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1.
Thirty-seven fluoroquinolone-resistant Escherichia coli strains from ruminants (according to Clinical and Laboratory Standards Institute guidelines) were screened by molecular methods for mutations in the quinolone resistance-determining region (QRDR) of the gyrA and parC genes and for the presence of the qnrA gene. One of the strains studied was an enterohemorrhagic E. coli (EHEC) strain potentially pathogenic for humans. Three E. coli strains resistant to enrofloxacin (minimal inhibitory concentration [MIC] = 2 microg/ml) but not to ciprofloxacin (MIC = 1 microg/ml) presented single mutations in the gyrA and parC genes, while 34 strains resistant to both fluoroquinolones presented double and single mutations in gyrA and parC, respectively (31 strains), or double mutations in gyrA and parC (3 strains). The EHEC strain presented a double amino acid substitution in the GyrA protein (Ser-83-->Leu and Asp-87-->Gly) and a double amino acid substitution in the ParC protein (Gly-78-->Cys and Ser-80-->Arg), one of which has not been previously described. The present study shows that most of the mutations in the QRDR of the gyrA and parC genes of fluoroquinolone-resistant E. coli strains from ruminants are the same as those seen in E. coli strains from other animal species and humans and that there are no differences in mutation patterns in the QRDR of E. coli strains from healthy ruminants and those with diarrhea. No strains carried qnrA, which indicates that this gene does not play an important role in the selection of fluoroquinolone-resistant E. coli strains from ruminants.  相似文献   

2.
鸡大肠杆菌O78对喹诺酮类药物高耐药株的分子鉴定   总被引：1，自引：0，他引：1  
就临床分离的鸡大肠杆菌O78对喹诺酮类药物的最低抑菌浓度（MIC）进行了测定，得到对喹诺酮类药物有不同耐药水平的细菌23株。根据GenBank已公布的QRDRs序列，设计了分剐扩增gyrA、gyrB、parC和parE基因的4对引物，以筛选的23株耐药菌DNA为模板，进行了PCR扩增。序列分析及AcrA的Western blotting检测结果表明，临床分离的鸡大肠杆菌对喹诺酮类药物的耐药水平与GyrA和ParC的突变密切相关，而AcrAB外输泵的表达水平无显著变化。提示临床分离的鸡大肠杆菌O78的耐药水平与喹诺酮类药物的选择性压力有关，它诱导了DNA旋转酶和拓扑异构酶IV的基因突变，可能不能激活AcrAB外输泵。  相似文献   

3.
The aim of this study were to detect the gyrA, parC and marR mutations and qnr genes (qnrA, qnrB and qnrS) in 120 strains of Escherichia coli isolated from animals. European Committee on Antimicrobial Susceptibility Testing and Clinical Laboratory Standards Institute disc diffusion and minimum inhibitory concentration (MIC) tests, respectively, were used to determine fluoroquinolone (FQ) resistance, and molecular methods were used to detect the mutations and the genes. E coli isolates with an MIC of ≥8 mg/l had mutation at Ser-80 in parC in addition to mutations at Ser-83, Asp-87 or both in gyrA. The nucleotide change was detected in marR (Ser-3?→?Asn, Ala-53?→?Glu, Gly-103?→?Ser, Tyr-137?→?His). Only four E coli isolates (3.3 per cent) contained qnrA and qnrS, and qnrB was not detected. Two E coli isolates from healthy calves also contained qnrA and qnrS. The MICs of enrofloxacin and danofloxacin for qnr-containing E coli isolates ranged from 32 mg/l to 256 mg/l. The results of this study indicated that the FQ-resistant E coli isolates presented an alteration in gyrA (Ser-83?→?Leu, Asp-87?→?Asn) and parC (Ser-80?→?Ile) with high MICs (8-256 mg/l), and there was a low prevalence of qnr genes among E coli isolated from animals.  相似文献   

4.
Quinolone-resistant (QR) mutants of Mycoplasma bovirhinis strain PG43 (type strain) were generated by stepwise selection in increasing concentrations of enrofloxacin (ENR). An alteration was found in the quinolone resistance-determining region (QRDR) of the parC gene coding for the ParC subunit of topoisomerase IV from these mutants, but not in the gyrA, gyrB, and parE gene coding for the GyrA and GyrB subunits of DNA gyrase and the ParE subunit of topoisomerase IV. Similarly, such an alteration in QRDR of parC was found in the field isolates of M. bovirhinis, which possessed various levels of QR. The substitution of leucine (Leu) by serine (Ser) at position 80 of QRDR of ParC was observed in both QR-mutants and QR-isolates. This is the first report of QR based on a point mutation of the parC gene in M. bovirhinis.  相似文献   

