ABSTRACT
Leptospirosis is a zoonosis that is related to potential respiratory, renal, neurological, and cardiovascular failure. At present, antibiotics are the recommended treatment, but due to the underlying cause of the disease, they may induce the Jarisch-Herxheimer reaction (JHR) within 24 hours. At the same time, we speculate that JHR may aggravate the natural course of leptospirosis. Considering that there are few available reports on this event, we will share a case of pulmonary hemorrhagic leptospirosis, where antibiotic treatment is suspected to have triggered the JHR. This report is expected to improve clinical attention to the relationship between leptospirosis and JHR.
ABSTRACT
In this study, we developed an in vivo method to determine drug effects on oxidation-induced apoptosis in the zebrafish brain caused by treatment with L-hydroxyglutaric acid (LGA). We confirmed that LGA-induced apoptosis was caused by oxidation by examining the presence of an oxidative product, nitrotyrosine. Next, we examined the effects of 14 characterized neuroprotectants on LGA-treated zebrafish, including: D-methionine (D-Met), Indole-3-carbinol, deferoxamine (DFO), dihydroxybenzoate (DHB), deprenyl, L-NAME (N(G)-nitro-L-arginine methyl ester), n-acetyl L-cysteine (L-NAC), 2-oxothiazolidine-4-carboxylate (OTC), lipoic acid, minocycline, isatin, cortisone, ascorbic acid and alpha-tocopherol. Eleven of 14 neuroprotectants and 7 of 7 synthetic anti-oxidants exhibit significant protection in zebrafish. Buthionine sulfoximine (BSO), used as a negative control, exhibited no significant protective effects. In addition, three blood-brain barrier (BBB) impermeable compounds exhibited no significant effects. Our results in zebrafish were similar to results reported in mammals supporting the utility of this in vivo method for identifying potential neuroprotective anti-oxidants.
