The Jarisch-Herxheimer reaction

The Jarisch-Herxheimer reaction resembles bacterial sepsis and can occur after initiation of antibacterials such as penicillin or tetracycline, or treatment of tick-borne relapsing fever. 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 manifests as fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), and exacerbation of skin lesions. The intensity of the reaction indicates the severity of inflammation. Reaction commonly occurs within two hours of drug administration, but is usually self-limiting. Prophylaxis and treatment with an anti-inflammatory agent may stop progression of the reaction. Oral aspirin every four hours for 1–2 days, or 60 mg of prednisone orally or intravenously has been used as an adjunctive treatment.

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.

Most women with primary syphilis and 50% of women with secondary syphilis develop JH reaction following penicillin therapy.