The sequence of events in the development of bilateral renal cortical necrosis accompanying the generalized Shwartzman reaction.

The generalized Shwartzman reaction, or Shwartzman-like conditions, were induced in a variety of experimental mammalian species by systemic injections of disintegrated cells of Gram negative bacteria, live Salmonella cholerae-suis or Liquoid. A comparative study of the renal lesions showed that the initial step in the development of bilateral cortical necrosis is stagnation and disintegration of red cells in glomerular capillaries. The glomerular “microthrombi” consist mainly of erythrocytic debris, which frequently has staining properties akin to those of fibrin; even wide-spread glomerular “thrombosis” is not accompanied by obvious destruction of renal parenchyma. A second step is necrotic mural lesions in afferent arteries, with ensuing thrombosis. These vascular lesions lead to the formation of individual infarcts which fuse to form total bilateral cortical necrosis in fulminant cases of the generalized Shwartzman reaction.     

Haemolytic-uraemic syndrome in a dog

An 11-year-old female German Shepherd dog presented with lethargy and anorexia, which progressed to haemorrhagic vomiting, diarrhoea and seizures. Serum biochemistry and haematology results showed azotaemia and mild thrombocytopaenia. Euthanasia was elected and the dog was submitted for necropsy examination. There were widespread serosal and mucosal petechial and ecchymotic haemorrhages within the abdomen, with ascites and multiple renal infarcts. The renal infarcts were associated with fibrinoid necrosis and thrombosis of inter-lobular arteries and arterioles. These arterial lesions and clinical signs are consistent with haemolytic-uraemic syndrome, which has not previously been reported in dogs in Europe.     

Fibrinonecrotic rhinitis caused by a concurrent infection of Fusobacterium necrophorum and Arcanobacterium pyogenes in a cow

An 8 year-old cow showing severe dyspnea and nasal mucosal necrosis immediately after parturition was subjected to pathological examination. The principal lesions were fibrinonecrotic rhinitis, necrotic bronchopneumonia and renal infarction. Fusobacterium necrophorum biotype A and Arcanobacterium pyogenes antigens were detected in the nasal and pulmonary lesions. These results suggest that the lesions were caused by a concurrent infection of the detected bacteria and that the pulmonary lesions were caused by the aspiration of infectious materials from the nasal ones. Mucosal coagulative necroses observed as the initial lesions in rhinitis were frequently associated with multiple thrombosis. The findings might suggest that thrombosis played an important role in the development of the nasal lesions.     

Vascular lesions in nine Göttingen minipigs with thrombocytopenic purpura syndrome

Tissues from 9 G?ttingen minipigs, aged 7 weeks to 1 year, with clinically diagnosed thrombocytopenic purpura syndrome were examined microscopically. All pigs had a history of spontaneous cutaneous purpura that was generally accompanied by disseminated visceral hemorrhages. Hematologic abnormalities included anemia (8 out of 9 pigs) and thrombocytopenia (7 out of 9 pigs), with platelet counts consistently below 20,000/microl. Microscopically, degenerative vascular lesions with morphologic features of arteriosclerosis were present in all 9 pigs. Vascular lesions affected small- to medium-sized muscular arteries and arterioles in various organs and extraparenchymal tissues; vessels of the renal pelvis and coronary arteries were consistently involved. Microscopic lesions in small- to medium-sized muscular arteries consisted of neointimal proliferation, medial thickening, luminal stenosis, thrombosis, disruption and fragmentation of the internal elastic lamina, necrosis of the tunica media, and medial deposits of myxoid matrix material. Microscopic lesions in arterioles included concentric laminar thickening of vessel walls (onion-skin pattern), endothelial cell hypertrophy, smooth muscle cell vacuolation, necrosis of the tunica media, thrombosis, and partial to complete luminal stenosis. Arteritis and/or periarteritis were also noted in 4 out of 9 pigs. Additional microscopic lesions included membranoproliferative glomerulonephritis (3 out of 9), myocardial microinfarcts (4 out of 7), renal interstitial fibrosis (2 out of 9), extramedullary hematopoiesis (6 out of 9), and intracapillary hyaline thrombi (2 out of 9). Degenerative vascular lesions have not been previously described in G?ttingen minipigs with thrombocytopenic purpura syndrome. The etiopathogenesis of both the vascular lesions and thrombocytopenic purpura syndrome is currently unknown.     

