Evaluation of central nervous system involvement in Lyme borreliosis patients with a solitary erythema migrans lesion.

To determine whether early dissemination of Borrelia burgdorferi to the central nervous system occurs in stage I of Lyme borreliosis, neurological and cerebrospinal fluid examination was performed in 48 consecutive patients in whom the only sign of infection was a solitary erythema migrans lesion. Long-term follow-up after treatment with tetracycline was carried out by telephone interview. At presentation, neurological findings were normal in all 48 patients. Cerebrospinal fluid samples were obtained from 29 (60%) patients. Mild pleocytosis and mild impairment of the blood-brain barrier were present in four and one of these patients, respectively. No significant amount of tumor necrosis factor or interleukin 6 was found in the cerebrospinal fluid samples. Culture results of 13 cerebrospinal fluid samples were negative. Borrelia burgdorferi DNA was only detected by the polymerase chain reaction in one of two aliquots of the cerebrospinal fluid sample of one patient. None of 46 patients who were interviewed 12 to 51 (median 25) months after antibiotic treatment developed manifestations consistent with disseminated or chronic Lyme borreliosis. Thus, no compelling evidence was found for the presence of asymptomatic central nervous system involvement in patients with clinically localized Lyme borreliosis.

Different genospecies of Borrelia burgdorferi are associated with distinct clinical manifestations of Lyme borreliosis.

Borrelia burgdorferi sensu lato has been subdivided into three genospecies: B. burgdorferi sensu stricto, B. garinii, and B. burgdorferi group VS461. Sixty-eight isolates cultured from patients and 26 strains from ticks were characterized with use of SDS-PAGE, western blotting, and rRNA gene restriction analysis. Fifty-seven of 58 strains obtained from the skin of 70 patients who had erythema migrams or acrodermatitis chronica atrophicans were of group VS461, whereas the genotype of the remaining strain was unidentifiable. Of 10 strains cultured from CSF (n = 3) and skin (n = 7) of 20 patients with extracutaneous symptoms of Lyme borreliosis, nine were B. garinii and one was B. burgdorferi sensu stricto. Of these 20 patients, 17 had neuroborreliosis, one had arthritis and carditis, one had myalgia, and one had erythema and arthralgia. All 26 isolates from ticks were of group VS461. In conclusion, infections due to group VS461 and B. garinii are associated with cutaneous and extracutaneous symptoms, respectively. Our findings suggest that B. burgdorferi genotypes have different pathogenic potentials.

Acquired sideroblastic anaemia after aplastic anaemia caused by D-penicillamine therapy for rheumatoid arthritis.

A 68 year old man with rheumatoid arthritis developed marrow aplasia during D-penicillamine treatment. Recovery of granulopoiesis and erythropoiesis was ineffective with features of a secondary sideroblastic anaemia. Absence of megakaryopoiesis persisted. Therapeutic measures failed, and the patient finally died. These events illustrate a haematopoietic stem cell injury induced by D-penicillamine.

Methylprednisolone pulse therapy in conjunction with azathioprine in rheumatoid arthritis.

In the management of rheumatoid arthritis two potentially useful roles for methylprednisolone (MP) pulse therapy are presently recognised: in patients in whom second line drugs have not led to a satisfactory remission or have caused side effects, and in bridging the gap between the start and the delayed onset of effect of a slow-acting antirheumatic drug. Recently it was shown that MP-pulse therapy was effective in accelerating the response to sulphasalazine and D-penicillamine. Nineteen patients with a persistently active rheumatoid arthritis, who had failed to respond to at least two slow-acting antirheumatic drugs, were treated with MP-pulse therapy in conjunction with azathioprine. Twelve patients continued this treatment for 6 months and 8 for 12 months. MP-pulse therapy resulted in an immediate improvement in Ritchie articular index, grip strength, ESR and CRP. However, this improvement lasted less than six weeks. After 6 months some improvement due to the effect of azathioprine became apparent. Some rather serious side effects were noted. It is concluded that MP-pulse therapy has a (short lasting) beneficial effect in persistently active rheumatoid arthritis. However MP-pulse therapy is not suitable to bridge the gap between the introduction of azathioprine-treatment and the delayed response to this drug.