scholarly journals Pulmonary hyalinosis in captive sugar gliders (Petaurus breviceps)

2017 ◽  
Vol 29 (5) ◽  
pp. 691-695 ◽  
Author(s):  
Set A. Sokol ◽  
Dalen W. Agnew ◽  
Anne D. Lewis ◽  
Teresa L. Southard ◽  
Andrew D. Miller

Pulmonary hyalinosis is an idiopathic, typically incidental lesion of old dogs, characterized by multifocal aggregates of epithelioid and multinucleate macrophages that surround periodic acid–Schiff (PAS)-positive hyaline material in airways. Lung lesions resembling pulmonary hyalinosis were observed in 6 captive adult sugar gliders ( Petaurus breviceps; 5 females and 1 male) in a retrospective review of 18 autopsied animals. Clinical signs for 3 of the sugar gliders included lethargy, tachypnea, and dyspnea. At autopsy, 5 of 6 animals had comorbid lesions that were the primary cause of death. Gross pulmonary lesions were characterized by mildly firm, discolored, vaguely nodular areas of parenchyma. Histologic examination of the lung revealed granulomatous inflammation with intracellular and extracellular amphophilic hyaline bodies within alveoli and airways. Hyaline bodies were positive for PAS and oil red O staining, blue via crystal violet staining, and displayed birefringence under polarized light, similar to findings in dogs with pulmonary hyalinosis.

1993 ◽  
Vol 5 (4) ◽  
pp. 585-590 ◽  
Author(s):  
K. Paige Carmichael ◽  
Elizabeth W. Howerth ◽  
John E. Oliver ◽  
Kurt Klappenbach

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.


2016 ◽  
Vol 54 (1) ◽  
pp. 178-187 ◽  
Author(s):  
T. K. Cooper ◽  
J. W. Griffith ◽  
Z. C. Chroneos ◽  
J. M. Izer ◽  
L. B. Willing ◽  
...  

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.


1976 ◽  
Vol 24 (6) ◽  
pp. 725-730 ◽  
Author(s):  
A B Johnson ◽  
H H Schaumburg ◽  
J M Powers

The straited accumulations in adrenal cortical cells and brain macrophages that are characteristic of adrenoleukodystrophy have been studied histochemically in cryostat sections to seek leads for the biochemical identification of the striated material. It stained pale pink with oil red O and did not stain with the Schultz cholesterol procedure or periodic acid-Schiff technique. By utilizing the birefringence of the accumulations as a marker, it was determined that, unlike natural cholesterol and cholesterol esters, the striated material was resistant to acetone and ethanol extraction. It was readily soluble, however, in nonpolar solvents such as n-hexane and chloroform. These findings indicated that the material was most probably a lipid, and they suggested that sequential extraction of adrenoleukodystrophy adrenal and brain with acetone and then n-hexane could be used to isolate this material in relatively pure form. Based on this lead, biochemical studies have just revealed a fatty acid abnormality in adrenoleukodystrophy which appears to be unique to this genetic disease.


2002 ◽  
Vol 39 (4) ◽  
pp. 494-496 ◽  
Author(s):  
C. J. Sigurdson ◽  
R. J. Basaraba ◽  
E. M. Mazzaferro ◽  
D. H. Gould

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.


2017 ◽  
Vol 55 (2) ◽  
pp. 298-302 ◽  
Author(s):  
Drew R. Magstadt ◽  
Amanda J. Fales-Williams ◽  
Jean-Sébastien Palerme ◽  
Heather Flaherty ◽  
Tracy Lindquist ◽  
...  

A 9-year-old female mixed breed dog presented for an acute onset of anorexia, vomiting, and cough. Initial examination and diagnostics revealed a large multilobular cranial mediastinal mass with unidentified fungal organisms on cytology. The disease progressed in spite of therapy until the dog was euthanized 8 months later. Gross necropsy findings were a large multilobular intrathoracic mass, mild pleuritis, and generalized lymphadenopathy. Histologic evaluation showed granulomatous inflammation and necrosis with numerous 20- to 70-micron, periodic acid–Schiff- and Gomori methenamine silver-positive spherules effacing lymph node parenchyma, as well as severe inflammation within the midbrain. Endosporulation was a common finding, and large numbers of fungal hyphae were also present in affected areas. Ribosomal RNA gene sequencing found 100% identity to published sequences of Phanerochaete chrysosporium, the teleomorph form of Sporotrichum pruinosum. This is the first published report of disease caused by natural infection with this basidiomycete organism in animals.