Vasculitis associated with ovine progressive pneumonia virus infection in sheep

Vasculitis, involving small muscular arteries and arterioles, was found in 5 of 18 sheep naturally infected with ovine progressive pneumonia (OPP) virus and in 5 of 11 sheep experimentally infected with OPP virus. In order of frequency, arterial lesions were seen in carpal joint capsules, kidneys, meninges, brains, lungs, and tracheas. The lesions were intramural edema and hemorrhage, mononuclear cell infiltration, fibrinoid necrosis of media, and thrombosis. The vascular lesions were frequently associated with interstitial pneumonitis, arthritis, and encephalitis also induced by OPP virus.     

Idiopathic arterial medial calcification of the thoracic arteries in an adult horse

A 6-year-old, gelded, Paint horse displayed clinical signs of muscle wasting and limb stiffness for a 6-month period. The horse's clinical signs abated with corticosteroid therapy, but returned upon cessation of treatment. Upon necropsy, severe lesions of aortic thickening and aortic valve rigidity were observed. Histologically, the tunica media of the aorta, coronary arteries, and pulmonary arteries were expanded by foci of elastin fiber calcification and extracellular matrix with lacunae formation. The vascular lesions are comparative to what has been described as medial arterial calcification, seen in humans suffering from chronic renal failure or diabetes mellitus. No exposure to vitamin D-containing plants or feedstuff could be documented at the time of onset or during the period of clinical signs. The current case describes dramatic lesions of arterial medial calcification of the aorta, coronary, and pulmonary arteries of undetermined cause.     

Renal microangiography and correlated histopathological observation of cows with nephropathy.

Seven Holstein-Friesian cows showing chronic nephropathy were studied by renal microangiography and its correlated histopathology. In cases of pyelonephritis associated with severe pathological lesions such as thickening of arterial walls, narrowing of the arterial and arteriolar lumen, and interstitial inflammation and abscess formation, patchy loss of the peritubular capillary plexus from the cortex to the medulla was clearly demonstrated by microangiography. Interlobular arteries were tortuous and attenuated or truncated. Opacification in the vasa rectae and interstitial capillaries was increased. Extensive non-perfused regions could be detected in the cortex. In cases of mild interstitial nephritis and moderate pyelonephritis, microangiography showed focal changes in the renal vasculature. Microangiography is thus shown to clearly demonstrate changes in the renal vasculature corresponding to the severity of the histopathological lesions.     

Pathological findings of hemorrhagic bowel syndrome (HBS) in six dairy cattle cases

Six adult dairy cows clinically diagnosed as hemorrhagic bowel syndrome (HBS) were the subjects of this study. The involved intestinal lesions were fixed in formalin and examined macroscopically and histopathologically. Pathological examinations revealed large intramural hematomas with necrotic foci, resulting in luminal obstruction. The mucosal layer in the lesions was detached from the intestinal wall, and there were no hemorrhagic changes in the lumen. The intramural hematomas were sometimes covered with histologically intact mucosal layer. These pathological findings were not consistent with those of “intraluminal blood clots” reported previously. Gram-positive and anti-Clostridium antibody-positive short bacilli were found in hemorrhagic necrotic areas. However, the exact relationship between Clostridium spp. observed in the lesions and HBS remains unclear, because this bacterium is a normal inhabitant in cattle.     

Cerebral arteriosclerosis in an aged captive polar bear (Ursus maritimus).

Cerebral arteriosclerosis was observed upon necropsy of a 36-yr-old female captive polar bear (Ursus maritimus) that developed a sudden onset of seizure-like activity and died. The medium and large cerebral arteries of the meninges had moderate to severe diffuse discoloration and mineralization of the matrix of the tunica media, with little or no associated cellular reaction. Scanning electron microscopy of the affected arteries showed discrete crystalline calcified deposits in the media and sclerosis of the arterial wall. There were no lesions in the brainstem. The findings suggested a sudden and rapidly fatal loss of blood flow to the brain caused by long-standing arterial lesions. Incidental findings included numerous 0.1- to 10-cm-diameter, hepatic cysts lined with hyperplastic biliary epithelium, a unilateral, unipolar, 3-cm-diameter renal tubular adenoma, and approximately 250 active Baylisascaris sp. nematodes in the intestines.     

Uremic gastropathy in the dog.

