scholarly journals Delayed peracute capture myopathy in a Himalayan Ibex Capra sibirica (Mammalia: Cetartiodactyla: Bovidae)

2018 ◽  
Vol 10 (10) ◽  
pp. 12363-12367
Author(s):  
Umar Nazir Zahid ◽  
Latief Mohammad Dar ◽  
Umar Amin ◽  
Showkat Shah ◽  
Rashid Yahya Naqash ◽  
...  
Keyword(s):  
Skeletal Muscles ◽  
Clinical Signs ◽  
Pathological Findings ◽  
Rescue Operation ◽  
Cortical Necrosis ◽  
Tubular Cells ◽  
Causes Of Mortality ◽  
Fatal Consequence ◽  
Myocardial Lesions ◽  
Capture Myopathy

The present study focused on the capture myopathy as a fatal consequence of capture and rescue operation in an endangered Himalayan Ibex kid. The Ibex died 48 hours after being captured without showing specific clinical signs.  Post-mortem examination revealed renal cortical necrosis, degeneration of tubular cells and congestion as the main histopathological findings in kidneys. Myocardial lesions consisted of multifocal degenerative changes of myofibres, hyalinization and nuclear degeneration with pyknosis. Skeletal muscles that appeared grossly normal showed mild to moderate degeneration and fragmentation with intermittent loss of striation. The pathological findings were indicative of delayed peracute capture myopathy. This is believed to be the first report of capture myopathy in an endangered Himalayan ibex from India underlining the importance of understanding the causes of mortality in such endangered wild species as a prerequisite to successful conservation programme.

STUDY OF CLINICAL CASES OF MYOCHE’S MYOPATHY AND DIFFERENTIAL DIAGNOSIS WITH OTHER TYPES OF ADVERSE MYOPATHIES

2021 ◽  
Author(s):  
K. Sarazhyna ◽  
Y. Solodovnikova ◽  
A. Son
Keyword(s):  
Case Report ◽  
Genetic Testing ◽  
Skeletal Muscles ◽  
Molecular Genetic ◽  
Clinical Signs ◽  
Lower Limbs ◽  
Molecular Genetic Testing ◽  
Membrane Repair ◽  
Rare Type ◽  
A Cell

Markesbery-Griggs myopathy, Miyoshi type (MM) is a rare type of myopathy, a form muscular dystrophy with the main involvement of the lower girdle and distal parts of the legs. Due to complexity of genetic testing, the diagnosis is mainly made on the neurological examination of the patient, which adds value to this case report. The childhood or adolescence onset of the disease is characterized initially by the calf muscles` wasting, accompanied by the severe elevation of the serum creatine kinase, as well as a slowly progressive ascending course. The disease refers to dysferlinopathies with various mutations in the DYSF gene. The dysferlin protein is localized in the plasma membrane and in the T-tubule system of skeletal muscles. Physiologically, skeletal muscles are constantly exposed to micromembrane lesions. Depending on the severity, these damages are restored using various complexes. One of the main reparative complexes is the dysferlin-dependent mechanism. Mutations can lead to a defect in the membrane repair, causing the influx of Ca 2+ into the cell, which leads to a cell`s destruction. There are three genetically identifiable types of Miyoshi myopathy: MMD1, MMD2, MMD3. The main clinical signs of the disease are the muscle weakness and atrophy, with predominant involvement of the distal parts of the lower limbs, especially in the gastrocnemius and plantar muscles. The MM causes tip toe walking disturbances and difficulties in climbing the stairs. Progression of the disease and further atrophy leads to the wasting of the lower girdle muscles, mainly gluteal ones. Peculiarity of these myopathies is the absence of cardiomyopathy, due to the immunity of cardiomyocytes to a deficiency of the protein dysferelin. Diagnosis is made on the basis of muscle biopsy and molecular genetic testing. The gold standard is immunoblotting or immunohistochemistry. One of treatment methods is the use of improperly folded dysferlin (treatment with a proteasome inhibitor MG-132) in fibroblasts with restoration of membrane sealing. The aim of this case report is to present an example of a possible clinical diagnosis of MM in a young man, in the absence of opportunities for molecular genetic testing.

