PubMed · 6991047
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W Brumfitt, J M Hamilton-Miller. 1980. Trimethoprim.. https://pubmed.ncbi.nlm.nih.gov/6991047/
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A capillary gas chromatographic method is described for the determination of methenamine hippurate residue in swabs collected from manufacturing equipment surfaces. Any residual methenamine hippurate remaining on process equipment after cleaning is removed by swabbing with one wet polyester Absorbond swab (4" x 4") pre-moistened with water followed by a dry Absorbond swab. The residual methenamine hippurate is chromatographed on a 30 x 0.32 mm (i.d.) Supelcowax-10 capillary column of 0.25-micron film thickness. The amount of residual methenamine hippurate is determined by comparing the ratio of methenamine hippurate peak area response to that of p-cresol (internal standard) obtained for the sample to a linear calibration curve obtained for a series of standard solutions. The method is demonstrated to be sufficiently linear, accurate, precise, sensitive and rugged for the determination of low levels of methenamine hippurate on equipment surfaces. Using this method, the mean recovery of methenamine hippurate from spiked Absorbond swab samples contained in high density polyethylene bottles was 105.2%, with a relative standard deviation (RSD) of +/- 7.1% (n = 25). The mean recoveries of methenamine hippurate from spiked test plates for '180 Grit' Stainless Steel, Teflon and WARCO White (neoprene and PVC) gasket material were 77.2, 96.1 and 50.6%, with RSDs of +/- 9.4 (n = 25), +/- 4.3 (n = 25) and +/- 36% (n = 20), respectively. Recovery correction factors have been incorporated into the method. The method was successfully applied to the assay of actual equipment cleaning validation swab samples. Stability studies demonstrate that methenamine hippurate is not very stable on the equipment surfaces or in the swabs. It is recommended that the surfaces be swabbed immediately after cleaning and the swabs analyzed within 24 h after sample collection. The results demonstrate that in order to fully validate the cleaning procedures, it is not only necessary to investigate the recovery of the drug from equipment surfaces and swabs but also that the stability of the drug on the surfaces and swabs be determined.
Urinary tract infection in women has its origin, predominantly, via ascending bacteria from the periurethral microflora. Asymptomatic bacteriuria, except for the pregnant patient, need not be treated. E. coli is the most common bacterium to cause UTIs, and is usually susceptible to oral antibiotics. Patients who are hospitalized with an indwelling Foley catheter or who have undergone instrumentation, tend to be infected with a bacterium other than E. coli. Patients with uncomplicated cystitis can effectively be treated with an oral antibiotic (Table 1) for 3 days. Patients who do not respond to empiric therapy have a recurrence within 2 weeks of treatment, or who have a recurrence within the first week after treatment, should have a pretreatment.
Five spontaneous nitrofurantoin-resistant mutants (one each of Clostridium leptum, Clostridium paraputrificum, two other Clostridium spp. strains from the human intestinal microflora, and Clostridium perfringens ATCC 3626) were selected by growth on a nitrofurantoin-containing medium. All of the Clostridium wild-type and mutant strains produced nitroreductase, as was shown by the conversion of 4-nitrobenzoic acid to 4-aminobenzoic acid. High-performance liquid chromatography (HPLC) analysis of the mutants during incubation with 50 microg of nitrofurantoin per ml showed the gradual disappearance of the nitrofurantoin peak. The nitrofurantoin peak also disappeared when cell-free supernatants instead of cultures of each of the resistant and wild-type bacteria were used, but it persisted if the cell-free supernatants had been inactivated by heat. At least two of the mutants converted nitrofurantoin to metabolites without antibacterial activity, as was shown by a bioassay with a nitrofurantoin-susceptible Bacillus sp. strain. Nitrofurantoin at a high concentration (50 microg/ml) continued to exert some toxicity, even on the resistant strains, as was evident from the longer lag phases. This study indicates that Clostridium strains can develop resistance to nitrofurantoin while retaining the ability to produce nitroreductase; the mutants metabolized nitrofurantoin to compounds without antibacterial activity.