Polysaccharide Storage Myopathy in Morgan, Arabian, and Standardbred Related Horses and Welsh-cross Ponies

2000 ◽  
Vol 37 (2) ◽  
pp. 193-196 ◽  
Author(s):  
B. A. Valentine ◽  
S. P. McDonough ◽  
Y.-F. Chang ◽  
A. J. Vonderchek
Keyword(s):  
Skeletal Muscle ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Neuromuscular Disorder ◽  
Periodic Acid Schiff ◽  
Exertional Rhabdomyolysis ◽  
Polysaccharide Storage Myopathy ◽  
Quarter Horse ◽  
Criteria For Diagnosis ◽  
Progressive Weakness

Polysaccharide storage myopathy is an equine neuromuscular disorder characterized by accumulation of glycogen-related polysaccharide inclusions within skeletal muscle fibers. The pathologic criteria for diagnosis of this disorder are somewhat controversial; however, periodic acid-Schiff-positive, amylase-resistant inclusions are considered pathognomonic. Although these inclusions are most often found in affected horses related to the Quarter Horse, draft horse, and Warmblood breeds, this report describes these characteristic inclusions in muscle of five horses from nonrelated breeds (two Morgans, one Arabian, one Arabian X Thoroughbred, and one Standardbred) and two Welsh cross ponies. Affected horses had histories of recurrent exertional rhabdomyolysis, and one developed progressive weakness leading to increased recumbency. The affected ponies were part of an unrelated research project and had no apparent clinical signs.

scholarly journals Phenotypic Modulation of Skeletal Muscle Fibers in LPIN1-Deficient Lipodystrophic (fld) Mice

2018 ◽  
Vol 56 (2) ◽  
pp. 322-331
Author(s):  
Rani S. Sellers ◽  
S. Radma Mahmood ◽  
Geoffrey S. Perumal ◽  
Frank P. Macaluso ◽  
Irwin J. Kurland
Keyword(s):  
Electron Microscopy ◽  
Skeletal Muscle ◽  
Fiber Type ◽  
Periodic Acid ◽  
Muscle Fibers ◽  
Myosin Atpase ◽  
Hybrid Fibers ◽  
Periodic Acid Schiff ◽  
Skeletal Muscle Fibers ◽  
Lipin 1

Lipin-1 ( Lpin1)–deficient lipodystrophic mice have scant and immature adipocytes and develop transient fatty liver early in life. Unlike normal mice, these mice cannot rely on stored triglycerides to generate adenosine triphosphate (ATP) from the β-oxidation of fatty acids during periods of fasting. To compensate, these mice store much higher amounts of glycogen in skeletal muscle and liver than wild-type mice in order to support energy needs during periods of fasting. Our studies demonstrated that there are phenotypic changes in skeletal muscle fibers that reflect an adaptation to this unique metabolic situation. The phenotype of skeletal muscle (soleus, gastrocnemius, plantaris, and extensor digitorum longus [EDL]) from Lpin1-/- was evaluated using various methods including immunohistochemistry for myosin heavy chains (Myh) 1, 2, 2a, 2b, and 2x; enzyme histochemistry for myosin ATPase, cytochrome-c oxidase (COX), and succinyl dehydrogenase (SDH); periodic acid–Schiff; and transmission electron microscopy. Fiber-type changes in the soleus muscle of Lpin1-/- mice were prominent and included decreased Myh1 expression with concomitant increases in Myh2 expression and myosin-ATPase activity; this change was associated with an increase in the presence of Myh1/2a or Myh1/2x hybrid fibers. Alterations in mitochondrial enzyme activity (COX and SDH) were apparent in the myofibers in the soleus, gastrocnemius, plantaris, and EDL muscles. Electron microscopy revealed increases in the subsarcolemmal mitochondrial mass in the muscles of Lpin1-/- mice. These data demonstrate that lipin-1 deficiency results in phenotypic fiber-specific modulation of skeletal muscle necessary for compensatory fuel utilization adaptations in lipodystrophy.

scholarly journals Histopathological findings in horses with and without clinical signs of rhabdomyolysis with special reference to polysaccharide storage myopathy

