Antibiotics and Steroids
From:
Lyme Disease 1991: Patient/Physician Perspectives from the U.S. and Canada
Lora Mermin, editor
by John Drulle, M.D.
"Corticosteroids, or steroids as they are commonly called, are very important drugs in a wide variety of medical conditions. They exert an anti-inflammatory effect and suppress the immune system. This may be life saving in some diseases such as asthma and malignancies. On the other hand, steroids are rarely curative, and are associated with harmful side effects if used for prolonged periods of time. These include bone loss, cataracts, sodium retention, weight gain, abnormal fat distribution and predisposition in other infections.
"The use of steroids in infectious diseases has always been controversial. It is well known that steroids can reactivate dormant tuberculosis infections.
Recent studies have shown that in meningitis infections steroids may decrease the incidence of post infectious complications. However, in cases of septic shock, their ability to improve survival rates is dubious. We have been traditionaly taught that in bacterial infections an intact, well-functioning immune system is necessary in order to recover. Steroids in the face of bacterial infections may alter the prognosis and in tuberculosis may actually increase the risk of fatality.
"Since Lyme is a bacterial infection, the question naturally arises as to what is the role of steroids in Lyme disease. Before the bacterial nature of Lyme was discovered, it was common to treat the arthritis complications and heart blocks with steroids. Early reports suggested that the heart blocks responded well to the steroids. However, in one report dealing with patients with Lyme arthritis, steroid injections into the joints prior to antibiotic therapy were associated with a worse prognosis when antibiotics were finally given. We have seen literally dozens of patients with Lyme who were initially treated with steroids who reported a dramatic worsening rather than improvement as would be expected. Dr. Joseph Burrascano has coined the expression, ' Steroid Disasters, ' to describe these patients.
"It is interesting to note that in dogs who had Lyme disease, injections of dexamethasone, a corticosteroid, enabled Borrelia burgdorferi to be cultured from blood drawn on the following day. This was done by Dr. Elizabeth Burgess at the University of Wisconsin. This suggests that the steroid suppresses a mechanism for keeping the bacteria out of the circulatory system, since ordinarily it is difficult to grow the Lyme organism from the blood. Entrance of the bacteria into the bloodstream can allow seeding of other organs.
"I have used steroids in Lyme patients, but only in very selected circumstances. In patients who have presented with eye involvement with rapidly deteriorating vision, such as optic neuritis or uveitis, the combination of high dose steroids appears to restore vision more rapidly than by using antibiotics alone. I have also used steroids in combination with antibiotics in patients who presented with a Lyme induced polymyalgia rheumatica (PMR). "PMR is a common disease of elderly people characterized by pain and stiffness in the muscles of the upper arms and legs, fevers, malaise and weight loss. The ESR, sedimentation rate is elevated. In its classic form, the cause of the condition is unknown, and the
dramatic response to steroids is in itself diagnostic. I have personally seen three cases of Lyme induced PMR, which did not respond to steroids alone or antibiotics alone, yet when the combination was given the response was dramatic.
"In conclusion, the decision to use the steroids in a Lyme patient must be given considerable thought and the possible benefits must be weighed against the risks. I would not use steroids unless the patient was also on antibiotics."
http://www.lymenet.de/literatur/steroids.htm
-------------------------------
Clin Diagn Lab Immunol. 2001 Mar;8(2):225-32.
Lyme borreliosis in rhesus macaques: effects of corticosteroids on spirochetal load and isotype switching of anti-borrelia burgdorferi antibody.
Pachner AR, Amemiya K, Bartlett M, Schaefer H, Reddy K, Zhang WF.
Department of Neurosciences, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, 185 S. Orange St., Newark, NJ 07103, USA. pachner@umdnj.edu
Experimental Borrelia burgdorferi infection of rhesus monkeys is an excellent model of Lyme disease and closely parallels the infection in humans.
Little is known about the interaction of host immunity with the spirochete in patients with chronic infection.
We hypothesized that rapid development of anti-B. burgdorferi antibody in immunocompetent nonhuman primates (NHPs) is the major determinant of the reduction of the spirochetal load in Lyme borreliosis. This hypothesis was tested by measurement of the spirochetal load by PCR in association with characterization of the anti-B. burgdorferi humoral immune response in immunocompetent NHPs versus that in corticosteroid-treated NHPs.
