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PubMed1981

Resistance and cross-resistance of guinea pigs to Dermacentor andersoni Stiles, D. variabilis (Say), Amblyomma americanum (Linnaeus), and Ixodes scapularis Say.

The ability of guinea pigs to acquire resistance to Dermacentor andersoni and Amblyomma americanum was determined by repeatedly infesting separate sets of guinea pigs with tick larvae. Resistance was measured in terms of reduced numbers successfully engorging and reduced weight of those ticks that engorged. An 83% reduction in numbers of larvae engorging and a 64.5% reduction in the weight of engorged larvae were seen between the first and second infestations with D. andersoni. Guinea pigs exhibited considerably less resistance to A. americanum the third time they were exposed to this species than did guinea pigs infested twice with D. andersoni. Feeding success was only 30.8% less than the initial percentage that engorged, and the percentage weight reduction was 35. During the challenge infestations, sizable fluid-filled vesicles formed on ears of the guinea pigs used as hosts for D. andersoni or A. americanum. Cross-resistance was evaluated by dividing D. andersoni-resistant animals into groups and challenging them with D. andersoni D. variabilis, A. americanum, or Ixodes scapularis. Appreciable cross-resistance was apparent between the two Dermacentor species. The weights of the A. americanum and I. scapularis were significantly reduced, but not the number that engorged. When A. americanum-resistant guinea pigs were challenged, they were cross-resistant to D. variabilis but not to D. andersoni. Skin tests on guinea pigs in which extracts of tick salivary glands were used as the antigens did not conclusively reflect the same patterns of cross-reactions noted in the tests of cross-resistance.

Animals↗

PubMed2006

Molecular cytogenetic characterization of doxorubicin-resistant neuroblastoma cell lines: evidence that acquired multidrug resistance results from a unique large amplification of the 7q21 region.

Neuroblastoma is a heterogeneous neural crest-derived embryonic childhood neoplasm that is the second most common solid tumor found in children. Despite recent advances in combined therapy, the overall survival of patients with high-stage disease has not improved in the last decades. Treatment failure is in part attributed to multidrug resistance. To address the mechanisms involved in the development of multidrug resistance, we have generated two doxorubicin-resistant neuroblastoma cell lines (IGRN-91R and LAN-1R). These cells were shown to overexpress the MDR1 gene coding for the P-glycoprotein and were resistant to other MDR1- and non-MDR1-substrate drugs. Indeed, the MDR1 inhibitor verapamil only partially restored sensitivity to drugs, confirming that P-glycoprotein-mediated drug efflux was not responsible for 100% resistance. High-resolution and array-based comparative genomic hybridization analyses revealed the presence of an amplicon in the 7q21 region as the unique genomic alteration common to both doxorubicin-resistant cell lines. In addition to the MDR1 locus, this large amplified region is likely to harbor additional genes potentially involved in the development of drug resistance. This study represents the first molecular cytogenetic and genomic approach to identifying genomic regions involved in the multidrug-resistant phenotype of neuroblastoma. These results could lead to the identification of relevant target genes for the development of new therapeutic modalities.

Antineoplastic Agents↗

PubMed2004

Reversal of breast cancer resistance protein (BCRP/ABCG2)-mediated drug resistance by novobiocin, a coumermycin antibiotic.

