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Case Reports
. 2021 May 29;21(1):182.
doi: 10.1186/s12890-021-01544-0.

Pulmonary Nocardia infection in a child with idiopathic pulmonary hemosiderosis

Affiliations
Case Reports

Pulmonary Nocardia infection in a child with idiopathic pulmonary hemosiderosis

Lu Qin et al. BMC Pulm Med. .

Abstract

Background: Idiopathic pulmonary hemosiderosis (IPH) encompasses a rare and agnogenic group of diffuse alveolar capillary hemorrhagic diseases. Corticosteroid treatment is the globally preferred therapeutic strategy for IPH; however, it can cause immunodeficiency. Nocardia infection often occurs in immunocompromised patients and primarily involves the pleura and lungs. Herein, we describe a case of pediatric pulmonary Nocardia infection after the corticosteroid treatment of IPH.

Case presentation: A 7-year-old girl presented with chief complaints of pale complexion persisting for 1 year and a cough for 20 days. Abundant hemosiderin-laden macrophages were detected in the gastric juice, which supported the diagnosis of IPH. Uninterrupted doses of corticosteroids were administered during the last hospitalization. After nearly 2 months of corticosteroids therapy, the patient began to cough and produce a purulent sputum. Next-generation sequencing of the bronchoalveolar lavage fluid revealed Nocardia abscessus (N. abscessus) DNA. Linezolid was administered with good response, and the patient was discharged after 18 days of hospitalization. Her symptoms and pulmonary lesions had recovered, and the IPH appeared to be well-controlled with low dose of corticosteroids in follow-up.

Conclusions: Nocardia infection should be considered in the differential diagnoses for IPH patients receiving corticosteroid therapy, especially in patients with poor response to conventional empirical antibiotic therapy. Next-generation sequencing of bronchoalveolar lavage fluid may be used to quickly identify the Nocardia. Sulfonamides or linezolid are effective for pediatric pulmonary Nocardia infection.

Keywords: Corticosteroid; Hemosiderin-laden macrophages; Idiopathic; Nocardia; Pulmonary hemosiderosis.

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Conflict of interest statement

There is no any competing interest.

Figures

Fig. 1
Fig. 1
Changes in chest imaging of the patient. a Diffuse fine granular shadows were observed in both lungs (2 months before admission). b Diffuse granular shadows in both lungs and round nodular high-density shadows in the right lung (14 days before admission). cd The transmittance of the disease into the bilateral lung decreased unevenly, and there were still fine particles in the lungs. The right lung contained scattered, circular lesions, and the boundaries were clear, the arrors showed two large lesions, the larger is about 30 × 42 × 27 mm (on the day of admission). e, f The lesions in the lower lobe of the right lung were improved, but cavity formation, new lesions in the left lung, and bilateral pleural thickening were observed (on the 9th day of admission). g, h The lesions in the inferior lobe of right lung with cavity were significantly reduced, and the changes of both lungs were improved (on the 16th day of discharge)
Fig. 2
Fig. 2
Pathological analysis. a Active erythroid hyperplasia, primarily in the late juvenile erythrocytes, was observed and the central globus pallidus of some mature erythrocytes was enlarged. b Multiple erythrocytes and large numbers of hemosiderin-laden macrophages were observed
Fig. 3
Fig. 3
Diagrammatic representation of the treatment and outcome
Fig. 4
Fig. 4
Chest radiography performed at 1, 15 and 21 months after discharge. The pulmonary lesions were significantly improved

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