RADIATION PNEUMONITIS IN THREE DOGS

Radiation pneumonitis developed within the radiation treatment field in three dogs with soft tissue sarcomas located on or adjacent to the thoracic wall. Radiographic signs compatible with a diagnosis of radiation pneumonitis developed from one (n = 2 dogs) to two (n = 1 dog) months after completion of therapy. The initial radiographic sign was an alveolar infiltrate in all three dogs. At subsequent examinations at variable time periods after treatment, radiographic findings included: bronchiectasis (n = 3 dogs), alveolar infiltrate (n = 2 dogs), decreased lung volume (n = 2 dogs), and unstructured interstitial opacification (n = 1 dog). Necropsy examination of one dog at fourteen months after the completion of radiotherapy showed evidence of pulmonary fibrosis within the irradiated lung. Necropsy examination of the second dog did not show any evidence of radiation induced changes. It is possible that histopathologic examination did not include irradiated lung. No clinical signs that could be attributed to the radiation pneumonitis were observed in any dog. It appears that approximately 25% of the lung can be safely irradiated to high doses, if indicated, in order to deliver an adequate dose of radiation to a primary tumor site.     

Experimentally induced parainfluenza type 3 virus infection in young lambs: pathologic response

Pulmonary changes in five 1-week-old, colostrum-deprived lambs transtracheally inoculated with parainfluenza type 3 virus were studied by immunofluorescent, microscopic, and ultrastructural techniques. The lambs were killed at postinoculation days (PID) 3, 5, and 7. Immunofluorescence specific for parainfluenza type 3 virus was first seen in small airways and alveolar epithelium and later in the lumens of airways and alveoli and, to a lesser extent, in the interstitium of the lungs. Grossly, there were multifocal areas of consolidation in all lobes of the lungs. These areas were characterized microscopically by bronchiolitis and interstitial pneumonitis. The bronchiolitis involved the terminal airways and consisted of necrosis and sloughing of epithelial cells followed by hyperplasia of the epithelium. The interstitial lesion comprised extensive infiltration of alveolar septa and alveoli with macrophages and the necrosis of alveolar epithelium. This was followed by hyperplasia of the epithelium. Degenerated bronchiolar and alveolar epithelium contained numerous intracytoplasmic inclusions early in the infection, but such inclusions were not seen in the lambs killed at PID 7. The degenerated changes were also seen with the electron microscope, as were numerous inclusions of viral nucleoprotein and a few viral buds at PID 3 and 5. Viral inclusions and buds were seen in ciliated and nonciliated bronchial epithelial cells and type I and type II alveolar epithelial cells.     

Interstitial lung disease in feline immunodeficiency virus (FIV) infected cats

Postmortem bronchoalveolar lavage of feline immunodeficiency virus-infected cats indicated an alveolitis process, and histological examination of their lungs confirmed the occurrence of alveolitis, parenchymatous lymphoplasmocytic infiltration and myomatosis. Similar lymphoid interstitial pneumonitis has been described in human and animal lentiviral diseases: lymphocytic interstitial pneumonitis in hiv-1-infected human beings, and maedi in sheep infected by the maedi-visna virus. Such lymphoid interstitial pneumonitis may thus be a common feature of lentiviral infections.     

Interstitial lung disease in feline immunodeficiency virus ( ) infected cats

Postmortem bronchoalveolar lavage of feline immunodeficiency virus-infected cats indicated an alveolitis process, and histological examination of their lungs confirmed the occurrence of alveolitis, parenchymatous lymphoplasmocytic infiltration and myomatosis. Similar lymphoid interstitial pneumonitis has been described in human and animal lentiviral diseases: lymphocytic interstitial pneumonitis in -1-infected human beings, and maedi in sheep infected by the maedi-visna virus. Such lymphoid interstitial pneumonitis may thus be a common feature of lentiviral infections.     

Differential production of proinflammatory cytokines in the pig lung during different respiratory virus infections: correlations with pathogenicity.

