Neuromyelitis Optica Spectrum Disorder (NMOSD) is a central nervous system disease. Blindness, paralysis, cognitive impairment, and even death can result from autoimmune inflammatory demyelination disorders. Most patients experience recurrent central nervous system inflammation (CNS inflammation), typically optic neuritis; long-term corticosteroid therapy can increase the risk of hypertension, diabetes, osteoporosis, cushing’s syndrome, and infections, while immunosuppressants increase the risk of infections, including viral, bacterial, and fungal opportunistic infections [9]. Although the precise etiology and pathogenesis of NMOSD remain elusive, it is believed that intricate interplay between genetic and environmental factors contributes to its development. The prevalence of NMOSD has increased overall, likely due to specific environmental factors such as changes in hygiene practices and antibiotic usage. Infectious diseases have been a focus of attention because they are believed to be triggers for many autoimmune diseases and may also contribute to the development or exacerbation of these conditions.10]. Infection may increase the risk of disease recurrence and progression in patients with NMOSD [11]. Scholars believe that tuberculosis bacillus, Helicobacter pylori, intestinal flora, herpes simplex virus, and EB virus may be linked to the prevalence of NMOSD, but more data is needed [10]. It has also been reported that COVID-19 can cause NMOSD relapse [12].

Nocardiosis is an opportunistic infection that usually affects immunocompromised individuals, particularly those with cellular immunodeficiency. Patients with malignant tumors, chronic glucocorticoid users, recipients of organ transplants and hematopoietic stem cell transplants, and HIV-positive individuals are the most frequently infected populations [13]. Normally, Nocardia species are absent in the respiratory tract, and their isolation from sputum samples may indicate infection. The lung is the primary site of Nocardia infection [2, 14]. Nocardiosis typically affects patients with compromised local pulmonary defenses or systemic immunosuppression, and rarely occurs in healthy individuals. Symptoms of Nocardia pneumonia include cough, fever, and breathing difficulties. Because the pathogenesis is `usually subacute or chronic granulomas, Nocardia pneumonia is often confused with other chronic suppurative lung diseases and malignancies, even when there is a high clinical suspicion of the disease. Nocardia can be rapidly diagnosed by examination of sputum, pleural fluid, bronchial lavage fluid, or percutaneous lung aspirate with Gram staining and modified acid-fast staining [15]. It has been reported that respiratory Nocardia isolates may not be pathogenic (i.e., colonizers), but this is extremely rare [14].

Pulmonary nocardiosis may be categorized as acute, subacute, or chronic onset and can not be distinguished by any specific signs or symptoms. However, fever, night sweats, fatigue, anorexia, weight loss, dyspnea, cough, hemoptysis, and pleuritic chest pain have all been reported [16, 17]. In this regard, we summarized the relevant cases of Nocardia pneumonia in children along with their clinical characteristics and treatments in Table 1.

All cases we reviewed had pulmonary Nocardia infection, with predisposing factors, including immunosuppression and/or pulmonary disease. Four of the cases had no predisposing factors, and most of the children had underlying diseases or a history of taking hormones, with three having known lung disease. Over a 24-year period, V Pintado et al. [27] summarized the characteristics of Nocardia infection in 34 patients (1978–2001). Immunosuppression and/or lung disease were predisposing factors in 85% of patients; twenty-one patients (62%) had some degree of immunodeficiency due to HIV infection (8 cases), immunosuppressive therapy (8 cases), diabetes (4 cases), or leukemia (1 case). Furthermore, nearly half of the patients (47%) had a prior lung condition, such as chronic obstructive pulmonary disease, silicosis, alveolar proteinosis, or pulmonary fibrosis. Only five patients (15%) did not have a known underlying disease. Attacks are frequently severe and recurring, with significant morbidity and mortality. Ten of the 106 patients died after an average of 4.5 relapses (range 1–10), with four of them succumbing to infection. Three patients died as a result of bronchopneumonia and one as a result of septicemia [28]. Lung Nocardia infections are clinically uncommon, even more so in children with neuromyelitis spectrum disorder, and the majority of these infections are severe. An acute necrotic inflammatory response and nonspecific clinical manifestations characterize Nocardia pulmonary. In our case, the child developed a cough, chest pain, fever, initial dry cough, progressive purulent sputum, and severe dyspnea that worsened despite the use of multiple antibiotics at the outset. Nocardia imaging in the lungs is also nonspecific, and Nocardia infection is difficult and time-consuming to diagnose. Bronchoscopic alveolar lavage with NGS may be the preferred method for rapid pathogen detection [29].

