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1.
Chronic bronchopneumonia associated with microlithiasis was diagnosed in a 9-year-old domestic shorthair cat with a 3-month history of coughing and dyspnea. Thoracic radiography revealed multifocal patchy alveolar infiltrates in all lung fields. Numerous acellular, concentrically laminated, periodic acid-Schiff-positive microliths were seen in mucus from tracheal washing. Microliths were composed primarily of calcium carbonate. A definite cause could not be identified. There was no response to treatment and the cat was euthanatized. Marked type-II alveolar cell proliferation, peribronchiolar smooth muscle proliferation, and alveolar microlithiasis were seen histologically. Microliths are rarely encountered in tracheal washings from companion animals. Their pathophysiologic properties and meaning remain to be established.  相似文献   

2.
Lung lesions of 60 Afghan pikas (Ochotona rufescens rufescens) were examined histologically; 38 cases of pulmonary alveolar microlithiasis were found. Neither sex was predominantly affected, and there was no predilection for age.  相似文献   

3.
A 9-year-old dog was presented with generalized extensive pulmonary mineralization associated with exertional dyspnea and cyanosis. The differential diagnosis for the pulmonary mineralization included metastaticand dystrophic pulmonary calcification, atypical pulmonary neoplasia, alveolar microlithiasis, idiopathic pulmonary mineralization, and idiopathic pulmonary ossification. The dog was euthanized at the owner's request. The histologic diagnosis was idiopathic pulmonary ossification. No previous report of generalized extensive idiopathic pulmonary ossification was found. Idiopathic pulmonary ossification occurs in man, usually involves a limited area of lung, and is functionally unimportant. The pulmonary ossification in the dog reported here was generalized and associated with severe pulmonary dysfunction. The disease in man and that in the dog in this report do not appear to be directly comparable.  相似文献   

4.
Six 3-month-old BALB/c Rag2-/- mice developed dyspnea 10 days after intravenous injection of wild type BALB/c CD45RB(high) lymphocytes to induce colitis as a model of inflammatory bowel disease. The lungs of all 6 mice were diffusely gray-purple and did not collapse completely. Microscopic findings were extensive coalescent patchy to diffuse alveolitis, characterized by macrophages and multinucleate giant cells, lymphocytes in alveolar lumina and septa, alveolar luminal of neutrophils, and alveolar proteinic material containing small black vesicular bodies characteristic of Pneumocystis sp. in methenamine silver stained sections. The morphologic diagnosis was diffuse granulomatous pneumonia with intra-alveolar organisms consistent with Pneumocystis sp., with an unusually aggressive inflammatory response related to the experimental procedure and possibly to the BALB/c genetic background.  相似文献   

5.
Six, 5- to 10-week-old male Holstein calves were inoculated intratracheally with 5 x 10(9) logarithmic growth phase Pasteurella haemolytica biotype A serotype 1 (A1). Immunohistochemical techniques in conjunction with the use of monoclonal antibodies directed against P. haemolytica A1-derived lipopolysaccharide (LPS), capsular polysaccharide, and a polyclonal rabbit anti-leukotoxin antibody were used to localize their respective antigens in tissue sections of pneumonic lung at the light and electron microscopic levels. We found the following: 1) LPS, capsular polysaccharide, and leukotoxin were released into the inflammatory exudate; 2) LPS was found within the cytoplasm of neutrophils (located in the alveolus and alveolar wall), alveolar macrophages, endothelial cells, pulmonary intravascular macrophages, and on epithelial cell surfaces; 3) capsular polysaccharide was found in the alveolus and alveolar macrophages but not in cells of the alveolar wall; and 4) leukotoxin was associated with cell membranes of degenerating inflammatory cells located in the alveolus. This is the first study that demonstrates the presence of leukotoxin in the pulmonary inflammatory lesions caused by P. haemolytica A1 and implicates endotoxin as an important factor in the genesis of the pulmonary lesions.  相似文献   