The acute stages of infection with swine influenza virus (SIV), porcine respiratory coronavirus (PRCV) and porcine reproductive-respiratory syndrome virus (PRRSV) were shown to differ in terms of clinical and lung inflammatory effects and proinflammatory cytokine profiles in bronchoalveolar lavage (BAL) fluids. Caesarian-derived colostrum-deprived pigs were inoculated intratracheally with one of the three viruses. SIV infection was followed within 1 day post inoculation (d PI) by characteristic respiratory and general signs, and excessive lung epithelial desquamation and neutrophil infiltration (38 to 56 per cent of BAL cells at 1 d PI vs 0 to 1 per cent in controls). High concentrations of bioactive interferon-alpha (IFN -alpha), tumour necrosis factor-alpha (TNF -alpha) and interleukin-1 (IL -1) coincided with peak symptoms and neutrophil infiltration. PRCV infection was asymptomatic and produced a mild bronchointerstitial pneumonitis and neutrophil infiltration (13 to 22 per cent of BAL cells at 4 d PI). IFN -alpha titres parallelled those found during SIV infection, TNF -alpha was negligible and IL -1 undetectable. PRRSV infection induced anorexia and lethargy between 3 and 5 d PI. There was marked infiltration with mononuclear cells in alveolar septa and BAL fluids between 7 and 10 d PI, while neutrophils remained at less than 11 per cent of BAL cells at any time. IL -1 was produced from three throughout 10 d PI, while IFN -alpha production was minimal and TNF -alpha undetectable. These data strongly suggest that proinflammatory cytokines can be important mediators of viral respiratory disease.     

肺炎支原体感染大鼠实验模型的建立

本试验旨在建立肺炎支原体感染的Wistar大鼠模型 ,为研究肺炎支原体的发病机制及药物治疗理论提供基础。采用滴鼻法对实验大鼠进行肺炎支原体感染 ,利用PCR法进行咽拭子检测 ,并以透射电镜和光学显微镜进行肺部病理组织学检查。结果发现 ,实验大鼠在感染肺炎支原体 1 0d时 ,咽拭子PCR检测结果为阳性 ;透射电镜观察到肺脏细胞膜破裂 ,线粒体变性 ,嵴断裂 ;光镜下可见到支气管及肺血管周围有明显的淋巴细胞浸润 ,形成斑片状间质性支气管肺炎。结果表明了Wistar大鼠对肺炎支原体较易感 ,并产生以间质性肺炎为主要特征的肺部和呼吸道感染 ,也说明本次造模试验成功     

Replication of parainfluenza type-3 virus and bovine respiratory syncytial virus in isolated bovine type-II alveolar epithelial cells.

The objectives of our research were to determine whether bovine pulmonary type-II alveolar epithelial cells could be isolated from bovine lung and maintained in tissue culture and to determine whether isolated bovine type-II alveolar epithelial cells would support productive viral replication of bovine parainfluenza type-3 virus and bovine respiratory syncytial virus. Type-II alveolar epithelial cells were isolated from lungs of 4- to 7-day-old male Holstein calves by enzymatic dissociation of pulmonary tissue with trypsin and by separation of cells with the use of filtration and centrifugation on continuous Percoll gradients. Cells were further separated by panning on IgG-coated plastic plates and by lectin binding. Isolated type-II alveolar cells were maintained on basement membrane-coated tissue cultured plates. In culture, type-II cells formed alveolar structures and maintained other cytologic features of type-II cells, including osmiophilic lamellar inclusions. Cell cultures were inoculated with and supported productive replication of bovine parainfluenza type-3 virus and bovine respiratory syncytial virus. This was determined by recovery of infectious viruses from inoculated cell cultures and by identification of viral structures in type-II alveolar epithelial cells by transmission electron microscopy.     

Bovine allergic pneumonitis: an acute outbreak associated with mouldy hay.

An outbreak of acute bovine atypical interstitial pneumonia is reported in association with feeding mouldy hay. Results of serological investigation and of provocation challenge indicated a hypersensitivity pneumonitis due to allergens of Micropolyspora faeni. Macroscopic and microscopic pulmonary changes were predominantly those of oedema and emphysema. These lesions were contrasted with more chronic changes reported in allergic pneumonitis of housed cattle.     