Breast cancer resistance protein (BCRP/ABCG2) of an ATP-binding cassette half-transporter confers resistance against mitoxantrone and camptothecin derivatives of topotecan and irinotecan. Novobiocin, a coumermycin antibiotic, is known to enhance anticancer drug sensitivity of cancer cells in vitro and in vivo, the mechanism of which remains undetermined. Here we focused on drug efflux pump and examined whether novobiocin reversed drug resistance in multidrug-resistant cells highly expressing BCRP. To explore the reversal mechanisms, intracellular drug accumulation was measured by flow cytometry, and a topotecan transport study using plasma membrane vesicles was performed. We used PC-6/SN2-5H2 small cell lung cancer and MCF-7/MX breast cancer cells selected with SN-38 of the active irinotecan metabolite and mitoxantrone, respectively, and the BCRP cDNA transfectant MCF-7/clone 8 cells. These cells expressed high levels of BCRP mRNA but not other known transporters. Compared to the parental PC-6 cells, PC-6/SN2-5H2 cells were 141-, 173- and 57.2-fold resistant to topotecan, SN-38 and mitoxantrone, respectively. Novobiocin at 60 microM decreased the degree of the above resistance by approximately 26-fold in PC-6/SN2-5H2 cells, and similarly reversed resistance in MCF-7/MX, MCF-7/clone 8 and un-selected NCI-H460 cells highly expressing BCRP. Furthermore, novobiocin increased the intracellular topotecan accumulation in these cells and inhibited the topotecan transport into the membrane vesicles of PC-6/SN2-5H2 cells. No effects of novobiocin in these assay were observed in the parental PC-6 and MCF-7 cells. The kinetic parameters in the transport study indicated that novobiocin was a inhibitor for BCRP, resulting in competitive inhibition of BCRP-mediated topotecan transport. These findings suggest that novobiocin effectively overcomes BCRP-mediated drug resistance at acceptable concentrations.

ATP Binding Cassette Transporter, Subfamily G, Mem↗

PubMed2004

[SARI: surveillance of antibiotic use and bacterial resistance in German intensive care units. Correlation between antibiotic use and the emergence of resistance].

Intensive care units (ICUs) are considered to be high-risk areas for the emergence and spread of multiresistant bacterial pathogens. In Germany, there are no representative epidemiological data on antibiotic resistance, on the use of antibiotics in ICUs, or on the correlation between antibiotic use and the emergence of resistance. Project SARI (surveillance of antibiotic use and bacterial resistance in ICUs), which as a part of the epidemiological network Spread of Nosocomial Infections and Resistant Pathogens (SIR) is supported by the German Ministry of Science and Education, started in February 2000 and meanwhile includes data on antibiotic use and resistance rates in 38 medical, surgical, and interdisciplinary ICUs. To date (February 2000-June 2003), a total of 1142 months, 413,065 patient days, and 550,288 defined daily doses (DDDs in accordance with the WHO) have been covered with a mean antibiotic usage density (AD) of 1335 DDDs/1000 patient days and resistance data on 37,612 isolates from ICUs. Ciprofloxacin use and MRSA correlate significantly, as do imipenem use and the rate of imipenemresistant P. aeruginosa. The genodiversity of P. aeruginosa is lower in ICUs with high resistance rates and low use of imipenem than in ICUs with high resistance rates and high use. This is an indirect parameter of transmission of identical strains. The epidemiological data of SARI form a basis for improved antibiotic and infection control management in ICUs (http://www.sari-antibiotika.de).

Anti-Bacterial Agents↗

PubMed2003

Cross-resistance to cisplatin in cells with acquired resistance to copper.

PURPOSE: Cells selected for resistance to cisplatin (DDP) demonstrate cross-resistance to copper (Cu) suggesting one or more common mechanisms of cellular defense. We sought to determine whether cells selected for resistance to Cu are cross-resistant to DDP. MATERIALS AND METHODS: Parental HuH7 human hepatoma cells and the CuR27 Cu-resistant subline were compared for sensitivity to Cu and DDP by clonogenic assay, and with respect to drug uptake and efflux by measuring cellular Cu and Pt content. RESULTS: CuR27 cells were found to be 1.8-fold resistant to Cu and 8.6-fold cross-resistant to DDP. Changes in the cellular pharmacokinetics of Cu in the CuR27 cells were paralleled by changes in the kinetics of DDP. The accumulations of Cu and DDP measured at 1 min were, respectively, 36% and 26% of those in the parental HuH7 cells. The initial rate of efflux from the CuR27 cells was 6.2-fold faster for Cu and 2.5-fold faster for DDP than from the HuH7 cells. Cu reduced the accumulation of DDP in the HuH7 cells in a concentration-dependent manner and vice versa. DDP also reduced the efflux of Cu. Western blot analysis demonstrated that expression of the Cu exporter ATP7B was increased 3.9-fold in the CuR27 cells. CONCLUSIONS: In this model system, cross-resistance between Cu and DDP was bidirectional and accompanied by parallel changes in the cellular pharmacokinetics of both compounds. The results are consistent with the idea that transporters and chaperones that normally mediate Cu homeostasis also directly or indirectly modulate the accumulation of DDP.

