甲素耐药黄金葡萄球菌和Candida spp. 的共同殖民. 在患有恶性瘤的儿童中
Raziyeh Baharvand1, Fatemeh Fallah2, Parvaneh Jafari3
1Department of Microbiology, Faculty of Science, Islamic Azad University, Arak branch, Arak, Iran.
AMB Express
|February 13, 2024
概括
在接受化疗的儿童中,口服共殖民性耐甲基金色葡萄球菌 (MRSA) 和Candida物种增加了关键毒性基因的表达. 这表明Candida可能促进MRSA感染,可能导致全身并发症.
科学领域:
- 医学微生物学 医学微生物学
- 传染性疾病 传染性疾病
- 儿科瘤学 儿科瘤学
背景情况:
- 接受化疗的儿童容易感染机会性感染.
- 在临床环境中,越来越多地认识到多微生物相互作用,特别是涉及金黄色葡萄球菌和菌种类的相互作用.
- 口腔是病原体的储存库,共同殖民可以改变毒性因子的表达.
研究的目的:
- 在儿童癌症患者的口腔中研究甲素耐药黄金葡萄球菌 (MRSA) 和Candida物种之间的相互作用.
- 在单一和共同殖民条件下评估MRSA中的mecA基因和Candida物种中的Als3p基因的表达水平.
- 确定Candida物种是否在这个脆弱群体中促进MRSA殖民或感染.
主要方法:
- 从接受化疗的儿科患者中采集口腔和鼻腔样本,使用无菌海绵拭子.
- 通过聚合酶链反应 (PCR) 确认MRSA和Candida物种,分别向mecA和Als3p基因.
- 定量实时PCR (基于SYBR绿色) 用于测量单个和共同殖民的场景中meca和Als3p基因的相对表达水平.
主要成果:
- 在14.1%的样本中检测到金黄色葡萄球菌,MRSA占口服分离物的58.3%.
- 最常见的Candida物种是Candida albicans (16.5%). 这是最常见的Candida物种.
- 在4.7%的患者中发生了MRSA和Candida物种的口腔共殖民. 基因表达分析显示了显著的上调:在联合殖民中,mecA表达增加了六倍,Als3p表达增加了两倍,而不是单个殖民.
结论:
- 这项研究突出显示了多微生物感染在免疫受损儿童中的临床意义.
- 坎迪达菌种可能在促进金黄色葡萄球菌感染方面发挥作用,可能会增加共殖民患者全身疾病的风险.
- 监测和理解这些微生物相互作用对于治疗儿科瘤患者的感染至关重要.
关键词:
在Candida Spp.孩子 孩子 孩子 孩子伊朗 伊朗 伊朗 伊朗恶性瘤是一种恶性瘤.甲素耐药的金黄色葡萄球菌 (Staphylococcus aureus) 是一种黄金葡萄球菌黄金葡萄球菌更多相关视频
相关概念视频
01:25Colonisation of Pathogens
Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
01:29Staphylococcal Skin Infections
Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
01:25Mechanism of Antibiotic Resistance in MRSA
Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
01:25Clinical Significance of Antibiotic Resistance
Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...