Fatal Pulmonary Infection With Respiratory Syncyti
Fatal Pulmonary Infection With Respiratory Syncyti
Fatal Pulmonary Infection With Respiratory Syncyti
OPEN
Abstract
Rationale: Respiratory syncytial virus (RSV) is a single-stranded negative-sense RNA virus that belongs to the family of
paramyxoviruses. RSV is the most common pathogen that causes acute lower respiratory tract infection in infants and young
children. However, its incidence in immunocompromised adults remains unclear. In the present study, we report an adult patient with
chronic nephropathy, who received long-term immunosuppressants and died of rapid respiratory failure due to RSV infection.
Patient concerns: A 54-year-old male patient with chronic nephropathy, who received long-term immunosuppressants, was
admitted to the Department of Respiratory Medicine due to the symptoms of fever, cough, expectoration, and dyspnea.
Diagnoses: Pulmonary radiology revealed multiple bilateral ground-glass opacity. Laboratory tests revealed elevated inflammation
indicators, implying infection with bacteria, viruses, and/or fungi. Furthermore, the patient was positive for RSV antibodies, without
positive results for other pathogens. Moreover, the patient was immunocompromised due to the long-term use of corticosteroids and
immunosuppressants, as evidenced by decreased total IgG levels and reduced CD4 and CD8 T-lymphocyte counts.
Interventions and outcome: Despite the intensive anti-infection treatment and respiratory support, the patient developed rapid
progression, and subsequently died of respiratory failure.
Lessons: RSV infection should be fully considered in adults who are immunocompromised or have underlying diseases, such as
nephropathy patients receiving long-term immunosuppressants, especially in the presence of respiratory symptoms and computed
tomography (CT) chest findings of diffuse ground-glass opacities.
Abbreviations: BMI = body mass index, CRP = C-reactive protein, CT = computed tomography, ESR = erythrocyte
sedimentation rate, RSV = respiratory syncytial virus, WBC = white blood cell.
Keywords: adult, ground-glass opacity, immunosuppression, respiratory syncytial virus
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Wang et al. Medicine (2018) 97:29 Medicine
However, rare cases of RSV infection that cause adult lower fever accompanied by progressive dyspnea, cough, and expecto-
respiratory tract infection, or even mortality, have been reported. ration for 5 days. On admission, the BMI of the patient was
In the present study, we present a 54-year-old patient, who was 24.5 kg/m2, and his body temperature was 39.0°C. Furthermore,
receiving immunosuppressants and admitted to a hospital with the patient had symptoms of tachypnea (35 bpm) and severe
symptoms of fever, cough, expectoration, and dyspnea, and hypoxemia (SaO2 86%). On auscultation, the patient had good
was subsequently diagnosed with RSV infection. This patient air entrance bilaterally with scattered diffuse crackles and
eventually died, emphasizing the precaution of RSV infection in rhonchi. Furthermore, the chest CT scan revealed multiple
immunocompromised adults, especially in presence of respirato- ground-glass opacities (Fig. 1F–H), and laboratory tests (Table 1)
ry symptoms and chest computed tomography (CT) findings of revealed normal white blood cell (WBC) count, but with elevated
diffuse ground-glass opacities of the lung. neutrophil count, C-reactive protein (CRP), erythrocyte sedi-
mentation rate (ESR), and (1→3)-b-D-glucan (Table 2). The
patient was diagnosed as RSV infection on the fourth day of
2. Case presentation
hospitalization when positive RSV-Ab was detected.
A 54-year-old male who had a medical history of membranous On admission, the patient was immediately given respiratory
nephropathy II with nephrotic syndrome (Fig. 1A and B) was monitoring and supplemental oxygen to improve the low oxygen
administered with long-term oral glucocorticoids and immuno- saturation, as well as antibiotics (moxifloxacin for 4 days,
suppressants. The patient had a 20 pack-year history of smoking, followed by cefminoxine for 8 days), and antifungal therapy
and denied a family history of hereditary diseases. Chest x-ray (voriconazole for 10 days). The dose of the glucocorticoids and
demonstrated normal findings at one month before admission immunosuppressants remained largely unchanged (Table 3).
(Fig. 1C–E). On August 8, 2016, the patient was hospitalized for After 10 days of treatment, the patient’s condition became worse.
Figure 1. (A) Histological analysis for renal biopsy (H&E staining) revealed focal segmental glomerulosclerosis with mild mesangial cell hyperplasia, endothelial cell
proliferation and thickening of the glomerular capillary walls, but with open glomerular tuft. Focal tubular epithelial cell atrophy was observed. (B) Periodic acid
methenamine–Masson staining revealed diffuse, segmental lesions as visible mesangial deposition, without “tram-track" appearance. (C–E) Chest CT scan at one
month before admission revealed normal findings. (F–H) Chest CT scan on admission revealed bilaterally diffuse ground-glass opacities in the lungs. (I–K) Chest CT
scan at the 10th day after admission indicated disease progression. (L) Chest x-ray at 15th days after admission revealed extensive diffuse ground-glass
opacification, which worsened compared to that of before. (M) Bronchoscopy pathology revealed pulmonary interstitial fibrosis, hyperplasia of the alveolar
epithelium and necrosis in the alveolar cavity.
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Wang et al. Medicine (2018) 97:29 Medicine
Figure 2. The clinical process for the diagnosis of widespread ground-glass opacity. BAL = bronchoalceolar lavage, COP = cryptogenic organizing pneumonia,
DAH = diffuse alveolar haemorrhage, ELISA = enzyme linked immunosorbent assay, ILD = interstitial lung disease, PCP = pneumocystis carinii pneumonia, PCR =
polymerase chain reaction.
the initial performance of diffuse ground-glass opacities was the patient presented with positive RSV-Ab without positive
accompanied by interstitial fibrosis, and this subsequently results for other pathogens. Considering the impairment of
gradually developed into pulmonary fibrosis and traction immunity in the patient, empiric broad-spectrum antibiotics were
bronchiectasis with a small amount of inflammatory exudates; used to ensure coverage of both typical and atypical organisms.
Table 3
Medical history and medications.
Time Description
Medical diagnosis 4 months before Nephrotic syndrome, membranous nephropathy II
Medications 4 months before Methylprednisolone (60 mg qd po, tapered 4 mg every 2 months); cyclophosphamide (50 mg bid po); Irbesartan felodipine (10 mg qd po)
At admission Methylprednisolone (48 mg qd po); cyclophosphamide (50 mg bid po)
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Table 4
Arterial blood gas analysis.
Admission 4 days 8 days 10 days 15 days Reference range
pH 7.52↑ 7.53↑ 7.50↑ 7.46↑ 7.36 7.35–7.45
PaCO2, mm Hg 31↓ 27↓ 30↓ 34↓ 52 35–45
∗
PaO2, mm Hg 60 53↓ 47↓ 27↓ 75 60–100
HCO3 , mmol/L 25.3 22.6 23.4 24.2 29.4↑ 21.3–27.3
Base excess, mmol/L 2.8 0.4 0.5 0.9 3.1↑ 3–+3
∗
The sample was collected at 3 hours after invasive ventilator-assisted ventilation therapy (SIMV, PEEP6, PS24, FiO2 85%, RR24/min, and RRspn16/min).