Duck Kidney Research Articles

Expression and Immunohistochemical Distribution of Duck Plague Virus Glycoprotein gE in Infected Ducks

To determine the distribution of duck plague virus (DPV) gE protein in paraformaldehyde-fixed, paraffin-embedded tissues of experimentally DPV-infected ducks, an indirect immunoperoxidase assay was established to detect glycoprotein E (gE) protein for the first time. The rabbit anti-His-gE serum, raised against the recombinant His-gE fusion protein expressed in Escherichia coli BL21 (DE3), was prepared and purified. Western blotting and indirect immunofluorescence analysis showed that the anti-His-gE serum had a high level of reactivity and specificity and could be used as the first antibody for further experiments to study the distribution of DPV gE protein in DPV-infected tissues. A number of DPV gE proteins were distributed in the bursa of Fabricius, thymus, spleen, liver, esophagus, duodenum, jejunum, ileum, and kidney of DPV-infected ducks and a few DPV gE were distributed in the Harders glands, myocardium, cerebrum, and lung, whereas the gE was not seen in the skin, muscle, and pancreas. Moreover, DPV gE was expressed abundantly in the cytoplasm of lymphocytes, reticulum cells, macrophages, epithelial cells, and hepatocytes. The present study may be useful not only for describing the characteristics of gE expression and distribution in infected ducks but also for understanding the pathogenesis of DPV.

Immunofluorescence Analysis of Duck plague virus gE protein on DPV-infected ducks

BackgroundIn previous studies, the expression and localization characteristics of duck plague virus (DPV) gE protein have been described in cultured cells, but the properties of DPV gE protein have not been reported in vivo. Immunofluorescence analysis had been used for the detection of virus antigen, but there was no report on the use of this technique for the detection of DPV gE. In this study, we investigated the distribution of DPV gE protein on DPV-infected ducks using polyclonal antibody raised against the recombinant His-gE fusion protein by indirect immunofluorescence assay (IFA).ResultsThe recombinant gE protein was highly immunogenicity by ELISA, and the gE was used as an antigen for the preparation of polyclonal antibody, which could be used the first antibody for further experiment to study the distribution of DPV gE protein in DPV-infected tissues by indirect immunofluorescence assay. DPV gE protein were distributed in the immune organs (thymus, bursa of fabricius (BF), Harders glands, spleen), the digestive organs (liver, duodenum, jejunum, ileum), and the other parenchymatous organs (kidney, myocardium, cerebrum, and lung) of DPV-infected ducks, but the positive immunofluorescence signal was not seen in the muscle and pancreas. The lymphocytes, reticulum cells, macrophages, epithelial cells, and hepatocytes served as the principal site for the localization of DPV gE antigen. Moreover, the intensity of fluorescence increased sharply from 12 to 216 h post-infection (p.i.).ConclusionsIn this work, the immunogenicity of the recombinant gE protein was analyzed by ELISA, and we presented the distribution properties of DPV gE antigen in infected ducks for the first time, which may be useful for understanding the pathogenesis of DPV. These properties of the gE protein provided the prerequisite for further functional analysis.

Sea ducks and aquaculture: the cadmium connection

Elevated concentrations of cadmium have been reported in the kidneys of sea ducks that forage along the Pacific Northwest, and cadmium has been postulated as a possible cause of population declines. The blue mussel (Mytilus spp.) which occurs in dense numbers on aquaculture structures and are a primary prey item for sea ducks also contain elevated cadmium concentrations. To determine if foraging on mussels associated with aquaculture structures could pose a toxicological risk to sea ducks, amounts of cadmium ingested per body weight per day by a representative sea duck species, the surf scoter (Melanitta perspicillata), were estimated and compared to the reported avian cadmium NOAEL (no observable adverse effect level) and LOAEL (lowest observable adverse effect level). Results indicate that in some locations within the Pacific Northwest, sea ducks could be exposed to toxicologically significant levels of cadmium associated with mussels foraged from aquaculture structures. This raises the possibility that such exposure could be contributing to observed population declines in these species.

