Faculty Opinions recommendation of Origin of the Mobile Di-Hydro-Pteroate Synthase Gene Determining Sulfonamide Resistance in Clinical Isolates.

2019 ◽  
Author(s):  
Didier Mazel
Keyword(s):  
Clinical Isolates ◽  
Sulfonamide Resistance

scholarly journals Novel Expansions of the Gene Encoding Dihydropteroate Synthase in Trimethoprim-Sulfamethoxazole-ResistantStreptococcus pneumoniae

1999 ◽  
Vol 43 (9) ◽  
pp. 2225-2230 ◽  
Author(s):  
Thanugarani Padayachee ◽  
Keith P. Klugman
Keyword(s):  
South African ◽  
Specific Region ◽  
Site Directed Mutagenesis ◽  
Clinical Isolates ◽  
Wild Type ◽  
Gene Encoding ◽  
Dihydropteroate Synthase ◽  
Sulfonamide Resistance ◽  
Resistant Strains ◽  
Chromosomal Mutations

ABSTRACT A study of eight sulfonamide-resistant clinical isolates ofStreptococcus pneumoniae revealed chromosomal mutations within the gene encoding dihydropteroate synthase that play a role in conferring resistance to sulfamethoxazole. The presence of thesuld mutation, found previously only in a laboratory mutant, was shown to occur in three of the wild-type clinical isolates. The duplication of Ser61, the other previously defined mutation in the dihydropteroate synthase gene of S. pneumoniae, was observed in only one of the isolates characterized. We report two previously unidentified amino acid alterations, namely, a duplication of Arg58 and Pro59 and an insertion of an arginine residue between Gly60 and Ser61 in trimethoprim-sulfamethoxazole-resistant strains. The significance of these mutations was confirmed by site-directed mutagenesis and by the transformation of a susceptible strain of S. pneumoniae to sulfamethoxazole resistance. Two resistant isolates did not contain any mutations within the gene encoding dihydropteroate synthase. The results presented suggest the independent generation of resistant mutations among South African clinical isolates. It is also proposed that the mechanism of sulfonamide resistance in S. pneumoniae involves the expansion of a specific region within dihydropteroate synthase, which probably forms part of the sulfonamide binding site.

scholarly journals Amino Acid Repetitions in the Dihydropteroate Synthase of Streptococcus pneumoniae Lead to Sulfonamide Resistance with Limited Effects on SubstrateKm

2001 ◽  
Vol 45 (3) ◽  
pp. 805-809 ◽  
Author(s):  
Ylva Haasum ◽  
Katrin Ström ◽  
Rahma Wehelie ◽  
Vicki Luna ◽  
Marilyn C. Roberts ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Washington State ◽  
Site Directed Mutagenesis ◽  
Clinical Isolates ◽  
Directed Mutagenesis ◽  
Aminobenzoic Acid ◽  
Kinetic Measurements ◽  
Dihydropteroate Synthase ◽  
Gene Coding ◽  
Sulfonamide Resistance

ABSTRACT Sulfonamide resistance in Streptococcus pneumoniae is due to changes in the chromosomal folP (sulA) gene coding for dihydropteroate synthase (DHPS). The first reported laboratory-selected sulfonamide-resistant S. pneumoniaeisolate had a 6-bp repetition, the sul-d mutation, leading to a repetition of the amino acids Ile66 and Glu67 in the gene product DHPS. More recently, clinical isolates showing this and other repetitions have been reported. WA-5, a clinical isolate from Washington State, contains a 6-bp repetition in the folP gene, identical to the sul-d mutation. The repetition was deleted by site-directed mutagenesis. Enzyme kinetic measurements showed that the deletion was associated with a 35-fold difference in Ki for sulfathiazole but changed the Km for p-aminobenzoic acid only 2.5-fold and did not significantly change theKm for 2-amino-4-hydroxy-6-hydroxymethyl-7,8-dihydropteridine pyrophosphate. The enzyme characteristics of the deletion variant were identical to those of DHPS from a sulfonamide-susceptible strain. DHPS from clinical isolates with repetitions of Ser61 had very similar enzyme characteristics to the DHPS from WA-5. The results confirm that the repetitions are sufficient for development of a resistant enzyme and suggest that the fitness cost to the organism of developing resistance may be very low.

Mechanism of Sulfonamide Resistance in Clinical Isolates of Streptococcus pneumoniae

2000 ◽  
Vol 44 (5) ◽  
pp. 1411-1411 ◽  
Author(s):  
Jeffrey P. Maskell ◽  
Armine M. Sefton ◽  
Lucinda M. C. Hall
Keyword(s):  
Streptococcus Pneumoniae ◽  
Clinical Isolates ◽  
Sulfonamide Resistance

Mechanism of sulfonamide resistance in clinical isolates of Streptococcus pneumoniae.

