Discoveries

Plastics Found in Petrel Chicks

Ocean plastic pollution is accidentally on the menu for southern giant petrel chicks. Even small nibbles of it may affect their physiology during development, according to a study from UC Davis and Argentina's National Research Council.

Southern giant petrels are not of high conservation concern globally, but they are particularly susceptible and useful sentinels for understanding how ocean plastic pollution affects wildlife.

With a range stretching from Antarctica to Chile, Argentina, Africa and Australia, these large birds frequently forage at the sea surface, where floating plastic tends to accumulate. Adults can accidentally transfer plastic they eat to their chicks when they regurgitate food.

The study—published in the journal Ecotoxicology and Environmental Safety—detected plastics in more than 71% of chicks, suggesting that they are inadvertently fed plastic by their parents.

To understand the effects of ingesting plastic on the chicks’ health, the researchers sampled and examined southern giant petrel chicks at two key stages of development during 2022 and 2023 in Patagonia, Argentina.

“We found that it doesn’t take a stomach full of plastic to leave a biological signal,” said corresponding author Marcela Uhart, a wildlife veterinarian with the school and its Karen C. Drayer Wildlife Health Center.

The amount of plastic recovered was small relative to the body mass of the chicks. Yet even at these low levels, eating plastic was associated with potentially adverse changes in the health of young chicks, especially for those around one month old. The health changes were related to nutrition, body condition, metabolism, liver and muscle function and immune response.
—Kat Kerlin, UC Davis News

Vision Loss Link Between Humans and Macaques

An inherited form of blindness directly comparable to a common inherited optic nerve disease in humans has been discovered in rhesus macaques at the National Biomedical Research Institute at UC Davis. The research, published in Proceedings of the National Academy of Sciences, could lead to a better understanding of autosomal dominant optic atrophy, or ADOA, and potentially to new treatments.

ADOA affects approximately 3 in 100,000 people worldwide, causing progressive vision loss and eventual blindness. Many patients are diagnosed between the ages of 10 and 30 and it is thus a significant cause of vision loss in children. People with the disease develop blind spots, or scotoma, and there is no available treatment, said Professor Sara Thomasy, senior author on the paper. As a comparative ophthalmologist, Thomasy holds dual appointments at the Weill School of Veterinary Medicine and the Department of Ophthalmology and Vision Science at UC Davis Health.

“The rhesus macaque could be a model to study gene therapy to prevent ADOA, or to test treatments that could slow or block progression in humans,” Thomasy said.

In humans, ADOA is related to mutations in a gene called OPA1 which affects mitochondria. While mitochondria are found throughout the body, the long nerve axons that run from the retina to the brain are particularly vulnerable to mitochondrial defects.

Rhesus macaques and other non-human primates have a very similar eye structure and vision system to humans. Thomasy and colleagues found that some of the monkeys at the research center had a spontaneous mutation in OPA1 that leads to changes in the eye very similar to those in people with ADOA.

The work was supported by grants from the National Institutes of Health. 
—Andy Fell, UC Davis News

Genetic Cause Identified for Fatal Foal Disease

UC Davis veterinary researchers led by Dr. Carrie Finno and graduate student Briana Brown have reported the genetic cause of a fatal neurologic disease—equine juvenile spinocerebellar ataxia (EJSCA)—in American Quarter Horse foals. The study was published in the Journal of Veterinary Internal Medicine.

Foals with EJSCA display incoordination within the first month of life. The disease damages axons, the nerve fibers that allow the brain and spinal cord to communicate. As these pathways deteriorate, communication is interrupted or lost, so foals do not know where their legs are in relation to the ground, leading to issues with movement and balance. The disease progresses rapidly, causing severe weakness in the hind limbs and difficulty standing. There is no treatment or cure, and affected foals are humanely euthanized.

“This is one of the most devastating diseases that I have seen in 20 years as an equine veterinarian,” said Finno, who serves as director of the Center for Equine Health (CEH). “These foals progress from looking completely normal, to slightly uncoordinated, to unable to stand in a matter of days.”

The American Quarter Horse is the most popular horse breed in North America, with more than 7 million horses registered worldwide. The low frequency of the variant in the breed, as well as the fact that all affected foals to date trace back to one prominent sire, suggest that this is a new genetic variant.

“There was an urgent need to identify the cause,” said Finno. “Fortunately, we were able to secure funding from the CEH to perform the genetic investigation. This highlights the strength of the CEH program and how it can rapidly solve research questions for horses and their owners.”
—Amy Young

A genetic test is available through the UC Davis Veterinary Genetics Laboratory.

Understanding Addison’s Disease in Dogs and Humans

Nova Scotia Duck Tolling Retrievers (Tollers) have an unusually high rate of Addison's disease, a condition in which the adrenal glands do not produce enough hormones, notably cortisol and aldosterone. In humans, Addison's disease is thought to occur when the body's immune system attacks the adrenal glands, making it a type of autoimmune disease.

Affected Tollers typically develop Addison's disease at a young age and the condition appears to be inherited. It often occurs with other autoimmune diseases, a condition called multiple autoimmune syndrome. Dogs with juvenile-onset Addison’s disease typically die within two years, even with treatment.

Researchers identified a gene variant in Tollers, RESF1, which is strongly associated with the disease in dogs and published their study in Scientific Reports. The team was led by Professor Danika Bannasch, Maxine Adler Endowed Chair of Genetics at the school, with graduate students Emily Brown and Scarlett Varney, and colleagues at UC Davis and internationally.

The RESF1 gene is very similar across other species, including humans, but has not previously been associated with Addison's disease or multiple autoimmune syndrome in people. The new study suggests that researchers could investigate it as a candidate gene for human Addison’s disease. Tollers could be a natural model for multiple autoimmune syndrome, potentially offering insights relevant to both veterinary and human medicine.
—Amy Young

A genetic test is available through the UC Davis Veterinary Genetics Laboratory.