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Biomedical subjects

A Dzhurov

Publications and source records attributed to A Dzhurov.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Clinical, morphological and biochemical changes in lambs caused by Fusarium toxins].

Studied was the effect of toxic trichotecenes and the F-2 toxin on the health status and the morphologic and biochemical changes in the blood on weaned lambs. It was shown that there was a drop of the hemoglobin content, rise of the leucocyte count, and decrease in the amount of the total proteins along with an increase in the activity of glutamate-oxalacetate and glutamate-pyruvate transaminases, alkaline phosphatase, and lactate-dehydrogenase. The morphologic changes appeared confined to the rumen, lymph nodes of the forestomach, duodenal mucosa, liver, and kidneys.

Animals↗
PubMed1981

[Clinical, morphological and biochemical changes in pigs caused by the toxic metabolites of Fusarium tricinctum].

Experiments were carried out with pigs in the course of 30 days with the use of dietary mixtures containing 10 and 20 per cent cultures of Fusarium tricinctum in rice. The treated animals showed higher sensitivity to trichotecenes. These moulds metabolites raised the activity of the serum glutamate oxaloacetate and glutamate-pyruvate transaminases, aldolase, lactate dehydrogenases, alkaline phosphatase, lipid level, and leukocyte count but lowered the amount of total protein and that of hemoglobin. The morphologic lesions seemed confined mainly to the stomach, intestines, and kidneys.

Animals↗
PubMed1981

[Histological changes in the liver of Benkovska breed geese during the fattening period].

Studies were carried out to follow up the histologic changes taking place in the liver of Benkovska breed geese during different periods of fattening. A correlation was established between the period of fattening and the severity of the liver lesions. During the preparatory period there was in the hepatocytes focal fatty infiltration, and by the 5th-10th day of the forced fattening diffuse fatty infiltration and fatty and granular degeneration were seen. On the 15th-20th day of the fattening period predominating in the dystrophic hepatocytes were the medium-sized fatty vacuoles, and on the 28th day - the larger vacuoles, which corresponds to Ist quality in terms of weight and macroscopic picture. The enrichment of the liver with fats was accompanied by lymphocytic and pseudoeosinophilic leukocyte infiltration of the interstitium.

Animals↗
PubMed1981

[Experiments to elucidate the role of Aspergillus fungi in the hemorrhagic syndrome in poultry].

Attempts were made to assess the role played by fungi of the Aspergillus genus in the occurrence of the hemorrhagic syndrome in birds. Groups of test birds were given continuously a forage mixture containing 30 per cent of ground nut cake which had aflatoxin at the rate of 1.5 ppm, a forage mixture 30 per cent of which was preliminarily contaminated with spores of Asp. fumigatus or Asp. flavus, and subtoxic amounts of nonpurified aflatoxin. Growth retardation was established along with the development of slightly manifested morphologic changes in some organs of the test birds. No morphologic picture characteristic of a hemorrhagic syndrome was found. In the authors' opinion the toxic Aspergillus fungi entering the body of the birds via the forage were not the sole factor contributing to the outbreak of such a syndrome.

Animal Feed↗
PubMed1981

[Toxicity of sodium monensin for pigs].

Studied were the acute and subchronic toxicity of monensin-Na in pigs. The investigations were carried out with elancoban-100, containing 10 per cent monensin-Na. A total of 46 pigs were used, weighing 15 to 60 kg. The preparation was applied individually via the nose or with the feed. It was found that nasally at 5 mg/kg the preparation did not lead to intoxication; rates of 10 and 20 mg/kg proved toxic, and a dose of 30 mg/kg was lethal. Feed containing 300 ppm of monensin-Na given but once led to intoxication and death with part of the animals. Pig tolerated well continuous (33 days) intake of feed that contained the sodium salt of monensin in concentrations of 120 and 240 ppm - no changes in the general status and behaviour were observed, nor were there any deviations in the morphologic and biochemical composition of the blood. It was demonstrated that the low amounts of monensin stimulated the weight gain of pigs. On the other hand, the clinical picture of the intoxication consisted in going off feed, higher pulse and respiration rates, involvement of the nervous system (depression of the nociceptive, eye closure, and ear reflexes, paresis of the hind limbs, and in severe cases - of the forelimbs too), hematuria in most of the animals, higher SGPT activity, and delayed ESR. Morphologically, there were vascular and slightly manifested degenerative changes in the parenchymal organs, red to brown urine in the bladder, strongly enlarged gallbladder, and catarrhal and hemorrhagic gastroenteritis. Histologically, there was granular and fatty degeneration of the kidneys, liver, and heart, hyperemia, perivascular and pericellular edema and degenerative changes in the glial cells of the berebrum, cerebellum, and medulla oblongata.

