Treating the Jarisch-Herxheimer

(JH) Flare Reaction

Stuart L. Weg, M.D. is certified by the American Board of Anesthesiology with added qualifications in pain management.

The observed temporary worsening of clinical status in patients undergoing anti-infective treatment is called the Jarisch-Herxheimer (JH) reaction. It may be referred to by some of the terms listed below.

This phenomenon, described in the cover article, is not just present in rheumatologic disease but is common to all forms of anti-infective therapies that I have used for most chronic painful states. This app arent common etiology of all chronic pain and arthritis is not within the scope of this discussion but will be covered in the future.

The JH reaction can take the mild form of sleepiness and fatigue to full blown anaphylactic shock. The timing varies from almost immediately, as is the case of IV antibiotics, to up to a week or two later. This depends on the rate that toxins are produced and how fast they can be metabolized or eliminated.

Drug levels are important, but often cannot explain the timin g of a reaction. In some cases an overwhelming, waterfall effect is present, while in other patients there is a slow, gradual building of symptoms. I have seen cases where adding another unrelated medication caused the antibiotic to become more bioavailable and that precipitated a JH.

There are cases where simply changing a single 100 mg daily dose of minocycline to two 50 mg split doses has provoked a JH due to an absorption increase. Reducing, suspending or changing the offending medication is the most obvious treatment. Patients must understand that early signs of the JH reaction may not be present; even the most conscientious and observant physicians may not stop or lower the medication in time to avoid patient discomfort.

The classical discuss ions of a JH describe the presence of bacterial debris or toxins from anti-infective therapies that cause this reaction. This is certainly true, but another byproduct is also formed when cell wall deficient bacteria or L forms are attacked. I have noticed that some JH present as a flu syndrome.

Other patients develop purulent drainage from the head and neck, urine and other areas. When I have cultured these patients, I have been able to isolate adult (non L-form) bacteria. Treatment with medications that favor the destruction of L-forms who are unwalled forms will also favor or select for the survival of adult or walled forms of bacteria.1

Microbiologists call this change of the form of bacteria pleomorphism. The induction of walled forms of bacteria has been studied and should be kept in mind when considering treating a JH reaction.

Treatment of a JH should be aimed at eliminating toxins from the killed bacteria and destruction of newly induced adult b acteria. Consideration should also be given to the possibility of overgrowth of endemic yeast infections.

Often there are symptoms that clinically indicate the presence of histamine. The physician's diagnostic skills and clinical judgment must be called into place to differentiate between a direct toxic reaction versus the appearance of an adult form organism or the more insidious development of yeast overgrowth.

For the ease of the reader, I am classifying the JH reaction into two categories:

1) Acute - life-threatening. These may also be called anaphilactoid.

2) Non-acute or non-life-threatening- not anaphilactoid.

Acute - Life Threatening

The severe acute reactions are probably related to a massive response of the immune system to toxins. There may be a large release of histamine as well. Such anaphilactoid reactions need immediate attention and should be considered life-threatening.

The most severe problems involve swelling of the neck areas and closure of the airway. This must be treated at once with epinephrine followed by transportation to a hospital. The management of severe anaphilactoid emergencies is well known by healthcare personnel and beyond the ability of the patients to handle at home.

A drop in blood pressure is also common along with skin changes due to dilation of the blood vessels. This can lead to cardiovascular collapse unless aggressively treated and also needs hospital management.

Milder cases featuring asthma may respond to inhaled broncodialator medications, but this can sometimes delay the patient from seeking early medical attention and avoiding catastrophe. Skin rashes are not life threatening but often are quite distressing. A more detailed

1 Mattman, Lida Cell Wall Deficient Forms, Stealth Pathogens 1993 CRC Press

Anti-infective therapies or approaches that can feature the JH

Antibiotic/antifungal therapies < LI>Oxidative therapies


Ultraviolet Blood Irradiation

Hydrogen Peroxide therapy

High dose vitamin C therapy

Induced Hyperthermia

Sunlight exposure

Various herbal therapies

Bee sting reactions

Iodine reactions

Terms in Use for JH

Herxheimer Reaction

Die Off Reaction

Flare Reaction

Coming Out Reaction

Summary of Tre atment Features of Life Threatening JH Reactions

Treatment of histaminic states

Acute life threatening histamine shock or airway swelling

Epinephrine with fluids for shock

Mild JH Reactions

Anti-histamine medication e.g.benadryl parenterally or by mouth

Supportive Care for Anaphylactic Type JH Reactions

Management of Bronchospasm (acute asthma) with Bronchodialators discussion of these kinds of problems is presented in most textbooks of medicine and all manuals for emergency care.

