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At least 19 recordsLinked to original sources
PubMed2026

Molecular Diagnostics for WHO Priority Bacterial Pathogens: A Bibliometric Mapping of Diagnostic Platforms, Resistance Markers, and Antimicrobial Resistance Research Trends.

Antimicrobial resistance (AMR) constrains effective treatment and carries implications for infection control, surveillance, and public health. The World Health Organization (WHO) priority bacterial pathogen framework has intensified the need for diagnostic innovation by redefining research priorities around organisms combining high disease burden with complex resistance profiles. Molecular diagnostics have accordingly moved beyond culture-based workflows, integrating rapid pathogen identification, resistance-marker detection, genomic surveillance, and clinical decision support. The present study conducted a bibliometric mapping of the literature on WHO priority pathogens. Rather than addressing resistance at a general level or a single pathogen or technology, it integrates priority pathogens, molecular platforms, and resistance markers within a single framework, tracing their joint thematic and temporal evolution along an explicit pathogen-platform-marker axis. Scopus-indexed articles and reviews (2000-2025) were retrieved, yielding 1746 publications after screening adapted from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Analyses used Bibliometrix/Biblioshiny, R, and VOSviewer. The literature expanded markedly after 2018, led by China and the United States. Methicillin-resistant Staphylococcus aureus (MRSA), Mycobacterium tuberculosis, Enterococcus faecium, and the Enterobacterales-carbapenemase axis constituted the principal thematic cores, whereas conventional polymerase chain reaction (PCR)/nucleic acid amplification testing (NAAT) and whole-genome sequencing were the dominant platforms. Overall, the field has evolved from pathogen detection into an AMR-centered translational domain encompassing resistance prediction, genomic epidemiology, surveillance, and clinical decision support. Diagnostic development, stewardship, and surveillance depend on hybrid workflows coupling rapid marker-targeted assays with genome-based characterization, delivering actionable resistance within clinically meaningful timeframes, and extending coverage to underrepresented pathogens and platforms.

Humans↗
PubMed2003

Different mutation patterns of atovaquone resistance to Plasmodium falciparum in vitro and in vivo: rapid detection of codon 268 polymorphisms in the cytochrome b as potential in vivo resistance marker.

BACKGROUND: Resistance of Plasmodium falciparum to atovaquone in vitro and in vivo has been associated to mutations in the parasite cytochrome b gene. METHODS: Cultures were sequentially subjected to increasing doses of atovaquone alone or in combination with cycloguanil and the cytochrome b gene was sequenced. Additionally, we investigated the parasite cytochrome b gene of a patient returning from Mali with Malarone treatment failure in vivo. RESULTS: All strains that survived atovaquone concentrations in vitro of 2 x 10(-8) to 2 x 10(7) M showed the M133I mutation and one strain with the highest atovaquone concentration the additional mutation L171F. Sequencing of the in vivo treatment failure revealed a point mutation at codon 268 resulting in an amino acid change from tyrosine to serine. Based on the repeated emergence of mutations at codon 268, but no detection of alterations at codon 133 in vivo, we developed a detection method for the diagnostic of codon 268 polymorphisms as a potential atovaquone/proguanil resistance marker. A nested PCR with 3 different pairs of primers for the second round was designed. Each product was digested with restriction enzymes, capable to distinguish the wild type from the two reported mutations at codon 268. CONCLUSION: Mutations at codon 268 of the parasite cytochrome bc1 gene are associated with atovaquone/proguanil treatment failure in vivo and can be used as potential resistance marker This method provides a novel and robust tool to investigate the relevance of codon 268 polymorphisms as resistance marker and to monitor the further emergence of atovaquone/proguanil resistance.

Animals↗
PubMedDate not supplied

[Presence of genetic exchange in Crithidia oncopelti (Trypanosomatidae) studied with drug resistance markers].