Animal Feed↗
PubMed1981

[Biochemical, electrocardiographic and pathomorphological studies the monensin poisoning of sheep].

Studies were carried out on the changes in the electrocardiogram, the content of sodium and potassium in the plasma and erythrocytes, and the morphology of the viscera of sheep spontaneously intoxicated with monensin. It was found that in the initial phases of poisoning the plasma level of Na and K strongly rose--410 +/- 12.57 mg% and 36.28 +/- 1.99 mg%, respectively, while after the tenth day it showed a trend of coming back to normal. The electrocardiogram of the poisoned sheep was inevitably deprived of the P deflection, while the QRST complex showed deformations characteristic of ischemia and degeneration of the myocardium. Morphologically, there were catarrhal abomasoenteritis, edomatized and fragile kidneys and liver, enlarged mucous membrane of the gallbladder, showing hyperemia and nodules, hemorrhages in the heart, and hyperemia and edema of the lungs. Histologically, there were dystrophic and necrotic nephrosis and focal glomerulonephritis, granular and fatty dystrophy and necroses of the liver, cholecystitis, granular and hyaline dystrophy of the myocardium, hyperemia, hemorrhages, and edema of the lungs as well as degenerative changes in the ganglion cells of the brain. The cadavers of animals that were ill for seven to ten days and died had multiple hemosiderosis in the kidneys, liver, lungs, and heart.

Animals↗
PubMed1981

[Liver diseases and their relationship to forestomach function in highly productive cows].

Studied were 12 cows with protracted, recurrent acidosis of the rumen, 4 cows with alkalosis, and 2 calves with experimental acidosis, following up the changes in the rumen content and their impact on the liver. The diseased animals were investigated both clinically and by laboratory tests with regard to alkaline phosphatase, plasma cholinesterase, SGOT, SGPT, alkali reserves, bilirubin, blood sugar, protein function of the liver (flocculation tests), biopsy of the liver, urine pH, urobilinogen, sedimentation test and ketone bodies, rumen pH, rumen infusoria, glucose-fermenting and cellulose-digesting activity, breakdown of nitrates, butyric acid, and ammonia gas. It was found that recurrent physiologic deviations of the rumen content play an essential pathogenetic role in liver injury. The more substantial and continuous the deviations the more severe the liver diseases. Studies revealed that along with other factors the recurrent acidosis and alkalosis of the rumen content could be claimed to be an immediate cause of the liver diseases in high producing cows. Histologically, the liver of cows with slightly expressed acidosis of the rumen showed granular degeneration, and of cows with protracted acidosis--fatty degeneration, activation of the reticulo-endothelial system, and leukocytes in the capillar sinusoids. Liver biopsy in the case of experimental acidosis demonstrated also decrease in the glycogen content of the hepatocytes.

Acidosis↗
PubMed1980

[Toxicity of hydroxyquinoline derivatives].

We studied a 90 day toxicity in dogs of the compound broxyquinoline + broxaldine--5:1 (enteroquin), applied orally and daily in doses of 0.1 and 0.2/kg t/24 h. We established the toxic manifestations during the period after the 15th day of the treatment: leukopenia, neutropenia and lymphocytosis (by 0.2 kg t/24 h). After the second and fifth day we observed a decrease of appetite, depression of the CNS, paralyses, arrhythmia, progressing loss in weight, proteinorrhea (more pronounced with those receiving 0.2/kg t (24 h); lethal consequence with some part of the animals 25% (ba 0.1/kg t) and 50% (by 0.2 kg t). We found out pathohistologically necrobiotic changes in the medulla oblongata and the kidneys, toxic distrophy of the liver, blood-vessel injuries. The toxic changes observed can be interpreted in connection with the presence of a species specific reaction.

