ICD-10 T78.2 DiseasesDB 32939 | ICD-9-CM 995.0 | |
A Jarisch–Herxheimer reaction ( /ˌjɑːrɪʃ ˈhɛərkshaɪmər/) is a reaction to endotoxin-like products released by the death of harmful microorganisms within the body during antibiotic treatment. The antibiotics are so successful at killing a lot of bacterial cells that now the contents of those burst cells provoke some irritation and must be cleared.
Contents
Jarisch–Herxheimer reactions are usually not life-threatening. Often they last only a few hours.
Signs and symptoms
It resembles bacterial sepsis and can occur after initiation of antibacterials, such as mild silver protein, penicillin or tetracycline, for the treatment of louse-borne relapsing fever (80–90% of patients) and in tick-borne relapsing fever (30–40%). An association has been found between the release of heat-stable proteins from spirochetes and the reaction. Typically, the death of these bacteria and the associated release of endotoxins or lipoproteins occurs faster than the body can remove the substances. It usually manifests within a few hours of the first dose of antibiotic as fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), exacerbation of skin lesions and anxiety. The intensity of the reaction indicates the severity of inflammation. Reaction commonly occurs within two hours of drug administration, but is usually self-limiting.
Causes
The Jarisch–Herxheimer reaction is classically associated with penicillin treatment of syphilis. Duration in syphilis is normally only a few hours. The reaction is also seen in other diseases caused by spirochetes, such as borreliosis (Lyme disease and tick-borne relapsing fever) and leptospirosis, and in Q fever. Similar reactions have also been reported to occur in bartonellosis (including cat scratch disease), brucellosis, typhoid fever, trichinosis, and cerebral trypanosomiasis.
Pathophysiology
The Herxheimer reaction has shown an increase in inflammatory cytokines during the period of exacerbation, including tumor necrosis factor alpha, interleukin-6 and interleukin-8. In an analogy to how the successful killing of a lot of undesirable cells by chemotherapy can present the corollary problem of tumor lysis syndrome, the successful killing of a lot of bacterial cells presents the resultant problem of clearing their constituents from the blood. The analogy is not precise because the cell contents differ; but the concept is instructive.
Treatments
Prophylaxis and treatment with an anti-inflammatory agent may stop progression of the reaction. Oral aspirin or ibuprofen every four hours for a day or 60 mg of prednisone orally or intravenously has been used as an adjunctive treatment. However, steroids are generally of no benefit. Patients must be closely monitored for the potential complications (collapse and shock) and may require IV fluids to maintain adequate blood pressure. If available, meptazinol, an opioid analgesic of the mixed agonist/antagonist type, should be administered to reduce the severity of the reaction. Anti TNF-a may also be effective.
History
Both Adolf Jarisch, an Austrian dermatologist, and Karl Herxheimer, a German dermatologist, are credited with the discovery of the Jarisch–Herxheimer reaction. Both Jarisch and Herxheimer observed reactions in patients with syphilis treated with mercury. The reaction was first seen following treatment in early and later stages of syphilis treated with Salvarsan, mercury, or antibiotics. Jarisch thought that the reaction was caused by a toxin released from the dying spirochetes. It is observed in 50% of patients with primary syphilis and about 90% of patients with secondary syphilis.