Here is some info for you...and I hope you will be feeling better soon.
Previoulsy posted by Pacbird.
What is a Herxheimer Reaction?
By Donna Herrell
Founder, Lyme Disease Information Resource
The herxheimer reaction, nicknamed "herx", otherwise referred to as Jarisch-Herxheimer (J-H) is a phenomenon originally observed in the treatment of Syphilis, but later found in other illness . In general terms, it is described as a temporary increase of symptoms when anti-syphilitic drugs (antibiotics) are administered.
What is known or speculated about Lyme disease herxheimers are based heavily on the reactions seen in Syphilis. [2-3] This is due to the fact both diseases are caused by a bacteria known as a spirochete, the former being Treponema pallidum, the latter Borrelia burgdoferi (B.b). However, the herxheimer reactions in Lyme disease are not identical to those seen in Syphilis, especially in terms of timing, frequency and duration as noted below. [1-5]
In Lyme disease it is thought that the cause of herxheimers are the result of endotoxin release. [2,5] That is toxin(s) within the spirochete that are released as the B.b are killed or broken down. This may be a result of the toxin(s) itself or the body's immune response to such.
As mentioned, the general description is a temporary increase in symptoms, but also included is the development of new ones. More specifically the most common events include: increased joint or muscle pain, headaches, chills, fever (usually low grade), hypotension, uticaria (hives) and rash. [1-5] A multitude of other symptoms have been described.
Worth noting is that hives and rash are sometimes mistaken for an allergic reaction.  It is up to one's physician to determine this. However, with close observation and proper treatment (see Treatment) may prevent unnecessary cessation of therapy.
In more severe cases of J-H, a reduction of the dosage or temporarily cessation of the treatment has been recommended .
Timing, Frequency and Duration:
This is individualistic and herxheimers can occur within days to weeks after the institution of antibiotic therapy. In some patients they occur only once or twice (if at all) and with others continue throughout the course of treatment, usually lessening in severity.
They can occur and are more often described in cycles (example: every 4 weeks) and have been reported to last from days to weeks. It can be very beneficial to document any exacerbation. Some physicians use this as a guideline for treatment. Further, it may help differentiate herxheimers from the normal symptoms or progression of Lyme disease.
Herxheimer reactions can be very difficult on patients and affect compliance with therapy so supportive measures should be sought or utilized to lessen discomfort if needed. The use of aspirin, NSAIDs (non-steroidal anti-inflammatory drugs), pain medication, muscle relaxers, hot baths or others remedies can be appropriate. Of note, some have found Benadryl helpful even in the absence of rash or hives.
The good news is that the herxheimer is thought to indicate that the antibiotics are indeed working and that following each worsening may bring about more improvement. Though the lack of a herxheimer reaction should not cause anxiety if symptoms are improving.
Something often overlooked but can present with similar symptoms is Candida (yeast) infection. Treatment with acidophilus and if needed prescription medications such as Nystatin or Diflucan can be utilized.
Sources of Information:
Lyme Disease 1991 - Patient/Physician Perspectives from the U.S. and Canada The Jarisch-Herxheimer Reaction James H. Katzel M.D.
Managing Lyme Disease 1996 Joseph J Burrascano M.D.
Principles and Practice of Infectious Diseases 4th Ed. Mandell, Douglas and Bennett
Seronegative chronic relapsing neuroborreliosis. Lawrence C, Lipton RB, Lowy FD, Coyle PK Eur Neurol 1995;35(2):113-117
The New Lyme Disease 1998 Joseph J Burrascano M.D.
See Jarisch-Herxheimer / Jarisch-Herxheimer-like Reactions
Lyme disease, Tick-borne Relapsing Fever and Allergy
Document and reference collection (in progress) November 15, 1999 http://www.x-l.net/Lyme/abstracts/herx/herx.collection.html
This document is for informational purpose only and not written by a medical professional. This article may be copied for personal use. For republication in any format please contact the author at [email protected]
Copyright � 1997
Lyme Disease Information Resource http://www.x-l.net/Lyme/HERX.html
And more info......previously posted by Shelley.
Jarisch-Herxheimer reaction, a transient, short-term immunologic reaction commonly seen following antibiotic treatment of early and later stages of syphilis and less often in other diseases, such as borreliosis, brucellosis, typhoid fever, and trichinellosis, which is manifested by fever, chills, headache, myalgias, and exacerbation of cutaneous lesions. The reaction has been attributed to liberation of endotoxin-like substances or of antigens from the killed or dying microorganisms, but its exact pathogenesis is unclear. Called also Herxheimer's r.