Stomachs of four dogs with uremia and four normal dogs were examined. Uremic stomachs represented four types of disease: atrophic, amyloidotic, ulcerative and necrotic gastropathy. Pathologic changes common to all uremic stomachs were expansion of the lamina propria, atrophy of gastric glands, and submucosal arteriopathy; lesions were limited to body and fundic zones. Lamina propria was markedly expanded by edema, mastocytosis, deposition of acidic mucosubstances, fibroplasia and mineralization. Capillaries in lamina propria had swollen endothelium and calcium salts were present extracellularly as amorphous granular laminae. Gastric glands were distorted and irregular and had fewer cells per unit of tissue. Parietal cells were swollen and had fragmentation of cytocavitary network and mitochondrial swelling with calcification. Chief cells were shrunken, agranular and atrophic with foci of glycogen and dilation of endoplasmic reticulum. Argentaffin cell content was diminished. Muscular arteries of submucosae had segmental degenerative lesions characterized by myocyte necrosis, calcification, and deposition of acidic mucosubstances and fibrin; thrombosis and obstructive arteriopathy were common. These studies suggest that uremic gastropathy is a disease of mucosal lamina propria and that lesions were due to anoxia caused by diffuse vascular injury and to altered parietal cell function.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. IV. Changes in the bronchial circulation demonstrated by C.T. scanning and microradiography

The purpose of this study was to use radiographic contrast techniques and special imaging methods to identify and high-light bronchial arterial involvement in lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses. The lungs from four horses with histories of EIPH were prepared for computerised tomographic scanning and microradiography by perfusing the broncho-oesophageal artery with a mixture of red latex and either barium or iodine contrast materials while the pulmonary supply received only blue latex. Computerised tomographic scan slices of the prepared inflated lungs were obtained from the caudal tip of the lung to the hilus. Microradiography of selected lung slices was also performed on a Faxitron. Diffuse areas of increased density, with preferential bronchial arterial supply noted on the computerised tomographic scans were confirmed by microradiography. Dense focal and diffuse plexuses of markedly hypertrophied and highly branched bronchial arterial networks were identified, centred around certain small airways. The vascular supply to these plexuses was recruited predominantly from neighbouring bronchial vessels, and in some cases, from the enlarged vasa vasorum of pulmonary arteries sending anastomoses to the affected areas. The authors conclude that bronchial vascular lesions in EIPH cases are the likely origin of haemorrhage; that small airway disease is the probable initiating stimulus for bronchial vascular proliferation in these lesions; and that the morphology and nature of the neovascular tissue in these lesions provides the conditions leading to haemorrhage in the lungs of horses with EIPH.     

Brain and spinal cord lesions in encephalitozoonosis in the blue fox

The central nervous system lesions in encephalitozoonosis were studied in 11 naturally infected blue foxes. Immunohistochemical staining was employed in the demonstration of the parasites and identification of host cells. Consistent findings in acute to subacute stages included granulomatous meningoencephalomyelitis and vasculitis, with arterial lesions similar to polyarteritis nodosa. Chronic stages were dominated by arteriosclerosis, perivascular mononuclear infiltrations and gliosis, with less prominent granulomatous reaction. Parasites were almost constantly observed in association with active lesions both in vessels and nervous tissue. Parasitophorous vacuoles (PV) occurred in endothelial cells and in the medial layer of arteries. Neurons, including even their processes, were widely parasitized, a fact that may account for the brain being an important target organ. PV also occurred in ependymal cells of the choroid plexus and occasionally in macrophages. A great number of parasites was demonstrated in phagolysosomes of macrophages, a fact that probably reflects a relative resistance to digestion, and may consequently contribute to the development of the prominent granulomatous reaction. It was concluded that the brain lesions, except in chronic stages of mild infections, seem to be pathognomonic for encephalitozoonosis in the blue fox.     

Granulomatous nephritis and meningoencephalomyelitis caused by Halicephalobus gingivalis in a pony gelding

A ten-year-old Shetland pony gelding showed low appetite, ataxia, peculiar swaying, clouding of consciousness, and ultimately died. At necropsy, multiple coalescing granulomatous foci were detected in the kidneys, and small necrotic lesions were found in the cerebellum. Histologic examination of the renal tissue sections revealed extensive granuloma, and Halicephalobus gingivalis-like nematodes were seen. Similar nematodes were found in the granulomatous or necrotic lesions of the renal lymph nodes and cerebellum, and were also frequently detected in cerebrospinal meningovascular lesions. Morphologic features together with partial ribosomal RNA gene sequences of the nematodes in the lesions revealed that they were H. gingivalis. The present results indicated that H. gingivalis caused granulomatous nephritis and meningoencephalomyelitis in this pony gelding.     

Pathological findings in dogs naturally infected with Angiostrongylus vasorum in Newfoundland and Labrador, Canada.