Strains resistant to 100 mkg/ml of cycloheximide (ChxR100) and to 2.5 mg/ml of chloramphenicol (CapR2.5) were used in studies for the presence of genetic interchange in C. oncopelti. Phenotypes of these strains were stable on the nonselective medium and specific. Strains ChxR100 and CapR2.5 were mixed in equal proportions, cultivated during 7 days and tested. Under consecutive effect of inhibitors the culture of strains mixture and clones isolated from it exhibited double resistance. Phenotypes of recombinant clones were stable on the nonselective medium during, at the minimum, 70 to 90 cell generations. At the same conditions control cultures of parental strains and clones did not exhibit resistance that excludes the possibility of origin of cells resistant to both antibiotics from Crithidia of one of the parental strains as a result of secondary mutation. Thus, the results obtained show convincingly the presence of genetic interchange between flagellates of ChxR100 and CapR2.5 strains.

Animals↗
PubMed1980

Conjugative transfer of multiple antibiotic resistance markers in Streptococcus pneumoniae.

Two antibiotic-resistant isolates of Streptococcus pneumoniae were investigated for conjugative transfer of their drug resistance markers into streptococcal (groups B and D) and pneumococcal (encapsulated and non-encapsulataed) recipients. Of these, 7 wild-type donor pneumococci transferred all their resistance markers (except Pc [penicillin], Su [sulfonamide], and Tp [trimethoprim]) into group D Streptococcus and non-encapsulated S. pneumoniae recipients at a low frequency (10(-5) to 10(-6)). The resistance markers transferred were Tc (tetracycline); Tc and Cm (chloramphenicol); Tc and MLS (macrolides, lincosamides, and streptogramin B); Tc, MLS, Km (kanamycin), and Cm. The transconjugants obtained retransferred their resistance markers into appropriate streptococcal or pneumococcal recipients or both. The resistance markers of streptococcal transconjugants could not be cured by chemical agents. All attempts to detect extra-chromosomal deoxyribonucleic acid from pneumococcal or streptococcal transconjugants were unsuccessful. The molecular weight of a streptococcal conjugative R plasmid (pIP501) was investigated after transfer into the non-encapsulated S. pneumoniae recipient and was found to be similar to that of the wild-type group B Streptococcus host (20 x 10(6)).

Acridine Orange↗
PubMed2025

Versatile and Portable Cas12a-mediated Detection of Antibiotic Resistance Markers.

Antibiotic-resistant bacteria are spreading in clinical, industrial, and environmental ecosystems. The spreading dynamics to and from the environment are unknown, largely due to the lack of appropriate (robust, fast, low-cost) analytical assays. In this study, we developed C12a, a versatile molecular toolbox to detect genetic markers of antibiotic resistance using CRISPR/Cas12a. Biochemical characterization show that the C12a toolbox can detect less than 100 attoMolar of pure DNA fragments from the blaCTX-M15 and floR genes, conferring resistance to b-lactams and amphenicols, respectively important for human and veterinary uses. In microbiological assays, C12a detected less than 102 CFU/mL and high concordance was observed if compared to antibiotic susceptibility tests, PCR, or to whole genome sequencing. Additionally, C12a confirmed a high prevalence of the integrase/integron system in E. coli isolates containing multiple antibiotic resistance genes (ARGs). The C12a toolbox shows equivalent detection performance in diverse laboratory settings, results redout (Fluorescence vs FLA) or input sample. Altogether, this work presents a comprehensive proof-of-concept, development description, and biochemical characterization of a collection of molecular tools to detect antibiotic resistance markers in a one health setup.

Antibiotic Resistance Gene↗
PubMed1982

Novobiocin resistance marker in Haemophilus influenzae that is not expressed on a plasmid.

The plasmid pNov2, carrying a cloned chromosomal marker conferring resistance to at least 2.5 micrograms of novobiocin per ml, was constructed with a new Haemophilus influenzae cloning vehicle, pDM2. The novobiocin marker of pNov2 was not normally expressed, but in Rec+ cells approximately one in 10(4) cells in a culture of a transformant became novobiocin resistant, a frequency about four orders of magnitude higher than the spontaneous mutation frequency. Variants of such cells that had lost the plasmid were also novobiocin resistant. Since Rec- cultures bearing pNov2 showed novobiocin resistance only at the normal mutation frequency, we concluded that the Rec+ novobiocin-resistant transformants arose because of a rare recombination between plasmid and chromosome in which the chromosome acquired the novobiocin marker from the plasmid. Evidence is presented that novobiocin sensitivity is dominant over this particular novobiocin resistance marker.

