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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, parasitological and pathological findings in a group of six donkeys naturally infected with D arnfieldi larvae are described. One animal had to be sacrificed at an early date because it developed pneumonia. The remaining five were unthrifty, showed mild clinical respiratory signs and had heavy strongyle infections. They had varying numbers of adult worms in the airways of the lungs and eggs were found coiled up in the smaller bronchi where they had apparently lead to an obstruction to airflow in that segment. The most striking gross pathological changes were circular discrete areas of over-inflation surrounding such bronchi. Histologically the infected bronchi exhibited a marked bronchiolitis with goblet cell hyperplasia and a mainly lymphoid inflammatory infiltrate. These areas also showed a localised bronchiolitus and overinflated alveolar tissue although true emphysema was not present. It is postulated that the parasite is well-adapted to its host and is able to survive for long periods within the lung without causing a debilitating amount of damage to the host. The immunological aspects of the infection are discussed briefly.
Vet Rec 1979 Jun 23
PMID:Lungworm: (Dictyocaulus arnfieldi) infection in donkeys. 15 90

In four outbreaks of indoor calf pneumonia, dyspnoea was a prominent clinical finding. At necropsy it was associated with pneumonia involving the cranial lobes of the lung and severe pulmonary emphysema. Histological examination of lung tissue revealed bronchiolitis and alveolitis with alveolar epithelial cell hyperplasia and multinucleate syncytium formation. Intraalveolar haemorrhage, intra-alveolar oedema and hyaline membrane formation were also noted. In all cases parainfluenza type 3 (PI3) virus was isolated from the lungs. In each of the four outbreaks there was evidence of PI3 virus and respiratory syncitial virus (RSV) infection.
Vet Rec 1979 Jan 20
PMID:Observations on outbreaks of respiratory disease in calves associated with parainfluenza type 3 virus and respiratory syncytial virus infection. 21 84

Broken wind is a syndrome characterised by chronic bronchitis and alveolar emphysema. Clinical signs include nasal catarrh, persistent coughing, dyspnoea and poor exercise tolerance. In racehorses, lung haemorrhages may result in epistaxis. Broken wind is a disease of domestication ascribed to pollution of the stable air with fungal spores from hay and straw. Treatment and prevention are based on the provision of fresh air and, if housing is unavoidable, the adoption of a permanent regime of dust-free stable management. If an early diagnosis is made and appropriate treatment instituted, the prognosis is considered to be reasonably good. The disease exemplifies the validity of the Royal Veterinary College motto Venienti occurrite morbo (treat the disease at its first appearance).
Vet Rec 1976 Dec 04
PMID:Chronic bronchitis and alveolar emphysema in the horse. 99 95

Nine calves between three and 18 weeks old with serologically confirmed natural bovine respiratory syncytial virus infection were examined clinically, radiographically and by radionuclide lung perfusion imaging. The results were compared with those from seven healthy calves. The diseased calves were euthanased and examined pathologically, virologically and bacteriologically. The clinical signs indicated that the disease was in an acute stage. Radiography of the diseased animals revealed cysts, corresponding morphologically with bullous emphysema, and infiltrations roughly corresponding in distribution with atelectatic and, or, pneumonic areas. Radionuclide lung perfusion imaging revealed no perfusion shifts between the left and right lungs and a normal perfusion pattern in five of the nine diseased calves. The abnormalities in the perfusion patterns of three calves were probably caused by anatomical disorders such as cysts and pleural adhesions, but no cause of the abnormality could be found in one calf. These findings suggest that in calves infected with bovine respiratory syncytial virus, the normal perfusion pattern is maintained until anatomical disorders occur. The pathological examination and radiography revealed that the cranioventral lung fields were particularly poorly ventilated. This finding and the normal perfusion pattern indicate that these parts of the lungs are probably the sites where shuntings and perfusion-ventilation mismatchings occur.
Vet Rec 1992 Nov 21
PMID:Radiographic and radionuclide lung perfusion imaging in healthy calves and calves naturally infected with bovine respiratory syncytial virus. 147 25

Four of eight red deer calves which had been artificially reared and were lungworm free were vaccinated with bovine lungworm oral vaccine when eight weeks old; the other four were not vaccinated. Three of each category were challenged daily with 500 Dictyocaulus viviparus infective stage larvae per kg liveweight for 17 days when six months old while one in each category was left as an unchallenged control. The effects of challenge were monitored and all challenged deer and one control were killed for post mortem assessment. Challenge with D viviparus was associated with reduced food intakes and weight gains but vaccinated calves were less affected than unvaccinated ones. The reaction of the alveolar tissue of red deer lung to D viviparus was mild in vaccinated and unvaccinated animals and differed from that of bovine lung in that alveolar epithelialisation was limited and hyaline membrane formation and interstitial emphysema were not seen. The disease was most evident in and around airways and was less in vaccinated calves. It was concluded that young red deer are tolerant to D viviparus but will readily acquire infection.
Vet Rec 1982 Aug 28
PMID:Experimental infections with Dictyocaulus viviparus in vaccinated and unvaccinated red deer. 621 59

A 16-day infection of Dictyocaulus viviparus in two groups of calves was treated with levamisole and fenbendazole respectively. Five days afterwards the calves were reinfected with 4000 larvae and necropsied 21 days later. Although the lungworm burdens of the two groups of calves were reduced by about 70 per cent compared to a control group the clinical signs of dyspnoea, tachypnoea and coughing were indistinguishable from a primary infection. This was due to pulmonary emphysema, oedema and an acute epithelialising pneumonia apparently associated with the death and disintegration of lungworms in situ, the result of an incompletely developed immune response. The results are compared with those obtained with the lungworm vaccine. It was concluded that the outcome of any system of "control" which depends on drug therapy and reinfection is unpredictable and that vaccination offers the only effective method of prophylaxis.
Vet Rec 1981 Feb 28
PMID:Control of parasitic bronchitis in calves: vaccination or treatment? 645 78