Expression and Distribution of the Duck Enteritis Virus UL51 Protein in Experimentally Infected Ducks

To determine the expression and distribution of tegument proteins encoded by duck enteritis virus (DEV) UL51 gene in tissues of experimentally infected ducks, for the first time, an immunoperoxidase staining method to detect UL51 protein (UL51p) in paraffin-embedded tissues is reported. A rabbit anti-UL51 polyclonal serum, raised against a recombinant 6-His-UL51 fusion protein expressed in Escherichia coli, was prepared, purified, and used as primary antibodies. Fifty-eight 30-day-old DEV-free ducks were intramuscularly inoculated with the pathogenic DEV CHv strain as infection group, and two ducks were selected as preinfection group. The tissues were collected at sequential time points between 2 and 480 hr postinoculation (PI) and prepared for immunoperoxidase staining. DEV UL51p was first found in the spleen and liver at 8 hr PI; in the bursa of Fabricius and thymus at 12 hr PI; in the Harders glands, esophagus, small intestine (including the duodenum, jejunum, and ileum), and large intestine (including the caecum and rectum) at 24 hr PI; in the glandularis ventriculus at 48 hr PI; and in the pancreas, cerebrum, kidney, lung, and myocardium at 72 hr PI. Throughout the infection process, the UL51p was not seen in the muscle. Furthermore, the intensity of positive staining of DEV UL51p antigen in various tissues increased sharply from 8 to 96 hr PI, peaked during 120-144 hr PI, and then decreased steadily from 216 to 480 hr PI, suggesting that the expressional levels of DEV UL51p in systemic organs have a close correlation with the progression of duck virus enteritis (DVE) disease. A number of DEV UL51p was distributed in the bursa of Fabricius, thymus, spleen, liver, esophagus, small intestine, and large intestine of DEV-infected ducks, whereas less DEV UL51p was distributed in the Harders glands, glandularis ventriculus, cerebrum, kidney, lung, pancreas, and myocardium of DEV-infected ducks. Moreover, DEV UL51p can be expressed in the cytoplasm of various types of cells, especially most abundantly in the cytoplasm of lymphocytes, reticulum cells, macrophages, epithelial cells, and hepatocytes. The present study may be useful not only for describing the characteristics of UL51p expression and distribution in vivo but also for a greater understanding of the pathogenesis of this DVE.

Two Novel Duck Antibacterial Peptides, Avian β-Defensins 9 and 10, with Antimicrobial Activity

Two novel avian beta-defensins (AvBDs) isolated from duck liver were characterized and their homologies with other AvBDs were analyzed. They were shown to be duck AvBD9 and AvBD10. The mRNA expression of the two genes was analyzed in 17 different tissues from 1-28-dayold ducks. AvBD9 was differentially expressed in the tissues, with especially high levels of expression in liver, kidney, crop, and trachea, whereas AvBD10 was only expressed in the liver and kidney of ducks at all the ages investigated. We produced and purified GST-tagged recombinant AvBD9 and AvBD10 by expressing the two genes in Escherichia coli. Both recombinant proteins exhibited antimicrobial activity against several bacterial strains. The results revealed that both recombinant proteins retained their antimicrobial activities against Staphylococcus aureus under a range of different temperatures (-70 degrees C -100 degrees C) and pH values (pH 3-12).

