The control of disinfection byproducts and their precursors in biologically active filtration processes.

While disinfection provides hygienically safe drinking water, the disinfectants react with inorganic or organic precursors, leading to the formation of harmful disinfection byproducts (DBPs). Biological filtration is a process in which an otherwise conventional granular filter is designed to remove not only fine particulates but also dissolved organic matters (e.g., DBP precursors) through microbially mediated degradation. Recently, applications of biofiltration in drinking water treatment have increased significantly. This review summarizes the effectiveness of biofiltration in removing DBPs and their precursors and identifies potential factors in biofilters that may control the removal or contribute to formation of DBP and their precursors during drinking water treatment. Biofiltration can remove a fraction of the precursors of halogenated DBPs (trihalomethanes, haloacetic acids, haloketones, haloaldehydes, haloacetonitriles, haloacetamides, and halonitromethanes), while also demonstrating capability in removing bromate and halogenated DBPs, except for trihalomethanes. However, the effectiveness of biofiltration mediated removal of nitrosamine and its precursors appears to be variable. An increase in nitrosamine precursors after biofiltration was ascribed to the biomass sloughing off from media or direct nitrosamine formation in the biofilter under certain denitrifying conditions. Operating parameters, such as pre-ozonation, media type, empty bed contact time, backwashing, temperature, and nutrient addition may be optimized to control the regulated DBPs in the biofilter effluent while minimizing the formation of unregulated emerging DBPs. While summarizing the state of knowledge of biofiltration mediated control of DBPs, this review also identifies several knowledge gaps to highlight future research topics of interest.

Systemic administration of the chemokine macrophage inflammatory protein 1alpha exacerbates inflammatory bowel disease in a mouse model.

INTRODUCTION: Exacerbations of inflammatory bowel disease are thought to be related to concurrent infections. As infections are associated with elevated local and serum concentrations of chemokines, we have determined whether systemic administration of the CC chemokine macrophage inflammatory protein 1alpha (MIP-1alpha) exacerbates colitis in a mouse model. METHODS: Colitis was induced in Balb/c mice using trinitrobenzene sulfonic acid (TNBS). Starting four days later, animals received daily intraperitoneal injections of recombinant MIP-1alpha. On day 7, mice were killed and pieces of colon taken for immunohistology and polymerase chain reaction analysis. The direct effects of MIP-1alpha on mucosal T cells and fibroblasts in vitro were also investigated. RESULTS: Systemic administration of MIP-1alpha markedly enhanced colitis with mice developing large transmural ulcers filled with granulation tissue. Treatment resulted in increased numbers of CD4 cells infiltrating the colonic lamina propria, increased interferon gamma (IFN-gamma) levels, and increased transcripts for tumour necrosis factor alpha (TNF-alpha) and matrix metalloproteinase 3 (MMP3). Isolated lamina propria lymphocytes from mice with TNBS colitis contained increased numbers of IFN-gamma and TNF-alpha transcripts when stimulated with MIP-1alpha in vitro. Colonic lamina propria fibroblasts also responded to MIP-1alpha with increased proliferation and decreased collagen 1 synthesis but fibroblast proliferation was not seen in vivo. CONCLUSIONS: These experiments show that increasing serum concentrations of a chemokine, MIP-1alpha, exacerbates immune mediated colitis. The effect seems to be due to the ability of MIP-1alpha to boost Th1 responses in the gut wall. Our findings also suggest a potential pathway by which peripheral infections can exacerbate inflammatory bowel disease.

Isolation and characterization of a bacterium capable of removing taste- and odor-causing 2-methylisoborneol from water.

2-Methylisoborneol (MIB), a metabolite of blue-green algae, has been implicated in causing unpalatable drinking water throughout the world. Current non-biological water treatment technologies are ineffective in removing MIB from potable water or are cost-prohibitive, and biological applications may address these problems. We have isolated and characterized a bacterium derived from lake water and capable of aerobically degrading MIB. Light microscopy and transmission electron microscopy revealed that this strain is a spore-forming, flagellated bacterium that is bacilloid in shape, and 16S rRNA phylogenetic analysis determined that it is most closely related to Bacillus fusiformis and Bacillus sphaericus, both members of the Bacillus sphaericus senso lato taxon. While the growth and oxidation potential of this strain was shown to be affected beyond certain MIB concentrations in the mg/l range, it was capable of depleting MIB at mg/l and ng/l concentrations and of removing MIB to concentrations yielding no observed odor.

Investigation of the role of CD8+ T cells in bovine tuberculosis in vivo.

Mycobacterium bovis is the causative agent of bovine tuberculosis (TB), and it has the potential to induce disease in humans. CD8(+) T cells (CD8 cells) have been shown to respond to mycobacterial antigens in humans, cattle, and mice. In mice, CD8 cells have been shown to play a role in protection against mycobacterial infection. To determine the role of CD8 cells in bovine TB in vivo, two groups of calves were infected with the virulent M. bovis strain AF2122/97. After infection, one group was injected with a CD8 cell-depleting monoclonal antibody (MAb), and the other group was injected with an isotype control MAb. Immune responses to mycobacterial antigens were measured weekly in vitro. After 8 weeks, the animals were killed, and postmortem examinations were carried out. In vitro proliferation responses were similar in both calf groups, but in vitro gamma interferon (IFN-gamma) production in 24-h whole-blood cultures was significantly higher in control cattle than in CD8 cell-depleted calves. Postmortem examination showed that calves in both groups had developed comparable TB lesions in the lower respiratory tract and associated lymph nodes. Head lymph node lesion scores, on the other hand, were higher in control calves than in CD8 cell-depleted calves. Furthermore, there was significant correlation between the level of IFN-gamma and the head lymph node lesion score. These experiments indicate that CD8 cells play a role in the immune response to M. bovis in cattle by contributing to the IFN-gamma response. However, CD8 cells may also play a deleterious role by contributing to the immunopathology of bovine TB.