There has been a growing consensus that whatever chronic Lyme disease is it’s not due to the bacteria. This concensus has been based on studies indicating that short term antibiotic treatment following an infection, causes a dramatic reduction in antibodies. That drop in antibody levels is believed to reflect the immune system turning itself off, because of the bacteria, Borrelia burgdorferi, is gone.
This study overturned that idea completely.
Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. Rebecca A. Elsner1,2¤a, Christine J. Hastey1,2¤b, Kimberly J. Olsen1, Nicole Baumgarth1,2,3* PLOS Pathogens | DOI:10.1371/journal.ppat.1004976 July 2, 2015
Borrelia has developed several tricks to evade the immune system. It can inhibit complement activity and disguise itself by varying the proteins found on its surface. How quickly the infection spreads may be a key factor in how easy it is to suppress. Infections that stay localized are more easily dealt with. Wider spreading infections are more difficult to contain. Studies suggest that adaptive or long term immunity is hard to come by.
Borrelia appears to head straight for the heart of the immune system – the lymph nodes – where, at least in mice, it inhibits the adaptive immune response by attacking the centers of T and B cell production. That, along with the antigen switching, helps explain the difficulty the immune response has in containing the infection.
First they gave the mice Borrelia. They observed the infection take hold and spread and then they treated the mice with antibiotics. They observed a strong antibody response. That, and antibiotics quickly brought the antibody levels down – suggesting that the infection had been resolved. (Tissue analyses done later indicated that antibiotic treatment had, in fact, vanquished Borrelia. In the non-antibiotic treated mice it was still present.)
Then they dug deeper into the post-bacterial infection stage. At the end of the antibiotic regimen they exposed the mice to Borrelia antigens again. The immune system, at that point, should be able to quickly jump on any hint of Borrelia and mount a huge immune response, but it refused to budge. When they challenged the mice with an actual Borrelia infection, all the mice – whether they’d been treated with antibiotics or not – came down with Borrelia. When they hit the mice an influenza vaccine, guaranteed to crank up the immune system, the antibody response to the influenza was weakened as well.
Somehow, during the initial infection, Borrelia had taken a hammer to the adaptive or long term immune response. Looking deeper they found structural alterations in the germinal centers that produce the long term immune response. Further study indicated that antibody response was significantly blunted, not just to Borrelia antigens – but to others as well.
They continued following the mice. They found significant immune suppression, lasting from a period about one month into the infection to about six months after it. During that period, immune system was essentially wide open to the Borellia bacteria and perhaps to other past infections. It did not respond to vaccines either.
The study found that antibiotics do appear to wipe out Borrelia and the immune system, in mice, at least, does appear to dust itself off after “many months” and get back to work. In the interim, though, people with Borrelia infections may be more vulnerable to further Borrelia or perhaps other infections (including infections that ticks carry.) ( Could Borrelia interfere with antibody response to herpesviruses? Could the immune suppression it invokes lead to herpesvirus reactivation?)
The Post Infection Period
Researchers are more and more recognizing that the effects of infection do not stop with an apparent vanquishing of the virus. A recent study found that measles infections suppress immune functioning for up to three years. The suppression occurs in a different way than Borrelia. Apparently the immune system gets so excited upon being confronted with measles that it throws all it’s memory cells at the virus – ignoring any other pathogens. The increased death rates seen in the three years following measles infections are not due to measles, but to other infections taking advantage of a weakened immune system.
The reports of post-Ebola fatigue and pain syndromes occurring in some Ebola survivors, are another compelling example of post-infectious problems. We know that cytomegalovirus infections reset the workings of much of the immune system for decades, even in healthy people. The point is that more understanding is slowly emerging of radical changes that can present themselves in the post-infection period. That’s good news for the infectious subset in ME/CFS and fibromyalgia.
This study introduced more uncertainty regarding Lyme diagnoses – an area that already comes with considerable uncertainty. It found that low levels of antibody titers to Borrelia in the six months or so following an infection are more indicative of a vanquished immune system than a vanquished bacteria. This suggests that antibody tests taken at a doctors office from a month to six months after a tick bite may be largely useless. Tests taken before or after this period, if I’m reading this study correctly, would likely be accurate.
It should be noted that this was a mouse study. While the mice did recapitulate the same up and down antibody responses known to occur in humans, the study findings have not been replicated in humans.
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