Entry of Duck Hepatitis B Virus into Primary Duck Liver and Kidney Cells after Discovery of a Fusogenic Region within the Large Surface Protein

Hepatitis B viruses exhibit a narrow host range specificity that is believed to be mediated by a domain of the large surface protein, designated L. For duck hepatitis B virus, it has been shown that the pre-S domain of L binds to carboxypeptidase D, a cellular receptor present in many species on a wide variety of cell types. Nonetheless, only hepatocytes become infected. It has remained vague which viral features determine host range specificity and organotropicity. By using chymotrypsin to treat duck hepatitis B virus, we addressed the question of whether a putative fusogenic region within the amino-terminal end of the small surface protein may participate in viral entry and possibly constitute one of the determinants of the host range of the virus. Addition of the enzyme to virions resulted in increased infectivity. Remarkably, even remnants of enzyme-treated subviral particles proved to be inhibitory to infection. A noninfectious deletion mutant devoid of the binding region for carboxypeptidase D could be rendered infectious for primary duck hepatocytes by treatment with chymotrypsin. Although because of the protease treatment mutant and wild-type viruses may have become infectious in an unspecific and receptor-independent manner, their host range specificity was not affected, as shown by the inability of the virus to replicate in different hepatoma cell lines, as well as primary chicken hepatocytes. Instead, the organotropicity of the virus could be reduced, which was demonstrated by infection of primary duck kidney cells.

Effects of fumonisins on liver and kidney sphinganine and the sphinganine to sphingosine ratio during chronic exposure in ducks

Sa and the Sa/So ratio are very sensitive biomarkers of exposure to fumonisins in several species. We previously demonstrated that increases in Sa and in the Sa/So ratio in serum were less pronounced when ducks ingested fumonisins for more than 7 weeks than when animals were exposed for only 1–2 weeks [S.T. Tran, D. Tardieu, A. Auvergne, J.D. Bailly, R. Babilé, S. Durand, G. Benard, P. Guerre, Serum sphinganine and the sphinganine to sphingosine ratio as biomarker of dietary fumonisins during chronic exposure in ducks, Chem. Biol. Interact., in press]. The aim of this study was to investigate the kinetics of Sa and of the Sa/So in both liver and kidney of ducks that have been previously tested for Sa and the Sa/So ratio in serum. Analysis were performed on treatment days 0, 7, 14, 28 and 77 in five groups of ducks fed fumonisins obtained from an extract of Fusarium verticillioides culture material by daily gavage to obtain an exposure equal to 0, 2, 8, 32 and 128 mg FB1/kg feed. Sa and the Sa/So ratio in tissues were then correlated with Sa and the Sa/So ratio previously obtained in serum. The amounts on sphinganine 1-phosphate (Sa1P) and sphingosine1-phosphate (So1P) in the liver were also investigated. On day 7 of treatment, 2 mg/kg FB1 in the feed were sufficient to increase Sa and the Sa/So ratio in liver (by 165 and 148%, respectively) and kidney (by 193 and 104%, respectively). At a rate of 128 mg/kg FB1 in the feed, a very high increase in Sa concentration was observed in both liver and kidney without mortality and/or signs of necrosis (respective increase of 2034 and 3768%). Although the precise mechanism of the resistance of ducks to fumonisin-induced hepatotoxicity is still uncertain, it might be linked to the rate at which the sphingoid bases sphinganine and sphingosine are converted to their 1-phosphate or other metabolite and eliminated from target tissues.

Plaque morphology of Italian H7N1 LPAI isolates in MDCK cells and in primary cells of different avian species.

The morphology of plaques induced by Italian, H7N1, low-pathogenic avian influenza (LPAI) viruses belonging to different lineages was investigated in primary chicken, turkey, Muscovy duck, and mallard duck kidney cells and in MDCK cells in the absence of trypsin. LPAI isolates were selected on the basis of the location in the phylogenetic tree: 977/V99 (located at the root, no additional glycosylation site [nAGS]), 2379N99 (AGS in position 123), and 3675/V99 (AGS in position 149). Different isolates did not induce plaques with a statistically significant different size in MDCK cells. However, in primary cells of different avian origin, the presence or absence of AGS significantly influenced plaque size. Generally speaking, 977N99 was the least efficient at plaquing in all cells, while 2379/V99 (AGS in position 123) plaqued more efficiently in turkey cells and 3675/V99 (AGS in position 149) in chicken cells. The presence of either AGS induced statistically significant larger plaques in cells of waterfowl origin.

