posted
Quick background first for those who haven't read my posts: 1 had a positive Lyme test with IgM 23 and 41 on October 14. I was treated with 21 days of doxy at 200mg/day. Started to feel better then the high fevers, chills, sweats, etc. came back about 13 days after I started Doxy. 2nd Lyme test negative with only 41 IgM and IgG positive. Finished out the doxy and then got sick again about 10 days after the first relapse.
So this wed my temp spiked to 103.7 while on Tylenol/Ibuprofen and my heart was beating very fast. These were symptoms during whole the 2nd relapse but this was worse. So I went to the ER.
I was pannicked and freaking out. Got there, HR 150. They rushed me back to see the doctors. They admitted me that night because my temp was so high and a cat scan revealed that my liver was a little enlarged.
This is my 3rd night here and they have no idea what is wrong with me. ID doesnt think it is Lyme or that I ever had Lyme. My primary team of docs is treating me with doxy but only 200mg/day and they are treating me with IV ceftriaxone too. They are starting to think likely not Lyme either.
They are look at all different viral infections, bacterial infections and then after that they have to go non-infectious disease and look for other things.
My blook tests changed a lot between the last time i had blood on the 31st of October - low platlets, low white blood cells but as of today those are back to normal and my red blood cells are coming back up. My platlets went down again.
My fevers are still high, heart rate still around 125, etc etc.
I don't know if I can use this dr.'s name but the Boston LLMD from the Chronicle episode's office called me Thursday while I was here. They wanted to offer me an appointment Monday but I can't because I don't know if I will have been released yet.
He said he would consult with my docs here but they don't think that is necessary. They say 21 days of doxy kills Lyme. Maybe I don't have Lyme, who knows!
I just wanted to let people know what was going on with me. Sorry for not answering PMS.
Posts: 24 | From Boston | Registered: Nov 2008
| IP: Logged |
lpkayak
Honored Contributor (10K+ posts)
Member # 5230
posted
do you have anyone supporting you? i would suggest you get to the real llmd.
-------------------- Lyme? Its complicated. Educate yourself. Posts: 13712 | From new england | Registered: Feb 2004
| IP: Logged |
posted
They tell me that if when they release me and we are still operating on the "unknown virus" assumption that of course I am free to go see a true Lyme specialist.
I've said before. If it is not Lyme I just need to know what it is but I don't want Lyme to be completely ruled out.
The ID docs are the ones that are adamant its not Lyme. They say the first test was a false positive because 23 IgM went away and never converted so the finding are minimal and not significant.
My primary doc team has not ruled it out which is why I am on antibiotics. I am feeling a little better after one day of the IV and doxy but the fever is still there. No chills with it this time though and I feel generally OK.
How can I get a "real" LLMD to help? I don't really know what to do. They say the first test was a false positive because 23 IgM went away and never converted so the finding are minimal and not significant.
Posts: 24 | From Boston | Registered: Nov 2008
| IP: Logged |
lymednva
Frequent Contributor (1K+ posts)
Member # 9098
posted
Most docs in hospitals have no clue about Lyme. You can leave against doctors orders. I would do that, if I were you and see that LLMD you mentioned.
Just my 2 cents here.
-------------------- Lymednva Posts: 2407 | From over the river and through the woods | Registered: Apr 2006
| IP: Logged |
posted
Hi Boston Wow - what a terrible time you are having! I'm so sorry for you! Look into a possible virus - but don't rule out Lyme just yet. When the doctors talk about 200mg Doxy for 21 days treatment will cure Lyme - they are following CDC guidelines - which have been thought to be undertreating the patient by many doctors and researchers who are just as competent as the ones attending you now. Some people - if just bit will recover after the std. CDC treatment. Some won't. Read Dr. Burrascano's treatment guideline for abx found in the newbie link on this site. Consider also co-infections. You got bit by a tick? My LLMD says seldon does anyone only get Lyme from a tick. Low white blood cell count - low platelet count and abnormal liver function, fever, chills, flu like symptoms could be a co-infection. HGA Anaplasma phagocytophilum comes to mind. So I think while you are seeking a diagnosis - I would try to get tested for co-infections as well. I really hope you feel better soon and get the proper help. Best wishes, -p
Posts: 641 | From So. CA | Registered: May 2008
| IP: Logged |
bettyg
Unregistered
posted
see MASS NAMES I'M SENDING BY PM NOW!!!!
so sorry you are so sick and no one will help find the culprit!
