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Edet E Udo - One of the best experts on this subject based on the ideXlab platform.
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Antibacterial resistance and their genetic location in MRSA isolated in Kuwait hospitals, 1994-2004
BMC Infectious Diseases, 2006Co-Authors: Edet E Udo, Noura Al-sweih, Eiman Mokaddas, Molly Johny, Rita Dhar, Huda H Gomaa, Inaam Al-obaid, Vincent O RotimiAbstract:Background Methicillin-resistant Staphylococcus aureus (MRSA) continues to be a major cause of serious infections in hospitals and in the community worldwide. In this study, MRSA isolated from patients in Kuwait hospitals were analyzed for resistance trends and the genetic location of their resistance determinants. Methods Between April 1994 and December 2004, 5644 MRSA isolates obtained from different clinical samples were studied for resistance to antibacterial agents according to guidelines from the National Committee for Clinical Laboratory Standards and the British Society for Antimicrobial Chemotherapy. The genetic location of their resistance determinants was determined by curing and transfer experiments. Results They were resistant to aminoglycosides, erythromycin, tetracycline, trimethoprim, fusidic acid, ciprofloxacin, chloramphenicol, rifampicin, mupirocin, cadmium acetate, mercuric chloride, Propamidine Isethionate and ethidium bromide but susceptible to vancomycin, teicoplanin and linezolid. The proportion of the isolates resistant to erythromycin, ciprofloxacin and fusidic acid increased during the study period. In contrast, the proportion of isolates resistant to gentamicin, tetracycline, chloramphenicol and trimethoprim declined. High-level mupirocin resistance increased rapidly from 1996 to 1999 and then declined. They contained plasmids of 1.9, 2.8, 3.0, 4.4, 27 and 38 kilobases. Genetic studies revealed that they carried plasmid-borne resistance to high-level mupirocin resistance (38 kb), chloramphenicol (2.8 – 4.4 kb), erythromycin (2.8–3.0 kb) and cadmium acetate, mercuric chloride, Propamidine Isethionate and ethidium bromide (27 kb) and chromosomal location for methicillin, the aminoglycosides, tetracycline, fusidic acid, ciprofloxacin and trimethoprim resistance. Thus, the 27 kb plasmids had resistance phenotypes similar to plasmids reported in MRSA isolates in South East Asia. Conclusion The prevalence of resistance to erythromycin, ciprofloxacin, high-level mupirocin and fusidic acid increased whereas the proportion of isolates resistant to gentamicin, tetracycline, chloramphenicol and trimethoprim declined during the study period. They contained 27-kb plasmids encoding resistance to cadmium acetate, mercuric chloride, Propamidine Isethionate and ethidium bromide similar to plasmids isolated in MRSA from South East Asia. Molecular typing of these isolates will clarify their relationship to MRSA from South East Asia.
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A chromosomal location of the mupA gene in Staphylococcus aureus expressing high-level mupirocin resistance
Journal of Antimicrobial Chemotherapy, 2003Co-Authors: Edet E Udo, Noura Al-sweih, B. C. NoronhaAbstract:OBJECTIVES To investigate the genetic location of the mupA gene in high-level mupirocin-resistant Staphylococcus aureus isolates. MATERIALS AND METHODS Antibiotic resistance was detected by disc diffusion. The Etest was used to determine mupirocin MIC. The presence of mupA was detected by PCR using specific primers. Curing, transfer experiments, pulsed-field gel electrophoresis (PFGE) and DNA hybridization were used to study the genetic location of mupA. RESULTS The isolates had mupirocin MICs > 1024 mg/L and were resistant to methicillin, gentamicin, kanamycin, streptomycin, erythromycin, tetracycline, ciprofloxacin, cadmium acetate, Propamidine Isethionate and ethidium bromide. They carried two plasmids of approximately 26 and 2.8 kb. Curing and transfer experiments demonstrated that the 26 kb plasmid encoded resistance to cadmium acetate, Propamidine Isethionate and ethidium bromide. Loss of mupirocin resistance corresponded to the loss of a 40 kb DNA fragment from a 175 kb SmaI chromosomal fragment. The mupA gene was detected only in the genomic DNA of the mupirocin-resistant strains and in their derivatives cured of the 26 kb plasmid. A labelled mupA probe hybridized to the 175 kb SmaI fragment only in the mupirocin-resistant isolates. CONCLUSION The absence of mupA on any of the plasmids and its detection only in the chromosomal DNA of the parents and in their derivatives cured of the 26 kb plasmid strongly supports a chromosomal location for mupA in these isolates.
