Laboratory Outbreak investigation of Sudden Death Syndrome in Broiler Chicken in Kathmandu Valley Nepal 2010

2011 ◽  
Vol 8 (2) ◽  
pp. 607-610
Author(s):  
Kedar Karki
Keyword(s):  
Sudden Death ◽  
Broiler Chicken ◽  
Sudden Death Syndrome ◽  
Outbreak Investigation ◽  
Kathmandu Valley

Diet, total plasma homocysteine concentrations and mortality rates in broiler chickens

2003 ◽  
Vol 83 (3) ◽  
pp. 601-604 ◽  
Author(s):  
S. E. Samuels
Keyword(s):  
Cardiovascular Disease ◽  
Sudden Death ◽  
Broiler Chickens ◽  
Independent Risk Factor ◽  
Total Mortality ◽  
Mortality Rates ◽  
Plasma Homocysteine ◽  
Sudden Death Syndrome ◽  
Total Plasma ◽  
Elevated Plasma

The aim of this study was to determine if total plasma homocysteine (HCY) concentrations and mortality rates due to ascites syndrome and (AS) sudden death syndrome (SDS) in broiler chickens could be lowered by diet. Elevated plasma HCY is an independent risk factor for cardiovascular disease in humans. A total of 828 day-old male broiler chickens (Arbor Acre) were fed, for 6 wk, either a basal practical diet or one supplemented with excess vitamins B6 and B12, folic acid and betaine to stimulate the degradation of HCY. The supplemented diet decreased plasma HCY by 17% (P < 0.05; n = 16 per diet). Total mortality due to AS and SDS was 18% lower in the supplemented diet but this difference was not statistically significant. Key words: Homocysteine, folate, chickens, cardiovascular disease, ascites, sudden death syndrome

scholarly journals The Genome Sequence of the Fungal Pathogen Fusarium virguliforme That Causes Sudden Death Syndrome in Soybean

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e81832 ◽  
Author(s):  
Subodh K. Srivastava ◽  
Xiaoqiu Huang ◽  
Hargeet K. Brar ◽  
Ahmad M. Fakhoury ◽  
Burton H. Bluhm ◽  
...  
Keyword(s):  
Sudden Death ◽  
Genome Sequence ◽  
Fungal Pathogen ◽  
Sudden Death Syndrome ◽  
Fusarium Virguliforme

Role of cardiac hypoxia in the pathogenesis of sudden death syndrome in broiler chickens – A metabolic and molecular study

2021 ◽  
Author(s):  
Pegah Safaei ◽  
Gholamhossein Khadjeh ◽  
Mohammad Reza Tabandeh ◽  
Keramat Asasi
Keyword(s):  
Sudden Death ◽  
Cardiac Muscle ◽  
Internal Control ◽  
Broiler Chickens ◽  
Sudden Death Syndrome ◽  
Pyruvate Dehydrogenase Kinase ◽  
Cardiac Insufficiency ◽  
Monocarboxylate Transporter ◽  
Pcr Analysis ◽  
Glucose Transporter 1

AbstractSudden death syndrome (SDS) is an economically important disorder in broiler chickens with unknown aetiology. The aim of the present study was to evaluate the metabolic and molecular alterations related to hypoxia in the myocardium of broiler chickens with SDS. Samples from the cardiac muscle of internal control broiler chickens (ICs) (n = 36) and chickens having died of SDS (n = 36) were obtained during the rearing period. The activities of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) and the concentration of lactate were measured in the cardiac tissue using available commercial kits. The expression of hypoxia-inducing factor 1α (HIF1α), glucose transporter 1 (GLUT1), pyruvate dehydrogenase kinase 4 (PDHK4) and monocarboxylate transporter 4 (MCT4) genes was determined in the myocardium by real-time PCR analysis. The results showed the elevation of lactate level and activities of LDH and CPK in the cardiac muscle of SDS-affected chickens compared with the IC birds (P < 0.05). The cardiac muscle expression of HIF1α, MCT4 and GLUT1 genes was increased, while the PDHK4 mRNA level was decreased in the SDS-affected group compared to those in the IC chickens (P < 0.05). Our results showed that metabolic remodelling associated with hypoxia in the cardiac tissues may have an important role in the pathogenesis of cardiac insufficiency and SDS in broiler chickens.

