Abstract
The transmission of chronic wasting disease (CWD) has largely been attributed to contact with infectious prions shed in excretions (saliva, urine, feces, blood) by direct animal-to-animal exposure or indirect contact with the environment. Less-well studied has been the role that mother-to-offspring transmission may play in the facile transmission of CWD, and whether mother-to-offspring transmission before birth may contribute to the extensive spread of CWD. We thereby focused on a population of free-ranging white-tailed deer from West Virginia, USA, in which CWD has been detected. Fetal tissues, ranging from 113 to 158 days of gestation, were harvested from the uteri of CWD+ dams in the asymptomatic phase of infection. Using serial protein misfolding amplification (sPMCA), we detected evidence of prion seeds in 7 of 14 fetuses (50%) from 7 of 9 pregnancies (78%), with the earliest detection at 113 gestational days. This is the first report of CWD detection in free ranging white-tailed deer fetal tissues. Further investigation within cervid populations across North America will help define the role and impact of mother-to-offspring vertical transmission of CWD.
Highlights
Investigations into the transmission dynamics of chronic wasting disease (CWD) have primarily focused on the presence of the infectious agent in bodily fluids and excretions of infected cervids [1,2,3,4]
The prevailing hypothesis is that contact with prions shed by CWD-infected cervids via animal-to-animal contact, or presumed ingestion of prions from contaminated environments represent the majority of CWD spread among cervids
CWD status was confirmed by immunohistochemistry (IHC) on medial retropharyngeal lymph node (RPLN) and obex according to standard protocols at the Southeastern Cooperative Wildlife Disease Study (SCWDS; University of Georgia, Athens, GA, USA)
Summary
Investigations into the transmission dynamics of chronic wasting disease (CWD) have primarily focused on the presence of the infectious agent (prions) in bodily fluids and excretions of infected cervids [1,2,3,4]. Further investigation led to reports of scrapie-associated aberrant prion protein (PrPScrapie ) deposition within maternal and fetal tissues [8,9,10,11,12,13,14,15], as well as the presence of prion infectivity within placental tissues [16,17], fetal tissues [18], embryos [14], and milk of scrapie-infected dams [19,20,21,22,23] This effectively demonstrated a role for maternal transmission, with increasing evidence for prebirth fetal exposure to scrapie. Further studies in our maternal infection model led to the discovery of the infectious agent within the pregnancy microenvironment (uterus, placentomes, amniotic fluid) [25] This piqued our interest to investigate the biological relevance of mother-to-offspring transmission in free-range cervid populations. For the first time, prion seeding activity within fetal tissues of naturally exposed free-ranging asymptomatic CWD+ white-tailed deer
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