Cadmium and lead in tissues of Mallards ( Anas platyrhynchos) and Wood Ducks ( Aix sponsa) using the Illinois River (USA)

Cadmium and lead concentrations were determined in the tissues of Mallards and Wood Ducks collected from two waterfowl management areas along the Illinois River, USA, during the autumn and late winter of 1997–1998. Lead concentrations in livers of Mallards were lower than previously reported, and, along with those in a small sample of Wood Duck livers, were within background levels (<2.0 μg/g wet weight). Mean concentrations of cadmium in the kidneys of Wood Ducks utilizing the Illinois River were four times greater than in after-hatch-year Mallards, and 14 times greater than in hatch-year Mallards. Concentrations of cadmium in the kidneys of Wood Ducks were comparable with those of specimens dosed with cadmium or inhabiting contaminated areas in previous studies. Wood Ducks utilizing wetlands associated with the Illinois River, and presumably other portions of the lower Great Lakes region, may be chronically exposed to cadmium.

Tissue residues of ractopamine and urinary excretion of ractopamine and metabolites in animals treated for 7 days with dietary ractopamine.

Ractopamine HCl is a beta-adrenergic leanness-enhancing agent recently approved for use in swine. Depletion of ractopamine in tissues, and elimination of ractopamine and its metabolites in urine, is of interest for the detection of off-label use. The objectives of this study were to measure the residues of ractopamine in livers and kidneys of cattle (n = 6), sheep (n = 6), and ducks (n = 9) after treatment with dietary ractopamine for seven (sheep, ducks) or eight (cattle) consecutive days and to measure the depletion of ractopamine from urine of cattle and sheep. Two cattle and sheep and three ducks were each slaughtered with withdrawal periods of 0, 3, and 7 d. Urine samples were collected daily from cattle and sheep. Tissue ractopamine concentrations were determined using the regulatory method (FDA approved) for ractopamine in swine tissues. Ractopamine residues in urine samples were measured before and after hydrolysis of conjugates. Analysis was performed with HPLC using fluorescence detection after liquid- (hydrolyzed samples) and(or) solid-phase extraction. No residues were detected in duck tissues. Liver residues in sheep averaged 24.0 and 2.6 ppb after 0- and 3-d withdrawal periods, respectively. Sheep liver residues after a 7-d withdrawal period were less than the limit of quantification (2.5 ppb). Sheep kidney residues were 65.1 and undetectable at 0- and at 3- and 7-d, withdrawal periods, respectively. Cattle liver residues were 9.3, 2.5, and undetectable after 0-, 3-, and 7-d withdrawal periods, respectively; kidney residues were 97.5, 3.4, and undetectable at the same respective withdrawal periods. Concentrations of parent ractopamine in sheep urine were 9.8+/-3.3 ppb on withdrawal d 0 and were below the LOQ (5 ppb) beyond the 2-d withdrawal period. After the hydrolysis of conjugates, ractopamine concentrations were 5,272+/-1,361 ppb on withdrawal d 0 and 178+/-78 ppb on withdrawal d 7. Ractopamine concentrations in cattle urine ranged from 164+/-61.7 ng/mL (withdrawal d 0) to below the LOQ (50 ppb) on withdrawal d 4. After the hydrolysis of conjugates in cattle urine, ractopamine concentrations were 4,129+/-2,351 ppb (withdrawal d 0) to below the LOQ (withdrawal d 6). These data indicate that after the hydrolysis of conjugates, ractopamine should be detectable in urine of sheep as long as 7 d after the last exposure to ractopamine and as long as 5 d after withdrawal in cattle.