scholarly journals A Gated Recurrent Units (GRU)-Based Model for Early Detection of Soybean Sudden Death Syndrome through Time-Series Satellite Imagery

2020 ◽  
Vol 12 (21) ◽  
pp. 3621
Author(s):  
Luning Bi ◽  
Guiping Hu ◽  
Muhammad Mohsin Raza ◽  
Yuba Kandel ◽  
Leonor Leandro ◽  
...  
Keyword(s):  
Time Series ◽  
Early Detection ◽  
Sudden Death ◽  
Near Infrared ◽  
Time Series Data ◽  
Sudden Death Syndrome ◽  
Plant Diseases ◽  
Series Data ◽  
Detection Accuracy ◽  
Test Accuracy

In general, early detection and timely management of plant diseases are essential for reducing yield loss. Traditional manual inspection of fields is often time-consuming and laborious. Automated imaging techniques have recently been successfully applied to detect plant diseases. However, these methods mostly focus on the current state of the crop. This paper proposes a gated recurrent unit (GRU)-based model to predict soybean sudden death syndrome (SDS) disease development. To detect SDS at a quadrat level, the proposed method uses satellite images collected from PlanetScope as the training set. The pixel image data include the spectral bands of red, green, blue and near-infrared (NIR). Data collected during the 2016 and 2017 soybean-growing seasons were analyzed. Instead of using individual static imagery, the GRU-based model converts the original imagery into time-series data. SDS predictions were made on different data scenarios and the results were compared with fully connected deep neural network (FCDNN) and XGBoost methods. The overall test accuracy of classifying healthy and diseased quadrates in all methods was above 76%. The test accuracy of the FCDNN and XGBoost were 76.3–85.5% and 80.6–89.2%, respectively, while the test accuracy of the GRU-based model was 82.5–90.4%. The calculation results show that the proposed method can improve the detection accuracy by up to 7% with time-series imagery. Thus, the proposed method has the potential to predict SDS at a future time.

scholarly journals First Report of Sudden Death Syndrome (Fusarium solani f. sp. glycines) of Soybean in Minnesota

Plant Disease ◽  
2003 ◽  
Vol 87 (4) ◽  
pp. 449-449 ◽  
Author(s):  
J. E. Kurle ◽  
S. L. Gould ◽  
S. M. Lewandowski ◽  
S. Li ◽  
X. B. Yang
Keyword(s):  
Sudden Death ◽  
Fusarium Solani ◽  
Growth Stage ◽  
Soybean Seed ◽  
Sudden Death Syndrome ◽  
South Central ◽  
Soil Temperatures ◽  
Glycine Max L ◽  
Pathogenicity Tests ◽  
Soybean Plants

