Idiopathic extramural coronary arteritis in beagle and mongrel dogs

Hearts obtained from 119 toxicological experiments on dogs during a 21-year period (1965-1986) were evaluated histologically to determine the incidence and characteristics of focal microscopic inflammatory lesions of the extramural coronary arteries. Lesions were encountered in 23% of 119 experiments. The average overall incidence was 2.3% of 1,905 control and chemically treated male and female beagle hearts (3.1% of male and 1.3% of female control beagles, and 1.8% of male and 2.8% of female treated beagles). Lesions were seen in 4.7% of 127 random-source mongrel dogs. Histologically, lesions were characterized by adventitial infiltrates of mononuclear cells, areas of mural necrosis, and inflammatory cell infiltrates in both mural and subendothelial regions. In the latter region, fibrosis developed separating the intima from the internal elastic membrane. Lesions occurred in the right and left coronary arteries and in the dorsal, circumflex, and ventral descending branches of the left coronary artery. Vascular lesions were not present in the intramural coronary vessels or in vessels of other organs in affected animals. More extensive sampling of the extramural coronary arteries revealed an incidence of 5-9%. The lesion of focal extramural coronary arteritis was idiopathic, and not a manifestation of the polyarteritis syndrome of dogs.     

Improvement in pulmonary arterial lesions after heartworm removal using flexible alligator forceps

Improvement of pulmonary arterial lesions after heartworm removal using flexible alligator forceps was investigated by measuring pulmonary arterial pressure (PAP), and by angiographic and histopathological examinations in 11 dogs. PAP obtained immediately after worm removal corresponded well with angiographic abnormalities. In 2 dogs, high PAP immediately after worm removal fell gradually by 12 weeks, and obstructions on angiogram were resolved at 4 to 12 weeks. In 4 dogs, slightly high PAP fell to the normal range at 4 weeks, and angiographic abnormalities were considerably reduced at 4 to 12 weeks. In 5 dogs, PAP returned to normal range immediately after worm removal, and angiographic changes almost disappeared at 4 to 8 weeks. On biopsy immediately after worm removal, samples of the main pulmonary arteries showed severe intimal proliferations with villous or papillary protrusion into the lumen. Autopsy at 12 to 20 weeks indicated that the intimal protrusions were remarkably reduced as compared with the biopsy samples in all cases. However, villous intimal protrusions were seen in the caudal lobar arteries in cases with remaining alive worms. New vessels seemed to develop into thromboemboli with time. From these findings, it is clear that the pulmonary arterial lesions improved after heartworm removal, and the clinical signs disappeared following the improvement in hemodynamics. Aspirin therapy (5 mg/kg/day) for 4 weeks after worm removal in 5 dogs did not improve the intimal lesions as compared to 3 control dogs.     

Extraglomerular lesions in kidneys of mink with encephalitozoonosis.

Extraglomerular renal lesions were studied by light and electron microscopy in 13 farmed mink which showed cataractous eyes associated with spontaneous encephalitozoonosis. The extraglomerular renal lesions consisted of multiple renal cysts, multifocal-to-coalescing interstitial nephritis and vasculitis. Tubular cysts of varying size were present in the corticomedullary junction and medulla. The inflammatory infiltrates were composed mostly of lymphocytes and plasma cells and usually accompanied an interstitial fibrosis. Vasculitis, perivasculitis and sclerotic arteries were frequently seen.     

Cutaneous histiocytosis in dogs

Multifocal cutaneous histiocytic lesions were recognized in 9 dogs. Clinically, the dogs had multiple erythematous plaques or nodules in the skin (1 to 5 cm diameter). Histologically, the lesions were comprised of dermal or pannicular infiltrates of large histiocytic cells, with varying numbers of other inflammatory cells intermixed. By electron microscopy, the cells resembled those of canine cutaneous histiocytoma. The lesions seemed to wax and wane and appeared in new sites, regardless of treatment. The dogs ranged in age from 2 to 13 years; 7 dogs were under 6 years of age. Both sexes and various breeds were represented. An infectious agent could not be identified.     