IP: Logged |
lpkayak
Honored Contributor (10K+ posts)
Member # 5230
posted
you posted this:
I don't know if I can use this dr.'s name but the Boston LLMD from the Chronicle episode's office called me Thursday while I was here. They wanted to offer me an appointment Monday but I can't because I don't know if I will have been released yet.
He said he would consult with my docs here but they don't think that is necessary. They say 21 days of doxy kills Lyme. Maybe I don't have Lyme, who knows!
the docs name starts with D and he is a real llmd. he is contacting you. i have never heard of that before but i know he is an excellent doc and with him calling you...it must mean he will get you in quick-he often has a long wait. sounds like angels are at work here
HOWEVER...if you are on iv abx that is great. i don't think i would rush out of there as long as that is happening.
what the idsa docs are telling you is what they tell everyone and that is why there are so many of us chroic lymies. in most cases 21 days of doxy does not kill lyme. occasionally-if everything goes right-yes, it can.
good for your primaries! but i doubt they will treat you long enough to make much difference. i'm not any kind of doc tho-just someone fighting this since 84
probably going from hosp to dr D is your best bet. you will get a good workup and know better where you stand. your abx will not be interupted.
all llmd's do not agree on tx either-and many of us go to one for a few years and then try another's protocols. many are better at one thing or another: neuro, psyc, ms ...depending on their research and experience. if you are not happy with dr D after awhile you can find one that is really up on viruses
i just kinda doubt if your primarys will go the distance with you unless they consult with an llmd or something
whenever you are in hosp it is good to have someone you trust close-who knows your wishes if things get bad and you have trouble making decisions. better to be ready.
-------------------- Lyme? Its complicated. Educate yourself. Posts: 13712 | From new england | Registered: Feb 2004
| IP: Logged |
posted
I was tested for babesia again at the hospital and that was negative. They are also testing me for Erlichia. Any other co-infections that you guys can think of?
I am considering have my PCP call Dr. Donta for a consult because I think she would do it. She has referred patients to him before and she is of the attitude that if long-term antibiotics work, they work.
TO be clear, I do not remember being bit by a tick, no rash and I do not go in to the woods, etc. I live in downtown Boston. That is why I am not convinced I ever had Lyme either.
But I want to take that possibility VERY seriously because I did have a positive by CDC standards. They think here that it was a false positive but from what I hear those are EXTREMELY rare.
I found it strange that Dr. Donta's office called me and offered me an opening on Monday when they are booking into February. Maybe he was very interested in my case? Maybe because I have a positive test that many never get? I don't know.
Posts: 24 | From Boston | Registered: Nov 2008
| IP: Logged |
lpkayak
Honored Contributor (10K+ posts)
Member # 5230
posted
there's lots of co infections but all testing is unreliable---a pos is a pos...but a neg means notheing
one of the biggest you didn't mention is bartonella-but testing is very bad
it responds to different abx than lyme
having your primary consult with dr D sounds great. it would be rally good to not interrupt your iv abx - many never get any
are you getting your pms? there is something important i would like to mention in private
Bless your heart. I'm sorry to hear that you are so sick.
I think your idea to have your PCP confer with Dr. D is a very, very good one. I think it's paramount, actually, given that you DO have a positive test for Lyme.
While I'm not hear to try and convince you that you have Lyme (that's not my place), I just thought I'd share with you some thoughts on the risk of exposure to Lyme.
A lot of people with Lyme do not ever remember having being bitten by a tick.
While the statistics have varied in the reading I've done, I've seen numbers of over 50% of the Lyme patients do not ever remember having a rash of any kind. And, many don't ever remember seeing a tick.
Since the ticks can be as small as a period at the end of a sentence, I can see why some never noticed them. Also, people can be bitten in areas of the body that they can't see (i.e., somewhere on the back of their bodies or on their scalps underneat the hair).
One does not have to have been in the woods for exposure. Virtually anywhere cats and dogs have been can be exposure enough. Cats and dogs, horses and another "domestic" pets are tick carriers. Birds are also carriers and they are everywhere.
As far as your question about additional testing for bacterium, below is what comes to my mind at the moment.
I know there is probably more testing -- I just can't think of it at the moment. Bear in mind that testing is limited because all of the pathogenic strains that are infecting people are not tested for. That is, there are plenty of vector borne infections that are transmitting to humans that the labs don't have the ability to test for right now. Clinical diagnosis from the physician is paramount.
