Spontaneous Lung Lesions in Aging Laboratory Rabbits (Oryctolagus cuniculus)

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.

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Histological and Immunohistochemical Characterization of Vascular Alterations in Meninges of Cats Infected with Gurltia paralysans

Pathogens ◽

10.3390/pathogens11010088 ◽

2022 ◽

Vol 11 (1) ◽

pp. 88

Author(s):

Svenja Hartung ◽

Angelika Weyrich ◽

Manuel Moroni ◽

Marcelo Gómez ◽

Christiane Herden

Keyword(s):

Spinal Cord ◽

South America ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Clinical Signs ◽

Vascular Lesions ◽

Alpha Smooth Muscle Actin ◽

Periodic Acid Schiff ◽

Tissue Samples

Gurltia paralysans, a metastrongyloid nematode, parasitizes in meningeal vessels in the thoracolumbar spinal cord of cats in South America and causes progressive paraparesis. Recently, the first report outside of South America described gurltiosis in a cat in Spain. As this parasitic disease has so far been largely neglected, especially outside of South America, the aim of the present case study was to add knowledge to the histologic and immunohistochemical characterization of central nervous lesions. To this purpose, formalin-fixed and paraffin-embedded (FFPE) tissue samples from the spinal cord and brain of five cats affected by clinical signs caused by Gurltia paralysans and of three control cats without CNS lesions were histopathologically examined using hematoxylin and eosin stain (HE), Elastica van Gieson stain, as well as periodic acid–Schiff (PAS) reaction. Moreover, immuno- histochemistry for alpha smooth muscle actin and Factor VIII-related antigen were performed to characterize vascular lesions. Lesions were consistent with previous descriptions and were mainly located in the spinal cord and consisted of chronic suppurative or lymphoplasmahistiocytic meningi tis as well as suppurative vasculitis, congestion and varicosis of meningeal veins. In view of the recent detection of this parasite in Europe and the increasing inner-European transport of rescued domestic cats, veterinarians in Europe should be aware of the clinical and pathomorphological presentation of this disease.

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A Case of Canine Apocrine Sweat Gland Adenoma, Clear Cell Variant

Veterinary Pathology ◽

10.1354/vp.42-2-215 ◽

2005 ◽

Vol 42 (2) ◽

pp. 215-218 ◽

Cited By ~ 10

Author(s):

K. Nibe ◽

K. Uchida ◽

T. Itoh ◽

S. Tateyama

Keyword(s):

Sweat Gland ◽

Clear Cell ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Alpha Smooth Muscle Actin ◽

Periodic Acid Schiff ◽

Clear Cells ◽

Apocrine Sweat Gland ◽

Cell Variant ◽

Clear Cell Variant

A cutaneous mass at the base of the retroauricular region of a 4-year-old, female Golden Retriever was examined pathologically. Histologically, the mass formed multiple nodules consisting of a proliferation of large clear cells with abundant cytoplasm. Mitotic figures among the neoplastic cells were very sparse. The large clear cells were intensely positive for cytokeratins (AE1/AE4, cytokeratin 8 and 18) and moderately positive for lysozyme and contained periodic acid-Schiff-positive granules in the cytoplasm. In addition, small flat cells lined the islands of neoplastic large clear cells, and these were strongly positive for alpha-smooth muscle actin and vimentin, and some were positive for cytokeratin (AE1/AE4), suggesting they were myoepithelial cells. No local recurrence or metastasis has been recognized during the 18 months since surgical excision. On the basis of these findings, the present tumor was diagnosed as apocrine sweat gland adenoma, clear cell variant. There have been few previous reports of canine apocrine adenomas showing a clear cell morphology.