Cardiovascular complications of chronic catheterization of the jugular vein in the dog

Cardiovascular changes associated with indwelling catheters were evaluated in 51 adult beagle dogs catheterized for 4 to 9 weeks. Pathologic changes consistent with traumatic injury were in the vena cava and endocardium of the right atrium of 88% of cannulated dogs. Lesions were characterized by surface denudation and diffuse intimal thickening due to myointimal hyperplasia and deposition of extracellular matrix. Affected intima was lined by hyperplastic, poorly differentiated endothelial cells and contained round to oval cells with characteristics of smooth muscle cells. After 9 weeks, thickened intima was vascularized and composed of spindle-shaped cells and fibrillar stroma. Intimal sclerosis and localized proliferative papillary projections in the vena cava cranial to areas of myointimal hyperplasia occurred infrequently. Traumatic lesions, regardless of location or severity, did not extend below the internal elastic membrane. Inflammatory cellular responses, when present, were minimal. The location, distribution, and morphogenesis of catheter-related cardiovascular lesions distinguishes them from those induced by chemical toxicity or pharmacotoxicity.     

Superficial eosinophilic gastritis in laboratory beagle dogs attributable probably to diet

Stomach tissues from 222 beagle dogs, which were used for toxicological studies, were examined histopathologically. Out of 190 dogs fed the same diet, 185 had gastric lesions, whereas all of 32 dogs fed another diet were free from them. The gastric lesions were noted as an accumulation of eosinophils, infiltration of inflammatory cells including lymphocytes, plasma cells and histiocytes in the gastric lamina propria, formation of foreign body type multinucleated giant cells, focal desquamation and papillary proliferation of mucosal epithelium. The lesions were confined to the superficial layer of the antral and pyloric mucosa, and neither desmoplasia nor clinical signs were seen. Multinucleated giant cells often contained amphophilic foreign bodies of varying appearance with inconsistent reaction for periodic acid-Schiff (PAS), but no definite causal agents were detected.     

Spontaneous aortic dissecting hematoma in two dogs.

This report describes 2 cases of spontaneous aortic dissecting hematoma in young Border Collie and Border Collie crossbred dogs. Histology was performed in one of the cases involving an unusual splitting of the elastin present within the wall of the aorta, consistent with elastin dysplasia as described in Marfan syndrome in humans. The first case involved a young purebred Border Collie that died suddenly and the second case involved a Border Collie crossbred dog that died after a 1-month history of seizures. Gross lesions included pericardial tamponade with dissection of the ascending aorta in the former case and thoracic cavity hemorrhage, mediastinal hematoma, and aortic dissection in the latter. Histologic lesions in the case of the Border Collie crossbred dog included a dissecting hematoma of the ascending aorta with elastin dysplasia and right axillary arterial intimal proliferation.     

Relationship between pulmonary arterial pressure and lesions in the pulmonary arteries and parenchyma, and cardiac valves in canine dirofilariasis.

The relationship between pulmonary hypertension and lesions was examined in 41 dogs infested naturally with heartworms, which consisted of 28 cases with pulmonary heartworm disease and 13 cases with caval syndrome. Pulmonary arterial pressure (PAP) was measured before and 1 or 7 days after heartworm removal with a flexible alligator forceps. In these dogs, lesions were examined after the last measurement of PAP. The mean PAP was 28.2 +/- 16.0 mmHg (10.9 to 81.4 mmHg in range) at post-removal phase. Pulmonary arterial intimal lesions, pulmonary thromboemboli, pneumonic lesions, tricuspid valvular lesions and mitral valvular lesions were macroscopically recognized in 95, 59, 39, 54 and 56% of cases, respectively. These lesions were classified by severity and the relationship with PAP was examined by the multiple correlation analysis. The multiple coefficient correlation was found the highest between PAP and thromboemboli, followed by mitral valvular lesion, tricuspid valvular lesion, and pneumonic lesion. There was no significant correlation between PAP and intimal lesions. The coefficient of determination showed the highest value in thromboemboli when one variable was used, and increased only very slightly when a variable of thromboemboli was added to those of other lesions. The cases with high PAP had fresh thromboemboli in large pulmonary arteries. From these evidences, it was concluded that thromboemboli following natural death of heartworm was the most important factor causing an increase in PAP and developing clinical signs in canine heartworm disease.     

