Possible Causes for Beak Deformities Active

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Current Research

After more than a decade of research, we have been able to rule out many probable causes of beak deformities in Alaskan birds. Recently, we used next generation sequencing (NGS) to investigate the hypothesis that a virus might be responsible for avian keratin disease (AKD). NGS is a powerful tool for studying new and emerging diseases because it can provide information about viruses and other pathogens that have not previously been described. In 2016 we detected a novel picornavirus (Poecivirus) in beak tissues of Black-capped Chickadees with AKD (Zylberberg et al. 2016). We detected this virus in 100% of birds with beak deformities; by comparison, the virus was present in only 20% of birds with apparently normal beaks. Subsequently, we sampled a larger number of chickadees from our field sites in south-central Alaska and confirmed a strong association between Poecivirus and beak deformities. Additionally, we have detected a closely related virus in other species from Alaska with beak deformities, providing further evidence for Poecivirus as a leading candidate cause of AKD. Other picornaviruses have been associated with keratin overgrowth, such as Seneca Valley virus in pigs (Vanucci et al. 2015). However, because Poecivirus is a newly discovered virus, we still have a lot to learn! Additional studies are currently underway to determine if this virus causes beak deformities in naïve birds, whether it is present outside of Alaska, and how it may be transmitted among wild birds.

Previous Investigations

Our previous research addressed a broad range of possible causes, including environmental contaminants, nutrient deficiencies, other diseases, parasites, and genetic abnormalities. None of these factors were clearly linked to avian keratin disorder (AKD) in Black-capped Chickadees or other affected species. However, we learned important information that pertains to the physiology and health of chickadees and other wild birds. See below for more information.

• Contaminants
• Nutrition
• Disease/Parasites
• Genetics

Contaminants

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Previous studies have documented associations between beak abnormalities and contaminant exposure in other species, but we have no direct evidence that contaminant exposure is responsible for Alaskan deformities.

Large clusters of birds with beak deformities are rare and those that have occurred have been associated with exposure to contaminants. Beginning in the 1970s, fish-eating birds in the Great Lakes region exhibited high rates of congenital deformities, including beak abnormalities. Evidence suggested that these birds were exposed to industrial sources of PCBs, PCDDs, and PCDFs (Gilbertson et al. 1991, Ludwig et al. 1996). Another cluster of deformities among aquatic birds occurred in the early 1980s in California. These deformities, including embryonic beak defects, were attributed to exposure to high concentrations of selenium from agricultural runoff (Ohlendorf et al. 1986, Hoffman et al. 1988).

We tested Black-capped Chickadee adults, eggs, and nestlings for contaminants, including metals and trace elements, organic pesticides, PCBs, PCDDs, and PCDFs. We found no evidence that selenium or any other element was responsible for the beak deformities, but some evidence that organochlorine compounds may be contributing factors. Adults with beak deformities had an elevated level of chromosomal damage, which was correlated with lipid level and concentrations of several organochlorine compounds. However, concentrations of these contaminants were relatively low in tissues and none is known to cause beak or keratin abnormalities. Laboratory tests for PCDDs and PCDFs, the most toxic of the organochlorine compounds, were not sensitive enough to detect potential differences between affected and unaffected birds and may warrant further study.

We also tested sunflower seeds, which are frequently used in backyard feeders, to determine if chickadees could be exposed to contaminants through human-supplied foods. Concentrations were low in the seeds, suggesting that sunflower seeds are not a significant source of ingested contaminants.

Nutrition

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Previous studies have documented associations between beak abnormalities and nutritional disorders in other species, but we have no direct evidence that nutritional deficiencies are responsible for Alaskan deformities.

Overgrowth of the beak can be caused by nutritional deficiencies of vitamin A, vitamin D3, or calcium, or by an imbalanced ratio of calcium and phosphorus (Altman 1986, Harrison and Harrison 1986). Vitamin D3, which is the form of vitamin D used by birds and is necessary for calcium regulation, is derived from sunlight and either absorbed through the skin or ingested through preening.  During short winter days, it is possible that birds may not get adequate sources of vitamin D3 from sunlight.  They could also develop nutritional deficiencies from incomplete diets, particularly if they are overly reliant on sunflower seeds at feeders or other human sources of food that are low in calcium and vitamin A and high in fat, which can interfere with calcium absorption. However, observed clinical signs in affected chickadees differ from those previously described for vitamin A, vitamin D3, or calcium imbalances, making these possibilities less likely.

We performed diet analysis with stable isotope analysis of blood and feathers in affected and unaffected chickadees to determine whether beak deformities were associated with differences in diet. While we found that affected birds consumed more foods from human-provided feeders, our results suggested that this difference was likely a consequence rather than a cause of the beak deformities. Because of physical limitations imposed by an elongated beak, affected birds have a difficult time foraging in the wild. Feeders provide more easily accessible food sources.

Disease/Parasites

Other types of beak deformities have been attributed to parasites or specific avian diseases, such as psittacine beak and feather disease.  However, laboratory examination and testing of Black-capped Chickadees with avian keratin disorder (AKD) largely ruled these out as contributing factors.

Overgrowth of the beak can be a symptom of liver disease (Harrison 1986). However, necropsy and histopathology of chickadees with AKD did not reveal any abnormal pathology of internal organs, including liver, spleen, and thyroid.  Blood serum biochemistry also did not provide evidence of acute infection. The parasitic scaly mite Cnemidocoptes pilae, which can cause lesions on the beak, was not detected.  Tests were negative for both avian polyomavirus and the circovirus that causes psittacine beak and feather disease, which is not currently known to infect passerine birds (Tully et al. 2000).

Genetics

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We sampled blood from all captured Black-capped Chickadees to determine sex of the birds, identify family relationships, and assess potential DNA damage.

We found no evidence to suggest that beak deformities among Black-capped Chickadees are heritable in nature.  However, the fact that deformities appeared in adult birds and not nestlings made it difficult to establish this conclusively.  Because we only recapture a small proportion of the adults in a population, we have a limited sample size of birds from known parents.  Additional analysis of genetic data will help determine if offspring from parents with beak deformities are more likely to have deformities themselves than offspring from parents with normal beaks.

In addition, genetic paternity analysis identified surprisingly high rates of “cheating” among pairs.  In many cases, the female, the male, or both adults mated with a different bird whose eggs subsequently ended up in the pair’s nest.  Occasionally, eggs from two completely different adults were “dumped” in a pair’s nest as well.  These complicating factors make genetic analysis especially important when examining effects across generations or relationships between the eggs or chicks in a nest.  Contaminant concentrations, for example, are often compared between siblings or between a female and her eggs.  Due to high rates of “cheating,” these relationships cannot be accurately determined without genetic fingerprinting of individuals.

We also tested for DNA damage in Black-capped Chickadees with a technique called flow cytometry.  Results from these tests indicated that chickadees with beak deformities had a significantly greater amount of DNA damage than normal chickadees (Easton 1999).  Such damage to the DNA can result from exposure to contaminants (Custer et al. 1994) or some other specific mutagen, such as a disease organism.