Sometimes the testing needs to be done by specialty labs like Igenex for example. Some of these tests, I know, you say you've already been tested for:
Lyme Babesia Bartonella Erhlichiosis (HGE, HME) and Anaplasmosis (HGA) Mycoplasmas Chlamydia Pneumonia Rocky Mountain Spotted Fever Tularemia Rickettsia Tick Relapsing Fever I assume the ID docs have tested you for Staph and MRSA and Strep?
Perhaps others might have recommendations on viral testing. I know there is HHV-6, Epstein Barr Virus (which is frequently transmitted and/or reactivated with Lyme), and West Nile Virus.
Do you have family or friends that can support you while you're so sick in hospital?
Finally, I'm going to include an article by Doc D on Late Stage and Chronic Lyme in case you'd like to give it to your PCP. It might help her to read this as she consults with him.
I'll just paste it in a new post here in it's entirety. I know you're unwell and it's probably hard to click on a bunch of links right now.
Hang in there!
Fuzzy
Posts: 503 | From Maryland | Registered: Oct 2007
| IP: Logged |
posted
Med Clin North Am 2002 Mar;86(2):341-9, vii.
*LATE AND CHRONIC LYME DISEASE*- Sam T. Donta, MD* Prof. of Medicine, Divisions of Infectious Disease and BioMolecular Medicine Director, Lyme Disease Unit Boston University Medical Center, Boston, Massachusetts Corresponding author for proof and reprints: Sam T Donta MD 508-539-6666
*INTRODUCTION*
- 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.
*PATHOGENESIS*
- 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.
*DIAGNOSIS*
- 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.
*TREATMENT*
- 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 (eg 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.
*FUTURE*
- 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.
*REFERENCES *
1. Asch ES, Bujak DI, Weiss M, et al. Lyme Disease: an infectious and postinfectious syndrome. J Rheum 21:454-61, 1994. 2. Bakken LL, Case KL, Callister SM, et al. Performance of 45 laboratories participating in a proficiency testing program for Lyme Disease serology. JAMA 268:891-5, 1992. 3. Brouqui P, Bodiga S, and Raoult D. Eucaryotic cells protect Borrelia burgdorferi from the action of penicillin and ceftriaxone but not from the action of doxycycline and erythromycin. Antimicrob Agents Chemother 40:1552-4, 1996. 4. Cadavid D, O'Neill T, Schaefer H, and Pachner AR. Localization of Borrelia burgdorferi in the nervous system and other organs in a nonhuman primate model of Lyme disease. Lab Investigation 80:1043-54, 2000. 5. Centers for Disease Control. Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR 44:590-1, 1995. 6. Choppa PC, Vojdani A, Tagle C, et al. Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis, and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome. Mol Cell Probes. 12:301-8, 1998. 7. Donta ST. Lyme Disease: A clinical challenge. J Spirochet and Tick Dis 2:50-51, 1995. 8. Donta ST. Tetracycline therapy of chronic Lyme Disease. Clin Infect Dis 25: S52-56, 1997. 9. Donta ST: Reactivation of latent Lyme Disease. X Annual LDF International Conference on Lyme Borreliosis, National Institutes of Health, April 1997. 10.. Donta ST. Treatment of chronic Lyme disease with macrolide antibiotics. In: Program and abstracts of the VIIIth International Conference on Lyme Borreliosis; June 20-24, 1999; Munich, Germany. Abstract P193. 11. Donta ST: Reactivation of Lyme Disease following OspA vaccine. Int J Antimicrob Agents 17:S116-7, 2001. 12. Donta ST: The existence of chronic Lyme Disease. Current Treatment Options in Infectious Diseases 3:261-2, 2001. 13. Dressler F, Whalen JA, Reinhardt BN and Steere AC. Western blotting in the serodiagnosis of Lyme disease. J Infect Dis 167:392-400, 1993. 14. Fallon B and Nields JA. Lyme disease: a neuropsychiatric illness. Am J Psych 141:1571-83, 1994. 15. Feder HM Jr, Gerber M, and Krause PJ. Early Lyme disease: a flu-like illness without erythema migrans. Pediatrics 91:456-9, 1993. 16. Fister RD, Weymouth LA, McLaughlin JC, et al. Comparative evaluation of three products for the detection of Borrelia burgdorferi antibody in human serum. J Clin Microbiol 37:2834-7, 1989. 17. Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. J Infect Dis166:440-4, 1992. 18. Gross DM, Forsthuber T, Tary-Lehman M, et al. Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis. Science 281:703-6, 1998. 19. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme Disease N Engl J Med. 345: 85-92, 2001. 