scholarly journals The Effects of Heart and Skeletal Muscle Inflammation and Cardiomyopathy Syndrome on Creatine Kinase and Lactate Dehydrogenase Levels in Atlantic Salmon (Salmo salarL.)

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Muhammad Naveed Yousaf ◽  
Mark D. Powell

Heart and skeletal muscle inflammation (HSMI) and cardiomyopathy syndrome (CMS) are putative viral cardiac diseases of Atlantic salmon. This study examined the levels and correlated the serum enzymes creatine kinase (CK) and lactate dehydrogenase (LDH) to the histopathology of clinical outbreaks of HSMI and chronic CMS in farmed Atlantic salmon. A total of 75 fish from 3 different HSMI outbreaks, 30 chronic CMS fish, and 68 fish from 3 nondiseased fish groups were used as the study population (N=173). Serum CK and LDH levels correlated significantly with the total inflammation and total necrosis scores for HSMI fish (P=0.001). However, no correlation was identified for enzyme levels and histopathology scores for chronic CMS fish. The significantly increased CK and LDH levels and their positive correlations to histopathology differentiate HSMI from CMS clinically suggesting the potential use of enzymes for screening for HSMI is promising.

Viruses ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 465 ◽  
Author(s):  
Kannimuthu Dhamotharan ◽  
Torstein Tengs ◽  
Øystein Wessel ◽  
Stine Braaen ◽  
Ingvild B. Nyman ◽  
...  

Heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon (Salmo salar) was first diagnosed in Norway in 1999. The disease is caused by Piscine orthoreovirus-1 (PRV-1). The virus is prevalent in farmed Atlantic salmon, but not always associated with disease. Phylogeny and sequence analyses of 31 PRV-1 genomes collected over a 30-year period from fish with or without HSMI, grouped the viral sequences into two main monophylogenetic clusters, one associated with HSMI and the other with low virulent PRV-1 isolates. A PRV-1 strain from Norway sampled in 1988, a decade before the emergence of HSMI, grouped with the low virulent HSMI cluster. The two distinct monophylogenetic clusters were particularly evident for segments S1 and M2. Only a limited number of amino acids were unique to the association with HSMI, and they all located to S1 and M2 encoded proteins. The observed co-evolution of the S1-M2 pair coincided in time with the emergence of HSMI in Norway, and may have evolved through accumulation of mutations and/or segment reassortment. Sequences of S1-M2 suggest selection of the HSMI associated pair, and that this segment pair has remained almost unchanged in Norwegian salmon aquaculture since 1997. PRV-1 strains from the North American Pacific Coast and Faroe Islands have not undergone this evolution, and are more closely related to the PRV-1 precursor strains not associated with clinical HSMI.


Pathogens ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1050 ◽  
Author(s):  
Øystein Wessel ◽  
Elisabeth F. Hansen ◽  
Maria K. Dahle ◽  
Marta Alarcon ◽  
Nina A. Vatne ◽  
...  

Piscine orthoreovirus 1 (PRV-1) is the causative agent of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon (Salmo salar). The virus is widespread in Atlantic salmon and was present in Norway long before the first description of HSMI in 1999. Furthermore, in Canada the virus is prevalent in farmed Atlantic salmon but HSMI is not and Canadian isolates have failed to reproduce HSMI experimentally. This has led to the hypothesis that there are virulence differences between PRV-1 isolates. In this study we performed a dose standardized challenge trial, comparing six PRV-1 isolates, including two Norwegian field isolates from 2018, three historical Norwegian isolates predating the first report of HSMI and one Canadian isolate. The Norwegian 2018 isolates induced lower viral protein load in blood cells but higher plasma viremia. Following peak replication in blood, the two Norwegian 2018 isolates induced histopathological lesions in the heart consistent with HSMI, whereas all three historical Norwegian and the Canadian isolates induced only mild cardiac lesions. This is the first demonstration of virulence differences between PRV-1 isolates and the phenotypic differences are linked to viral proteins encoded by segment S1, M2, L1, L2 and S4.


2020 ◽  
pp. 3-10
Author(s):  
V. P. Melnikov ◽  
V. V. Pronin

Heart and skeletal muscle inflammation (HSMI) is one of the most widespread economically relevant diseases of farmed Atlantic salmon (Salmo salar), and it poses serious danger to its aquaculture. The disease was first reported in Norway in 1999. In 2006, the Norwegian researchers demonstrated its viral etiology. Heart and skeletal muscle inflammation is a novel and understudied highly contagious transboundary disease of Salmonidae characterized by erythrocyte damage, blood circulation failure, jaundice and aggregated signs of heart and skeletal muscle inflammation. The disease associated economic damage to aquaculture is enormous. Total cumulative mortality can reach 30% and morbidity can amount to 100%. Loss of quality of the commercial fish products due to melanised foci in the salmons’ muscles further increases the disease-associated economic losses. Aquacultured Atlantic salmon is the most susceptible to HSMI. Rainbow trout, chub salmon and bull trout are also susceptible species and the list is still being continued. The disease is caused by the virus belonging to genus Orthoreovirus in the family Reoviridae. Currently Piscine orthoreovirus demonstrates the tendency towards its global spread. The virus-induced disease is reported in Norway, Scotland, Ireland, Iceland, France, Germany, Italy, Denmark and Alaska. The majority of the outbreaks are registered in Central and Northern parts of Norway, which borders the Murmansk Oblast. The vicinity of the affected areas to Russia, the Gulf Stream passing the Norwegian shore while moving towards the Murmansk Oblast as well as wild Salmonidae migration to the Barents Sea, White Sea and Pechora Sea through the Norwegian territorial waters coupled with high stability of the virus compose high threat of Piscine orthoreovirus introduction to the Russian Federation from the adjacent countries.


