Diagnosis and therapy of Lyme disease in childhood. Recommendation of German-Society of Pediatric Infectious Diseases

Lyme borreliosis is the most frequent tickborne disease of man in the North ern Hemisphere. A variety of systems may be involved. The most frequent man ifestations in childhood include erythema migrans, meningitis, cranial nerv e palsy and arthritis. Erythema migrans is usually easily recognized and de termination of antibodies to Borrelia burgdorferi should not be performed. Childhood neuroborreliosis is characterized mostly by aseptic meningitis wi th or without cranial nerve palsy, in most cases facial palsy. Basic CSF fi ndings often show combined evidence of lymphocytic pleocytosis, IgM-class d ominance in intrathecal humoral immune response, and blood-CSF barrier dysf unction. Calculation of the B. burgdorferi-specific antibody index (accordi ng to Reiber) has proved to be the most sensitive method for detecting intr athecal synthesis of specific antibodies. Lyme arthritis presents initially as episodic oligoarthritis, mostly involving the knee joint, and may turn into chronic monoarthritis of the knee; usually high titers of IgG antibodi es to B. burgdorferi are found. Rarer manifestations such as encephalomyeli tis, chronic arthritis, carditis and inflammatory eye disease may be diffic ult to diagnose due to clinical ambiguity and problems in the interpretatio n of serological results. Antibodies to B. burgdorferi found by the sensiti ve Elisa test must always be confirmed by immunoblot analysis, but sometime s immunoblot analysis is more sensitive than the Elisa. Treatment is by ant ibiotics, amoxicillin for erythema migrans, and i.v. third-generation cepha losporins for all other manifestations. Discussion: Even after successful antibiotic therapy,antibodies may persist for months and years, and no further antibiotic treatment is necessary in the absence of attributable clinical manifestations. The differentiation be tween a persisting immune response and a persisting infection therefore has to be based upon the clinical symptoms, non-specific laboratory data and t he development of antibody titers.