In August 2002, soybean (Glycine max (L.) Merr.) plants exhibiting foliar and root symptoms typical of sudden death syndrome were observed in Blue Earth and Steele counties in south-central Minnesota. Leaf symptoms ranging from small chlorotic spots to prominent interveinal necrosis were present on soybean plants at the R6 to R7 growth stage. As plants matured, complete defoliation took place with only petioles remaining. Symptomatic plants had necrotic secondary roots, truncated taproots, and discolored cortical tissue at the soil line. Blue sporodochia containing macroconidia were observed on the taproot of affected plants at both locations (3,4). Multiple cultures from both locations were obtained by transferring macroconidia from the sporodochia to potato dextrose agar (PDA) and modified Nash-Snyder Medium (NSM) (3). After 14 days, isolations were made from fungal colonies exhibiting bluish pigmentation and masses of bluish macroconidia (4). The isolates grew slowly, developed a bluish color, and formed sporodochia containing abundant macroconidia on NSM. These isolates were identified as Fusarium solani (Mart.) Sacc. f. sp. glycines based on colony characteristics and morphology of macroconidia (2). Pathogenicity tests were conducted with a single isolate from each location. The isolate from Blue Earth County was inoculated as mycelia in a plug of media onto taproots of plants of susceptible cvs. Williams 82 and Spencer at the V2 growth stage. Chlorotic spots appeared on leaves after 12 days of growth at 22 to 25°C in the greenhouse. Interveinal necrosis appeared after 15 days (4). The isolate from Steele County was used to inoculate the susceptible cv. Great Lakes 3202. Sorghum seed (3 cm3) infested with mycelia of the isolate were placed 2 to 3 cm below soybean seed planted in Cone-Tainers. Noninfested sorghum seed was used as a control. Plants were maintained for 21 days at 22 to 28°C in the greenhouse. Chlorotic spots appeared on leaves of inoculated plants within 21 days after planting followed by the development of interveinal chlorosis and necrosis (1). Molecular analysis further supported the identification of the Steele County isolate as F. solani f. sp. glycines. Polymerase chain reaction with specific primers Fsg1 and Fsg2 of total genomic DNA extracted from the Steele County isolate amplified a 438-bp DNA fragment identical with that extracted from previously identified isolates of F. solani f. sp. glycines (1). In 2002, symptoms of sudden death syndrome were also reported in Olmsted, Freeborn, and Mower counties. Although studies are needed to determine the distribution of sudden death syndrome in the state, the occurrence of the symptoms at multiple locations suggests that F. solani f. sp. glycines is widely distributed in southeast and south-central Minnesota. The counties where sudden death syndrome symptoms were reported are located in the most productive soybean-growing region of Minnesota. Sudden death syndrome could be a serious threat to soybean production in this area since poorly drained, heavy, clay soils are common, and soil temperatures 18°C or less are normal before the end of May. References: (1) S. Li et al. Phytopathology 90:491, 2000. (2) K. W. Roy. Plant Dis. 81:566, 1997. (3) K. W. Roy et al. Plant Dis. 81:1100, 1997. (4) K. W. Roy. Plant Dis. 81:259, 1997.

scholarly journals A Fine mapping quantitative trait loci that underlie resistance to soybean sudden death syndrome using NILs and SNPs.

2018 ◽  
pp. 583-591
Author(s):  
Yi Chen Lee ◽  
M Javed Iqbal ◽  
Victor N Njiti ◽  
Stella Kantartzi ◽  
David A. Lightfoot
Keyword(s):  
Quantitative Trait Loci ◽  
Sudden Death ◽  
Candidate Genes ◽  
Quantitative Trait ◽  
Soybean Cyst Nematode ◽  
Snp Markers ◽  
Sudden Death Syndrome ◽  
Isogenic Line ◽  
Trait Loci ◽  
Glycine Max L

Soybean (Glycine max (L.) Merr.) cultivars differ in their resistance to sudden death syndrome (SDS), caused by Fusarium virguliforme. Breeding for improving SDS response has been challenging, due to interactions among the 18-42 known resistance loci. Four quantitative trait loci (QTL) for resistance to SDS (cqRfs–cqRfs3) were clustered within 20 cM of the rhg1 locus underlying resistance to soybean cyst nematode (SCN) on Chromosome (Chr.) 18. Another locus on Chr. 20 (cqRfs5) was reported to interact with this cluster. The aims here were to compare the inheritance of resistance to SDS in a near isogenic line (NIL) population that was fixed for resistance to SCN but segregated at two of the four loci (cqRfs1 and cqRfs) for SDS resistance; to examine the interaction with the locus on Chr. 20; and to identify candidate genes underlying QTL. Used were; a NIL population derived from residual heterozygosity in an F5:7 recombinant inbred line EF60 (lines 1-38); SDS response data from two locations and years; four segregating microsatellite and 1,500 SNP markers. Polymorphic regions were found from 2,788 Kbp to 8,938 Kbp on Chr. 18 and 33,100 Kbp to 34,943 Kbp on Chr. 20 that were significantly (0.005 < P > 0.0001) associated with resistance to SDS. The QTL fine maps suggested that the two loci on Chr. 18 were three loci (cqRfs1, cqRfs, and cqRfs19). Candidate genes were inferred.  An epistatic interaction was inferred between Chr. 18 and Chr. 20 loci. Therefore, SDS resistance QTL were both complex and interacting.

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