Adenosine Triphosphatases↗

PubMed1998

High-level mupirocin resistance among Spanish methicillin-resistant Staphylococcus aureus.

Twelve strains of methicillin-resistant Staphylococcus aureus with high-level resistance to mupirocin were studied. The MIC of methicillin was 16 to 128 mg/l and the MIC of mupirocin > or = 512 mg/l. All of the isolates carried a plasmid of about 30 MDa, and one strain lost resistance to mupirocin when the plasmid was cured. Three different resistance patterns were found: six strains were resistant to ciprofloxacin, kanamycin, and 10 mg/l of cadmium sulfate; two strains were resistant to these agents as well as to gentamicin, erythromycin, clindamycin, mercury chloride, and ethidium bromide; and four strains were resistant to the previously named agents as well as to rifampicin and tetracycline. The use of this valuable topical antibiotic, especially in long-term-care facilities, should be monitored to avoid dissemination of resistance.

Anti-Bacterial Agents↗

PubMedDate not supplied

Correlative interpretation of staphylococcal resistance to penicillinase-resistant penicillins by ceftizoxime disk susceptibility test using Showa disks.

The Showa disk susceptibility test (Showa Yakuhin Kako Company, Japan) was evaluated to discriminate between the strains of Staphylococcus aureus resistant to penicillinase-resistant penicillins (PRPs) and those susceptible. When we tested 129 PRP-resistant and 112 susceptible strains, many PRP-resistant strains were interpreted to be false susceptible to methicillin and oxacillin, especially when incubated at 37 degrees C. Growth at 30 degrees C and when NaCl was added to the medium improved the test reliability for detection of PRP resistance. Ceftizoxime disk (30 micrograms) susceptibility test results highly correlated with reference PRP resistance when incubated at 35 degrees C. All the PRP-resistant strains produced no zone of inhibition, whereas all of the PRP-susceptible strains were categorized as susceptible to ceftizoxime (greater than or equal to 22 mm, less than or equal to 3.13 micrograms/ml), for example, 100% correlation. It was concluded that the Showa ceftizoxime disk, in replacement of PRPs, will provide a reliable, alternative method to predict PRP resistance in S. aureus pending reevaluation of the Show PRP disk tests.

Ceftizoxime↗

PubMed2005

Molecular analysis of methicillin-resistant Staphylococcus aureus reveals an absence of plasmid DNA in multidrug-resistant isolates.

The number, diversity and restriction enzyme fragmentation patterns of plasmids harboured by 44 multidrug-resistant hospital-acquired methicillin-resistant Staphylococcus aureus (MR-HA-MRSA) isolates, two multidrug-resistant community-acquired MRSA (MR-CA-MRSA), 50 hospital-acquired MRSA (HA-MRSA) isolates (from the University Hospital Birmingham, NHS Trust, UK) and 34 community-acquired MRSA (CA-MRSA) isolates (from general practitioners in Birmingham, UK) were compared. In addition, pulsed-field gel electrophoresis (PFGE) type following SmaI chromosomal digest and SCCmec element type assignment were ascertained for each isolate. All MR-HA-MRSA and MR-CA-MRSA isolates possessed the type II SCCmec, harboured no plasmid DNA and belonged to one of five PFGE types. Forty-three out of 50 HA-MRSA isolates and all 34 CA-MRSA isolates possessed the type IV SCCmec and all but 10 of the type IV HA-MRSA isolates and nine CA-MRSA isolates carried one or two plasmids. The 19 non-multidrug-resistant isolates (NMR) that did not harbour plasmids were only resistant to methicillin whereas all the NMR isolates harbouring at least one plasmid were resistant to at least one additional antibiotic. We conclude that although plasmid carriage plays an important role in antibiotic resistance, especially in NMR-HA-MRSA and CA-MRSA, the multidrug resistance phenotype from HA-MRSA is not associated with increased plasmid carriage and indeed is characterised by an absence of plasmid DNA.