Fifty-six dogs from St. John's, Newfoundland, Canada, were evaluated for Angiostrongylus vasorum infection. Small numbers of nematodes were found within pulmonary arteries of 6 dogs. Larvae were identified in fecal samples in 2 of 6 dogs. All 6 dogs had multifocal granulomatous pneumonia and sometimes foci of chronic thrombosis, which varied from very mild to severe. One dog had extensive pulmonary lesions resulting in cor pulmonale. Right heart failure was characterized by right ventricular hypertrophy, hepatic congestion, ascites, and hydrothorax. Microscopically, in most cases, eggs, larvae, and sometimes intravascular adults, were present within lung tissue sections. Small foci of granulomatous inflammation with and without larvae were present in kidney and brain in 4 dogs. An additional dog, diagnosed antemortem with angiostrongylosis via fecal examination, was also examined. Pathological findings consisted of severe pyogranulomatous interstitial pneumonia with myriad eggs, larvae, and numerous intravascular pulmonary adult nematodes with extensive arterial thrombosis. Five hundred and seventy-two adult worms were removed from pulmonary arteries. Foci of granulomatous inflammation, often associated with larvae and/or eggs, were present in tracheobronchial lymph nodes, adrenal gland, brain, and kidneys. Severe seizuring noted antemortem was attributed to several large, discrete areas of acute hemorrhagic infarction within the cerebrum and cerebellum. Natural A. vasorum infection in domestic dogs in eastern Newfoundland causes lung pathology of variable severity, which in some cases, may progress to cor pulmonale and which may be associated with extrapulmonary lesions and clinical signs.     

The Vascular Architecture of the Porcine Small Intestine

The vascular anatomy of the porcine small intestine was studied by injection of intestinal vessels with India Ink. Examination of transverse and longitudinal serial sections of the injected intestine facilitated a three-dimensional interpretation of the vascular pattern. An artery from the mesentery penetrated the tunica muscularis, supplied muscular branches and passed on to the submucosa where it formed an arterial rete. From the submucosal arteries, arterioles arose and followed a direct axial course to the tips of villi where they ramified into a subepithelial capillary plexus. Some of the capillaries, at the midpoint of the villus, fused into paraxial venules, which emptied into a “transverse venule” at the base of the villus. Other villus capillaries were continuous with those of the crypts. The pericryptal capillary plexus received a few arterial branches from the submucosal arteries. The transverse venule and the pericryptal capillary plexus emptied into large, segmentally dilated veins in the submucosa. The submucosal veins formed an extensive anastomosing network drained by large venous trunks which passed through the muscle layers to the mesentery.

The observations suggest possible relationships between the vascular pattern and intestinal fluid movement.

     

Brain and spinal cord lesions in encephalitozoonosis in mink

Central nervous system lesions were studied by light microscopy in 43 farmed mink, aged 5 months to 2 1/2 years, with spontaneous encephalitozoonosis and showing cataractous eye changes. Lesions were found in the brain and spinal cord of all animals examined but were generally mild and chronic. The lesions were consistent with those previously described in spontaneous encephalitozoonosis in other carnivores. Parasites in parasitophorous vacuoles and free or phagocytosed in necrotic and granulomatous lesions were demonstrated in animals aged 5 months to 1 year. The occurrence of arterial lesions of the polyarteritis nodosa type found in the youngest animals probably indicates fetal infection. In animals aged 1 1/2 and 2 1/2 years active lesions were usually lacking and the changes were characterized by arterial sclerosis, sometimes with aneurysmal formations, small perivascular lympho-plasmacytic cuffings and focal gliosis.     

Arterial Vascularization and Morphological Characteristics of Adrenal Glands in the Pampas Deer (Ozotoceros bezoarticus,Linnaeus 1758)

This research presents morphological characteristics of adrenal glands and a demonstration of arterial vascularization in the Pampas deer, which is considered to be in extreme danger of extinction. A total of ten deer constituted the material of the study. Vascularization of organs was investigated by using latex injection technique. Left adrenal glands were basically supplied by coeliac, cranial mesenteric, renal and lumbal arteries. The arterial vascularization of the left adrenal glands was very complex in comparison with right adrenal glands. In two examples, branch of the lumbal artery was divided into phrenic caudal artery and cranial adrenal artery. In six examples, it was observed that the caudomedial and ventral regions of the left adrenal glands were also supplied by thinner branches that stemmed from second left lumbal artery. Besides, coeliac and cranial mesenteric arteries also gave off shorter branches supplying the cranial region of the left adrenal glands in five examples. It was determined that two branches originated from abdominal aorta directly for supplying left adrenal glands in only two examples. In four examples, two caudal adrenal arteries stemmed separately from left renal artery in a short distance. Arterial vascularization of right adrenal glands was more constant and supplied by lumbal and renal arteries. The adrenal glands were generally oval or round shaped. In only two examples, left adrenal glands were ‘V‐’ or heart‐shaped. There was no significant difference (P > 0.05) in sizes between right and left adrenal glands.