Although anti-B. burgdorferi immunoglobulin G (IgG) antibody was effectively inhibited in dexamethasone (Dex)-treated NHPs, anti-B. burgdorferi IgM antibody levels continued to rise after the first month and reached levels in excess of IgM levels in immunocompetent NHPs.
This vigorous production of anti-B. burgdorferi IgM antibodies was also studied in vitro by measurement of antibody produced by B. burgdorferi-stimulated peripheral blood mononuclear cells. Despite these high IgM antispirochetal antibodies in Dex-treated NHPs, spirochetal loads were much higher in these animals.
These data indicate that Dex treatment results in interference with isotype switching in this model and provide evidence that anti-B. burgdorferi IgG antibody is much more effective than IgM antibody in decreasing the spirochetal load in infected animals.
PMID: 11238200 [PubMed - indexed for MEDLINE]
Full PDF version:
http://cvi.asm.org/cgi/reprint/8/2/225
The full paper concludes:
In human infections, corticosteroids are sometimes used for the treatment of clinical syndromes such as facial paralysis or arthritis, when these problems are thought to be idiopathic.
The data presented above demonstrate the interplay between host immunity and spirochetal infection in Lyme borreliosis and the importance of a competent immune response in limiting the spirochetal load. Since the diagnosis of Lyme borreliosis may sometimes be difficult to make, there is a risk in areas of endemicity of using corticosteroids as therapy in inflammatory syndromes that could represent Lyme disease.
[Also noteworthy is the chart on page 7 showing that the highest spirochetal load was found in the apex of the heart and the base of the heart.]
---------------------------------
Copied from "Lyme disease and the Heart" and posted here because this paper addresses both topics. The paper above and this one contain different comments about steroid effects on IgG.
Both were signed by Andrew Pachner.
Laboratory Investigation (2004) 84, 1439–1450,
27 September 2004; doi:10.1038/labinvest.3700177
Cardiac involvement in non-human primates infected with the Lyme disease spirochete Borrelia burgdorferi
Diego Cadavid1,2, Yunhong Bai1,2, Emir Hodzic3, Kavitha Narayan1, Steven W Barthold3 and Andrew R Pachner1
Abstract
To investigate cardiac involvement in the non-human primate (NHP) model of Lyme disease, we inoculated 39 adult Macaca mulatta with Borrelia burgdorferi sensu stricto strains N40 (BbN40) by needle (N=22, 14 immunocompetent (IC), seven permanently immunosuppressed (IS), and four transiently immunosuppressed (TISP)) or by tick-bite (N=4, all TISP) or strain 297 (Bb297) by needle (N=2 IS), or with B. garinii strains Pbi (N=4, 2 TISP and 2 IS), 793 (N=2, TISP) or Pli (N=2, TISP).
Five uninfected NHPs were used as controls. Infection and inflammation was studied in the hearts and the aorta removed at necropsy 2–32 months after inoculation by (1) H&E and trichrome-staining; (2) immunohistochemistry and digital image analysis; (3) Western blot densitometry; and (4) TaqMan RT-PCR.
All NHPs inoculated with BbN40 became infected and showed carditis at necropsy. The predominant cells were T cells, plasma cells, and macrophages.
There was increased IgG and IgM in the heart independent of immunosuppression.
The B-cell chemokine BLC was significantly increased in IS-NHPs. There was increased deposition of the complement membrane attack complex (MAC) in TISP and IS-NHPs. The spirochetal load was very high in all BbN40-inoculated IS-NHPs but minimal if any in IC or TISP NHPs. Double-immunostaining revealed that many spirochetes in the heart of BbN40-IS NHPs had MAC on their membranes.
We conclude that carditis in NHPs infected with B. burgdorferi is frequent and can persist for years but is mild unless they are immunosupressed.
http://www.nature.com/labinvest/journal ... 00177a.pdf
[Some selections from the full version:]
During infection of immunosuppressed NHPs inoculated with the sensu stricto strain N40 of B. burgdorferi (BbN40), we found that the heart had the most severe injury of all tissues examined and one of the highest spirochetal loads.
These results showed that in steroid-treated NHPs heavily infected with BbN40, MAC binds to but does not kill spirochetes.
Another possibility for the higher spirochetal load in steroid-treated animals is impaired complement activation that is required for efficient spirochetal killing. In the absence of specific antibody B. burgdorferi is resistant to the bactericidal activity of complement.
