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尼日利亚迈杜古里地区人类免疫缺陷病毒感染者的肺曲霉病表型特征及相关细胞免疫

Phenotypic profile of pulmonary aspergillosis and associated cellular immunity among people living with human immunodeficiency virus in Maiduguri, Nigeria.

作者信息

Nasir Idris Abdullahi, Shuwa Halima Ali, Emeribe Anthony Uchenna, Adekola Hafeez Aderinsayo, Dangana Amos

机构信息

Department of Medical Laboratory Services, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria.

Department of Medical Microbiology and Parasitology, University of Ilorin, Ilorin, Nigeria.

出版信息

Tzu Chi Med J. 2019 Jul-Sep;31(3):149-153. doi: 10.4103/tcmj.tcmj_46_18.

DOI:10.4103/tcmj.tcmj_46_18
PMID:31258289
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6559025/
Abstract

OBJECTIVE

causes many forms of pulmonary infectious diseases ranging from colonization (noninvasive) to invasive aspergillosis. This largely depends on the underlying host's lung health and immune status. Pulmonary aspergillosis (PA), especially the invasive form, occurs as opportunistic to human immunodeficiency virus (HIV) as a result of cluster of differentiation (CD)4+ lymphopenia. The majority of patients with comorbid HIV and aspergillosis go undiagnosed. This study aimed to isolate, identify the etiologies, and determine the prevalence of PA among HIV-infected persons with a productive cough (at least <2 weeks) at the HIV Clinics of the University of Maiduguri Teaching Hospital, Nigeria.

MATERIALS AND METHODS

After ethical approval, three consecutive early morning sputum samples were collected from patients with negative tuberculosis results. The samples were individually inoculated onto Sabouraud dextrose agar supplemented with chloramphenicol and cycloheximide in duplicate for 7 days at 37°C and 25°C, respectively. The fungal isolates were examined morphologically and microscopically and identified using the standard biochemical reagents. CD4+ cell counts were performed using flow cytometry. Self-administered questionnaires were used to assess the patients data. All patients were antiretroviral naïve.

RESULTS

The prevalence of PA was 12.7% in these 150 patients. Of the 19 fungal culture-positive individuals, accounted for the highest proportion of the isolates (8, 42.1%) followed by (5, 26.3%), (4, 21.1%), and (2, 10.5%). Based on the assessment of functionality of cellular immunity, HIV participants who were negative for PA (131/150) had significantly higher mean ± standard deviation CD4 T-cell counts (245.65 ± 178.32 cells/mL) than those with aspergillosis (126.13 ± 105.27 cells/mL) ( = 0.0051). PA was relatively highest among patients with CD4+ cell counts <200 cells/mL (12. 34.3%) followed by those with CD4+ cell counts between 200 and 350 cells/mL (5, 9.6%) and least among those with CD4+ cell counts >350 cells/mL (2, 3.2%). The Chi-square test showed a significant association between the prevalence of PA and the CD4+ cell count, age, and gender ( < 0.05) but not with occupation or education level ( > 0.05).

CONCLUSION

The findings from this study indicate that spp. is a significant etiology of acute productive cough in people living with HIV and this is related to the CD4+ cell count of coinfected persons.

摘要

目的

引发多种形式的肺部感染性疾病,范围从定植(非侵袭性)到侵袭性曲霉病。这在很大程度上取决于宿主潜在的肺部健康状况和免疫状态。肺曲霉病(PA),尤其是侵袭性形式,由于分化簇(CD)4 +淋巴细胞减少,作为人类免疫缺陷病毒(HIV)的机会性感染而发生。大多数合并感染HIV和曲霉病的患者未被诊断出来。本研究旨在分离、鉴定病因,并确定在尼日利亚迈杜古里大学教学医院HIV诊所出现干咳(至少<2周)的HIV感染者中PA的患病率。

材料与方法

经伦理批准后,从结核病检测结果为阴性的患者中连续采集三份清晨痰液样本。将样本分别接种到添加有氯霉素和放线菌酮的沙氏葡萄糖琼脂上,一式两份,分别在37°C和25°C下培养7天。对真菌分离株进行形态学和显微镜检查,并使用标准生化试剂进行鉴定。使用流式细胞术进行CD4 +细胞计数。通过自行填写问卷来评估患者数据。所有患者均未接受过抗逆转录病毒治疗。

结果

这150名患者中PA的患病率为12.7%。在19例真菌培养阳性个体中, 占分离株的比例最高(8例,42.1%),其次是 (5例,26.3%)、 (4例,21.1%)和 (2例,10.5%)。基于细胞免疫功能的评估,PA检测为阴性的HIV参与者(131/150)的平均±标准差CD4 T细胞计数(245.65±178.32细胞/毫升)显著高于患有曲霉病的参与者(126.13±105.27细胞/毫升)( = 0.0051)。CD4 +细胞计数<200细胞/毫升的患者中PA相对最高(12例,34.3%),其次是CD4 +细胞计数在200至350细胞/毫升之间的患者(5例,9.6%),而CD4 +细胞计数>350细胞/毫升的患者中最少(2例,3.2%)。卡方检验显示PA患病率与CD4 +细胞计数、年龄和性别之间存在显著关联( < 0.05),但与职业或教育水平无关( > 0.05)。

结论

本研究结果表明, 属是HIV感染者急性干咳的重要病因,这与合并感染患者的CD4 +细胞计数有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f54c/6559025/0b31e53ba387/TCMJ-31-149-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f54c/6559025/0b31e53ba387/TCMJ-31-149-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f54c/6559025/0b31e53ba387/TCMJ-31-149-g001.jpg

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