Brown Ducks Research Articles

Mottled ducks, feral mallards, and their hybrids in Florida

AbstractThe nonmigratory and endemic Florida mottled duck (Anas fulvigula fulvigula) is facing conservation threats from the combined effects of urbanization and introgressive hybridization with feral mallards (Anas platyrhynchos) and mallard x mottled duck hybrids. In the past, the status of the Florida mottled duck population was assessed during annual aerial surveys and most brown ducks (mottled ducks, mallards, and hybrids of them) detected during the survey would have been mottled ducks. But the release of domesticated mallards for aesthetic purposes has led to increases in the prevalence of mallards‐hybrids (mallards or mallard x mottled duck hybrids) throughout peninsular Florida, USA, and because it is impossible to differentiate among mottled ducks, female mallards, and hybrids during aerial surveys, helicopter surveys were halted in 2009 until state researchers could conduct a range‐wide study to determine what proportion of brown ducks are mottled ducks versus mallards‐hybrids. We used plumage keys and high‐resolution photography to categorize brown ducks from 557 wetland grid points as either mottled ducks or mallards‐hybrids. Of the 5,179 brown ducks categorized, 40.1% were mottled ducks and 59.9% were mallards‐hybrids. We used logistic regression analysis to model the interactive effect of a site's latitude and level of urbanization (urban gradient value within a 2‐km buffer) to generate a predictive raster surface (1‐km resolution) of the study area with values corresponding to the probability that a brown duck observed within a cell is a pure mottled duck. Predicted values will be used as correction factors when estimating final mottled duck population abundance from brown‐duck survey data. Additionally, the predictive raster surface will be used to identify wetlands where mottled ducks remain predominant so that these sites can be targeted for preservation. Overall, mallards‐hybrids outnumbered mottled ducks throughout most of peninsular Florida, especially in more urbanized regions, and their current prevalence rate presents a serious conservation threat, via hybridization, to extant mottled duck populations.

Molecular characterization of duck hepatitis B virus isolated from Hubei brown ducks

The objective of this study was to characterize the genome structure of duck hepatitis B virus (DHBV) isolated from Hubei brown ducks. The natural carrier rate of DHBV in adult ducks from Hubei area was investigated and the DHBV DNA-positive serum screened out. The complete genome of a DHBV strain was amplified by polymerase chain reaction (PCR) and cloned into T vector and sequenced. The results showed that the carrier rate of DHBV in Hubei brown ducks was 10 %. This strain (GenBank accession number DQ276978) had a genome of 3024 nucleotides with three overlapping open reading frames encoding the surface, core and polymerase proteins respectively. Comparison of the strain with 17 DHBV strains registered in GenBank revealed a homology from 89.3 % to 93.5 % at the nucleotide level. The sequences of the structural and functional domains of these proteins were highly conserved. The strain was found to share more signature amino acids in the polymerase genes with the "Chinese" DHBV strains than those of the "Western" country strains. This finding was also corroborated by a phylogenetic tree analysis. Therefore, the DQ276978 might belong to a subtype of the Chinese DHBV strains.

Mutations outside the YMDD motif in the P protein can also cause DHBV resistant to Lamivudine

To observe the Lamivudine resistance character of a DHBV strain in vitro and in vivo, and to analyze if the Lamivudine resistance character is caused by gene mutation or by abnormity of the Lamivudine metabolism. Congenitally DHBV-negative Guangdong brown ducks and duck embryo liver cells were respectively taken as animal and cell model. The Lamivudine-susceptive DHBV and Lamivudine-resistant DHBV (LRDHBV) were infected and Lamivudine was administrated according to the divided groups. The changes of DHBV quantity in the animal and cell model were tested. Three Lamivudine-resistant and two Lamivudine-susceptive DHBV complete genomes were successfully amplified, sequenced and then submitted to GenBank. All the DHBV complete sequences in the GenBank at present were taken to align with the three LRDHBV to analyze the mutational points related to the Lamivudine-resistant mutation. Both the animal and cell model showed that the large and the small dosage Lamivudine have no significant inhibitory effect on the LRDHBV. Five sequences of DHBV complete genomes were successfully cloned. The GenBank accession numbers of the three sequences of LRDHBV are AY521226, AY521227, and AY433937. The two strains of Lamivudine-susceptive DHBV are AY392760 and AY536371. The correlated mutational points are KorR86Q and AorE591T in the P protein. The Lamivudine resistance character of this DHBV strain is caused by genome mutation; the related mutational points are KorR86Q and AorE591T and have no relations with the YMDD motif mutation.

