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Resistant Strains (resistant + strain)
Selected AbstractsDetection of quinolone-resistance genes in Photobacterium damselae subsp. piscicida strains by targeting-induced local lesions in genomesJOURNAL OF FISH DISEASES, Issue 8 2005M-J Kim Abstract Quinolone-resistant strains of the fish-pathogenic bacterium, Photobacterium damselae subsp. piscicida are distributed widely in cultured yellowtail, Seriola quinqueradiata (Temminck & Schlegel), in Japan. The quinolone resistance-determining region (QRDR) was amplified with degenerate primers, followed by cassette ligation-mediated PCR. Open reading frames encoding proteins of 875 and 755 amino acid residues were detected in the gyrA and parC genes, respectively. Resistant strains of P. damselae subsp. piscicida carried a point mutation only in the gyrA QRDR leading to a Ser-to-Ile substitution at residue position 83. No amino acid alterations were discovered in the ParC sequence. A mutation in the gyrA gene was also detected in nalidixic acid-resistant mutants of strain SP96002 obtained from agar medium containing increased levels of quinolone. These results suggest that GyrA, as in other Gram-negative bacteria, is a target of quinolone in P. damselae subsp. piscicida. Furthermore, we attempted to detect a point mutation using targeting-induced local lesions in genomes (TILLING), which is a general strategy used for the detection of a variety of induced point mutations and naturally occurring polymorphisms. We developed a new detection method for the rapid and large-scale identification of quinolone-resistant strains of P. damselae subsp. piscicida using TILLING. [source] Microbiology of postoperative peritonitisBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2000A. Röhrborn Background The microbiology of secondary peritonitis is well known and standards of antibiotic therapy are established. In contrast, little is known about the bacteriology of postoperative peritonitis. Resistant strains could be involved and patients may have had previous antibiotic treatment. Methods The intraoperative and postoperative bacteriology (10 days after operation) of all 88 cases of postoperative peritonitis occurring between September 1994 and May 1999 were documented. Resistances were used to determine effective antibiotic therapy. Results Compared with secondary peritonitis, enterococci outnumbered Escherichia coli in postoperative peritonitis. While E. coli showed no advanced resistance, the different pattern of bacterial findings (e.g. enterococci, Enterobacter, Gram-positive bacteria) leads to failures of standard therapy for secondary peritonitis. Imipenem,cilastatin failed in 20 per cent, piperacillin,tazobactam in 31, aminoglycosides in 31, ciprofloxacin in 37 and third-generation cephalosporins in 47 per cent (the latter three combined with metronidazole). Conclusion Cephalosporins, the ,gold standard' in secondary peritonitis, fail in postoperative cases. Carbapenems are the drugs of choice. Aminoglycosides should be avoided in these patients. © 2000 British Journal of Surgery Society Ltd [source] Inheritance of resistance and cross resistance pattern in indoxacarb-resistant diamondback moth Plutella xylostella L.ENTOMOLOGICAL RESEARCH, Issue 1 2010Sarita NEHARE Abstract Leaf-dip assay of Plutella xylostella against indoxacarb showed that the concentration that produced 50% mortality (LC50) of indoxacarb ranged from 20.1 to 11.9 ppm, with highest in Nasik and lowest levels in Coimbatore strains. In selection studies, the LC50 of indoxacarb was 18.5 ppm at generation 1 (G1), which increased to 31.3-fold (167.8 ppm) resistance after ten exposed generations (G10) as compared to unexposed. The LC50 of quinalphos was 74.4 ppm, which increased to 10.0-fold (631.5 ppm) resistance after G10. The LC50 of cypermethrin resistant strain resulted in an 11.5-fold increase in resistance after G10. In P. xylostella, heritability (h2) after ten generations of selection was estimated at 0.4. The number of generations required for tenfold increase in LC50 (1/R) were 6.7. The response to indoxacarb selection in P. xylostella was 0.2 and the selection differential was estimated as 0.4. The phenotypic standard deviation was 0.2. Reciprocal crosses between indoxacarb-resistant and susceptible strains showed that the inheritance of indoxacarb resistance was autosomal. The degree of heritability (DLC) (0.4, 0.4) indicated incomplete recessive inheritance of indoxacarb resistance. [source] Over expression of a Cytochrome P450 (CYP6P9) in a Major African Malaria Vector, Anopheles Funestus, Resistant to PyrethroidsINSECT MOLECULAR BIOLOGY, Issue 1 2008D. A. Amenya Abstract Anopheles funestus Giles is one of the major African malaria vectors. It has previously been implicated in a major outbreak of malaria in KwaZulu/Natal, South Africa, during the period 1996 to 2000. The re-emergence of this vector was associated with monooxygenase-based resistance to pyrethroid insecticides. We have identified a gene from the monooxygenase CYP6 family, CYP6P9, which is over expressed in a pyrethroid resistant strain originating from Mozambique. Quantitative Real-Time PCR shows that this gene is highly over expressed in the egg and adult stages of the resistant strain relative to the susceptible strain but the larval stages showed almost no difference in expression between strains. This gene is genetically linked to a major locus associated with pyrethroid resistance in this A. funestus population. [source] Molecular characterization of the amplified carboxylesterase gene associated with organophosphorus insecticide resistance in the brown planthopper, Nilaparvata lugensINSECT MOLECULAR BIOLOGY, Issue 6 2000Graham J. Small Abstract Widespread resistance to organophosphorus insecticides (OPs) in Nilaparvata lugens is associated with elevation of carboxylesterase activity. A cDNA encoding a carboxylesterase, Nl-EST1, has been isolated from an OP-resistant Sri Lankan strain of N. lugens. The full-length cDNA codes for a 547-amino acid protein with high homology to other esterases/lipases. Nl-EST1 has an N-terminal hydrophobic signal peptide sequence of 24 amino acids which suggests that the mature protein is secreted from cells expressing it. The nucleotide sequence of the homologue of Nl-EST1 in an OP-susceptible, low esterase Sri Lankan strain of N. lugens is identical to