Acute Toxicity of Ingested Zinc Shot to Game-farm Mallards

We conducted a 30-day acute toxicity test of zinc (Zn) shot using 6- to 8-month-old wild-type game-farm Mallards (Anas platyrhynchos), 40 of which (20 males and 20 females) were dosed with 6 No. 4 candidate shot pellets containing 98% Zn and 2% tin (Sn); the remaining 40 ducks were dosed with 6 No. 4 steel (Fe) shot and served as controls. The Zn shot resulted in high mortality, with a greater proportion of females dying than males. For the 30-day study, survival averaged 18 and 23 days for female and male Zn-dosed ducks, respectively; all Fe-dosed ducks survived to Day 30. Ataxia/paresis and other signs of intoxication were noted in a large portion of Zn-dosed ducks. For all ducks retaining 6 shot pellets, including those that survived &lt; 30 days, shot retention, percent of the original shot weight dissolved, and dissolution rates were similar for Zn- and Fe-dosed ducks. For those ducks that retained 6 pellets and survived to Day 30, percent loss of the original shot weight and the dissolution rate were higher in Zn-dosed ducks. Mean body weight in Zn-dosed ducks decreased between Days and 15, and between Days 15 and 30 in Zn-dosed females. Zn-intoxicated ducks lost a considerable proportion of their body weight between dosing and death. The kidneys of Zn-dosed ducks as a group were heavier, and the pancreases, livers, and gizzards lighter, as compared with Fe-dosed ducks. The liver (males) and kidneys of Zn-dosed ducks that died as a result of Zn intoxication were heavier, whereas thegonads (females) and gizzards were lighter, as compared with those that survived. The liver, pancreas, and kidneys increased, whereas the gonads (males) and gizzards decreased, as a proportion of total body weight in Zn-dosed ducks that died prior to Day 30. Mean packed cell volume (PCV) decreased between Days and 15 and increased between Days 15 and 30 in male and female Zn-dosed ducks. PCV values changed little in Fe-dosed ducks over the course of the study; however, PCV decreased dramatically in Zn-intoxicated ducks. A variety of gross lesions was observed, most often associated with the gastrointestinal tract. Grossly, cecal lesions were the most consistent and dramatic changes observed. No macroscopic lesions were observed in the Fe-dosed ducks, and histologic lesions in this group were considered within normal limits for game-farm ducks. Histologic lesions observed in Zn-dosed Mallards most often included pancreatic apoptosis, splenic lymphoid depletion and/or lympholysis, necrohemorrhagic typhlitis, and necrosis of the epithelial cells of the renal tubules. We detected high concentrations of Zn, and alterations in levels of other elements, in the tissues of Zn-dosed ducks relative to Fe-dosed controls. Mean Zn concentrations were greater in Zn-dosed ducks for all tissues examined, and levels in the kidneys, livers, and pancreases of Zn-intoxicated Mallards were similar to levels associated with toxic effects reported in other studies. Mean tissue tin (Sn) concentrations were below the Method Detection Limit (MDL) in all cases; few individual Sn values were above MDLs. Changes in tissue element concentrations tended to be more dramatic in ducks that died as a result of Zn intoxication than in Zn-dosed ducks that survived the experiment. Gender differences in analyte concentrations were detected for some tissues. These results indicated that dosing of 6- to 8-month-old game-farm Mallards with 6 No. 4 shot comprised of 98% Zn and 2% Sn produced toxic effects under the test conditions.

Accumulation and effects of lead and cadmium on wood ducks near a mining and smelting complex in Idaho