Histologic examination of selected areas of canine pulmonary arteries

Selected areas of pulmonary arteries from 18 healthy mixed-breed dogs were examined using histologic staining techniques. Smooth muscle cell, collagen, and elastin content of the tunica intima and tunica media were assessed. Fifteen dogs had abnormalities of tunica intima or tunica media in at least one arterial section examined. Of all arterial sections examined, 40% had histologic changes of the tunica intima or tunica media, and 42% of these vascular lesions were in the main pulmonary artery. The most commonly occurring pathologic change was loss of smooth muscle cells and elastin of the tunica media and replacement by collagen. This lesion is similar to cystic medionecrosis of the aorta. Seemingly, a high frequency of spontaneous vascular lesions exist in pulmonary arteries of young dogs.     

Pulmonary Lymphomatoid Granulomatosis in Seven Dogs (1976–1987)

Seven dogs with pulmonary lymphomatoid granulomatosis were reviewed. The disease occurred in six large-breed and one small-breed dogs. The dogs were five to 14 years old (mean, 8.4; median, 7), and four of seven dogs were males. Three dogs had been previously treated with adulticide therapy for canine dirofilariasis. Clinical histories included a progressive respiratory disease characterized by varying degrees of cough, dyspnea, exercise intolerance, and weight loss. Thoracic radiographic features included hilar lymphadenopathy, pulmonary masses of varying sizes, and mixed pulmonary patterns of lobar consolidation with ill-defined interstitial and alveolar pulmonary infiltrates. Cardiovascular changes compatible with chronic dirofilariasis were present in three dogs. The clinical course was usually progressive and fatal. The survival time ranged from six days to four years (mean, 12.5 mos; median, 3 mos). Gross and histologic features included mass lesions with areas of necrosis that replaced normal pulmonary architecture. Cytologically, these lesions were characterized by infiltration with pleomorphic, angioinvasive mononuclear cells that often resulted in vascular obliteration. The infiltrating cells resembled large lymphoid cells that possessed large hyperchromatic nuclei and small amounts of cytoplasm. Systemic lymphoid neoplasia with peripheral lymphadenopathy was diagnosed in two dogs. In both cases, lymph-node cytology was similar to the cellular infiltrates found in the lungs and consistent with a diagnosis of lymphomatoid granulomatosis. These features are compared with previously reported cases of canine lymphomatoid granulomatosis and those features identified in a similar disease described in man.     

Note on Onchocerca armillata in the Sudanese camel (C. dromedarius). A histological and anatomo-pathological approach

Aortic onchocercosis due to O. armillata was diagnosed in 45 (41%) out of 109 Sudanese camels. Although the thoracic aorta was regularly affected, involvement of other vessels such as the abdominal aorta, brachiocephalic, pulmonary and costocervical arteries was not excluded. Gross examination of the affected blood vessels revealed tortuous tunnels of parasitic tracks readily visible in the intimal surface of the vessels. Nodular lesions were more common on the adventitia. Microscopically, the lesions showed irregulary elevated intimal surfaces. The underlying tunica media contained a varying number of encapsulated and partially mineralized parasitic fragments. The inflammatory response varied in intensity and location and consisted of eosinophils, lymphocytes, macrophages and occasional giant cells.     