6.
旨在研究被动吸烟对小白鼠肺部组织结构的影响。对小白鼠进行烟熏处理后,取其肺部组织,制作石蜡切片,进行HE染色,借助显微镜观察小白鼠肺部组织结构的变化。研究结果表明,烟熏后小白鼠肺部出现肺泡扩充,肺泡壁变薄;肺泡隔出现不同程度的组织增生;肺泡囊、肺泡管扩大或受损;细支气管管壁受损,黏膜上皮柱状纤毛细胞数量增多,排列凌乱,管腔内有异物积累,管腔变窄;终末细支气管黏膜皱襞受损严重,管壁增厚。并且通过比较可观察到香烟烟雾对成年小白鼠肺部组织结构的影响变化较幼年小白鼠更明显。由该试验结果可以得出,随着烟熏时间的延长,香烟烟雾中的某些物质会引起小白鼠肺部组织结构发生明显变化,且被动吸烟对成年小鼠肺部组织结构造成的影响较幼年小鼠严重。  相似文献   

7.
为探究构建急性肺损伤模型的条件,本试验选用健康昆明小鼠,经腹腔注射递增剂量脂多糖（LPS）（0、2、4、6、8、10 mg/kg）,观察不同条件下小鼠呼吸频率、死亡率、肺脏干湿重比值及组织结构变化,检测炎症因子IL-10、TNF-α、IL-1β及IFN-γ在不同程度肺损伤中的表达量变化。结果显示,4 mg/kg LPS组肺脏干湿重比值显著高于对照组（P<0.05）;6、8和10 m/kg LPS组肺脏干湿重比值极显著高于对照组（P<0.01）。病理切片分析显示,6 mg/kg LPS组小鼠肺脏出现充血,肺泡腔及肺间质出现渗出,肺泡隔增厚,出现少量中性粒细胞浸润;8、10 mg/kg LPS组小鼠肺脏充血明显,肺泡腔及肺间质出现渗出,肺泡明显隔增厚,出现中性粒细胞浸润;与对照组相比,6、8、10 mg/kg LPS组肺组织中胶原纤维大量增多,且多出现在肺气管周围,10 mg/kg LPS组现象最明显。炎症因子检测分析结果显示,与对照组相比,2、4、6、8、10 mg/kg LPS组炎症因子均极显著增加（P<0.01）。结合病理组织切片及相关检测指标表明,昆明小鼠腹腔注射8 mg/kg LPS并作用12 h,可成功构建急性肺损伤模型。  相似文献   

8.
In order to explore the building conditions of acute lung injury, healthy Kunming mice were selected, by intraperitoneal injection of cascade dose of LPS (0, 2, 4, 6, 8, 10 mg/kg) to observe the mice respiratory frequency, mortality, lung W/D value and the changes of tissue structure in different conditions, and detect the expression changes of inflammation cytokine, IL-10,TNF-α, IL-1β and IFN-γ. The results showed that compared with control group, lung W/D value in 4 mg/kg LPS group significantly increased (P<0.05) and lung W/D values in 6, 8 and 10 mg/kg LPS groups extremely significantly increased (P<0.01). Pathological analysis showed that 6 mg/kg LPS group appeared lung congestion, alveolar luminal and pulmonary interstitial exudation, alveolar septal thickening, and a small amount of neutrophil infiltration. 8 and 10 mg/kg LPS groups appeared pulmonary congestion, alveolar and pulmonary interstitial exudation, alveolar septal thickening and neutrophil infiltration. Compared with control group, collagen fibers of the lung tissue in 6, 8, 10 mg/kg LPS group increased, and more appeared in the lung around the trachea, 10 mg/kg LPS group was the most obvious. The inflammatory factors in 2, 4, 6, 8 and 10 mg/kg LPS groups had extremely significantly increased compared with control group (P<0.01). Pathological biopsy and related indicators showed that the model of mice could be successfully constructed by intraperitoneal injection of 8 mg/kg LPS for 12 h.  相似文献   