一例体细胞克隆黄牛肺脏的组织结构观察

作者应用石蜡切片及HE染色技术对体细胞克隆黄牛的肺脏及其细胞类型和形态进行了详细的观察。结果表明,光镜下,该体细胞克隆黄牛肺脏的组织结构与自然繁殖的黄牛肺脏的组织结构基本一致,包括支气管、细支气管、终末细支气管、呼吸性细支气管、肺泡管、肺泡囊及肺泡等结构,但体细胞克隆黄牛的细支气管管壁内的皱壁消失,其黏膜以单层立方上皮为主;肺泡处于半充容状态,肺泡腔狭小,肺泡膈较厚,其中含有较多胶原纤维和弹性纤维。肺泡壁的细胞结构不清,肺泡腔内有内容物,可能是发生病变引起。     

Necrotizing meningoencephalitis and pneumonitis in a simian immunodeficiency virus-infected rhesus macaque due to Acanthamoeba

Free-living amoebae of the genus Acanthamoeba can cause a fatal disease of the brain in humans called granulomatous amoebic encephalitis. We present a case of meningoencephalitis and pneumonitis in a simian immunodeficiency virus (SIV)-infected rhesus macaque caused by Acanthamoeba sp. The animal became ill 176 days after intravenous inoculation with SIVmac251 after a short history of weight loss and a sudden onset of hind limb paresis and abnormal head movements. Histopathologic examination of hematoxylin and eosin-stained tissues revealed multifocal to coalescing necrotizing neutrophilic meningoencephalitis and pneumonitis. Immunofluorescence and polymerase chain reaction were used to identify the genus of amoeba as Acanthamoeba. Immunohistochemistry of immune cell markers was used to characterize the animal's immune response to the opportunistic amoebic infection with features of both innate and adaptive cell-mediated immunity. Although not previously reported, the potential transmission to humans, either through environmental contamination or contact with an infected animal, makes this disease a threat to laboratory animal care staff and pathologists.     

In vitro phagocytosis and killing of Corynebacterium equi by alveolar macrophages of foals

Bronchoalveolar lavage was performed 5 times, sequentially, on 3 healthy foals while each foal was 6 to 63 days of age. Phagocytosis and bactericidal assays were performed on recovered alveolar macrophages. Corynebacterium equi and alveolar macrophages at a ratio of 10:1 were incubated for 1 hour in medium containing 1% heat-inactivated rabbit anti-C equi serum. After incubation, greater than 90% of the alveolar macrophages contained at least 1 ingested bacterium and each alveolar macrophage contained 9.4 +/- 1.0 bacteria (mean +/- SE). After alveolar macrophages and C equi were incubated for 1 hour in medium containing heat-inactivated pooled normal horse serum, approximately 24% of the alveolar macrophages contained at least 1 bacterium and each alveolar macrophage contained 0.8 +/- 0.7 bacteria. From 6 to 61 days of age, each foal had significantly (P less than 0.05) decreased phagocytic activity by alveolar macrophages, but a significant change in killing of C equi by alveolar macrophages was not found in the foals from 21 to 61 days of age. After incubating alveolar macrophages and C equi for 4 hours in vitro, approximately 75% of ingested C equi remained viable.     

Continuous positive airway pressure therapy for aspiration pneumonia in a dog

A 14-year-old mixed-breed dog aspirated a large amount of liquid barium sulfate. Calculation of the alveolar arterial oxygen tension difference (34 mm of Hg; normal, less than 7.5 mm of Hg) from the alveolar gas equation and the arterial blood gas analysis indicated impaired pulmonary gas exchange. The dog was treated for 5 days with continuous positive airway pressure and supplemental oxygen administered by a simple apparatus connected to a tracheostomy tube. Continuous positive airway pressure was believed to improve gas exchange and to increase pulmonary compliance by decreasing alveolar collapse in this dog.     