Causes of Mortality and Pathological Findings in European Hedgehogs (Erinaceus europaeus) Admitted to a Wildlife Care Centre in Southwestern France from 2019 to 2020

2022 ◽  
Vol 190 ◽  
pp. 19-29
Author(s):  
Maria Zacharopoulou ◽  
Elise Guillaume ◽  
Guillaume Coupez ◽  
Céline Bleuart ◽  
Guillaume Le Loc'h ◽  
...  
Keyword(s):  
Pathological Findings ◽  
Care Centre ◽  
Erinaceus Europaeus ◽  
Causes Of Mortality

Cardiomyopathy caused by avocado (Persea Americana Mill) leaves

1991 ◽  
Vol 62 (1) ◽  
pp. 21-22 ◽  
Author(s):  
Rina Grant ◽  
P. A. Bassson ◽  
Hellen H. Booker ◽  
J. B. Hofherr ◽  
M. Anthonissen
Keyword(s):  
Clinical Signs ◽  
Persea Americana ◽  
Myocardial Lesions

Six of 21 goats feeding on fresh avocado (Persea americana) leaves from pruned trees, showed clinical signs of cardiac distress. Some sheep subsequently dosed experimentally at different dosage rates with the same and other avocado varieties, showed clinical signs of respiratory or cardiac distress and myocardial lesions at autopsy.

Effects of Jatropha curcas on Calves

1979 ◽  
Vol 16 (4) ◽  
pp. 476-482 ◽  
Author(s):  
O. M. M. Ahmed ◽  
S. E. I. Adam
Keyword(s):  
Jatropha Curcas ◽  
Total Protein ◽  
Aspartate Aminotransferase ◽  
Clinical Signs ◽  
Pathological Findings

Jatropha curcas seed was fed to six calves at doses of 2.5, 1 and 0.25 g/kg once and to two other calves at 0.025 g/kg up to 14 days. The onset of toxic manifestations in the six calves was rapid and death occurred within 19 hours of administration. The two calves that received daily the lowest dose of J. curcas showed signs of poisoning and died within 10 to 14 days. The clinical signs of diarrhoea, dyspnoea, dehydration and loss of condition were well correlated with the pathological findings. There was an increase in aspartate aminotransferase, ammonia and potassium and a decrease in total protein and calcium in the serum of jatrophapoisoned calves.

scholarly journals Light and Electron Microscopic Changes in Cardiac and Skeletal Muscle of Sheep with Experimental Monensin Toxicosis

1983 ◽  
Vol 20 (5) ◽  
pp. 590-602 ◽  
Author(s):  
A. W. Confer ◽  
D. U. Reavis ◽  
R. J. Panciera
Keyword(s):  
Skeletal Muscles ◽  
Ultrastructural Change ◽  
Creatine Phosphokinase ◽  
Interstitial Fibrosis ◽  
Light And Electron Microscopy ◽  
Clinical Signs ◽  
Electron Microscopic ◽  
Initial Exposure ◽  
Serum Creatine Phosphokinase ◽  
Cardiac Muscles

Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.

scholarly journals Clinical, laboratory and anatomopathological study of caudal vena cava thrombosis in cattle

2021 ◽  
Vol 41 ◽  
Author(s):  
Luiz T. Coutinho ◽  
Jomel F. Santos ◽  
Rodolfo José C. Souto ◽  
Nivan A.A. Silva ◽  
José Cláudio A. Souza ◽  
...  
Keyword(s):  
Respiratory Distress ◽  
Clinical Laboratory ◽  
Vena Cava ◽  
Clinical Signs ◽  
Pathological Findings ◽  
Mild Anemia ◽  
Liver Abscesses ◽  
Left Shift ◽  
Vena Cava Thrombosis ◽  
Epidemiological Information

ABSTRACT: This paper aimed to describe the main clinico-epidemiological, laboratory, and anatomopathological findings in 10 cattle affected with caudal vena cava thrombosis. The main clinical signs observed were decreased milk production, reduced appetite, apathy, impairment of ruminal motility, cardiorespiratory disorders (tachycardia and tachypnea), epistaxis, hemoptysis, and ascites. Intercurrent diseases such as mastitis, metritis, and phlebitis were verified. The hematological findings were mild anemia, leukocytosis due to neutrophilia with regenerative left shift, and hyperfibrinogenemia. The pathological exams revealed thrombi in the caudal vena cava, hepatomegaly, ascites, liver abscesses, pulmonary edema and emphysema, and abscesses in the lungs. The association of epidemiological information, clinical signs such as respiratory distress, epistaxis or hemoptysis, in addition to anemia and leukocytosis due to neutrophilia, as well as the occurrence of thrombus in the caudal vena cava as pathological findings, are indicative elements of the clinical picture of vena cava thrombosis in cattle. It is reiterated that this disease has an unfavorable prognosis and, when diagnosed, the animal must be culled.

scholarly journals Cerebrospinal fluid analysis in 58 ruminants showing neurological disorders

