Ceftriaxone and Doxycycline induced Seroconversion in Previously Seronegative Patient with Clinically Suspected Disseminated Lyme Disease: Case Report.

We present a case of middle-aged woman whose health problems began 3 months after a registered tick bite in endemic area of Lyme borreliosis. First symptoms included fatigue, chills, cervical lymphadenopathy, neck pain and stiffness. Patient was afebrile. Lyme disease was excluded due to lack of erythema migrans and negative enzyme immunoassay test results for anti-Borrelia antibodies. During the next few months, her condition was getting worse and symptoms were accompanied with brain fog, dizziness, palpitations, irregular menstrual cycles, insomnia, panic attacks, headaches, and muscle aches. This led to multiple medical tests and examinations, but the diagnosis failed to be established. Finally, after occurrence of paresthesia and weakness of leg muscles, clinical diagnosis of disseminated Lyme borreliosis with nervous system involvement was suspected and antibiotic therapy was initiated. After the second dose of ceftriaxone, patient got fever and her condition worsened. However, ceftriaxone therapy was continued for a total of 5 days and was followed by 4 weeks of doxycycline therapy. Upon completion of antibiotic therapy, high specific anti-Borrelia antibodies were detected by Western blot and SeraSpot. Appearance of anti-Borrelia antibodies, in contrast to negative test results performed immediately before the therapy started, indicated seroconversion. 18 months after the therapy, patient was completely without the symptoms. This paper emphasizes importance of clinical evaluation of Lyme disease and shows a unique case of seroconversion in patient with symptoms of disseminated Lyme disease. Seroconversion was likely triggered by release of lipoproteins and other immunogenic molecules from Borrelia once the bacterial die-off began due to antibiotic therapy.

Chronic iron overload induces gender-dependent changes in iron homeostasis, lipid peroxidation and clinical course of experimental autoimmune encephalomyelitis.

To analyze iron- and gender-dependent mechanisms possibly involved in pathogenesis of multiple sclerosis (MS) in this study we evaluated the effects of iron overload (IO) on iron status and lipid peroxidation processes (LPO) in tissues of female and male DA rats during chronic relapsing experimental autoimmune encephalomyelitis, a well-established MS animal model. Rats were treated by iron sucrose (75mg/kg bw/day) or with saline solution during two weeks before the sensitization with bovine brain homogenate in complete Freund's adjuvant. Clinical signs of EAE were monitored during 29 days. Serum and tissues of CNS and liver were sampled before immunization and at day 13th post immunization (during acute phase of EAE). The determination of ferritin, iron, malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) and evaluation of histopathology were performed by ELISA, ICP spectrometry and immunohistochemistry. Results showed that IO in female EAE rats accelerated the onset of disease. In contrast, in male rats it accelerated the progression of disease and increased the mortality rate. During acute phase of EAE female IO rats sequestered more Fe in the liver, spinal cord and in the brain and produced more ferritin than male EAE rats. Male rats, however, reacted on IO by higher production of MDA or 4-HNE in the neural tissues and showed greater signs of plaque formation and gliosis in spinal cord. The data point to sexual dimorphism in mechanisms that regulate peripheral and brain iron homeostasis and imply that men and women during MS might be differentially vulnerable to exogenous iron overload.