5.
Nine quinolone resistant (minimal inhibitory concentration [MIC] was > 32 microg/mL for nalidixic acid, > 1 microg/mL for ciprofloxacin) isolates of Escherichia coli have been found in wild birds with septicemia. All of the isolates were aerobactin positive. The mechanisms of resistance were characterised by sequencing the quinolone resistance-determining region (QRDR) of the gyrA, gyrB, parC, and parE genes. Sequence analysis of the gyrA gene in all isolates identified only 1 nucleotide substitution at codon Serine-83 for Leucine-83. Sequence analysis of the gyrB, parC, and parE QRDR genes revealed no mutations in any of the isolates. This study was conducted to determine the importance of these genes in the susceptibility of E. coli strains isolated from wild birds to quinolones.  相似文献   

6.
The aim of this study was to determine antimicrobial resistance of Aeromonas hydrophila isolated from farmed Nile Tilapia. A total of 50 A. hydrophila isolates from clinical cases were screened for the presence of class 1, 2 and 3 integrons and all the strains resistant to enrofloxacin and/or ciprofloxacin (n=19) examined for mutation in the quinolone resistance-determining regions (QRDRs) of gyrA and parC. The intI1 gene was detected in 23 A. hydrophila strains (46%) but no intl2 and intl3 were detected. Among these, 14 isolates (60.8%) carried gene cassettes inserted in variable regions i.e., partial aadA2, aadA2, dfrA1-orfC and dfrA12-aadA2, of which the most common gene cassette array was dfrA12-aadA2 (26.09%). Conjugal transfer of class 1 integrons with resistance gene array was detected. All the A. hydrophila strains resistant to enrofloxacin and/or ciprofloxacin possessed mutations in the QRDRs of gyrA and parC. Only a Ser-83-Ile substitution was identified in GyrA and only a Ser-80-Ile amino change was found in ParC. The data confirms that A. hydrophila from farm-raised Nile Telapia serve as a reservoir for antimicrobial resistance determinants.  相似文献   

7.
The antibacterial activity, selection of Escherichia coli (E. coli) mutants and mechanisms of fluoroquinolone resistance were investigated by integrating the minimum inhibitory concentration (MIC), mutant prevention concentration (MPC) and in vitro dynamic model approaches. Difloxacin and orbifloxacin, for which the above information has been scarce, were used. A range of area under curve over a 24h interval (AUC(24h))/MIC ratios and selected E. coli strains were investigated using the dynamic models. Continuous incubation for three days in the presence of difloxacin or orbifloxacin resulted in losses in E. coli susceptibility. An AUC(24h)/MIC (AUC(24h)/MPC)-dependent fluoroquinolone activity and selection of E. coli mutants was confirmed. Maximum losses in susceptibility occurred at AUC(24h)/MIC ratios of 54 (orbifloxacin) and 57.3 (difloxacin). AUC(24h)/MIC ratios of 169.8 (orbifloxacin) and 199.5 (difloxacin) were estimated to be protective against the selection of E. coli mutants, and the corresponding ratios based on AUC(24h)/MPC predictions were 34 (orbifloxacin) and 36.3 (difloxacin). When integrating our in vitro data with pharmacokinetic data in dogs, the conventional clinical doses of both drugs were found to be inadequate to attain the above protective values for 90% of the mutant subpopulation (AUC(24h)/MPC(90)). Both target mutations, esp. at codon 83 (Ser to Leu) of gyrA, and overexpression of efflux pumps contributed to resistance development, with mutants also showing decreased susceptibility to enrofloxacin and marbofloxacin. Additional studies would determine the role of mutations found outside the QRDR, at codon 24 of gyrA, and at codon 116 of parC, and establish the significance of these observations in vivo.  相似文献   

