Dilated Cardiomyopathy in a Rio Grande Wild Turkey (Meleagris gallopavo intermedia) in Southern Utah, USA, 2013 Author(s): David D. Frame, E. Jane Kelly, and Arnaud Van Wettere Source: Journal of Wildlife Diseases, 51(3):790-792. Published By: Wildlife Disease Association DOI: http://dx.doi.org/10.7589/2014-09-228 URL: http://www.bioone.org/doi/full/10.7589/2014-09-228
BioOne (www.bioone.org) is a nonprofit, online aggregation of core research in the biological, ecological, and environmental sciences. BioOne provides a sustainable online platform for over 170 journals and books published by nonprofit societies, associations, museums, institutions, and presses. Your use of this PDF, the BioOne Web site, and all posted and associated content indicates your acceptance of BioOne’s Terms of Use, available at www.bioone.org/page/ terms_of_use. Usage of BioOne content is strictly limited to personal, educational, and non-commercial use. Commercial inquiries or rights and permissions requests should be directed to the individual publisher as copyright holder.
BioOne sees sustainable scholarly publishing as an inherently collaborative enterprise connecting authors, nonprofit publishers, academic institutions, research libraries, and research funders in the common goal of maximizing access to critical research.
DOI: 10.7589/2014-09-228
Journal of Wildlife Diseases, 51(3), 2015, pp. 790–792 # Wildlife Disease Association 2015
Dilated Cardiomyopathy in a Rio Grande Wild Turkey (Meleagris gallopavo intermedia) in Southern Utah, USA, 2013 David D. Frame,1,2,4 E. Jane Kelly,1,2 and Arnaud Van Wettere1,3 1Animal, Dairy, and Veterinary Sciences Department, Utah State University, 4815 Old Main Hill, Logan, Utah 84322-4815, USA; 2Utah Veterinary Diagnostic Laboratory, Central Utah Branch, 1451 S Main, Nephi, Utah 84648, USA; 3Utah Veterinary Diagnostic Laboratory, 950 E 1400 N, Logan, Utah 84341, USA; 4Corresponding author (email: [email protected])
et al. 2007). In Wild Turkeys, a possible DCM-sparing variant of the inhibitory subunit troponin I (Tnl) of the troponintropomyosin system that governs skeletal muscle contraction in vertebrates has been reported (Biesiadecki et al. 2004). It is possible that the compensatory variant of the Tnl subunit of the filament-based troponin-tropomyosin system may selectively spare the Wild Turkey population from an appreciable incidence of DCM. In at least three Wild turkey disease surveys from various areas of the US, cardiac abnormalities are not mentioned (Trainer et al. 1968; Davidson et al. 1985; Peterson et al. 2002). We describe an unusual occurrence of DCM in a mature male Rio Grande Wild Turkey (Meleagris gallopavo intermedia) found dead in March 2013 by Utah Division of Wildlife Resources (DWR) personnel in southern Utah (37u289460N, 113u189350W). To our knowledge, this is the first report describing DCM in a Wild Turkey. The turkey was submitted for necropsy to the Utah Veterinary Diagnostic Laboratory-Central Utah Branch (UVDLCUB) with a history of sudden death. The turkey had been living in semidomestication on the premises of a recently retired DWR employee. It was submitted to UVDL-CUB with concern that the turkey may have died from infectious contagious causes that might endanger the free-living turkey flock nearby. The turkey was severely emaciated. Upon necropsy, the peritoneal cavity contained an abundance of yellow serous fluid. Lungs were fluid filled and contained areas of dark red to black consolidation. The spleen was moderately enlarged, and the capsule appeared thickened. There was
ABSTRACT: A male Rio Grande Wild Turkey (Meleagris gallopavo intermedia) living in semidomestication was submitted for necropsy. Emaciation, a greatly enlarged heart, and chronic passive congestion of the liver were present. Dilated cardiomyopathy occurs in domestic turkey flocks but has not been reported in Wild Turkeys.