2008 ◽  
Vol 53 (No. 12) ◽  
pp. 660-667 ◽  
Author(s):  
E. Ludvikova ◽  
I.D. Wijnberg ◽  
P. Fictum ◽  
Z. Lukas ◽  
J.H. van der Kolk ◽  
...  
Keyword(s):  
Special Reference ◽  
Clinical Signs ◽  
Size Variation ◽  
Clinical History ◽  
Histopathological Findings ◽  
Exertional Rhabdomyolysis ◽  
Fibre Size ◽  
Significant Difference ◽  
Polysaccharide Storage Myopathy ◽  
History Of

Objective of the study was to assess histopathological changes in horses with a clinical history of exertional rhabdomyolysis (ER) with special reference to polysaccharide storage myopathy and to compare histopathological findings in horses with and without a clinical history of ER. In total 39 muscle samples were collected, from horses with a history of repeated episodes of exertional rhabdomyolysis (test group, 10 horses) and from horses without clinical signs of muscular disorders in their history (control group, 29 horses). Frozen muscle samples were stained with haematoxylin and eosin and periodic acid-Schiff with and without amylase digestion. Histopathologic changes (amylase resistant polysaccharide, subsarcolemmal glycogen, intracytoplasmic masses, subsarcolemmal vacuoles, fibre size variation and internal nuclei) were evaluated. There was a statistically significant difference between groups in the presence of subsarcolemmal amylase sensitive glycogen deposits (P ≤ 0.0001), the risk ratio was 5.22. Statistically significant differences between groups were not found regarding the presence of intracytoplasmic masses, subsarcolemmal vacuoles, amylase resistant polysaccharide, fibre size variation and internal nuclei. Presence of amylase resistant polysaccharide within muscle fibres of apparently healthy horses could be a manifestation of different phenotype expression of PSSM but also the insufficient specificity of this diagnostic criterion.

scholarly journals Actinomycosis is not Frequent in the Periapex But is a Persistent Lesion

2017 ◽  
Vol 28 (6) ◽  
pp. 688-693 ◽  
Author(s):  
Lucas Senhorinho Esteves ◽  
Águida Cristina Gomes Henriques ◽  
Carolina Ávila Varginha de Moraes e Silva ◽  
Maria Cristina Teixeira Cangussu ◽  
Eduardo Antônio Gonçalves Ramos ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Periodic Acid ◽  
Lesion Size ◽  
Periapical Lesion ◽  
Periodic Acid Schiff ◽  
Bacterial Colony ◽  
Periapical Lesions ◽  
Criteria For Diagnosis ◽  
Hematoxylin Eosin

Abstract Periapical actinomycosis caused by a gram-positive anaerobic pathogen characterizes a typical extra-radicular infection. This study determined the frequency and correlated the content of bacteria colonies with the of periapical actinomycosis size. The study comprised a total of 218 periapical lesions (PL) (cysts, granulomas or abscess). The specimens embedded in paraffin were sliced into 4-µm sections and stained with hematoxylin-eosin, Gram, Periodic Acid-Schiff (PAS) and Grocott’s stain. The presence of bacterial colonies composed of filamentous structures labeled with the histochemical stains were described as Actinomyces, and for each case, the bacterial colonies were counted and measured. The correlation between the number and size of bacterial colonies and the size of PL was tested using Pearson’s adjusted correlation coefficient. From 218 PL, bacterial colonies were identified in 64 biopsies. Seven cases (0.3%) fulfill the criteria for diagnosis of periapical actinomycosis. All of cases were therapy-resistant and did not showed periapical repair after 12 months of follow-up. Periapical surgery or dental extraction was performed. The correlation test indicated no correlation between the number of bacterial colonies and the lesion size (p=0.752, r=-0.148). However, a larger bacterial colony size generally resulted in a larger periapical lesion (P=0.000, r=0.657). The frequency of periapical actinomycosis was low, and this lesion should be included in the differential diagnosis of PL. The size of the Actinomyces colonies seemed to contribute to increase the size of the periapical lesion.

scholarly journals Neuroaxonal Dystrophy in a Group of Related Cats

1993 ◽  
Vol 5 (4) ◽  
pp. 585-590 ◽  
Author(s):  
K. Paige Carmichael ◽  
Elizabeth W. Howerth ◽  
John E. Oliver ◽  
Kurt Klappenbach
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Coat Color ◽  
Amorphous Material ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Neuroaxonal Dystrophy ◽  
Periodic Acid Schiff ◽  
Dystrophic Axons ◽  
Positive Core

