SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Clostridium botulinum type B toxicosis was diagnosed as the cause of generalized weakness and death in a group of cows and mules fed from the same batch of rye silage. One severely affected cow was treated and recovered, as did other less severely affected cows. All affected mules died. The remaining cattle in the herd were then vaccinated before continued feeding of the silage.
From 1974 to 1977, 62 wild mule deer (Odocoileus hemionus) fawns from Steens Mountain, Ore were euthanatized in autumn (23 deer), winter (21 deer), and spring (18 deer). The number of sarcocysts of Sarcocystis spp was counted in histologic sections of various muscular organs. Sarcocysts were seen in the muscle specimens of 14 of the 23 deer euthanatized in autumn (September to November) and in specimens from all 39 deer euthanatized in winter (December and January) and spring (March and April). The sarcocyst burden was greatest in the spring (736/deer), less in the winter (150/deer), and least in autumn (12/deer). Most sarcocysts collected from 3- to 5-month-old deer in autumn were immature, whereas most sarcocysts collected from 9- and 10-month-old deer in the spring were mature. More sarcocysts were seen in sections of muscles from limbs than in those of tongue, esophagus, and other skeletal muscles; the fewest sarcocysts were seen in the heart. Degenerating sarcocysts were seen in deer examined in the spring, but not in deer examined in autumn and winter. Sarcocystis was the only infectious agent found in unthrifty deer fawns. Of the 18 fawns (6 in autumn, 1974; 6 in winter, 1974; and 6 in spring, 1975) examined for helminths, only mild infections were seen in the deer examined in the spring of 1975. From 1974 to 1977, from the Crooked Creek area of Oregon, 48 mule deer fawns (12 in autumn, 18 in winter, and 18 in spring) were euthanatized and evaluated for Sarcocystis infections.(ABSTRACT TRUNCATED AT 250 WORDS)
Cutaneous fibromas of white-tailed deer (Odocoileus virginianus), when compared with normal skin of the same species, had a thinner basement membrane; thickened stratum spinosum with numerous melanocytes, desmosomes, polyribosomes, and tonofilaments; focal hyperplasia of the stratum granulosum containing numerous large, electron-dense keratohyalin granules with irregular borders and containing occasional cells with diffuse intranuclear virus particles; and a moderately thickened stratum corneum with (although rarely) small crystalline arrays of virus particles. Normal mule deer (Odocoileus hemionus) skin was structurally similar to that of the white-tailed deer. Mule deer fibromas were similar to those in white-tailed deer, except for diffuse thickening of the stratum granulosum (the cells of which contained large keratohyalin granules of various electron densities with occasional composite granules) and except for a markedly thickened stratum corneum that contained numerous intranuclear viral inclusions. In negatively stained homogenates of tumors from both deer species, viral particles resembled papillomaviruses.
Four mule foals received anti-RBC antibody from their dam's colostrum. Two foals developed anemia, 1 developed severe thrombocytopenia, and 1 did not develop any clinical or laboratory abnormalities. All foals had the same donkey sire. Seven mares, including the dams of foals 1 to 4, bred to the donkey sire produced anti-RBC antibody. Two mares produced anti-RBC antibody to the donkey RBC on the first mating. The donkey sire and 18 of its offspring were found to have an RBC antigen unique to mules and donkeys. Thus, all matings of this donkey to horse mares were incompatible. The reason for the high rate of sensitization of mares bred to this donkey is unknown.
Eleven-day-old female Mule ducks (Cairina moschata x Anas platyrhynchos) were individually infected per os with a single inoculation containing 10(4), 10(5) or 10(6) sporulated oocysts of E mulardi, or kept as uninfected controls. No mortality was observed. Growth rate was not modified at lower doses, but was reduced in the other 2 groups, with weight loss on d 7 post inoculation (PI). Blood was detected in feces by chemical characterization of hemoglobin as early as d 3 PI with the highest infecting dose, while oocyst excretion began on d 6 PI in all infected groups. With 10(5) and 10(6) oocysts, the authors observed a significant increase in sedimentation rate and a slight anemia. Total protein and lipid concentrations in the plasma decreased in the 3 infected groups. These results show the pathogenic effect of E mulardi in Mule duckling, with dose-dependent changes. All parameters, except sedimentation rate, showed maximal variations during the acute phase of infection, between d 6 and d 9 PI, and returned to normal values early, in relation to the infecting dose, except that the weight remained lower than in the uninfected group at the final control (d 28 Pl). These perturbations have been described in avian coccidiosis.