9.
Pulmonary alveolar microlithiasis (PAM) is a rare, familial disease of unknown aetiology characterised by intra‐alveolar formation and accumulation of microliths. Multiple formalin‐fixed tissues were submitted from a 5‐month‐old female alpaca that died suddenly without significant clinical signs. No gross abnormalities were observed on postmortem examination. Histological findings included PAM and severe centrilobular hepatic necrosis. Although the hepatic lesion was the likely cause of death, PAM was an incidental finding that has not been reported previously in alpacas. An overview of PAM, including pathogenesis and histopathological characteristics, are discussed in relation to the concurrent hepatic disease in the present case.  相似文献   

10.
Pulmonary alveolar macrophages are considered to be the main phagocytic cell of the pulmonary defense mechanism. However recent studies indicate that neutrophils may also participate in the defense against inhaled bacteria. The aim of this investigation was to study in mice the correlation between numbers of phagocytic cells in the bronchoalveolar space and the pulmonary clearance of bacteria. White mice were exposed to aerosols of Pasteurella haemolytica (n = 129) or Staphylococcus aureus (n = 129) in three different experimental replicates. Another group of mice (n = 22) was sham exposed to an aerosol of sterile phosphate buffered solution in a single replicate. Animals were sacrificed at various times postaerosolization. The numbers of neutrophils and alveolar macrophages in lung lavages and the pulmonary bacterial clearance rates were determined and statistically analysed. No significant differences (p greater than 0.05) were observed in the rates of pulmonary clearance between the two genera of bacteria, but P. haemolytica had a significant (p less than 0.05) replicate effect. The number of alveolar macrophages was not significantly affected by either bacteria or phosphate buffered solution. Exposure to P. haemolytica resulted in dramatic, significant (p less than 0.01) but transient increases in neutrophils in the bronchoalveolar space as well as a significant (p less than 0.01) increase in the weights of lung. The correlation between neutrophils and clearance was positive for P. haemolytica but negative for S. aureus. These results indicate that both species of bacteria are rapidly eliminated from the lung despite a rather different cellular response.  相似文献   

11.
This study was conducted to investigate the in vivo effect of a single intratracheal inoculation of Pasteurella haemolytica cytotoxin on the rat lung. Changes in the biochemical and cytological composition of bronchoalveolar lavage fluid were used to estimate the magnitude of pulmonary cell injury, inflammatory response, vascular permeability and functional status of pulmonary alveolar macrophages. Effect of treatment was compared with rats intratracheally inoculated with supernatants of Pasteurella multocida or with sterile physiological saline solution (vehicle). Results indicated that Pasteurella haemolytica supernatants were not significantly toxic for the lungs of rats.  相似文献   

12.
The sequential pulmonary changes in dermatosis vegetans were studied in pigs aged one, seven, 14, 17, 21 and 28 days, and two and a half, four and 12 months. At one day old the lung tissues appeared normal. At seven days old there was a moderate infiltration of mononuclear inflammatory cells in the alveolar structures, and proliferation of type II pneumocytes was also observed. At 14 and 17 days old the alveolar structures were intensely infiltrated with mononuclear inflammatory cells. At 21 days old, loosely arranged epithelioid and multinucleate giant cell granulomas appeared, and there was a proliferation of alveolar epithelial cells. By four and 12 months old the inflammatory changes diminished, and small granulomas and moderate alveolar fibrosis were present. The initial lesions were characterised by an alveolitis, developing into loosely arranged granulomas by four months old, and persisting to the age of 12 months. These observations suggest that the interpretation of the lung changes and the disease in general should be revised.  相似文献   