Anti-Bacterial Agents↗

PubMed1999

pH and drug resistance. I. Functional expression of plasmalemmal V-type H+-ATPase in drug-resistant human breast carcinoma cell lines.

A major obstacle for the effective treatment of cancer is the phenomenon of multidrug resistance (MDR) exhibited by many tumor cells. Many, but not all, MDR cells exhibit membrane-associated P-glycoprotein (P-gp), a drug efflux pump. However, most mechanisms of MDR are complex, employing P-gp in combination with other, ill-defined activities. Altered cytosolic pH (pHi) has been implicated to play a role in drug resistance. In the current study, we investigated mechanisms of pHi regulation in drug-sensitive (MCF-7/S) and drug-resistant human breast cancer cells. Of the drug-resistant lines, one contained P-gp (MCF-7/DOX; also referred to as MCF-7/D40) and one did not (MCF-7/MITOX). The resting steady-state pHi was similar in the three cell lines. In addition, in all the cell lines, HCO3- slightly acidified pHi and increased the rates of pHi recovery after an acid load, indicating the presence of anion exchanger (AE) activity. These data indicate that neither Na+/H+ exchange nor AE is differentially expressed in these cell lines. The presence of plasma membrane vacuolar-type H+-ATPase (pmV-ATPase) activity in these cell lines was then investigated. In the absence of Na+ and HCO3-, MCF-7/S cells did not recover from acid loads, whereas MCF-7/MITOX and MCF-7/DOX cells did. Furthermore, recovery of pHi was inhibited by bafilomycin A1 and NBD-Cl, potent V-ATPase inhibitors. Attempts to localize V-ATPase immunocytochemically at the plasma membranes of these cells were unsuccessful, indicating that V-ATPase is not statically resident at the plasma membrane. Consistent with this was the observation that release of endosomally trapped dextran was more rapid in the drug-resistant, compared with the drug-sensitive cells. Furthermore, the drug-resistant cells entrapped doxorubicin into intracellular vesicles whereas the drug-sensitive cells did not. Hence, it is hypothesized that the measured pmV-ATPase activity in the drug-resistant cells is a consequence of rapid endomembrane turnover. The potential impact of this behavior on drug resistance is examined in a companion manuscript.

Antineoplastic Agents↗

PubMed1998

High-level chloroquine resistance of Plasmodium berghei is associated with multiple drug resistance and loss of reversal by calcium antagonists.

The chloroquine resistance of Plasmodium falciparum is reversed in vitro by numerous compounds, including calcium antagonists, which could enhance the accumulation of the drug in the parasite food vacuole. However, this mechanism of resistance could be insufficient when the resistance level increases. Using in vitro drug trials on strains of Plasmodium berghei displaying various chloroquine-resistance levels, we confirmed previous results obtained in vivo in the chloroquine-resistant strains of P. berghei are cross-resistant to related drugs (amodiaquine, quinine and mefloquine), the resistance levels to these drugs being related to their analogy to chloroquine. Furthermore, we showed that high-level resistant lines were associated with a loss of drug potentiation by verapamil and nicardipine in vivo, but that the reversal rates obtained in vitro are of low significance. We conclude that the parasite is able to escape the activity of these reversing agents.

