Correction methods for organic carbon artifacts when using quartz-fiber filters in large particulate matter monitoring networks: the regression method and other options.

Sampling and handling artifacts can bias filter-based measurements of particulate organic carbon (OC). Several measurement-based methods for OC artifact reduction and/or estimation are currently used in research-grade field studies. OC frequently is not artifact-corrected in large routine sampling networks (e.g., U.S. Environmental Protection Agency (EPA)'s Chemical Speciation Network). In some cases, the OC artifact has been corrected using a regression method (RM) for artifact estimation. In this method, the gamma-intercept of the regression of the OC concentration on the fine particle (PM2.5) mass concentration is taken to be an estimate of the average OC sampling artifact (net of positive and negative artifacts). This paper discusses options for artifact correction in large routine sampling networks. Specifically, the goals are to (1) articulate the assumptions and limitations inherent to the RM, (2) describe other artifact correction approaches, and (3) suggest a cost-effective method for artifact correction in large monitoring networks. The RM assumes a linear relationship between measured OC and PM mass: a constant slope (OC mass fraction) and a constant intercept (RM artifact estimate). These assumptions are not always valid. Additionally, outliers and other individual data points can have a large influence on the RM artifact estimates. The RM yields results within the range of measurement-based methods for some datasets and not for others. Given that the adsorption of organic gases increases with atmospheric concentrations of organics, subtraction of an average artifact from all samples (e.g., across multiple sites) will underestimate OC for lower-concentration samples (e.g., clean sites) and overestimate OC for higher-concentration samples (e.g., polluted sites). For relatively accurate, simple, and cost-effective artifact OC estimation in large networks, the authors suggest backup filter sampling on at least 10% of sampling days at all sites with artifact correction on a sample-by-sample basis as described herein.

Cholera in Ethiopia in the 1990 s: epidemiologic patterns, clonal analysis, and antimicrobial resistance.

In 1993, after 6 years of absence, cholera re-emerged in the Horn of Africa. Following its introduction to Djibouti, the disease spread to the central and southern areas of Ethiopia reaching Somalia in 1994. Cholera outbreaks persisted in Ethiopia with a recrudescence of cases in 1998. Twenty-two Vibrio cholerae O1 strains, selected to represent the 1998 history of cholera in Ethiopia, were characterized by random amplified polymorphic DNA patterns, BglI ribotyping and antimicrobial susceptibility. All isolates showed a unique amplified DNA pattern and a prevalent ribotype B8a. All strains were multidrug-resistant and harboured an IncC plasmid which conferred resistance to ampicillin, chloramphenicol, streptomycin, sulfamethoxazole and trimethoprim. These findings indicate that a group of closely related V. cholerae O1 strains was responsible for the cholera epidemic in Ethiopia in 1998.

Clonal relationship among Vibrio cholerae O1 El Tor strains isolated in Somalia.

One hundred and three Vibrio cholerae O1 strains, selected to represent the cholera outbreaks which occurred in Somalia in 1998-1999, were characterized by random amplified polymorphic DNA patterns, ribotyping, and antimicrobial susceptibility. All strains showed a unique amplified DNA pattern and 2 closely related ribotypes (B5a and B8a), among which B5a was the more frequently identified. Ninety-one strains were resistant to ampicillin, chloramphenicol, spectinomycin, streptomycin, sulfamethoxazole, and trimethoprim, conferred, except for spectinomycin, by a conjugative plasmid IncC. These findings indicated that the group of strains active in Somalia in the late 1990s had a clonal origin.

Molecular epidemiology and origin of cholera reemergence in Italy and Albania in the 1990s.

In 1994 a cholera epidemic occurred in Italy and Albania after more than a decade of case absence. To investigate genotypic characteristics and the origin of the epidemic strains, 110 Vibrio cholerae O1 El Tor isolates from Italy and Albania were studied by randomly amplified polymorphic DNA analysis (RAPD), BglI ribotyping, and pulsed-field gel electrophoresis (PFGE) of genomic DNA. The Italian and Albanian strains were all ribotype 6 and their RAPD and PFGE patterns were identical as well. These findings indicated that the 1994 isolates belonged to the same clone and that the clone was part of the larger global spread of epidemic ribotype 6 strains, which started in southern Asia in 1990.

Susceptibility to rifaximin of Vibrio cholerae strains from different geographical areas.

Four hundred and eight clinical strains of Vibrio cholerae isolated from different geographical areas and with different antimicrobial resistance patterns were tested for susceptibility to rifaximin, a non-absorbable antibiotic active in vitro against Gram-negative bacteria. The MICs ranged from 0.5 to 4 mg/l for all strains. These values and the pharmacokinetic properties suggest rifaximin as an attractive antimicrobial agent for cholera.