Section 11: The Herxheimer Reaction
In a field in which clinical findings can be vague and imprecise, and where helpful monitoring laboratory tests are lacking, the Herxheimer reaction is an indispensable clinical tool in the treatment of persistent LD, or neuroborreliosis. In theory, Herxheimer reactions occur when an administered antimicrobial agent has successfully led to lyses of certain organisms (107). By definition this phenomenon is not unique to Bb. Fortunately, however, the Herxheimer reaction appears to provide a highly reliable barometer of therapy in Bb, so much so that a treatment course which lacks the Herxheimer response places the diagnosis of persistent Bb in serious doubt.
The reaction was first described in 1895 by an Austrian dermatologist Jarisch Adolf Herxheimer, who was practicing in Vienna, and later confirmed by his brother Karl Herxheimer, who was also a dermatologist, practicing in Frankfort (108,109). During these times, both physicians were responsible for treating syphilitic lesions and employed various preparations of mercury, arsenic and bismuth in these therapies. The key observation noted by both physicians was that, shortly after treatment of syphilitic skin lesions had been administered, many of their patients developed fever accompanied by rigors, drenching sweats, and nausea and vomiting. In addition, they found that the syphilitic skin lesions flared and became larger before healing; results were best in the patients that experienced this reaction, which typically lasted for 2 to 3 days.
The debate about the cause and nature of this predictable reaction has raged on for decades. Various theories have ranged from a vascular reflex mediated by the autonomic nervous system (110) to a direct toxic effect of the antimicrobial on tissues (111). In 1943 Mahoney described the first Jarisch-Herxheimer reaction in syphilitic patients treated with the relatively new antibiotic penicillin (112 ). Classically, the Jarisch-Herxheimer reaction occurred when treating the secondary stage of syphilis, at a time when a widespread rash may occur and the spirochetal burden is high. Even today, medical students are taught that a Jarisch-Herxheimer reaction occurs as a result of treatment of secondary syphilis. Most physicians are not aware that the Herxheimer reaction occurs in Bb infections and has been described in a variety of other diseases, many of them caused by spirochetal organisms such as Treponema pallidum (syphilis) and Bb in LD. A short list of treated spirochetal infections noted to manifest Herxheimer reactions includes Relapsing Fever (Borrelia recurrentis), Yaws (a subspecies of Treponema pallidum), Rat Bite Fever (spirullum minus), and perhaps Vincents Angina (spirochetal mouth forms) (113). Non-spirochetal infections manifesting the Herxheimer event after treatment include Brucellosis, Glanders, Anthrax, and even Leprosy (mycobacterium leprae) (113).
In 1972 Gudjonsson reported on a summary of experiments that entailed almost a decade of work (114). He concluded that the Herxheimer effect was not allergic in nature and was likely caused by a leukocyte pyrogen released at the time of phagocytosis. Most now believe that the pyrogens in question are exogenous pyrogens, or endotoxins, derived from components of the bacterial cell wall. In the case of Bb, the pyrogen is most likely the lipoprotein moiety which comprises the outer coat of the organism. These lipoproteins, specifically OspA and Osp B, have been shown to have potent B cell mitogenic and cytokine-stimulatory properties (78). It is widely recognized that antibiotic therapy may promote endotoxin release by virtue of its microbicidal effect which leads to the disintegration of the bacterial organism and exposure, or presentation, of endotoxin. On recognition of the endotoxin, polypeptides such as IL-1, interferons, or tumor necrosis factor (TNF), otherwise referred to as endogenous pyrogen (EP) or pyrogenic cytokines, are released by the monocyte/macrophage system(115). It should be pointed out that only minute quantities of EP are needed in order to generate fever and other systemic symptoms. In the extreme case, such as gram negative bacterial sepsis, high and persistent levels of endotoxin are present and lead to sepsis syndrome with capillary leak syndrome and vascular collapse. In the Bb model, with a relatively low number of organisms present and with limited and inconsistent die-off with each round of antibiotic therapy, one could conceive a model in which constitutional complaints, mediated by pyrogenic cytokines, are manifested in an ongoing and rather unpredictable manner. This then would represent the defining principle for the Herxheimer reaction in Bb infection. In predicting a pattern of response based on our knowledge of Bb infection, we would expect these symptoms to be worse initially, depending on die-off rates, and to not be life threatening, but likely to be life altering. Our clinical experience supports these precepts.