Tilmicosin reduces lipopolysaccharide-stimulated bovine alveolar macrophage prostaglandin E(2) production via a mechanism involving phospholipases

Tilmicosin is a potent antimicrobial with broad-spectrum activity against the bacterial agents involved in the bovine respiratory disease complex. Recent studies indicate that in addition to being bactericidal, tilmicosin is capable of modulating inflammation in the lung. A series of experiments were designed to determine whether tilmicosin alters alveolar macrophage-prostaglandin E(2) (PGE(2)) production induced by Escherichia coli (O55:B5) lipopolysaccharide (LPS). Twenty-two healthy Holstein bull calves were used to study the effects of LPS-induced PGE(2) production of alveolar macrophages after in vivo or in vitro treatment with tilmicosin. In Experiment 1, tilmicosin was given by subcutaneous injection (15 mg/kg) twice, 48 hours apart, to four calves; four control calves received no treatment. Twenty-four hours after the second treatment, alveolar macrophages were stimulated with LPS in vitro. In Experiment 2, alveolar macrophages from five untreated calves were harvested and treated in vitro with tilmicosin, followed by LPS stimulation. In Experiment 3, the ability of in vitro tilmicosin treatment to alter the expression of LPS-induced cyclooxygenase-2 (COX-2) mRNA was evaluated. In Experiments 4 and 5, secretory phospholipase A(2) activity was examined in untreated calves. Treatment of calves with tilmicosin resulted in reduced LPS-induced alveolar macrophage PGE(2) production. Similar reductions in PGE(2) by LPS-stimulated alveolar macrophages after in vitro tilmicosin treatment were noted. This in vitro tilmicosin treatment was not associated with reduction of the expression of LPS-induced COX-2. Alveolar macrophage phospholipase A(2) activity induced by LPS was significantly reduced by prior tilmicosin treatment in vitro. Tilmicosin (in vivo and in vitro) appears to reduce the PGE(2) eicosanoid response of LPS-stimulated alveolar macrophages by reducing the in vitro substrate availability without altering in vitro COX-2 mRNA expression.     

PAS-positive inclusions in the alveolar type II cells of the caprine lung.

Histochemical analysis of inclusions in the alveolar type II cells was done with the alcian blue-PAS technique. PAS-positive inclusions, which were absent in the sheep and buffalo, were detected in the alveolar type II cells of the goat lung. Mixed diamine-sodium chloride did not stain these inclusions which also showed orthochromatic blue reaction with toluidine blue. The high percentage of alveolar type II cells showing these inclusions suggested that this difference could be explained by the environmental habitat of the goat.     

不同发育阶段高原牦牛肺泡超微结构的研究

利用透射电镜和计算机图像分析系统对1日龄、30日龄、180日龄和成年4个年龄组的高原牦牛肺泡超微结构进行观测,并与同日龄平原黄牛进行比较。结果表明:不同发育阶段高原牦牛和平原黄牛肺泡壁均由扁平的肺泡I型上皮细胞和立方的肺泡II型上皮细胞组成,气-血屏障均由肺泡I型上皮、基膜和肺泡隔毛细血管内皮3层结构组成,但高原牦牛肺泡I型上皮处可见一些凹陷和空泡状结构。此外,1日龄高原牦牛肺泡II型细胞明显多于同日龄黄牛;除1日龄外,其余年龄段高原牦牛的气-血屏障算术平均厚度和调和平均厚度均显著小于同日龄平原黄牛(P<0.05)。高原牦牛气-血屏障的算术平均厚度和调和平均厚度随年龄增加不断减小,这不同于平原黄牛随年龄增加不断增大的特点。结论:高原牦牛出生后肺泡迅速发育,在超微结构方面表现出较多适应高原低氧环境的组织学结构特点。     

In vitro and in vivo 2',5'-oligoadenylate synthetase activity induced by recombinant DNA-derived bovine interferon alpha I1 in bovine alveolar macrophages and blood mononuclear cells.