20. Levin JM, Nelson JA, Segretti J, et al. In vitro susceptibilities of Borrelia burgdorferi to 11 antimicrobial agents. Antimicrob Agents Chemother 37:1444-6, 1993. 21. Luft BJ, Dattwyler RJ, Johnson RC, et al. Azithromycin compared with amoxicillin in the treatment of erythema migrans. A double blind, randomized, controlled trial. Ann Int Med 124:785-91, 1996. 22. Maurin M, Benoliel AM, Bongrand P, and Raoult D. Phagolysosomal alkalinization and the bactericidal effect of antibiotics: the Coxiella burnetii paradigm. J Infect Dis 166:1097-102, 1992. 23. Nicolson GL, and Nicolson NL. Chronic infections as a common etiology for many patients with chronic fatigue syndrome, fibromyalgia, and Gulf War Illness. Intern J Med 1:42-6, 1998. 24. Pachner AR, Delaney E, O'Neill T, and Major E. Inoculation of nonhuman primates with the N40 strain of Borrelia burgdorferi leads to a model of Lyme neuroborreliosis faithful to the human disease. Neurology 45:165-72, 1995. 25. Preac-Mursic V, Wilske B, Schierz G, et al. In vitro and in vivo susceptibility of Borrelia burgdorferi. Eur J Clin Microbiol 6:424-6, 1987. 26. Roberts ED, Bohm RP Jr, Lowrie RC Jr, et al. Pathogenesis of Lyme neuroborreliosis in the Rhesus monkey: the early disseminated and chronic phases of disease in the peripheral nervous system. J Infect Dis 178:722-32, 1998. 27. Seltzer EG, Gerber MA, Carter ML, et al. Long-term outcomes of persons with Lyme disease. JAMA 283:609-616, 2000. 28. Shadick NA, Phillips CB, Logigian EL, et al. The long-term clinical outcomes of Lyme Disease. Ann Intern Med 121:560-7, 1994. 29. Steere AC, Malawista SE, Hardin JA, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med 86:685-98, 1977. 30. Steere AC. Lyme Disease. NEJM 345:115-25, 2001. 31. Straubinger RK. PCR-based quantification of Borrelia burgdorferi organisms in canine tissues over a 500-day postinfection period. J Clin Microbiology 38:2191-9, 2000. 32. Wormser G, Nadelman RB, Dattwyler RJ, et al. Practice guidelines for the treatment of Lyme disease. Clin Infect Dis 31(S1):S1-S14, 2001. 33. Ziska MH, Donta ST, and Demarest FC. Physician preferences in the diagnosis and treatment of Lyme Disease in the U.S. Infection 23:1-5, 1995.
Posts: 503 | From Maryland | Registered: Oct 2007
| IP: Logged |
posted
Also, just in case it might help you or your PCP, here is a short-list breakdown of symptoms that are sometimes seen with Lyme and some Co-Infections.
Taken from /Diagnostic Hints And Treatment Guidelines For Lyme And Other Tick Borne Illnesses/ /, by Dr. B.
/Short list:/
*/Borrelia/* *(Borreliosis, neuroborreliosis; also known as Lyme Disease)* /Spread primarily though the bite of infected ticks that live on a wide range of mammalian species; secondary human-to-human transmission through semen, breast milk, and possibly in utero/
Bladder dysfunction Burning or stabbing sensations Cardiac impairment Change in bowel function Chest pain Confusion Depression Difficulty thinking Difficulty with concentration and reading Difficulty with speech, writing Difficulty finding words; name blocking Disorientation: getting lost, going to wrong places Disturbed sleep: too much, too little, fractionated, early awakening Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity Exaggerated symptoms or worse hangover from alcohol Eyes/Vision: double, blurry, increased floaters, light sensitivity Facial paralysis (Bell's palsy) Fatigue, tiredness, poor stamina Forgetfulness Headache Heart block Heart murmur Heart palpitations Heart valve prolapse Increased motion sickness Irritability Irritable bladder Joint pain or swelling Lightheadedness Mood swings Muscle pain or cramps Neck creaks & cracks Neck stiffness, pain Numbness Pelvic pain Poor attention Poor balance Poor short-term memory Problem absorbing new information Pulse skips Rib soreness Sexual dysfunction or loss of libido Shooting pains Shortness of breath; cough Skin hypersensitivity Sore throat Stiffness of the joints or back Swollen glands Testicular pain Tingling Tremor Twitching of the face or other muscles Unavoidable need to sit or lay down Unexplained breast pain Unexplained fevers, sweats, chills or flushing Unexplained hair loss Unexplained menstrual irregularity' Unexplained milk production Unexplained weight loss or gain Upset Stomach or abdominal pain Vertigo Wooziness
*/Babesia/* *(Babesiosis)* Babesia is a protozoan spread by ticks, blood transfusion, and in utero. Despite there being 13 known forms to date, current testing only looks for two of them.