A syndrome resembling previously described feline hereditary neuroaxonal dystrophy (FHND) was diagnosed in a litter of cats. The disorder was characterized by a sudden onset of hind limb ataxia that slowly progressed to hind limb paresis and paralysis. The cats were between 6 and 9 months old when clinical signs were first noted. Histologically, there was marked ballooning of axonal processes, with spheroid formation and vacuolation in specific regions of the brain and spinal cord. Some dystrophic axons contained a central periodic acid-Schiff (PAS)-positive core. Neuronal loss and gliosis were seen in certain brain stem nuclei, spinal cord nuclei, and the cerebellum. Ultrastructurally, there was hypomyelination and dysmyelination of affected axons. The PAS-positive core in dystrophic axons corresponded ultrastructurally with accumulations of electrondense, flocculent, amorphous material. In addition, these axons contained membrane-bound osmiophilic bodies and large nonmembrane-bound vacuoles. The syndrome in this report differs from the previously described FHND in that no inner ear involvement was seen and onset of clinical signs occurred at a later age. In addition, although some of the affected cats did have diluted coat colors, abnormal coat color was not always associated with clinical disease. This disease is similar to juvenile neuroaxonal dystrophy in children and to neuroaxonal dystrophies described in horses, dogs, cattle, and sheep.

scholarly journals Spontaneous Lung Lesions in Aging Laboratory Rabbits (Oryctolagus cuniculus)

2016 ◽  
Vol 54 (1) ◽  
pp. 178-187 ◽  
Author(s):  
T. K. Cooper ◽  
J. W. Griffith ◽  
Z. C. Chroneos ◽  
J. M. Izer ◽  
L. B. Willing ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Periodic Acid ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Heterotopic Bone ◽  
Alpha Smooth Muscle Actin ◽  
Periodic Acid Schiff ◽  
Lung Lesions ◽  
Age Related

Spontaneous age-related lesions of laboratory rabbits are not well documented in the contemporary scientific literature. A retrospective study of diagnostic necropsies of 36 rabbits >2 years of age found a number of common lung lesions. Fibromuscular intimal hyperplasia affected medium and to a lesser extent large pulmonary arteries and was present to a variable extent in all 36 rabbits >2 years of age. The lesions were characterized by fragmentation and/or reduplication of the internal elastic lamina (IEL), proliferation of smoothelin+/alpha-smooth muscle actin (α-SMA)+/vimentin− smooth muscle cells and fewer smoothelin−/α-SMA+/vimentin+ myofibroblasts, and intimal deposition of collagen without thrombosis, embolism, or evidence of pulmonary hypertension. Pulmonary emphysema, present in 30/36 rabbits, was characterized by the loss of alveolar septa; most affected rabbits did not have clinical signs of respiratory disease. In 8/13 rabbits of the inbred EIII/JC audiogenic strain, we identified a unique syndrome of granulomatous pneumonia containing hyaline brown to gray, globular to ring-like acellular material that was Alcian blue and periodic acid-Schiff positive. The material was immunoreactive for surfactant protein-A and had the ultrastructural appearance of multilamellar vesicles, suggesting a genetic defect in surfactant metabolism. Additionally, we found small benign primary lung tumors (fibropapillomas, 5 rabbits) not previously described. Other findings included heterotopic bone (5 rabbits), subacute to chronic suppurative bronchopneumonia, pyogranulomatous pneumonia with plant material, and pulmonary artifacts from barbiturate euthanasia solution.

scholarly journals Histochemical and Morphometric Evaluation of Skeletal Muscle from Horses with Exertional Rhabdomyolysis (Tying-up)

1986 ◽  
Vol 23 (4) ◽  
pp. 400-410 ◽  
Author(s):  
S. A. McEwen ◽  
T. J. Hulland
Keyword(s):  
Skeletal Muscle ◽  
Clinical Signs ◽  
Gluteus Medius ◽  
Control Group ◽  
Type Ii ◽  
Cross Sectional ◽  
Gluteus Medius Muscle ◽  
Exertional Rhabdomyolysis ◽  
Exercise Period ◽  
Type Ii Fibers

