Douterelo, J. Boxall, P. Deines, R. Sekar, K. Fish, C. Biggs, Methodological approaches for studying the microbial ecology of drinking water distribution systems, Water Res. Nair, J.
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Disseminated Avian Mycobacteriosis in a Free-Living Grey Heron (Ardea cinerea)
Lee, J. Miller, B. Freeman, J. McGrath, R. Paul, Water purification membranes: The role of polymer science. Ubomba-Jaswa, C. Navntoff, I. Polo-Lopez, P. Zhang, X. Xie, M. Tang, C. Criddle, Y.
Cui, S. Wang, Magnetically ultraresponsive nanoscavengers for next-generation water purification systems Nature Communications Volume: 1 4 doi: Block, Eds. Litton Aondale Navy Shipyard Report, Field scale demonstration of electrocoagulation and enhanced media filtration for treatment of shipyard storm water, M.
Pulido, E. La Motta, R. Nandipati, J. Josse, Eds. Kozar, K. Tanner, F. Kamel, G. Ross, J. Reliable access to their DNA is only achieved during sample processing by combining exposure to stringent lysis buffers with an additional optimised mechanical disruption step. The organisms have been cultured and detected in blood showing that, as in animals, the infection in humans is systemic [ 35 — 37 ]. When validated methodologies have been used most people with CD have been found to be infected with MAP [ 39 ].
In simple words, most people with chronic inflammation of the intestine of the CD type are infected with a mycobacterium which is a proven specific cause of chronic inflammation of the intestine. There are no data which demonstrate that MAP are harmless to humans.
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The overwhelming balance of probability and public health risk favours the conclusion that MAP are also pathogenic for people. MAP infects the gut widely in CD and is found both in the more normal looking intestine and the grossly inflamed and diseased segments of intestine [ 33 ].
Mannans released by MAP inhibit intracellular killing of internalised bacteria [ 41 ]. The MAP infection causes a primary microscopic inflammation accompanied by a specific immune dysregulation and enteric neuropathy [ 33 ]. Mucosal integrity and other critical functions of the intestine are impaired. The visible segments of gross inflammatory disease result from the perturbed neuroimmune response to the secondary penetration into the gut wall of gut flora containing both normal intestinal bacteria and those which have undergone transformations leading to a more invasive phenotype like AIEC.
It is important to note that genomic loci in the host conferring genetic susceptibility to Crohn's disease have the potential to operate at the levels of both primary and secondary pathogens. The entry of food residues into the gut wall contributes an allergic component to the inflammatory mess. Although MAP has been found in intestinal granulomas in humans [ 42 ], the presence or absence of these and other features of the variable histopathological picture of CD are principally determined by the large scale response to the secondary co-pathogens including especially other granulomatous species like M.
Thus the three lines of contemporary research inquiry come together in a two tiered co-operative pathogenic mechanism. Imagine the collective human enteric microbiome in, say, a crowded Europe.
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A vast composite structure made up of millions of individual highly mobile microbial reservoirs variably interconnected in time and space and degree. A dynamic structure possessing an inherent self governing order and stability not easily displaced. Into this cellular system is progressively introduced a slowly growing specific mycobacterial pathogen which has acquired the genetic machinery necessary to cloak itself with a predicted fucosylated surface [ 43 ] so that it conforms with the familiar molecular environment particularly of the host's epithelial cells and mucosal compartment [ 44 ].
It has come from the parallel universe of the collective enteric microbiome of human food animals and before that from the soil. It causes a microscopic inflammation and perturbs the microenvironment of the mucosa and gut wall. To survive and prosper it minimises its confrontation with the human immune system.
It causes a variable immune dysregulation but it also inflames the fine structure and function of the enteric nervous system. More than a hundred years go by.
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Both animal and human total microbiomes swell with increasing population density. The mycobacterial pathogen acquires additional properties resulting in an evolution in its behaviour with an increase in pathogenicity and species range. Some normal inhabitants of the enteric microbiome adapt to the disturbed intestinal microenvironment and they too acquire characteristics which make them more invasive. Chronic enteric disease emerges and spreads particularly in individuals with an inherited or acquired susceptibility.
Humans responsible for controlling and managing these diseases, blind to what is really happening are distracted by detail and dismissive. The required remedial measures are not designed and applied and the problems get worse. Left undisturbed, maybe the education in hostility already received by increasingly aggressive members of the former normal gut flora will progress to the point where they too can emerge from background to become primary independent pathogens in their own right. When they do so more new diseases will emerge. The answer to this question supported by a correct interpretation of data both from open label studies [ 45 — 48 ] and the Australian controlled clinical trial is a qualified yes [ 49 — 51 ].
It can in some people with CD some of the time. When it does so in 'responders' receiving treatment with drug combinations including rifabutin and clarithromycin the clinical and pathological improvement can be dramatic and has been associated with the conversion of pre-treatment MAP positive tests in blood [ 52 ] and gut mucosa my own unpublished observations to negative. Furthermore, some of the clinical benefit resulting from treatment of CD with conventional 'immunosuppressive' agents such as 6-mercaptopurine or methotrexate may actually be a consequence of their demonstrable direct anti-MAP action [ 53 — 55 ].
But MAP infections are difficult to eradicate. The organisms are generally resistant in vivo to drugs conventionally used in the treatment of tuberculosis. Treatment is prone to all the problems of microbial drug resistance and latency encountered in the management of chronic lung disease caused by other members of the M. Avium Complex. Rich clinical and commercial rewards are out there for those who do so successfully.