Nl-EST1. Southern analysis of genomic DNA from the Sri Lankan OP-resistant and susceptible strains suggests that Nl-EST1 is amplified in the resistant strain. Therefore, resistance to OPs in the Sri Lankan strain is through amplification of a gene identical to that found in the susceptible strain. [source] cDNA sequence, mRNA expression and genomic DNA of trypsinogen from the Indianmeal moth, Plodia interpunctellaINSECT MOLECULAR BIOLOGY, Issue 1 2000Y. C. Zhu Abstract Trypsin-like enzymes are major insect gut enzymes that digest dietary proteins and proteolytically activate insecticidal proteins produced by the bacterium Bacillus thuringiensis (Bt). Resistance to Bt in a strain of the Indianmeal moth, Plodia interpunctella, was linked to the absence of a major trypsin-like proteinase (Oppert et al., 1997). In this study, trypsin-like proteinases, cDNA sequences, mRNA expression levels and genomic DNAs from Bt-susceptible and -resistant strains of the Indianmeal moth were compared. Proteinase activity blots of gut extracts indicated that the susceptible strain had two major trypsin-like proteinases, whereas the resistant strain had only one. Several trypsinogen-like cDNA clones were isolated and sequenced from cDNA libraries of both strains using a probe deduced from a conserved sequence for a serine proteinase active site. cDNAs of 852 nucleotides from the susceptible strain and 848 nucleotides from the resistant strain contained an open reading frame of 783 nucleotides which encoded a 261-amino acid trypsinogen-like protein. There was a single silent nucleotide difference between the two cDNAs in the open reading frame and the predicted amino acid sequence from the cDNA clones was most similar to sequences of trypsin-like proteinases from the spruce budworm, Choristoneura fumiferana, and the tobacco hornworm, Manduca sexta. The encoded protein included amino acid sequence motifs of serine proteinase active sites, conserved cysteine residues, and both zymogen activation and signal peptides. Northern blotting analysis showed no major difference between the two strains in mRNA expression in fourth-instar larvae, indicating that transcription was similar in the strains. Southern blotting analysis revealed that the restriction sites for the trypsinogen genes from the susceptible and resistant strains were different. Based on an enzyme size comparison, the cDNA isolated in this study corresponded to the gene for the smaller of two trypsin-like proteinases, which is found in both the Bt-susceptible and -resistant strains of the Indianmeal moth. The sequences reported in this paper have been deposited in the GenBank database (accession numbers AF064525 for the RC688 strain and AF064526 for HD198). [source] Differential mRNA expression levels and gene sequences of carboxylesterase in both deltamethrin resistant and susceptible strains of the cotton aphid, Aphis gossypiiINSECT SCIENCE, Issue 3 2008Chuan-Wang Cao Abstract Extensive use of insecticides on cotton has prompted resistance development in the cotton aphid, Aphis gossypii (Glover) in China. A deltamethrin-selected population of cotton aphids from Xinjiang Uygur Autonomous Region, China with 228.59-fold higher resistance to deltamethrin was used to examine how carboxylesterase conferred resistance to this pyrethroid insecticide. The carboxylesterase activity in the deltamethrin-resistant strain was 3.67-, 2.02- and 1.16-fold of the susceptible strain when using ,-naphthyl acetate (,-NA), ,-naphthyl acetate (,-NA) and ,-naphthyl butyrate (,-NB) as substrates, respectively. Carboxylesterase cDNA was cloned and sequenced from both deltamethrin-resistant and susceptible strains. The cDNA contained 1581 bp open reading frames (ORFs) coding a 526 amino acid protein. Only one amino acid substitution (Val87 -Ala) was observed between deltamethrin-resistant and susceptible strains but it is not genetically linked to resistance by the catalytic triad and signature motif analysis. The real-time polymerase chain reaction analysis indicated that the resistant strain had a 6.61-fold higher level of carboxylesterase mRNA than the susceptible strain. The results revealed that up-regulation of the carboxylesterase gene, not modified gene structure, may be responsible for the development of resistance in cotton aphids to deltamethrin. [source] Mechanisms of resistance to spinosad in the western flower thrip, Frankliniella occidentalis (Pergande) (Thysanoptera: Thripidae)INSECT SCIENCE, Issue 2 2008Shu-Yun Zhang Abstract Cross-resistance, resistance mechanisms, and mode of inheritance of spinosad resistance were studied in the western flower thrip, Frankliniella occidentalis (Pergande). Spinosad (naturalyte insecticide) showed low cross-resistance to prothiophos (organophosphorus insecticide) and chlorphenapyr (respiratory inhibitor) showed some cross-resistance to thiocyclam (nereistoxin). The synergists PBO (piperonyl butoxide), DEM (diethyl maleate), and DEF (s, s, s-tributyl phosphorotrithioate) did not show any synergism on the toxicity of spinosad in the resistant strain (ICS), indicating that metabolic-mediated detoxification was not responsible for the spinosad resistance, suggesting that spinosad may reduce sensitivity of the target site: the nicotinic acetylcholine receptor and GABA receptor. Following reciprocal crosses, dose-response lines and dominance ratios indicated that spinosad resistance was incompletely dominant and there were no maternal effects. The results of backcross showed that spinosad resistance did not fit a single-gene hypothesis, suggesting that resistance was influenced by several genes. [source] Altered mating behaviour in a Cry1Ac-resistant strain of Helicoverpa armigera (Lepidoptera: Noctuidae)JOURNAL OF APPLIED ENTOMOLOGY, Issue 5 2008X. C. Zhao Abstract Randomness of mating between susceptible and resistant individuals is a major factor that closely relates to the refuge strategy of resistance management for Helicoverpa armigera (Hübner) to Bacillus thuringiensis cotton. The mating behaviour of Cry1Ac-susceptible and Cry1Ac-resistant strains of H. armigera was compared to investigate the randomness of their mating. The percentage of mating was lower for Cry1Ac-resistant H. armigera compared with that of the susceptible strain under both no-choice and multiple-choice conditions. The low percentage of mating in the resistant strain indicates a reduced incidence