Air hunger Cough Fatigue Fevers Headache Hemolysis Imbalance without true vertigo Mild encephalopathy Shaking chills Sweats
*/Bartonella/* *(Bartonellosis, also known as cat scratch fever)* /Spread by bites from infected ticks and in utero/
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
If you can get into the LLMD on Monday - do it! Even if you leave the hospital for a couple of hours, do it! You still have your freedom. Even if you have a IV line in you, go! Even if you have to take a taxi, go! Please.
You have every right to sign yourself out for a 2nd opinion and come back if you want. Appointments with LLMDs are a rare chance.
To clear up a few things: 21 days of doxy will not cure lyme.
False positives are very rare - they are uneducated about lyme and testing. With your symptoms and the positive test, you need an expert. Anything less and your life is truly on the line.
LLMDs test and evaluate for other things besides lyme. They are much more educated in matters of all the other tick-borne diseases and other chronic or acute stealth infections as described below.
You say you live in downtown Boston. Well, you have the Boston Commons. Boston has birds. Boston has rodents. Do you ever garden? Have you? Have you ever been camping or walking in the woods or gardens?
With severe symptoms and a positive test it really seems that a seasoned expert would be the best way to go. Someone who has seen thousands of other patients with similar symptoms. You need that experience. You have a chance to see a LLMD on Monday. I hope you can make it. Do all you can, please.
On a similar note, when you said the hospital tested for other things, too, and came up empty, I wonder if they did the right tests at the right labs.
I think your current doctors are giving up too easily. And, oh, Tylenol can cause a liver to enlarge. It would not cause a fever, but the effect of Tylenol on a liver that may be dealing with toxins form infection should not be overlooked
--------
For thought concerning other possibilities with A "reprint" of an excellent post from Timaca:
I would encourage EVERY person who has received a lyme diagnosis to get the following tests.
This is because (1) you may really have a different pathogen causing your problem besides lyme, and it would be good to find that out.
(2) Lyme (as well as other pathogens) can cause the immune system to malfunction, allowing other pathogens to reactive. Thus you may be fighting lyme and other pathogens. This is what happened to me.
It really helps to get a thorough evaluation...then treat what is most obviously wrong.
Here's the info. I apologize ahead of time, for I don't know how to copy and past the long webpage links into the URL...and I'm sure not going to type the entire link in... I feel it is important to direct you right to the link.
Best, Timaca
========
If you have been ill with various multi-systemic symptoms and the doctors have run many tests on you and cannot figure out what is wrong, then consider getting these tests done.
40678 Lyme C6 peptide 2034 Lyme IgG and IgM western blot
Tick borne disease tests (Q-Fever through Lyme tests) can also be run at Igenex: www.igenex.com
Getting tested at Focus Diagnostics Lab can be a bit of a problem, unless your doctor has signed up for an account with them. Here's some links as to how to get the testing done. These links are at the HHV-6 website, and you must sign in to view the posts.
posted
Thank you everyone for all of your suggestions. They are not totally giving up on Lyme, just not their primary focus. I am still getting doxy and IV antibiotics.
My temps have been trending downward. My red and white blood cells are normal and my platlets are rising but still only around 80. They would ideally like to see 150 but would be happy with 100.
To the person that suggested candida and fungus - they just came a little bit ago to take blood to do a culture to check for a fungal infection. So thats a possibility too.
They are concious of the fact that the amount of tylenol I took may have caused the liver enlargement. My liver values are not seriously elevated and they did come down somewhat today.