1997 ◽  
Vol 41 (10) ◽  
pp. 2121-2126 ◽  
Author(s):  
J P Maskell ◽  
A M Sefton ◽  
L M Hall
Keyword(s):  
Streptococcus Pneumoniae ◽  
Genetic Basis ◽  
Laboratory Strain ◽  
Clinical Isolates ◽  
Gene Exchange ◽  
Gene Encoding ◽  
Dihydropteroate Synthase ◽  
Loss Of Resistance ◽  
Sulfonamide Resistance

The genetic basis of sulfonamide resistance in six clinical isolates of Streptococcus pneumoniae was demonstrated to be 3- or 6-bp duplications within sulA, the chromosomal gene encoding dihydropteroate synthase. The duplications all result in repetition of one or two amino acids in the region from Arg58 to Tyr63, close to but distinct from the sul-d mutation, a duplication previously reported in a resistant laboratory strain (P. Lopez, M. Espinosa, B. Greenberg, and S. A. Lacks, J. Bacteriol. 169:4320-4326, 1987). Six sulfonamide-susceptible clinical isolates lacked such duplications. The role of the duplications in conferring sulfonamide resistance was confirmed by transforming 319- or 322-bp PCR fragments into the chromosome of a susceptible recipient. Two members of a clone of serotype 9V, one susceptible and one resistant to sulfonamide, which are highly related by other criteria, were shown to have sulA sequences that differ in 7.2% of nucleotides in addition to the duplication responsible for resistance. It is postulated that horizontal gene exchange has been involved in the acquisition (or loss) of resistance within this clone. However, five of the six resistant isolates have distinct duplications and other sequence polymorphisms, suggesting that resistance has arisen independently on many occasions.

Antimicrobial Resistance of Salmonella in Raw Retail Chickens, Imported Chicken Portions, and Human Clinical Specimens

2004 ◽  
Vol 67 (6) ◽  
pp. 1220-1225 ◽  
Author(s):  
I. G. WILSON
Keyword(s):  
Saint Paul ◽  
Clinical Isolates ◽  
Chicken Breast ◽  
Multiple Resistance ◽  
Routine Examination ◽  
Clinical Specimens ◽  
Sulfonamide Resistance ◽  
Resistance Patterns ◽  
Salmonella Virchow ◽  
Resistance Rates

Salmonella isolates from raw, chilled, retail chickens (n = 434) sampled between 1998 and 2000 were tested for resistance to 12 antibiotics. Of 23 salmonellas isolated, 30% were susceptible and 30% were resistant or intermediately resistant to one antibiotic, 26% to two, and 13% to four or more. One Salmonella Saint-Paul and two Salmonella Typhimurium isolates were resistant to more than four antibiotics. Highest resistance rates were sulfonamide (52%), streptomycin (26%), tetracycline (22%), and ampicillin (17%). Isolates (n = 27) from frozen chicken portions (n = 150) imported from Brazil and Thailand (generally for manufacturing and catering) were also tested. Brazilian salmonellas showed no multiple resistance, but an isolate of Salmonella Virchow from Thai chickens was resistant to two antibiotics. This compared with 39% resistance to two or more antibiotics in nonimported isolates. Resistance patterns of both sets of chicken isolates were compared with human fecal clinical isolates (n = 274) submitted for routine examination at this hospital, and a greater similarity was found between the clinical and local isolates than with imported salmonellas. Sulfonamide resistance in imported salmonellas was lower than that of nonimported and clinical isolates. Resistance to one or more antimicrobial was found in 70% of nonimported raw retail chickens, 52% of imported chicken breast fillets, and 84% of human fecal isolates. Multiple resistance (to four or more antibiotics) is a much more limited problem.

Molecular Characterisation of ESBL producer E. coli

2018 ◽  
Vol 1 (2) ◽  
pp. 40-57
Author(s):  
Abdulghani Alsamarai ◽  
Shler Khorshed ◽  
Imad Weli
Keyword(s):  
Urinary Tract Infection ◽  
Urinary Tract ◽  
Tract Infection ◽  
Female Student ◽  
Clinical Problem ◽  
Clinical Isolates ◽  
Molecular Characterisation ◽  
M Gene ◽  
Esbl Producer ◽  
E Coli

Background: Antibiotic resistance emerged as clinical problem challenge the effective treatment of infections. Virulence factor may play an important role in the influence of antimicrobial resistance. Objective: To determine the frequency of resistance gene in E. coli clinical isolates from women with urinary tract infection. Materials and Methods: Fifteen E.coli clinical isolates were tested by PCR to determine their molecular characterization. Results: The bla CTX –M gene was not detected in 6.7% out of the tested 15 E. coli clinical isolates from women with urinary tract infection. However, bla OXA gene was detected in all E. coli tested clinical isolates from pregnant women, female student and diabetic women with urinary tract infection. While bla TEM gene and bla SHV gene were not detected in 33.3% and 40% out of the tested E. coli clinical isolates respectively. Conclusions: Four types of ESBL genes were detected, and shows new trend of distribution, which indicated the predominance of OXA and CTX-M genes.

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