8.
The prevalence of qnr genes was investigated in veterinary clinical isolates of Escherichia coli in Guangdong province, China, and the aac (6')-Ib gene and the mutations in QRDRs of gyrase and topoisomerase IV were examined in qnr-positive strains. A total of 232 E. coli strains isolated from pig and poultry were screened for the presence of the qnrA, qnrB and qnrS genes by PCR and sequencing. The aac (6')-Ib gene was detected in qnr-bearing strains by PCR and sequencing. For all strains carrying qnr, MICs for six quinolones were determined. Mutations within the gyrase and topoisomerase were analyzed by PCR and sequencing for all the QRDRs of gyrA, gyrB, parC and parE. Among 232 E. coli isolates, 14 (6%) isolates were positive for the qnr gene, including one for qnrB, 13 for qnrS, but no qnrA was identified in this population. Detection of the aac (6')-Ib gene showed that one qnrS-positive isolate from pig and one qnrB-positive isolate from duck carried aac (6')-Ib gene, and both were the cr variant allele of aac (6')-Ib. All of the 14 isolates had MICs of ciprofloxacin more than 0.25 mg/L. Mutations in the QRDR of gyrA mutations were observed in 5 (35.7%) of the 14 strains. Three fluoroquinolone-resisting strains showed one mutation S83L of gyrA, while one S83I. One high-level resistance strains harboured gyrA S83L and A87N of gyrA. A singe mutation in site 58 of parC was detected in 3 (21.4%) strains. None mutations were found in QRDRs of gyrB and parE. The emergence of qnr genes in veterinary clinical E. coli isolates is described for the first time. This is also the first report of aac (6')-Ib-cr gene in E. coli isolates from food-producing animals.  相似文献   

9.
沙门氏菌耐药株gyrA基因和parC基因突变特征分析   总被引：3，自引：0，他引：3  
提取沙门氏菌染色体DNA，设计引物扩增gyrA基因和parC基因片段，克隆测序寻找耐药菌株的突变位点，通过系统的比较，分析氟喹诺酮类药物（以环丙沙星为代表）对各沙门氏菌MIC和耐药突变位点之间的关系。通过对耐药突变位点的研究，可以为下一步研究耐药性监测的快速方法提供理论基础。  相似文献   

10.
通过药敏实验检测了鸡鲍氏、人鲍氏和人福氏三株志贺菌对12种常用抗生素的耐药情况,发现三者均未产生对喹诺酮类药物的耐药性。用聚合酶链反应(PCR)分别扩增三株志贺菌的DNA旋转酶A亚单位(gyrA)和拓扑异构酶ⅣC亚单位(parC)基因,并对其中的耐喹诺酮类决定区(QRDR)进行了分析。发现鸡和人鲍氏志贺菌QRDR区的序列没有发生任何碱基突变,这与药敏试验结果相吻合。人福氏志贺菌虽然也对喹诺酮类无耐药性,但其gyrA基因存在83位Ser83(TCG)→Leu(TTG)的突变,由于只有83位点一处突变,所以尚未表现出耐药性表征,parC基因中存在58位Ser58(AGC)→Ile(ATC)的突变,该突变点与常见的80、84位氯基酸的改变有所不同,却仍在QRDR区域之中,虽然暂时还无法根据这一结果判断该突变与喹诺酮类耐药性之间的关系,但至少表明该菌株正处在耐药性演变进程之中,其在志贺菌耐药性中的确切作用还有待进一步研究。  相似文献   

11.
The minimum inhibitory concentrations (MICs) of oxytetracycline, cephapirin, cephapirin/mecillinam, cefquinome, ceftiofur and enrofloxacin, candidate antibiotics for the principal bacteria associated with uterine infections: Escherichia coli, Arcanobacterium pyogenes and the anaerobic bacteria Fusobacterium necrophorum and Prevotella melaninogenicus, were determined by the agar dilution method. The bacteria were isolated from animals with clinical metritis and/or endometritis. For E coli, cefquinome and enrofloxacin had the lowest MIC90 and MIC50 values (< 0.06 microg/ml), and oxytetracycline and cephapirin had the highest values. For A pyogenes, oxytetracycline had the highest MIC50 value (16 microg/ml), but all the cephalosporins had values below 0.06 microg/ml. For the anaerobic bacteria, enrofloxacin and oxytetracycline had the highest MIC50 values but all the cephalosporins had values of 0.06 microg/ml or below.  相似文献   

12.
旨在了解猪链球菌对氟喹诺酮类药物耐药性与parC、gyrA基因突变的相关性,通过微量稀释法测定34株猪链球菌对4种氟喹诺酮类药物的MIC值,采用PCR方法扩增并测序分析了临床分离的猪链球菌对氟唪诺酮类约物10株耐药株和9株敏感株的parC和gyrA基因喹诺酮耐药决定区(QRDRs).在氟喹诺酮类药物耐药菌株parC基因QRDRs发生Ser79→Phe、Arg 87→Leu的氨基酸突变,在4株高度耐药菌株gyrA基因QRDRs发生Arg66→Ser,Ser81→Arg氨基酸突变;当菌株对氟喹诺酮类药物敏感时,parC和gyrA基因的QRDR区均未有突变;而当MIC≥32 μg·L-1 时,parC的氨基酸发生了 Ser79→Phe的突变,同时发生gyrA氨基酸Arg66→Ser,Set81→Arg突变.结果表明,猪链球菌对氟喹诺酮类药物低水平类耐药是由parC单一位点突变引起,而高水平耐药是由parC和gyrA双位点突变引起.  相似文献   

