Objective
To determine the sensitivity of 4 strains of Oxalobacter formigenes (OxF) found in humans, HC1, Va3, CC13, and OxK, to varying concentrations of commonly-prescribed antibiotics. OxF gut colonization has been associated with a decreased risk of forming recurrent calcium oxalate kidney stones.
Methods
For each strain and each antibiotic concentration, 100 μL of an overnight culture and 100 μL of the appropriate antibiotic were added to a 7 mL vial of oxalate culture media containing 20 mM oxalate. On the fourth day, vials were visually examined for growth, and a calcium oxalate precipitation test was performed to determine whether OxF grew in the presence of the antibiotic.
Results
All 4 OxF strains were resistant to amoxicillin, amoxicillin/clavulanate, ceftriaxone, cephalexin, and vancomycin while they were all sensitive to azithromycin, ciprofloxacin, clarithromycin, clindamycin, doxycycline, gentamicin, levofloxacin, metronidazole, and tetracycline. One strain, CC13, was resistant to nitrofurantoin while the others were sensitive. Differences in minimum inhibitory concentration between strains were demonstrated.
Conclusions
Four human strains of OxF are sensitive to a number of antibiotics commonly utilized in clinical practice; however, minimum inhibitory concentrations differ between strains.
Fragile X syndrome (FXS), a neurodevelopmental disorder with no known cure, is caused by a lack of expression of the fragile X mental retardation protein (FMRP). As a singlegene disorder, FXS is an excellent candidate for viral-vectorbased gene therapy, although that is complicated by the existence of multiple isoforms of FMRP, whose individual cellular functions are unknown. We studied the effects of rat and mouse orthologs of human isoform 17, a major expressed isoform of FMRP. Injection of neonatal Fmr1 knockout rats and mice with adeno-associated viral vectors (AAV9 serotype) under the control of an MeCP2 mini-promoter resulted in widespread distribution of the FMRP transgenes throughout the telencephalon and diencephalon. Transgene expression occurred mainly in non-GABAergic neurons, with little expression in glia. Early postnatal treatment resulted in partial rescue of the Fmr1 KO rat phenotype, including improved social dominance in treated Fmr1 KO females and partial rescue of locomotor activity in males. Electro-encephalogram (EEG) recordings showed correction of abnormal slow-wave activity during the sleep-like state in male Fmr1 KO rats. These findings support the use of AAV-based gene therapy as a treatment for FXS and specifically demonstrate the potential therapeutic benefit of human FMRP isoform 17 orthologs.
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