[Show abstract][Hide abstract] ABSTRACT: We report the case of a healthy 36 year old man who suffered from foot pain lasting for weeks, without having a specific medical history relating to it. The clinical evaluation was interpreted as a transfer metatarsalgia caused by a splayfoot. The radiographs revealed no pathology except the splayfoot deformity. Due to persistent pain and swelling of the entire forefoot, after two weeks of conventional treatment, magnet resonance images (MRI) and a blood sample were taken. The laboratory investigation showed raised levels of white blood cell count and C-reactive protein. The MRI showed up oedema in the metatarsal heads II-IV, as well as soft tissue swelling of the forefoot without any signs of decomposition.
Because of this atypical inflammation of the forefoot a laboratory investigation to check for rheumatology disease was done and revealed borrelia burgdorferi infection. On the basis of these findings, antibiotic treatment was started and maintained over three weeks. The symptoms disappeared after 2 weeks, and the patient was able to resume his sports activities.
Journal of Medical Case Reports 02/2007; 1:44. DOI:10.1186/1752-1947-1-44
[Show abstract][Hide abstract] ABSTRACT: Borrelia spielmanii sp. nov. has recently been shown to be a novel human pathogenic genospecies that causes Lyme disease in Europe. In order
to elucidate the immune evasion mechanisms of B. spielmanii, we compared the abilities of isolates obtained from Lyme disease patients and tick isolate PC-Eq17 to escape from complement-mediated
bacteriolysis. Using a growth inhibition assay, we show that four B. spielmanii isolates, including PC-Eq17, are serum resistant, whereas a single isolate, PMew, was more sensitive to complement-mediated
lysis. All isolates activated complement in vitro, as demonstrated by covalent attachment of C3 fragments; however, deposition
of the later activation products C6 and C5b-9 was restricted to the moderately serum-resistant isolate PMew and the serum-sensitive
B. garinii isolate G1. Furthermore, serum adsorption experiments revealed that all B. spielmanii isolates acquired the host alternative pathway regulators factor H and factor H-like protein (FHL-1) from human serum. Both
complement regulators retained their factor I-mediated C3b inactivation activities when bound to spirochetes. In addition,
two distinct factor H and FHL-1 binding proteins, BsCRASP-1 and BsCRASP-2, were identified, which we estimated to be approximately
23 to 25 kDa in mass. A further factor H binding protein, BsCRASP-3, was found exclusively in the tick isolate, PC-Eq17. This
is the first report describing an immune evasion mechanism utilized by B. spielmanii sp. nov., and it demonstrates the capture of human immune regulators to resist complement-mediated killing.
Infection and Immunity 11/2007; 75(10):4817-25. DOI:10.1128/IAI.00532-07 · 3.73 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We report the identification of isolates of Borrelia burgdorferi strain B31 that exhibit an unusual macrolide-lincosamide (ML) or macrolide-lincosamide-streptogramin A (MLS(A)) antibiotic resistance pattern. Low-passage isolates were resistant to high levels (>100 microg/mL) of erythromycin, spiramycin and the lincosamides but were sensitive to dalfopristin, an analogue of streptogramin B. Interestingly, the high-passage erythromycin-resistant strain B31 was resistant to quinupristin, an analogue of streptogramin A (25 microg/mL). Biochemical analysis revealed that resistance was not due to antibiotic inactivation or energy-dependent efflux but was instead due to modification of ribosomes in these isolates. Interestingly, we were able to demonstrate high-frequency transfer of the resistance phenotype via conjugation from B. burgdorferi to Bacillus subtilis (10(-2)-10(-4)) or Enterococcus faecalis (10(-5)). An intergeneric conjugal system in B. burgdorferi suggests that horizontal gene transfer may play a role in its evolution and is a potential tool for developing new genetic systems to study the pathogenesis of Lyme disease.
International Journal of Antimicrobial Agents 01/2008; 30(6):496-504. DOI:10.1016/j.ijantimicag.2007.07.013 · 4.30 Impact Factor
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