13.
Minimum inhibition concentrations (MICs) were determined for ampicillin, ceftiofur, cephalothin, chloramphenicol, enrofloxacin, gentamicin, lincomycin, lincospectin (lincomycin/spectinomycin), neomycin, premafloxacin, spectinomycin, sulfamethoxazole/trimethoprim, and tetracycline against a total of 180 isolates of Actinobacillus pleuropneumoniae, Escherichia coli, and Salmonella choleraesuis (60 each) clinically isolated from pigs on farms in Taiwan from 1994 to 1996. No more than 3 isolates per farm were used. Ceftiofur had the highest activity in vitro against isolates of A. pleuropneumoniae, E. coli, and S. choleraesuis, with MIC90 values of 0.03, 2, and 1 microg/ml, respectively. Premafloxacin was highly active against isolates of A. pleuropneumoniae, E. coli, and S. choleraesuis, with MIC90 values of 2, 8, and 0.5 microg/ml, respectively, which were lower than those with enrofloxacin (MIC90 8, 32, and 2 microg/ml, respectively). Neomycin was moderately active against A. pleuropneumoniae and E. coli, with MIC90 values of 8 and 64 microg/ml, respectively, but was inactive with S. choleraesuis. Gentamicin showed high activity against A. pleuropneumoniae (MIC90 of 2 microg/ml) but was only moderately active with E. coli and S. choleraesuis (MIC90 of 64 and 32 microg/ml). Cephalothin was highly active against isolates of A. pleuropneumoniae (MIC90 of 1 microg/ml) but was inactive with E. coli (MIC90 of 128 microg/ml). Lincomycin had moderate activity (MIC90 of 32 microg/ml) against A. pleuropneumoniae. Chloramphenicol, lincomycin, and tetracycline were inactive with E. coli and S. choleraesuis (MIC90 > 128 microg/ml). In conclusion, ceftiofur and premafloxacin were highly active against isolates of A. pleuropneumoniae, E. coli, and S. choleraesuis, enrofloxacin and gentamicin were highly to moderately active; cephalothin was highly active against A. pleuropneumoniae and moderately active against S. cholearesuis; chloramphenicol, lincomycin, and tetracycline were active only with A. pleuropneumoniae; neomycin was moderately active against A. pleuropneumoniae and E. coli. The other antimicrobials tested were inactive.  相似文献   

14.
Niwa H  Hobo S  Anzai T 《Veterinary microbiology》2006,115(1-3):264-268
In this study, the quinolone resistance-determining region (QRDR) in gyrA and gyrB of in vitro fluoroquinolone-resistant Rhodococcus equi mutants was sequenced. These mutants were selected from four R. equi strains on blood agar plates containing ciprofloxacin or enrofloxacin. Each mutant became 8- to 64 or greater-fold resistant to fluoroquinolones compared with their parent strains. From the results of sequence analysis of QRDR in gyrA and gyrB, a nucleotide mutation of codon GAC for GGC in gyrA was detected in all mutants, but no mutation was observed in gyrB. This mutation leads to amino acid substitution of Asp for Gly in putative GyrA in R. equi. The position of this substitution corresponds to position 87 of GyrA in Escherichia coli. Our results suggest that the mutation of QRDR in gyrA, which was observed in in vitro fluoroquinolone-resistant R. equi mutants in this study, is closely associated with fluoroquinolone resistance.  相似文献   