A single endotracheal instillation of elastase initiates a series of changes in animal lungs that results in a condition resembling human panlobular emphysema. An ultrastructural examination of this series of changes was conducted on the lungs of male golden hamsters exposed to 3H-methylated pancreatic elastase and sacrificed at intervals between 4 hour and 24 days after exposure to enzyme. Lung tissue between 4 and 48 hours showed evidence of hemorrhage and progressive degradation of elastic fibers. Very little indication of epithelial cell damage accompanied these changes. Four days after exposure to elastase, synthesis of new elastic fibers began with the appearance of small clumps of microfibrils in close association with interstitial cells, fibroblasts, and smooth muscle cells. There was also evidence of alterations in alveolar type II cells at this time. Small fibrillar elastic fibers continued to be present in the lung through twenty-four days and may represent a slow repair process or may indicate a structural difference in elastic fibers synthesized after exposure to elastase. Evidence of the continued degradation of elastic fiber could be found up to 16 days after exposure to elastase, revealing that repair processes were occurring in some areas of the lung while destructive process still predominated in other areas.
Anat Rec 1981 Nov
PMID:Ultrastructural changes in hamster lung four hours to twenty-four days after exposure to elastase. 691 32

Indole and 3-methylindole (3MI) are ruminal metabolites of L-tryptophan (TRP) and have similar physical and chemical properties. 3-Methylindole causes acute bovine pulmonary emphysema (ABPE). The effects of indole when administered orally to cows were determined. Four mature Holstein cows were given increasing doses of 0.05, 0.1 and 0.2 g indole per kg body-weight orally at two-week intervals. The animals were killed one week after the last dose. Plasma indole concentrations peaked three house after administration at 4.5, 8.8 and 19.8 microgram per ml after the 0.05, 0.1 and 0.2 doses, respectively. Detectable concentrations of indole (more than 0.02 microgram per ml) persisted in the plasma from three to 25 hours after dosing. Packed cell volume was decreased (P less than 0.01) at 48 and 72 hours after the 0.2 g per kg dose and at 72 hours after the 0.1 g per kg dose. Plasma haemoglobin was increased (P less than 0.05) at 48 hours after the 0.2 and 0.1 g per kg doses. By 72 hours after the 0.2 g per kg dose, all cows had mild diarrhoea and haemolysis and two of the cows had haemoglobinuria. At necropsy, microscopic lesions of haemoglobinuric nephrosis were seen in all four cows. No lesions of ABPE were found in any of the animals.
Vet Rec 1980 Oct 11
PMID:Indole toxicity in cattle. 721 Apr 36

In recent outbreaks of infectious bovine rhinotracheitis (IBR) in Britain a proportion of the animals affected developed a severe clinical disease characterised, at necropsy, by widespread damage to the respiratory tract. They had necrotising rhinitis, pharyngitis, laryngotracheobronchitis with extensive pseudomembrane formation and severe pneumonia with or without interstitial emphysema. Renal infarction was seen in approximatley half of the cases. The central nervous system was not affected in any of the 25 animals with severe IBR examined in this study. Tissues from the respiratory tract of 14 animals were examined for the presence of bovine herpesvirus 1 and the virus was isolated from the nasal passages of 11 and the lungs of four. Mycoplasma bovis was frequently isolated in large numbers from both the upper and lower respiratory tract.
Vet Rec 1980 Nov 08
PMID:The pathological features of severe cases of infectious bovine rhinotracheitis. 745 96

The pathogenesis of acute bovine pulmonary oedema and emphysema (ABPE) is related to the ruminal formation of 3-methylindole (3MI) from L-tryptophan (TRP), a naturally occurring amino acid and constituent of forage. The objectives of the present study were to determine whether monensin and lasalocid, both polyether antibiotics, were effective in reducing ruminal conversion of TRP to 3MI in vivo and to confirm that reduction in ruminal conversion of TRP to 3MI prevented tryptophan induced ABPE. Sixteen mature Hereford cows were assigned to one of four groups and given TRP to induce ABPE. Group 1 was given 100 mg monensin orally twice daily starting one day before and ending four days after TRP dosing. Group 2 was given 200 mg monensin once daily and group 3 was given 100 mg lasalocid twice daily. Group 4, the control, was given only TRP without further treatment. All control cows developed clinical signs of respiratory disease and lesions of ABPE; one control cow died of ABPE. Mean ruminal 3MI concentrations in control cows reached a peak of 36.4 micrograms per ml. Clinical signs of pulmonary disease appeared in two cows treated with lasalocid and one died. Mean ruminal 3MI in these animals peaked at 38.8 micrograms per ml. No clinical signs of respiratory disease were observed in any of the monensin treated cows and at necropsy there were no pulmonary lesions of ABPE. Mean ruminal 3MI concentrations in monensin treated cows did not exceed 8.9 micrograms per ml. In all groups plasma 3MI concentrations generally reflected ruminal 3MI concentrations but at lower concentrations. The results of this experiment demonstrate that reduction in ruminal 3MI formation by monensin prevents tryptophan induced ABPE.
Vet Rec 1980 Oct 04
PMID:Prevention of tryptophan-induced acute bovine pulmonary oedema and emphysema (fog fever). 746 89


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