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J L Vegad

Publications and source records attributed to J L Vegad.

At least 37 records · Page 2Linked to original sources

Pathology of the active Arthus reaction in the chicken.

It was possible to produce an active Arthus reaction in chicken skin which resulted in gross and microscopic lesions. Histologically, the reaction was predominantly thrombotic in nature and restricted to the upper dermis. The thrombi appeared to develop as a consequence of immune complex deposition with adherence and aggregation of thrombocytes at the vascular endothelium. Thrombosis induced widespread necrosis and haemorrhage and vasculitis occurred in the lower dermis. Up to four hours after inoculation, the cell population comprised an infiltration of heterophils, monocytes and basophils, suggesting an immediate hypersensitivity reaction. This was followed by an Arthus type reaction for four to 12 hours involving both heterophils and monocytes. A characteristic feature was the development of early perivascular lymphoid foci. After 12 hours the reaction resembled a delayed hypersensitivity. The use of colloidal carbon suggested that whereas phagocytic activity of the heterophils and basophils appeared sensitisation dependent, that of thrombocytes and monocytes was independent of it. The findings indicate that in the Arthus reaction in the chicken the thrombocyte appears to be the principal cell producing tissue damage by thrombosis. A comparison was made with the active Arthus reaction in the rabbit.

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Observations on the pathology of experimental avian spirochaetosis.

In experimental infection of chickens with a virulent strain of Borrelia anserina, peak spirochaetaemia was recorded from 72 to 96 hours. Progressive enlargement of the spleen with mottling was the predominant gross finding. Spleen, liver and small intestine showed extensive erythrophagocytosis, which continued even after the disappearance of spirochaetes from blood and tissues. While haemosiderosis was mild in the lungs, it was absent from the heart, kidney and brain. Spirochaetes were demonstrable in the spleen, liver, intestine, kidney and to a lesser extent in the lungs, but absent from the heart and brain. Widespread erythrophagocytosis and extravascular haemolysis suggest involvement of an immune mechanism in the pathogenesis of splenomegaly.

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Studies on acute inflammation in the chicken using turpentine-induced pleuroperitonitis as a test system.

An acute inflammatory reaction was induced in chickens by intraperitoneal injection of turpentine. The birds were then killed at various intervals and the peritoneal exudate sampled. The antihistamine mepyramine maleate was administered to another group of birds and the procedure repeated. Following turpentine injections there was a biphasic increase in vascular permeability, the early phase apparently mediated by histamine.

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Haematological studies on normal lactating Indian water buffaloes.

Haematological studies were conducted on 50 clinically normal lactating Murrah buffaloes in India. The range and mean (with one standard deviation), respectively, for the parameters examined were: red blood cells, 5.07 to 8.27, 6.54 +/- 0.77 million per microliter; haemoglobin, 9 to 13.5, 11.1 +/- 0.96 g/dl; packed cell volume, 0.26 to 0.34, 0.31 +/- 0.02; mean corpuscular volume, 40.6 to 55.2, 48.2 +/- 4.6 fl; mean corpuscular haemoglobin concentration, 30.9 to 38.5, 35.2 +/- 2.34 g/dl; mean corpuscular haemoglobin, 13.5 to 20.5, 17.10 +/- 1.85 pg; icterus index, 2 to 5, 2 +/- 1.25 units; erythrocyte sedimentation rate, 17 to 69, 53 +/- 12.3 mm at one hour; plasma protein, 6 to 9, 7.8 +/- 0.7 g/dl; fibrinogen, 0.2 to 0.8, 0.37 +/- 0.2 g/dl; reticulocytes, 0 per cent; white blood cells, 6250 to 13,050, 9676 +/- 1789 microliters; band cells, 0 to 1, 0.2 +/- 0.34 or 0 to 106, 18 +/- 40/microliters; neutrophils, 13 to 54, 32.9 +/- 8.74 per cent or 1285 to 6893, 3257 +/- 1262/microliters; lymphocytes, 26 to 75, 52.7 +/- 12.0 per cent or 2554 to 9637, 5065 +/- 1595/microliters; monocytes 1 to 11.5, 5.9 +/- 2.63 per cent or 63 to 1349, 584 +/- 301/microliters; eosinophils, 2 to 14.0, 6.9 +/- 4.64 per cent or 170 to 1471, 592 +/- 452/microliters and basophils, 0 to .5, 1.4 +/- 1.02 per cent or 0 to 326, 131 +/- 98 microliters. Normal species characteristics evident from this investigation included average size of the erythrocytes similar to that in cattle, low icterus index, conspicuous erythrocyte sedimentation rate, absence of reticulocytes and predominance of lymphocytes over neutrophils.

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Microscopic study of increased vascular permeability and leucocyte emigration in the chicken wing web.

The components of an acute inflammatory response in the chicken were investigated using a combination of histological and colloidal carbon techniques. The experimental model was the inflammatory reaction induced by the subcutaneous injection of turpentine or carrageenin into the wing web. Increased vascular permeability was shown to be mainly venular in origin. There did not appear to be an ordered migration of heterophils and monocytes and the process was unrelated to altered vascular permeability. Special features distinct from acute mammalian inflammation included a basophilic response, giant cell formation and the development of perivascular lymphoid foci.

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Demonstration of the phagocytic activity of chicken thrombocytes using colloidal carbon.

Chicken thrombocytes showed marked phagocytosis of carbon particles in both in vivo and in vitro systems. Initially, in both systems, thrombocytes containing carbon particles tended to form clumps. In the later stages, however, clumping was less obvious in the in vivo system. In addition to the thrombocytes, monocytes also contained carbon particles but heterophils did not. The present findings suggest that thrombocytes play a useful role in helping to clear the blood of foreign materials.

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Studies on acute inflammation in the chicken using mesentery as a test system.

An acute inflammatory response was produced in the chicken by the intraperitoneal injection of turpentine and vascular permeability was assessed by the technique of carbon labelling. This revealed a biphasic pattern of increased permeability which comprised an immediate transient reaction and a delayed more prolonged response. In both phases, the increased permeability remained confined to venules only. The vascular permeability was dissociated in time from leucocyte emigration. The pattern of leucocyte emigration revealed that heterophils and monocytes emigrated concurrently. Participation of basophils in significant numbers in the early stages indicated their possible role in avian inflammation. Examination of mast cells revealed morphological changes of degranulation and disruption. There was a coincident reduction in the population of these cells. It was thought likely that vasoactive amines released from the degranulated mast cells and the basophils might initiate the early vascular changes by acting on the venules.

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A topographical study of increased vascular permeability in acute inflammatory reaction in the chicken skin.

An inflammatory reaction was produced in the skin of the chicken by various stimuli. Then the colloidal carbon technique was used to identify vessels showing an increased permeability. The type of vessel affected, the extent and duration of reaction after each procedure were compared. Intradermal histamine, 5-hydroxytryptamine and bradykinin caused extensive but transient carbon labelling which was confined to venules. Topical application of xylol produced a more persistent delineation of venules. Intradermal turpentine and carrageenin affected extensive and restricted portions, respectively, of venules, and to a lesser extent capillaries. Following thermal injury of 65 degrees C for 30 sec, the superficial capillary network was initially involved but the venular response persisted for up to 18 h. These findings are compared and contrasted with those reported in laboratory animals. The possibility of distinction between direct vascular injury and chemical mediation is discussed.

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Dissecting aneurysm and cardiac tamponade.

A Gir cow which died suddenly had a dissecting aortic aneurysm. Death was caused by cardiac tamponade which followed rupture of the intrapericardial aorta after it had been damaged by onchocercosis.

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