There has been a longstanding debate between the IDSA and ILADS regarding Lyme symptoms which persist after standard doses of antibiotics as defined by the IDSA. They take the position that standard therapy eradicates the organism. Furthermore, they take the stance that symptoms which persist after standard therapy should be called "post Lyme," not chronic Lyme, because the cause relates to an autoimmune process. ILADS posits that persistent Lyme symptoms after IDSA recommended treatment are due to persistence of the organism. The following case should be written up and submitted to a peered reviewed journal for publication since it clearly sheds much light on this debate.
A 51 year old woman presented to my clinic on April 1, 2008. At that time she complained of multiple symptoms which she related to tick borne illness. She was in good health until August 2006. At that time she reported occupational exposure to Ixodes ticks and EM rash. She was evaluated by and infectious disease specialist in September 2006. This physician noted that symptoms started 3 to 4 days prior to the initiation of antibiotic therapy. She had received 6 weeks of doxycyline. The dose had ranged from 200mg to 400mg per day. This physician recommended two more weeks of doxycycline and follow up care. She subsequently went to another physician who had experience treating Lyme and tick born infections. He treated her with 5 weeks of Rocephin. The Rocephin was stopped due to an allergic reaction. She was treated with long term continuous oral antibiotics. These included: Zithromax, Mepron, Flagyl and Bactrim.
When I first saw her it was noted that an MRI of the brain was positive for WMD.
She complained of memory loss, headaches, fevers, swollen glands, muscle and joint pains, fatigue and numbness and tingling of the extremities. She had severe cognitive deficits and was fully disabled. Her neuro exam showed cognitive processing delay and evidence of peripheral neuropathy. It was noted that Lyme serology had been negative.
She was started on antimicrobial therapy including: Zithromax, Amoxil, Flagyl and Plaquenil. On May 7, 2008 the Flagyl was stopped and the other meds continued. On May 9, 2007 she was still on the same antibiotics. On May 16, 2008 the dose of Amoxil was increased. On May 21 she continued to have disabling symptoms. Intravenous antibiotic therapy was recommended. The results of a second Lyme serology Western Blot from IgeneX showed seroconversion. Her Bb IgM bands were positive in positions: 18,23,31,34,41,58 and 66. She was positive by both CDC and IgeneX criteria. Her IgG bands were positive by IgeneX internal criteria.
IV antibiotics were not covered by her insurance company. Therapeutic doses of oral antibiotic combinations were administered continuously through July 2008. She continued to have disabling muti-system symptoms and clinical neuroborreliosis. The IV antibiotics were finally approved in August 20008. While awaiting this approval she received a single dose of Bicillin 2.4 million units on August 1, 2008. On August 3, 2008 she was started on IV Primaxin, 500mg every 8 hours. This second line drug was picked because of a previous adverse reaction to Rocephin. The Primaxin was augmented with oral antibiotics including Zithromax and Flagyl. She also was re-treated for Babesia with Mepron. She symptomatically improved significantly for the first time. The intravenous therapy was only approved for 8 weeks. After this she was still symptomatic and oral antibiotics were continued.
On October 14, 2008, while still on oral antibiotics, she came into the office complaining of swelling and pain in both knees. An arthrocentesis was performed and the fluid was sent for analysis.
This patient's synovial fluid was PCR positive for Borrelia burdorferi.
Here is a very ill patient with chronic Lyme symptoms. After receiving standard therapy as defined by the IDSA, she was treated with very aggressive long term antibiotic therapy, both oral and intravenous, in accordance with ILADS' principals.
After more than two years of continuous antibiotic therapy this patient clearly demonstrates persistence of Borrelia burdorferi, the agent responsible for Lyme disease, presenting in synovial fluid. It should also be noted that prolonged therapy in this patient was associated with marked clinical improvement over time.
These findings refute the hypothesis that persistent symptoms are due to an autoimmune process. In fact they demonstrate the ability of the organism to persist in the face of massive anti-microbial therapy.
These findings provide evidence based support for ILADS based protocols for the management of chronic Lyme disease.