Expression of the B-cell chemokine BLC [CXCL13] was increased accordingly to the spirochetal load.
In humans with Lyme disease, carditis is found in up to 25%, but only rarely pathology specimens are available for examination.
---------------------------------
Pachner, 2001:
"Although anti-B. burgdorferi immunoglobulin G (IgG) antibody was effectively inhibited in dexamethasone (Dex)-treated NHPs, anti-B. burgdorferi IgM antibody levels continued to rise after the first month and reached levels in excess of IgM levels in immunocompetent NHPs."
Pachner, 2004:
"There was increased IgG and IgM in the heart independent of immunosuppression. "
----------------------------------
Med Mal Infect. 2007 Jul-Aug;37(7-8):473-8. Epub 2007 Mar 21. Links
[Non antibiotic treatments of Lyme borreliosis]
[Article in French]
Puéchal X.
Service de rhumatologie, centre hospitalier du Mans, 194, avenue Rubillard, 72037 Le Mans cedex 09, France. xpuechal@ch-lemans.fr
Non-antibiotic treatment of Lyme borreliosis is only indicated in a few specific clinical situations. In chronic Lyme arthritis, intra-articular steroids are useful to immediately relieve symptomatic joint effusion. Nevertheless, 4 studies with weak methodological evidence were convergent enough to recommend not proposing intra-articular injection before or even immediately after antibiotic treatment. The injection can only be recommended in the treatment of patients whose joint effusion persists despite 2 courses of oral antibiotherapy or one course of IV antibiotherapy. For some experts, the injection can only be made after negative PCR assessment of the joint fluid for spirochetes. This recommendation, although logical, has never been evaluated. Radiation synovectomy may be indicated in persistent synovitis after antibiotherapy and before surgical synovectomy. Further studies are mandatory to confirm the role of radiation synovectomy in the local therapy. Arthroscopic synovectomy can reduce the period of joint inflammation when persistent synovitis is associated with significant pain or limited function. Several experts recommend using the procedure only if synovitis persists after 2 months of antibiotherapy and a negative PCR joint fluid assessment. Non-steroidal anti-inflammatory drugs are often prescribed for their symptomatic effects. Experimental data is consensual on the deleterious consequences of systemic corticosteroid therapy. Corticosteroids are not indicated in Lyme's disease. In post Lyme's disease syndrome, patient complaints may lead to a multidisciplinary therapeutic management and the use of neuro-psychiatric drugs.
PMID: 17376627
-----------------------------------
Steroids and Lyme Disease a recipe of disaster
Doctors tell you that steroids (cortisone, prednisone, etc.) only cause side effects after many years of use. But new research shows that permanent damage is immediate and devastating. Studies show that steroids can cause permanent, debilitating effects after a single dosage. Inflammation contributes to more pain, disease, and disability than any other condition.
Far from being a wonder drug 'cure all', steroids cannot cure one single condition. All they do is suppress your body's ability to express a normal response. In a few instances, this type of suppression will give the body a chance to heal itself. But more often, the effect is immediate, devastating and permanent damage. And we are only now realizing just how quickly damage can occur. Despite
http://www.shirleys-wellness- cafe.com/steroids.htm
article regarding Lyme and steroids:
http://www.lymenet.de/ literatur/steroids.htm
"Steroid Disaster" is a term coined by the pioneer of Lyme Treatment, Dr. Burrascano (see link at bottom of page).
Corticosteroids supress the immune system, the last thing a Lyme patient needs is to lower immunity. Can you imagine, your body trying hard to fight off the spirochete bacteria and suddenly and immunosuppressants is introduced, "freezing" your immune system, rendering it unable to battle, giving great advantage now to the Lyme bacteria to spread and go wherever it wants and it does!
Corticosteroids can last in the body for months, usually around 6 months. With LD this gives many months for the bacteria to spread, possibly cause damage & according to Dr. Burrascano the prognosis can be much worse.
Many Lyme patients (such as myself) triggered LD with cortisone shots, pills, inhalers, etc. I can tell you, it is a nightmare I wouldn't wish on my worst enemy.
It is important to list on all medical charts and pharmacies that you have an allergy to corticosteroids. If surgery is in your future or an unexpected ER visit, make it known without a doubt you do not want any corticosteroids due to "allergic reaction".