Chloramphenicol↗
PubMed1986

Conjugative transfer of staphylococcal antibiotic resistance markers in the absence of detectable plasmid DNA.

Eleven Staphylococcus aureus clinical isolates were tested for transfer of resistance markers by transduction and filter mating. The resistance markers of six of the strains could be transferred only by transduction; however, the five remaining strains transferred their resistance both by transduction and filter mating. The resistance markers that were cotransferred in filter matings (transfer of resistance to penicillin and streptogramin A was accompanied, in each case, by the transfer of one or more markers, i.e., resistance to aminoglycosides, cadmium, or tetracycline, depending on the donor) were not cotransduced. The filter mating transfers were recA independent and were observed with both Staphylococcus aureus and Staphylococcus epidermidis recipients. Experiments to elucidate the mechanism of transfer by filter mating suggested that conjugation requiring cell-to-cell contact may have been involved. These transfers occurred in the absence of detectable plasmid DNA.

Anti-Bacterial Agents↗
PubMed1980

[Drug-resistance markers from Salmonellae in Pasteurella multocida].

A transfer of resistance was effected of S. haidelberge strain, having 7 medicinal resistance markers, onto 2 Pasteurella multocida strains No. 10 and Vladislavovo. In strain No. 10 were found 20% of recombinations, whereas in Vladislavovo their number was 10%, hence the different pasteurella strains can be recipients at a higher or lower degree. The recombinations obtained are not stable and during their short conservation in bouillon they spontaneously get rid of the markers of resistance acquired.

Drug Resistance, Microbial↗
PubMed1983

A bovine papilloma virus vector with a dominant resistance marker replicates extrachromosomally in mouse and E. coli cells.

We describe the construction of a bovine papilloma virus-based vector (pCGBPV9) which contains a dominant selectable marker and replicates autonomously in both mouse and Escherichia coli cells. This vector contains the complete bovine papilloma virus genome, a ColE1 replication origin and a dominant selectable marker conferring resistance to kanamycin in bacteria and G418 in eukaryotic cells. A high number of G418R colonies are obtained after transfer of pCGBPV9 into mouse C127 cells. These G418R colonies contain vector DNA which replicates autonomously at approximately 10-30 copies per cell. The molecules are in most cases unrearranged and can be rescued into E. coli cells by bacterial transformation.

Animals↗
PubMed1993

Variable stability of antibiotic-resistance markers in Bacillus cereus UW85 in the soybean rhizosphere in the field.

We compared the stability of antibiotic-resistance markers in strains derived from Bacillus cereus UW85 in culture media and in the soybean rhizosphere in a growth chamber and in the field. We studied two independent, spontaneous mutants resistant to neomycin, three independent, spontaneous mutants resistant to streptomycin, and strains carrying plasmid pBC16, which encodes tetracycline resistance. Antibiotic-resistance markers were maintained in populations of all UW85 derivatives in culture and in the rhizosphere of soybeans grown in soil in a growth chamber. In two field experiments, antibiotic resistance was substantially lost in rhizosphere populations of B. cereus as early as 14 or as late as 116 days after planting. To distinguish between death of the inoculated strain and loss of its marker, we tested populations of B. cereus for other phenotypes (orange pigmentation, plasmid-borne resistance to tetracycline, and biocontrol activity) that are typical of UW85-derivatives used as inoculum, but atypical of the indigenous populations of B. cereus, and these phenotypes were maintained in populations from which the marker was lost. In general, neomycin-resistance markers were maintained at a higher frequency than streptomycin-resistance markers, and maintenance of antibiotic-resistance markers varied with position on the root and with the year of the experiment. In a semi-defined medium, the UW85 derivatives grew at the same rate as the wild type at 28 degrees C, but most grew more slowly than the wild type at 16 degrees C, demonstrating that antibiotic resistance can affect fitness under some conditions. The results suggest that the stability of antibiotic-resistance markers should be assessed in the ecosystems in which they will be studied.

