The etiology of acute interstitial pneumonia (AIP) remains elusive since its original description. It has only recently described that rotavirus may cause interstitial pneumonia. We describe a case of fatal acute interstitial pneumonia in which rotaviral RNA was isolated by reverse transcription in-situ-PCR in alveolar macrophages and pneumocytes.
A 57-year-old white female with a 3-week history of progressive dyspnea on exertion preceded by 2 days of diarrhea and malaise. Her medical history was significant for ischemic cardiomyopathy and diabetes. She denied alcohol, illegal drugs or cigarrete smoking.Vitals on admission: respiratory rate 22 breaths/min, blood pressure 105/54 mmHg, heart rate 75 beats/min temperature 96.8 F, O2sat 98% room air. There was no jugular venous distention. She had bilateral coarse crackles. Heart exam disclosed regular rate and rhythm. There was no hepato-splenomegaly. She had bilateral lower extremity edema. Laboratory data: WBC 8,500 cells/ul, hemoglobin 10 mg/dl, arterial blood gas on room air revealed a pH of 7.49, pCO2 37 mmHg, pO2 74 mmHg. Chest X-ray showed interstitial pattern and bilateral pleural effusions.After a 6-day therapy with furosemide and empiric antibiotics her hypoxemia progressed. All subsequent cultures remained negative. A chest CT showed thickening of both inter and intralobular septa. A bronchioalveolar lavage showed 71% alveolar macrophages, 27% neutrophils, 2% lymphocytes and negative bacterial, fungal and viral cultures. Autoimmune panel was negative.The open lung biopsy showed extensive acute interstitial pneumonitis in an organizing fibroblastic phase with predominant type II pneumocyte hyperplasia. Reverse transcriptase in-situ-PCR studies were negative for adenovirus, Epstein-Barr virus, cytomegalovirus and herpes virus but strikingly positive for rotavirus RNA in macrophages and pneumocytes. After the biopsy the patient remained hypoxemic and despite treatment with high dose steroids she expired.
Acute interstitial pneumonia is characterized by diffuse alveolar damage similar to the Acute Respiratory Distress Syndrome. It has an initial exudative phase that progresses to a proliferative phase within one week. As in the majority of reported cases, our patient’s biopsy showed prominent type II pneumocyte proliferation. Although AIP is idiopathic a number of clinical situations such as infections, drugs, connective tissue diseases, and vasculitides may cause a pattern of diffuse alveolar damage similar to AIP. Viral infections may cause pneumonitis, however there have been only two reported cases of fatal pneumonits in which rotaviral RNA was isolated in the lungs. One had a similar clinical presentation, an upper respiratory illness that progressed to a fatal respiratory failure over several weeks. His biopsy showed acute interstitial pneumonitis in the proliferative phase, and rotaviral RNA was localized in alveolar macrophages and pneumocytes. The other reported patient had a more acute course and he died 2 days after admission. His autopsy showed marked septal capillaritis and prominent denudement of the alveolar lining. Viral RNA was found in endothelial cells, pneumocytes and alveolar macrophages. Although all cultures were negative for viruses a recent study demonstrated that RT-PCR was more sensitive identifying viruses causing lower respiratory infections compared with the traditional cell culture methods. In our patient the presence of viral RNA most likely represents an acute infection, as rotavirus does not cause latent infections.
The strong presence of rotaviral RNA in alveolar macrophages and pneumocytes suggests its pathogenic role in our patient’s AIP. However the virus could only be an innocent bystander or a contributing factor in the progression to respiratory failure in a patient with established idiopathic interstitial pneumonia. More studies using RT in- situ-PCR would be helpful to understand the roll of viruses in the pathogenesis of AIP.
Martin Valdivia-Arenas, None.