It is imperative to NEVER take corticosteroid for pain if you know you have a bacterial infection. Some bacterial infections are so severe that a shot of cortisone could kill you, although that would be unlikely with Lyme, but rule of thumb, bacterial infections and immunosuppressants do not mix!
If you ever do any shots to relieve pain, tell the Md to leave out the steroid and use lidocaine or procaine only should be safe, ask your LLMD. Many Md's mainstream Md's are shying away from corticosteroid use, I noticed this when I was searching for pain relief and 2 doctor's were extremely hesitant and then refused to give me corticosteroids of any kind. I didn't know I had LD at the time and looking back, I was hell bent to get a cortisone shot, I was hurting! I found the Md that would do it and basically I can only tell you the pain that followed I never knew existed. Like a grenade had gone off internally and shrapnel flying, every part of me hurt, every tendon, muscle and nerve scalp to feet. I write this at 3.5 years after those shots were given to me. I have a long, long way to go...if I ever recover. Scary and extremely painful is my world, so I warn you PLEASE don't risk corticosteroids.
Having had steroid injections before realizing I had LD, I consider myself lucky to be alive today, so much "exploded" in me, I am amazed as I sit and type this I am able to do so. So many who have used corticosteroids wish they never had, but didn't know better, it has activated lyme, disseminated it and made it much harder to treat, not to mention again PAIN that you could not imagine!
The main thing always overlooked that is most important - corticosteroids release dormant viruses (we ALL have dormant viruses residing in our spine) especially if IV, trigger point injections or facet joint injections are done near the spine. Mine were in the shoulder blade area. Viruses released as well and spread everywhere in my body 4 in all, they can make pain much worse and mixed w/Ld a nightmare. We have all been exposed to viruses in our lifetime through saliva, contact with others infected or even airborne, for instance Chicken Pox reactivated can be something entirely different, shingles, shingles can be localized or systemic (internally and body wide) Mono from the Epstein Barr virus reactivated can cause pain and neuropathy just as an example. You have dormant viruses, it is fact.
Once released they can be dangerous. If you have had corticosteroids at all, especially if you have pain that is not manageable, insist upon viral testing.
Know how to read a viral report, if either the IgG or IgM show out range you ARE infected w/viruses, many doctor's only look at the IgM (meaning active - IgG meaning past exposure) and may be wrong. There is much argument in the medical community as to the meaning of IgG...IgM is clearly active, IgG positive tests, the line blurs as to whethr you are actively infected or not.
An ID MD at Standford explains that doctor's often are mistaken in believing that the IgM needs to be positive to prove active infections. More information is here under our viral link.
Also what viruses to test for: viewtopic.php?f=6&t=55
An extremely high profile LLMD (lyme literate Md) who worked with HIV patients in the 80's has told me personally that "the IgM must be positive for active infection". I must admit both Md's make valid points.
Dr. Burrascano makes it clear in his treatment guidelines that steroid treatment is detrimental, these are excerpts from his guidelines:
"More evidence has accumulated indicating the severe detrimental effects of the concurrent use of immunosuppressants including steroids in the patient with active B. burgdorferi infection.. Never give steroids or any other immunosuppressant to any patient who may even remotely be suffering from Lyme, or serious, permanent damage may result, especially if given for anything greater than a short course. If immunosuppressive therapy is absolutely necessary, then potent antibiotic treatment should begin at least 48 hours prior to the immunosuppressants. The severity of the clinical illness is directly proportional to the spirochete load, the duration of infection, and the presence of co-infections.
These factors also are proportional to the intensity and duration of treatment needed for recovery.
More severe illness also results from other causes of weakened defenses, such as from severe stress, immunosuppressants medications, and severe intercurrent illnesses. This is why steroids and other immunosuppressants medications are absolutely contraindicated in Lyme. This also includes intra-articular steroids." (definiton of intra-articular: situated within, occurring within)
See page 12 paragraph 3 for this quote in Burrascano's treatment guidelines.
http://www.ilads.org/files/ burrascano_0905.pdf
An easy explanation. Your immune system are the "soldiers" of your body constantly standing by to attack any foreign invader. When an immunosuppressant is used, it is like killing off or knocking out most of your "army", now your body is open to all foreign invasion and while your immune system is knocked out, those invaders can go anywhere, your heart, liver, brain - everywhere. Steroids to a lyme patient are like kryptonite to Superman.