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Mast cell infiltration associated with tubulointerstitial fibrosis in chronic Aristolochic Acid Nephropathy

Human & Experimental Toxicology ◽

10.1191/0960327105ht502oa ◽

2005 ◽

Vol 24 (2) ◽

pp. 41-47 ◽

Cited By ~ 6

Author(s):

Yichao Wu ◽

Zhihong Liu ◽

Weixin Hu ◽

Leishi Li

Keyword(s):

Mast Cell ◽

Aristolochic Acid ◽

Interstitial Fibrosis ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Basement Membranes ◽

Cell Infiltration ◽

Alpha Smooth Muscle Actin ◽

Periodic Acid Schiff ◽

Aristolochic Acid Nephropathy

Aristolochic Acid Nephropathy (AAN) is regarded as a kind of toxic nephropathy caused by the formation of DNA- aristolochic acid adducts in renal parenchymal cells. However, the underlying mechanisms driving the progression of renal interstitial fibrosis in AAN still remains unclear. This study aims to elucidate the role of some immunological factors, especially mast cells (MCs), in the pathogenesis of AAN. Sixteen patients with AAN were enrolled in this study, including five acute and 11 chronic AAN. Monoclonal antibodies against human tryptase, alpha smooth muscle actin (α-SMA), and CD68 were applied on serial sections, which were further counterstained with Periodic Acid-Schiff. It was found that massive tryptase-positive MCs were observed in the fibrotic areas in chronic AAN, especially around thickened tubular basement membranes where myofibroblasts accumulated too. In contrast, MCs infiltrated to a less extent in acute AAN, and were barely found in normal control kidneys. In chronic AAN, the number of MCs in the tubulointerstitium was positively correlated with the degree of renal fibrosis ( r=0.64, P<0.05), but not with serum creatinine levels. Meanwhile, the recruitment of MCs into the renal interstitium is accompanied with local proliferation of myofibroblasts. Macrophages were not abundant, neither in acute nor in chronic AAN. Our findings show for the first time that mast cell infiltration seems to be associated with the progression of fibrosis in the renal tubulointerstitium in chronic AAN.

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Hypertrophic gastropathy associated with gastric sarcoma in a dog

Journal of Veterinary Diagnostic Investigation ◽

10.1177/1040638720966972 ◽

2020 ◽

Vol 33 (1) ◽

pp. 112-115

Author(s):

Mariarita Romanucci ◽

Paolo E. Crisi ◽

Maria Veronica Giordano ◽

Morena Di Tommaso ◽

Francesco Simeoni ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Neuron Specific Enolase ◽

Partial Gastrectomy ◽

Abdominal Ultrasound ◽

Gastric Body ◽

Gastric Glands ◽

Periodic Acid Schiff ◽

Gastric Lumen

A 14-y-old spayed female Labrador Retriever was presented with an 8-mo history of chronic vomiting. Abdominal ultrasound and gastrointestinal endoscopy revealed a mass protruding into the gastric lumen, with cytologic features suggestive of sarcoma. A partial gastrectomy was performed; the gastric body and antrum were thickened, with a cerebriform appearance of the mucosal surface. Histologic examination revealed a submucosal neoplastic proliferation of fusiform cells variably arranged in irregular bundles and scattered whorls. Fusiform cells strongly reacted to antibodies against vimentin, S100, and neuron-specific enolase; glial fibrillary acidic protein was moderately and multifocally expressed. Pancytokeratin, KIT, α–smooth muscle actin, and desmin were nonreactive. Histologic and immunohistochemical findings suggested a diagnosis of gastric sarcoma with features referable to a non-GIST (gastrointestinal stromal tumor), non–smooth muscle NIMT (non-angiogenic, non-lymphogenic intestinal mesenchymal tumor). The overlying gastric mucosa was thickened by elongated and dilated gastric glands, predominantly lined by intensely periodic acid-Schiff–stained mucous cells. This altered mucosal architecture was suggestive of Ménétrier-like disease. Although this disease has been hypothesized to predispose to gastric adenocarcinoma in dogs, an association with gastric sarcoma has not been documented previously in the veterinary literature, to our knowledge.

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The presence of LPS in OVA inhalations affects airway inflammation and AHR but not remodeling in a rodent model of asthma

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00208.2011 ◽

2012 ◽

Vol 303 (1) ◽

pp. L54-L63 ◽

Cited By ~ 21

Author(s):

Kimitake Tsuchiya ◽

Sana Siddiqui ◽

Paul-André Risse ◽

Nobuaki Hirota ◽

James G. Martin

Keyword(s):

Smooth Muscle ◽

Airway Inflammation ◽

Airway Remodeling ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Brown Norway ◽

