So what causes fish flavor in brown-shelled eggs? In a word - trimethylamine (TMA). This compound is a normal component of fishmeal, which is seldom, if ever, added to layer diets in the U.S. Trimethylamine is also synthesized from the nutrients choline and betaine following bacterial fermentation in the cecum and terminal intestine. Canola meal contains the protein sinapine which is degraded to TMA in the intestine, resulting in absorption and ultimately deposition in the yolk.
The problem of accumulation of TMA with resulting fish flavor in brown-shelled eggs is due to a genetic abnormality in up to 10% of brown-feathered hens. Normally TMA is oxidized in the liver to an innocuous compound by the action of an enzyme trimethylamine oxidase a flavin-containing monooxygenase isoform.
The synthesis of the enzyme is dependent on the expression of the gene FM03 located on chromosome 8. In the case of the non-synonymous mutation in the FM03 gene (designated T3295) hens are unable to oxidize TMA which accumulates in yolk. Irrespective of the source of TMA whether from fishmeal, canola meal or endogenous synthesis, hens bearing the gene defective FM03 will produce eggs with tainted yolks given sufficient precursor products in their diets.
Identifying the problem
Intensive research by the major primary breeders in cooperation with universities in Germany and Finland during 2003 and 20041 confirmed the specific genetic mutation responsible for the quality defect. Subsequently tests applying PCR technology were developed in Sweden2 to identify lines which carried the mutant gene.
The primary breeders of brown-feathered strains modified their programs to exclude affected families at the elite level. The test involves identifying affected hens and heterozygous carriers using a sample of blood from quill feathers. All primary breeders have made progress in ensuring that successive generations are free of the mutant FM03 gene, allowing normal oxidation of TMA.
Solution by 2012
It is anticipated that all commercial-level hens will be derived from breeding programs incorporating the commercially available screening procedure by 2012 although parents without the defect were available in the EU and the U.S. in 2007. It is emphasized that the defective FM03 gene has never been identified in white-shelled strains so no specific dietary restrictions on inclusion of canola meal are necessary.
It has been determined that trimethylamine oxidase can be partly inactivated by high levels of dietary tannins and glucosinolates which are found in non-traditional U.S. ingredients for poultry including pulses (field beans, peas), linseed and canola meals. Since these ingredients are not generally included in diets for hens in the U.S. the problem of fish taint was more common in the EU especially where rapeseed or canola meals are fed. Fermentation of betaine and choline by abnormal intestinal flora (dysbiosis) may result in accumulation of TMA, which should be oxidized by all white-shelled strains and brown hens with an unaffected FM03-gene.
Other flavors and odors
The inclusion of non-deodorized fish oils and some vegetables oils in diets for hens may result in “off-flavored” yolks due to the presence of oxidized long chain polyunsaturated fatty acids.
Administration of antibiotics to producing hens, which is permitted in some countries, could result in an imbalanced flora favoring synthesis of TMA.
Exposing unpacked eggs to volatile compounds including gasoline, cresylic disinfectants and paint solvents will result in abnormal odors. Nest-run eggs are apparently susceptible to acquiring unusual flavors and odors during storage or transport.
Some green vegetables containing volatile components may also taint eggs including cabbages, onions, leeks and according to anecdotal reports, potatoes and apples.
1 Honkatukia, M., Reese, K., Preisinger, A., et al. (2005) Fishy taint in chicken eggs is
associated with a substitution within a conserved motif of the FM03 gene.
Genomics. 86 : 225-232.
2 U.S. Patent 7273703