The Use of Kaolin as a Prophylactic Treatment to Prevent Columnaris Disease (Flavobacterium covae) in Commercial Baitfish and Sportfish Species.

Aquaculture farms in Arkansas, USA routinely battle columnaris disease caused by Flavobacterium covae. Columnaris is prevalent during stressful events such as feed training and when fish are stocked at high densities in holding vats before sale. Kaolin clay was effective in laboratory trials as a treatment for columnaris in catfish. As a result, fish farmers are interested in applying kaolin products but were hesitant as they feared that the high doses of kaolin clay in vats might negatively affect the gills and overall health of fish. Therefore, we evaluated potential clay concentrations that might be used to prophylactically treat fish in vats. The effects of low to excessively high doses (0, 1, 2, 4, or 8 g/L) of kaolin clay (AkuaProTM, Imerys, GA, USA) were evaluated using a 72 h bioassay conducted in static tanks using Micropterus salmoides, Pomoxis nigromaculatus, Lepomis macrochirus, Ictalurus punctatus, Notemigonus crysoleucas, and Pimephales promelas. Results of these trials revealed a 100% survival rate across all six fish species exposed to kaolin clay at concentrations of up to 8 g/L for 48 h (followed by a 24 h recovery period in clean water) with no adverse effects to eyes, skin, gastrointestinal tract, or liver histology noted at any treatment. In addition, Micropterus salmoides analyzed for heavy metals due to exposure to the clay indicated that concentrations did not differ from control fish.

Cocaine enhances HIV-1-induced CD4(+) T-cell apoptosis: implications in disease progression in cocaine-abusing HIV-1 patients.

Substance abuse is a major barrier in eradication of the HIV epidemic because it serves as a powerful cofactor for viral transmission, disease progression, and AIDS-related mortality. Cocaine, one of the commonly abused drugs among HIV-1 patients, has been suggested to accelerate HIV disease progression. However, the underlying mechanism remains largely unknown. Therefore, we tested whether cocaine augments HIV-1-associated CD4(+) T-cell decline, a predictor of HIV disease progression. We examined apoptosis of resting CD4(+) T cells from HIV-1-negative and HIV-1-positive donors in our study, because decline of uninfected cells plays a major role in HIV-1 disease progression. Treatment of resting CD4(+) T cells with cocaine (up to 100 µmol/L concentrations) did not induce apoptosis, but 200 to 1000 µmol/L cocaine induced apoptosis in a dose-dependent manner. Notably, treatment of CD4(+) T cells isolated from healthy donors with both HIV-1 virions and cocaine significantly increased apoptosis compared with the apoptosis induced by cocaine or virions alone. Most important, our biochemical data suggest that cocaine induces CD4(+) T-cell apoptosis by increasing intracellular reactive oxygen species levels and inducing mitochondrial depolarization. Collectively, our results provide evidence of a synergy between cocaine and HIV-1 on CD4(+) T-cell apoptosis that may, in part, explain the accelerated disease observed in HIV-1-infected drug abusers.