15.
The mutant prevention concentration (MPC) is a new concept meant to face the increased prevalence of antibiotic resistance by using antibiotic concentrations able to prevent the selection of single-step resistant mutants. In the present study, the MPCs of ciprofloxacin and enrofloxacin were evaluated against fully susceptible strains of Escherichia coli, Salmonella Typhimurium and Pseudomonas aeruginosa. Additionally, representative single-step mutants arising after exposure to sub-MPC antibiotic concentrations were investigated for molecular basis of their fluoroquinolone resistance phenotypes. MPC value was recorded when more than 1010 CFU/mL were spread on Muëller Hinton Agar supplemented with different antibiotic concentrations (from 1X to 16X MIC value). MICs of original strains as well as single-step mutants were determined in presence or absence of the Efflux Pump Inhibitor Phe-Arg-β-naphthylamide (PAβN). Moreover point mutations in the QRDR of the gyrA and parC genes were investigated by sequencing. The enrofloxacin MPC values were 4–16-fold higher than ciprofloxacin values. E. coli and S. Typhimurium representative single-step mutants showed reduced susceptibilities associated with point mutations in the QRDR of the gyrA gene or efflux pump system. P. aeruginosa mutants showed resistance phenotypes associated predominantly with efflux pump system activity. According to in vitro MPC data, ciprofloxacin showed a better efficacy than enrofloxacin, in preventing the selection of E. coli, S. Typhimurium and P. aeruginosa single-step mutants. However, in relation to AUC/MPC ratio, the MPC concept can be applied in vivo to ciprofloxacin and enrofloxacin for E. coli and S. Typhimurium but not for P. aeruginosa.  相似文献   

16.
The epidemiology of an enrofloxacin-resistant Escherichia coli clone was investigated during two separate outbreaks of colibacillosis in the Danish broiler production. In total five flocks were reported affected by the outbreaks. Recorded first-week mortalities were in the range of 1.7-12.7%. The clone was first isolated from dead broilers and subsequently demonstrated in samples from associated hatchers and the parent flock with its embryonated eggs, suggesting a vertical transmission from the parents. The second outbreak involved two broiler flocks unrelated to the affected flocks from the first outbreak. However, the clone could not be demonstrated in the associated parent flock. Furthermore, samplings from grand-parent flocks were negative for the outbreak clone. The clonality was evaluated by plasmid profiling and pulsed-field gel electrophoresis. None of the recognized virulence factors were demonstrated in the outbreak clone by microarray and PCR assay. The molecular background for the fluoroquinolone-resistance was investigated and point mutations in gyrA and parC leading to amino-acid substitutions in quinolone-resistance determining regions of GyrA and ParC were demonstrated. Vertical transmission of enrofloxacin-resistant E. coli from healthy parents resulting in high first-week mortality in the offspring illustrates the potential of the emergence and spreading of fluoroquinolone-resistant bacteria in animal husbandry, even though the use of fluoroquinolones is restricted.  相似文献   

17.
In total, 83 avian pathogenic Escherichia coli (APEC) isolates from avian colibacillosis during a period from 2001 to 2006 in Japan were investigated for serogroups, typical virulence factors, antimicrobial susceptibility, and genetic relatedness. The most common serogroup was O78 (30.1%); 80.7% of isolates harbored the iss gene and 55.4% of isolates harbored the tsh gene. Antimicrobial resistance of the isolates was found for ampicillin (77.1%), oxytetracycline (75.9%), kanamycin (36.1%), fradiomycin (33.7%), trimethoprim (25.3%), enrofloxacin (21.7%), and florfenicol (6.0%). Although multiple antimicrobial-resistant phenotypes (three or more antimicrobials) accounted for 54.2% of isolates, no isolate exhibited resistance to all agents tested. The fluoroquinolone-resistant isolates had point mutations in GyrA (Ser83 --> Leu, Asp87 --> Asn) and ParC (Ser80 --> Ile, Glu84 --> Gly). Of 18 enrofloxacin-resistant E. coli isolates, nine isolates belonged to serotype O78. In PFGE analysis, eight of the nine enrofloxacin-resistant O78 isolates were classified into an identical cluster. This suggests that a specific genotype of fluoroquinolone-resistant O78 APEC may be widely distributed in Japan.  相似文献   

