]. Comparison of culture-confirmed EM caused by B. afzelii with EM caused by B. burgdorferi showed differences in epidemiological, clinical, and laboratory findings, suggesting 2 distinct syndromes that are caused by different agents .
Two other studies have demonstrated several differences between EM due to B. afzelii and B. garinii [11, 12]. The primary aim of the present study was to further assess the idea that the characteristics of individual clinical manifestations of Lyme borreliosis depend on the species of B. burgdorferi sensu lato; by comparison of findings for adult patients with either B. afzelii or B. garinii isolated from CSF, we tested the hypothesis that the features of Lyme neuroborreliosis in the 2 groups differ.
For full paper go to: http://www.journals.uchicago.edu/doi/pdf/10.1086/506936
Slide show by Burrascano
Immunoblots and Lyme disease: a review
NB link now broken but have kept on file for information..
Despite the multiplicity of symptoms – Lyme neuroborreliosis has been named “the great simulator” – all adult patients have something in common: pains. These burning pains often exacerbated during the night are not related to movements. Therefore, most patients will consult without delay their general practitioner who will be faced with a difficult diagnosis in an emotional context.
At the first visit, pain may be the only symptom: subacute, irradiating to the extremities, chest or abdomen, pain is definitely described by the patient as a new symptom. It can be confused with a disc problem, VZV infection, acute myocardial infarction, kidney stones or polymyalgia rheumatica.
Days or weeks after the onset of these symptoms, the clinical picture tends to become more clearly associated with a neurological problem. Headache, photophobia, extreme fatigue, memory troubles, emotional lability are common and suggest CNS involvement. Any of the cranial nerves can be affected but sixth and seventh nerve palsy are the most frequent. Unilateral or bilateral peripheral palsy (Bell’s palsy) can be caused by borreliosis but should never be viewed as its most frequent cause. Lyme disease should be considered in case of facial peripheral palsy but is responsible for less than 5% of all cases. Blurred vision also can be seen during this stage secondary to papilledema, optic atrophy, optic or retrobulbar neuritis, or pseudotumor cerebri. Optic nerve disease may be unilateral or bilateral, and solitary or associated with other neurologic or neuro-ophthalmologic manifestations.