Parainfluenza Virus Type 3 Post Stem Cell Transplant: High Prevalence but Low Mortality.

Parainfluenza virus type 3 (PIV 3) is a well recognised cause of respiratory illness after stem cell transplant (SCT) with an estimated incidence of 2–7%.(Wendt et al. N Engl J Med1992; 326: 921–926, Nichols et al. Blood2001; 98: 573–578). Persistently high mortality rates have been documented in this population. The largest series to date reported 75% mortality from PIV 3 lower respiratory tract infection.(Nichols et al). Treatment options are limited. There are anecdotal reports of successful use of ribavirin treatment but no randomised controlled trials have been undertaken.We undertook a retrospective review of 23 cases of PIV 3 occurring in adult SCT recipients over a 12 month period. A total of 145 patients had received a SCT in the same time period and 20 developed PIV3 infection (13.8%). The frequency of infection was 36.1% (13 of 36) in matched unrelated donor SCT recipients, 23.8% (5 of 21) in sibling allogenic SCT recipients and only 2.3% (2of 88) in autologous transplant recipients. Fourteen patients had received Campath 1-H as part of their conditioning regimen. The remaining three PIV 3 cases had a transplant date prior to the 12 month period. The median time from transplant to PIV 3 diagnosis was 54 days (range −7 to 2037 days). Only 6 cases were inpatients at diagnosis. Seventeen cases were outpatient or community acquired despite standard infection control procedures. Cases were identified by nasopharyngeal aspirate taken at the first sign of coryzal symptoms. Immunofluorescence (IF) identified PIV 3 in 13 patients and the virus was cultured in the remaining 10 cases. Eleven patients developed only upper respiratory tract symptoms and all survived. Lower respiratory tract symptoms and signs developed in 12 patients, of which 8 had a new infiltrate on chest X-ray. Four patients required invasive ventilation and one required non-invasive ventilation. Overall mortality at 30 days from PIV3 diagnosis was 4% (1 of 23). Three patients died in total but PIV 3 was not believed to be the primary cause of death in any of these patients. Autopsy confirmed post transplant lymphoproliferative disorder in one patient. The second case had septicaemia from a multiresistant coliform. Bronchoscopy in the remaining patient revealed invasive aspergillosis but IF and culture were negative for PIV 3. Early ribavirin treatment was administered in 8 patients. The primary indication for ribavirin treatment was lower respiratory tract infection. Six cases received aerosolised treatment, one intravenous and one patient received both aerosolised and IV therapy. Only one patient who received ribavirin treatment died. These results suggest a higher prevalence of PIV 3 but lower mortality than previously documented particularly in allogenic transplant recipients. We propose that the high prevalence reflects our unit policy of active surveillance for respiratory viruses and the difficulty in preventing transmission of PIV 3 especially in the outpatient setting. Ribavirin treatment may improve outcome in patients with lower respiratory tract infection but is not required in all patients with PIV 3 infection.