Has been reported as early
as 1 week and as late as 12 weeks after exposure (1,2).
Proposed mechanisms
for the development of fetal hydrops include:
Fetal anemia. The
virus infects erythroid precursor cells resulting in erythroid
hypoplasia, shortened red cell survival and hemolysis (3). Fetal anemia
as low as 1.7 g/l has been reported (4).
Cardiac failure
secondary to a viral myocarditis. Parvovirus has been reported in
cardiac muscle of infected fetuses (5). The anemia results in tissue
hypoxia when results in a compensatory compensatory increase in cardiac
output and hydrops (6).
Spontaneous resolution
of the hydrops, although rare has been reported (7).
Public Health Laboratory
Service Working Party on Fifth Disease: Prospective study of human
parvovirus (B19) infection in pregnancy. Br Med J 1990;300:1166-1170.
Bond PR, Caul EO, Usher J
et.al. Intrauterine infection with human parvovirus. Lancet
1986;1:448-449.
Burron PA, Caul EO. Fetal
cell trophism of human parvovirus B19. Lancet 1988;1:767 (letter).
Anderson MJ, Khousam MN,
Fleming KA. Human parvovirus B19 and hydrops fetalis. Lancet 1988;1:535.
Porter HJ, Quantrill AM,
Fleming KA. B19 parvovirus infection of myocardial cells (letter). Lancet
1988;1:535-536.
Pryde PG, Nugent CE, Pridjian
et.al. Spontaneous resolution of nonimmune hydrops fetalis secondary to
human parvovirus B19 infection. Obstet Gynecol 1992;79:859-861.
Bhal PS, Davies NJ,
Westmoreland D et.al. Spontaneous resolution of non-immune hydrops fetalis
secondary to transplacental parvovirus B19 infection. Ultrasound Obstet
Gynecol 1996;7:55-57.