Application of QMRA to prioritise water supplies for Cryptosporidium risk in New South Wales, Australia.

A Quantitative Microbial Risk Assessment (QMRA) framework was applied to assess 312 drinking water supply systems across regional New South Wales (NSW). The framework was needed to support the implementation of a recommendation in the Australian Drinking Water Guidelines (ADWG) for appropriate treatment barriers to be operating in systems 'at risk' for Cryptosporidium. The objective was to prioritise systems so that those with the highest risk could be identified and addressed first. The framework was developed in a pilot study of 30 systems, selected to represent the range of water supplies across regional NSW. From these, source water categories were defined to represent local conditions with reference to the literature and Cryptosporidium risk factors. Values for Cryptosporidium oocyst concentration were assigned to the categories to allow quantification of the health risk from those water sources. The framework was then used to assess the risks in all 312 regional drinking water supply systems. Combining the disciplined approach of QMRA with simple catchment and treatment information and categorical risk outputs provided a useful and transparent method for prioritising systems for further investigation and potential risk management intervention. The risk rankings for drinking water supplies from this QMRA process have been used to set priorities for a large State Government funding program.

Cryptosporidiosis in the immunocompromised: weighing up the risk.

Cryptosporidiosis has been increasingly recognised as a cause of diarrhoeal illness in both immunocompetent and immunocompromised people. Massive outbreaks have been linked to municipal drinking water supplies in North America and Europe, but so far none have been reported in Australia. There is evidence that modes of transmission other than drinking water are more important. There can be no guarantee that infective Cryptosporidium oocysts will not contaminate an Australian water supply. Therefore, a permanent "boil water" warning may be warranted on medical advice in severely immunocompromised people, for whom cryptosporidiosis could be persistent and life threatening.

Fish oil feeding delays influenza virus clearance and impairs production of interferon-gamma and virus-specific immunoglobulin A in the lungs of mice.

Ingestion of fish oil can suppress the inflammatory response to injury and may impair host resistance to infection. To investigate the effect of a diet containing fish oil on immunity to viral infection, 148 BALB/c mice were fed diets containing 3 g/100 g of sunflower oil with either 17 g/100 g of fish oil or beef tallow for 14 d before intranasal challenge with live influenza virus. At d 1 and d 5 after infection, the mice fed fish oil had higher lung viral load and lower body weight (P < 0.05). In addition to the greater viral load and weight loss at d 5 after infection, the fish oil group consumed less food (P < 0.05) while the beef tallow group was clearing the virus, had regained their preinfection weights and was returning to their preinfection food consumption. The fish oil group had impaired production of lung interferon-gamma (IFN-gamma), serum immunoglobulin (Ig) G and lung IgA-specific antibodies (all P < 0. 05) although lung IFN-alpha/beta and the relative proportions of bronchial lymph node CD4+ and CD8+ T lymphocytes did not differ between groups after infection. The present study demonstrates a delay in virus clearance in mice fed fish oil associated with reduced IFN-gamma and antibody production and a greater weight loss and suppression of appetite following influenza virus infection. However, differences observed during the course of infection did not affect the ultimate outcome as both groups cleared the virus and returned to preinfection food consumption and body weight by d 7.

Increased saturated triacylglycerol levels in plasma membranes of human neutrophils stimulated by lipopolysaccharide.

Neutrophils isolated from patients with bacterial infections or stimulated in vitro with lipopolysaccharide (LPS) produce a high resolution, lipid-dominated spectrum on 1H-NMR spectroscopy (May et al, 1993. J. Infect. Dis. 168: 386-392). We have investigated the origin of this lipid signal using NMR and chemical analyses of both whole neutrophils and purified plasma membranes. Plasma membranes from neutrophils that had been stimulated with 50 microg/ml LPS exhibited the high resolution 1H-NMR signal, and contained double the triacylglycerol (TAG) content of plasma membranes isolated from resting cells. Chemical analysis of the whole cells indicated that the TAG also increased at the cellular level (1.7-fold) after stimulation with LPS. Diradylglycerol increased 2- to 3-fold in both whole cells and plasma membranes after stimulation, but was only a minor component compared with TAG. The plasma membrane protein/phospholipid ratio increased 2.6-fold, whereas cholesterol (free and esterified) was unchanged. The membranes from LPS-stimulated neutrophils exhibited increased fluidity, as judged by increased merocyanine 540 binding, consistent with a 2-fold reduction in cholesterol/phospholipid ratio. LPS induced a shift in fatty acid content of whole cell polar lipids towards more oleic acid and less palmitic acid, whereas the neutral lipid fraction contained increased amounts of palmitic and stearic acids. The TAG fraction of plasma membrane lipids contained increased amounts of palmitic acid when prepared from cells stimulated with LPS. We conclude that the 1H-NMR signal in LPS-stimulated neutrophils arises from increased amounts of plasma membrane TAG with an elevated content of palmitic acid.