Animals↗

PubMed2003

[Antibiotic resistance of Staphylococcus aureus at north Lebanon: place of the methicillin resistance and comparison of detection methods].

The aim of this study was to evaluate the susceptibility of 100 Staphylococcus aureus strains isolated from the laboratory of Microbiology of the Islami Hospital of Tripoli (Lebanon) to 19 antibiotics, and to determine the prevalence of methicillin resistant strains. 30% of strains studied were methicillin resistant, 96% were resistant to the penicillin G. Clavulanic acid restaurated the amoxicillin activity to 29%. The resistance level was 34% for amikacin, 3% for gentamycin and tobramycin, 10% for chloramphenicol, 44.33% for tetracyclin, 7% for erythromycin, 4.04% for clindamycin, 20% for trimethoprim-sulfametoxasol and 0% for vancomycin and teicoplanin. The methicillin-resistant Staphylococcus aureus possess more important resistant level in comparison with the methicillin sensitive strains. We compared the ability of latex agglutination test (Slidex(R) SARM, bioMérieux, France) to detect the production of penicillin-binding protein 2' (PBP 2') in 100 clinical isolates of S. aureus with two reference methods: the oxacillin disk diffusion test and the MIC determination by the E-test (AB BIODISK, Sweden). The two reference methods give the same results for the detection of methicillin resistant S. aureus. The Slidex test was positive for all 30 isolates determined to be methicillin resistant by the reference methods (sensitivity 100%). The latex test was negative for 42 of 70 isolates determined to be methicillin susceptible by the reference methods, and the latex test was positive for 28 isolates determined to be susceptible (specificity 60%).

Drug Resistance, Bacterial↗

PubMed2003

Emergence of phenotypic resistance to ciprofloxacin and levofloxacin in methicillin-resistant and methicillin-sensitive Staphylococcus aureus strains.

The emergence of phenotypic resistance to ciprofloxacin and levofloxacin in methicillin-sensitive and methicillin-resistant Staphylococcus aureus (MRSA) strains was studied. Twenty MRSA and 77 methicillin-sensitive S.aureus (MSSA) strains susceptible to both quinolones were investigated for resistance after single step or serial passages. No growth of 20 MRSA strains was observed at 4xMIC of levofloxacin after 48 h incubation, but 4 of 77 (5%) MSSA strains grew at the same concentration. At 4xMIC concentration of ciprofloxacin, 10 MSSA (13%) and five MRSA (25%) strains were grown. In the serial passages of MRSA strains, resistance to ciprofloxacin was 75 and 5% for levofloxacin by the third passage. In the seventh passage this resistance was 100 and 15%, respectively. In MSSA strains, resistance to ciprofloxacin was 75 and 19% to levofloxacin at the third passage and at the seventh passage, 100 and 61%, respectively. Emergence of ciprofloxacin resistance was more common and developed more rapidly than resistance to levofloxacin in both MRSA and MSSA strains.

Ciprofloxacin↗

PubMed2026

Super enhancer-driven transcriptional reprogramming promotes abiraterone resistance via neuroendocrine transition and ferroptosis evasion in castration-resistant prostate cancer.

Abiraterone resistance represents a major clinical challenge in the management of castration-resistant prostate cancer (CRPC), yet the epigenetic mechanisms that sustain this resistance remain poorly understood. In particular, how super enhancers (SEs) reprogram transcriptional networks to promote this therapy resistance has not been fully elucidated. Here, by integrating chromatin immunoprecipitation sequencing and transcriptome profiling, we identified aberrantly activated oncogenic SEs that drive the transcriptional upregulation of the transcription factors ELF3 and JUNB in abiraterone-resistance CRPC cells. Importantly, SE-driven activation of the ELF3/JUNB axis promotes abiraterone resistance by inducing WNT11-mediated neuroendocrine transition. In parallel, this transdifferentiated state is closely associated with ferroptosis resistance, as evidenced by the upregulation of key ferroptosis-protective genes, including FTH1 and GPX4. In contrast, disruption of the ELF3/JUNB-WNT11 axis markedly restored abiraterone sensitivity and triggered ferroptotic cell death in CRPC cells both in vitro and in vivo. Collectively, our findings highlight targeting SE-driven transcriptional programs as a promising strategy for overcoming abiraterone resistance in CRPC.

