Jarisch-Herxheimer Reaction

Although RA is discussed in particular, patients with other inflammatory rheumatic diseases will recognize many issues mentioned here.

The Jarisch -Herxheimer, or Herxheimer reaction, was named for the German dermatologist, Karl Herxheimer (1844-1947). Dorlands Medical Dictionary refers to the Herxheimer reaction as a transient, short-term, immunological reaction commonly seen following antibiotic treatment of early and later stage [infectious] diseases which [may be] manifested by fever, chills, headache, myalgias (muscle pain), and exacerbations of cutaneous lesions. The reaction has been attributed to liberation of endotoxins-like substances or of antigens (a substance which causes an immune reaction) from the killed or dying microorganisms.

A TRANSIENT SHORT-TERM, IMMUNOLOGICAL REACTION

What does this mean in layman's terms? The Herxheimer flare reaction may be the first indication that the antibiotic is reaching its target and is therefore considered a good sign. In his original book, The Road Back, the late Thomas McPherson Brown, MD noted that the reaction caused a temporary worsening of symptoms.

The amount of medication may be directly related to the intensity of the flare. Medications which have no effect on mycoplasma (or other microbes) do not provoke this reaction nor do these medications generally have a favorable long-term effect on the disease. Unlike the RA flare, which can last for weeks or even months, the Herxheimer flare reaction is often of short duration. (Scleroderma patients who do not exhibit inflammatory components to their disease generally do not report a Herxheimer of clinical significance.)

Large doses of antibiotics may initially caused a worsening or flare reaction in many of the rheumatic diseases. The rheumatic diseases which are most hypersensitive (rheumatoid arthritis, lupus, psoriatic arthritis, etc.) have shown similar, distinct and often severe flare reactions from even a low dose of antibiotic. According to Dr. Brown, when the resulting released toxins go to the joints, joint pain is the result; when they go to the brain, depression may result.

Dr. Brown found the Herxheimer effect showed a number of important principles at work. It demonstrated that the disease was a hypersensitive reaction, not to the drug itself, but to the toxins that a microbe creates in response to the drug's presence. And, it opened the way to a chemical attack (with medications) on the whole area of arthritis and rheumatic diseases.

Dr. Brown found that rheumatic diseases are often associated with a high degree of tissue sensitivity. It was soon observed that a more potent antibiotic would produce a more marked flare reaction because of this tissue sensitivity. By keeping the dosage low, it was possible to gradually remove the microorganisms from the tissues without causing major clinical worsening of the disease. If these microorganisms were truly present and responsible for the hypersensitivity reaction, long term, low dose treatment would result in clinical improvement of symptoms in patients.

Dr. Brown recognized he was not dealing with an ordinary infectious problem where microbial invasion was the prominent feature. The reaction of the patient to the infectious organism was as important as the organism itself.

In the historical protocol as determined by Dr. Brown, the use of low dosage cortisone in conjunction with the antibiotics, either prevented or modified such flare reactions. Chemical worsening of the blood figures in lab testing was not generally noticeable until much larger doses of the antibiotics were given.

Usually the first clinical changes to occur are those of lessening of the duration of morning stiffness. In many patients under long term management, the morning stiffness disappears altogether.

When the severity of the arthritic condition begins to lessen, either from a spontaneous improvement or as a result of the continued treatment with a carefully measured dose of antibiotic, a greater tolerance of the antibiotic is generally noticed and larger doses are tolerated without the return of the Herxheimer flare reaction. If the dose has been increased too rapidly at any time, the initial flare reaction may occur again. However, some patients need to remain on a low, intermittent dose and respond well.

The standard prescription for antibiotic use in non-rheumatic diseases is a high dose for a short period of time. The overall guidelines for rheumatic diseases for avoiding too severe a Herxheimer flare are dependent on careful use of low dose and attention to frequency of administration. This treatment methodology calls for low dose antibiotics prescribed over a long period of time-- a very different protocol than usual for the prescribing of antibiotics.

TREATING THE FLARE

Since the Herxheimer is a drug related flare, treating the symptoms and allowing the flare to run its course will enable the antibiotic to attack the offending microorganism and hasten recovery. Treat the pain symptoms with pain medications which don't block the effect of the antibiotic and which don't suppress the immune system ( i.e.: not high doses of steroids.) The pain of the Herxheimer will diminish as the reaction runs its course, making the need for pain medications or those which address increased inflammation less needed over time. Remember, a Herxheimer is a reaction to the effects of an antibiotic on the microorganism causing the disease, while an RA flare is a worsening of disease.

The Road Back Foundation does not engage in the practice of medicine. Consult with a physician to assess any medical treatment that is being considered. The Road Back Foundation encourages healthcare consumers to thoroughly investigate and understand all treatments and medications before proceeding. This material is for educational purposes only.

The Road Back Foundation
P.O. Box 410184
Cambridge, MA 02141
614-227-1556
www.roadback.org