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A primary-structure analysis of the 16s rRNA gene was performed with 10 strains representing five described and one unidentified species of the genus Microcystis. The phylogenies determined illustrate the evolutionary affiliations among Microcystis strains, other cyanobacteria, and related plastids and bacteria. A cluster of 10 strains that included hepatotoxic isolates identified as Microcystis aeruginosa formed a monophyletic group. However, the genus Microcystis appeared to be polyphyletic and contained two strains that clustered with unicellular cyanobacteria belonging to the genus Synechococcus. The clustering of related Microcystis strains, including strains involved in the production of the cyclic peptide toxin microcystin, was consistent with cell morphology, gas vacuolation, and the low G+C contents of the genomes. The Microcystis lineage was also distinct from the lineage containing the unicellular genus Synechocystis and the filamentous, heterocystforming genus Nostoc. The secondary structure of a Microcystis 16s rRNA molecule was determined, and genus-specific sequence signatures were used to design primers that permitted identification of the potentially toxic cyanobacteria belonging to the genus Microcystis via DNA amplification.The Cyanobacteria is a diverse bacterial phylum with respect to form, function, and habitat. On the basis of microfossil and geochemical evidence the origin of cyanobacterium-like organisms has been dated to the late Precambrian era. On the basis of the results of phylogenetic studies workers have inferred that the cyanobacterial phylum is 1 of the 11 bacterial phyla (32,42). The possibility that eukaryotic chloroplasts arose from a cyanobacterial ancestor by a symbiotic event has also been inferred on the basis of molecular data (8, 38).Members of the genus Microcystis are a major cause of freshwater noxious cyanobacterial blooms, which have a broad geographical distribution. The microcystins, a family of cyclic heptapeptide toxins that are not synthesized ribosomally (3) and are produced by most members of this genus, cause acute hepatotoxicity in agricultural livestock. Recent epidemiological data have also linked chronic subacute consumption of microcystins to human liver tumor promotion (5). The increasing occurrence of Microcystis blooms in major sources of human drinking water makes identification and prediction of these toxic blooms very important.Due to the variably expressed and minor morphological and developmental characteristics used for identification, classification of cyanobacterial strains at the genus or species level may be ambiguous (29), particularly when laboratory cultures and environmental isolates are compared (7). The current cyanobacterial taxonomy does not provide an unequivocal system for identification of the toxigenic and bloom-forming genus Microcystis (20). Depending on the taxonomic treatises used for classification, which differ in their emphasis on the cell size, shape, buoyancy, and toxicity of the planktonic, freshwater cyanobacteria, d...

A fecal analysis survey was undertaken to quantify animal inputs of pathogenic and indicator microorganisms in the temperate watersheds of Sydney, Australia. The feces from a range of domestic animals and wildlife were analyzed for the indicator bacteria fecal coliforms and Clostridium perfringens spores, the pathogenic protozoa Cryptosporidium and Giardia, and the enteric viruses adenovirus, enterovirus, and reovirus. Pathogen and fecal indicator concentrations were generally higher in domestic animal feces than in wildlife feces. Future studies to quantify potential pathogen risks in drinking-water watersheds should thus focus on quantifying pathogen loads from domestic animals and livestock rather than wildlife.The current trend in minimizing pathogen health risks to water supplies is to use a risk management-based approach to ensure delivery of high-quality water. This approach utilizes multiple barriers within the water system, including effective control of contaminant inputs through watershed management. One potential source of these pathogens in drinkingwater watersheds is the feces of domestic and wildlife animal populations. Pathogens from animal feces may enter waterways by direct deposition or as a result of overland runoff containing fecal material deposited in the watershed. To construct a source material budget of pathogen inputs, it is necessary to estimate the potential impact of animal populations on surface water quality (15). Subsequent analysis can then be performed to estimate the proportion of the source material that will be inactivated through natural decay and environmental stressors, how much may be transported to the stream network, and the proportion that represents a risk of human infection.The initial requirement for the development of a source material budget is to estimate the concentration of potential pathogens in animal feces (shedding intensity). There is limited published information on the concentration and input load of potential waterborne pathogens and fecal indicator bacteria in wildlife (native and feral animal) populations (2,3,8,19). Yet it is these animals that often have the greatest access to the riparian zones and reservoir surrounds in watersheds, since, by definition, their movements are largely uncontrolled, making surface water protection difficult. By comparison, data for potential pathogen concentrations in the feces of domestic animals are more abundant, particularly for the enumeration and prevalence of the protozoan parasites Cryptosporidium and Giardia spp. (4-7, 18, 24, 25).This study was undertaken to provide a cross-sectional estimate of the intensity of shedding of pathogenic and indicator microorganisms in animal feces present in a large, semiprotected drinking-water watershed. The study quantified potentially pathogenic protozoa (Cryptosporidium and Giardia), enteric viruses (adenovirus, enterovirus, and reovirus), and indicator organisms (fecal coliforms and Clostridium perfringens spores) in fecal samples from watershed animals. The latter are t...

We report a case of measles inclusion-body encephalitis (MIBE) occurring in an apparently healthy 21-month-old boy 8.5 months after measles-mumps-rubella vaccination. He had no prior evidence of immune deficiency and no history of measles exposure or clinical disease. During hospitalization, a primary immunodeficiency characterized by a profoundly depressed CD8 cell count and dysgammaglobulinemia was demonstrated. A brain biopsy revealed histopathologic features consistent with MIBE, and measles antigens were detected by immunohistochemical staining. Electron microscopy revealed inclusions characteristic of paramyxovirus nucleocapsids within neurons, oligodendroglia, and astrocytes. The presence of measles virus in the brain tissue was confirmed by reverse transcription polymerase chain reaction. The nucleotide sequence in the nucleoprotein and fusion gene regions was identical to that of the Moraten and Schwarz vaccine strains; the fusion gene differed from known genotype A wild-type viruses.

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