Resistance to Trimethoprim and Other Antibiotics in Ontario Shigellæ

Bannatyne, Robert M.; Toma, S; Cheung, Rose; Hu, Gerard; Taylor, Denise; Keystone, J. S.; Devlin, Hannah

doi:10.1016/s0140-6736(80)90977-0

Cited by 18 publications

(5 citation statements)

References 6 publications

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“…In the 1970s and the early 1980s, TMP resistance occurred in only a minority of Shigella isolates (8,11,21,50,55,64,95,116,122). In 1983 and 1984, about 4 to 17% of the isolates were TMP or TMP-SUL resistant (21,50,64), in 1985 7 to 21% were resistant, and later, TMP resistance even increased to 52%, depending on the Shigella sp.…”

Section: Spread Of Tmp and Sul Resistancementioning

confidence: 99%

Trimethoprim and sulfonamide resistance

Huovinen¹,

Sundström²,

Swedberg³

et al. 1995

Antimicrob Agents Chemother

441

314

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Section: Spread Of Tmp and Sul Resistancementioning

confidence: 99%

Trimethoprim and sulfonamide resistance

Huovinen¹,

Sundström²,

Swedberg³

et al. 1995

Antimicrob Agents Chemother

441

314

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“…Similar incidences of the emergence of bacteria resistant to the combination, and to trimethoprim alone, have been reported during treatment of urinary tract infections (Huovinon and Toivanen, 1980;Pearson et. a\., 1979), while the emergence of Shigella strains which are resistant to trimethoprim-sulphamethoxazole may represent a significant clinical problem (Bannatyne et a\., 1980;Taylor et a\., 1980). Trimethoprim was selected for the combination because of its high broad spectrum of antibacterial activity (Roth et aI., 1962).…”

mentioning

confidence: 99%

Clinical Pharmacokinetics of Co-trimoxazole (trimethoprim-sulphamethoxazole)

Patel

Welling

1980

Clinical Pharmacokinetics

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The combillalioll trimethoprim-sulphametllOxazole (co-trimoxazole) is used c1illical(v for the treatmelll of a \'Oriety of illfectiolls due to Gram-positil'e alld Gram-llegatipe orgallisms; particular(I' for urillary alld respiratory tract il(fectiolls While both trimet/wprim alld sulphametlwxazole are mainly bacteriostatic when used alone. their combilled effect tellds to be bactericidal. SYllergism is due to sequelltial blockade at two separate steps ill bacterial folate metabolism. resultillg ill illhibitioll of deoxyribollllcleic acid sylllhesis.The optimum collcelltralioll ratio of trimetllOprim:sulphametllOxazole {i)r a bactericidal effect paries betwf:ell 1:5 alld I :40. which is collsistellt with their relatipe minimum inhibitory concellIration (MIC) palues against susceptible organisms. The combination is administered principal(I' by the oral route. although it is also giwlI parellleralb' and rectalb'. A single oral dose of 160mg trimetllOprim and 800mg sulphametllOxazole gives peak sertlm lel'els at approximately 411 of 1.2 to 2}Jg / ml trimetllOprim alld 26 to 63}Jg / ml sulpl1ametl1oxazole. After repeated 12 -I/Our(v doses. minimum sertlm /el'e/s are 1.3 to 2.8}Jg / ml and 32 to 63}Jg/ ml {i)r trinll;'tllOprim and slllphametllOxazole respectil'e(I'. The high con celli ration of slllphametllOxazole in serum re/atil'e to that of trimethoprim is dlle to the greater tisslle penetration of trimetllOprim. The high sulphametlwxazole:trimethoprim cOllcentration ratio in serum does Iwt always occur in extral'ascular tissues. However, this is partially compensated {i)r by tile higl1 bacteriostatic actil'ity of trimethoprim alone in tissues.The 2 compounds are bound to plasma proteins to similar extellIs. Both trimethoprim and sulphamethoxazole obey first order absorption. distributioll. alld elimination killetics. The disposition t!f sulphamethoxazole in the body after oral doses has been described ill .terms of onecompartment model kinetics, while both Olle-compartmelll and lII'o-compartment model kinetics hOl'e been IIsed to describe the disposition of trimetllOprim.Both compoullds are cleared from the body predominantly via the kidneys. slIlphametllOxazole being excreted mainly ill the acetylated {i)rm. Average elimillatioll half-lives of trimetllOprim and slIlphamethoxazole are II alld 9h respectively, althollgh there is considerable illdividual variatioll ill these I'ailles. The clearance of both compoullds is not marked(1' affected by declining rellal function until creatinille clearance falls be/ow 30ml/ min. /n severe renal failure, the elimination ha(f-/ives of both drugs may increase to 45 to 60h and adJustment of dosage is necessary to avoid renal toxicity. Both trimetlwprim alld sulphamet!Joxazole appear

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“…The first trimethoprim-resistant plasmid was described in England in 1972 [24]. Subsequently, plasmid-mediated trimethoprim resistance has become widely disseminated, according to reports from the UK [25], France, Italy [20], Finland, Canada and Bangladesh [26,27].…”

Section: Discussionmentioning

confidence: 99%

The distribution of the DHFR genes in trimethoprim-resistant urinary tract isolates from Taiwan

Chang¹,

Chang²,

Chow

et al. 1992

Epidemiol. Infect.

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Between July 1987 and June 1989, 1054 urinary isolates of enterobacteria from Kaohsiung, Taiwan were studied for their trimethoprim resistance. Trimethoprim resistance was defined as MIC greater than 4 micrograms/ml and high-level resistance by MIC greater than 1000 micrograms/ml. The incidence of trimethoprim resistance increased from 33.6% in 1987 to 42.1% in 1989. Among the resistant strains studied, 90% were resistant to high levels of trimethoprim. An increase in the proportion of resistant strains (33.9-46.3%) exhibiting high-level non-transferable trimethoprim resistance was noted. The distribution of the dihydrofolate reductase (DHFR) genes by colony hybridization in 374 trimethoprim-resistant isolates revealed the presence of type I and type V DHFR genes in most of these isolates (45.4% and 10.4% respectively). Type I was predominant in Escherichia coli whereas type V was frequently seen in Enterobacter spp. None showed homology with the type II and type III DHFR probe DNA. In addition, transposon Tn7 was present in 7.8% of 374 trimethoprim-resistant enterobacteria.

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Resistance to Trimethoprim and Other Antibiotics in Ontario Shigellæ

Cited by 18 publications

References 6 publications

Trimethoprim and sulfonamide resistance

Trimethoprim and sulfonamide resistance

Clinical Pharmacokinetics of Co-trimoxazole (trimethoprim-sulphamethoxazole)

The distribution of the DHFR genes in trimethoprim-resistant urinary tract isolates from Taiwan

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