黑金梭菌是一种腐生植物,dematiary,酵母样真菌很少涉及人类感染。这里,我们报告了第一例30周龄早产的黑原真菌血症,极低出生体重的新生儿出生在有妊娠糖尿病史的primigravida,妊娠高血压和羊水过少。婴儿出现呼吸窘迫,低血压,心动过缓,出生后不久的凝血病和感染性休克,最终在生命的第9天死于多器官功能障碍综合征。配对的血液培养物显示出一种脱脂性酵母样真菌的生长,通过rDNA内部转录间隔区(ITS)测序将其鉴定为黑色素A。分离物的抗真菌药敏试验显示氟康唑的最低抑菌浓度高(32µg/mL),表明阻力。黑原真菌血症的诊断很困难,因为在生长的初始阶段,它很容易与革兰氏染色涂片中的念珠菌和相似的菌落形态混淆。此外,传统的诊断方法,如VITEK2和MALDI-TOFMS对于该病原体的鉴定是不可靠的。使用分子技术进行准确鉴定对于做出治疗决定至关重要,因为黑色素A.显示出实质性的抗真菌抗性。临床医生应该意识到,血液培养中的酵母样细胞不仅表明念珠菌属物种,但也是罕见的病原体,如A.melanogenum和应谨慎,而开始氟康唑治疗。目前,没有确定的金黄色葡萄球菌的易感性断点。需要进一步的研究来确定此类感染的最佳治疗方法。
Aureobasidium melanogenum is a saprophytic, dematiaceous, yeast-like fungus rarely implicated in human infections. Here, we report the first
case of A. melanogenum fungemia in a 30-week-old preterm, very low birth weight neonate born to a primigravida with history of gestational diabetes, pregnancy induced hypertension and oligohydramnios. The baby developed respiratory distress, hypotension, bradycardia, coagulopathy and septic shock shortly after birth, and eventually succumbed to multiple organ dysfunction syndrome on day 9 of life. Paired blood culture showed growth of a dematiaceous yeast-like fungus which was identified as A. melanogenum by rDNA internal transcribed spacer (ITS) sequencing. Antifungal susceptibility testing of the isolate showed high minimum inhibitory concentration of fluconazole (32 µg/mL), indicating resistance. Diagnosis of A. melanogenum fungemia is difficult as it is easily confused with Candida species in Gram stained smears and similar colony morphology during the initial stages of growth. Also, the conventional diagnostic methods, such as VITEK 2 and MALDI-TOF MS are unreliable for identification of this pathogen. Accurate identification using molecular techniques is crucial for making treatment decisions as A. melanogenum shows substantial antifungal resistance. Clinicians should be aware that yeast-like cells in blood culture are not only indicative of Candida species, but also rare pathogens like A. melanogenum and should exercise caution while starting fluconazole therapy. At present, there are no established susceptibility breakpoints for
Aureobasidium spp. Further studies are needed to determine the optimal treatment for such infections.