Does anyone know if magnesium is related to Lyme. They gave me a magnesium IV yesterday because they said my numbers were low.
Here is the problem about the appointment Monday. I couldn't take it. I didn't know if I could go and she wasn't OK with me cancelling. I didn't want to not show up and then have them never see me. So, I'm going to call as soon as I get out of here and beg for them to see me soon and/or have my PCP talk with his office.
Thank you for the list of viruses to be checked for. They are running several different types of tests on each virus they are checking. I think that they are testing me for most. They said they can't do anything for some things - like HHV-6 so they don't test for it.
About my exposure to ticks. I do not leave the city of Boston much. I walk Lilly, my dog, around the common and downtown and she sometimes goes to my boyfriends parents house in the western burbs of Boston. We also did a charity MSPCA dog walk mid-september where we were around tons of dogs.
Lilly also had fleas. My bf found one on her about a week or two before I got sick but didn't know what it was and flicked it off of her. Then I found two more little black bugs on her (too big to be a tick). I gave her Frontline and now they are gone but there were def fleas on my dog during this process.
Its just frustrating to have a positive test for something but have that possibly not be what is making you sick!
Posts: 24 | From Boston | Registered: Nov 2008
| IP: Logged |
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
Fleas can spread lyme.
Magnesium IV are wonderful and should help the liver be able to detox, calm nerve fibers and help in other ways.
Lyme depletes magnesium. Seriously, that is one of the big problems. Lyme is a magnesium magnet, so to speak, taking it away from the body being able to use it.
I am VERY impressed that they considered a magnesium IV.
lpkayak
Honored Contributor (10K+ posts)
Member # 5230
posted
magnesium is VERY related to lyme. low mag is diagnostic in some ways
i can't explain the interaction-keets eat it or something...dr D will know this. is it melanie on here that could explain it? i forget.
don't rely on testing too much-unless it is done right it means nothing and costs a lot. even fungal or parasite testing in a hosp will probably not be done right
good luck. hope you get the consult going. there really is something i need to tell you about dr D and the way he treats-it is important
-------------------- Lyme? Its complicated. Educate yourself. Posts: 13712 | From new england | Registered: Feb 2004
| IP: Logged |
Keebler
Honored Contributor (25K+ posts)
Member # 12673
Bacterial zoonoses: emerging concepts - [Article in French]
Philippon A.
Service de bact�riologie, H�pital Cochin, 27 rue du faubourg Saint-Jacques, 75014 Paris.
Bacterial zoonoses are evolving with changes in society, climate and lifestyles. . . .
The creation of specific networks and reference centers has provided the means to monitor the emergence (or re-emergence) of zoonoses such as brucellosis and Q fever.
Molecular tools have facilitated the detection of bacteria that are transmitted by arthropod vectors (ticks, fleas, etc.) and that cause diseases such as Lyme borreliosis, bartonellosis and ehrlichiosis.
PMID: 17140097
==============
Clin Rheum Dis. 1986 Aug;12(2):343-67.
Lyme disease. By Goldings EA, Jericho J.
Although initially considered a localized epidemic form of arthritis. Lyme disease is now known to have protean manifestation (skin, joint, heart, nervous system) and worldwide distribution.
*** It is caused by infection with the spirochaete Borrelia burgdorferi and is transmitted by a variety of hard ticks and, in some localities, fleas. ***
Antigenic variation between isolates may determine the differences in clinical expression observed between cases in North America and Europe. The reservoir in the animal kingdom is primarily in deer and mice but house pets have also been implicated.
Prompt diagnosis assures the best outcome. . . . .
PMID: 3542350
--
Note: the treatment listed for lyme in this abstract is outdated, however the fact that pets and fleas can carry lyme is still not known by many. There is more literature that connects fleas - and pets - with lyme. I have come across it many times. However, I don't have the energy to continue searching.
There are also cases of lyme in patients in NYC who have rarely left the city - one who had never left. But he walked his dog in a park.
Good luck. I hope you feel better soon. Please keep us posted on how the appointment goes on Monday with the LLMD. I so hope you can call on his experience and assessment.
Well, you might have your answer. Fleas do transmit Lyme and other diseases as others have mentioned here in this thread. I know that they also transmit Bartonella -- a co-infection that is commonly seen with Lyme. There are quite a few published medical articles that speak to fleas and transmission of disease. Keebler has provided you with evidence of some above.
