Institutional designs to face the dark side of total allowable catches

Setting total allowable catches (TACs) is an endogenous process in which different agents and institutions, often with conflicting interests and opportunistic behaviour, try to influence policy-makers. Such policy-makers, far from being the benevolent social planners many would wish them to be, may also pursue self-interest when making final decisions. Although restricted knowledge of stock abundance and population dynamics, and weakness in enforcement, have effects, these other factors may explain the reason why TAC management has failed to guarantee sustainable exploitation of fish resources. Rejecting the exogeneity of the TAC and taking advantage of fruitful debate on economic policy (i.e. the rules vs. discretion debate, and that surrounding the independence of central banks), two institutional developments are analysed as potential mechanisms to face up to misconceptions about TACs: long-term harvest control rules, and a central bank of fish.

Multi-drug resistance profiles and the genetic features of Acinetobacter baumannii isolates from Bolivia

Introduction: Acinetobacter baumannii is opportunistic in debilitated hospitalised patients. Because information from some South American countries was previously lacking, this study examined the emergence of multi-resistant A. baumannii in three hospitals in Cochabamba, Bolivia, from 2008 to 2009. Methodology: Multiplex PCR was used to identify the main resistance genes in 15 multi-resistant A. baumannii isolates. RT-PCR was used to measure gene expression. The genetic environment of these genes was also analysed by PCR amplification and sequencing. Minimum inhibitory concentrations were determined for key antibiotics and some were determined in the presence of an efflux pump inhibitor, 1-(1-napthylmethyl) piperazine. Results: Fourteen strains were found to be multi-resistant. Each strain was found to have the bla(OXA-58) gene with the ISAba3-like element upstream, responsible for over-expression of the latter and subsequent carbapenem resistance. Similarly, ISAba1, upstream of the bla(ADC) gene caused over-expression of the latter and cephalosporin resistance; mutations in the gyrA(Ser83 to Leu) and parC (Ser-80 to Phe) genes were commensurate with fluoroquinolone resistance. In addition, the adeA, adeB efflux genes were over-expressed. All 15 isolates were positive for at least two aminoglycoside resistance genes. Conclusion: This is one of the first reports analyzing the multi-drug resistance profile of A. baumannii strains isolated in Bolivia and shows that the over-expression of thebla(OXA-58), bla(ADC) and efflux genes together with aminoglycoside modifying enzymes and mutations in DNA topoisomerases are responsible for the multi-resistance of the bacteria and the subsequent difficulty in treating infections caused by them.