Male↗

PubMed1999

Testing for tumor drug resistance in the age of molecular medicine. A contribution to the Debate Round-Table on Phenotypic and Genotypic Analyses of Multidrug Resistance (MDR) in Clinical Hospital Practice.

The detection of multidrug resistance (MDR) in clinical hospital practice represents an important strategy to combat clinical tumor drug resistance. Predicting the response of tumors to cytostatic drugs is of prognostic value. The 'Debate Round-Table on Phenotypic and Genotypic Analyses of Multidrug Resistance (MDR) in Clinical Hospital Practice' was launched in 1997 to address specific questions on this topic. The results published thus far are a rich source to learn about the promises and pitfalls of methods, eg surrogate and functional tests and protein or mRNA expression assays as well. In the present paper, some requirements are discussed for applications of drug resistance testing in clinical routine diagnostics. To improve the detection of low-level resistance, established methodologies may be strengthened with respect to: (1) standardization of sample handling, antibodies, PCR primers, and detection reagents; (2) standardization of protocols and far reaching automation in performance and evaluation of results to ensure high quality control criteria. Sophisticated new techniques will feature: (1) high-throughput analyses for the 'horizontal screening' of single drug resistance genes in large numbers of patient samples at economically fair costs; (2) 'vertical screening' of a large number of resistance mechanisms operating upstream or downstream of the actual drug-target interaction sites, in order to detect more complex and multifaceted genotypes and phenotypes of multidrug resistance.

Drug Resistance, Multiple↗

PubMed2003

Influence of tetracycline exposure on tetracycline resistance and the carriage of tetracycline resistance genes within commensal Escherichia coli populations.

AIMS: To assess the influence of incremental tetracycline exposure on the genetic basis of tetracycline resistance within faecal Escherichia coli. METHODS AND RESULTS: Through the adoption of a novel combination of multiple breakpoint selection, phenotypic characterization and the application of a polymerase chain reaction based gene identification system it proved possible to monitor the influence of antibiotic exposure on resistance gene possession. Using tetracycline as a case study a clear hierarchy was revealed between tet genes, strongly influenced by host antimicrobial exposure history. CONCLUSIONS: The antimicrobial exposure regime under which an animal is produced affects both the identity and magnitude of resistance gene possession of a selected bacterial population within its enteric microflora. Among the ramifications associated with such resistance gene selection is the degree of resistance conferred and the carriage of linked resistance determinants. This selection is applied by exposure to antibiotic concentrations well below recognized minimum inhibitory tetracycline concentration breakpoints widely adopted to characterize bacterial 'susceptibility'. SIGNIFICANCE AND IMPACT OF THE STUDY: This study confirms the ability of minimal antibiotic exposure to select for the continued persistence of resistance genes within the enteric microflora. It is clearly demonstrated that different antimicrobial regimes select for different resistance genes, the implications of which are discussed.

Animals↗

PubMed2006

Enhanced expression of multidrug resistance-associated protein 2 and reduced expression of aquaglyceroporin 3 in an arsenic-resistant human cell line.