Bacillus cereus↗
PubMed1998

Chemosensitivity of advanced larynx carcinoma cells in vitro and significance of multidrug resistance markers in these tumors.

Thirty cases of previously untreated advanced larynx carcinoma were checked for in vitro chemosensitivity and presence of the resistance markers viz. P-glycoprotein (P-gp) glutathione-S-transferase-pi (GST-pi) and protein kinase C (PKC) overexpression. The cytotoxicity testing was done using MTT assay and the resistance markers were checked by immunohistochemical methods using monoclonal antibodies. The drug combinations employed in MIT assay were 5FU* + MTX*, 5FU + cisPt*, 5FU + Mito*, cisPt + Mito and MTX + Mito (*5FU = 5Fluorouracil, MTX-methotrexate, cisPt-cisplatin and Mito = mitomycin C). No statistically significant correlation was observed between resistance to the above drug combinations and presence of the resistance markers under consideration. A statistically significant correlation was observed between node positivity and expression of resistance markers which indicates that presence of one or more of these markers in these tumors may be considered as a negative prognosis marker. CisPt-Mito was found to be the most effective drug combination in vitro, in the cases studied.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Antibiotic resistance markers in genetically modified plants: a risk to human health?

Cotransformation with an antibiotic-resistance marker is often necessary in the process of creating a genetically modified (GM) plant. Concern has been expressed that the release of these markers in GM plants may result in an increase in the rate of antibiotic resistance in human pathogens. For such an event to occur, DNA must not be totally degraded in field conditions, and the antibiotic-resistance marker must encounter potential recipient bacteria and be taken up by them, before being integrated into the bacterial genome, and the genes then expressed. In addition, the new recombinant must overcome the physiological disadvantage of acquisition of a piece of foreign DNA, probably in conditions where the new gene does not provide a selective advantage. We review each of these stages, summarising the investigations that have followed each of these steps. We contrast the potential increase in the antibiotic resistance reservoir created by antibiotic-resistance markers in GM plants with the current situation created by medical antibiotic prescribing. We conclude that, although fragments of DNA large enough to contain an antibiotic-resistance gene may survive in the environment, the barriers to transfer, incorporation, and transmission are so substantial that any contribution to antibiotic resistance made by GM plants must be overwhelmed by the contribution made by antibiotic prescription in clinical practice.

Drug Resistance↗
PubMed1983

Induction and expression of mutations at multiple drug-resistance marker loci in Chinese hamster ovary cells.

We have observed quantitative and qualitative differences in the mutability and mutagen-specificity of various drug-resistance marker loci in Chinese hamster ovary (CHO) cells, which suggest that mammalian gene loci may differ in their relative mutability by a given mutagenic agent. We have used the CHO-AT3-2 multiple-marker mutagenesis assay system to examine the dose-dependent induction and kinetics of expression of mutations at four well-characterized, drug-resistance marker loci, after treatment with chemical agents which produce various types of DNA damage. The CHO-AT3-2 subline allows simultaneous quantitation and direct comparison of induced mutation frequencies at the hgprt, oua (Na+/K+ ATPase), aprt, and tk loci. The agents tested in this study included ethyl methanesulfonate, methyl methanesulfonate, mitomycin C, ICR-191, benzo[a]pyrene, and dimethylnitrosamine. The expression kinetics and optimal expression times for each drug-resistance marker were determined in dose-response experiments in which cells from mutagen-treated populations were plated at 1-2-day intervals over a period of 10 days following mutagenesis. Comparison of induced mutation frequencies for each drug-resistance marker after mutagen treatments yielding equivalent cell survivals (equitoxic doses resulting in relative cell survivals of 0.37) revealed locus-specific differences in the relative mutagenicities of the agents tested. These results indicate that the apparent mutagenicity of a particular agent at a single genetic locus may not necessarily be an accurate indicator of that agent's mutagenic potential for the genome as a whole.

