Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome
Wg. Nichols et al., Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome, BLOOD, 98(3), 2001, pp. 573-578
Parainfluenza virus (PIV) infections may be significant causes of morbidity
and mortality in patients undergoing stem cell transplantation, but data r
egarding their impact on transplant-related mortality is limited. This stud
y sought to determine the risk factors of PIV acquisition and progression t
o lower respiratory tract infection, their Impact on transplant-related mor
tality, and the effectiveness of antiviral therapy. A total of 3577 recipie
nts of hematopoietic stem cell transplantation (HSCT) between 1990 and 1999
were studied. PIV infections occurred in 253 patients (7.1%); 78% of these
infections were community acquired. Multivariable analysis identified the
receipt of an unrelated transplant as the only risk factor for PIV acquisit
ion; the dose of corticosteroids at the time of PIV infection acquisition w
as the primary factor associated with the development of PIV-3 pneumonia, b
oth among allogeneic and autologous HSCT recipients. Both PIV-3 upper respi
ratory infection and pneumonia were associated with overall mortality. Pulm
onary copathogens were isolated from 29 patients (53%) with pneumonia. Mort
ality was highly influenced by the presence of copathogens and the need for
mechanical ventilation. Aerosolized ribavirin with or without intravenous
immunoglobulin did not appear to alter mortality from PIV-3 pneumonia, nor
did such therapy decrease the duration of viral shedding from the nasophary
nx among patients with pneumonia. Corticosteroid administration thus drives
the development of PIV pneumonia in a dose-dependent fashion, even among a
utologous HSCT recipients. Both upper and lower tract PIV infections are pr
edictors of mortality after HSCT. Currently available antiviral therapy app
ears to be inadequate in reducing viral shedding or mortality once pneumoni
a is established.