of successful mating. The percentage of spermatophore-containing mated female H. armigera in the crossing of susceptible females × resistant males was significantly lower than in the crossing of resistant females × susceptible males, but the observed mating frequencies of these two types of cross were similar to each other. This indicates that resistant males reduce the incidence of mating paternity more than they do their mating frequency. The percentages of heterogametic matings (susceptible females × resistant males, resistant females × susceptible males) in the multiple-choice experiment were lower than those of homogametic matings (susceptible × susceptible, resistant × resistant) on peak mating nights. However, the difference between heterogametic and homogametic mating was not significant, indicating that there was a random mating between susceptible and resistant strains. The results presented here do not reflect reality in mating associated with Cry1Ac resistance but can provide insight into variable expression. [source] Strong genetic influence on IPN vaccination-and-challenge trials in Atlantic salmon, Salmo salar L.JOURNAL OF FISH DISEASES, Issue 8 2008A Ramstad Abstract Two series of experimental challenge trials were performed for evaluation of multivalent oil-adjuvanted vaccines with and without an infectious pancreatic necrosis virus (IPNV) antigen component. In both the trial series, Atlantic salmon were hatched, reared, vaccinated and subjected to temperature and light manipulation to induce smoltification. When ready for sea the fish were transported to the VESO Vikan experimental laboratory for bath or cohabitant challenge with IPNV. In the first series, four vaccination and bath challenge trials involving 2-year classes of experimental fish were conducted. In the second series, three groups of eyed eggs of Atlantic salmon allegedly differing in their innate resistance to IPNV were used (Storset, Strand, Wetten, Kjøglum & Ramstad 2007). Hatching, rearing and smoltification were synchronized for each group, and fish from each genetic group were randomly allocated IPN vaccine, reference vaccine or saline before being placed into parallel tanks for bath or cohabitant challenge. In the first series of trials, IPN-specific mortality commenced on day 10,12 after bath challenge. Replicates showed similar results. In trials 1 and 2 belonging to the same experimental fish year class, the average cumulative control mortality reached 60.6% and 79.5%, respectively, whereas in trials 3 and 4 belonging to the following year class the control mortality was consistently below 50%. In the second series of trials, the experimental fish originating from allegedly IPN susceptible parents consistently showed the highest cumulative mortality among the unvaccinated controls (>75%) whereas smolts derived from allegedly IPNV resistant parents showed only 26,35% control mortality. The IPN-vaccinated fish experienced significantly improved survival vs. the fish immunized with reference vaccine, with RPS values above 75% in the IPN susceptible strain. In the IPN resistant strain, the protection outcomes were variable and in part non-significant. The outcome of both the trial series suggests that control mortalities above 50% are necessary to reliably demonstrate specific protection with IPN vaccines. [source] Screening for Alternative Antibiotics: An Investigation into the Antimicrobial Activities of Medicinal Food Plants of MauritiusJOURNAL OF FOOD SCIENCE, Issue 3 2010M.F. Mahomoodally ABSTRACT:, The present study was designed to evaluate the antimicrobial activities of 2 endemic medicinal plants; Faujasiopsis flexuosa,(Asteraceae) (FF) and Pittosporum senacia,(Pittosporaceae) (PS) and 2 exotic medicinal plants, Momordica charantia,(Cucurbitaceae) (MC) and Ocimum tenuiflorum,(Lamiaceae) (OT) that forms part of local pharmacopoeia of Mauritius and correlate any observed activity with its phytochemical profile. Aqueous and organic fractions of the leaves, fruits, and seeds of these plants were subjected to antimicrobial testing by the disc diffusion method against 8 clinical isolates of bacteria and 2 strains of fungus. It was found that MC, OT, and FF possessed antimicrobial properties against the test organisms. The MIC for MC ranged from 0.5 to 9 mg/mL and that of FF from 2 to 10 mg/mL and the lowest MIC value (0.5 mg/mL) was recorded for the unripe fruits of MC against E. coli. On the other hand, higher concentration of the unripe MC fruit extract of 9 mg/mL was needed to be effective against a resistant strain of Staphylococcus aureus,(MRSA). The antimicrobial effect against MRSA was lost upon ripening of the fruits. The methanolic extract of both MC and FF showed highest MIC values compared to the corresponding aqueous extract, which indicates the low efficacy and the need of higher doses of the plant extract. Phytochemical screening of the plants showed the presence of at least tannins, phenols, flavonoids, and alkaloids, which are known antimicrobial phyto-compounds. In conclusion, the observed antimicrobial properties would tend to further validate the medicinal properties of these commonly used endemic medicinal and food plants of Mauritius. [source] STAT1 and STAT3 ,/, splice form activation predicts host responses in mouse hepatitis virus type 3 infectionJOURNAL OF MEDICAL VIROLOGY, Issue 3 2003Qin Ning Abstract Signal transducer and activator of transcription 1, (STAT1 ,) is reported to be essential for IFN-, and IFN-, regulated gene expression, while STAT1 ,, an alternate splice-form, mediates only IFN-,-dependent gene expression. STAT3 , and STAT3 , splice forms are also differentially activated in response to cytokines including IL-6 and IL-10. The aim of this study was to investigate whether the STAT activation will predict the host immune response to viral infection and possibly a therapeutic target for the treatment of viral infection. Mouse hepatitis virus type 3 (MHV-3) resistant strain (A/J) and sensitive mouse strains (BalB/cJ) were infected intraperitoneally (i.p.) with 100 plaque form units (pfu) of MHV-3. The mice were sacrificed at the indicated times, and livers and spleens were immediately frozen in liquid nitrogen. Nuclear extracts proteins were detected by immunoblotting. STAT1 and STAT3 activation in spleen increased 24 to 72 hr following MHV-3 infections in both sensitive and resistant mouse strains. However, over this time period, the ratio of activated , to , splice-form for STAT1 and STAT3 increased above 1.0 in resistant A/J mice, while the ratio fell to <0.3 in MHV-3 sensitive Balb/cJ and C3H/HeJ strains. Activated STAT1 ,/, and STAT3 ,/, ratio in liver were similar in resistant and sensitive mouse strains. Treatment of sensitive Balb/cJ mice with neutralizing anti-TGF-, antibody could increase the STAT1 ,/, ratio to <1.0 in spleens, predicting enhanced rates of survival. These results suggested that ratio of activated STAT1 ,/, and STAT3 ,/, in mixed leukocytes from spleen predict the outcome to MHV-3 infection, and may be an important marker and therapeutic target for modification of host immune response to virus infection. J. Med. Virol. 