---------------------------
From:
Lyme Disease 1991: Patient/Physician Perspectives from the U.S. and Canada
Lora Mermin, editor
by John Drulle, M.D.
"Corticosteroids, or steroids as they are commonly called, are very important drugs in a wide variety of medical conditions. They exert an anti-inflammatory effect and suppress the immune system. This may be life saving in some diseases such as asthma and malignancies. On the other hand, steroids are rarely curative, and are associated with harmful side effects if used for prolonged periods of time. These include bone loss, cataracts, sodium retention, weight gain, abnormal fat distribution and predisposition in other infections.
"The use of steroids in infectious diseases has always been controversial. It is well known that steroids can reactivate dormant tuberculosis infections.
Recent studies have shown that in meningitis infections steroids may decrease the incidence of post infectious complications. However, in cases of septic shock, their ability to improve survival rates is dubious. We have been traditionaly taught that in bacterial infections an intact, well-functioning immune system is necessary in order to recover. Steroids in the face of bacterial infections may alter the prognosis and in tuberculosis may actually increase the risk of fatality.
"Since Lyme is a bacterial infection, the question naturally arises as to what is the role of steroids in Lyme disease. Before the bacterial nature of Lyme was discovered, it was common to treat the arthritis complications and heart blocks with steroids. Early reports suggested that the heart blocks responded well to the steroids. However, in one report dealing with patients with Lyme arthritis, steroid injections into the joints prior to antibiotic therapy were associated with a worse prognosis when antibiotics were finally given. We have seen literally dozens of patients with Lyme who were initially treated with steroids who reported a dramatic worsening rather than improvement as would be expected. Dr. Joseph Burrascano has coined the expression, ' Steroid Disasters, ' to describe these patients.
"It is interesting to note that in dogs who had Lyme disease, injections of dexamethasone, a corticosteroid, enabled Borrelia burgdorferi to be cultured from blood drawn on the following day. This was done by Dr. Elizabeth Burgess at the University of Wisconsin. This suggests that the steroid suppresses a mechanism for keeping the bacteria out of the circulatory system, since ordinarily it is difficult to grow the Lyme organism from the blood. Entrance of the bacteria into the bloodstream can allow seeding of other organs.
"I have used steroids in Lyme patients, but only in very selected circumstances. In patients who have presented with eye involvement with rapidly deteriorating vision, such as optic neuritis or uveitis, the combination of high dose steroids appears to restore vision more rapidly than by using antibiotics alone. I have also used steroids in combination with antibiotics in patients who presented with a Lyme induced polymyalgia rheumatica (PMR). "PMR is a common disease of elderly people characterized by pain and stiffness in the muscles of the upper arms and legs, fevers, malaise and weight loss. The ESR, sedimentation rate is elevated. In its classic form, the cause of the condition is unknown, and the
dramatic response to steroids is in itself diagnostic. I have personally seen three cases of Lyme induced PMR, which did not respond to steroids alone or antibiotics alone, yet when the combination was given the response was dramatic.
"In conclusion, the decision to use the steroids in a Lyme patient must be given considerable thought and the possible benefits must be weighed against the risks. I would not use steroids unless the patient was also on antibiotics."
http://www.lymenet.de/literatur/steroids.htm
-------------------------------
Clin Diagn Lab Immunol. 2001 Mar;8(2):225-32.
Lyme borreliosis in rhesus macaques: effects of corticosteroids on spirochetal load and isotype switching of anti-borrelia burgdorferi antibody.
Pachner AR, Amemiya K, Bartlett M, Schaefer H, Reddy K, Zhang WF.
Department of Neurosciences, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, 185 S. Orange St., Newark, NJ 07103, USA. pachner@umdnj.edu
Experimental Borrelia burgdorferi infection of rhesus monkeys is an excellent model of Lyme disease and closely parallels the infection in humans.
Little is known about the interaction of host immunity with the spirochete in patients with chronic infection.
We hypothesized that rapid development of anti-B. burgdorferi antibody in immunocompetent nonhuman primates (NHPs) is the major determinant of the reduction of the spirochetal load in Lyme borreliosis. This hypothesis was tested by measurement of the spirochetal load by PCR in association with characterization of the anti-B. burgdorferi humoral immune response in immunocompetent NHPs versus that in corticosteroid-treated NHPs.
