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.

Globoid Cell Leucodystrophy in Polled Dorset Sheep

1980 ◽  
Vol 17 (4) ◽  
pp. 399-405 ◽  
Author(s):  
D. H. Pritchard ◽  
D. V. Napthine ◽  
A. J. Sinclair
Keyword(s):  
White Matter ◽  
Hind Limb ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Periodic Acid Schiff ◽  
Histologic Changes ◽  
The Brain ◽  
Globoid Cell Leucodystrophy ◽  
Globoid Cell ◽  
Globoid Cells

Globoid cell leucodystrophy (Krabbe's disease) was diagnosed in two Polled Dorset sheep from a stud farm. Clinical signs were hind limb incoordination progressing to tetraplegia. Histologic changes in white matter of the brain were myelin destruction, loss of oligodendroglia, astrogliosis and accumulation of distinctive periodic acid-Schiff (PAS)-positive globoid cells. The activities of galactocerebroside β-galactosidase, the lysosomal enzyme specifically deficient in globoid leucodystrophy, and of three other glycosidase enzymes were compared in brain tissue of one affected and six unaffected sheep. Activities of the three nonspecific glycosidases were similar in all seven brains. Galactocerebrosidase activity was similar in the six control sheep, but in the affected brain was less than 6% of the control mean.

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 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 Krabbe disease: the importance of early diagnosis for prognosis

2012 ◽  
Vol 10 (2) ◽  
pp. 233-235 ◽  
Author(s):  
Tatiana Suemi Sano
Keyword(s):  
Early Diagnosis ◽  
Early Onset ◽  
Late Onset ◽  
Krabbe Disease ◽  
Globoid Cell Leukodystrophy ◽  
Nervous Systems ◽  
Clinical Forms ◽  
Peripheral Nervous Systems ◽  
Globoid Cell

Krabbe disease (globoid cell leukodystrophy) is an inherited recessive autosomal leukodystrophy caused by deficiency of the enzyme galactocerebrosidase. The lack of this enzyme leads to the build-up of galactolipids that will promote the death of oligodendrocytes and the demyelination of the central and peripheral nervous systems. There are two clinical forms: early onset and late onset. This article reports a case of late onset Krabbe disease and discusses the importance of early diagnosis for its prognosis.

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.

scholarly journals Bronchoalveolar lavage (BAL) in tapirs (Tapirus terrestris) with Mycobacterium tuberculosis

2014 ◽  
Vol 66 (6) ◽  
pp. 1643-1646 ◽  
Author(s):  
J.S. Biava ◽  
R.C. Gonçalves ◽  
M.L. Javorouski ◽  
M. Bonat ◽  
O. Lacerda ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Lower Respiratory Tract ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Clinical Information ◽  
Inflammatory Cells ◽  
Periodic Acid Schiff ◽  
Chemical Restraint ◽  
Tapirus Terrestris

This paper describes the in vivo Bronchoalveolar lavage (BAL) technique by endoscopy in tapirs (Tapirus terrestris) with clinical signs of tuberculosis. The technique was performed in two tapirs, male and female, from Curitiba Zoo, Paraná, Brazil. A flexible endoscope and a polyethylene catheter were used after the chemical restraint of the animals. For BAL technique, 60mL of saline 0.9% were infused with a polyethylene catheter, introduced by the endoscope's working channel, and 15mL of BAL were recovered, analyzed and submitted to cytocentrifugation. Slides were stained by Papanicolaou, periodic acid-Schiff (PAS) and Ziehl-Neelsen methods contained high quantity of inflammatory cells on light microscopy (macrophages 27.5%, lymphocytes 0.5%, neutrophis 67% and eosinophis 5%). BAL samples were submitted to culture, bacilloscopy and PCR and were negative for both animals. Based on this study, it was concluded that the bronchoalveolar lavage technique in tapirs is feasible, simple, noninvasive, practical and fast, providing an important clinical information in vivo regarding the functional status of the lower respiratory tract.

Myocardial protein aggregates in pet guinea pigs

2021 ◽  
pp. 030098582110425
Author(s):  
Teresa Southard ◽  
Kathleen Kelly ◽  
Anibal G. Armien
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Guinea Pigs ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Body Burden ◽  
Ventricular Myocardium ◽  
Right Ventricular Free Wall ◽  
Periodic Acid Schiff ◽  
The Right

A retrospective study of guinea pigs submitted for necropsy revealed intracytoplasmic inclusions in the cardiomyocytes of 26 of 30 animals. The inclusions were found with approximately the same frequency in male and female guinea pigs and were slightly more common in older animals. In most cases, the animals did not have clinical signs or necropsy findings suggestive of heart failure, and the cause of death or reason for euthanasia was attributed to concurrent disease processes. However, the 4 guinea pigs with the highest inclusion body burden all had pulmonary edema, sometimes with intra-alveolar hemosiderin-laden macrophages, suggestive of heart failure. The inclusions were found in both the left and right ventricular myocardium, mainly in the papillary muscles, but were most common in the right ventricular free wall. No inclusions were detected in the atrial myocardium or in skeletal muscle. The inclusions did not stain with Congo red or periodic acid–Schiff. Electron microscopy revealed dense aggregates of disorganized myofilaments and microtubules that displaced and compressed the adjacent organelles. By immunohistochemistry, there was some scattered immunoreactivity for desmin and actin at the periphery of the inclusions and punctate actin reactivity within the aggregates. The inclusions did not react with antibodies to ubiquitin or cardiac myosin, but were variably reactive for alpha B crystallin, a small heat shock chaperone protein. The inclusions were interpreted as evidence of impaired proteostasis.

A Neoplasm of Globule Leukocytes in a Cat

1986 ◽  
Vol 23 (3) ◽  
pp. 287-292 ◽  
Author(s):  
D. J. Honor ◽  
D. B. De Nicola ◽  
J. J. Turek ◽  
J. A. Render ◽  
D. A. Serra
Keyword(s):  
Lymph Nodes ◽  
Electron Density ◽  
Single Unit ◽  
Mononuclear Cells ◽  
Phosphotungstic Acid ◽  
Periodic Acid ◽  
Domestic Cat ◽  
Unit Membrane ◽  
Periodic Acid Schiff ◽  
Tracheobronchial Lymph Nodes

A neoplasm involving the ileo-cecal-colic junction, thymus, and tracheobronchial lymph nodes of a 7-year-old domestic cat was composed of dense sheets of round to oval mononuclear cells with oval to indented nuclei, moderate amounts of cytoplasm, and variable numbers of round eosinophilic granules. These granules are brown to black in phosphotungstic acid hematoxylin-stained sections and stain variably with the periodic acid-Schiff stain. They are 0.8 to 1.5 μm in diameter, limited by a single unit membrane, and have variable electron density. Light microscopic cellular morphology and staining characteristics as well as ultrastructural features of these cells are consistent with feline globule leukocytes. Morphologic features of the neoplastic cells in the present case are similar to those of the only other reported neoplasm of globule leukocytes which also involved the intestine of a cat.

Sign in / Sign up

Export Citation Format

Share Document