: A study of wood ducks (Aix sponsa) was conducted along the Coeur d'Alene River system in northern Idaho in 1986 and 1987. Most of this area has been subjected to severe contamination from lead and other metals from mining and smelting since the 1880s. In 1986, a preliminary study of wood duck nesting was conducted in the contaminated area; incubating hens captured in nest boxes were bled and weighed. Blood samples were used to determine lead and cadmium concentrations and physiological characteristics. In 1987, an intensive study of wood ducks involved trapping and monitoring nest boxes in the contaminated area. Blood and tissue samples were also taken from wood ducks from a reference area without known contamination from metals. Lead levels in blood and tissues of most wood ducks from the contaminated area frequently exceeded those considered hazardous to birds; maximum levels (wet weight) of lead were 8 μg g(-1) in blood and 14 μg g(-1) in liver. Changes in physiological characteristics constituted the only evidence of potentially adverse effects from lead. In the contaminated area, nesting success (55% unadjusted, 35% Mayfield estimate) was less than in other areas where predation was low and nest boxes were used; but lead concentrations and physiological characteristics of blood were similar in successful and unsuccessful hens.Values of ALAD, hemoglobin, and body mass were negatively correlated with blood concentrations of lead, whereas protoporphyrin was positively correlated with lead levels in the blood. Some of the protoporphyrin values (1,091 μg dl(-1) in a male and 756 μg dl(-1) in a female) equalled those associated with lead toxicosis in experimental birds. ALAD activity was low in most birds from the contaminated area; values of 0 were obtained from 11 birds. Lead levels in blood, ALAD, protoporphyrin, and hemoglobin were significantly different between birds from the contaminated and reference areas. Concentrations of lead in ingesta of wood ducks ranged from 0.9 to 610 μg g(-1) in the contaminated area and 0.2 to 0.6 μg g(-1) in the reference area. Levels of cadmium in kidneys of wood ducks ranged from 1μg g(-1) to 20 μg g(-1) in the contaminated area and from only to 0.1 μg g(-1) to 1 μg g(-1) in the reference area. Cadmium concentrations were less than known effect levels.

The identification and characterization of 125I-labelled iodomelatonin-binding sites in the duck kidney

The melatonin-binding sites in membrane preparations of duck kidney were demonstrated by utilizing 125I-labelled iodomelatonin as a radioligand. Binding at these sites was found to be reversible, saturable, specific and of high affinity. Scatchard analysis of the specific binding revealed an equilibrium binding constant (Kd) of 44.6 +/- 4.4 pmol/l (n = 6) and a total number of binding sites (Bmax) of 6.43 +/- 0.60 fmol/mg protein (n = 6) at the mid-point of the light period (mid-light). The Hill coefficient approached 1.0, suggesting a single class of 125I-labelled iodomelatonin-binding site in the duck kidney. Diurnal variation in 125I-labelled iodomelatonin binding showed that the Bmax was 53.4% higher at mid-light than at mid-point of the dark period (P < 0.05), with no significant variation in Kd. The Kd value determined from kinetic analysis was 22.5 pmol/l in birds at mid-light, which was comparable with values determined from equilibrium studies. The order of pharmacological affinity for 125I-labelled iodomelatonin-binding sites in the duck kidney membrane preparations was: 2-iodomelatonin > melatonin > 6-chloromelatonin > 6-hydroxymelatonin > N-acetylserotonin >> 5-methoxytryptamine, 5-methoxytryptophol, 5-hydroxytryptamine, tryptamine, 1-acetylindole-3-carboxaldehyde, 5-hydroxyindole-3-acetic acid, L-tryptophan, 5-methoxyindole-3-acetic acid, 3-acetylindole, acetylcholine, epinephrine, norepinephrine and harmaline. The pharmacological characteristics indicated that 125I-labelled iodomelatonin-binding sites are highly specific for melatonin. Our finding of 125I-labelled iodomelatonin-binding sites in the kidney suggests that melatonin may regulate kidney function.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of some inducers on hepatic and extrahepatic drug metabolism in the mallard duck ( Anas platyrhynchos)

1. Cytochrome P-450-dependent activities were measured in the liver, duodenum and kidney of mallard ducks ( Anas platyrhynchos) after pretreatment with known inducers of these enzymes (phenobarbital, β-naphthoflavone, polychlorobiphenyls, and two imidazole fungicides, prochloraz and imazalil). 2. Liver enzymes were highly induced by phenobarbital, and to a lesser extent by β-naphthoflavone. Considerable differences were found between ducks and rodents in the nature of monooxygenase acivities expressed after pretreatment with these two compounds. PCBs and fungicides caused only minor modifications in cytochrome P-450 level and enzymatic activities. 3. Extrahepatic enzyme activities were induced by phenobarbital, and were modified only slightly by other compounds.