Arsenic-resistant cells (R15), derived from a human lung adenocarcinoma cell line (CL3), were 10-fold more resistant to sodium arsenite (As(III)). Because R15 cells accumulated less arsenic than parental CL3 cells, this arsenic resistance may be due to higher efflux and/or lower uptake of As(III). We therefore compared expression of the multidrug resistance-associated proteins MRP1, MRP2, and MRP3 in these two cell lines. MRP2 expression was 5-fold higher in R15 cells than in CL3 cells, whereas MRP1 and MRP3 expression levels were similar. Furthermore, verapamil and cyclosporin A, inhibitors of multidrug resistance transporters, significantly reduced the efflux of arsenic from R15. Thus, increased arsenic extrusion by MRP2 may contribute to arsenic resistance in R15 cells. We also examined the expression of several aquaglyceroporins (AQPs), which mediate As(III) uptake by cells. Little AQP7 or AQP9 mRNA was detected by reverse transcription-PCR in either cell line, whereas AQP3 mRNA expression was 2-fold lower in R15 cells than in CL3 cells. When AQP3 expression in CL3 cells was knocked down by RNA interference, CL3 cells accumulated less arsenic and became more resistant to As(III). Conversely, overexpression of AQP3 in human embryonic kidney 293T cells increased arsenic accumulation, and the cells were more susceptible to As(III) than 293T cells transfected with vector alone. These results suggest that AQP3 is involved in As(III) accumulation. Taken together, our results suggest that enhanced expression of MRP2 and lower expression of AQP3 are responsible for lower arsenic accumulation in arsenic-resistant R15 cells.

Aquaglyceroporins↗

PubMed2026

Chlorfenapyr-pyrethroid nets for pyrethroid-resistant malaria vectors: efficacy, resistance risks, and policy implications.

The Global Technical Strategy for Malaria 2016-2030 aims to reduce malaria incidence and mortality by 90%, yet widespread pyrethroid resistance among major malaria vectors in sub-Saharan Africa threatens this goal. Thus, the World Health Organization recommends chlorfenapyr-pyrethroid combination nets as a priority intervention where pyrethroid resistance undermines vector control. This systematic review synthesizes evidence on the performance, emerging resistance risks, and policy implications of these next-generation insecticide-treated nets. A structured search of literature from 2010 to 2024 across PubMed, Embase, WHO IRIS, and Google Scholar identified 31 eligible studies from 113 records. Evidence shows that chlorfenapyr-pyrethroid nets consistently outperform pyrethroid-only nets against resistant Anopheles populations, demonstrating a 1.8-fold increase in mosquito mortality (95% CI: 1.5-2.1). Community trials report 40-60% reductions in malaria infection incidence and entomological inoculation rates following deployment. However, early signs of chlorfenapyr resistance have emerged in Anopheles gambiae populations in Central Africa (RR: 2.4, p = 0.01), linked to CYP6P4 metabolic overexpression. A significant correlation was also observed between agricultural pesticide use and vector resistance patterns (r = 0.62, p < 0.05). Although chlorfenapyr-pyrethroid nets provide an important short-term tool for managing pyrethroid resistance, their long-term effectiveness depends on integrated resistance management. Rotational deployment with other insecticide classes, strengthened genetic and phenotypic surveillance, and a coordinated 'One Health' approach involving both public health and agriculture are essential to sustain gains and advance progress toward the 2030 malaria targets.

Pyrethrins↗

PubMed2003

Quinupristin-dalfopristin resistance in gram-positive bacteria: mechanism of resistance and epidemiology.

Antimicrobial resistance in gram-positive bacteria is a continuing problem resulting in significant morbidity, mortality, and cost. Because of this resistance, new antimicrobial agents have been needed. Quinupristin-dalfopristin is a recently approved agent for treatment of these infections. Shortly after its introduction into clinical medicine, resistance was reported. Resistance can occur by one or more of several mechanisms, including enzymatic modification, active transport of efflux mediated by an adenosine triphosphate-binding protein, and alteration of the target site. Resistance is rare in isolates of staphylococci and Enterococcus faecium from humans. Resistance is common in isolates recovered from food animals and is related to the use of virginiamicin as a feed additive. Considering the effect antimicrobial resistance has on human health, as well as its economic impact, measures to preserve the usefulness of these agents and delay the development of resistance are urgently needed.

Anti-Bacterial Agents↗