Whether Borrelia burgdorferi, the causative agent of Lyme disease, can persist for long periods in the human body has been a controversial question. The objective of this study was to see if we could find B. burgdorferi in a Lyme disease patient after a long clinical course and after long-term antibiotic treatment. Therefore, we investigated the potential presence of B. burgdorferi antigens and DNA in human autopsy tissues from a well-documented serum-, PCR-, and culture-positive Lyme disease patient, a 53-year-old female from northern Westchester County in the lower Hudson Valley Region of New York State, who had received extensive antibiotic treatments during extensive antibiotic treatments over the course of her 16-year-long illness. We also asked what form the organism might take, with special interest in the recently found antibiotic-resistant aggregate form, biofilm. We also examined the host tissues for the presence of inflammatory markers such as CD3+ T lymphocytes. Autopsy tissue sections of the brain, heart, kidney, and liver were analyzed by histological and immunohistochemical methods (IHC), confocal microscopy, fluorescent in situ hybridization (FISH), polymerase chain reaction (PCR), and whole-genome sequencing (WGS)/metagenomics.
We found significant pathological changes, including borrelial spirochetal clusters, in all of the organs using IHC combined with confocal microscopy.
The aggregates contained a well-established biofilm marker, alginate, on their surfaces, suggesting they are true biofilm.
We found:
B. burgdorferi DNA by FISH, polymerase chain reaction (PCR), and an independent verification by WGS/metagenomics, which resulted in the
detection of B. burgdorferi sensu stricto specific DNA sequences
IHC analyses showed significant numbers of infiltrating CD3+ T lymphocytes present next to B. burgdorferi biofilms
In summary, we provide several lines of evidence that suggest that B. burgdorferi can persist in the human body, not only in the spirochetal but also in the antibiotic-resistant biofilm form, even after long-term antibiotic treatment. The presence of infiltrating lymphocytes in the vicinity of B. burgdorferi biofilms suggests that the organism in biofilm form might trigger chronic inflammation. View Full-Text
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**Comment**
When will there be enough evidence for mainstream medicine?
Many people with and without Lyme are fearful of Coronavirus also called Covid-19. In my Seattle Lyme practice, I am answering questions about what one should do to protect themselves and to boost their immune systems. Many wonder if immune dysregulation, caused by Lyme, increases their chances of acquiring the virus, having a severe case, or even death. (See link for article)
IS SUPPRESSING IMMUNE SYSTEM HARMFUL TO LYME PATIENTS?
There have only been a few published reports detailing the outcome of treatment on Lyme disease patients who are immunocompromised. Now, a study by Maraspin and colleagues¹ evaluates the impact of tumour necrosis factor-alpha (TNF-α) inhibitors, medications that suppress the immune system, on Lyme disease patients.
The authors compared 16 individuals receiving TNF-α inhibitors with 32 healthy controls. The individuals had confirmed Lyme disease with an erythema migrans rash manifestation. The patients received immune-suppressing medications, which included adalimumab, infliximab, etanercept, golimumab. These were often combined with other immunosuppressant drugs for rheumatic (13 patients) or inflammatory bowel (3 patients) disease.
Investigators found that, when compared to controls, patients receiving immunosuppressants had:
frequent comorbidities other than immune-mediated diseases (62.5% vs. 25%)
symptoms/signs of disseminated Lyme borreliosis (18.8% vs. 0%)
treatment failure (25% vs. 0%.)
In fact, 4 out of 16 (25%) Lyme disease patients treated with immunosuppression therapy failed treatment. Three of these four patients required retreatment. One of them was quite ill.
“The immunocompromised patients were also more likely to fail treatment than patients who were not immunocompromised,” writes Maraspin.
The fourth patient, a 44-year-old man, remained well until his 6-month follow-up visit. But, “7 months after beginning antibiotic treatment he developed severe arthralgia, fatigue and back pain,” writes Maraspin in the Journal of Clinical Medicine.
A specialist was consulted but could not confirm whether the man had a relapse of rheumatoid arthritis. He remained ill for the next 5 months. And tests revealed his IgG antibody to VlsE borrelial antigens rose from 542.1 to 1462.0 AU/mL.
His symptoms improved following re-treatment with the antibiotic, ceftriaxone.
The authors recommended regular follow-up visits to carefully monitor immunocompromised Lyme patients.
The exact cocktail of a tick’s saliva proteins changes every few hours, Ribeiro says. The thousands of proteins in its saliva are highly redundant in function, and the tick cycles through them as a way of circumventing a host’s immune system. Immune systems take time to recognize and react to a foreign tick protein, and this strategy simply doesn’t give a host’s cells a chance to do that. Suppose, Ribeiro says, “Monday a tick starts feeding on you and injecting the saliva in you.” By Friday, when your body can mount a proper immune response against those first proteins, “the tick has already changed the repertoire.”
Taken together, these results suggest that Ip-sL1 and Ip-sL2 confer immunosuppressive functions and appear to be involved in the transmission of pathogens by suppressing host immune responses, such as cytokine production and dendritic cell maturation.