Although anti-B. burgdorferi immunoglobulin G (IgG) antibody was effectively inhibited in dexamethasone (Dex)-treated NHPs, anti-B. burgdorferi IgM antibody levels continued to rise after the first month and reached levels in excess of IgM levels in immunocompetent NHPs.
This vigorous production of anti-B. burgdorferi IgM antibodies was also studied in vitro by measurement of antibody produced by B. burgdorferi-stimulated peripheral blood mononuclear cells. Despite these high IgM antispirochetal antibodies in Dex-treated NHPs, spirochetal loads were much higher in these animals.
These data indicate that Dex treatment results in interference with isotype switching in this model and provide evidence that anti-B. burgdorferi IgG antibody is much more effective than IgM antibody in decreasing the spirochetal load in infected animals.
PMID: 11238200 [PubMed - indexed for MEDLINE]
Full PDF version:
http://cvi.asm.org/cgi/reprint/8/2/225
The full paper concludes:
In human infections, corticosteroids are sometimes used for the treatment of clinical syndromes such as facial paralysis or arthritis, when these problems are thought to be idiopathic.
The data presented above demonstrate the interplay between host immunity and spirochetal infection in Lyme borreliosis and the importance of a competent immune response in limiting the spirochetal load. Since the diagnosis of Lyme borreliosis may sometimes be difficult to make, there is a risk in areas of endemicity of using corticosteroids as therapy in inflammatory syndromes that could represent Lyme disease.
[Also noteworthy is the chart on page 7 showing that the highest spirochetal load was found in the apex of the heart and the base of the heart.]
---------------------------------
Copied from "Lyme disease and the Heart" and posted here because this paper addresses both topics. The paper above and this one contain different comments about steroid effects on IgG.
Both were signed by Andrew Pachner.
Laboratory Investigation (2004) 84, 1439–1450,
27 September 2004; doi:10.1038/labinvest.3700177
Cardiac involvement in non-human primates infected with the Lyme disease spirochete Borrelia burgdorferi
Diego Cadavid1,2, Yunhong Bai1,2, Emir Hodzic3, Kavitha Narayan1, Steven W Barthold3 and Andrew R Pachner1
Abstract
To investigate cardiac involvement in the non-human primate (NHP) model of Lyme disease, we inoculated 39 adult Macaca mulatta with Borrelia burgdorferi sensu stricto strains N40 (BbN40) by needle (N=22, 14 immunocompetent (IC), seven permanently immunosuppressed (IS), and four transiently immunosuppressed (TISP)) or by tick-bite (N=4, all TISP) or strain 297 (Bb297) by needle (N=2 IS), or with B. garinii strains Pbi (N=4, 2 TISP and 2 IS), 793 (N=2, TISP) or Pli (N=2, TISP).
Five uninfected NHPs were used as controls. Infection and inflammation was studied in the hearts and the aorta removed at necropsy 2–32 months after inoculation by (1) H&E and trichrome-staining; (2) immunohistochemistry and digital image analysis; (3) Western blot densitometry; and (4) TaqMan RT-PCR.
All NHPs inoculated with BbN40 became infected and showed carditis at necropsy. The predominant cells were T cells, plasma cells, and macrophages.
There was increased IgG and IgM in the heart independent of immunosuppression.
The B-cell chemokine BLC was significantly increased in IS-NHPs. There was increased deposition of the complement membrane attack complex (MAC) in TISP and IS-NHPs. The spirochetal load was very high in all BbN40-inoculated IS-NHPs but minimal if any in IC or TISP NHPs. Double-immunostaining revealed that many spirochetes in the heart of BbN40-IS NHPs had MAC on their membranes.
We conclude that carditis in NHPs infected with B. burgdorferi is frequent and can persist for years but is mild unless they are immunosupressed.
http://www.nature.com/labinvest/journal ... 00177a.pdf
[Some selections from the full version:]
During infection of immunosuppressed NHPs inoculated with the sensu stricto strain N40 of B. burgdorferi (BbN40), we found that the heart had the most severe injury of all tissues examined and one of the highest spirochetal loads.
These results showed that in steroid-treated NHPs heavily infected with BbN40, MAC binds to but does not kill spirochetes.
Another possibility for the higher spirochetal load in steroid-treated animals is impaired complement activation that is required for efficient spirochetal killing. In the absence of specific antibody B. burgdorferi is resistant to the bactericidal activity of complement.
Expression of the B-cell chemokine BLC [CXCL13] was increased accordingly to the spirochetal load.