Thirteen horses with histories of exertional rhabdomyolysis were exercised for 20 minutes to induce clinical signs of lameness, elevated serum creatine kinase (CK), and aspartate aminotransferase (AST) activities and skeletal muscle morphologic lesions. The clinical signs exhibited by affected horses included trembling, sweating, increased rate of respiration, and restricted limb movement. Serum CK reached maximal activity between 4 and 8 hours after the exercise period and serum AST activity peaked between 24 and 48 hours. Histologically, the skeletal muscle lesions in muscle biopsies 24 hours after the exercise period consisted of segmental muscle fiber degeneration. Damaged muscle fibers were repaired by myoblastic regeneration. Horses with moderate (>1,500 U/liter) to severe (>5,000 U/liter) elevations of serum CK activity accompanied by clinical signs of muscle soreness induced by exercise, had visible muscle fiber degeneration microscopically. Frozen sections of biopsies of the gluteus medius muscle from affected ( n = 13) and control ( n = 11) groups of horses were processed to demonstrate myofibrillar ATPase activity. These sections were then used to determine fiber types, area percentages, and mean cross sectional fiber sizes. The mean type I, type II, and intermediate fiber sizes were significantly larger in the affected group than in the control group. In the gluteus medius muscles of the affected group, there was a significantly greater percentage of intermediate fibers and a significantly greater percentage of area occupied by intermediate fibers than in the control group. In the muscle samples with acute lesions of exertional rhabdomyolysis, type II fibers were selectively but not exclusively affected. In one horse which was subsequently necropsied 24 hours after the exercise period, lesions were present in several postural muscles, the masseter muscle and the heart. We conclude that the gluteus medius muscle fibers of affected horses are larger in cross sectional area than those of control horses and that there is preferential degeneration of type II fibers in acute lesions of exertional rhabdomyolysis.

Globoid Cell-like Leukodystrophy in a Domestic Longhaired Cat

2002 ◽  
Vol 39 (4) ◽  
pp. 494-496 ◽  
Author(s):  
C. J. Sigurdson ◽  
R. J. Basaraba ◽  
E. M. Mazzaferro ◽  
D. H. Gould
Keyword(s):  
Mononuclear Cells ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Krabbe Disease ◽  
Periodic Acid Schiff ◽  
Nervous Systems ◽  
Central Nervous Systems ◽  
Mental Regression ◽  
Globoid Cell ◽  
Globoid Cells

Globoid cell leukodystrophy (GLD; Krabbe disease), is a rare heritable metabolic disorder in humans, dogs, mutant twitcher mice, and rhesus monkeys that is caused by a deficiency in the lysosomal enzyme galactocerebrosidase (GALC). GALC deficiency results in the accumulation of psychosine, which is toxic to oligodendrocytes and Schwann cells of the central and peripheral nervous systems. Clinical signs include hypotonia, mental regression, and death by 2 years of age in most human patients. Here we describe a domestic longhaired kitten with rapidly progressive neurologic disease and brain and spinal cord lesions characteristic of GLD. Pathologic hallmarks of the disease reflect the loss of oligodendrocytes and include myelin loss, gliosis, and the perivascular accumulation of large mononuclear cells with fine cytoplasmic vacuoles (globoid cells) in the peripheral and central nervous systems. Globoid cells were CD68 and ferritin positive, confirming their monocytic origin, and cytoplasmic contents were nonmetachromatic and periodic acid-Schiff positive.

scholarly journals Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology

2020 ◽  
Vol 7 ◽  
Author(s):  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Esther C. Peters ◽  
Patrick W. Wilson ◽  
Noretta Perry ◽  
...  
Keyword(s):  
Body Wall ◽  
Chromatin Condensation ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Host Cells ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Crystalline Inclusion ◽  
Periodic Acid Schiff ◽  
Stony Coral