Spectrum of liver disease and duck hepatitis B virus infection in a large series of chinese ducks with hepatocellular carcinoma

The striking difference in the geographical distribution of liver cancer in ducks raised the question of whether duck hepatitis B virus (DHBV), like mammalian hepadnaviruses, could be an oncogenic agent. Hepatocellular carcinomas (HCCs) have been found only in domestic ducks in Qidong, China, where hepatitis B virus infection and aflatoxin B 1 (AFB 1) are both risk factors and where a high frequency of human HCCs has been reported. To date, the study of liver pathology occurring in Chinese ducks has been hampered by the small number of samples available. We describe here a series of 59 Chinese brown duck livers that were collected in Qidong more than 20 years ago and formalin fixed. Thirty-six HCCs, which ranged from well-differentiated trabecular to highly anaplastic type, were identified in relatively young ducks (average age, 3.3 years). Several unique features not previously reported, such as tumor giant cells, tumor necrosis, tumor thrombi in blood vessels, and inactive cirrhosis, were observed. Bile ductule proliferation, known to be a prominent feature of AFB 1 exposure in ducks, was present in 86% of livers. Using polymerase chain reaction (PCR) and two primer pairs, located within conserved portions of the DHBV S and C genes, we demonstrated the presence of DHBV DNA in 23 of 34 HCCs analyzed (68%). The spectrum of liver pathology that we report in brown ducks from Qidong was never observed in Pekin ducks of the same age chronically infected with DHBV and followed under controlled conditions outside China, suggesting that causative factors other than virus infection may be involved in duck liver carcinogenesis observed in this area. However, because DHBV DNA was present in most HCCs, and given the lower sensitivity of PCR in formalin-fixed tissue, we cannot rule out the importance of DHBV infection in the liver disease of ducks from this study. The specific role of Chinese DHBV isolates and brown duck breed in liver pathology and oncogenesis observed in Qidong ducks should be further investigated in controlled experimental transmission studies with long-term follow-up in the absence of external carcinogens.

Spectrum of liver disease and duck hepatitis B virus infection in a large series of chinese ducks with hepatocellular carcinoma

The striking difference in the geographical distribution of liver cancer in ducks raised the question of whether duck hepatitis B virus (DHBV), like mammalian hepadnaviruses, could be an oncogenic agent. Hepatocellular carcinomas (HCCs) have been found only in domestic ducks in Qidong, China, where hepatitis B virus infection and aflatoxin B1 (AFB1) are both risk factors and where a high frequency of human HCCs has been reported. To date, the study of liver pathology occurring in Chinese ducks has been hampered by the small number of samples available. We describe here a series of 59 Chinese brown duck livers that were collected in Qidong more than 20 years ago and formalin fixed. Thirty-six HCCs, which ranged from well-differentiated trabecular to highly anaplastic type, were identified in relatively young ducks (average age, 3.3 years). Several unique features not previously reported, such as tumor giant cells, tumor necrosis, tumor thrombi in blood vessels, and inactive cirrhosis, were observed. Bile ductule proliferation, known to be a prominent feature of AFB1 exposure in ducks, was present in 86% of livers. Using polymerase chain reaction (PCR) and two primer pairs, located within conserved portions of the DHBV S and C genes, we demonstrated the presence of DHBV DNA in 23 of 34 HCCs analyzed (68%). The spectrum of liver pathology that we report in brown ducks from Qidong was never observed in Pekin ducks of the same age chronically infected with DHBV and followed under controlled conditions outside China, suggesting that causative factors other than virus infection may be involved in duck liver carcinogenesis observed in this area.(ABSTRACT TRUNCATED AT 250 WORDS)

Molecular cloning and sequence analysis of duck hepatitis B virus genomes of a new variant isolated from Shanghai ducks

The genomes of duck hepatitis B virus (DHBV) from a brown duck (S5) and a white duck (S31) kept independently in Shanghai, China, were cloned and the complete nucleotide sequence of each virion DNA (DHBV-S5 and DHBV-S31) was determined. DHBV-S5 and DHBV-S31 were both 3027 by in length and 6 by longer than the other two DHBVs analyzed previously, DHBV16 and DHBV3. The genomes of DHBV-S5 and DHBV-S31 encoded three long overlapping open reading frames designated as P, S, and C. A possible new open reading frame was found in a complementary strand of each viral genome, as 336 by for DHBV-S5 and 306 by for DHBV-S31, respectively. A pair of 3-bp insertions were found in the overlapping region of pre-S2 and P and so two amino acids were inserted in this region in DHBV-S5 and DHBV-S31. The nucleotide sequence variation between DHBV-S5 and DHBV-S31 (4.9%) was similar to that between DHBV16 and DHBV3 (5.6%), and less than the variations between either of these Shanghai clones and DHBV16 or DHBV3 (9.5–10.4%). The amino acid sequence was also conserved in the two Shanghai clones but showed group difference from DHBV16 or DHBV3. Thus these two independent Shanghai clones of DHBV showed geographical characteristics of genomic structure.