Abstract Nitrate can control biogenic souring by lowering sulfate reducing bacteria (SRB) metabolic activity and shifting the microbial community such that nitrate-reducing bacteria (NRB) out-compete SRB for nutrients. Nitrate was applied in a laboratory study using a 20-cc packed bed upflow reactor to determine kinetic rate of H2S removal. The objectives of the testing were to (1) enrich for nitrate-reducing, sulfide-oxidizing microorganisms derived from produced water and (2) determine the kinetic rate of H2S removal at 60˚C in a synthetic medium with an H2S:nitrate molar ratio of 2, and (3) describe the microbial community involved in nitrate-mediated souring control in this system. Sulfide was measured at the face and at the discharge of the column to determine the sulfide oxidation rate. Residence time in the reactor was varied by changing flow rate but a removal rate of nearly 50% H2S was achieved across the column in one hour residence time. This paper provides a description of the microbial community cultivated at high temperature using 16S rRNA to profile the population dynamics resulting from nitrate treatment. Phospholipid fatty acid analysis was also used for taxonomic evaluation and quantifying physiological changes in the biomass due to nitrate treatment.
A model flow cell system was designed to investigate pitting corrosion in pipelines associated with microbial communities. A microbial inoculum producing copious amounts of H2S was enriched from an oil pipeline biofilm sample. Reservoirs containing a nutrient solution and the microbial inoculum were pumped continuously through six flow cells containing mild steel corrosion coupons. Two cells received corrosion inhibitor "A", two received corrosion inhibitor "B", and two ("untreated") received no additional chemicals. Coupons were removed after 1 month and analyzed for corrosion profiles and biofilm microbial communities. Coupons from replicate cells showed a high degree of similarity in pitting parameters and in microbial community profiles, as determined by 16S rRNA gene sequence libraries but differed with treatment regimen, suggesting that the corrosion inhibitors differentially affected microbial species. Viable microbial biomass values were more than 10-fold higher for coupons from flow cells treated with corrosion inhibitors than for coupons from untreated flow cells. The total number of pits > 10 mils diameter and maximum pitting rate were significantly correlated with each other and the total number of pits with the estimated abundance of sequences classified as Desulfomicrobium. The maximum pitting rate was significantly correlated with the sum of the estimated abundance of Desulfomicrobium plus Clostridiales, and with the sum of the estimated abundance of Desulfomicrobium plus Betaproteobacteria. The lack of significant correlation with the estimated abundance of Deltaproteobacteria suggests not all Deltaproteobacteria species contribute equally to microbiologically influenced corrosion (MIC) and that it is not sufficient to target one bacterial group when monitoring for MIC.
Film forming corrosion inhibitors are often selected to control CO2 corrosion and their effectiveness versus microbiologically influenced corrosion (MIC) is desirable in systems that suffer from both forms of corrosion. Traditional corrosion inhibitor tests (e.g., bubble tests) have unfavorable conditions for microbial activity and are inadequate for evaluating MIC control. Biocide screening test methods have been used to evaluate microbial kill with toxic chemicals added batch wise, providing very little direct information about controlling corrosion. Once-through flow cells containing corrosion coupons were inoculated with a field consortium enriched in synthetic produced water to simulate MIC field activity. Maximum pitting rate on the coupons was the key performance indicator for screening inhibitors. Results indicated that many of the corrosion inhibitors tested increased the maximum MIC pitting rates when compared to untreated controls. In at least one case, a less toxic inhibitor provided better MIC control than a more toxic inhibitor. Data suggest that the field microbial consortia used in the testing developed a resistance to an incumbent inhibitor that has been used for many years. The results indicate that inhibitor selection based on MIC control is not simply a function of their ability to control bacterial growth and activity.