背景:慢性胆囊炎,以胆囊持续发炎为特征,主要源于胆结石的长期存在。结石性胆囊炎的发病率随着时间的推移而持续增加。胆囊结石已被认为是胆道感染发展的诱发因素。同时,引起胆道感染的病原微生物的分布和耐药性发生了重大变化。及时采集胆汁样本进行病原体分析至关重要,鉴于其在指导明智的临床药物治疗和改善患者预后方面的关键作用。
方法:我们介绍了一例66岁的女性患者,该患者先前因弥漫性大B细胞淋巴瘤而接受了胃大部切除术。患者因腹痛而入院。随后的诊断评估显示并发胆总管结石和胆囊结石。患者接受了手术胆囊切除术作为治疗方法。切除的胆囊的组织病理学检查揭示了表明慢性胆囊炎的特征性特征。随后对患者胆汁标本的实验室分析产生革兰氏阳性球菌,随后通过生化测定鉴定,质谱,和16SrRNA分析为流感球菌。使用圆盘扩散和微流体稀释进行的进一步体外抗菌敏感性测试表明,该菌株对26种抗生素的抑制作用范围为12.0至32.0mm,包括氨苄青霉素,头孢唑啉,头孢呋辛,头孢噻肟,头孢曲松,头孢吡肟,氨苄西林/舒巴坦,哌拉西林,环丙沙星,头孢哌酮/舒巴坦,亚胺培南,美罗培南,哌拉西林/他唑巴韦,青霉素,红霉素,氯霉素,万古霉素,甲氨蝶呤/磺胺甲恶唑,替考拉宁,利奈唑胺,替加环素,头孢西丁,头孢他啶,左氧氟沙星,米诺环素和妥布霉素。然而,阿米卡星的抑菌圈直径为6.0mm,苯唑西林,克林霉素,还有四环素.患者术前及术后24h内接受头孢他啶抗感染治疗,术后1周成功出院。
结论:在这项研究中,我们介绍了从结石性胆囊炎患者的胆汁标本中首次分离和鉴定出的流球菌。这项新发现为指导临床合理的抗微生物治疗和推进有关感染的相关致病机制的探索奠定了坚实的实验基础。
BACKGROUND: Chronic cholecystitis, characterized by persistent inflammation of the gallbladder, predominantly stems from the prolonged presence of gallstones. Calculous cholecystitis has demonstrated a consistent escalation in its incidence over time.Gallbladder stones have been recognized as a predisposing factor for the development of biliary tract infections.Concomitantly, there have been substantial shifts in the distribution and resistance profiles of pathogenic microorganisms responsible for biliary tract infections. The timely acquisition of
bile samples for pathogen analysis is of paramount importance, given its critical role in guiding judicious clinical pharmacotherapy and enhancing patient prognosis.
METHODS: We present a
case involving a 66-year-old female patient who had previously undergone subtotal gastrectomy due to diffuse large B-cell lymphoma. The patient was admitted to our institution with complaints of abdominal pain. Subsequent diagnostic evaluation revealed concurrent choledocholithiasis and cholecystolithiasis. The patient underwent surgical cholecystectomy as the therapeutic approach. Histopathological examination of the excised gallbladder disclosed characteristic features indicative of chronic cholecystitis. Subsequent laboratory analysis of the patient\'s
bile specimen yielded Gram-positive cocci, subsequently identified through biochemical assays, mass spectrometry, and 16 S rRNA analysis as Vagococcus fluvialis. Further in vitro antimicrobial susceptibility testing using disk diffusion and microfluidic dilution showed that this strain exhibited inhibition zone diameters ranging from 12.0 to 32.0 mm in response to 26 antibiotics, including ampicillin, cefazolin, cefuroxime, cefotaxime, ceftriaxone, cefepime, ampicillin/sulbactam, piperacillin, ciprofloxacin, cefoperazone/sulbactam, imipenem, meropenem, piperacillin/tazobarb, penicillin, erythromycin, chloramphenicol, vancomycin, methotrexate/sulfamethoxazole, teicoplanin, linezolid, tigecycline, cefoxitin, ceftazidime, levofloxacin, minocycline and tobramycin. However, the inhibition zone diameters were 6.0 mm for amikacin, oxacillin, clindamycin, and tetracycline. The patient received ceftazidime anti-infective therapy both preoperatively and within 24 h postoperatively and was discharged successfully one week after surgery.
CONCLUSIONS: In this study, we present the inaugural isolation and identification of Vagococcus fluvialis from
bile specimens of patients afflicted with calculous cholecystitis. This novel finding lays a substantial experimental groundwork for guiding clinically rational antimicrobial therapy and advancing the exploration of relevant pathogenic mechanisms pertaining to Vagococcus fluvialis infections.