Animals↗
PubMed1980

[Toxicological studies of Bulgarian activated bentonite].

We studied the endurance of calves, lambs and pigs as well as the acute, subchronic and chronic toxicity for chickens with regard to bentonite of local origin, extra activated in a physico-chemical way. It was proved that the medicine was rather endurable with calves, lambs and pigs without causing intoxication or death after a single internal introduction in doses respectively 4138, 4130 and 1860 mg/kg t. LD0 of the activated bentonite for the chickens in the case of intra-crop application was over 18000 mg/kg t. During a 33-day extra addition to the fodder of chickens in quantities of 2 and 6% and during a 90-day introduction into concentrations 1, 3 and 5% the activated bentonite and not provoke any changes in the behaviour, overall state and in the clinical biochemical and electrolytic composition (Ca, P, K, Na) of the blood, but it caused suppression of growth ranging from 6 to 27% and brought about a higher expenditure of food for a single growth unit ranging from 4.7 to 12.1%. This was also observed when it was added to the morning ration of pigs in doses 1 and 5% (6 and 30 d/pig) without any influence over the health state of the pigs, but it slowed down growth ranging from 17.2 to 21.3% and a lower utilization of the fodder taken by 19 to 26%.

Animal Feed↗
PubMed1980

[Acute and subchronic monensin toxicity for lambs].

The acute and subchronic toxicity of monenzine (preparation Elancoban -- 100 of Elanco Co., USA) to male lambs for fattening aged 3-4 months and weighing 16-28.5 kg was studied. It was established that the single per oral dose of 5 mg/kg weight of the natrium monoenzine salt causes a temporary lack of appetitie but no changes in the behavior and the general state of the animals. The use of a 10 and 30 mg/kg weight dose of the preparation led to death of the lambs on the 72nd-120th hour. The toxicity was clinically manifested by anurexia, arumination, ataxia, paresis, and paralysis of the limbs, tachicardia, taxipnea, hypothermia and showed down and weakened rumen movements. Erosive rumitis and abomasis, catharrhalhemorrhagis duodenitis, hemorrhages on the epicardis, hyperremia and parenchymal organ oedema, 3-4 times increased gall-bladder with numerous nodes having a sunken center on its walls were observed pathologo-anatomically, while microscopically blood vessel disturbances (hyperremia, hemorrhages and oedema) of the lungs, heart, spleen, endocrinal glands (thyroid, adrenal and hypophysis), the brain, and the leptomeninges, liver distrophy, distrophic nephrosis and necrotic holecystitis were obvious. Following a long term (30 days) application to the fodder in 10 and 50 g/t doses, monenzine-natrium does not have a negative effect on the behaviour, general condition, clinical and biochemical blood composition and the structural build up of the inner organs, but in the first 5-10 days of the treatment it causes loss of appetite. Additional specific investigations are needed to elucidate the effect of the preparation on body gain.

Animals↗
PubMed1979

[Effect of high doses of the toxins from Bacillus thuringiensis strains on mice and sheep].

The investigation on Bac. thuringiensis toxines applied orally and subcutaneously on experimental white mice and on sheep proved that high doses of the dipel endotoxin are most toxic for mice of all strains (No. 862, 2E, 171) and spores and crystals of strain ND-1 used in dipel injection. The endotoxin of strain 862 applied orally to sheep at a dose of 10 cm3/kg body weight caused slight changes only to some paraclinical indices, namely: total protein, carotene, etc. Exotoxin had none or only slight toxic effect. The remaining strains applied to high doses proved almost harmless to mice.

Animals↗
PubMed1978

[Pathomorphological studies in experimental simazine poisoning of sheep].

Studied were the morphologic changes in the viscera of 14 sheep and 2 goats experimentally intoxicated via the oral administration of simasin at various rates. The gross lesions consisted of catarrhal and hemorrhagic typhlitis, liver dystrophia, and enlargement of the gallbladder. Histologically, the acute cases presented granular degeneration of the liver and kidneys, oedema of the lungs, fatty infiltration of the myocardium, oedema, hyperemia, and hemorrhages in the brain. In the cases of chronic intoxication there were fatty degeneration of the liver as well as dystrophic changes in the testes, cerebrum, and cerebellum and diffuse granular degeneration of the kidney. Chronic intoxication of sheep with simasin at 1.4 and 3.0 mg per kilogram led to hypofunction of the thyroid; doses of 6.0 and 25 mg kg caused colloid struma while acute toxicity with 250 mg/kg (once and twice treated animals) caused parenchymal struma. A drop in the content of liver glycogen and degranulation of the mastocytes of the mesentery were also observed.