Management of Non-life Threatening JH Reactions or Clinical Flares

The more typical JH reactions to anti-infective therapies are: worsening of symptoms, febrile states such as night sweats, flu-like picture, hot swollen joints, mental depression and fatigue. I recommend home therapies designed to clear the blood and make the patient more comfortable.

My routine calls for baths in hydrogen peroxide and Epsom salts. These baths are very effective and have tremendous anti-infective effects. They may work for only a short time at first and may need to be repeated. The peroxide easily enters the body through the skin and rapidly detoxifies and sterilizes the blood.

There will be a marked reduction in tight muscles that can be a part of a JH reaction.

Unfortunately peroxide can have a JH reaction of its own, but this is more pronounced when it is used IV rather than in a bath. Magnesium in the Epsom salts also passes easily systematically; it has a local anesthetic, antispasmodic effect and an overall improvement in the performance of most systems. Oral peroxide is available but not discussed here.

The IV route for both peroxide and magnesium is used to stop the JH reaction in office management. The same benefit of blood detoxification and general enhanced clearing of tissue toxins and bacteria can be claimed for high dose ascorbic acid (20-50 GMs IV). Vitamin C can be given in oral form too.

Ascorbic acid powder equals about 5 grams per level teaspoon. This dose can be taken with water or juice as often as needed or until there is GI intolerance such as diarrhea. The clinical effects are similar to peroxide.

In fact, the two can be given to a patient on the same day with excellent results. It must be remembered however; the vitamin C will also neutralize peroxide and thus should always be given after the bath.

Mild JH reactions are also seen with vitamin C therapy again mainly when given IV. Such therapies as peroxide baths and vitamin C are easy to do at home and extremely effective at helping patients make a quick, safe recovery from a JH reaction.

Other oxidative office therapies can be alternated with these modalities or with antibiotics to hasten detoxification of bacterial toxins. Ultraviolet blood irradiation (UBI) involves removing a small portion of the circulating blood and cleaning it under UV light before returning it to the patient. The mechanism of action is not well known, but such treatment has been used for over fifty years mostly outside the United States for improvement in immunologic function. This treatment also ameliorates the JH phase of anti infective therapy.

It is further noticed that direct exposure to sunlight has a similar effect to UBI in many patients. Therefore my patients are asked to get sun exposure if the climate allow s not using sunscreen up to the point of mild burning. I caution them that minocycline will cause them to be sensitive, but that they can go out with care and receive great benefit.

And as I had expected, I do see stable patients develop mild JH re actions after such activities as fishing trips which cause a huge UV sun dose and large destruction of circulating bacteria.

Another approach to treating worsening of symptoms after oral antibiotic or other anti-infective therapy is the use of IV a ntibiotics. I have used IV doxycycline for quelling such problems. Other physicians have used IV minocycline, IV clindamycin and others for this purpose.

In my practice the antibiotics are the drugs of last resort. The most preferred treatments involve the home remedies with peroxide and vitamin C.

I have tried to avoid the use of anti-inflammatory remedies for the JH reaction. The corticosteroids will control a rash, but I have noted a general deterioration of the patient's condition weeks later.

Such topical steroids as are given in inhaled or skin medications are certainly absorbed. Their use will be a quick fix at a high cost due to the setback they cause. The nonsteroidal anti-inflammatories that are used orally have the effect of irritating the GI system and are implicated as one of the causes of the leaky gut syndrome also linked to many of the chronic pain states.

Again they are drugs of a last resort. Topical soothing lotions such as aloe vera can do no harm and may make a rash feel better.

Yeast overgrowth must be considered when new symptoms develop after antibiotics are started. I put all chronic pain patients on continuous oral acidophilus supplements before starting any anti-infective therapy.

We were noticing yeast emergence in nearly 100% of the patients. With the addition of acidophilus, this problem is becoming a lot less common.


Worsening or flaring of symptoms after the commencement of anti-infective therapy should be expected and considered a JH reaction. The patient should be cautioned about the signs of a potentially life threatening anaphilactoid reaction and urged to seek medical attention at once.

The more common clinical non-life threatening flares should not cause undo concern to the patient and may be treated by altering the medication dosage and with some of the suggested therapies above. Abandoning of the anti-infective approach to chronic pain and arthritic disease would be unfortunate simply because of these expected temporary setbacks.

For educational purposes only. Consult your physician before you make any changes in your treatment. Source Here

Lucy Barnes