In humans with Lyme disease, carditis is found in up to 25%, but only rarely pathology specimens are available for examination.
---------------------------------
Pachner, 2001:
"Although anti-B. burgdorferi immunoglobulin G (IgG) antibody was effectively inhibited in dexamethasone (Dex)-treated NHPs, anti-B. burgdorferi IgM antibody levels continued to rise after the first month and reached levels in excess of IgM levels in immunocompetent NHPs."
Pachner, 2004:
"There was increased IgG and IgM in the heart independent of immunosuppression. "
----------------------------------
Med Mal Infect. 2007 Jul-Aug;37(7-8):473-8. Epub 2007 Mar 21. Links
[Non antibiotic treatments of Lyme borreliosis]
[Article in French]
Puéchal X.
Service de rhumatologie, centre hospitalier du Mans, 194, avenue Rubillard, 72037 Le Mans cedex 09, France. xpuechal@ch-lemans.fr
Non-antibiotic treatment of Lyme borreliosis is only indicated in a few specific clinical situations. In chronic Lyme arthritis, intra-articular steroids are useful to immediately relieve symptomatic joint effusion. Nevertheless, 4 studies with weak methodological evidence were convergent enough to recommend not proposing intra-articular injection before or even immediately after antibiotic treatment. The injection can only be recommended in the treatment of patients whose joint effusion persists despite 2 courses of oral antibiotherapy or one course of IV antibiotherapy. For some experts, the injection can only be made after negative PCR assessment of the joint fluid for spirochetes. This recommendation, although logical, has never been evaluated. Radiation synovectomy may be indicated in persistent synovitis after antibiotherapy and before surgical synovectomy. Further studies are mandatory to confirm the role of radiation synovectomy in the local therapy. Arthroscopic synovectomy can reduce the period of joint inflammation when persistent synovitis is associated with significant pain or limited function. Several experts recommend using the procedure only if synovitis persists after 2 months of antibiotherapy and a negative PCR joint fluid assessment. Non-steroidal anti-inflammatory drugs are often prescribed for their symptomatic effects. Experimental data is consensual on the deleterious consequences of systemic corticosteroid therapy. Corticosteroids are not indicated in Lyme's disease. In post Lyme's disease syndrome, patient complaints may lead to a multidisciplinary therapeutic management and the use of neuro-psychiatric drugs.
PMID: 17376627
-----------------------------------
Steroids and Lyme Disease a recipe of disaster
Doctors tell you that steroids (cortisone, prednisone, etc.) only cause side effects after many years of use. But new research shows that permanent damage is immediate and devastating. Studies show that steroids can cause permanent, debilitating effects after a single dosage. Inflammation contributes to more pain, disease, and disability than any other condition.
Far from being a wonder drug 'cure all', steroids cannot cure one single condition. All they do is suppress your body's ability to express a normal response. In a few instances, this type of suppression will give the body a chance to heal itself. But more often, the effect is immediate, devastating and permanent damage. And we are only now realizing just how quickly damage can occur. Despite
what doctors say, that steroids only have side effects after many years of use, there is no such thing as a safe dose. Full article at this link:
http://www.shirleys-wellness- cafe.com/steroids.htm
article regarding Lyme and steroids:
http://www.lymenet.de/ literatur/steroids.htm
"Steroid Disaster" is a term coined by the pioneer of Lyme Treatment, Dr. Burrascano (see link at bottom of page).
Corticosteroids supress the immune system, the last thing a Lyme patient needs is to lower immunity. Can you imagine, your body trying hard to fight off the spirochete bacteria and suddenly and immunosuppressants is introduced, "freezing" your immune system, rendering it unable to battle, giving great advantage now to the Lyme bacteria to spread and go wherever it wants and it does!
Corticosteroids can last in the body for months, usually around 6 months. With LD this gives many months for the bacteria to spread, possibly cause damage & according to Dr. Burrascano the prognosis can be much worse.
Many Lyme patients (such as myself) triggered LD with cortisone shots, pills, inhalers, etc. I can tell you, it is a nightmare I wouldn't wish on my worst enemy.
It is important to list on all medical charts and pharmacies that you have an allergy to corticosteroids. If surgery is in your future or an unexpected ER visit, make it known without a doubt you do not want any corticosteroids due to "allergic reaction".