69:306,312, 2003. © 2003 Wiley-Liss, Inc. [source] Insecticide resistance in the malarial mosquito Anopheles arabiensis and association with the kdr mutationMEDICAL AND VETERINARY ENTOMOLOGY, Issue 1 2007T. S. MATAMBO Abstract A colony of Anopheles arabiensis Patton (Diptera: Culicidae) from the Sennar region of Sudan was selected for resistance to dichlorodiphenyltrichloroethane (DDT). Adults from the F-16 generation of the resistant strain were exposed to all four classes of insecticides approved for use in malaria vector control and showed high levels of resistance to them all (24-h mortalities: malathion, 16.7%; bendiocarb, 33.3%; DDT, 12.1%; dieldrin, 0%; deltamethrin, 24.0%; permethrin, 0%). Comparisons between the unselected base colony and the DDT-resistant strain showed elevated glutathione- S -transferase (P < 0.05) in both sexes and elevated esterases (P < 0.05) in males only. The Leu-Phe mutation in the sodium channel gene was detected by polymerase chain reaction and sequencing, but showed no correlation with the resistant phenotype. These results do not provide any explanation as to why this colony exhibits such widespread resistance and further studies are needed to determine the precise mechanisms involved. The implications for malaria vector control in central Sudan are serious and resistance management (e.g. through the rotational use of different classes of insecticides) is recommended. [source] EmtA, a rRNA methyltransferase conferring high-level evernimicin resistanceMOLECULAR MICROBIOLOGY, Issue 6 2001Paul A. Mann Enterococcus faecium strain 9631355 was isolated from animal sources on the basis of its resistance to the growth promotant avilamycin. The strain also exhibited high-level resistance to evernimicin, a drug undergoing evaluation as a therapeutic agent in humans. Ribosomes from strain 9631355 exhibited a dramatic reduction in evernimicin binding, shown by both cell-free translation assays and direct-binding assays. The resistance determinant was cloned from strain 9631355; sequence alignments suggested it was a methyltransferase and therefore it was designated emtA for evernimicin methyltransferase. Evernimicin resistance was transmissible and emtA was localized to a plasmid-borne insertion element. Purified EmtA methylated 50S subunits from an evernimicin-sensitive strain 30-fold more efficiently than those from a resistant strain. Reverse transcription identified a pause site that was unique to the 23S rRNA extracted from resistant ribosomes. The pause corresponded to methylation of residue G2470 (Escherichia coli numbering). RNA footprinting revealed that G2470 is located within the evernimicin-binding site on the ribosome, thus providing an explanation for the reduced binding of the drug to methylated ribosomes. [source] Molecular analysis of pyrethroid resistance conferred by target insensitivity and increased metabolic detoxification in Plutella xylostellaPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 5 2010Shoji Sonoda Abstract BACKGROUND: The pyrethroid resistance of the diamondback moth Plutella xylostella (L.) is conferred by increased gene expression of cytochrome P450 to detoxify the insecticide and/or through gene mutation of the sodium channel, which makes the individual insensitive to pyrethroids. However, no information is available about the correlation between the increased metabolic detoxification and the target insensitivity in pyrethroid resistance. RESULTS: Frequencies of pyrethroid-resistant alleles (L1014F, T929I and M918I) and two resistance-related mutations (A1101T and P1879S) at the sodium channel and expression levels of the cytochrome P450 gene CYP6BG1 were examined individually using laboratory and field strains of P. xylostella. Real-time quantitative PCR analysis using the laboratory strains revealed that levels of larval expression of the resistant strain, homozygous for the pyrethroid-resistant alleles other than the M918I, are significantly higher than those of the susceptible strain. In the field strains, the expression levels in insects having the same resistant alleles as those of the resistant strains varied greatly among individuals. The expression levels were not significantly higher than those in the heterozygotes. CONCLUSION: Significant correlation between the target insensitivity and the increased metabolic detoxification in pyrethroid resistance of P. xylostella was observed in the laboratory but not in the field. Copyright © 2010 Society of Chemical Industry [source] Cross-resistance study and biochemical mechanisms of thiamethoxam resistance in B-biotype Bemisia tabaci (Hemiptera: Aleyrodidae)PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 3 2010Yuntao Feng Abstract BACKGROUND: B-biotype Bemisia tabaci (Gennadius) has invaded China over the past two decades. To understand the risks and to determine possible mechanisms of resistance to thiamethoxam in B. tabaci, a resistant strain was selected in the laboratory. Cross-resistance and the biochemical mechanisms of thiamethoxam resistance were investigated in the present study. RESULTS: A 66.3-fold thiamethoxam-resistant B. tabaci strain (TH-R) was established after selection for 36 generations. Compared with the susceptible strain (TH-S), the selected TH-R strain showed obvious cross-resistance to imidacloprid (47.3-fold), acetamiprid (35.8-fold), nitenpyram (9.99-fold), abamectin (5.33-fold) and carbosulfan (4.43-fold). No cross-resistance to fipronil, chlorpyrifos or deltamethrin was seen. Piperonyl butoxide (PBO) and triphenyl phosphate (TPP) exhibited significant synergism on thiamethoxam effects in the TH-R strain (3.14- and 2.37-fold