13.
Experimental inoculations of 1000 Toxocara cati larval eggs were carried out in 18 BALB/c mice. The T. cati eggs used for inoculation were collected from the faeces of naturally infected cats. Euthanasia was performed on two mice on days 1, 2, 3, 4, 5, 6, 14, 21 and 28 post-inoculation (p.i.). Tissue samples were taken for digestion and histopathology. Larvae were recovered from all infected mice and the average of all larvae recovered was 28.3% (95%; CI: 14.1-42.4). Maximum number was obtained from liver on days 1 and 2 p.i.; from the lung on day 2 p.i. and from the brain on day 28 p.i. In muscle, the recovery was high as from day 3 p.i., with the maximum obtained on day 28 p.i. Superficial foci of congestion and haemorrhage were macroscopically observed in the lungs between days 2 and 5 p.i. and in the brain between days 3 and 6 p.i. Microscopic lesions were observed in the liver between days 2 and 14 p.i., with periportal and subcapsule inflammatory infiltrates. In the lungs, haemorrhages and inflammatory infiltrates can be observed in the alveolar parenchyma, close to bronchioles and large blood vessels. In the brain, congestive areas without inflammatory reactions were seen. In muscle, the presence of inflammatory infiltrates and degenerated muscle can be observed surrounding a parasite larva. These same lesions were observed in myocardium and pericardium. The kidneys were congested with inflammatory infiltrates. The inflammatory cells present in all the tissues studied were lymphocytes, neutrophils and a few eosinophils. Formation of granulomas or signs of larva encapsulation were not observed. The migratory pattern of T. cati larvae in BALB/c mice and its tendency to become concentrated in the muscle reinforce the importance of the mouse as a paratenic host for the parasite's cycle in the environment.  相似文献   

14.
The two objectives of this research were 1) to describe the ultrastructural morphogenesis of pulmonary damage and repair induced in calves after treatment with 4-ipomeanol and 2) to characterize infiltrating pulmonary inflammatory cells by bronchoalveolar lavage. Interstitial edema was observed as early as 4 hours after intravenous injection of 4-ipomeanol (5 mg/kg body weight) and progressed to severe alveolar edema by 72 hours. Damage to type I alveolar epithelial cells and terminal bronchiolar nonciliated cells included dilation of endoplasmic reticulum and perinuclear envelopes and was present at 4 hours after treatment. Necrosis and sloughing of these cells from basement membranes occurred at times from 12 to 96 hours after treatment. Alveolar capillary endothelial cells had mild dilation of endoplasmic reticulum at times from 12 to 72 hours after treatment. Necrosis of endothelial cells was not observed. Inflammatory cell infiltrates in bronchioles and alveoli were dominated by macrophages and neutrophils. Significant elevations (P less than 0.05) in numbers of neutrophils and macrophages were recovered by bronchoalveolar lavage at times from 24 to 96 hours after 4-ipomeanol-treatment. Hyperplasia of nonciliated bronchiolar epithelial cells and of type II alveolar epithelial cells were observed at 72 and 96 hours after treatment. The results indicate that type I alveolar epithelial cells and nonciliated bronchiolar epithelial cells are most susceptible to 4-ipomeanol-induced damage and necrosis in calves. 4-ipomeanol-induced pulmonary edema in calves occurs prior to ultrastructurally-demonstrable, mild, alveolar capillary endothelial cell damage.  相似文献   

15.
Eosinophilic crystalline pneumonia is an idiopathic disease that occurs in many strains and stocks of mice, more commonly in strains on a C57BL/6 background. The disease occurs sporadically in most strains of mice and varies from mild and subclinical to severe and fulminating, sometimes resulting in respiratory distress and death. In this study, 94 aged male and female 129S4/SvJae mice were evaluated for eosinophilic crystalline pneumonia lesions. There was an 87% incidence, with females overrepresented. Histologically, there were multifocal to coalescing inflammatory infiltrates composed of numerous large eosinophilic macrophages and multinucleate cells admixed with eosinophils, neutrophils, lymphocytes, and plasma cells within alveolar and bronchiolar spaces, associated with refractile, brightly eosinophilic, angular crystals. Alveolar macrophages and multinucleate cells contained fine needlelike to rectangular intracytoplasmic crystalline material. Similar crystals were often free within alveoli and conducting airways, often associated with mucous metaplasia of bronchiolar epithelium. This disease may occur spontaneously or in concert with other pulmonary lesions, such as pulmonary adenomas, lymphoproliferative disease, allergic pulmonary disease, and parasitic or fungal infections. The characteristic crystals morphologically resemble Charcot-Leyden crystals, which represent eosinophil breakdown products in humans with eosinophil-related disease. However, crystals in eosinophilic crystalline pneumonia are composed predominantly of Ym1 protein, a chitinase-like protein associated with neutrophil granule products and secreted by activated macrophages. The function of Ym1 protein is not fully understood but is believed to be involved in host immune defense, eosinophil recruitment, and cell-cell and cell-matrix interactions consistent with tissue repair. The mechanism of induction of eosinophilic crystalline pneumonia with Ym1 crystal formation is unknown.  相似文献   