The receptivity and susceptibility of the Muscovy duck, the domestic duck, and their hybrid, the mule duck, toward an experimental infection by Eimeria mulardi were studied. To appraise their susceptibility, female ducklings were infected with a dose of 75,000 oocysts per duckling (bringing about a clinical coccidiosis). In another group, to compare the multiplication rates of the parasite in the three species of ducks, thus assessing their receptivity, an infection with 750 oocysts per duckling was realized. Eimeria mulardi develops in the three species of ducks. In each case, a significant decrease in growth in the contaminated group vs. the control group was noted, even though the Muscovy and the mule ducks were more susceptible to the contamination.
The limb bones of cursorial mammals may exhibit regional structural/material variations for local mechanical requirements. For example, it has been hypothesized that mineral content (%ash) and secondary osteon population density (OPD) progressively change from proximal (e.g., humerus) to distal (e.g., phalanx), in accordance with corresponding progressive changes in stress and mechanical/metabolic cost of functional use (both greatest in the distal limb). We tested this hypothesis in wild-shot Rocky Mountain mule deer by examining transverse segments from mid-diaphyses of medial proximal phalanges, principal metacarpals, radii, and humeri, as well as the lateral aspects of sixth ribs from each of 11 mature males. Quantified structural parameters included the section modulus (Z), polar moment of inertia (J), cortical area/total area ratio (CA/TA), bone girth, and cortical thickness. In addition, %ash and the prevalence of in vivo microcracks were measured in each bone. Thin sections from seven animals were further examined for OPD and population densities of new remodeling events (NREs). Results showed a significant progressive decrease in %ash from the humerus (75.4% +/- 0.9%) to the phalanx (69.4% +/- 1.1%) (P < 0.0001), with general proximal-to-distal increases in OPD and general decreases in J and Z. Thirteen microcracks were identified in the rib sections, and only two were observed in the limb bones. Although the ribs had considerably greater NREs, no significant differences in NREs were found between the limb bones, indicating that they had similar remodeling rates. Equivalent microcrack prevalence, but nonequivalent structural/material organization, suggests that there are regional adaptations that minimize microcrack production in locations with differences in loading conditions. The progressive proximal-to-distal decrease in %ash (up to 6%); moderate-to-high correlations between OPD, %ash, J, and CA/TA; and additional moderate-to-high correlations of these parameters with each bone's radius of gyration support the possibility that these variations are adaptations for regional loading conditions.
It has been known for some time that plant transposons can capture and mobilize cellular genes. Recent work by Jiang and coworkers((1)) has revealed that this process has happened on a massive scale. They found that portions of more than 1000 genes in rice have been captured and mobilized by members of the MULE family of transposons. In rice, and perhaps other plants as well, it appears that thousands of genes and portions of genes have been duplicated, transposed and rearranged. These results have fascinating implications for our understanding of the mode and tempo of gene evolution in plants.
Chronic wasting disease (CWD), a progressive and uniformly fatal neurological disorder, is characterized neuropathologically by intraneuronal vacuolation, spongiform change of the neuropil and astrocytic hyperplasia and hypertrophy. Ultrastructural neuropathological findings consist of (1) extensive vacuolation in neuronal processes, within myelin sheaths, formed by splitting at the major dense lines or within axons; (2) dystrophic neurites (dendrites, axonal preterminals and myelinated axons containing degenerating mitochondria and pleomorphic, electron-dense inclusion bodies); (3) prominent astrocytic gliosis; (4) amyloid plaques; and (5) giant neuronal autophagic vacuoles. Other findings include activated macrophages and occasional spheroidal structures containing densely packed fibrillar material of unknown origin, abundant structures suggestive of degenerating microtubules entrapped in filamentous masses, vacuoles and myelin figures. Similar findings have been previously observed in scrapie-infected hamsters and Creutzfeldt-Jakob disease (CJD)-infected mice, bovine spongiform encephalopathy, and CJD indicating that CWD in captive mule deer belongs to the subacute spongiform encephalopathies (transmissible brain amyloidoses).