Samples from eight species of corals (Colpophyllia natans, Dendrogyra cylindrus, Diploria labyrinthiformis, Meandrina meandrites, Montastraea cavernosa, Orbicella faveolata, Pseudodiploria strigosa, and Siderastrea siderea) that exhibited gross clinical signs of acute, subacute, or chronic tissue loss attributed to stony coral tissue loss disease (SCTLD) were collected from the Florida Reef Tract during 2016–2018 and examined histopathologically. The hallmark microscopic lesion seen in all eight species was focal to multifocal lytic necrosis (LN) originating in the gastrodermis of the basal body wall (BBW) and extending to the calicodermis, with more advanced lesions involving the surface body wall. This was accompanied by other degenerative changes in host cells such as mucocyte hypertrophy, degradation and fragmentation of gastrodermal architecture, and disintegration of the mesoglea. Zooxanthellae manifested various changes including necrosis (cytoplasmic hypereosinophilia, pyknosis); peripheral nuclear chromatin condensation; cytoplasmic vacuolation accompanied by deformation, swelling, or atrophy; swollen accumulation bodies; prominent pyrenoids; and degraded chloroplasts. Polyhedral intracytoplasmic eosinophilic periodic acid–Schiff-positive crystalline inclusion bodies (∼1–10 μm in length) were seen only in M. cavernosa and P. strigosa BBW gastrodermis in or adjacent to active lesions and some unaffected areas (without surface lesions) of diseased colonies. Coccoidlike or coccobacilloidlike structures (Gram-neutral) reminiscent of microorganisms were occasionally associated with LN lesions or seen in apparently healthy tissue of diseased colonies along with various parasites and other bacteria all considered likely secondary colonizers. Of the 82 samples showing gross lesions of SCTLD, 71 (87%) were confirmed histologically to have LN. Collectively, pathology indicates that SCTLD is the result of a disruption of host–symbiont physiology with lesions originating in the BBW leading to detachment and sloughing of tissues from the skeleton. Future investigations could focus on identifying the cause and pathogenesis of this process.

scholarly journals Granulomatous colitis: more than a canine disease? A case of Escherichia coli-associated granulomatous colitis in an adult cat

2017 ◽  
Vol 3 (2) ◽  
pp. 205511691773116
Author(s):  
Rodolfo Oliveira Leal ◽  
Kenny Simpson ◽  
Mélanie Fine ◽  
Jean-Charles Husson ◽  
Juan Hernandez
Keyword(s):  
Escherichia Coli ◽  
Periodic Acid ◽  
Diagnostic Testing ◽  
In Situ Hybridisation ◽  
Clinical Signs ◽  
Fluorescence In Situ Hybridisation ◽  
Granulomatous Colitis ◽  
Periodic Acid Schiff ◽  
E Coli ◽  
Adult Cat

Case summary This report describes a 4-year-old cat with chronic intermittent haematochezia and faecal incontinence of 7 months’ duration. Investigation revealed severe colonic multifocal mucosal ulcerations and infiltration of the mucosal lamina propria by large numbers of periodic acid–Schiff-positive macrophages. Fluorescence in situ hybridisation analysis of colonic biopsies revealed multifocal clusters of intracellular Escherichia coli. Treatment with fluoroquinolones for 6 weeks led to a complete resolution of clinical signs. Relevance and novel information The findings reveal that mucosally invasive E coli can also be associated with granulomatous colitis in cats and indicate the need for diagnostic testing of mucosal samples for E coli and other infectious agents.

scholarly journals Gastric B-Cell Lymphoma with Mott Cell Differentiation in a Dog

2009 ◽  
Vol 21 (5) ◽  
pp. 715-719 ◽  
Author(s):  
Gabrita De Zan ◽  
Valentina Zappulli ◽  
Laura Cavicchioli ◽  
Linda Di Martino ◽  
Eriberta Ros ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cell ◽  
Gastrointestinal Disease ◽  
Periodic Acid ◽  
Palliative Therapy ◽  
Clinical Signs ◽  
B Cell Lymphoma ◽  
Surgical Excision ◽  
Periodic Acid Schiff ◽  
Regional Lymph Nodes

A gastric lymphoid tumor with involvement of regional lymph nodes and spleen was diagnosed in an 8-year-old crossbreed male dog with a 6-month history of gastrointestinal disease. Despite surgical excision and palliative therapy (prednisolone and cimetidine), the dog was euthanized due to worsening of clinical signs. At necropsy, multiple white, solid, nodular, infiltrative masses were observed in the stomach, duodenum, spleen, liver, and lungs in association with generalized lymph node enlargement. Cytology, histology, histochemistry, immunohistochemistry, and electron microscopy revealed that the neoplastic cell population was composed of B lymphocytes that contained variable amounts of round periodic acid-Schiff-positive cytoplasmic globules consistent with Russell bodies. The tumor most likely represented a variant of B-cell neoplasia with extensive Mott cell differentiation.

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