Vaccines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 230
Author(s):  
Muhammad Salman Malik ◽  
Lena H. Teige ◽  
Stine Braaen ◽  
Anne Berit Olsen ◽  
Monica Nordberg ◽  
...  

Heart and skeletal muscle inflammation (HSMI), caused by infection with Piscine orthoreovirus-1 (PRV-1), is a common disease in farmed Atlantic salmon (Salmo salar). Both an inactivated whole virus vaccine and a DNA vaccine have previously been tested experimentally against HSMI and demonstrated to give partial but not full protection. To understand the mechanisms involved in protection against HSMI and evaluate the potential of live attenuated vaccine strategies, we set up a cross-protection experiment using PRV genotypes not associated with disease development in Atlantic salmon. The three known genotypes of PRV differ in their preference of salmonid host species. The main target species for PRV-1 is Atlantic salmon. Coho salmon (Oncorhynchus kisutch) is the target species for PRV-2, where the infection may induce erythrocytic inclusion body syndrome (EIBS). PRV-3 is associated with heart pathology and anemia in rainbow trout, but brown trout (S. trutta) is the likely natural main host species. Here, we tested if primary infection with PRV-2 or PRV-3 in Atlantic salmon could induce protection against secondary PRV-1 infection, in comparison with an adjuvanted, inactivated PRV-1 vaccine. Viral kinetics, production of cross-reactive antibodies, and protection against HSMI were studied. PRV-3, and to a low extent PRV-2, induced antibodies cross-reacting with the PRV-1 σ1 protein, whereas no specific antibodies were detected after vaccination with inactivated PRV-1. Ten weeks after immunization, the fish were challenged through cohabitation with PRV-1-infected shedder fish. A primary PRV-3 infection completely blocked PRV-1 infection, while PRV-2 only reduced PRV-1 infection levels and the severity of HSMI pathology in a few individuals. This study indicates that infection with non-pathogenic, replicating PRV could be a future strategy to protect farmed salmon from HSMI.


1979 ◽  
Vol 25 (6) ◽  
pp. 943-947 ◽  
Author(s):  
G P James ◽  
R L Harrison

Abstract We measured creatine kinase (EC 2.7.3.2) activity in 1009 serum samples from 538 patients in the intensive-care units of the University of Texas Medical Branch hospitals. Creatine kinase isoenzymes migrating cathodal to skeletal muscle creatine kinase (CK-MM) on cellulose acetate electrophoresis were found in sera from 14 of the 538 patients. Creatine kinase, lactate dehydrogenase (EC 1.1.1.27), aspartate aminotransferase (EC 2.6.1.1), and alanine aminotransferase (EC 2.6.1.2) activities were abnormally increased in these 14 patients. Liver lactate dehydrogenase isoenzyme (LDH5) and cardiac creatine kinase isoenzyme (CK-MB) were abnormally increased in 12 and eight of these patients, respectively. Ten of the 14 patients died during their hospital admission. We believe the creatine kinase isoenzymes that migrated cathodal to skeletal muscle creatine kinase (CK-MM) were of mitochondrial origin.


Author(s):  
J. Krafft ◽  
R. Fink ◽  
S. B. Rosalki

Serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities were abnormal in 76, 50, and 28% respectively of 50 patients studied within 26 hours of surgery. No patient showed clinical evidence of myocardial infarction. Creatine kinase MB isoenzyme elevation, and lactate dehydrogenase LD1 activity greater than LD2 (LD1 > LD2) were infrequent (6 and 10% respectively). No patient showed the combination of transient MB isoenzyme elevation and LD1 > LD2, although their rare association without infarction after surgery is to be anticipated.


1981 ◽  
Vol 241 (3) ◽  
pp. C98-C105 ◽  
Author(s):  
G. Suarez-Kurtz ◽  
A. B. Eastwood

Isolated, intact frog muscles bathed in control saline release creatine kinase (CK) and lactate dehydrogenase (LDH) at constant rates for several hours. The basal rates of release from “toe” muscles (CK 0.087%/min; LDH 0.105%/min) were one order of magnitude greater than those from semitendinosus muscles. This is attributed to differences in muscle mass and geometry, and to the smaller diameter of toe muscle fibers. Enzyme release rates were not affected by Na-free or Cl-free solutions, whereas LDH release rate doubled during exposure to Ca-free (EGTA-containing) saline or in the presence of isosmotic solutions containing 120 mM KCl or potassium propionate. Following mechanical injury or detergent treatment (Brij 58), the enzyme release rates into Ca-free medium reached peak values 4 and 16 times (toe muscle), and 16 and 20–30 times (semitendinosus), respectively, the control rates. The greater effect of detergent treatment is ascribed to a larger area of sarcolemmal damage plus possible changes in the state of the enzymes in the sarcoplasm.


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