A medium has been developed which permits the isolation and growth of Borrelia hermsi, an organism that causes relapsing fever.

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Conventional aerobic nitrification was adversely affected by single pulse inputs of six different classes of industrially relevant chemical toxins: an electrophilic solvent (1-chloro-2,4-dinitrobenzene, CDNB), a heavy metal (cadmium), a hydrophobic chemical (1-octanol), an uncoupling agent (2,4-dinitrophenol, DNP), alkaline pH, and cyanide in its weak metal complexed form. The concentrations of each chemical source that caused 1 5, 25, and 50% respiratory inhibition of a nitrifying mixed liquor during a short-term assay were used to shock sequencing batch reactors containing nitrifying conventional activated sludge. The reactors were monitored for recovery over a period of 30 days or less. All shock conditions inhibited nitrification, but to different degrees. The nitrate generation rate (NGR) of the shocked reactors recovered overtime to control reactor levels and showed that it was a more sensitive indicator of nitrification inhibition than both initial respirometric tests conducted on unexposed biomass and effluent nitrogen species analyses. CDNB had the most severe impact on nitrification, followed by alkaline pH 11, cadmium, cyanide, octanol, and DNP. Based on effluent data, cadmium and octanol primarily inhibited ammonia-oxidizing bacteria (AOB) while CDNB, pH 11,and cyanide inhibited both AOB and nitrite-oxidizing bacteria (NOB). DNP initially inhibited nitrification but quickly increased the NGR relative to the control and stimulated nitrification after several days in a manner reflective of oxidative uncoupling. The shocked mixed liquor showed trends toward recovery from inhibition for all chemicals tested, but in some cases this reversion was slow. These results contribute to our broader effort to identify relationships between chemical sources and the process effects they induce in activated sludge treatment systems.

A method for the quantitation of neuraminidase in the presence of N-acetylneuraminic acid aldolase is described. The neuraminidase content of Diplococcus pneumoniae was found to be dependent on the media employed for growth; the highest enzyme activity per milligram of bacterial protein was obtained with Todd-Hewitt broth. Neuraminidase production was stimulated in D. pneumoniae by the addition of N-acetylneuraminlactose, N-acetylneuraminic acid, or N-acetylmannosamine to the growth medium. Three rough strains of D. pneumoniae, which were nonpathogenic for mice, lacked neuraminidase activity. Seven of 12 smooth strains contained neuraminidase; enzyme activity was not detected in the remaining 5 smooth strains. There was no correlation between the presence of neuraminidase activity and the capsular type or between neuraminidase production and animal virulence.

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The effects of shock loads of 1‐chloro‐2,4‐dinitrobenzene (CDNB); cadmium; 1‐octanol; 2,4‐dinitrophenol (DNP); weakly complexed cyanide; pH 5, 9, and 11; and high ammonia levels on activated sludge biomass growth, respiration rate, flocculation, chemical oxygen demand removal, dewaterability, and settleability were studied. For all chemical shocks, except ammonia and pH, concentrations that caused 15, 25, and 50% respiration inhibition were used to provide a single pulse shock to sequencing batch reactor systems containing a nitrifying or non‐nitrifying biomass. Cadmium and pH 11 shocks were most detrimental to all processes, followed by CDNB. The DNP and cyanide primarily affected respiration, while pH 5, pH 9, octanol, and ammonia did not affect the treatment process to a significant extent. A chemical source–process effect matrix is provided, which we believe will aid in the development of methods that prevent and/or attenuate the effects of toxic shock loads on activated sludge systems.

Sterile sonic-treated materials of pneumococci grown in media containing N -acetylmannosamine as the carbohydrate source were lethal for mice. Purification of the toxic factor led to its identification as the enzyme neuraminidase.