A male aged 61 years was admitted to our hospital for intermittent fever and cough on August 16, 2019.In the past 4 years, the patient had developed pulmonary infection repeatedly, which all improved after anti-infection treatment. He had a history of hypertension, coronary heart disease and bronchiectasia. In the past one year, the patient intermittently developed cough, sputum, accompanied by fever, with a body temperature of about 38.0℃, without afternoon low fever, night sweats and hemoptysis. He was hospitalized for many times, discharged after anti-infection treatment. The patient continued to cough and fever intermittently outside the hospital.
On admission, the patient was conscious, with no enlargement of superficial lymph nodes, slightly coarse breathing sounds in both lungs, and a little moist crackles could be heard. On June 19, 2019, chest CT (computed tomograph) indicated space occupation in the right upper lung, bilateral lung infective lesion with bronchiectasis, emphysema, bullae of the lung, right pleural effusion Fig. 1A. On August 16, chest CT indicated that the lesion area of the right upper lung mass was significantly larger than before, accompanied by bronchiectasis, emphysema, and pulmonary bulla Fig. 1B. After admission, the patient underwent CT-guided percutaneous lung puncture examination, and the tissues were performed histomathology and microbial culture examination. Histopathology showed chronic inflammatory changes accompanied by mild hyperplasia of alveolar epithelium. No bacterial was observed in lung tissue culture. Bronchoscope alveolar lavage fluid (BALF) examination revealed bronchial inflammation. Cytology of lavage fluid exfoliation: no cancer cells detected;mTB-DNA was not detect in BALF by Gene Xpert. No acid-fast bacilli were found in lavage fluid and sputum by acid-fast staining, and no hyphae and spores of bacteria and fungi were found by gram staining. Mycobacterium culture was negative. IgA, IgG, IgM, C3 and C4 were normal. Blood tests for white blood cells (WBC) 13.6×109/L (reference range:3.5–9.5×109/L),C-reactive protein (CRP) 64.67 mg/L (reference range < 6.0 mg/L), PCT 0.053mg/L (reference range: 0-0.046 ng/ml).
After treatment with cefoperazone sodium + sulbactam sodium + amikacin, the patient's symptoms(fever, cough and sputum) improved, but neurological symptoms such as headache, delirium and memory loss appeared on August 16.A magnetic resonance imaging (MRI) scan of the brain suggested space occupation in the left frontal lobe, the maximum cross-sectional area of the lesion was about 35mm×52mm, brain abscess was considered(Fig. 2.A).On August 28, the patient underwent minimally invasive puncture drainage under CT-guidance, and about 10mL yellow purulent fluid was extracted. The puncture fluid was sent to the microorganism laboratory for testing, after cultured for 48 hours, white cotton-like colonies grew. Aftersmear staining, branching and uneven staining of filamentous bacilli could be seen under the microscope (Fig. 3A-C). The mycelia could be wound into clusters to form actinomycetes like particles, gram stain and the weak acid-fast staining was positive. The bacteria were identified as Nocardia Farcinica by mass spectrometry,99.9% credibility. Then, the patient was diagnosed withNocardia farcinica brain abscess. After 16 days of treatment with trimethoprim/sulfamethoxazole (TMP/SMX)(1.2g − 5.0g, po, bid) and intravenous amikacin (0.4g, iv, qd), the patient’s temperature returned to normal and his headache completely disappeared, intracranial mass was significantly reduced(Fig. 2.B) and the right upper lung mass was significantly absorbed(Fig. 1.C).During subsequent treatment, the patient developed nausea and vomiting for many times, which was considered to be caused by cerebral edema. After treatment with mannitol dehydration, the symptoms were relieved. Re-examination of head MRI on October 23(Fig. 2.B), it showed that the brain abscess lesions were smaller than before, the brain edema was significantly better than before. Continue with the previous anti-infection treatment regimen.
On December 8, the patient had occasional mild chest tiredness, which relieved spontaneously, intermittent cough, nausea and retching, chest CT showed significant increase in lung lesions, partial bronchiectasis, emphysema and bullious lungs appeared. The patient developed dyspnea on December 12accompanied by wheezing sound in both lungs, sputum culture suggested Candida tropicalis, antifungal treatment with itraconazole and doxotheophylline for dyspnea. On December 15,the patient developed ARDS, blood pressure(BP): 100/75mmHg,arterial blood oxygen saturation (SaO2) 79%.After a series of treatments, including assistant respiration(mask oxygen inhalation), anti-inflammatory(methylprednisolone), antiasthmatic (doxofylline, salbutamol, ipratropium bromide), hyperensort(dopamine), the patient's dyspnea symptoms were not relieved and blood pressure did not rise(BP 77/52mmHg).The patient's family gave up the rescue. Subsequently, the patient goes into a deep coma, loses consciousness, and the heart rate drops. The patient died on the morning of the 16th.