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) in captive and free-ranging cervids in the USA; its origin is obscure. Archival formalin-fixed and paraffin-embedded specimens of 16 captive mule deer brains with CWD were analyzed using immunocytochemistry for the disease-associated prion protein (PrP). The most prominent pattern of PrP deposition were plaque-like structures, a substantial proportion of which were florid plaques surrounded by a rim of spongiform vacuoles. The percentage of florid plaques was highly variable according to region, ranging from 0% to 52.7%. The highest percentage was observed in the medulla and basal ganglia, the lowest in the cerebral cortex. Only three brains contained no florid plaques. There were also punctate synaptic-type and perivascular deposits, particularly in areas of severe spongiform change, and subpial and subependymal plaque-like deposits, whereas cerebellar involvement was mild. Thus, CWD brain pathology prominently features florid PrP plaques, as does variant Creutzfeldt-Jakob disease (vCJD), but differs in other characteristics from vCJD.
An electron microscopic study of the endogenous development of Eimeria mulardi Chauve, Reynaud and Gounel, 1994 was carried out in mule ducks which are hybrids of the domestic duck (Anas platyrhynchos) and the muscovy duck (Cairina moschata). All of the endogenous stages were seen within the nucleus of the host cell. Merozoites arose from ectomerogony and three mutually similar merogonies were noted. The asexual stages were found in leukocyte-like cells in the lamina propria of the jejunum, ileum and caecum, while the gamonts developed in glandular epithelial cells in the same part of the intestine.
Amyloid plaques were demonstrable in central nervous system tissues of adult captive mule deer affected with chronic wasting disease, a transmissible primary spongiform encephalopathy. Plaques were detected in tissues of 13 of 21 (62 per cent) spontaneously affected animals from 2 to 4 years of age or older, but were not found in 16 unaffected deer of from a few months to 12 years of age.
An experimental Eimeria mulardi coccidiosis was reproduced in mule ducks. A single dose of toltrazuril (7 mg per kg) was administered at two different endogenous stages: Day 2 (first meronts) or Day 5 (last meronts and gamonts). The efficacy of the drug was assessed on four criteria (body weight, oocyst counts, macroscopic lesions, and presence of the meronts and gamonts). To have a curative effect, a single dose of toltrazuril should be administered early on. However, a single treatment on Day 5 had a prophylactic effect.
The purpose of this study was to investigate if carotenoids could alleviate the adverse effects caused by aflatoxin with respect to growth performance and immune response. In two experiments, a total of 320 mule ducklings were assigned to 5 treatments, i.e. control, aflatoxin B(1) (AFB(1)) 200 ppb, AFB(1) +beta-carotene (BC) 200 ppm, AFB(1)+BC 400 ppm, and AFB(1)+astaxanthin (AS) 200 ppm. In experiment 1, the addition of beta-carotene or astaxanthin in the diet containing AFB(1) 200 ppb resulted in a significant decrease in average daily gain as compared with the control. AFB(1) 200 ppb alone and the addition of BC or AS on top of AFB(1) resulted in a significantly lower daily feed intake than for the control group. There were no significant differences in relative organ weights among treatment groups. Both treatments of BC 400 ppm and AS 200 ppm had significantly more macrophages harvested per duck than the control and AFB(1) 200 ppb treatments. However, there were no significant differences among treatments in percentages of phagocytotic macrophages and number of Candida albican phagocytized by phagocytotic macrophages. In experiment 2, blood biochemical parameters and antibody titers were evaluated. There were no significant differences among treatments in total bilirubin content and alkaline phosphatase activity in the serum or in antibody titers against fowl cholera. However, AFB(1) treatment had the highest activities of AST and ALT in the serum. The addition of BC 400 ppm on top of AFB(1) significantly reduced ALT activity as compared with the AFB(1) 200 ppb treatment. These results suggest that carotenoids could provide a slightly toxic alleviating effect on growth performance, enhance the chemotaxis ability of macrophages, and reduce ALT activity elevated by AFB(1).