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Genetic analysis of methicillin-resistant Staphylococcus aureus expressing high- and low-level mupirocin resistance.
Journal of Medical Microbiology, 2001Co-Authors: Edet E Udo, L. E. Jacob, Bindu MathewAbstract:Clinical strains of methicillin-resistant Staphylococcus aureus (MRSA) expressing high- and low-level mupirocin resistance were studied to determine the genetic location of mupirocin and other resistance determinants. Mupirocin resistance was confirmed by MIC determination with E-test strips. Curing and transfer experiments were used to establish the genetic location of the resistance determinants and the PCR with mupAp-specific primers was used to detect the presence of mupA genes. High-level mupirocin- resistant isolates had MICs >10245mumg/L, whereas the low-level resistant isolates had MICs of 32–1285mumg/L. The isolates carried plasmids ranging from 2.8 to 38 kb in size. All of them carried 26- and 3.0-kb plasmids, but only the high-level mupirocin-resistant isolates carried a 38-kb plasmid. Curing and transfer experiments revealed that the 26-kb plasmid encoded resistance to cadmium, mercuric chloride, Propamidine Isethionate and ethidium bromide and the 38-kb plasmid was a conjugative plasmid encoding high-level mupirocin resistance. One isolate, IBN287, carried both plasmid-borne high-level and chromosomal low-level mupirocin resistance. The mupA gene was detected on the 38-kb plasmid DNA but not in the genomic DNA of the low-level mupirocin-resistant isolates. The genomic DNA of strain IBN287 cured of the 38-kb mupirocin resistance plasmid did not contain mupA. The results suggest that different genes encoded low-and high-level mupirocin resistance in these isolates.
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Persistence of a clone of methicillin-resistant Staphylococcus aureus in a burns unit.
Journal of Medical Microbiology, 2001Co-Authors: A.m. Al-haddad, Edet E Udo, E.m. Mokadas, S.c. Sanyal, Warren B. GrubbAbstract:A total of 128 MRSA isolates from a burns unit in 1992 and 1997 was studied by resistotyping, plasmid analysis and pulsed-field gel electrophoresis (PFGE) of SmaI-digested chromosomal DNA to ascertain whether a clone of MRSA had persisted in the unit or whether different clones had been introduced at different times. All the MRSA isolates produced β-lactamase and had high MICs to methicillin (>2565mumg/L). All were resistant to tetracycline, kanamycin, cadmium acetate and mercuric chloride. Most were resistant to gentamicin, neomycin, erythromycin, chloramphenicol, trimethoprim, ciprofloxacin, Propamidine Isethionate and ethidium bromide, and were susceptible to minocycline, vancomycin and teicoplanin. None of the 1992 isolates was resistant to mupirocin, but 56% and 19% of the 1997 isolates expressed high- and low-level mupirocin resistance, respectively. Many of the 1997 isolates had acquired a 38-kb plasmid encoding high-level mupirocin resistance. The 1992 isolates had two main PFGE patterns; 82% of them belonged to PFGE pattern 1. The 1997 isolates had PFGE pattern 1, the same as the majority of the 1992 isolates. All MRSA isolates from both years carried the mecA gene in the same SmaI fragment. These findings demonstrated that a clone of MRSA that was prevalent in the burns unit in 1992 had persisted and became the predominant clone in 1997.
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Characterisation of methicillin-resistant Staphylococcus aureus from Kuwait hospitals with high-level fusidic acid resistance.
