National Reference Laboratory for Toxoplasmosis, Center for Parasitic Zoonoses, Institute for Medical Research, University of Belgrade, Belgrade, Serbia.
J Clin Microbiol. 2013 Aug;51(8):2686-90. doi: 10.1128/JCM.01077-13. Epub 2013 Jun 12.
In immunocompromized patients, including hematopoietic stem cell transplant (HSCT) recipients, life-threatening toxoplasmosis may result from reactivation of previous infection. We report a case of severe disseminated toxoplasmosis that developed early after allogeneic HSCT for T-cell lymphoblastic leukemia/lymphoma in a 15-year-old Toxoplasma gondii-seropositive boy with Nijmegen breakage syndrome, a rare genetic DNA repair disorder associated with immunodeficiency. The donor was the patient's HLA-identical brother. Prophylaxis with cotrimoxazole was discontinued a day before the HSCT procedure. Signs of lung infection appeared as early as day 14 post-HSCT. The presence of tachyzoite-like structures on Giemsa-stained bronchoalveolar lavage (BAL) fluid smears suggested toxoplasmosis. Real-time PCR targeted at the T. gondii AF146527 gene revealed extremely high parasite burdens in both blood and BAL fluid. Although immediate introduction of specific treatment resulted in a marked reduction of the parasite load and transient clinical improvement, the patient deteriorated and died of multiple organ failure on day 39 post-HSCT. Direct genotyping of T. gondii DNA from blood and BAL fluid with the PCR-restriction fragment length polymorphism method revealed type II alleles with SAG1, SAG2, and GRA6 markers but alleles of both type I and type II with GRA7. Additional analysis with 15 microsatellite markers showed that the T. gondii DNA was atypical and genetically divergent from that of the clonal type I, II, and III strains. This is the first report of increased clinical severity of toxoplasmosis associated with an atypical strain in the setting of immunosuppression, which emphasizes the need to diagnose and monitor toxoplasmosis by quantitative molecular methods in cases of reactivation risk.
在免疫功能低下的患者中,包括造血干细胞移植(HSCT)受者,先前感染的弓形虫再激活可能导致危及生命的弓形体病。我们报告了一例严重播散性弓形体病,发生在一位 15 岁 T 细胞淋巴母细胞白血病/淋巴瘤的异基因 HSCT 后早期,该患者为 Toxoplasma gondii 血清阳性,患有尼曼匹克氏症,这是一种罕见的与免疫缺陷相关的 DNA 修复障碍遗传疾病。供者是患者 HLA 完全相同的兄弟。HSCT 前一天停用复方磺胺甲噁唑预防。HSCT 后 14 天出现肺部感染迹象。吉姆萨染色支气管肺泡灌洗液(BAL)液涂片上的速殖子样结构提示弓形体病。针对 T. gondii AF146527 基因的实时 PCR 显示血液和 BAL 液中寄生虫载量极高。尽管立即引入特异性治疗导致寄生虫负荷明显减少和短暂的临床改善,但患者在 HSCT 后第 39 天因多器官衰竭而恶化和死亡。通过 PCR-限制性片段长度多态性方法直接从血液和 BAL 液中弓形虫 DNA 的基因分型显示 SAG1、SAG2 和 GRA6 标记的 II 型等位基因,但 GRA7 有 I 型和 II 型等位基因。使用 15 个微卫星标记的进一步分析表明,弓形虫 DNA 是非典型的,与克隆 I 型、II 型和 III 型菌株的遗传差异很大。这是首例在免疫抑制背景下与非典型株相关的弓形体病临床严重程度增加的报告,强调了在再激活风险的情况下需要通过定量分子方法诊断和监测弓形体病。