Dilated cardiomyopathy (DCM), formerly known as spontaneous cardiomyopathy of turkeys, occurs frequently in commercial domestic turkeys (Meleagris gallopavo). An enlarged heart in commercial turkeys was first described in 1962 (Magwood and Bray 1962) and subsequently in 1968 (Sautter et al. 1968). Incidence may be higher in flocks raised at moderate to high elevations (Frame et al. 2001). Reducing the sodium and increasing the chloride concentration in the diet significantly decreased mortality attributable to DCM in poults up to 3 wk of age (Frame et al. 2001). Simply reducing the salt concentration in the starter diet accomplished similar results (Clark et al. 1995). Rapid growth rate is a factor in occurrence of DCM, as well as the interaction of multiple determinants and risk factors (Frame 1991; Frame et al. 2010). The majority of mortality in affected commercial flocks occurs within the first 3 wk of life when the rate of growth is high. However, DCM has also been seen frequently in tom (male) flocks at 6–8 wk of age, and even sporadically in individual toms as old as 18 wk (D.D.F. pers. obs.). Wild Turkeys (also M. gallopavo) do not experience dramatically accelerated growth rates. Genes from the turkey have been studied as models to better understand human dilated cardiomyopathies (Lin 790
LETTERS
widespread congestion of intestinal vasculature. The most striking lesions were a greatly enlarged heart and a firm liver with markedly rounded edges. Right and left ventricular dilatation were present; however, measurements were not taken (Fig. 1). Culture of heart sac, liver, and spleen yielded no bacterial growth. No microscopic lesions were detected in the myocardium; however, histologic lesions in the liver were supportive of chronic passive congestion with moderate to severe bridging fibrosis, especially prominent in the centrilobular areas. Moderate to marked vacuolation (mostly lipid type) of hepatocytes was also present. Diffuse pulmonary congestion with presumptive mild pulmonary edema, as well as prominent congestion in the kidneys and intestinal tract was observed. Living in semidomestication may have allowed this turkey to continue surviving with a severely compromised heart. A turkey in this condition would probably not survive in the wild and, consequently, would not be detected on surveys. Any case of sudden death in Wild Turkeys must be taken seriously because of the risk
FIGURE. 1. Rio Grande Wild Turkey (Meleagris gallopavo intermedia) found dead in southern Utah in 2013 and diagnosed with dilated cardiomyopathy. Note enlarged heart, firm liver with markedly rounded edges, and atrophied pectoral muscle (i.e., emaciation).
791
of harboring and transmitting serious diseases, such as avian influenza or exotic Newcastle disease, into wild or domestic turkey populations. The cause of DCM in this Wild Turkey is unknown. The diet of this semidomesticated bird was probably different than that of wild flocks and may have been a contributing factor in the pathogenesis. LITERATURE CITED Biesiadecki BJ, Schneider KL, Yu Z-B, Chong SM, Jin JP. 2004. An R111C polymorphism in wild turkey cardiac troponin I accompanying the dilated cardiomyopathy-related abnormal splicing variant of cardiac troponin T with potentially compensatory effects. J Biol Chem 279:13825– 13832. Clark FD, Frame DD, Warnick RE, Kelly EJ, Roeder BL. 1995. Effects of lowered dietary sodium chloride on spontaneous cardiomyopathy mortality in turkeys. In: Proceedings of the 44th western poultry disease conference, Western Poultry Disease, Sacramento, California, 5–7 March, pp. 22–23. Davidson WR, Nettles VF, Couvillion CE, Howerth EH. 1985. Diseases diagnosed in wild turkeys (Meleagris gallopavo) of the southeastern United States. J Wildl Dis 21:386–390. Frame DD. 1991. Roundheart disease in Utah turkey flocks. In: Proceedings of the 40th western poultry disease conference, Western Poultry Disease, Acapulco, Guerrero, Mexico, 24–27 April, pp. 95–96. Frame DD, Buckner RE, Anderson GL. 2010. Causes and control of spontaneous cardiomyopathy or roundheart disease in Utah turkeys. Utah State University Extension Publication. http:// extension.usu.edu/files/publications/publication/ AG_506.pdf. Accessed January 2014. Frame DD, Hooge DM, Cutler R. 2001. Interactive effects of dietary sodium and chloride on the incidence of spontaneous cardiomyopathy (round heart) in turkeys. Poult Sci 80:1572– 1577. Lin QC, Xu J, Kamara D, Geng T, Gyenai K, Reed KM, Smith EJ. 2007. DNA sequence and haplotype variation in two candidate genes for dilated cardiomyopathy in the turkey Meleagris gallopavo. Genome 50:463–469. Magwood SE, Bray DF. 1962. Disease condition of turkey poults characterized by enlarged and rounded hearts. Can J Comp Med Vet Sci 26:268–272. Peterson MJ, Aguirre R, Ferro PJ, Jones DA, Lawyer TA, Peterson MN, Silvy NJ. 2002. Infectious
792
JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 3, JULY 2015
disease survey of Rio Grande wild turkeys in the Edwards Plateau of Texas. J Wildl Dis 38: 826–833. Sautter JH, Newman JA, Kleven SH, Larsen CT. 1968. Pathogenesis of the roundheart syndrome in turkeys. Avian Dis 12:614–628.