It is imperative to NEVER take corticosteroid for pain if you know you have a bacterial infection. Some bacterial infections are so severe that a shot of cortisone could kill you, although that would be unlikely with Lyme, but rule of thumb, bacterial infections and immunosuppressants do not mix!
If you ever do any shots to relieve pain, tell the Md to leave out the steroid and use lidocaine or procaine only should be safe, ask your LLMD. Many Md's mainstream Md's are shying away from corticosteroid use, I noticed this when I was searching for pain relief and 2 doctor's were extremely hesitant and then refused to give me corticosteroids of any kind. I didn't know I had LD at the time and looking back, I was hell bent to get a cortisone shot, I was hurting! I found the Md that would do it and basically I can only tell you the pain that followed I never knew existed. Like a grenade had gone off internally and shrapnel flying, every part of me hurt, every tendon, muscle and nerve scalp to feet. I write this at 3.5 years after those shots were given to me. I have a long, long way to go...if I ever recover. Scary and extremely painful is my world, so I warn you PLEASE don't risk corticosteroids.
Having had steroid injections before realizing I had LD, I consider myself lucky to be alive today, so much "exploded" in me, I am amazed as I sit and type this I am able to do so. So many who have used corticosteroids wish they never had, but didn't know better, it has activated lyme, disseminated it and made it much harder to treat, not to mention again PAIN that you could not imagine!
The main thing always overlooked that is most important - corticosteroids release dormant viruses (we ALL have dormant viruses residing in our spine) especially if IV, trigger point injections or facet joint injections are done near the spine. Mine were in the shoulder blade area. Viruses released as well and spread everywhere in my body 4 in all, they can make pain much worse and mixed w/Ld a nightmare. We have all been exposed to viruses in our lifetime through saliva, contact with others infected or even airborne, for instance Chicken Pox reactivated can be something entirely different, shingles, shingles can be localized or systemic (internally and body wide) Mono from the Epstein Barr virus reactivated can cause pain and neuropathy just as an example. You have dormant viruses, it is fact.
Once released they can be dangerous. If you have had corticosteroids at all, especially if you have pain that is not manageable, insist upon viral testing.
Know how to read a viral report, if either the IgG or IgM show out range you ARE infected w/viruses, many doctor's only look at the IgM (meaning active - IgG meaning past exposure) and may be wrong. There is much argument in the medical community as to the meaning of IgG...IgM is clearly active, IgG positive tests, the line blurs as to whethr you are actively infected or not.
An ID MD at Standford explains that doctor's often are mistaken in believing that the IgM needs to be positive to prove active infections. More information is here under our viral link.
Also what viruses to test for: viewtopic.php?f=6&t=55
An extremely high profile LLMD (lyme literate Md) who worked with HIV patients in the 80's has told me personally that "the IgM must be positive for active infection". I must admit both Md's make valid points.
Dr. Burrascano makes it clear in his treatment guidelines that steroid treatment is detrimental, these are excerpts from his guidelines:
"More evidence has accumulated indicating the severe detrimental effects of the concurrent use of immunosuppressants including steroids in the patient with active B. burgdorferi infection.. Never give steroids or any other immunosuppressant to any patient who may even remotely be suffering from Lyme, or serious, permanent damage may result, especially if given for anything greater than a short course. If immunosuppressive therapy is absolutely necessary, then potent antibiotic treatment should begin at least 48 hours prior to the immunosuppressants. The severity of the clinical illness is directly proportional to the spirochete load, the duration of infection, and the presence of co-infections.
These factors also are proportional to the intensity and duration of treatment needed for recovery.
More severe illness also results from other causes of weakened defenses, such as from severe stress, immunosuppressants medications, and severe intercurrent illnesses. This is why steroids and other immunosuppressants medications are absolutely contraindicated in Lyme. This also includes intra-articular steroids." (definiton of intra-articular: situated within, occurring within)
See page 12 paragraph 3 for this quote in Burrascano's treatment guidelines.
http://www.ilads.org/files/ burrascano_0905.pdf
An easy explanation. Your immune system are the "soldiers" of your body constantly standing by to attack any foreign invader. When an immunosuppressant is used, it is like killing off or knocking out most of your "army", now your body is open to all foreign invasion and while your immune system is knocked out, those invaders can go anywhere, your heart, liver, brain - everywhere. Steroids to a lyme patient are like kryptonite to Superman.
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