A 50-year-old man with a high fever, non-productive cough, and progressive dyspnea for three days was admitted to our hospital. The body temperature was between 39.4 C and 40 C, accompanied by chills. He was a healthy man before the onset. He denied tuberculosis infection history or other infectious disease exposure history and no history of smoking or alcohol abuse. After moxifloxacin 0.4 g, I.V., qd in an external hospital for two days, his symptoms did not relieve. A chest CT scan was performed 24 hours before admission showing pulmonary infiltrate and consolidation in the lower lobe of the right lung (Figure 1A-C). 
His vital signs of physical examinations at admission were as follows: temperature 39.5 C, pulse rate 118 beats/ min, blood pressure 128 / 80mmHg, respiratory rate 34 breaths/min. He was tachypnea, and his lips were cyanotic. His saturation of peripheral oxygen was 88% with mask oxygen inspiration (5L/min). Wet rales could be heard in the lower lobe of the right lung. The rest of the physical examination was roughly normal.
Laboratory tests on admission showed white cell count 10.7x10^9/L (reference range:4-10x10^9/L), neutrophil ratio 95% (50-70%), hemoglobin 151 g/L (120-160 g/L), and platelet count 221x10^9/L (100-300x10^9/L). C reactive protein was 272mg/L (0-3mg/L). Erythrocyte sedimentation (ESR) was 38mm/1h (0-20 mm/1h). Procalcitonin (PCT) was 0.62ng/mL (<0.5ng/mL). His renal function was normal. He had severe liver function damage. His aspartate aminotransferase (AST) was 195 IU/L (8-40 IU/L), alanine aminotransferase (ALT) 112 IU (5-40 IU/L), albumin 23 g/L (35-55 g/L). The laboratory tests revealed electrolyte disorders- hyponatremia and hypochloremia. Serum sodium concentration was 128mmol/l (130-150mmol/l), chloride concentration 95mmol/l (96-106mmol/l).
No etiological evidence was found. Sputum culture results, acid-fast bacilli stain, and GeneXpert MTB/RIF assay was negative. Nasal swabs for detection of Covid-19, influenza virus, adenovirus, and respiratory syncytial virus also found nothing.
Intravenous infusion of moxifloxacin 0.4g was continued after admission. A chest CT scan was reexamined the next day after admission. The lung shadow progressed rapidly, showing multiple patchy ground-glass opacity and consolidation in both lungs (Figure 1D-F). The patient's condition deteriorated, with persistent high fever (39-40 C), and worsening dyspnea. With mask oxygen inhalation of 10L/min, arterial blood gas analysis revealed pH 7.52, PO2 40 mmHg (83-108mmHg), PCO2 25 mmHg (35-48mmHg), and HCO3- 24.5 mmol/L (18-23mmol/L). He was treated with non-invasive mechanical ventilation in S/T mode with IPAP 15cmH2O, EPAP 6cmH2O, and FiO2 60%, which could achieve a tidal volume of about 450mL and minute ventilation of 9L/min and peripheral oxygen saturation of 94%. The patient progressed rapidly and was diagnosed with progressive pneumonia. We considered that the disease progressed rapidly, and the risk of death was high. We adjusted the anti-infection therapy regime according to common pathogens of progressive pneumonia. Moxifloxacin was discontinued and upgraded to tigecycline 100mg, I.V., q12h to cover for atypical pathogens, gram-positive cocci, and drug-resistant bacteria. At the same time, extended-spectrum antibiotic meropenem 1.0g, I.V. q8h was combined. In addition, oseltamivir 75mg, P.O., bid was administered to cover the influenza virus.
While adjusting the anti-infective regimen, we performed fiberoptic bronchoscopy alveolar lavage in the basal segment of the lower lobe of the right lung and sent the bronchoalveolar lavage fluid (BALF) for mNGS detection. We also conducted tests related to rheumatic connective tissue disease. Connective tissue assays including immunoglobulin levels (IgG, IgM, IgA, and IgE), anti-ARS antibodies (anti-Jo-1, anti-MDA-5, anti-PL-7, anti-PL-12, anti-EJ, anti-KS antibodies), antinuclear antibodies (ANA), rheumatoid factor, cyclic citrullinated peptide antibodies, cytoplasmic antineutrophil cytoplasmic antibodies (cANCA), and perinuclear antineutrophil cytoplasmic antibodies (p-ANCA) antibody titers were all within normal parameters, which provided no clue to rheumatic connective tissue disease.
On the seventh day of admission, mNGS of BALF indicated C. psittaci (sequence reads: 205) and Candida albicans (sequence reads: 50). Upon close investigation, the patient had kept a pet bird a week before the onset of the disease. Until the patient was admitted to hospital, the bird did not appear abnormal. On the second day after tigecycline, the fever had gone down, and dyspnea was alleviated. After the mNGS results were reported, we adjusted the treatment regimen: we stopped meropenem and oseltamivir, and doxycycline 0.1g, P.O., q12h was successively administered for 14 days after 7 days of tigecycline administration. After 21 days of anti-psittacosis treatment, the patient's general condition was significantly improved, and there was no complaint of comfort. The patient's body temperature changes and treatment process were shown in Figure 2. A reexamination of chest CT revealed that the infiltrate was obviously absorbed (Figure 1G-I).