Possible role of histamine in the genesis of pulmonary arterial disease in cats infected with Toxocara cati

Kittens between 12 and 20 weeks of age were orally dosed with 6000 infective ova of Toxocara cati. Animals were sacrificed at intervals between one and eight weeks after infection to study the development of pulmonary arterial lesions. After two weeks, marked leucocyte infiltration and mild thickening of the media of some of the smaller arteries was apparent histologically . Cellular inflammatory activity progressively increased up to four weeks after infection when intimal proliferation was evident in many of the arteries. After six weeks, the arterial walls were grossly thickened with pronounced intimal proliferation which after eight weeks had resulted in complete occlusion of some vessels. The progressive arterial occlusion was associated with a three- to four-fold increase in the parenchymal mast cell population and a corresponding increase in lung histamine content. The possible role of histamine in the genesis of the arteriopathy is discussed.     

Gastroenteritis of basenji dogs

Intestinal digestive and absorptive function and the gross and histologic appearance of the gastrointestinal tract were evaluated in Basenji dogs with chronic diarrhea, asymptomatic Basenji dogs, and healthy control dogs. Gastric rugal hypertrophy, lymphocytic gastritis, and gastric mucosal atrophy occurred in asymptomatic and affected Basenji dogs. All affected dogs had moderate or severe intestinal lesions characterized by villous clubbing and fusion, increased tortuosity of intestinal crypts, and diffuse infiltration of mononuclear inflammatory cells. Intestinal lesions in asymptomatic Basenji dogs invariably were less severe than those in affected dogs, but the small intestinal lamina propria of asymptomatic Basenji dogs consistently contained greater numbers of mononuclear inflammatory cells than did that of control dogs. The proportion of cells containing each immunoglobulin isotype (IgG, IgM, IgA) was similar among affected Basenji dogs, asymptomatic Basenji dogs, and control dogs. As compared to healthy beagle controls, intestinal function was abnormal in both affected and asymptomatic Basenji dogs evaluated by combined N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test, but malabsorption and maldigestion were most pronounced in affected Basenji dogs.     

Relationship between pulmonary arterial pressure and pulmonary thromboembolism associated with dead worms in canine heartworm disease.

To examine effects of thromboemboli due to dead worms on pulmonary arterial pressure (PAP), 20 to 50 dead heartworms were inserted into the pulmonary arteries of 4 heartworm uninfected dogs (uninfected group) and 11 dogs infected with heartworms (infected group). In the uninfected group, the mean PAP rose 1 week after worm insertion (10.9 to 166. mmHg), but it recovered by the 4th week. Clinical signs, hemodynamics and blood gas findings also deteriorated at the 1st week, but recovered at the 4th week. Angiographic and pathological findings indicated that blood flow recovered through the spaces between thromboemboli and vessel walls at the 4th week. The infected dogs were divided into three groups. In the infected-I group (5 dogs), the intimal lesions of the pulmonary arteries were slight, and clinical and laboratory findings showed changes similar to those of the uninfected group. In the infected-II group (4 dogs), the pulmonary arterial lesions were severe and the mean PAP was higher (25.7 mmHg) than in the uninfected group before worm insertion. An increase in PAP (34.1 mmHg) and worsening of clinical and laboratory findings were noticed till the 4th week. Thromboemboli adhered extensively to the vessel walls. Two dogs in the infected-III group died of severe dyspnea on the 9th and 10th day, and the mean PAP rose remarkably at the 1st week (from 19.4 to 28.2 mmHg). Severe pulmonary parenchymal lesions with edema or perforation were observed. From the above results, it was clarified that effects of dead worms on PAP and clinical signs depended on the severity of pulmonary arterial lesions before worm insertion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidemiology, clinical signs, histopathology and molecular characterization of canine leproid granuloma: a retrospective study of cases from Brazil