In other words, there are immunosuppressants within tick saliva that makes it easier for transmission to occur.
It only follows that giving patients immunsuppressants (or those patients infected with numerous pathogens) will function similarly in the body – allowing for pathogen proliferation which will be demonstrated by more severe disease.
TOUCHED BY LYME: Proxy votes violate spirit of TBD Working Group
The federal Tick-Borne Disease Working Group held two days of meetings in Philadelphia this week. I watched the live-streamed proceedings via YouTube both days. On the second day, I gave the following public comments via telephone:
My name is Dorothy Leland and I am vice-president of LymeDisease.org
I have two points regarding yesterday’s meeting. The first speaks to “process integrity” – how this Working Group should operate.
Why in the world did David Walker cast proxy votes for Eugene Shapiro?
The point of the Working Group is for people from diverse scientific viewpoints to listen to each other, discuss the issues, and THEN decide how to vote. Dr. Shapiro wasn’t in the room and didn’t take part by phone. Yet, Dr. Walker cast votes on his behalf.
Why is this even allowed? If it doesn’t technically violate a rule, it certainly violates the spirit of the Working Group. It mocks the concept of the healthy exchange of ideas. Here, somebody doesn’t have to participate at all…and still has a vote.
When Dr. Shapiro was first named to this group, LymeDisease.org protested vociferously—because of his flagrant financial conflicts of interest. More than 37,000 members of the Lyme community signed our petition to remove him from this panel. It fell on deaf ears.
Dismissing the needs of chronic Lyme patients
My second point about yesterday’s meeting concerns Ben Beard’s defense of the CDC website—and his dismissal of questions about the validity of Lyme disease testing.
Beard stated—and I quote—
“The vast majority of Lyme disease patients are served quite well by the guidance we have on our website. The diagnostic test is reliable in terms of it telling you what you expect to hear.”
Here’s my response: It’s true that some people get Lyme, get treated, and get well—in short order. But many people don’t get well. They stay desperately sick for years, often losing their jobs, their homes, their marriages, their families. Children lose their childhoods, often too impaired to go to school.
The CDC acknowledges that 10 to 20 percent of Lyme patients remain ill after treatment. Over 20 years, that could mean up to three MILLION people with persistent symptoms of Lyme disease–using the CDC’s own figures.
And that doesn’t count people who remain undiagnosed and untreated. They are the ones most ill-served by the CDC’s “guidance”—and a lousy lab test.
Another process irregularity
Beard’s comment highlighted another process irregularity with the Working Group. 2018’s group had three representatives of the Lyme patient community. This 2020 group has only one—Pat Smith.
Meaningful patient representation requires more than a single voice crying in the wilderness.
When Pat raised questions about patients with persistent Lyme disease, the CDC spokesman dismissed those concerns—and there was nobody else willing to support the patient point of view.
This Working Group was created due to the efforts of patients with persistent Lyme disease—not people who got well quickly. Those folks don’t NEED a Working Group. I urge you not to forget your core constituency.
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Here is a two-minute clip of Pat Smith taking representatives of the CDC and the NIH to task for their cavalier attitudes towards chronic Lyme patients. If you’ve got hours to spend, you can watch both meetings in their entirely. Day One and Day Two.
I hate to say it, but I saw this coming a mile away. Shapiro and his ilk stick together. It’s a “Good ol’ Boys Club.” I also heard Mr. Beard at a conference. He’s not a friend of patients but a status quo CDC employee afraid of losing his job if he doesn’t follow the narrative. https://www.hhs.gov/ash/advisory-committees/tickbornedisease/members/index.html
It takes cajones to be a whistleblower. Just ask Peter Gotzsche, Andrew Wakefield, Judy Mikovitz, and William Thompson. These people are vilified, have their character torn to shreds, and are continually persecuted on the cross of truth.
Increases in tick-borne disease prevalence and transmission are important public health issues. Efforts to control these emerging diseases are frustrated by the struggle to control tick populations and to detect and treat infections caused by the pathogens that they transmit. This review covers tick-borne infectious diseases of nonrickettsial bacterial, parasitic, and viral origins. While tick surveillance and tracking inform our understanding of the importance of the spread and ecology of ticks and help identify areas of risk for disease transmission, the vectors are not the focus of this document.
Here, we emphasize the most significant pathogens that infect humans as well as the epidemiology, clinical features, diagnosis, and treatment of diseases that they cause. Although detection via molecular or immunological methods has improved, tick-borne diseases continue to remain underdiagnosed, making the scope of the problem difficult to assess. Our current understanding of the incidence of tick-borne diseases is discussed in this review. An awareness of the diseases that can be transmitted by ticks in specific locations is key to detection and selection of appropriate treatment. As tick-transmitted pathogens are discovered and emerge in new geographic regions, our ability to detect, describe, and understand the growing public health threat must also grow to meet the challenge.
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**Of Note**
This article has a delayed release (embargo) and will be available in PMC on January 2, 2021.
I pray to God that their inference to “ticks in specific locations” doesn’t continue the 40 year old narrative which placates doctors into looking at maps to determine if patients are infected or not.