2020 ◽  
Vol 40 (5) ◽  
pp. 346-354
Author(s):  
Antônio Carlos L. Câmara ◽  
Mariana C. Gonzaga ◽  
Thaís M. Ziober ◽  
Cintia Regina R. Queiroz ◽  
Tayná C.M. Fino ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurological Disorders ◽  
Viral Infections ◽  
Experimental Studies ◽  
Clinical Signs ◽  
Pathological Findings ◽  
Cerebrospinal Fluid Analysis ◽  
Cns Diseases ◽  
Fluid Analysis ◽  
Csf Analysis

ABSTRACT: Ruminants may be affected by a wide variety of central nervous system (CNS) diseases. Cerebrospinal fluid (CSF) analysis forms the basis for ante mortem diagnostic evaluation of ruminants with clinical signs involving the CNS. Despite its importance as a tool to aid diagnosis, data regarding CSF examinations in spontaneous cases of CNS diseases in ruminants from Brazil are limited, and most reports involve experimental studies. Therefore, this study aimed to report the results of CSF analysis in 58 ruminants showing signs of neurological disorders. CSF samples for analysis were obtained from 32 cattle, 20 sheep, and 6 goats by cerebello-medullary cistern (n=54) or lumbosacral space (n=4) puncture. These ruminants showed neurological signs related to viral (n=13), mycotic (n=3), or bacterial (n=15) infections, and toxic (n=21), traumatic (n=4), or congenital disorders (n=2). CSF analysis from ruminants with viral infections presented lymphocytic pleocytosis, even though CSF showed no changes in several cases of rabies. Neutrophilic pleocytosis, cloudiness, presence of fibrin clots, and abnormal coloration were evident in the CSF of most cases of CNS bacterial infection, such as meningoencephalitis, meningitis, abscesses, myelitis, and a case of conidiobolomycosis. On the other hand, CSF was unchanged in most cases of toxic disorders, as botulism and hepatic encephalopathy. Elevated CSF density was observed in 60% of ruminants diagnosed with polioencephalomalacia. Our findings show that evaluation of CSF is a valuable diagnostic tool when used in association with epidemiological, clinical and pathological findings for diagnosis of CNS diseases in ruminants.

scholarly journals Clinical and Pathological Findings in SARS-CoV-2 Disease Outbreaks in Farmed Mink (Neovison vison)

2020 ◽  
Vol 57 (5) ◽  
pp. 653-657 ◽  
Author(s):  
Robert Jan Molenaar ◽  
Sandra Vreman ◽  
Renate W Hakze-van der Honing ◽  
Rob Zwart ◽  
Jan de Rond ◽  
...  
Keyword(s):  
Viral Antigen ◽  
Clinical Signs ◽  
Disease Outbreaks ◽  
Immunohistochemical Detection ◽  
Pathological Findings ◽  
Chain Reaction ◽  
Pathological Characteristics ◽  
Acute Interstitial Pneumonia ◽  
Polymerase Chain ◽  
Postmortem Finding

SARS-CoV-2, the causative agent of COVID-19, caused respiratory disease outbreaks with increased mortality in 4 mink farms in the Netherlands. The most striking postmortem finding was an acute interstitial pneumonia, which was found in nearly all examined mink that died at the peak of the outbreaks. Acute alveolar damage was a consistent histopathological finding in mink that died with pneumonia. SARS-CoV-2 infections were confirmed by detection of viral RNA in throat swabs and by immunohistochemical detection of viral antigen in nasal conchae, trachea, and lung. Clinically, the outbreaks lasted for about 4 weeks but some animals were still polymerase chain reaction–positive for SARS-CoV-2 in throat swabs after clinical signs had disappeared. This is the first report of the clinical and pathological characteristics of SARS-CoV-2 outbreaks in mink farms.

Fatal reexpansion pulmonary edema in a kitten following surgical correction of pectus excavatum

1995 ◽  
Vol 31 (2) ◽  
pp. 133-136 ◽  
Author(s):  
MJ Soderstrom ◽  
SD Gilson ◽  
N Gulbas
Keyword(s):  
Literature Review ◽  
Pulmonary Edema ◽  
Pectus Excavatum ◽  
Clinical Signs ◽  
Surgical Correction ◽  
Pathological Findings ◽  
Reexpansion Pulmonary Edema

Fulminant, fatal pulmonary edema developed in an eight-week-old kitten following external splint correction of severe pectus excavatum. History, signalment, onset of clinical signs, and gross pathological findings were most compatible with a diagnosis of reexpansion pulmonary edema (RPE). This report presents case findings and a literature review of RPE.

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