The latest study published in the journal presented a case report of an elderly man with severe community-acquired pneumonia (CAP) caused by human metapneumovirus (hMPV).
hMPV was first identified in 2001 and is increasingly recognized as a respiratory pathogen with significant health consequences. It is associated with a variety of respiratory diseases, such as lower and upper respiratory tract infections, and causes symptoms similar to other respiratory viruses. Therefore, the overlapping clinical findings of hMPV and other pathogens highlight the need for precise diagnostics.
hMPV is spread mainly through sneezing, coughing, close personal contact and exposure to contaminated surfaces. These modes of transmission pose risks in healthcare settings where appropriate control measures are necessary to prevent nosocomial transmission. As highlighted in the case report, the virus remains infectious for up to a week after the onset of symptoms, requiring vigilance among healthcare workers.
Severe symptoms often occur in young children, the elderly and people with weakened immune systems. Studies on severe hMPV infection have mainly been conducted in pediatric populations. Therefore, data in the adult population remain limited. CAP is a significant cause of morbidity and mortality worldwide. Vaccination programs have successfully reduced bacterial CAP. However, there are still gaps in knowledge about the microbiological etiology of severe CAP requiring hospitalization, especially in the case of respiratory viruses such as hMPV.
Investigation and findings
In this study, researchers from Brazil reported a case of severe hMPV-induced pneumonia in an immunocompetent older adult. The patient was a 68-year-old man, chronically taking aspirin, with a history of dyslipidemia and mild systemic arterial hypertension. The subject was physically active, a non-smoker, without obesity, diabetes or other comorbidities, and had gradually worsening respiratory symptoms.
Initial symptoms (on day 1, D1) were intermittent dry cough and mild odynophagia, which progressed to nasal congestion, rhinorrhea, night sweats, and allodynia on D2. Self-administered nasopharyngeal swab tested negative for severe acute respiratory syndrome virus 2 (SARS-CoV-2). The patient was then started on treatment with amoxicillin with clavulanic acid, prednisone and clarithromycin.
Nevertheless, the patient’s condition deteriorated with intense cough, bronchospasm, myalgia, fatigue and headache, resulting in admission to the emergency department on D7. Laboratory test results showed elevated inflammatory markers, including C-reactive protein (7.6 mg/dl) and D-dimer (870 ng/ml), thrombocytopenia, a mild increase in transaminases, and normal procalcitonin and leukocyte levels, suggesting an etiology viral. Imaging studies showed significant lung involvement.
Chest computed tomography (CT) showed mild bilateral pleural effusions, ground glass opacities interspersed with areas of consolidation, and small centrilobular opacities. These findings were consistent with viral pneumonia and mainly involved the left lower and upper lobes. Moreover, computed tomography of the paranasal sinuses revealed thickening of the mucosa of the frontal sinus.
During hospitalization, the patient received nebulization with oxygen, intravenous moxifloxacin, salbutamol, ipratropium bromide and physiotherapy. The patient’s condition stabilized within 24 hours and he was discharged home on oral treatment with moxifloxacin. Over the next week, the patient’s condition gradually improved, achieving recovery by day 14 after discharge from the hospital. During hospitalization, other diagnostic evaluations included molecular testing using a multiplex reverse transcription polymerase chain reaction (RT-PCR) panel, which identified hMPV.
No other viral or bacterial pathogens were detected. Venous blood gas analysis showed metabolic compensation, with a venous blood pH of 7.41 and a bicarbonate level of 30.4 mmol/L. Hematological test results showed normal white blood cell counts, with a predominance of neutrophils and mild thrombocytopenia. Platelet levels stabilized the next day, and there were minimal fluctuations in hematological and inflammatory markers throughout the hospital stay.
Conclusions
The present study highlights that hMPV can cause severe pneumonia in immunocompetent adults without comorbidities. This highlights the growing recognition of hMPV as a common cause of CAP across age groups, particularly as bacterial infections decline. Radiological findings such as ground glass opacities and bilateral consolidations are characteristic of viral pneumonia, further confirming this disease diagnosis. Of note, despite molecular tests demonstrating hMPV as the sole pathogen, antibiotic therapy was initiated due to continued diagnostic uncertainty in differentiating between bacterial and viral infections.
Overall, this case report highlights the importance of rapid molecular diagnosis of hMPV, improving treatment and reducing unnecessary antibiotic use. The study also highlights the worldwide problem of underdiagnosis of hMPV in adult populations, emphasizing the need to include it in routine diagnostic procedures. Incorporating hMPV testing into routine clinical protocols could improve diagnosis and resource utilization. Furthermore, addressing the global burden of hMPV requires continued investment in diagnostics and therapies to improve outcomes and reduce morbidity.
Additionally, vaccine development, such as the investigational bivalent IVX-A12 vaccine targeting both hMPV and RSV, holds promise for reducing disease burden and improving prevention strategies.
Magazine number:
Carmo, R., Saddy, F., Costa, J. L., Tavares, L. R., & Caire, H. (2024). The silent threat of human metapneumovirus: clinical challenges and diagnostic insights in severe pneumonia. Microorganisms, 13(1), 73. DOI: 10.3390/microorganisms13010073, https://www.mdpi.com/2076-2607/13/1/73