No abstract

The biodegradation, photolysis, and adsorption of pentachlorophenol (PCP) in outdoor, aquatic environments were examined with man-made channels built by the U.S. Environmental Protection Agency at a field station on the Mississippi River near Monticello, Minn. Four channels were used, each channel being approximately 520 m long and receiving river water that flowed through the channels for about 10 h before reentering the river. The channels were dosed continuously during the summer of 1982 with various concentrations of PCP (approximately 0, 48, 144, and 432 micrograms/liter). We monitored the biotic and abiotic degradation of PCP in these channels for approximately 16 weeks. Photolysis of PCP was rapid at the water surface, but greatly attenuated with depth. Depending on sunlight conditions, photolysis accounted for a 5 to 28% decline in initial PCP concentration. Adsorption of PCP by sediment and uptake by biota accounted for less than 15% and probably less than 5% in unacclimated water. Microbial degradation of PCP became significant about 3 weeks after the initiation of dosing and eventually became the primary mechanism of PCP removal, accounting for a 26 to 46% (dose-dependent) decline in initial PCP. Most of the PCP-mineralizing microorganisms that developed in the channels were either attached to surfaces (e.g., rocks and macrophytes) or associated with surface sediments. Total bacterial numbers (direct microscopic counts) in the various channels were not affected significantly by PCP concentrations of micrograms per liter. Numerous strains of bacteria able to grow at the expense of PCP were isolated from the adapted channels. The experiments reported here will help predict the responses of flowing aquatic ecosystems to contamination by biocides such as pentachlorophenol.

Both Ehrlichia chaffeensis and Ehrlichia ewingii are causative agents of human ehrlichiosis. Both pathogens are transmitted to humans through the bite of an infected lone star tick (Amblyomma americanum). Since Missouri has a high incidence of human monocytic ehrlichiosis, we investigated the prevalence of E. chaffeensis- and E. ewingii-infected A. americanum and Dermacentor variabilis (American dog tick) ticks to help assess the relative risk for humans exposed to these vectors. We used a nested polymerase chain reaction assay for the detection of ehrlichial DNA in the collected ticks. Infection rates for both ehrlichial species were calculated from the assay results for each of the tick species. E. chaffeensis was found to be present in 9.8% of adult A. americanum ticks (57 of 579) and 6.7% of D. variabilis ticks (eight of 120). E. ewingii DNA was present at an infection rate of 5.4% in adult A. americanum (31 of 579) and 3.3% of D. variabilis ticks (four of 120). A minimum infection rate for nymph pools of A. americanum was 1.7% for E. chaffeensis and 0.6% for E. ewingii.

The purine regulon repressor protein, PurR, was shown to be a purine component involved in glyA regulation in Escherichia coli. Expression of glyA, encoding serine hydroxymethyltransferase activity, was elevated in a purR mutant compared with a wild-type strain. When the purR mutant was transformed with a plasmid carrying the purR gene, the serine hydroxymethyltransferase levels returned to the wild-type level. The PurR protein bound specifically to a DNA fragment carrying the glyA control region, as determined by gel retardation. In a DNase I protection assay, a 24-base-pair region was protected from DNase I digestion by PurR. The glyA operator sequence for PurR binding is similar to that reported for several pur regulon genes.

A pentachlorophenol (PCP)-degrading Flavobacterium sp. was tested for its ability to dechlorinate other chlorinated phenols by using resting cells that had been grown in the presence or absence of PCP. Phenols with chlorine atoms at positions 2 and 6 of the phenol ring were dechlorinated completely by PCP-induced cells. Other chlorinated phenols were not significantly mineralized. When PCP was added to a culture growing on L-glutamate, there was a lag period before the start of PCP degradation. When similar cells were treated with chloramphenicol prior to the addition of PCP, they did not degrade added PCP, even after prolonged incubations. Thus, the enzymes necessary for PCP degradation appeared to be inducible. Suspensions of cells grown in the presence of 2,4,6-trichlorophenol or 2,3,5,6-tetrachlorophenol did not show a lag period for mineralization of PCP, 2,4,6-trichlorophenol, or 2,3,5,6-tetrachlorophenol, indicating that one enzyme system probably was induced for the biodegradation of all three compounds. Nondegradable chlorophenols were toxic toward the Flavobacterium sp., probably acting as uncouplers of oxidative phosphorylation.