Modulation of kidney function in conscious Pekin ducks by atrial natriuretic factor.

The influence of avian atrial natriuretic factor (ANF) on renal function was examined in conscious saltwater-acclimated Pekin ducks undergoing a steady state diuresis maintained by iv infused isotonic avian Krebs-Ringer solution at a rate of 1.0 ml/min. Synthetic chicken ANF (chANF) was applied iv at doses of 10, 50, and 90 ng/min.kg BW for 10 min and caused dose-dependent transient increases in urine flow, osmolal excretion, glomerular filtration rate, effective renal plasma flow, and fractional water clearance at decreased urinary osmolality. Using receptor autoradiography, binding sites for [125I]Bolton-Hunter-labeled chANF [( 125I]BH-chANF) were localized in both the reptilian-type glomeruli and the collecting duct system throughout the duck kidney. A RRA for [125I]BH-chANF, established using an enriched kidney membrane fraction, indicated that unlabeled chANF and human ANF competitively displaced [125I]BH-chANF with comparable potencies. ANF-induced modulation of renal salt and water elimination via glomerular and tubular receptor interactions is consistent with the concept that this hormone has a physiological role in avian volume homeostasis.

Manganese, copper, zinc, iron, cadmium, mercury and lead in muscle meat, liver and kidneys of poultry, rabbit and sheep slaughtered in the northern part of Poland, 1987

Manganese, copper, zinc, iron, cadmium, mercury and lead concentrations have been determined in muscle meat, livers and kidneys of ducks, geese, chickens, hens, rabbits and sheep slaughtered in the northern part of Poland in 1987. The mean values obtained related to wet weight for muscle meat, livers and kidneys of animals were: 0.11-0.27, 0.73-3.3 and 0.90-1.9 mg/kg Mn; 0.52-7.3, 3.8-88 and 2.8-15 mg/kg Cu; 5.7-40, 20-45 and 21-30 mg/kg Zn; 10-35, 27-83 and 50-180 mg/kg Fe; less than 5-5, 16-140 and 250-5100 micrograms/kg Cd; less than 1-3, 2-10 and 5-12 micrograms/kg Hg; and less than 10-20, 100-210 and 120-1300 micrograms/kg Pb, respectively. Substantial differences have been found in the mean copper concentration in muscle meat, livers and kidneys, zinc and iron in muscle meat, and cadmium in kidneys, between some of the species examined. The mean and maximum concentrations of mercury and lead found in muscle meat and organs of animals in the present study were low, and only in the case of cadmium were somewhat higher values found in kidneys of rabbit and hen. The results obtained are compared with the literature data on the concentrations of the metals examined in muscle meat, livers and kidneys of poultry, rabbit and sheep in Poland or elsewhere.

Combined nephrotoxicity of methylmercury, lead, and cadmium in Pekin ducks: metallothionein, metal interactions, and histopathology.