Trainer DO, Glazener WC, Hanson RP, Nassif BD. 1968. Infectious disease exposure in a wild turkey population. Avian Dis 12:208–214. Submitted for publication 5 September 2014. Accepted 8 January 2015.
BioOne (www.bioone.org) is a nonprofit, online aggregation of core research in the biological, ecological, and environmental sciences. BioOne provides a sustainable online platform for over 170 journals and books published by nonprofit societies, associations, museums, institutions, and presses. Your use of this PDF, the BioOne Web site, and all posted and associated content indicates your acceptance of BioOne’s Terms of Use, available at www.bioone.org/page/ terms_of_use. Usage of BioOne content is strictly limited to personal, educational, and non-commercial use. Commercial inquiries or rights and permissions requests should be directed to the individual publisher as copyright holder.
BioOne sees sustainable scholarly publishing as an inherently collaborative enterprise connecting authors, nonprofit publishers, academic institutions, research libraries, and research funders in the common goal of maximizing access to critical research.
DOI: 10.7589/2014-09-228
Journal of Wildlife Diseases, 51(3), 2015, pp. 790–792 # Wildlife Disease Association 2015
Dilated Cardiomyopathy in a Rio Grande Wild Turkey (Meleagris gallopavo intermedia) in Southern Utah, USA, 2013 David D. Frame,1,2,4 E. Jane Kelly,1,2 and Arnaud Van Wettere1,3 1Animal, Dairy, and Veterinary Sciences Department, Utah State University, 4815 Old Main Hill, Logan, Utah 84322-4815, USA; 2Utah Veterinary Diagnostic Laboratory, Central Utah Branch, 1451 S Main, Nephi, Utah 84648, USA; 3Utah Veterinary Diagnostic Laboratory, 950 E 1400 N, Logan, Utah 84341, USA; 4Corresponding author (email: [email protected])
et al. 2007). In Wild Turkeys, a possible DCM-sparing variant of the inhibitory subunit troponin I (Tnl) of the troponintropomyosin system that governs skeletal muscle contraction in vertebrates has been reported (Biesiadecki et al. 2004). It is possible that the compensatory variant of the Tnl subunit of the filament-based troponin-tropomyosin system may selectively spare the Wild Turkey population from an appreciable incidence of DCM. In at least three Wild turkey disease surveys from various areas of the US, cardiac abnormalities are not mentioned (Trainer et al. 1968; Davidson et al. 1985; Peterson et al. 2002). We describe an unusual occurrence of DCM in a mature male Rio Grande Wild Turkey (Meleagris gallopavo intermedia) found dead in March 2013 by Utah Division of Wildlife Resources (DWR) personnel in southern Utah (37u289460N, 113u189350W). To our knowledge, this is the first report describing DCM in a Wild Turkey. The turkey was submitted for necropsy to the Utah Veterinary Diagnostic Laboratory-Central Utah Branch (UVDLCUB) with a history of sudden death. The turkey had been living in semidomestication on the premises of a recently retired DWR employee. It was submitted to UVDL-CUB with concern that the turkey may have died from infectious contagious causes that might endanger the free-living turkey flock nearby. The turkey was severely emaciated. Upon necropsy, the peritoneal cavity contained an abundance of yellow serous fluid. Lungs were fluid filled and contained areas of dark red to black consolidation. The spleen was moderately enlarged, and the capsule appeared thickened. There was
ABSTRACT: A male Rio Grande Wild Turkey (Meleagris gallopavo intermedia) living in semidomestication was submitted for necropsy. Emaciation, a greatly enlarged heart, and chronic passive congestion of the liver were present. Dilated cardiomyopathy occurs in domestic turkey flocks but has not been reported in Wild Turkeys.
