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.
