Steroids Contraindicated In Lyme Disease

Chronic Lyme Disease: A Working Case Definition https://thescipub.com/pdf/10.3844/ajidsp.2018.1.44

“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.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC96041/

"In this study, risk factors such as delayed diagnosis and exposure to inappropriate antibiotics and steroids prior to appropriate treatment occurred in over half the PTLDS patients." https://www.frontiersin.org/articles/10.3389/fmed.2017.00224/full?&

"Moreover, initial exposure to non-recommended antibiotics or steroids has also been associated with worse clinical outcomes." https://www.frontiersin.org/articles/10.3389/fmed.2017.00224/full?&u

"An association between corticosteroid use in acute LDFP and worse long-term facial function outcomes has been demonstrated." https://www.frontiersin.org/articles/10.3389/fmed.2017.00224/full?&u

“Sixteen specific-pathogen-free beagles were infected with Borrelia burgdorferi. Three groups of 4 dogs were treated with antibiotics for 30 consecutive days starting 120 days after tick exposure; 4 dogs were untreated controls. At day 420 after tick exposure and again before euthanasia, 2 dogs of each group were treated with prednisone for 14 days. All dogs contracted infection and 11 developed acute arthritis 50-120 days after exposure. After day 120, one of 12 antibiotic-treated dogs and 2 of 4 untreated dogs became lame. Antibiotic therapy reduced the frequency of Borrelia-positivity in subsequent skin biopsy samples. After prednisone treatment, both control dogs developed severe polyarthritis. At euthanasia, single tissues of the antibiotic-treated dogs and multiple tissues of all control dogs were Borrelia-positive by polymerase chain reaction. Viable spirochetes were not recovered from antibiotic-treated dogs.” https://www.ncbi.nlm.nih.gov/pubmed/10720533

“In three separate experiments, B. burgdorferi-infected dogs received antibiotic treatment (amoxicillin; azithromycin; ceftriaxone; doxycycline) for 30 consecutive days. Two subclinical persistently infected dogs received oral prednisone for 14 consecutive days starting at day 420 post-infection. Dogs developed acute arthritis in the joints closest to the tick bites after a median incubation period of 68 days. Synovial membranes of lame and non-lame dogs produced the chemokine IL-8 in response to B. burgdorferi. Antibiotic treatment prevented or resolved episodes of acute arthritis, but failed to eliminate the bacterium from infected dogs. Corticosteroid treatment reactivated Lyme disease in persistently infected dogs, which had not received antibiotics previously. B. burgdorferi disseminates through tissue by migration following tick inoculation, produces episodes of acute arthritis, and establishes persistent infection. The spirochete survives antibiotic treatment and disease can be reactivated in immunosuppressed animals.” https://www.ncbi.nlm.nih.gov/pubmed/10048169

“Also, we discuss the responsibility of corticosteroids in clinical worsening of Lyme disease if they are prescribed without concomitant antibiotics.” https://www.ncbi.nlm.nih.gov/pubmed/22365471

“In our study, the spirochetal load was much higher in NHPs whose anti-B. burgdorferi antibody response was blunted by dexamethasone than in immunocompetent animals.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC96041/

“The mechanisms of impaired immunity induced by corticosteroid administration are complex and not completely understood. Many cells have intracellular steroid receptors complexed to a heat shock protein, hsp90. Steroids displace hsp90 from the receptor, allowing the receptor to enter the nucleus and bind to the gene regulatory sequences. Corticosteroids have effects on a wide variety of cellular processes and cell types. Thus, the precise steroid effect or combination of effects that to increased spirochetal loads in the corticosteroid-treated NHPs in this study was not determined. However, given previous studies that have demonstrated the importance of anti-B. burgdorferi antibodies in protection from infection, it is likely that the much lower level of specific antibody in the dexamethasone-treated NHPs contributed significantly to the higher spirochetal loads in those animals. Any combination of the lymphoid cells critical to antibody generation (APCs, helper T cells, or B cells) could have been affected.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC96041/

“We assumed at the initiation of the experiment that anti-B. burgdorferi IgM antibody production in the dexamethasone-treated NHPs would be impaired similarly to IgG isotype production. However, the IgM titers in these animals continued to climb through the course of the experiment, surpassed the levels in the immunocompetent animals, and remained high. The IgM antibody produced in the immunosuppressed NHPs, although quantitatively high, did not have the complexity of the IgG response in immunocompetent NHPs. That is, IgM antibody, when tested by immunoblotting, bound predominantly to the 39- and 41-kDa proteins of the spirochete, while the IgG antibody response at the same time p.i. in the immunocompetent NHPs bound to a broader spectrum of spirochetal proteins.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC96041/

“Transient suppression of the anti-B. burgdorferi immune response in the human could occur in instances of co-infection, i.e. simultaneous transmission via the tick of another pathogen other than B. burgdorferi. Thus, mild immunosuppression as accomplished in our NHPs with corticosteroids was designed to mimic conditions in the human host which allow B. burgdorferi in the natural state to gain a firm foothold in the central nervous system in the 10-15% of B. burgdorferi-infected patients who develop clinically symptomatic nervous system disease.” https://www.ncbi.nlm.nih.gov/pubmed/10048168

“Healing was less favorable in the Borrelia group despite an equal rate of palsy at onset and adequate antibiotic treatment. Corticosteroid treatment used in 44% of the patients did not significantly improve the functional outcome.” https://www.ncbi.nlm.nih.gov/pubmed/8393307

Comments By Lyme Treating Physicians:

"Even a single dose of steroids, if large enough, can negatively impact TBDs. After all, any dose and or duration strong enough to suppress inflammation is also strong enough to suppress immunity."

"Steroids contribute to the chronicity of the disease. They just sweep the problem under the table. Because the patient has "improved tremendously on antibiotics" - as you say - steroids are absolutely contraindicated."

"Only if these measures do not work will I add steroids (which, BTW, don't always work to relieve pains)."

Last Updated- October 2019

Lucy Barnes

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