Maternal Infection with Chronic Wasting Disease Reduces Fetal Head Size

Chronic wasting disease (CWD) is a fatal neurological disease of cervids caused by an infectious protein (prion) that has been detected in Illinois’ wild white-tailed deer herd since 2002¹. Transmission of CWD is usually through direct contact with an infected animal and its bodily fluids². Still, consumption of prion-contaminated plants³, water⁴, or soil⁵ or vertical transmission from mother to fetus may also cause infection⁶. That means a fawn could be born infected with CWD, but even if infection does not occur in utero, CWD impacts an animal’s ability to eat, thus a CWD-positive female deer may suffer from nutritional deficiencies⁷ before the onset of visible signs and the characteristic wasting (weight loss). This raises the question of whether fetal growth is impacted by CWD, particularly the brain and other neurological tissues. To explore this possibility, we used data collected from 18 counties in Illinois (Figure 1) to examine the impact of maternal CWD infection and other variables on fetal head size⁸, which is directly proportional to brain size⁹.

We selected fetuses from known CWD-positive and CWD-negative deer. It should be noted that whether the fetuses were infected was unknown due to difficulties with detecting low prion concentrations at early stages of disease. Three different head measurements were examined in this study: (1) distance between the tip of the nose and the occipital bone, (2) distance from the frontal to the occipital bone, and (3) the circumference of the head from the crown (top) to the jaw (bottom) (Figure 2).

The first step in the analysis was identifying factors that may impact fetal head size, and selecting eight variables: (1) fetal weight, (2) fetal body length, (3) fetal sex, (4) maternal age, (5) maternal weight, (6) number of fetuses in the litter, (7) deer habitat quality and quantity (land cover utility score)¹⁰, and (8) the day of the year the female deer died. We also included a ninth variable to account for CWD status. A regression model used the eight variables as the “control variables” to account for differences in head sizes between fetuses (due to fetal, maternal, and environmental characteristics) other than maternal CWD status, isolating the effect of the ninth variable (maternal CWD infection). The results of the model showed that fetal head size increased with fetal body size, and when maternal age and weight increased. Fetal head size also increased with deer habitat quality and quantity, but decreased with larger litters. The model also found that fetuses of CWD-positive female deer had smaller heads than those of CWD-negative deer. Specifically, fetuses of CWD-infected females had nose-occipital lengths and crown-jaw circumferences smaller (6.76% and 11.31% respectively) than their CWD-negative counterparts⁸.

This finding could have serious implications for fawn survival and success after birth. Though no studies have evaluated the impact of smaller brains on cervids, studies in humans have found delayed and/or impaired cognitive development and problems with vision and hearing^11,12. A study of prion diseases in non-human primates suggests that, because smaller brains have less neural tissue, prion-infected animals with smaller brains may die faster¹³; which may shorten the lifespan of fawns born with CWD or infected soon after birth. This study demonstrates an additional impact of CWD infection, suggesting long-term consequences for the newborn and the herd.

References

1. Illinois Department of Natural Resources. (2003). Chronic Wasting Disease Surveillance Summary: Status of CWD in Illinois.
2. Pritzkow, S. (2022). Transmission, strain diversity, and zoonotic potential of chronic wasting disease. Viruses, 14(7), 1390.
3. Carlson, C. M., Thomas, S., et al. (2023). Plants as vectors for environmental prion transmission. Iscience, 26(12).
4. Nichols, T. A., Pulford, B., et al. (2009). Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. Prion, 3(3), 171-183.
5. Kuznetsova, A., Ness, A., et al. (2024). Detection of chronic wasting disease prions in prairie soils from endemic regions. Environmental Science & Technology, 58(25), 10932-10940.
6. Sandoval, A. M., Nalls, A. V., et al. (2025). Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations. Scientific Reports, 15(1), 28553.
7. Williams, E. S. (2005). Chronic wasting disease. Veterinary Pathology, 42(5), 530-549.
8. Mori, J., Perez-Girones, S. V., et al. (2026). Maternal chronic wasting disease infection restricts fetal head size in white-tailed deer (Odocoileus virginianus). Prion, 20(1), 18-30.
9. Lesciotto, K. M., & Richtsmeier, J. T. (2019). Craniofacial skeletal response to encephalization: How do we know what we think we know?. American Journal of Physical Anthropology, 168, 27-46.
10. Mori, J., Brown, W., et al. (2024). An updated framework for modeling white‐tailed deer (Odocoileus virginianus) habitat quality in Illinois, USA. Ecology and Evolution, 14(11), p.e70487.
11. Gordon-Lipkin, E., Gentner, M. B., et al. (2017). Neurodevelopmental outcomes in 22 children with microcephaly of different etiologies. Journal of Child Neurology, 32(9), 804-809.
12. Nawathe, A., Doherty, J., & Pandya, P. (2018). Fetal microcephaly. Bmj, 361.
13. Mortberg, M. A., Minikel, E. V. & Vallabh, S. M. Analysis of non-human primate models for evaluating prion disease therapeutic efficacy. PLoS Pathog. 18, e1010728 (2022).