respectively). However, diethyl maleate (DEM) did not act synergistically with thiamethoxam. Biochemical assays showed that cytochrome P450 monooxygenase activities increased 1.21- and 1.68-fold respectively, and carboxylesterase activity increased 2.96-fold in the TH-R strain. However, no difference was observed for glutathione S -transferase between the two strains. CONCLUSION: B-biotype B. tabaci develops resistance to thiamethoxam. Cytochrome P450 monooxygenase and carboxylesterase appear to be responsible for the resistance. Reasonable resistance management that avoids the use of cross-resistance insecticides may delay the development of resistance to thiamethoxam in this species. Copyright © 2009 Society of Chemical Industry [source] Biochemical mechanisms of methoxyfenozide resistance in the cotton leafworm Spodoptera littoralisPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 7 2009Hadi Mosallanejad Abstract BACKGROUND: Methoxyfenozide is a lepidopteran-specific insecticide that belongs to a new group of insecticides, the non-steroidal ecdysteroid agonists, also called moulting accelerating compounds (MACs). To investigate the risk of resistance and possible mechanisms conferring resistance to methoxyfenozide, the authors selected in the laboratory for a resistant strain of the cotton leafworm Spodoptera littoralis (Boisd.), which is a representative lepidopteran model and an important pest in cotton and vegetables worldwide, with a high risk for resistance development. RESULTS: After selection with methoxyfenozide during 13 generations, toxicity data showed that the selected strain developed fivefold resistance to methoxyfenozide in comparison with the susceptible strain. Measurement of the detoxification enzymes demonstrated that the monooxygenase (MO) activity was 2.1 times higher in the selected strain, whereas there was no change for esterases and glutathione- S -transferases. When the inhibitors piperonyl butoxide (PBO), S,S,S -tributyl phosphorotrithioate (DEF) and diethyl maleate were tested as synergists, the respective synergistic ratios were 0.97, 0.96 and 1.0 for the susceptible strain, and 2.2, 0.96 and 1.1 for the resistant strain. The significant synergistic effect by PBO concurs with the increased MO activity in the selected strain. CONCLUSION: Taken overall, the present study supports the importance of MO-mediated metabolism in resistance to methoxyfenozide, directing tactics to fight against resistance development for this novel group of insecticides. Copyright © 2009 Society of Chemical Industry [source] Inheritance mode and realized heritability of resistance to imidacloprid in the brown planthopper, Nilaparvata lugens (Stål) (Homoptera: Delphacidae)PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 6 2009Yan Hua Wang Abstract BACKGROUND: The brown planthopper, Nilaparvata lugens (Stål), is a serious pest that causes enormous losses to the rice crop in Asia. The genetic basis of imidacloprid resistance was investigated in N. lugens. RESULTS: The resistant strain, selected for imidacloprid resistance from a field population of N. lugens collected from Nanjing, Jiangsu Province, China, showed a 964-fold resistance compared with the laboratory strain. Progenies of reciprocal crosses (F1 and F1,) showed similar dose,mortality responses (LC50) to imidacloprid, and also exhibited a similar degree of dominance (D), 0.58 for F1 and 0.63 for F1,. Chi-square analyses of self-bred and backcross progenies (F2, F2, and BC respectively) rejected the hypothesis for a single gene control of the resistance. The estimated realized heritability (h2) of imidacloprid resistance was 0.1141 in the resistant strain of N. lugens. CONCLUSION: The results showed that imidacloprid resistance in N. lugens was autosomal and was expressed as an incompletely dominant trait, probably controlled by multiple genes. Copyright © 2009 Society of Chemical Industry [source] Lack of fitness costs associated with pyriproxyfen resistance in the B biotype of Bemisia tabaciPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 3 2009David W Crowder Abstract BACKGROUND: The insect growth regulator pyriproxyfen has provided effective control of the whitefly Bemisia tabaci Gennadius in many countries. Here, whether or not fitness costs were associated with pyriproxyfen resistance in a laboratory-selected resistant strain (QC02-R) of the B biotype was determined. RESULTS: Mortality caused by pyriproxyfen and fitness traits over time were measured in unselected and selected hybrid strains, which were created by crossing individuals of the resistant strain with individuals of a susceptible strain. Fitness costs were not associated with resistance in QC02-R, as mortality caused by pyriproxyfen did not increase over time in unselected hybrid strains and fitness traits were similar in unselected and selected hybrid strains. Using a new method to examine the inheritance of resistance, based on data from fitness cost experiments, it was estimated that pyriproxyfen resistance is controlled by two loci in the QC02-R strain. CONCLUSION: The lack of fitness costs associated with pyriproxyfen resistance could promote the evolution of resistance in field populations with similar traits to QC02-R. Copyright © 2008 Society of Chemical Industry [source] Inheritance of beta-cypermethrin resistance in the housefly Musca domestica (Diptera: Muscidae)PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 2 2008Lan Zhang Abstract BACKGROUND: Beta-cypermethrin, a synthetic pyrethroid insecticide, was applied frequently in the control of health pests including houseflies, Musca domestica L., in China. However, different levels of resistance to beta-cypermethrin were monitored in field strains of houseflies. A strain of M. domestica, 4420-fold resistant to beta-cypermethrin after continuous 25 generations of selection, was used in this paper to determine the mode of inheritance of pyrethroid resistance. RESULTS: The estimated realized heritability (h2) of beta-cypermethrin resistance was 0.30 in this resistant strain. Results of bioassays showed no significant difference in values of LD50 and slope of log dose-probit lines between reciprocal progenies F1 and F,1, and yielded values of , 0.10 (F1) and , 0.11 (F,1) for the degree of dominance (D). Chi-square analysis from responses of self-bred and backcross progenies (F2, BC1 and BC2 respectively) indicated that