A real-time quantitative Polymerase Chain Reaction (PCR) method has been developed for the quantitation of mule duck (Anas platyrhynchos x Cairina moschata) in binary duck/goose foie gras mixtures. The method combines the use of real-time PCR with duck-specific and endogenous control "duck + goose" primers to measure duck content and total foie gras content, respectively. Both PCR systems (duck-specific and duck + goose) were designed on the mitochondrial 12S ribosomal RNA gene (rRNA). The duck-specific system amplifies a 96 bp fragment from duck DNA, whereas the duck + goose system amplifies a 120 bp fragment from duck and goose DNA. The method measures PCR product accumulation through a FAM-labeled fluorogenic probe (TaqMan). The C(t) (threshold cycle) values obtained from the duck + goose system are used to normalize the ones obtained from the duck-specific system. Analysis of experimental duck/goose foie gras binary mixtures demonstrated the suitability of the assay for the detection and quantitation of duck in the range of 1-25%. This genetic marker can be very useful to avoid mislabeling or fraudulent species substitution of goose by duck in foie gras.
Epidemics of contagious prion diseases can be perpetuated by horizontal (animal to animal) and maternal (dam to offspring, before or after birth) transmission, but the relative importance of each mechanism is unclear. Here we compare the incidence of chronic wasting disease (CWD) in captive mule deer (Odocoileus hemionus) that is attributable to horizontal or maternal transmission. We find that horizontal transmission is remarkably efficient, producing a high incidence of disease (89%) in a cohort of deer in which maternal transmission was improbable. Our results indicate that horizontal transmission is likely to be important in sustaining CWD epidemics.
The equilibrium O2-binding properties of the hybrid haemoglobin (Hb) present in vivo in erythrocytes from mule and of its parent Hbs from horse and donkey were compared with special reference to the effect of heterotropic ligands such as Cl-, D-glycerate 2,3-bisphosphate (DPG) and inositol hexakisphosphate. All these Hbs display a decreased effect by polyphosphates, confirming that what has been observed for horse Hb [Giardina, Brix, Clementi, Scatena, Nicoletti, Cicchetti, Argentin & Condò (1990) Biochem. J. 266, 897-900] is common to other equine species, at least from a qualitative standpoint. However, different quantitative aspects can be detected, which can be accounted for by a different role for the two types of chain in characterizing the binding free energy for the various heterotropic effectors. In particular, it is shown that the binding mode of DPG and inositol hexakisphosphate displays different features since long-range effects can be observed clearly for inositol hexakisphosphate but not for DPG. In general terms, in spite of a different intrinsic O2 affinity, the modulation of functional properties by third ligands leads these Hbs to behave, under physiological conditions, similarly to human HbA. It might represent an interesting example of how different species with similar functional needs find different ways to produce a similar functional behaviour.
Overfeeding of some waterfowl species results in obesity, which is mainly characterized by a dramatic hepatic steatosis induced by strong accumulation of lipids synthesized from dietary glucose in the liver. In mammals, fructose is known to be able to raise plasma triacylglycerol concentrations significantly; consequently, this may induce obesity. The aim of this study was to assess the effect of partial replacement of dietary glucose provided by corn starch with fructose on metabolism and fatty liver production in the Mule ducks. On the basis of 9.5 kg maize (132,920 kJ) given twice a day for 14 days, a supplementation of 9,800 kJ was provided in form of glucose, sucrose or high fructose corn syrup (HFCS: 50 % glucose, 42 % fructose and 8 % other saccharides). Fatty liver weight in ducks fed with glucose supplementation was 499 +/- 21 g. Sucrose or HFCS supplementation brought about a significant increase in liver weight (+ 18.7 % and + 16.3 % vs. glucose supplementation respectively, p < 0.05). These results suggest that the dietary fructose favors the liver steatosis by increasing hepatic lipogenesis. Postprandial plasma insulin concentrations were similar in ducks fed diets with or without fructose, suggesting that the effect of fructose on liver steatosis is not mediated by insulin.