The severity of pulmonary involvement varies from transient infections to fully consolidated bronchopneumonia. Nocardia can cause lung lesions or spread to other organs, particularly in immunocompromised patients following organ or bone marrow transplant or in patients with acquired immunodeficiency syndrome (AIDS). Spread to the bones, joints, skin, kidneys, liver, spleen, and brain can result in serious complications and a high mortality rate. Patients who have received chemotherapy or high-dose corticosteroids are also at risk for developing metastatic infections. Additional risk factors include malignancies (e.g., lymphoma, leukemia) and tuberculosis [16, 30]. A study of 1050 cases of nocardiosis found that systemic infection was responsible for about 32% of the cases. In contrast, pulmonary involvement accounted for 39%, central nervous system involvement for 9%, and skin or lymphatic involvement in 8% of the cases [16]. A single site outside the lung, such as the eye or bone, was involved in 12% of cases. In total, 793 strains of Nocardia were isolated from Observatoire Français des Nocardioses, with the majority coming from the lungs (53.8%). Nocardia farcinica (20.2%), Nocardia abscessus complex (19.9%), and Nocardia nova complex (19.5%) were the most prevalent species. The percentage of N. farcinica increased significantly over time, rising from 13% in 2010 to 27.6% in 2014. Linezolid, amikacin, trimethoprim-sulfamethoxazole, minocycline, and imipenem are the most widely used antimicrobials [31, 32]. The ideal first-line treatment for nocardiosis should include a wide range of species as well as adequate antibiotic concentrations in all involved organs. However, determining the best treatment strategy is difficult because most current antibiotic regimens rely on microbiological data, such as species identification and antimicrobial susceptibility testing (AST) [33,34,35]. In this case report, the child had nonspecific signs and symptoms and had been taking tacrolimus and hormones for a long time due to Neuromyelitis Optica Spectrum Disorders. The child’s condition developed rapidly and continued to aggravate even with combined anti-infection, leading to difficulty in breathing; as a result, his illness was almost misdiagnosed as a tumor. This is a lesson we should take away from this diagnosis and treatment process.Identifying the causative agent is the most crucial step to rule out infection. Long-term antimicrobial treatment is required for N. asteroids, and possible medications include trimethoprim-sulfamethoxazole, minocycline, amoxicillin-clavulanic acid, cefuroxime, third-generation cephalosporins, amikacin, and imipenem [27]. Excluding patients who died, the average duration of treatment was 6.3 months (range: 3–13 months, median: 6 months). Forty-three patients were administered TMP-SMZ alone (23 patients) or in combination with other antibiotics (20 patients). The most common combination was TMP-SMZ along with imipenem/meropenem (11 patients), of which 5 patients received amikacin at the same time. Linezolid was administered to 3 patients (alone to 2 patients and in combination with meropenem to one patient) Nocardia was suspected as a result of secondary effects on TMP-SMZ (rash and renal tubular acidosis) or in vitro bacteria resistance to TMP-SMZ. Two patients were treated with linezolid alone for 5 and 7 months [36]. Systemic corticosteroid therapy is closely related to pulmonary nocardiosis [37].

Finally, patients with pulmonary nocardiosis frequently have nonspecific clinical symptoms, laboratory tests, and imaging results that are frequently misdiagnosed as other diseases such as actinomycosis, tuberculosis, fungal pneumonia, and even lung tumors and metastases. The risk of nocardiosis must be considered when immunocompromised individuals develop acute, subacute, or chronic pulmonary infections or central nervous system and soft tissue infections. If chest CT shows bilateral consolidation, multiple nodules, or cavity formation, the doctor should consider the possibility of pulmonary Nocardiosis and report any suspicions to the microbiology laboratory to reduce the risk of disease and provide early diagnosis and treatment.