Husain Shahid, McCurry Kenneth, Dauber James, Singh Nina, Kusne Shimon
Division of Infectious Diseases, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
J Heart Lung Transplant. 2002 Mar;21(3):354-9. doi: 10.1016/s1053-2498(01)00394-1.
Nocardia is responsible for infection in both normal and immunocompromised hosts. Organ transplant recipients are increasingly recognized as a sub-group of immunocompromised patients in whom nocardia is an important pathogen. The frequency of nocardia in organ transplant recipients varies between 0.7% and 3%. Nocardia infection has largely been reported in heart, kidney and liver transplant recipients. Presentations of nocardia in lung transplant recipients have been restricted primarily to case reports. The present study reviews the clinical and epidemiologic characteristics of nocardia infection in lung transplant recipients at our institution.
A retrospective cohort study of 473 lung transplant recipients from January 1991 to November 2000 was done at a university hospital. Patient demographics, immunosuppressive regimen at the time of isolation of nocardia species, use of trimethoprim-sulfamethoxazole for Pneumocystis carinii prophylaxis, rejection episodes in the preceding 6 months, concurrent pathogens, site of infection, radiologic findings and treatment and outcome were recorded.
Nocardia infection was found in 2.1% (10 of 473) of our lung transplant recipients. Median time of onset was 34.1 months after transplantation. Nocardia species included N farcinica in 30% (3 of 10), N nova in 30% (3 of 10), N asteroides complex in 30% (3 of 10) and N brasiliensis in 10% (1 of 10) of patients. Post-transplant diabetes was present in 50% (5 of 10) of patients. The primary indication for lung transplantation was emphysema in 40% (4 of 10). Native lung involvement was noted in 75% (3 of 4) of patients with single lung transplant. Breakthrough nocardia infection were noted in 6 patients who were receiving trimethoprim-sulfamethoxazole prophylaxis for P carinii pneumonia; all breakthrough isolates remained susceptible to trimethoprim-sulfamethoxazole. Overall mortality was 40% (4 of 10). All patients (3 of 3) with infection due to N farcinica, except 1 (1 of 7) with infection due to other nocardia species, died. Seventy-five percent (3 of 4) of deaths were attributable to nocardia infection.
Nocardia infection tended to involve the native lung in single lung transplant recipients. Trimethoprim-sulfamethoxazole for P carinii prophylaxis at the doses given was not protective against nocardiosis in these patients. Infection with N farcinica was associated with poor outcome. Thus, species identification and extended courses of antibiotics based on antimicrobial susceptibility testing are important in management of these patients.
诺卡菌可导致正常宿主和免疫功能低下宿主发生感染。器官移植受者越来越被视为免疫功能低下患者的一个亚组，诺卡菌是其中的一种重要病原体。器官移植受者中诺卡菌感染的发生率在0.7%至3%之间。诺卡菌感染主要在心脏、肾脏和肝脏移植受者中报道。肺移植受者中诺卡菌感染的表现主要局限于病例报告。本研究回顾了我院肺移植受者中诺卡菌感染的临床和流行病学特征。
在一所大学医院对1991年1月至2000年11月期间的473例肺移植受者进行了一项回顾性队列研究。记录患者的人口统计学资料、分离出诺卡菌属时的免疫抑制方案、用于预防卡氏肺孢子虫肺炎的甲氧苄啶-磺胺甲恶唑的使用情况、前6个月的排斥反应发作、并发病原体、感染部位、影像学表现以及治疗和结局。
在我们的肺移植受者中，2.1%（473例中的10例）发现有诺卡菌感染。发病的中位时间为移植后34.1个月。诺卡菌属包括豚鼠耳炎诺卡菌，占30%（10例中的3例）；新星诺卡菌，占30%（10例中的3例）；星状诺卡菌复合体，占30%（10例中的3例）；巴西诺卡菌，占10%（10例中的1例）。50%（10例中的5例）的患者存在移植后糖尿病。肺移植的主要指征为肺气肿，占40%（10例中的4例）。单肺移植患者中，75%（4例中的3例）有原肺受累。6例接受甲氧苄啶-磺胺甲恶唑预防卡氏肺孢子虫肺炎的患者发生了诺卡菌突破性感染；所有突破性分离株对甲氧苄啶-磺胺甲恶唑仍敏感。总体死亡率为40%（10例中的4例）。所有豚鼠耳炎诺卡菌感染的患者（3例中的3例）均死亡，除1例（7例中的1例）为其他诺卡菌属感染的患者。75%（4例中的3例）的死亡归因于诺卡菌感染。
单肺移植受者中，诺卡菌感染倾向于累及原肺。给予的剂量用于预防卡氏肺孢子虫肺炎的甲氧苄啶-磺胺甲恶唑对这些患者的诺卡菌病没有保护作用。豚鼠耳炎诺卡菌感染与不良结局相关。因此，在这些患者的管理中，菌种鉴定和基于药敏试验的延长抗生素疗程很重要。