Yes, magnesium deficiency is seen with Lyme infection.
Please tell your physicians at the hospital, your PCP and any LLMD that you consult with about the "bugs" on your dog and the fleas.
This could be really important. You might have your answer to your "risk of exposure" right there.
Please let us know how you get on, k?
Fuzzy
Posts: 503 | From Maryland | Registered: Oct 2007
| IP: Logged |
posted
What hospital are you at?? I ask only because while under the care of Dr. D, I was hospitalized at Boston hospital and made a number of contacts. My test results were EXACTLY the same as yours and I had similar discussions with the ID team at the hospital that you are having. Anyway, depending, I might be able to offer you some help/resources!!
Another thought....have them test you for Brucella...
Please feel free to PM me.
Kristin
Posts: 561 | From mass | Registered: Jul 2007
| IP: Logged |
posted
cleaned it out.....
Posts: 561 | From mass | Registered: Jul 2007
| IP: Logged |
gemofnj
Frequent Contributor (1K+ posts)
Member # 15551
posted
Boston,
At least your current doctors are ruling out other possibile serious disease, but...
Hoping you are going to the LLMD tomorrow!!
drs. dont usually use the CD 57 test to diagnose lyme, but you might consider getting it. It should be done by Labcorp and it is a specific marker for lyme. If it is lower than 60 it may help diagnose lyme.
My ID doctor told me I had a false positive too. They tested me for all coinfections and it came up negative. Never found a tick.
In the past, my heart was beating very irregular which is not uncommon in lyme patients. My PCP thought I had a heart attack.
I am still undergoing treatment for lyme after 6+ months. Have remarkably improved to 95%.
Lyme patients are commonly low in magnesium.
21 days of doxy does not kill lyme.
Even tho you live in Boston, is it possible you visited a relative that lives in an area that does have ticks? or a relative with a pet from that area visit you? or traveled on business to one?
I guess you know your pet can also transmit ticks or fleas with lyme.
Coinfections sometimes dont show up unless you get tested by more reliable labs that specialize in coinfections.
I do hope you get to your LLMD visit tomorrow. GOOD LUCK hope you feel better SOON.
Posts: 1127 | From atlantic city, nj | Registered: May 2008
| IP: Logged |
is it possible you visited a relative that lives in an area that does have ticks? or a relative with a pet from that area visit you? or traveled on business to one?
Gemofny and others (Boston03 has already heard this):
I just want to point out that we do not have to live or visit the 'burbs or the Cape to contract lyme, necessarily.
I live in Somerville, MA-- the most-densely populated city outside Manhattan and the industrial NJ cities---
and there are ticks galore in the bushes outside my condo complex. Last year they weren't even noticeable.
I was presumably bitten by one this past July (found engorged tick in my house) as we were tracking the ticks hanging out at the end of the tendrils (overhanging a stone wall! yes, a STONE wall!) into my house. I saw one on the ceiling a couple weeks ago.
This is in the dead of the city. I wish I could provide photos to everyone so you can see the ideal habitat on a city street. I and another person on my street have lyme, along with my sister.
There are infected ticks in the small parks in London, England. So why not in parks here?
Where there are rodents, there are ticks, and there are rodents and birds to carry them--- and there is tick-borne disease.
The rodent population has burgeoned since the depression of the central artery in Boston, along with other major construction, and replacement of old pipes in the streets in Boston, Cambridge and Somerville neighborhoods. Their habitat was displaced and they are wandering the streets in broad daylight.
Where they are dogs and people brushing against branches---there is transmission to pets and humans.
Boston03 participated in a dog walk with 1000 dogs? My PCP would check off the list next to "Exposure" without missing a beat.
It's a very scary situation for her and it really seems like co-infections are in the mix. Which are not treated with Antibiotics necessarily (Babesia) and for which, like lyme, there are no definitive tests. I don't know about mycoplasma. Y'all would know more about the co-s than me.
I really don't know why ID doctors look to tests when EVEN the CDC itself states that it is a clinical diagnosis and that testing should be used for surveillance, not diagnosis. Seriously, I just don't get it.
I hope it's actually an infection that is easier to cure than TBD. We can only hope.
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
![[group hug]](graemlins/grouphug.gif)
![[kiss]](graemlins/kissing.gif)
![[Eek!]](eek.gif)
![[Smile]](smile.gif)
Printer-friendly view of this topic