Clinical characteristics of Chlamydia psittaci pneumonia

Psittacosis is a zoonosis caused by Chlamydia psittaci, a Gram-negative intracellular bacterium. This condition is caused by the ingestion of contaminated fecal matter and nasal secretions from infected birds. The severity of human psittacosis varies from mild flu-like symptoms to life-threatening severe pneumonia.[1] Given that C. psittaci is not a part of the traditional microbiological diagnosis’ human psittacosis is often underreported, misdiagnosed, and inadequately diagnosed. In this study, the clinical data of C. psittaci pneumonia patients were retrospectively analyzed. Specifically, we analyzed five consecutive cases of C. psittaci pneumonia, who were admitted to The Fourth Affiliated Hospital of Zhejiang University School of Medicine, between December 2019 and May 2020. We screened the hospital's electronic case system and extracted data on demographics, symptoms, signs, laboratory tests, disease severity, dynamic computed tomography, tracheoscopy, and clinical course of each case. We also collected data on treatment prescription, treatment response, and prognosis. The study was approved by the Ethics Committee of the Fourth Affiliated Hospital of Zhejiang University School of Medicine (Approval No. K2020079). We had obtained written informed consent from all enrolled patients, and concealed their identifiable information as well as relevant images. Before enrolment, patients diagnosed with C. psittaci pneumonia had to meet the following three inclusion criteria: first, they complied with criteria for community-acquired pneumonia[2]; second, metagenomic next-generation sequencing (mNGS) from bronchoalveolar lavage fluid (BALF) revealed a specific deoxyribonucleic acid (DNA) fragment in C. psittaci; and third, all routine etiological tests, including blood, sputum, BALF smear, and cultures, were negative, with no other causative organisms present. We detected C. psittaci DNA fragments in all cases. A summary of copy numbers for C. psittaci nucleic acid in BALF detected by mNGS is shown in Table 1. C. psittaci was the dominant infection across all five cases. However, we simultaneously detected herpes simplex virus type 1 in one severe case, although its immunoglobulin M was negative, suggesting possible colonization or pollution. Two patients (40%) were positive for Chlamydia abortus, albeit with low copy numbers, whereas other patients exhibited low copies of Candida parapsilosis complex, Candida albicans, Staphylococcus epidermidis, Haemophilus influenzae, Burkholderia cepacia, or Acinetobacter baumannii, indicating colonization or pollution. Table 1 - Demographical and basic clinical features of the five patients. Case# Severity Age (years)/Sex Underlying diseases Poultry exposure Onset time (days) mNGS results and specific reads (n) Symptoms Signs 1 Severe 57/Female None Indirect∗ 7 Chlamydia psittaci (55307); herpes simplex virus type 1 (17392); Staphylococcus epidermidis (126); Haemophilus influenzae (9); Candida parapsilosis complex (9) High-feverCoughDyspnea 40.0°CApathyMoist ralesRelatively slow pulse 2 Severe 69/Male None Pigeon feces 7 Chlamydia psittaci (1233); Chlamydia abortus (61); Candida albicans (12) High-feverChillsCoughDyspnea 39.7°CApathyMoist rales 3 Non-severe 71/Male None None 3 Chlamydia psittaci (21); Haemophilus parainfluenzae (17) High-fever chills 40.5°CMoist ralesRelatively slow pulse 4 Non-severe 64/Male Hypertension Chicken 3 Chlamydia psittaci (362); Chlamydia abortus (18) High-feverCoughDyspnea 41.5°C 5 Non-severe 65/Female Hypertension, hyperlipidemia Pigeon 5 Chlamydia psittaci (73435); Burkholderia cepacia (99); Acinetobacter baumannii (85) High-feverNauseaVomitingWeak 40.0°C Case# Arterial blood gas analysis (mmHg) Inflammatory biomarkers Biochemistry Imaging Antibiotics Respiratory support Fever time(d)† Hospital stays (d) Outcome 1 FiO2:221PCO2:23.8 WBC:5500/μLNE:91.3%CRP:316.5 mg/LPCT:3.47 ng/L Lac:1.8 mmol/LLDH:679 U/LCK-MB:18.4 U/LCK:705 U/L Consolidation air bronchogram Moxifloxacin tigecycline Intubation ventilator 10 23 Cured 2 FiO2: 250PCO2:30.6 WBC:11500/μLNE:96.9%CRP:303 mg/LPCT:5.24 ng/L Lac:1.4 mmol/LLDH:1039 U/LCK-MB:57 U/LCK:1919 U/L Consolidation air bronchogram Moxifloxacin tigecycline Intubation ventilator 5 20 Cured 3 FiO2: 361PCO2:30.2 WBC:5200/μLNE:88.3%CRP:176.7 mg/LPCT:1.58 ng/L Lac:1.2 mmol/LLDH:265 U/LCK-MB:17.4 U/LCK:472 U/L Consolidation air bronchogram Moxifloxacin Oxygen 1.25 11 Cured 4 FiO2: 384PCO2:30.1 WBC:8700/μLNE:87.7%CRP:191.5 mg/LPCT:0.474 ng/L Lac:1.5 mmol/LLDH:216 U/LCK-MB:8.2 U/LCK:147 U/L Consolidation air bronchogram Moxifloxacin Oxygen 3 8 Cured 5 FiO2: 275PCO2:29.9 WBC:13200/μLNE:92.7%CRP:278.9 mg/LPCT:1.54 ng/L Lac:1.2 mmol/LLDH:265 U/LCK-MB:17.4 U/LCK:57 U/L Consolidation air bronchogram Moxifloxacin Oxygen 2 9 Cured ∗Workplace of case 1 was located upstairs of a farmers’ market (including poultry market areas). †Days from initiation of moxifloxacin therapy until patients’ body temperature returns to normal. ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; CK: Creatine kinase; CK-MB: Creatine kinase isoenzyme; CRP: C-reactive protein; FiO2: Oxygenation index; Lac: Lactic acid; LDH: Lactate dehydrogenase; mNGS: Metagenomic next-generation sequencing; NE%: Proportion of neutrophils; PCO2: Partial pressure of carbon dioxide; PCT: Procalcitonin; WBC: White blood cell. The study group comprised of two (40%) females and three (60%) males, with a median age of 65 (57–71) years. Among the enrolled patients, two (40%) had hypertension, one presented multiple disease states, including hyperlipidemia, hypertension, and pacemaker implantation status, whereas the other three (60%) were healthy. Medical records showed that three (60%) patients had a history of direct contact with domestic poultry before the onset of the disease. Here, one case had been fertilized with pigeon manure, one had newly reared chickens at home, one had reared pigeons, and one had a possible indirect environmental contact because her workplace was located upstairs of a farmers’ market (including poultry market areas), consistent with poultry transmissible zoonoses.[3] The median time from the onset of the first symptoms to admission was 5 (3–7) days. High fever was recorded in five patients. Cough and dyspnea were recorded in three patients, respectively. Fatigue was recorded in two (40%) patients. One patient manifested nausea and vomiting. Relatively slow pulse was recorded in two patients. Mental changes, presented as apathy was recorded in two severe patients. A few moist rales could be heard in three patients (60%). In this group, patients complained of neither headache nor muscle soreness, which was inconsistent with results from the previous reports.[4,5] Arterial blood gas analysis revealed type I respiratory failure in three patients (60%). The proportion of neutrophils was increased in five patients, while white blood cell count was increased in two patients. C-reactive protein (CRP) was high in five patients, whereas elevated levels of procalcitonin (PCT) were recorded in four cases. CRP and PCT were significantly higher in severe cases. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme elevated in all five patients. Hyponatremia was recorded in five patients, and hypokalemia and hypocalcemia were recorded in four patients. Chest CT showed air-containing bronchial shadow consolidation in all five (100%) patients. Specifically, scalloped or oval lesions originated from their pleura or interlobar fissures. As the disease progressed, these lesions incorporated the hilum and other lobes, including the contralateral lung lobe. In addition, the lesions originated from the left lower lung in four patients. Multi-lobe lesions recorded in two severe cases, whereas these lesions were confined to one lobe in three non-severe cases. Two patients had a little pleural effusion. Tracheoscopy revealed that all five patients were clean, with no additional secretions. All five patients were intravenously injected with 0.4 g moxifloxacin, once a day within 24 h of admission, in combination with β-lactam antibiotics. The three non-severe cases got better within 72 h. Two severe cases had aggravated respiratory failure, at 76 and 88 h after admission. They were intubated for ventilator-assisted breathing and admitted to intensive care unit (ICU). The two severe cases were intravenously injected with tigecycline 50 mg (first dose 100 mg) every 12 h in ICU, and they were cured at last. This indicated that non-severe cases respond better to moxifloxacin compared with severe ones. Our study has some limitations. First, we analyzed a small sample size that may not fully represent the clinical features of C. psittaci pneumonia. Second, this was a retrospective study. Future studies should analyze prospective clinical cases with larger samples. We conclude that C. psittaci pneumonia is common. History of poultry exposure, high fever, elevated inflammatory biomarkers, elevated LDH, coupled with air-containing bronchial shadow consolidation with little or no secretions may guide early clinical diagnosis of C. psittaci pneumonia. Metagenomic sequencing of BALF is an important method for diagnosing this condition. Conflicts of interest None.