Animals↗
PubMed1975

[Suppresion of the R-factor transduction transmission of antibiotic resistance markers in E. coli by distamycin A].

Some mechanisms of inhibition by distamycin A of transduction of antibiotic resistance markers of R-factors (RI drd and R222) with the moderate phage PI kc in E. coli were studied. The kinetics of the transduction of the R-factor markers was investigated in comparison with the stages of interaction of PI kc phage particles with bacterial cells of E. coli K-12 carrying the R-factors such as RI and R222 -- phage PI kc -- E. coli C6000. Later the effect of distamycin A on transduction of the above R-factors was studied using the same system. It was shown that distamycin A in concentrations of 75 gamma/ml suppressed the transduction of the R-markers when added to the transduction mixture simultaneously with the phage. The transduction rate decreased 15 times if the drug was added 5 minutes after beginning of the phage contact with the recipient culture. Addition of distamycin A at the 20th minute of the experiment induced no inhibition of the transduction of the R-factor markers. Preliminary 18-hour exposure to distamycin A of the recipient culture and phagolysates possessing transduction capacity resulted in decreased rates of the transduction of the antibiotic resistance markers 35 to 40 times. No inhibitory effect of distamycin A on the process of phenotypic manifestation of the antibiotic resistance markers of the R-factors was noted. The experiments showed that distamycin A affected the early stages of interaction of the transducing particles with the recipient culture, possibly the process of penetration of the transducing DNA of the R-factors into the cells of the recipient culture.

Anti-Bacterial Agents↗
PubMed1999

Mass mating method in combination with G418- and aureobasidin A-resistance markers for efficient selection of hybrids from homothallic strains in Saccharomyces cerevisiae.

We have developed a mass mating method using the spore suspensions of homothallic yeasts of Saccharomyces cerevisiae in combination with dominant selective drug resistance markers, Tn601(903) against geneticin and AUR1-C against aureobasidin A for the selection of the hybrids. To examine the effectiveness of these markers in the mass mating method, each marker was introduced into a homothallic wine yeast. Using a mixed culture of spore suspensions from the resultant transformants, many hybrids were screened by the drug resistance markers. This method is more practical than the spore-to-spore mating method because it does not require the use of a micromanipulator and many hybrids are obtained at one time. The resultant hybrids could be utilized for industrial brewing because plasmids, which are used to confer resistance markers, are easily eliminated from the hybrids by cultivation in a medium without drugs. We propose that the mass mating method using spore suspensions in combination with dominant selective geneticin- and aureobasidin A-resistance markers is useful for the selection of hybrids from industrial homothallic yeasts.

Journal Article↗
PubMed1998

Localization of auxotrophic and benomyl resistance markers through the parasexual cycle in the beauveria bassiana (Bals.) vuill entomopathogen.

Genetic studies to localize auxotrophic markers and resistance to benomyl fungicide and to analyze gene transfer on the Beauveria bassiana deuteromycete were carried out using the parasexual cycle. Parasexual crosses among strains with complementary genetic markers resulted in vigorous heterocaryons. Selection of the segregant products was made using two methodologies: total isolation and parental elimination. Colonies with recombinant traits were recovered directly from the heterocaryon in all crosses, and no diploid colony was isolated. This shows the high instability of the diploid nucleus in this species. Among the parasexual segregant products preferential recovery of markers in one of the parental strains involved in the crosses was detected, probably because of an inhibition of conidiogenesis from one parental strain to another. Genetic markers were localized in four linkage groups by the parasexual crosses. In the first group markers nic4, nic3, thi2, bio3, ade2, ths2, and ben1R were localized; in the second, the marker met1; in the third, pab1; and in the fourth, bio1. The parental strain 196/A11/3 is a carrier of translocation among the linkage groups I and III.

Benomyl↗