18.
Ninety-five avian pathogenic Escherichia coli (APEC) isolates recovered from diagnosed cases of avian colibacillosis from North Georgia between 1996 and 2000 were serotyped and examined for typical virulence-factors, susceptibility to antimicrobials of human and veterinary significance, and genetic relatedness. Twenty different serotypes were identified, with O78 being the most common (12%). The majority of the avian E. coli isolates (60%), however, were non-typeable with standard O antisera. Eighty-four percent of isolates were PCR positive for the temperature-sensitive hemagglutinin (tsh) gene and 86% positive for the increased serum survival (iss) gene. Multiple antimicrobial-resistant phenotypes (> or =3 antimicrobials) were observed in 92% of E. coli isolates, with the majority of isolates displaying resistance to sulfamethoxazole (93%), tetracycline (87%), streptomycin (86%), gentamicin (69%), and nalidixic acid (59%). Fifty-six E. coli isolates displaying resistance to nalidixic acid were co-resistant to difloxacin (57%), enrofloxacin (16%), gatifloxacin (2%), and levofloxacin (2%). DNA sequencing revealed point mutations in gyrA (Ser83-Leu, Asp87-Tyr, Asp87-Gly, Asp87-Ala), gyrB (Glu466-Asp, Asp426-Thr), and parC (Ser80-Ile, Ser80-Arg). No mutations were observed in parE. Twelve of the quinolone-resistant E. coli isolates were tolerant to cyclohexane, a marker for upregulation of the acrAB multi-drug resistance efflux pump. Quinolone-resistant isolates were further genetically characterized via ribotyping. Twenty-two distinct ribogroups were identified, with 61% of isolates clustering into four major ribogroups, indicating that quinolone resistance has emerged among multiple avian pathogenic E. coli serogroups and chromosomal backgrounds.  相似文献   

19.
OBJECTIVES AND DESIGN: 1) A prospective study to determine in vitro concentrations for a range of fluoroquinolones, gentamicin and amoxycillin-clavulanate required to inhibit growth of recently collected, feline and canine Escherichia coli and canine Staphylococcus intermedius isolates. 2) A comparative retrospective study to compare the minimum inhibitory concentrations (MICs) of ciprofloxacin, enrofloxacin and amoxycillin-clavulanate for archived canine E coli and S intermedius isolates collected ten to twenty years earlier, with those for recently collected isolates. PROCEDURE: Susceptibility was assessed using disk diffusion, agar dilution susceptibility testing and Epsilometer tests (E-tests) for both recently collected and archived isolates. RESULTS: All feline E coli isolates and recently collected canine S intermedius isolates were susceptible to all fluoroquinolones. There was a statistically significant increase in the MIC range of ciprofloxacin and enrofloxacin for recently collected E coli, and in the MIC range of amoxycillin-clavulanate for recently collected S intermedius isolates compared to archived isolates. Twelve of 59 recently collected canine E coli isolates were resistant to both ciprofloxacin and enrofloxacin. Resistant canine E coli isolates were associated with complicating host or infection site factors. CONCLUSION: This is the first report comparing the MICs for all veterinary fluoroquinolones currently available in Australia for a representative sample of canine and feline E coli and canine S intermedius isolates. Importantly, this study identified 12 of 59 canine E coli isolates resistant to fluoroquinolones and identified the development of low level resistance in canine E coli to ciprofloxacin and enrofloxacin and canine S intermedius to amoxycillin-clavulanate.  相似文献   

20.
OBJECTIVE: To evaluate the pharmacokinetic-pharmacodynamic parameters of enrofloxacin and a low dose of amikacin administered via regional IV limb perfusion (RILP) in standing horses. ANIMALS: 14 adult horses. PROCEDURES: Standing horses (7 horses/group) received either enrofloxacin (1.5 mg/kg) or amikacin (250 mg) via RILP (involving tourniquet application) in 1 forelimb. Samples of interstitial fluid (collected via implanted capillary ultrafiltration devices) from the bone marrow (BMIF) of the third metacarpal bone and overlying subcutaneous tissues (STIF), blood, and synovial fluid of the radiocarpal joint were collected prior to (time 0) and at intervals after tourniquet release for determination of drug concentrations. For pharmacokinetic-pharmacodynamic analyses, minimum inhibitory concentrations (MICs) of 16 microg/mL (amikacin) and 0.5 microg/mL (enrofloxacin) were applied. RESULTS: After RILP with enrofloxacin, 3 horses developed vasculitis. The highest synovial fluid concentrations of enrofloxacin and amikacin were detected at time 0; median values (range) were 13.22 microg/mL (0.254 to 167.9 microg/mL) and 26.2 microg/mL (5.78 to 50.0 microg/mL), respectively. Enrofloxacin concentrations exceeded MIC for approximately 24 hours in STIF and synovial fluid and for 36 hours in BMIF. After perfusion of amikacin, concentrations greater than the MIC were not detected in any samples. Effective therapeutic concentrations of enrofloxacin were attained in all samples. CONCLUSIONS AND CLINICAL RELEVANCE: In horses with orthopedic infections, RILP of enrofloxacin (1.5 mg/kg) should be considered as a treatment option. However, care must be taken during administration. A dose of amikacin > 250 mg is recommended to attain effective tissue concentrations via RILP in standing horses.  相似文献   

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