Thirty-eight cases of canine leproid granuloma were diagnosed between 2000 and 2008. Diagnosis was based upon clinical and histopathological findings and the presence of acid-fast bacilli in skin sections. The clinical lesions were localized predominantly on the pinnae and included papules, plaques and nodules, with or without ulceration. Boxer dogs were the breed most affected. Histopathological findings included nodular to diffuse pyogranulomatous, lymphoplasmocytic inflammatory infiltrates, with or without necrosis, localized in the dermis or subcutaneous tissue. The bacillary loading and morphology were variable among the lesions analysed. There was no significant correlation between bacterial load and histopathological pattern, dominant type of inflammatory infiltration or the amount of necrosis or giant cells. No correlation was observed between giant cells and histopathological pattern. In the majority of cases where a PCR-based assay was done, a novel mycobacterium species as the main aetiological agent was identified, as reported in previous studies.     

Dermal arteritis of the nasal philtrum in a Giant Schnauzer and three Saint Bernard dogs

Arteritis of the nasal philtrum is described in four dogs. Two of the Saint Bernards were related. The lesions were solitary, well-circumscribed, linear ulcers that were neither pruritic nor painful. The age of the dogs at the time the owners first noticed the lesion ranged from 3 to 6 years. The ulcers had been present for 0.5-5 years before diagnosis was pursued. Three of the dogs experienced repeated, mild episodes of arterial bleeding from the ulcers. Two dogs also experienced a severe episode of bleeding that required surgical intervention. Histopathological findings included a V-shaped ulcer, neutrophilic dermal inflammation subjacent to the ulcer and lymphoplasmacytic dermatitis bordering the ulcer. The most remarkable pathological findings were present in the deep dermal arteries and arterioles subjacent to the ulcer. The changes were characterized by subendothelial spindle cell proliferation with marked extracellular matrix deposition that stained blue with Alcian Blue (mucin) and Masson's trichrome (collagen) and resulted in intimal thickening, and stenosis of dermal arteries and arterioles. Immunohistochemical studies suggested that the proliferating spindle cells were of either myofibroblast or smooth muscle origin (actin and vimentin positive). Anti-inflammatory therapy (glucocorticoids; tetracycline and niacinamide; fish oil) may be beneficial for long-term control of this condition, however, long-term maintenance treatment appears to be necessary.     

End-stage kidney disease probably due to reflux nephropathy with segmental hypoplasia (Ask-Upmark kidney) in young Boxer dogs in Norway. A retrospective study

This paper is a retrospective morphologic study of 7 young Boxer dogs, showing end-stage kidney lesions compatible with chronic pyelonephritis with severe segmental cortical atrophy and fibrosis, associated with chronic tubulointerstitial inflammation of varying degree. Azotemia was observed in 6 of the 7 cases. The gross kidney lesions were as follows: bilateral small kidneys with numerous segmental cortical scars causing depression of the renal cortical surface. Histologic examination revealed salient atrophy of nephrons, including paucity of glomeruli, glomerulocystic lesions, colloid-filled tubular microcysts, and a conspicuously increased occurrence of arteries with narrowed lumina caused by intimal thickening. These segmental abnormalities were accompanied by pronounced interstitial fibrosis. All but 1 dog showed salient tubulointerstitial lympho-plasmacytic infiltration, which in 3 cases also included diffuse infiltration of polymorphonuclear neutrophilic leukocyte (PMN)-cells and occurrence of tubular PMN-casts. Morphologic signs of abnormal metanephric differentiation (renal dysplasia) were observed in all cases in the form of atypical tubules or asynchronous nephronic development (immature glomeruli) or both. However, other morphologic primary dysplastic features were absent. Based on the morphologic features, it is concluded that the end-stage kidney disease in these young Boxer dogs was the result of chronic atrophic nonobstructive pyelonephritis, most probably caused by vesico-ureteral reflux, compatible with reflux nephropathy causing segmental hypoplasia (Ask-Upmark kidney) in man. It is proposed that atypical tubular epithelium in the form of adenomatoid proliferation of collecting duct epithelial cells should be considered an acquired compensatory lesion, rather than the result of disorganized metanephric development.     

