BackgroundLymphatic filariasis (LF), a global public health problem affecting approximately 120 million people worldwide, is a leading cause of disability in the developing world including the South Pacific. Despite decades of ongoing mass drug administration (MDA) in the region, some island nations have not yet achieved the threshold levels of microfilaremia established by the World Health Organization for eliminating transmission. Previously, the generation of a novel Aedes polynesiensis strain (CP) infected with an exogenous type of Wolbachia has been described. The CP mosquito is cytoplasmically incompatible (i.e., effectively sterile) when mated with wildtype mosquitoes, and a strategy was proposed for the control of A. polynesiensis populations by repeated, inundative releases of CP males to disrupt fertility of wild females. Such a strategy could lead to suppression of the vector population and subsequently lead to a reduction in the transmission of filarial worms.Methodology/Principal FindingsCP males and F1 male offspring from wild-caught A. polynesiensis females exhibit near equal mating competitiveness with F1 females under semi-field conditions.Conclusions/SignificanceWhile laboratory experiments are important, prior projects have demonstrated the need for additional testing under semi-field conditions in order to recognize problems before field implementation. The results reported here from semi-field experiments encourage forward progression toward small-scale field releases.

Immersion of knives momentarily in hot water (82 degrees C) was ineffective in destroying salmonellas on knives used in a meatworks to carry out the bung dropping operation. Laboratory experiments confirmed that knives covered with meat products required 10 or more seconds to be effectively decontaminated at this temperature. Examination of knives used for slaughtering and for dressing beef carcases showed that knives coming into contact with hides had higher counts for salmonella and a higher percentage positive than knives used for other cutting operations. Knives used for cutting the skin of the forelegs and hindlegs had the highest counts.

The ability of the pathogenic fungus Candida albicans to cause disease requires rapid adaptation to changes in the host environment and to an evolving host immune response. The identification of 'virulence factors' using in vitro characterization of mutant strains has traditionally relied on a common set of phenotypic and biochemical assays (most often performed at 30 6C) and the subsequent correlation with their corresponding virulence in mouse models of disease. Utilizing a panel of isogenic mutants for the multifunctional signal-modulating 14-3-3 protein (Bmh1p), we have found that specific mutations affect a variety of different pathways currently associated with virulence, including those involved with the formation of filaments, as well as interaction with host immune cells. Surprisingly, our studies revealed that deficiencies in many of these pathways do not always correlate with virulence in a mouse model of disseminated infection. Mutations within the binding pocket of Bmh1p that affect the ability of the protein to efficiently bind ligand had varying effects on the results of a number of in vitro and in vivo assays. The capability, in vitro, to filament in embedment conditions, and to filament and form chlamydospores under microaerophilic conditions on cornmeal agar, does not correlate with virulence. It is likely that only a subset of hyphal signalling pathways is actually required for the establishment of infection in the disseminated mouse model. Most importantly, our results suggest that the delayed onset of lagphase growth in vitro at 37 6C, and not at 30 6C, results in an inability of these mutants to rapidly adjust to environmental changes in vivo and may be responsible for their increased clearance and reduced virulence. It is critical, therefore, that future in vitro studies of putative virulence factors in C. albicans include careful characterization at physiological temperatures.

A method similar to that used by Board and Board (1967) was used to determine the numbers of eggs penetrated by bacteria on 3 poultry farms in south-east Queensland. Significant differences in the percentages of penetrated eggs between the eggs of layer birds (9.7%) and the eggs of meat birds (16.1%) and between nest eggs (10.5%) and floor eggs (15.3%) were detected. The distribution of the numbers of penetration points was similar for nest and floor eggs for both types of bird and was independent of shell surface area or thickness.

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