the null hypothesis, a single gene responsible for resistance, was accepted. The minimum number of independent segregation genes was 0.93 for F1 by Lande's method. CONCLUSION: It was concluded that beta-cypermethrin resistance in the housefly was inherited as a single, major, autosomal and incompletely recessive factor. These results would provide the basic information for pest management programmes. Copyright © 2007 Society of Chemical Industry [source] Temporal synergism can enhance carbamate and neonicotinoid insecticidal activity against resistant crop pestsPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 1 2008Georgina Bingham Abstract BACKGROUND: Piperonyl butoxide (PBO) effectively synergises synthetic pyrethroids, rendering even very resistant insect pests susceptible, provided a temporal element is included between exposure to synergist and insecticide. This concept is now applied to carbamates and neonicotinoids. RESULTS: A microencapsulated formulation of PBO and pirimicarb reduced the resistance factor in a clone of Myzus persicae (Sulzer) from > 19 000- to 100-fold and in Aphis gossypii (Glover) from > 48 000- to 30-fold. Similar results were obtained for a strain of Bemisia tabaci Gennadius resistant to imidacloprid and acetamiprid, although a second resistant strain did not exhibit such a dramatic reduction, presumably owing to the presence of target-site insensitivity and the absence of metabolic resistance. Synergism was also observed in laboratory susceptible insects, suggesting that, even when detoxification is not enhanced, there is degradation of insecticides by the background enzymes. Use of an analogue of PBO, which inhibits esterases but has reduced potency against microsomal oxidases, suggests that acetamiprid resistance in whiteflies is largely oxidase based. CONCLUSION: Temporal synergism can effectively enhance the activity of carbamates and neonicotinoids against resistant insect pests. Although the extent of this enhancement is dependent upon the resistance mechanisms present, inhibition of background enzymes can confer increased sensitivity against target-site resistance as well as increased metabolism. Copyright © 2007 Society of Chemical Industry [source] Synergism and stability of acetamiprid resistance in a laboratory colony of Plutella xylostellaPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 8 2005Kodwo D Ninsin Abstract The involvement of metabolic enzymes in the resistance of a laboratory colony of diamondback moth, Plutella xylostella (L), to the neonicotinoid insecticide acetamiprid was determined with the synergists piperonyl butoxide (PBO), which suppresses the activity of cytochrome P-450 monooxygenases, and S,S,S -tributyl phosphorotrithioate (DEF), an inhibitor of esterases, using the leaf-dipping method. Both PBO and DEF enhanced the insecticidal activity of acetamiprid significantly in the resistant P xylostella strain but not in a reference strain, suggesting that cytochrome P-450 monooxygenases and esterases play an important role in the resistance of P xylostella to acetamiprid. The resistant P xylostella strain was also reared without further exposure to acetamiprid to determine the stability of resistance. Maintaining the resistant strain for seven generations in the absence of selection pressure resulted in a drop in resistance ratio from 110 to 2.42, indicating that acetamiprid resistance in P xylostella is not stable. Copyright © 2005 Society of Chemical Industry [source] Biorational insecticides: Mechanism and cross-resistance ,ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 4 2005Isaac Ishaaya Abstract Potency and cross-resistance of various biorational insecticides, exemplified by the whitefly Bemisia tabaci, have been studied. Bemisia tabaci were exposed to the juvenile hormone mimic pyriproxyfen for the past 12 years resulting in an over 2,000-fold resistance, but there was no appreciable cross-resistance with the benzoylphenyl urea novaluron. Similarly, no cross-resistance was found between pyriproxyfen and the two neonicotinoids, acetamiprid and imidacloprid. On the other hand, a slight cross-resistance of 5,13-fold was observed with another neonicotinoid thiamethoxam. Among the neonicotinoids, a resistant strain of B. tabaci to thiamethoxam (,100-fold) showed no appreciable cross-resistance to either acetamiprid or imidacloprid, while another strain 500-fold resistant to thiamethoxam resulted in a mild of 4,6-fold resistance to acetamiprid and imidacloprid. In other assays, B. tabaci strain resistant to thiamethoxam (,100-fold) had no cross-resistance to pyriproxyfen. Our findings indicate that no appreciable cross-resistance was observed between the benzoylphenyl urea novaluron, the juvenile hormone mimic pyriproxyfen, and the neonicotinoids acetamiprid and imidacloprid. Hence, these compounds could be used as components in insecticide resistance management programs. Arch. Insect Biochem. Physiol. 58:192,199, 2005. © 2005 Wiley-Liss, Inc. [source] Proteome mapping of overexpressed membrane-enriched and cytosolic proteins in sodium antimony gluconate (SAG) resistant clinical isolate of Leishmania donovaniBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 4 2010Awanish Kumar WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT Over 60% of patients with visceral leishmaniasis (VL) in India and Sudan have become unresponsive to treatment with pentavalent antimonials, the first line of drugs for over 60 years. The drug resistance mechanism, studied so far in in vitro selected laboratory strains, has been attributed to various biochemical parameters. The resistance to Sb (V) in Leishmania field isolates is still unexplored. WHAT THIS STUDY ADDS In order to elucidate for the first time the mechanism of drug resistance in field isolates, this study was done in those clinically relevant field isolates which were either responsive or non responsive to SAG. A comparison of proteome profiles of membrane-enriched as well as cytosolic protein fractions of these isolates has pinpointed the multiple overexpressed proteins in resistant isolates. This study has indicated their possible essential role in antimony resistance of the parasite and provides a vast field to be exploited to find much needed novel treatment strategies against VL. AIMS This study aimed to identify differentially overexpressed membrane-enriched as well as cytosolic proteins in SAG