Cell Hyperplasia ◽

Periodic Acid Schiff ◽

Th2 Cytokine ◽

Ifn Γ

Ovalbumin (OVA) is the most frequently used allergen in animal models of asthma. Lipopolysaccharide (LPS) contaminating commercial OVA may modulate the evoked airway inflammatory response to OVA. However, the effect of LPS in OVA on airway remodeling, especially airway smooth muscle (ASM) has not been evaluated. We hypothesized that LPS in commercial OVA may enhance allergen-induced airway inflammation and remodeling. Brown Norway rats were sensitized with OVA on day 0. PBS, OVA, or endotoxin-free OVA (Ef-OVA) was instilled intratracheally on days 14, 19, 24. Bronchoalveolar lavage (BAL) fluid, lung, and intrathoracic lymph node tissues were collected 48 h after the last challenge. Immunohistochemistry for α-smooth muscle actin, Periodic-Acid-Schiff staining, and real-time qPCR were performed. Airway hyperresponsiveness (AHR) was also measured. BAL fluid macrophages, eosinophils, neutrophils, and lymphocytes were increased in OVA-challenged animals, and macrophages and neutrophils were significantly lower in Ef-OVA-challenged animals. The ASM area in larger airways was significantly increased in both OVA and Ef-OVA compared with PBS-challenged animals. The mRNA expression of IFN-γ and IL-13 in lung tissues and IL-4 in lymph nodes was significantly increased by both OVA and Ef-OVA compared with PBS and were not significantly different between OVA and Ef-OVA. Monocyte chemoattractant protein (MCP)-1 in BAL fluid and AHR were significantly increased in OVA but not in Ef-OVA. LPS contamination in OVA contributes to the influx of macrophages and MCP-1 increase in the airways and to AHR after OVA challenges but does not affect OVA-induced Th1 and Th2 cytokine expression, goblet cell hyperplasia, and ASM remodeling.

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Histopathologic Spectrum of Neuromuscular and Vascular Hamartoma With Special Reference to the Vasculopathic Phenomenon

International Journal of Surgical Pathology ◽

10.1177/1066896919890129 ◽

2019 ◽

Vol 28 (4) ◽

pp. 382-392

Author(s):

Pavithra Ayyanar ◽

Suvendu Purkait ◽

Tushar Subhadarshan Mishra ◽

Susama Patra ◽

Suvradeep Mitra

Keyword(s):

Smooth Muscle ◽

Intestinal Obstruction ◽

Smooth Muscle Actin ◽

Periodic Acid ◽

Stricture Formation ◽

Periodic Acid Schiff ◽

Mesenchymal Tissue ◽

Unusual Lesion ◽

Submucosal Fibrosis ◽

Vascular Hamartoma

Neuromuscular and vascular hamartoma (NMVH) is an unusual lesion presenting as intestinal obstruction by stricture formation. It is characterized by a hamartomatous mass comprising haphazardly arranged mesenchymal tissue native to the intestinal mucosa and submucosa. We aimed to characterize the clinicohistopathological spectrum of NMVH in adult subjects with a search for an etiological clue. We reviewed 84 resected specimens (adult cases) of intestinal obstruction in our institute and diagnosed 4 cases with NMVH. A panel of special stains (Masson trichrome, Verhoeff-van-Gieson, and periodic acid–Schiff) and immunohistochemistry (smooth muscle actin, S100, Bcl2, CD34, vimentin, desmin, CD117, and CD3) were performed in all cases. All cases of NMVH showed characteristic hamartomatous mounds comprising haphazardly arranged smooth muscle, nerves, ganglia, vessels, and collagen with overlying mucosal ulceration. Adjacent bowel showed submucosal fibrosis, muscularis mucosae thickening, and duplication along with vasculopathy. A typical vasculopathy (“vessel-in-vessel” appearance) was seen in the submucosal and/or subserosal veins. Besides, different other forms of vasculopathic changes like obliterative venopathy and concentric myohypertrophy were also seen. One case had vasculitis and the patient died despite successful surgery. One other case was associated with lymphocytic ganglioneuronitis and granulomatous etiology. We conclude that NMVH can be multifactorial in origin although ischemia resulting from vasculopathy appears to be directly causative. The characteristic vasculopathy in the submucosal location may aid in the diagnosis of NMVH in small biopsy samples.

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