16.
The relationship between acute pulmonary cell injury and inflammatory response was investigated in rats killed 1, 3, and 7 days after intratracheal inoculation with bacterial lipopolysaccharide (LPS). Activities of lactate dehydrogenase (LDH) and alkaline phosphatase (AP) in bronchoalveolar lavage (BAL) fluid and bronchoalveolar cell (BAC) lysate supernatants were used as indicators of cell injury in the lung. Concentrations of protein in BAL fluid and the number and types of BAC were used as indicators of pulmonary inflammatory response. The magnitude of inflammation and cell injury was calculated as the percentage difference of cellular and biochemical values, compared with values of nontreated controls. Inoculation with LPS induced a significant and dramatic (greater than 18,000%) influx of polymorphonuclear leukocytes (PMN) and a mild (approx 250%) increase in pulmonary alveolar macrophages. A moderate, significant and time-dependent increase in LDH (up to approx 260%) and AP (up to approx 220%) was detected in BAL fluid and BAC lysate supernatants after LPS inoculations. Inoculation with saline solution alone resulted in increased PMN (approx 975%), but did not alter LDH and AP values. In all rats evaluated, protein concentrations did not change. Numbers of PMN significantly and positively correlated with activities of LDH and AP. Protein concentrations and PMN counts had a negative nonsignificant association. Evidence of further cell injury was not detected after massive influx of PMN into the bronchoalveolar space. Therefore, the cellular influx of PMN induced by LPS probably was disproportionate to the magnitude of pulmonary cell injury.  相似文献   

17.
The role of neutrophils in the development of peracute lung lesions of bovine pneumonic pasteurellosis was investigated. Eight calves were divided into two groups of four calves each. Group I was treated with intravenous phosphate-buffered saline and served as the neutrophil sufficient calves. Group II was treated with intravenous hydroxyurea which produced a state of neutropenia. When peripheral blood neutrophil numbers dropped below 300 cells/microL in group II, all calves were challenged with an intrabronchial bolus of Pasteurella haemolytica in the log phase of growth. An acute inflammatory process occurred in both groups of calves indicated by a rise in body temperature. While pulmonary lesions occurred in both groups by six hours postinoculation, they varied in pathological characteristics. Pulmonary lesions in the neutrophil sufficient calves consisted of fibrinopurulent alveolitis-bronchiolitis with associated alveolar septal necrosis, interlobular edema, and intravascular thrombi. The neutrophil deficient calves had extensive intra-alveolar edema, interlobular edema, intraalveolar hemorrhage, atelectasis, and focal areas of alveolar septal necrosis. These results show that P. haemolytica can induce severe pulmonary tissue damage through both neutrophil dependent and neutrophil independent mechanisms.  相似文献   

18.
宁夏某肉牛场牛支原体分离鉴定及病理组织学观察   总被引：1，自引：0，他引：1  
为了分离鉴定宁夏某肉牛场牛支原体和分析该病原对靶器官的损伤,采用Thiaucourt's液体筛选培养基和固体培养基进行病原分离,设计牛支原体16SrRNA通用引物和uvrC特异性引物进行基因序列扩增并测序,使用DNA Star软件将分离菌株测序结果与GenBank中的标准株序列进行同源性比较,采用MEGA6.0软件中的邻接法(Neighbor-joining,NJ)依据16SrRNA和uvrC序列构建分离株系统发育树并进行遗传进化分析,采用石蜡切片,HE染色,病理组织学观察。结果表明,病原菌落呈油煎蛋样,16S rRNA和uvrC扩增片段与阳性对照一致,16S rRNA和uvrC基因序列构建的系统发育树与牛支原体在同一分支;肺组织结构消失,部分肺泡腔实变、塌陷,局灶性肺出血,肺泡腔内可见炎性细胞浸润;肺泡隔增厚、出血,肺泡内有少量脱落的上皮细胞;肺泡壁断裂,肺泡腔可见红色的炎性渗出物,有纤维结缔组织增生。  相似文献   