2020 ◽  
Vol 7 ◽  
Author(s):  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Esther C. Peters ◽  
Patrick W. Wilson ◽  
Noretta Perry ◽  
...  

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.


2017 ◽  
Vol 3 (2) ◽  
pp. 205511691773116
Author(s):  
Rodolfo Oliveira Leal ◽  
Kenny Simpson ◽  
Mélanie Fine ◽  
Jean-Charles Husson ◽  
Juan Hernandez

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.


2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Brittany N. Robles ◽  
Catherine Shea ◽  
Ghadir Salame

Sarcoidosis is an inflammatory disease that affects one or multiple organs, most commonly the lungs and lymph nodes. This disease can present in a variety of ways which often makes diagnosis difficult. A 54-year-old postmenopausal African American female with a history of omental carcinomatosis of unknown origin was referred to the gynecology-oncology service at a local community hospital following a laparoscopic incarcerated hernia repair where multiple abdominal lesions suspicious of ovarian carcinomatosis were visualized. She was brought to the operating room for a diagnostic laparoscopy at which point the intra-abdominal survey revealed white tubercle-like lesions that were consistent with peritoneal tuberculosis. The lesions were excised and sent to pathology. The omentum biopsy was originally reported as adipose tissue showing focal fibrosis, focal mild acute inflammation, few cyst formation, and multiple granulomatous chronic inflammation, with multinucleated giant cells. Periodic acid-Schiff stain and acid fast bacilli stain were negative, and a diagnosis of peritoneal tuberculosis was made. The patient was started on an antituberculosis treatment regimen; however, she was not improving. The pathology slides were reexamined and revealed nonnecrotizing granulomatous inflammation consistent with sarcoidosis. The patient was immediately referred to the department of pulmonology and rheumatology, at which point she was started on corticosteroids and had an improvement in her condition.


2009 ◽  
Vol 21 (5) ◽  
pp. 715-719 ◽  
Author(s):  
Gabrita De Zan ◽  
Valentina Zappulli ◽  
Laura Cavicchioli ◽  
Linda Di Martino ◽  
Eriberta Ros ◽  
...  

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.


2019 ◽  
Vol 55 (5) ◽  
pp. 261-265
Author(s):  
Caroline Benzimra ◽  
Chloé Job ◽  
Quentin Pascal ◽  
Stéphane Bureau ◽  
Anaïs Combes ◽  
...  

ABSTRACT A 4 mo old female Staffordshire bull terrier puppy was presented with chronic Escherichia coli cystitis. Ultrasound and cystoscopic examination revealed innumerable, intraluminal, finger-like proliferations arising from the dorsal urinary bladder (UB) wall. Histological examination of mucosal biopsies obtained by cystoscopy was suggestive of granulomatous cystitis. The proliferative lesions were removed surgically and submitted for histological examination. The UB submucosa was heavily infiltrated by macrophages with periodic acid-Schiff–positive cytoplasm exhibiting rare Michaelis-Gutmann bodies, leading to the diagnosis of malakoplakia. The puppy was prescribed with sulfamethoxazole-trimethoprim. The urinary signs disappeared despite the persistent UB wall thickening revealed by abdominal ultrasound. Urine culture performed during the ninth week of treatment showed a persistent infection by E coli resistant to sulfamethoxazole-trimethoprim. The dog was switched to doxycycline but was then lost to follow-up. Malakoplakia is a chronic granulomatous inflammation well documented in humans. Its pathophysiology is not fully understood, but bacterial infection, immunodepression, and a defective lysosomal function may lead to the intracytoplasmic accumulation of partially degraded bacteria that can subsequently mineralize to form the Michaelis-Gutmann bodies. Malakoplakia should be suspected when UB mass lesions are identified in a young dog with bacterial cystitis.


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