The Jarisch-Herxheimer reaction in Borrelia infection
Unfortunately, JHR is very rarely described in Lyme disease. There are scattered case studies, but I cannot name any reliable sources.
The JHR is much more clearly described and more pronounced in syphilis. In syphilis, the pathogen is less fragile, and when the patient is in stage III, meaning that larger quantities of the pathogen are present in the blood, the quantity is greater than that of Borrelia in Lyme disease.
This is why there is still a belief that Borrelia does not remain in the blood for long: in the case of recurrent fever and syphilis, the enormous amount of pathogen in the blood correlates well with the patient’s symptoms and is visible in a microscopic smear without concentration. However, this is approximately two orders of magnitude greater than spirochaetaemia in the case of Borrelia.
We discuss these in our latest article, stating that: (i) it is rather stupid for a pathogen to spread via bloodsuckers and not want to remain in the blood, when this cannot harm it, (ii) Borrelia burgdorferi is orders of magnitude less abundant than B. recurrentis, and this is already below the limit of microscopic detectability (without concentration or culture), (iii) Borrelia completely changes its genetics in 3 weeks, so if we search for it based on multiple genome sequences, we will see the modification in the first round, i.e. it is present in the same quantity with different genetics, and then after 1-2-3 generations it “disappears from the map”, meaning that even PCR cannot measure it. This cannot be interpreted as meaning that the pathogen disappears, as Éva Sápi and Eva Ruzic, among others, successfully cultivate the pathogen from blood plasma at any time using completely different methods.
But back to JHR. So we are not even sure that it will appear at all during the first successful antibiotic treatment, or that it will appear.
Even if it does appear, it is a transient phenomenon and it is almost certain that it will not return. For example, a doctor I know who treats patients with a non-standard device proudly reports that his patients “herx” after every treatment. I asked: does that mean they feel unwell after every treatment? He replied: yes. Well, I say, that is very unlikely; I would rather look for another type of real discomfort. We know that there are devices that cause physical harm to patients if they vary with certain vital signs.
JHR can be avoided.
With the LB Foundation’s preparatory and supplementary programme, this almost never happens. Proper preparation of the intestinal and immune systems is necessary and possible. So it is likely that not all of the discomfort can be attributed to JHR.
If we look into it further, we cannot find a precise definition of what this reaction is.
The general opinion is that JHR is either a cytokine reaction (“cytokine storm”) or the effect of a toxin released by the bacterium. Well, the latter, whether toxins can be released in the case of Borrelia, is controversial in the first place, and the current consensus is that there is no specific toxin that can be released from Borrelia because it does not contain any. Of course, certain glyco- or lipoproteins can still be triggers for the body.
A relatively thorough article on the pathophysiology of JHR:
https://www.ncbi.nlm.nih.gov/books/NBK557820/
“Pathophysiology
Despite advances in medical science, the exact mechanism of JHR is still unclear and is considered to be multifactorial. The breakdown of spirochetes after antibiotic treatment causes the release of toxins (??) and cytokines. JHR is thought to be caused by an acute inflammatory reaction when cytokines and lipoproteins enter the patient’s bloodstream. JHR causes an increase in inflammatory cytokines, including interleukin-6, interleukin-8 and tumour necrosis factor-alpha levels, which lead to body aches, fever, rashes, nausea, flushing and other symptoms. Symptoms usually begin 2 hours after administration of the antibiotic and subside within 24 hours.
However, we still encounter discomfort in some patients when they start a course of doxycycline, even though B. garinii is the dominant cause of infection in that patient.
I have encountered several such cases where Doxy made the patient worse, while Amox made them better. Of course, there are still very few cases where DualDur and Bózsik Western blot tests are available, from which the Borrelia strain is conclusive and we also know the patient’s treatment.
Is it possible that JHR is actually saying, “the patient is not properly prepared” or “it is time to use a different antibiotic”?