19.
The purpose of this study was to describe the clinical, radiographic, and computed tomographic findings in dogs and cats with migrating intrathoracic grass awns. Thirty-five dogs and five cats with visual confirmation of a grass awn following surgery, endoscopy or necropsy, and histology were assessed. The medical records and all diagnostic imaging studies were reviewed retrospectively. Labrador Retrievers or English Pointers < 5 years of age, with a history of coughing and hyperthermia, were the most common presentations. Seventeen animals had an inflammatory leukogram of which 14 had a left shift or toxic neutrophils. Radiographs were performed in 38 animals and computed tomography (CT) in 14. Thoracic radiographs were characterized by focal pulmonary interstitial to alveolar opacities (n = 26) that occurred most commonly in the caudal (n = 19) or accessory lobes (n = 8). Additional findings included pneumothorax (n = 9), pleural effusion (n = 8), and pleural thickening (n = 7). Pulmonary opacities identified on radiographs correlated to areas of pneumonia and foreign body location. CT findings included focal interstitial to alveolar pulmonary opacities (n = 12) most commonly in the right caudal lung lobe (n = 9), pleural thickening (n = 11), mildly enlarged intrathoracic lymph nodes (n = 10), soft tissue tracking (n = 7) with enhancing margins (n = 4), pneumothorax (n = 6), pleural effusion (n = 4), and foreign body visualization (n = 4). Histologic diagnoses included pulmonary and mediastinal granulomas or abscesses, bronchopneumonia, and pleuritis. Migrating intrathoracic grass awns should be considered as a differential diagnosis in coughing, febrile animals with focal interstitial to alveolar pulmonary opacities, pleural effusion, pleural thickening, and/or pneumothorax on radiographs or CT.  相似文献   

20.
OBJECTIVE: To evaluate the efficacy of inhaled nitric oxide (NO) in anesthetized healthy newborn foals with experimentally induced pulmonary hypertension. ANIMALS: Five 1- to 3-day-old foals. PROCEDURE: Anesthesia was induced and maintained with propofol, and foals were intubated and mechanically ventilated. Systemic pressure and pulmonary arterial pressure (P(PA)) were recorded every 30 seconds. Hypertension was induced via a hypoxic gas mixture or chemical vasoconstriction, using the thromboxane mimetic U46619. Nitric oxide was added at a concentration of 80 parts per million (ppm) for 6 minutes under baseline conditions and during pulmonary hypertension-induced alveolar hypoxia (inspired oxygen concentration = 0.08). Nitric oxide (20, 40, 80, and 160 ppm) was evaluated during U46619-induced hypertension. Samples for determination of arterial blood gas tensions were collected before and after each NO treatment. RESULTS: Inhaled NO (approx 80 ppm) did not have an effect on baseline variables. Infusion of U46619 (0.35 +/- 0.04 microg/kg of body weight/min) or alveolar hypoxia resulted in increased P(PA) and decreased arterial oxygenation (PaO2) and hemoglobin saturation (HbSat). The increase in P(PA) was attenuated, in a dose-dependent manner, by NO during U46619 infusion and reversed by NO during induced hypoxemia. The PaO2 and HbSat were significantly improved at all NO doses during U44619 infusion but not during alveolar hypoxia. For all inhaled NO concentrations, nitrogen dioxide and methoglobin values were < 5 ppm and 3%, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Nitric oxide is a potent, selective vasodilator of the pulmonary circulation in healthy newborn foals. Inhaled NO may have value as a therapeutic agent in foals with pulmonary hypertension.  相似文献   

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