Animals↗
PubMed1975

[Chronic zinc-bacitracin toxicity in chickens].

The administration of zink-bacitracin, mainly bacipharmin, at rates of 300 mg per kg with the feed did not produce toxic effects in birds: there were no changes in the general condition and the blood picture, the activity of SGPT and SGOT, the blood level of sugar, and the microstructure of the viscera over a period of 90 days. However, doses of 1000 mg/kg of the preparation given with the feed to chickens led to sporadic cases of slightly expressed karyopycnosis in the renal tubules. Established was a growth-stimulating effect. By the end of the experimental period the relaive weight of the adrenal glands, kidneys, liver, and heart in the treated birds was lower in most of the cases as compared with the weight of the same organs in the control birds.

Alanine Transaminase↗
PubMed1975

[Pathomorphologic changes in calves with ruminal acidosis for fattening].

Studied were the morphologic changes in the organs of 17 calves for fattening with massive acute and subacute acidosis of the rumen. The disease broke out as the result of an abrupt change in the regime of feeding and tending. The gross observations consisted of hemorrhagic and necrotic foci in the rumen, hemorrhages and hyperemia in the omasum and reticulum, and ulcera in the abomasum. Established was also enlargement of the lymph nodes in the forestomach as well as odemas in the liver and kidneys. Histologically, there were necrotic inflammation of the rumen, serous and fibrinous exudate, leukocyte infiltration, hyphae, thrombuses, and arteritis. The omasum and reticulum presented desquamation of the cutaneous mucosal membrane, and the abomasum--necrotic foci, edema, and leukocyte infiltrations. There was also hepatitis, and fatty infiltration of the kidneys and heart and an activation of the interstitium. Degenerative process and hyperemia were observed in the thyroid gland, and fatty infiltration--in the pancreas. The kidneys, the adrenal glands, and the liver had higher alkalinephosphatase activity.

Acidosis↗
PubMed1975

[Histochemical tracing of the iron in the body of piglets injected with an iron-dextran preparation].

A comparative study was carried out with thirteen pigs, aged 1 to 3 days, to follow up the resorption and distribution of the Bulgarian iron-dextran preparations Ferdex-100, Dextrofer-75, A-100, and Miofer-100 in the body. Histochemically, an activation of the reticulo-endothelial system was established. Most macrophages that had phagocytised iron were established in the regional lymph nodes, followed by the liver, kidneys, marrow, while in the spleen their count was negligible. Using the histochemical reaction for the demonstration of iron in the viscera it was established that the A-100 preparation was best utilized by the organism. It was concluded that by the amounts of iron found in some organs it even exceeded Miofer-100.

Animals↗
PubMed1975

[Pathomorphological changes in a disease in swine caused by feeding bacterial-contaminated 1-lysine].

Studied were the lesions in the parenchymal organs and the hormonal glands in 20 pigs spontaneously died as a result of feeding with 1-lysine that had been contaminated with bacteria. The gross changes consisted of the enlargement and dark red coloration of the liver, gastroenteritis, hyperemia and hemorrhages in the kidneys and heart, oedema of the lungs and the wall of the gall bladder. Histologically, in the acute cases the liver showed hyperemia, pericapillary oedema, and granular dystrophia; in the subacute cases there were toxic dystrophy with the activation of the reticulo-endothelial system and subserous oedema in the gall bladder. The kidneys presented hyperemia, hemorrhages, and decreased volume of the glomeruloses in the subacute course of the disease. In terms of their function the heart, lungs, and kidneys displayed hemodynamic disturbances, and in the thyroid there were histologically changes characteristic of a follicular collapse. It is believed that the morphologic changes in the viscera investigated were due not to the intake of lysine itself, but to the effect of toxins produced by the concomitant microflora and the toxic amins (metabolites of the amino acids).

Animal Feed↗