Ž nencephaly in cattle is analogous to that in sheep MacLachlan and Osburn, 1983;
. MacLachlan et al., 1985 . The severity of the cerebral malformation is inversely
proportional to the gestational age of the fetus at infection. Fetuses inoculated very early Ž
. in gestation between 70 and 85 days of gestation , if they survived infection, had the
Ž .
most severe CNS malformations hydranencephaly, cerebellar destruction at birth,
whereas fetuses inoculated within a few weeks of parturition had mild encephalitis but Ž
. no malformations Waldvogel et al., 1992 . The critical period would appear to range
from approximately 70 to 130 days of gestation, with fetuses inoculated at the later stage of this period having only cerebral cysts and dilated lateral ventricles.
4.3. BTV-induced abortion in ruminants BTV infection of both fetal cattle and sheep can occasionally result in abortion, but
teratogenesis is more common. Although definitive studies are lacking, it is likely that BTV-induced abortion utilizes the same pathway as for normal delivery. However, fetal
death also may, depending on the stage of gestation and the source of hormonal control of pregnancy result in the expulsion of the uterine contents. It is to be emphasized that
pregnant sheep and cattle can abort in the absence of any fetal infection or disease, presumably as a direct consequence of maternal stress.
5. EAV infection of the equine fetus
5.1. Introduction Ž
. EAV was first isolated in 1953 in the US Doll et al., 1957 . The virus can cause
abortion of pregnant mares, interstitial pneumonia in foals, and a generalized influenza- like illness in adult horses that is characterized by fever, peripheral edema, and nasal
Ž .
discharge Huntington et al., 1990; Timoney and McCollum, 1993 . Outbreaks of equine viral arteritis have been reported in both North America and Europe, and serological
surveys indicate that the virus is widespread. Although confirmed occurrences of clinical viral arteritis have increased in recent years, the majority of infections are subclinical
and asymptomatic infection is especially prevalent among Standardbred and the Warm-
Ž .
blood breeds of horses Timoney and McCollum, 1993 . The pathogenesis of EAV infection of the horse has been described. After respiratory infection, the virus first
replicates in pulmonary macrophages, it then proliferates in macrophages and endothe- lial cells in the lungs and bronchial lymph nodes, and then it rapidly spreads in the
Ž circulation to infect endothelial cells and macrophages throughout the body McCollum
. et al., 1971; MacLachlan et al., 1996 . Although endothelial cells and macrophages are
the principal sites of virus replication, selected epithelial cells, mesothelium, and smooth Ž
muscle cells of the media of arteries and the myometrium may also be infected Henson .
and Crawford, 1974; Wada et al., 1994 . Although EAV infection of pregnant mares can result in abortion, the pathogenesis of fetal infection and the mechanism responsible for
Ž abortion are not adequately understood Coignoul and Cheville, 1984; Cole et al., 1986;
. Johnson et al., 1991 . Strains of EAV appear to vary in their abortigenic potential.
Abortion can occur during either the acute or early convalescent stage of infection, and abortions have been described at anywhere between 3 months of gestation to nearly
term. Aborting mares usually exhibit no obvious signs of viral arteritis, and aborted Ž
. fetuses are delivered in either an autolyzed or non-autolyzed fresh state.
5.2. EAV-induced abortion The major concern and adverse impact of equine viral arteritis is abortion of pregnant
Ž .
mares Huntington et al., 1990; Timoney and McCollum, 1993 . Transplacental viral infection of the fetus does occur during EAV infection of pregnant mares, however,
Ž histologic lesions are seldom present in fetal tissues including placenta Jones et al.,
. 1957; Coignoul and Cheville, 1984; Cole et al., 1986; Johnson et al., 1991 . Myometrial
necrosis can be a feature of EAV infection, and some workers have attributed EAV-in- duced fetal death to decreased blood supply to the fetus as a consequence of virus-in-
duced injury to the myometrium, rather than to any direct effect of the virus on the fetus
Ž .
itself Coignoul and Cheville, 1984; Wada et al., 1994 . It was also proposed that virus in the fetus reflected only contamination attributable to increased permeability of the
Ž .
placenta Coignoul and Cheville, 1984 . More recent data clearly indicates that EAV does infect the fetus, although histologic changes in fetal tissues can be subtle or
Ž .
etiologically non-specific MacLachlan et al., 1996 . The fact that titers of EAV in fetal blood can be considerably higher than those in maternal blood would suggest that virus
in the fetus does not reflect mere ‘‘contamination’’ from the dam. Similarly, the relative abundance of viral antigen in fetal tissues, as compared to those of the dam, confirms
that the presence of EAV in fetal tissues does not reflect simple contamination.
6. Conclusions