Dilated cardiomyopathy (DCM), formerly known as spontaneous cardiomyopathy of turkeys, occurs frequently in commercial domestic turkeys (Meleagris gallopavo). An enlarged heart in commercial turkeys was first described in 1962 (Magwood and Bray 1962) and subsequently in 1968 (Sautter et al. 1968). Incidence may be higher in flocks raised at moderate to high elevations (Frame et al. 2001). Reducing the sodium and increasing the chloride concentration in the diet significantly decreased mortality attributable to DCM in poults up to 3 wk of age (Frame et al. 2001). Simply reducing the salt concentration in the starter diet accomplished similar results (Clark et al. 1995). Rapid growth rate is a factor in occurrence of DCM, as well as the interaction of multiple determinants and risk factors (Frame 1991; Frame et al. 2010). The majority of mortality in affected commercial flocks occurs within the first 3 wk of life when the rate of growth is high. However, DCM has also been seen frequently in tom (male) flocks at 6–8 wk of age, and even sporadically in individual toms as old as 18 wk (D.D.F. pers. obs.). Wild Turkeys (also M. gallopavo) do not experience dramatically accelerated growth rates. Genes from the turkey have been studied as models to better understand human dilated cardiomyopathies (Lin 790
LETTERS
widespread congestion of intestinal vasculature. The most striking lesions were a greatly enlarged heart and a firm liver with markedly rounded edges. Right and left ventricular dilatation were present; however, measurements were not taken (Fig. 1). Culture of heart sac, liver, and spleen yielded no bacterial growth. No microscopic lesions were detected in the myocardium; however, histologic lesions in the liver were supportive of chronic passive congestion with moderate to severe bridging fibrosis, especially prominent in the centrilobular areas. Moderate to marked vacuolation (mostly lipid type) of hepatocytes was also present. Diffuse pulmonary congestion with presumptive mild pulmonary edema, as well as prominent congestion in the kidneys and intestinal tract was observed. Living in semidomestication may have allowed this turkey to continue surviving with a severely compromised heart. A turkey in this condition would probably not survive in the wild and, consequently, would not be detected on surveys. Any case of sudden death in Wild Turkeys must be taken seriously because of the risk
FIGURE. 1. Rio Grande Wild Turkey (Meleagris gallopavo intermedia) found dead in southern Utah in 2013 and diagnosed with dilated cardiomyopathy. Note enlarged heart, firm liver with markedly rounded edges, and atrophied pectoral muscle (i.e., emaciation).
791
of harboring and transmitting serious diseases, such as avian influenza or exotic Newcastle disease, into wild or domestic turkey populations. The cause of DCM in this Wild Turkey is unknown. The diet of this semidomesticated bird was probably different than that of wild flocks and may have been a contributing factor in the pathogenesis. LITERATURE CITED Biesiadecki BJ, Schneider KL, Yu Z-B, Chong SM, Jin JP. 2004. An R111C polymorphism in wild turkey cardiac troponin I accompanying the dilated cardiomyopathy-related abnormal splicing variant of cardiac troponin T with potentially compensatory effects. J Biol Chem 279:13825– 13832. Clark FD, Frame DD, Warnick RE, Kelly EJ, Roeder BL. 1995. Effects of lowered dietary sodium chloride on spontaneous cardiomyopathy mortality in turkeys. In: Proceedings of the 44th western poultry disease conference, Western Poultry Disease, Sacramento, California, 5–7 March, pp. 22–23. Davidson WR, Nettles VF, Couvillion CE, Howerth EH. 1985. Diseases diagnosed in wild turkeys (Meleagris gallopavo) of the southeastern United States. J Wildl Dis 21:386–390. Frame DD. 1991. Roundheart disease in Utah turkey flocks. In: Proceedings of the 40th western poultry disease conference, Western Poultry Disease, Acapulco, Guerrero, Mexico, 24–27 April, pp. 95–96. Frame DD, Buckner RE, Anderson GL. 2010. Causes and control of spontaneous cardiomyopathy or roundheart disease in Utah turkeys. Utah State University Extension Publication. http:// extension.usu.edu/files/publications/publication/ AG_506.pdf. Accessed January 2014. Frame DD, Hooge DM, Cutler R. 2001. Interactive effects of dietary sodium and chloride on the incidence of spontaneous cardiomyopathy (round heart) in turkeys. Poult Sci 80:1572– 1577. Lin QC, Xu J, Kamara D, Geng T, Gyenai K, Reed KM, Smith EJ. 2007. DNA sequence and haplotype variation in two candidate genes for dilated cardiomyopathy in the turkey Meleagris gallopavo. Genome 50:463–469. Magwood SE, Bray DF. 1962. Disease condition of turkey poults characterized by enlarged and rounded hearts. Can J Comp Med Vet Sci 26:268–272. Peterson MJ, Aguirre R, Ferro PJ, Jones DA, Lawyer TA, Peterson MN, Silvy NJ. 2002. Infectious
792
JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 3, JULY 2015
disease survey of Rio Grande wild turkeys in the Edwards Plateau of Texas. J Wildl Dis 38: 826–833. Sautter JH, Newman JA, Kleven SH, Larsen CT. 1968. Pathogenesis of the roundheart syndrome in turkeys. Avian Dis 12:614–628.
Trainer DO, Glazener WC, Hanson RP, Nassif BD. 1968. Infectious disease exposure in a wild turkey population. Avian Dis 12:208–214. Submitted for publication 5 September 2014. Accepted 8 January 2015.