sensitive and resistant clinical strains of L. donovani isolated from VL patients which are involved in the drug resistance mechanism. METHODS The proteins in the membrane-enriched as well as cytosolic fractions of drug-sensitive as well as drug-resistant clinical isolates were separated using two-dimensional gel electrophoresis and overexpressed identified protein spots of interest were excised and analysed using MALDI-TOF/TOF. RESULTS Six out of 12 overexpressed proteins were identified in the membrane-enriched fraction of the SAG resistant strain of L. donovani whereas 14 out of 18 spots were identified in the cytosolic fraction as compared with the SAG sensitive strain. The major proteins in the membrane-enriched fraction were ABC transporter, HSP-83, GPI protein transamidase, cysteine,leucine rich protein and 60S ribosomal protein L23a whereas in the cytosolic fraction proliferative cell nuclear antigen (PCNA), proteasome alpha 5 subunit, carboxypeptidase, HSP-70, enolase, fructose-1,6-bisphosphate aldolase, tubulin-beta chain have been identified. Most of these proteins have been reported as potential drug targets, except 60S ribosomal protein L23a and PCNA which have not been reported to date for their possible involvement in drug resistance against VL. CONCLUSION This study for the first time provided a cumulative proteomic analysis of proteins overexpressed in drug resistant clinical isolates of L. donovani indicating their possible role in antimony resistance of the parasite. Identified proteins provide a vast field to be exploited for novel treatment strategies against VL such as cloning and overexpression of these targets to produce recombinant therapeutic/prophylactic proteins. [source] Characterization of alanyl aminopeptidase from insecticide resistant and susceptible strains of Musca domestica L.ENTOMOLOGICAL RESEARCH, Issue 3 2008Sohail AHMED Abstract To investigate the high activity of intracellular proteases in insecticide resistant strains of Musca domestica L., purification by anion-exchange chromatography and gel filtration of one of the enzymes, alanyl aminopeptidase (Ala AP), in three strains of Musca domestica was carried out. The fractions collected by gel filtration of soluble homogenates of the three strains (571ab, 17bb and Cooper) showed a single peak of Ala AP activity. Partially purified Ala AP of the three strains showed high activity at pH 7.5. The presence or absence of Ca2+ in the assay medium did not produce any difference in activity of Ala AP in the 571ab and Cooper strains, but there was a significant difference in the 17bb strain. The activity of Ala AP in all three strains was essentially unaltered in the presence of inhibitors of serine (PMSF), cysteine (E-64) proteases and carboxypeptidases (pepstatin). Ala AP hydrolyzed alanine amino methylcoumarin (Ala-AMC) maximally, followed by phenyl alanine amino methylcoumarin (Phe-AMC), leucyl amino methylcoumarin (Leu-AMC) and ornithine amino methylcoumarin (Orn-AMC). Ala AP from the three strains showed differential activity towards various substrates. The comparison of alanyl aminopeptidase's activity from different sources is discussed. [source] Anti-adhesion therapy of bacterial diseases: prospects and problemsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2003Itzhak Ofek Abstract The alarming increase in drug-resistant bacteria makes a search for novel means of fighting bacterial infections imperative. An attractive approach is the use of agents that interfere with the ability of the bacteria to adhere to tissues of the host, since such adhesion is one of the initial stages of the infectious process. The validity of this approach has been unequivocally demonstrated in experiments performed in a wide variety of animals, from mice to monkeys, and recently also in humans. Here we review various approaches to anti-adhesion therapy, including the use of receptor and adhesin analogs, dietary constituents, sublethal concentrations of antibiotics and adhesin-based vaccines. Because anti-adhesive agents are not bactericidal, the propagation and spread of resistant strains is much less likely to occur than as a result of exposure to bactericidal agents, such as antibiotics. Anti-adhesive drugs, once developed, may, therefore, serve as a new means to fight infectious diseases. [source] Current status of malaria chemotherapy and the role of pharmacology in antimalarial drug research and developmentFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2009Kesara Na-Bangchang Abstract Antimalarial drugs have played a mainstream role in controlling the spread of malaria through the treatment of patients infected with the plasmodial parasites and controlling its transmissibility. The inadequate armory of drugs in widespread use for the treatment of malaria, development of strains resistant to currently used antimalarials, and the lack of affordable new drugs are the limiting factors in the fight against malaria. In addition, other problems with some existing agents include unfavorable pharmacokinetic properties and adverse effects/toxicity. These factors underscore the continuing need of research for new classes of antimalarial agents, and a re-examination of the existing antimalarial drugs that may be effective against resistant strains. In recent years, major advances have been made in the pharmacology of several antimalarial drugs both in pharmacokinetics and pharmacodynamics aspects. These include the design, development, and optimization of appropriate dosage regimens of antimalarials, basic knowledge in metabolic pathways of key antimalarials, as well as the elucidation of mechanisms of action and resistance of antimalarials. Pharmacologists have been working in close collaboration with scientists in other disciplines of science/biomedical sciences for more understanding on the biology of the parasite, host, in order to exploit rational design of drugs. Multiple general approaches to the identification of new antimalarials are being pursued at this time. All should be implemented in parallel with focus on the rational development of new agents directed against newly identified parasite targets. With major advances in our understanding of malaria parasite biology coupled with the completion of the malaria genome, has presented exciting opportunities for target-based antimalarial drug discovery. [source] The mechanisms of resistance to