Lyme disease, treatment

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:

  1. frequent comorbidities other than immune-mediated diseases (62.5% vs. 25%)
  2. symptoms/signs of disseminated Lyme borreliosis (18.8% vs. 0%)
  3. 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.
  1. Bransfield RC, Friedman KJ, Differentiating Psychosomatic, Somatopsychic, Multisystem Illnesses and Medical Uncertainty. Healthcare 2019, 7(4), 114.



I would argue that ALL Lyme/MSIDS patients are immune suppressed even if they are not taking immune suppressing drugs, which means the outcome would be similar.  This issue desperately needs to be addressed as mainstream medicine and research continues to approach this as a singular pathogen illness when recent research shows 65% of TBD patients produce immune responses to various microbes:

Here’s a study shows patients with EM who were receiving rituximab (an immune suppressant) for underlying disease show more borrelia isolated in the blood and that their cases are more often disseminated than in immunocompetent patients :

And here we see ticks have immunosuppressive proteins in their saliva:

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.