This report describes the metallothionein (MT) levels and accumulation of mercury, lead, and cadmium, as well as their interaction with tissue zinc, copper, and iron, and the histopathological changes in kidneys of ducks exposed to methylmercury chloride (MeHgCl), lead acetate (PbAc), and cadmium chloride (CdCl2), singly or in combination for 13 wk. Forty-eight female Pekin ducks, divided into 8 groups of 6 birds each, were fed diets containing no added metals (control), 8 mg MeHgCl/kg feed, 80 mg PbAc/kg feed, 80 mg CdCl2/kg feed, 8 mg MeHgCl + 80 mg PbAc/kg feed, 8 mg MeHgCl + 80 mg CdCL2/kg feed, 80 mg PbAc + 80 mg CdCl2/kg feed, and 8 mg MeHgCl + 80 mg PbAc + 80 mg CdCL2/kg feed. Cadmium (Cd) when administered alone or in combination caused a 60-fold increase in kidney MT levels, while methylmercury (MeHg) or lead (Pb) administration caused a threefold increase in kidney MT levels. No significant changes in kidney MT levels were observed when metals were administered concurrently when compared with single-treatment groups. Residue analysis revealed accumulation of administered metals in kidney tissue. However, lead administration resulted in accumulation of small amounts of this element in kidney tissue. Simultaneous administration of MeHgCl and PbAc significantly increased the accumulation of lead in kidney when compared with PbAc-treated group. Cadmium when administered alone or in combination caused an increase in the levels of zinc and copper in kidney. Administration of MeHgCl or PbAc either alone or in combination caused increased iron levels in kidney, while cadmium administration either alone or in combination caused decreased iron levels. Administration of cadmium either alone or in combination caused degenerative changes in kidney proximal tubules. The severity of degenerative lesions increased when cadmium was simultaneously administered with other metals. These results indicate that combined administration of MeHg, Pb, and Cd has no significant effect on kidney MT levels or on essential elements in kidney tissue when compared with single metal groups. However, there appears to be an increase in the severity of histopathologic changes.

Processing of colloidal gold particles in the glomerular mesangium and macula densa of the duck kidney

Bovine-serum-albumin coated colloidal gold particles were injected intravenously into healthy, adult domestic ducks. The fate of these tracer particles was followed in a timesequence up to 4–5 days in the renal glomerular mesangium—distal tubule macula densa junction with transmission electron microscopy. The bulk of particle aggregates is ‘trapped’ in the mesangial channel system, phagocyted by mesangial cells, exocyted back into the mesangial channels, transported extracellularily towards the vascular hilus, rephagocyted by macula densa cells and expelled into the tubular lumen. This process requires about nineteen hours in the experimental model chosen, although it continues to take place to a much lower extent even 4–5 days after administration of the tracer. This mode of macromolecular excretion may be of interest in connection with the pathogenesis of several forms of glomerulonephritis.

Duck virus enteritis (anatid herpesvirus infection) in mute swans(Cygnus Olor)

An outbreak of duck virus enteritis (DVE) in mute swans (Cygnus olor) is described. Ninety-nine captive swans in a flock of 440 died within 3 months. The origin was obscure. The infection did not spread to other species on the same premises. Clinical signs included polydypsia, photophobia, inappetance, drooping wings, watery nasal discharge and yellowish diarrhoea. Necropsies were made on eight swans. All showed a diphtheritic oesophagitis especially near the oesophageal-proventricular junction. Whitish, necrotic plaques from 1 mm to 3 cm in extent affected the epithelium of the small intestine. Other lesions were present but less consistent. Histological examination of livers showed typical lesions of DVE associated with intranuclear inclusions. The virus was propagated in duck kidney cell cultures and on second passage caused a cytopathic effect with intranuclear inclusions typical of DVE. Presence of virus was confirmed by electron microscopy. Experimentally the virus infected susceptible, unvaccinated ducklings, but not those vaccinated against DVE.

脚弱鶏の関節材料からのトリレオウイルスの分離および分離株の性状

Avian reoviruses were isolated from the tendons and tendon sheaths of 19 chickens of 7 flocks out of 127 tested birds of 22 flocks with clinical evidence of leg weakness. Biological andserological characteristics were examined in 7 isolates selected from the 7 flocks each.All the isolates produced cytopathic effect (CPE) in chicken kidney and chicken embryo liver and lung cells. Some of them failed to produce CPE in chicken embryo fibroblasts, duck kidney cells, duck embryo fibroblasts and Vero cells. All the isolates produced plaques of differentsizes in chicken kidney cells. Two of the 7 isolates killed all chicken embryos when inoculated viayolksac, allantoic sac and chorioallantoic membrane. Crossneutralization test revealed that the isolates could be divided into three serogroups.