Journal of Medical Microbiology, 2000Co-Authors: Edet E Udo, L. E. JacobAbstract:Forty-seven fusidic acid- and methicillin-resistant Staphylococcus aureus isolates from clinical samples in four hospitals in Kuwait were studied for their relatedness by biotyping and pulsed-field gel electrophoresis (PFGE) and for the genetic location of their resistance determinants. Forty-four isolates were resistant to gentamicin, kanamycin and neomycin. Forty-one isolates were resistant to erythromycin and trimethoprim, 10 were resistant to chloramphenicol and four were resistant to ciprofloxacin. They contained two or three plasmids of c. 28, 2.8 and 1.8 kb. Genetic studies demonstrated that resistance to cadmium, Propamidine Isethionate and ethidium bromide were linked and were carried on the c. 28-kb plasmid. Chloramphenicol resistance was encoded by the 2.8-kb plasmid in resistant isolates. No resistance was associated with the 1.8-kb plasmid and this was considered to be a cryptic plasmid. Resistance to fusidic acid, methicillin, benzylpenicillin, gentamicin, kanamycin, neomycin, tetracycline, trimethoprim, erythromycin and ciprofloxacin were located on the chromosome. All the isolates produced urease, but varied in the production of haemolysins, pigments, lipase and lecithinase and were classified into nine biotypes. In contrast, PFGE divided the isolates into two major patterns with one PFGE type constituting the majority of isolates in all four hospitals. The presence of the dominant PFGE pattern in all four hospitals suggests that it is an epidemic MRSA clone with the capacity to spread. Infection control measures should be directed towards restricting the further spread of this clone.
Dorothy K.l. Xing - One of the best experts on this subject based on the ideXlab platform.
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investigation of synergism with combinations of dibromoPropamidine Isethionate or Propamidine Isethionate and polymyxin b
Journal of Pharmacy and Pharmacology, 1994Co-Authors: Michael R E Richards, Dorothy K.l. XingAbstract:— Combinations of polymyxin B and dibromoPropamidine Isethionate exhibited synergistic inhibitory and bactericidal activity against Pseudomonas aeruginosa, Enterobacter cloacae, Proteus mirabilis, Escherichia coli and Staphylococcus aureus. Similar results were obtained with polymyxin B plus Propamidine combinations except that Propamidine was not as active as dibromoPropamidine and the combination of polymyxin B plus Propamidine against S. aureus only had additive activity. The antibacterial agents were tested in solutions and in a cream formulation. The findings indicate a potential for the use of selected combinations of these antibacterial agents in the treatment of wound and superficial eye infections.
Michael R E Richards - One of the best experts on this subject based on the ideXlab platform.
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investigation of synergism with combinations of dibromoPropamidine Isethionate or Propamidine Isethionate and polymyxin b
Journal of Pharmacy and Pharmacology, 1994Co-Authors: Michael R E Richards, Dorothy K.l. XingAbstract:— Combinations of polymyxin B and dibromoPropamidine Isethionate exhibited synergistic inhibitory and bactericidal activity against Pseudomonas aeruginosa, Enterobacter cloacae, Proteus mirabilis, Escherichia coli and Staphylococcus aureus. Similar results were obtained with polymyxin B plus Propamidine combinations except that Propamidine was not as active as dibromoPropamidine and the combination of polymyxin B plus Propamidine against S. aureus only had additive activity. The antibacterial agents were tested in solutions and in a cream formulation. The findings indicate a potential for the use of selected combinations of these antibacterial agents in the treatment of wound and superficial eye infections.
Peter J Mcdonnell - One of the best experts on this subject based on the ideXlab platform.