antimalarial drugs in Plasmodium falciparumFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 2 2003Jacques Le Bras Abstract Drug-resistant malaria is primarily caused by Plasmodium falciparum, a species highly prevalent in tropical Africa, the Amazon region and South-east Asia. It causes severe fever or anaemia that leads to more than a million deaths each year. The emergence of chloroquine resistance has been associated with a dramatic increase in malaria mortality among inhabitants of some endemic regions. The rationale for chemoprophylaxis is weakening as multiple-drug resistance develops against well-tolerated drugs. Plasmodium falciparum drug-resistant malaria originates from chromosome mutations. Analysis by molecular, genetic and biochemical approaches has shown that (i) impaired chloroquine uptake by the parasite vacuole is a common characteristic of resistant strains, and this phenotype is correlated with mutations of the Pfmdr1, Pfcg2 and Pfcrt genes; (ii) one to four point mutations of dihydrofolate reductase (DHFR), the enzyme target of antifolates (pyrimethamine and proguanil) produce a moderate to high level of resistance to these drugs; (iii) the mechanism of resistance to sulfonamides and sulfones involves mutations of dihydropteroate synthase (DHPS), their enzyme target; (iv) treatment with sulphadoxine,pyrimethamine selects for DHFR variants Ile(51), Arg(59), and Asn(108) and for DHPS variants Ser(436), Gly(437), and Glu(540); (v) clones that were resistant to some traditional antimalarial agents acquire resistance to new ones at a high frequency (accelerated resistance to multiple drugs, ARMD). The mechanisms of resistance for amino-alcohols (quinine, mefloquine and halofantrine) are still unclear. Epidemiological studies have established that the frequency of chloroquine resistant mutants varies among isolated parasite populations, while resistance to antifolates is highly prevalent in most malarial endemic countries. Established and strong drug pressure combined with low antiparasitic immunity probably explains the multidrug-resistance encountered in the forests of South-east Asia and South America. In Africa, frequent genetic recombinations in Plasmodium originate from a high level of malaria transmission, and falciparum chloroquine-resistant prevalence seems to stabilize at the same level as chloroquine-sensitive malaria. Nevertheless, resistance levels may differ according to place and time. In vivo and in vitro tests do not provide an adequate accurate map of resistance. Biochemical tools at a low cost are urgently needed for prospective monitoring of resistance. [source] High Level of Antimicrobial Resistance in French Helicobacter pylori IsolatesHELICOBACTER, Issue 1 2010Josette Raymond Abstract Background: Helicobacter pylori is a human pathogen responsible for serious diseases including peptic ulcer disease and gastric cancer. The recommended triple therapy included clarithromycin but increasing resistance has undermined its effectiveness. It is therefore important to be aware of the local prevalence of antimicrobial resistance to adjust treatment strategy. Materials and Methods: Overall, 530 biopsies were collected between 2004 and 2007. The antimicrobial susceptibility of H. pylori was determined by E-test and molecular methods. Results: Among these, 138/530 (26%) strains were resistant to clarithromycin, 324/530 (61%) to metronidazole and 70/530 (13.2%) to ciprofloxacin. Whereas no resistance against amoxicillin and tetracycline was observed, only one strain was resistant to rifampicin. Compared to the patients never treated for H. pylori infection, the prevalence of resistance was significantly higher in patients previously treated (19.1% vs 68% for clarithromycin; 13.2% vs 53.3% for both clarithromycin and metronidazole). The trend analysis revealed an increase of primary resistance to ciprofloxacin between 2004 and 2005 (7.3%) vs 2006,2007 (14.1%) (p = .04) and the secondary resistance reached 22.7% in 2007. Interestingly, 27 biopsies (19.6%) contained a double population of clarithromycin-susceptible and -resistant strains. Conclusions: The reported high prevalence of clarithromycin and multiple resistances of H. pylori suggest that the empiric therapy with clarithromycin should be abandoned as no longer pretreatment susceptibility testing has assessed the susceptibility of the strain. As culture and antibiogram are not routinely performable in most clinical laboratories, the use of molecular test should be developed to allow a wide availability of pretreatment susceptibility testing. [source] Amoxicillin Resistance in Helicobacter pylori: Studies from Tokyo, Japan from 1985 to 2003HELICOBACTER, Issue 1 2005Kazuhiro Watanabe ABSTRACT Background., Previous reports revealed no resistant strains of amoxicillin (AMPC), which is usually used in eradication therapy for H. pylori infection. However, the frequency and evolution of natural AMPC-resistant strains in the Japanese population remains unknown. Aim., To assess the prevalence of H. pylori resistance against AMPC in the Tokyo area, a collection of 648 H. pylori strains isolated from patients with GI diseases from 1985 to 2003 was tested for their sensitivity to AMPC. Methods., The susceptibility of the strains was assessed by determination of the minimal inhibitory concentration (MIC) using the E -test and/or the Dry-plate method. The susceptibility breakpoints of AMPC for H. pylori were: sensitive (AMPC-S); MIC < 0.04 µg/ml, intermittent resistance (AMPC-I); 0.04,1, resistant (AMPC-R); > 1. Results., No AMPC-R strains were detected in the strains isolated between 1985 and 1996, while the rate of resistance was determined to be 1.1%, 2.1%, 5.4%, 5.6%, 0%, 8.8%, and 1.5% every year, respectively, from 1997 to 2003. The percentage of AMPC-I strains increased from 2000 to 2003. The total eradication rate of H. pylori in the patients who received triple therapy containing AMPC was 81.4% (214/263). Classified as above, the rates of AMPC-S, AMPC-I, and AMPC-R were 84.6%, 77.8%, 25%, respectively. Conclusion.,H. pylori resistance to AMPC is still rare in Japan, although the percentage of AMPC-I strains has increased over the last 4 years. The frequency of isolation of strains showing true resistance to AMPC may increase in the future, along with an increase in the frequency of isolation of AMPC-I strains. [source] | |||||||||||||||||||||||||||||||