Biological responses to recombinant DNA-derived bovine interferon alpha (rBoIFN-alpha I1) by bovine alveolar macrophages were examined by measuring viral yield reduction and 2',5'-oligoadenylate synthetase (2',5'-OAS) production by IFN-treated cells. In vitro IFN pretreatment of alveolar macrophages reduced viral yield in cultures challenged exposed with parainfluenza-3 virus, compared with control cultures. In vitro treatment of alveolar macrophages with IFN also resulted in increased 2',5'-OAS activity. The 2',5'-OAS activity was measured in alveolar macrophages and blood mononuclear leukocytes of calves injected IM with 3.6 x 10(6) U of rBoIFN-alpha I1/kg of body weight. The IFN action was monitored by measuring 2',5'-OAS activity of blood mononuclear leukocytes beginning 6 days before and ending 24 hours after IFN treatment. The 2',5'-OAS activity in the blood mononuclear leukocytes sharply increased 24 hours after IFN treatment, indicating response to IFN. The alveolar macrophages collected from the same calves 24 hours after IFN administration also had increased 2',5'-OAS activity, compared with alveolar macrophages from the same calves collected 6 days before treatment. Increased 2',5'-OAS activity indicates: a possible mechanism of IFN action in cattle that may be responsible for viral yield reduction; potential use of high enzyme activity as a marker for IFN induction; and potential use of 2',5'-OAS activity as a marker for determining effects of IFN on bovine macrophages and other cells of the bovine immune system.     

Pulmonary lesions induced by 3-methylindole and bovine respiratory syncytial virus in calves

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P less than 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arthritis and systemic disease caused by Borrelia burgdorferi infection in a cow

Infection with Borrelia burgdorferi caused arthritis, myocarditis, glomerulonephritis, and pneumonitis in a cow. Spirochetes were detected by use of immunofluorescent staining in liver and lung specimens and were isolated from the liver. The carpal, stifle, and tarsal joints had marked synovial proliferation, and synovial fluid obtained from these joints had high antibody titers against B burgdorferi. The cow was from an area of Wisconsin that is not endemic for borreliosis.     

Normal blood supply to the canine mandible and mandibular teeth

The normal blood supply to the canine mandible and mandibular teeth was determined by microangiography and correlated histology. Branches of the inferior alveolar artery supplied the cortical bone of the mandibular body. Vessels from the periosteal and endosteal surfaces supplied symphyseal cortical bone. Direct vascular anastomoses were not found to cross the fibrous mandibular symphysis. Blood supply to the mandibular teeth was via dental arteries derived from the inferior alveolar artery, with interdental and interradicular arteries supplying the alveolar bone and periodontal ligament.     

Public health aspects of dirofilariasis in the United States

Coin lesions in the human lung present significant differential diagnostic problems to the physician. There are at least 20 known causes of such lesions, including neoplastic lesions, infectious diseases, and granulomas. The human medical literature contains many misconceptions about the life cycle of Dirofilaria immitis, including the method of entry of the infective-stage larvae and the development of the young adult worm. These misconceptions have obscured the recognition of the clinical presentation of pulmonary dirofilariasis and the potential for D. immitis to lodge in many other areas of the human body besides the lung. Exposure to infective larvae of D. immitis is more common in humans than is currently recognized. Reported cases in humans reflect the prevalence in the canine population in areas of the United States. The veterinary literature provides compelling evidence that D. immitis is a vascular parasite, not an intracardiac one. Its presence in the right ventricle is a post-mortem artifact, because it has never been shown to be there by echocardiography or angiography in a living dog, even though these techniques have demonstrated adult D. immitis in the pulmonary, femoral, and hepatic arteries; posterior vena cava; and right atrium of live dogs. Physicians have taken the name "heartworm" literally, believing that the worm lives in the heart and only after it dies does it embolize to the pulmonary artery. However, the coin lesion is spherical in shape, not pyramidal, as embolic infarcts to the lung in humans are known to be. The coin lesion is an end-stage result of the parasite's death in the vascular bed of the lungs and the stimulation of a pneumonitis followed by granuloma formation. This pneumonitis phase of human pulmonary dirofilariasis is often not recognized by the radiologist because of the way pneumonitis is diagnosed and treated and because the developing nodule is obscured by the lung inflammation. Serologic methods for use in humans are needed for clinical evaluations of patients with pneumonitis living in highly enzootic D. immitis regions. As well, epidemiological surveys are needed to determine the real extent of this zoonotic infection.