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assessing efficacy of combined riboflavin and uv a light 365 nm treatment of acanthamoeba trophozoites
Investigative Ophthalmology & Visual Science, 2011Co-Authors: Renata T Kashiwabuchi, Fabio Ramos De Souza Carvalho, Yasin A Khan, Denise De Freitas, Annette Silva Foronda, Flavio E Hirai, Mauro Campos, Peter J McdonnellAbstract:PURPOSE: To assess the Acanthamoeba trophozoite viability in vitro and treatment of Acanthamoeba keratitis in a hamster model using ultraviolet light A (UV-A) and riboflavin (B2). METHODS: A sample of Acanthamoeba sp. cultured was transferred to a 96-well plate and exposed to B2 and the UV-A light (365 nm wavelength) at a power density of 3 mW/cm(2), 8 mm spot diameter, for 30 minutes. The exposure was done in triplicate. Control groups were prepared in triplicate as well: blank control, UV-A only, riboflavin only, and dead control. Cell viability assessment was done using the trypan blue dye exclusion method. Acanthamoeba keratitis was induced in Chinese hamsters; who were randomly assigned to one of the animal groups: UV-A + B2, Propamidine Isethionate (Brolene; Sanofi-Aventis, Ellerslie, Auckland, Australia), UV-A + B2 + Propamidine Isethionate (Brolene), only UV-A, only B2, and blank. Throughout the 14 days after treatment the animals were examined clinically. Histology and clinical scores of all groups were compared. RESULTS: The in vitro study showed no difference between the treatment group UV-A + B2 and the control groups. In the hamster keratitis model a significant improvement of clinical score was observed for the groups Propamidine Isethionate (Brolene) and UV-A + B2 + Propamidine Isethionate (Brolene) (P = 0.0067). Also a significant worsening of clinical score was observed in the other groups: UV-A + B2 group (P = 0.0084), only UV-A (P = 0.0078), B2 only (P = 0.0084), and blank (P = 0.0082). No difference was observed between Propamidine Isethionate (Brolene) and UV-A + B2 + Propamidine Isethionate (Brolene). CONCLUSIONS: The adjunctive use of UV-A and B2 therapy did not demonstrate antitrophozoite activity; in vivo UV-A and B2 did not demonstrate efficacy in this model.
Annette Silva Foronda - One of the best experts on this subject based on the ideXlab platform.
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assessing efficacy of combined riboflavin and uv a light 365 nm treatment of acanthamoeba trophozoites
Investigative Ophthalmology & Visual Science, 2011Co-Authors: Renata T Kashiwabuchi, Fabio Ramos De Souza Carvalho, Yasin A Khan, Denise De Freitas, Annette Silva Foronda, Flavio E Hirai, Mauro Campos, Peter J McdonnellAbstract:PURPOSE: To assess the Acanthamoeba trophozoite viability in vitro and treatment of Acanthamoeba keratitis in a hamster model using ultraviolet light A (UV-A) and riboflavin (B2). METHODS: A sample of Acanthamoeba sp. cultured was transferred to a 96-well plate and exposed to B2 and the UV-A light (365 nm wavelength) at a power density of 3 mW/cm(2), 8 mm spot diameter, for 30 minutes. The exposure was done in triplicate. Control groups were prepared in triplicate as well: blank control, UV-A only, riboflavin only, and dead control. Cell viability assessment was done using the trypan blue dye exclusion method. Acanthamoeba keratitis was induced in Chinese hamsters; who were randomly assigned to one of the animal groups: UV-A + B2, Propamidine Isethionate (Brolene; Sanofi-Aventis, Ellerslie, Auckland, Australia), UV-A + B2 + Propamidine Isethionate (Brolene), only UV-A, only B2, and blank. Throughout the 14 days after treatment the animals were examined clinically. Histology and clinical scores of all groups were compared. RESULTS: The in vitro study showed no difference between the treatment group UV-A + B2 and the control groups. In the hamster keratitis model a significant improvement of clinical score was observed for the groups Propamidine Isethionate (Brolene) and UV-A + B2 + Propamidine Isethionate (Brolene) (P = 0.0067). Also a significant worsening of clinical score was observed in the other groups: UV-A + B2 group (P = 0.0084), only UV-A (P = 0.0078), B2 only (P = 0.0084), and blank (P = 0.0082). No difference was observed between Propamidine Isethionate (Brolene) and UV-A + B2 + Propamidine Isethionate (Brolene). CONCLUSIONS: The adjunctive use of UV-A and B2 therapy did not demonstrate antitrophozoite activity; in vivo UV-A and B2 did not demonstrate efficacy in this model.
