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1.
MEDICC Rev ; 24(2): 20-25, 2022 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-35648059

RESUMO

INTRODUCTION: Urinary tract infection is the second-leading reason for consults in primary health care. Bacterial urinary tract infections are the most common, of which Escherichia coli is the main etiologic agent. Antimicrobial resistance and multidrug resistance complicate effective community treatment, especially if resistance is caused by extended-spectrum beta-lactamase production. WHO recommends that antimicrobial susceptibility be evaluated in different regions of the world at different times. Community-acquired E. coli's susceptibility to colistin has not yet been studied in Cuba, and mcr-1 gene screening is necessary. OBJECTIVE: Evaluate community-acquired uropathogenic E. coli isolates' susceptibility to antibiotics, including colistin, and identify extended-spectrum beta-lactamase-producing bacteria. METHODS: We conducted a descriptive cross-sectional study that included 281 community-acquired uropathogenic E. coli isolates (153 from the Isle of Youth Special Municipality's Hygiene, Epidemiology, and Microbiology Center and 128 from Microbiology Laboratories of 7 institutions in Havana) from June 2016 through July 2018. We used the disk diffusion method to determine susceptibility to ampicillin, ampicillin/sulbactam, cefazolin, trimethoprim/sulfamethoxazole, ciprofloxacin, nitrofurantoin and fosfomycin. The disk elution method was used to determine susceptibility to colistin. The combined disk method was used to identify extended-spectrum beta-lactamases. Estimates were made regarding the frequency and percentages of antimicrobial susceptibility and resistance, as well as multidrug-resistance patterns. RESULTS: Of the 281 isolates, 68.3% (192/281) were resistant to ampicillin, 54.8% (154/281) were resistant to ciprofloxacin, and 49.5% (139/281) were resistant to trimethoprim/sulfamethoxazole. Resistance to colistin was not detected. On the other hand, 14.2% (40/281) were susceptible to the 8 antibiotics we evaluated, 22.1% (62/281) showed resistance to only 1 antibiotic, and 63.7% (179/281) were resistant to 2 or more antibiotics. In the extended-spectrum beta-lactamase determination, 34.5% (97/281) had inhibition zones ≤14 mm with cefazolin. Of those with inhibition zones, 64.9% (63/97) were positive in the phenotype test, and 35.1% (34/97) were negative. In extended-spectrum beta-lactamase-producing bacteria, 1.6% (1/63) were resistant to fosfomycin, and 3.2% (2/63) were resistant to nitrofurantoin. The most common multidrug-resistance pattern (22.9%; 30/131) was to ampicillin/sulbactam, ampicillin, cefazolin, ciprofloxacin, and trimethoprim/sulfamethoxazole. CONCLUSIONS: Uropathogenic E. coli resistance to the antibiotics most frequently used in community medical practice is quite common, and extended-spectrum beta-lactamase-producing bacteria is the mechanism for beta-lactam antibiotic resistance. Multidrug-resistance patterns include resistance to the antibiotics most used in community-acquired infections. Fosfomycin and nitrofurantoin are the most active in extended-spectrum beta-lactamase producing bacteria. All the isolates were susceptible to colistin.


Assuntos
Fosfomicina , Infecções Urinárias , Escherichia coli Uropatogênica , Ampicilina/uso terapêutico , Antibacterianos/farmacologia , Antibacterianos/uso terapêutico , Cefazolina/uso terapêutico , Ciprofloxacina/uso terapêutico , Colistina/farmacologia , Colistina/uso terapêutico , Estudos Transversais , Cuba , Proteínas de Escherichia coli , Fosfomicina/farmacologia , Fosfomicina/uso terapêutico , Humanos , Testes de Sensibilidade Microbiana , Nitrofurantoína/uso terapêutico , Sulbactam/uso terapêutico , Sulfametoxazol/uso terapêutico , Trimetoprima/uso terapêutico , Infecções Urinárias/tratamento farmacológico , Infecções Urinárias/epidemiologia , Infecções Urinárias/microbiologia , beta-Lactamases/uso terapêutico
2.
Iran J Basic Med Sci ; 20(4): 368-379, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28804607

RESUMO

OBJECTIVES: Buprenorphine is a common analgesic in experimental research, due to effectiveness and having few side-effects, including a limited influence in the immune and endocrine systems. However, how buprenorphine affects cytokine levels and the adrenal and thyroid response during general anesthesia and surgery is incompletely understood. This study aimed to assess whether buprenorphine modulated significantly those responses in rats submitted to general anesthesia, mechanical ventilation, and surgical insertion of intravascular catheters. MATERIALS AND METHODS: Animals were anesthetized with isoflurane, mechanically ventilated, and surgically instrumented for carotid artery and the femoral vein catheter placement. The test group (n=16), received buprenorphine subcutaneously before surgery, whereas the control group (n=16) received normal saline. Blood sampling to determine plasma levels of adrenocorticotropic hormone (ACTH), corticosterone (CS), total thyroxine (TT4), total triiodothyronine (TT3), thyroid-stimulating hormone (TSH), TNF-α, IL6, IL10, TNF-α, IL6, and IL10 mRNA was performed at 10 min after completion of all surgical procedures and at 90, 150, 240, and 300 min thereafter, with the animals still anesthetized and with mechanical ventilation. RESULTS: Buprenorphine-treated animals had higher levels of ACTH, CS, and TT4 at several time points (P<0.05) and TSH and TT3 at all-time points (P<0.05). They also had increased IL10, TNF-α, and IL10 mRNA levels. CONCLUSION: In this model, buprenorphine significantly modulated the intra-operative cytokine and endocrine response to anesthesia, mechanical ventilation, and surgical placement of intravascular catheters. The mechanism and significance of these findings remain undetermined. Researchers should be aware of these effects when considering the use of buprenorphine for analgesic purposes.

3.
Biol Reprod ; 83(6): 901-8, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20720169

RESUMO

Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. However, their influence on luteal steroidogenesis is not clearly understood. The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. Protein expression and FASL mRNA transcription increased in the late CL. Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). FASL clearly inhibited in vitro progesterone and prostaglandin E(2) (PGE(2)) production by equine luteal cells but increased prostaglandin F(2alpha) (PGF(2alpha)). Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis.


Assuntos
Corpo Lúteo/metabolismo , Proteína Ligante Fas/metabolismo , Fase Luteal/metabolismo , Luteólise/metabolismo , Receptor fas/metabolismo , Animais , Apoptose , Sobrevivência Celular , Células Cultivadas , Corpo Lúteo/citologia , Dinoprosta/metabolismo , Dinoprostona/metabolismo , Proteína Ligante Fas/genética , Feminino , Regulação da Expressão Gênica , Cavalos , Imuno-Histoquímica , Interferon gama/metabolismo , Progesterona/metabolismo , RNA Mensageiro/metabolismo , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismo , Receptor fas/genética
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