A 7-year-old boy was admitted to the hospital for a fever with a maximum temperature of 38.1 C and paroxysmal coughing, dyspnea, and cyanosis of the lips for two days, without spasmodic coughing, wheezing, digestive symptoms, or joint pain. Self-measured SPO2 was 89%. Therefore, he was admitted to a hospital and underwent intravenous administration of amoxicillin and clavulanate potassium for one day, meropenem once, and nebulization, mask, and high-flow oxygen therapy. Still, his condition did not improve, so he was transferred to our hospital for treatment.
Past medical history: The patient had a history of multiple episodes of wheezing and "asthma " but had not experienced wheezing attacks in the past two years. He underwent tonsil and adenoidectomy surgery three years ago. There was no history of immunodeficiency, no use of immunosuppressive drugs, and no contact with patients infected with T whipplei.
Physical examination on admission: temperature 38.1 C, pulse 136 bpm, respiratory rate 34 bpm, blood pressure 118/67 mmHg, SPO2 96% (mask oxygen inhalation 6 L/min), clear consciousness, low spirit, rapid breathing, three depressions sign, low breath sounds in the left lung, no rhonchi and crackles heard in both lungs and no abnormalities found in cardiac and abdominal examinations.
The laboratory test in another hospital revealed blood routine: white blood cell 20.1 x 10 9/L, neutrophil 92.6%, lymphocyte 4.3%, C-reactive protein 1.2 mg/L. Blood gas analysis in another hospital showed a PH 7.387, PaCO2 39.2 mmHg, PaO2 56 mmHg, HCO3- 21.9 mmol/L, BE -0.31, Lac 2.1 mmol/L. The chest CT from our emergency department revealed consolidation in the left lung and occlusion of the left upper lobe bronchus (Figure 1).
After admission, several examinations were completed. Complete blood count showed white blood cell 21.11 x 109/L, with 96.4% neutrophil and 2.3% lymphocyte, and C-reactive protein 11.81 mg/L. Arterial blood gas analysis showed a pH of 7.42, PaCO2 34.4 mmHg, PaO2 78.9 mmHg, HCO3- 22 mmol/L, BE -1.8, and Lac 4.3 mmol/L. The patient's procalcitonin level was 0.325 ng/ml. Immunoglobulin and lymphocyte subgroup tests were normal, suggesting no immunodeficiency. Pathogen tests examinations for influenza A and B, respiratory syncytial virus, adenovirus, Chlamydia, coronavirus, rhinovirus, Mycoplasma pneumoniae, human metapneumovirus, Bocavirus, parainfluenza virus, Ureaplasma urealyticum, and Chlamydia trachomatis were negative. EB virus antibody and tuberculosis-related tests were negative. The G and GM tests were negative, and the pharyngeal swab and lavage culture was normal.
The patient received nasal high-flow warm and humidified oxygen therapy upon admission. On the same day, bronchoalveolar lavage was performed, and sputum plugs were removed. Metagenomic Next-Generation Sequencing was performed on the lavage fluid, and a follow-up chest x-ray showed increased transparency in the left lung (Figure 2). Subsequently, the patient received intravenous azithromycin to fight off infection, methylprednisolone to suppress inflammation, ambroxol to liquefy sputum, and nebulized inhalation. The results on day 3 showed T whipplei (with a sequence count of 261) and Streptococcus mitis (with a sequence count of 6) in the lavage fluid. So azithromycin was discontinued (after three days of administration) and replaced with intravenous piperacillin-tazobactam for five days (150 mg/kg.d). After five days of anti-infection treatment, the patient's blood test results were normal. The patient was discharged on the eighth day of treatment. The re-examed chest x-ray on the day of discharge suggested that the left lung lesion had significantly improved (Figure 3). The patient continued to take oral amoxicillin and clavulanate potassium for four days after discharge.
Discharge diagnoses were respiratory failure, severe pneumonia, and plastic bronchitis. One-month follow-up after discharge showed no cough and fever and normal symmetrical breathing sounds in the lungs, and the condition did not recur.
Ct scan on the day of admission (complete consolidation of the left upper lobe, bronchial obstruction of the left upper lobe, and large areas of high-density shadows in the left lower lobe).