Israel Medical Association Journal

A fundamental challenge for multiple sclerosis (MS) therapy is to promote repair and remyelination beyond their limited spontaneous extent. Glatiramer acetate (GA, Copaxone®), an approved treatment for MS, has been shown to induce immunomodulation as well as neuroprotection in the inflamed central nervous system (CNS) in MS and in its model, experimental autoimmune encephalomyelitis (EAE). Using electron microscopy, immunohistochemistry, and advanced magnetic resonance imaging, we have demonstrated diminished myelin damage in GA-treated mice, in both relapsing-remitting and chronic EAE, even when treatment was applied late after the disease exacerbation, suggesting repair. Furthermore, quantitative analysis indicated significant elevation in remyelinated axons in GA-treated compared to untreated EAE mice. To further prove that GA can promote myelination, we studied its effect in the developing naïve CNS, when injected postnatally. Immunohistochemical and ultrastructural analyses revealed significant increase in the number of myelinated axons, the thickness of the myelin encircling them, and the resulting g-ratios in the spinal cords of GA-injected mice compared to their phosphate-buffered saline-injected littermates. A prominent elevation in the amount of progenitor oligodendrocytes and their proliferation, as well as in mature oligodendrocytes, implied that the effect of GA is linked to the differentiation along the oligodendroglial cascade. Furthermore, a functional advantage in rotating rod test was exhibited by GA-injected mice over their littermates. These cumulative findings indicate that GA treatment affects myelination under inflammatory as well as non-inflammatory conditions, supporting the notion that the repair process in the CNS can be up-regulated by therapy.

Background: Due to increasing antimicrobial resistance there has been renewed interest in old drugs that have fallen into disuse because of toxic side effects.

Objectives: To evaluate the susceptibility profile, in our hospital, of Enterobacteriaceae and Streptococcus pneumoniae isolates to chloramphenicol and to compare them with the susceptibility to amoxicillin-clavulanate.

Methods: All isolates of Enterobacteriaceae and S. pneumoniae recovered in our lab during a one year period were tested for susceptibility to chloramphenicol and amoxicillin-clavulanate or penicillin, respectively.

Results: Of 413 Enterobacteriaceae isolates, 182 (44.1%) were resistant to amoxicillin-clavulanate, but only 76 (18.4%) were resistant to chloramphenicol. Of 189 isolates of S. pneumoniae, 4 (2.1%) were highly resistant to penicillin and 73 (38.8%) were partially resistant, while only 2 (1.1%) were resistant to chloramphenicol. None of the 24 S. pneumoniae isolates causing invasive diseases exhibited resistance to chloramphenicol.

Conclusions: In an era of increasing resistance to many antibiotic preparations, chloramphenicol might have a role in the treatment of intraabdominal and respiratory tract infections.