Apoptosis, inflammatory response and parasite load in skin of Leishmania (Leishmania) chagasi naturally infected dogs: A histomorphometric analysis

The skin has an important role in infection by Leishmania chagasi. Apoptosis modulates the inflammatory response acting distinctively either on the progression or regression of the lesions. The parasites interact with multiple regulatory systems inducing apoptosis in host cells, during cell invasion, stabilization and multiplication of pathogens. In this context, the aim of this study was to evaluate cell death within the inflammatory infiltrates, and to correlate these results with parasite load and clinical features of dogs naturally infected with L. chagasi. Fragments of skin pinnas (8 symptomatic+8 asymptomatic+6 negative controls) were used to characterize and measure the inflammatory response, parasite load and apoptosis. Diagnosis of canine leishmaniasis was confirmed by the detection of anti-Leishmania antibodies by IFA and ELISA in serum, direct visualization of the parasite and culture in spleen, liver, pinna, bone marrow and lymph nodes, and PCR (pinna). Histomorphometry was performed with images obtained from 20 representative histological fields in a light microscope. Ultra-thin sections were mounted over a 300 mesh grids, contrasted with 2% uranyl acetate and lead citrate and examined under a Transmission Electronic Microscopy. Amastigotes were only found in the skin of symptomatic animals (31.94±18.81). The number of foci and cellularity of the inflammatory infiltrates in symptomatic dogs were higher than in other groups and in asymptomatics were higher than in controls (p<0.05; Tukey). The average area, perimeter and extreme diameters of the inflammatory infiltrates obtained in symptomatic dogs were higher than in controls (p<0.05; Tukey). The apoptotic index was higher in symptomatic than in other groups and there was no difference between asymptomatics and controls (p<0.05; Tukey). Ultrastructurally, apoptotic cells were shrunken, with condensed nuclear chromatin and cytoplasm. Condensed nuclei were frequently fragmented. Internucleosomal DNA fragmentation occurred only in symptomatic cases. Amastigotes were observed within neutrophils and macrophages. Apoptosis is directly related to parasite load, intensity of inflammatory response and clinical manifestations in L. chagasi naturally infected dogs.     

美洛昔康片对比格犬的靶动物安全性评价

为研究美洛昔康片对靶动物比格犬的安全性,选取24只健康的比格犬随机分成4组,每组6只。各组试验犬分别以0、推荐剂量(0.2 mg/kg bw)、3倍推荐剂量(0.6 mg/kg bw)、5倍推荐剂量(1.0 mg/kg bw)口服美洛昔康片,每日1次,连续给药7 d。对一般临床状况、采食量、增重、饲料转化率、血液生理和生化指标、病理组织学等进行观察和检测。结果显示,除5倍推荐剂量对犬的肾脏和胃有一定的病理性影响外,其他各项指标与空白对照组相比差异均不显著。表明美洛昔康片毒性小,在犬体内耐受性高,以推荐剂量给药对靶动物犬是安全的。     

Intestinal crypt lesions associated with protein-losing enteropathy in the dog

Six dogs were diagnosed with protein losing enteropathy (PLE). There was no evidence of inappropriate inflammatory infiltrates or lymphangiectasia in multiple mucosal biopsies of the small intestine of 4 of the dogs. The 5th and 6th dogs had obvious lymphangiectasia and a moderate infiltrate of inflammatory cells in the intestinal mucosa. All 6 dogs had a large number of dilated intestinal crypts that were filled with mucus, sloughed epithelial cells, and/or inflammatory cells. Whether PLE occurs in these dogs because of protein lost from the dilated crypts into the intestinal lumen or whether the dilated crypts are a mucosal reaction due to another undetermined lesion that is responsible for alimentary tract protein loss is unknown. However, when large numbers of dilated intestinal crypts are present, they appear to be associated with PLE even if there are no other remarkable lesions in the intestinal mucosa.