Published reviews have suggested a periodicity exists for Bb activity or replication, specifically that symptoms of fever and malaise, etc. occur at 4 week intervals (116). Others have created so called mathematical models to support this hypothesis. While we respect this author's opinion, we find it difficult to understand how there could be synchronicity in any given polymorphic Bb population (often consisting of multiple strains) in any given host. The matter merits further study and validation. In females, increased symptoms and increased urinary shedding of Bb has been documented in the perimenstrual period, suggesting a hormonal influence (personal communication Dr. Nick Harris), and so it would seem possible that periodicity may exist in menstruating females (although our more seriously ill female LD patients routinely develop menstrual irregularity).
In our clinic, prior to starting any antimicrobial therapy, especially if our patient is na�ve to treatment, we emphasize to the patient that they may notice certain significant clinical events while on therapy. In the occasional patient in whom we have no firm diagnosis but where we are suspicious enough to offer short-term empiric oral therapy, we are intentionally a bit vague about providing information to the patient about the Herxheimer effect, as we do not wish to influence a response by suggestion. We have found the Herxheimer response in LD to be as myriad as the course of persistent LD itself. It is na�ve for one to expect to witness simply a flu-like syndrome, although this certainly happens. Instead, generally one sees an intensification of pre-existing symptoms, e.g. increased brain fog or muscle/joint pain, where these symptoms were reported prior to therapy. On the other hand, it is equally common to take reports of new symptoms, e.g. headache in a patient who previously reported symptoms other than headache. In general, the Herxheimer reaction is worse in our most seriously ill patients and most violent at the onset of therapy. The Herxheimer response typically occurs within 3 to 5 days, but may take up to 2 weeks to appear. These symptoms may persist for days or weeks and often become a major management concern as our patient may suffer considerably in the process of treatment. Eventually, as therapy progresses, we tend to witness a dampening of the intensity of the Herxheimer response, as well as some reports of positive clinical gains. Introduction of new therapy, as we cycle antibiotics through our treatment schedule (see treatment program to follow), invariably leads to intensification or new symptoms, all of which are unpleasant. In fact, if we do not observe a new response when therapy is added or substituted, we question the efficacy of our program. Later in this report, we refer to dermal or neurologic Herxheimer phenomena, which we feel reflect local manifestations of pyrogenic cytokines in response to treatment.
Regrettably, but not unexpectedly, we have treated a number of individuals whose Herxheimer experience is so intense and prolonged that continued treatment is virtually impossible. After exhausting all customary supportive and treatment measures, which incidentally never includes the use of systemic steroids, we have resorted to the off-label use of infliximab (Remicade) in these cases, with positive results in a significant majority of those treated. Therapy with infliximab is not continued if the initial treatment does not provide significant relief. Where relief is provided, however, we are convinced that judicious use of this approach, in the occasional situation where it may be needed, has allowed Bb treatment to continue. Undoubtedly, as other cytokine blockade therapies become available, we will evaluate their potential role in this setting as well.
The escalating headache symptoms experienced by some patients on intensive antibiotic treatment is a Herxheimer effect that merits special attention. This ``Lyme'' headache is thought to be linked to cerebral edema brought about by Bb die-off and the ensuing creation of inflammatory microfoci in the leptomeninges. In our experience, severe CNS symptoms, such as incapacitating headache, are more likely to occur when the patient has had prominent CNS symptoms or findings pre-therapy, e.g. encephalopathy, aseptic meningitis, optic neuritis, and so on. In 2-3% of our treated cases, we have had to resort to one or more therapeutic lumbar punctures to provide relief by lowering intracranial pressure.
Given the miserable experience which we may exact on our patients during therapy, we would perhaps be better off if we followed the advice of Russell McMillan, DDS, DPH, who wrote the Arthritis Trust of America in 1994 with his personal remedy for the Herxheimer reaction. ``I take a saltz bath which consists of adding 1 cup salt, 1 cup soda, 1 cup Epsom salts, 1 cup aloe vera, to a hot bath which I remain in and keep hot for about 11/2 hours all the while consuming about 2 quarts of warm water. Evidently the perspiration and osmotic pressure removes the causative toxins. I find it quite helpful'' (117). Hey, sounds ok to us.