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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bobwhite quails (Colinus virginianus) were inoculated with 10(6) mean tissue-culture infective dose of quail bronchitis virus at 1, 3, 6, or 9 weeks of age by intratracheal, intraperitoneal, or subcutaneous routes. Quails developed necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia; multifocal necrotizing hepatitis; necrotizing splenitis, with or without hyperplasia of splenic mononuclear phagocytes; bursal lymphoid necrosis; and bursal atrophy. Lesions were more extensive and severe in quails inoculated at 1 or 3 weeks of age than in older quails. Large intranuclear inclusions, characteristic of adenovirus infection, were identified in trachea, lung, liver, and bursa of Fabricius. This is the first report of the histopathology of experimentally induced quail bronchitis.
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PMID:Pathology of experimentally induced quail bronchitis. 215 96

An adenovirus (isolate 1452) associated with inclusion body hepatitis of bobwhite quails (Colinus virginianus) was characterized as a group I, serotype 1 avian adenovirus and was indistinguishable from quail bronchitis virus. Bobwhite quails were inoculated via the intratracheal or intraperitoneal route with 10(6) mean tissue-culture infective dose of isolate 1452 at 1, 3, 6, or 9 weeks of age. Lesions produced by either route of inoculation were similar to those of quail bronchitis and included necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia, and multifocal necrotizing hepatitis, necrotizing splenitis with or without hyperplasia of splenic macrophages, and lymphoid necrosis and atrophy of the bursa of Fabricius. Basophilic intranuclear viral inclusions were present in respiratory mucosal epithelium, hepatocytes and occasionally bile duct epithelium, and the mucosal epithelium overlying follicles of the bursa. Results indicate that isolate 1452 is a field isolate of quail bronchitis virus and that inclusion body hepatitis of bobwhite quails is a manifestation of quail bronchitis.
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PMID:Further characterization of an avian adenovirus associated with inclusion body hepatitis in bobwhite quails. 217 32

Pyogranulomatous pneumonia was detected in two koalas (Phascolarctos cinereus). Nocardia asteroides was isolated from one koala with extensive pneumonia, pleurisy and splenitis. Staphylococcus epidermidis was isolated from a second koala with pneumonia restricted to the left cranial lobe. Both koalas were in poor condition and had underlying urogenital disease. It was concluded that each organism had acted as an opportunistic pathogen in its compromised host.
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PMID:Pyogranulomatous pneumonias due to Nocardia asteroides and Staphylococcus epidermidis in two koalas (Phascolarctos cinereus). 268 45

The lesions and etiologic agents associated with 13 outbreaks of respiratory disease in commercial chickens were investigated. Adenoviruses were isolated from tracheal and lung tissues of affected chickens in all 13 outbreaks. Escherichia coli was isolated from the lung of an occasional bird. The tracheal specimens were consistently negative for Bordetella avium, but E. coli and occasionally Staphylococcus aureus were isolated. There was also serological evidence in one outbreak, and pathological evidence in another, of a concurrent infectious bursal disease virus (IBDV) infection of chickens affected with the disease. Gross and microscopic alterations in the tracheas and lungs of affected chickens were similar in all outbreaks and consisted of catarrhal tracheitis and occasionally multifocal pneumonia with mononuclear cell infiltrates. Hepatitis and splenitis with heterophil infiltrates occasionally were seen in birds with coliform septicemia. The tracheal and lung lesions in the present investigation were considered primarily of adenovirus etiology, complicated by secondary bacterial infection.
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PMID:Adenovirus infection associated with respiratory disease in commercial chickens. 282 79

The presumed route of human infection by Legionella pneumophila is inhalation. We investigated possible oral transmission of legionellosis in guinea pigs. Fifty-six guinea pigs (group 1) were given virulent L. pneumophila, serogroup 1, in drinking water. Fifty-nine guinea pigs (group 2) were inoculated with L. pneumophila via gastric intubation. Nineteen guinea pigs (group 3) were given heat-killed L. pneumophila in drinking water. Twenty-four guinea pigs (group 4, positive control) were inoculated intraperitoneally with L. pneumophila. Twenty-seven guinea pigs (group 5, negative control) were either intubated gastrically with phosphate-buffered saline or given drinking water without L. pneumophila. Sixty-six of 115 (57%) of the guinea pigs orally inoculated with viable L. pneumophila (groups 1 and 2) had a temperature greater than or equal to 103 degrees F and 8 of 115 (7%) had diarrhea, compared with 0 of 19 (0%) and 0 of 19 (0%), respectively, in group 3 and 1 of 27 (4%) and 0 of 27 (0%), respectively, in group 5. There were no fatalities in groups 1, 2, 3, and 5 compared with 15 of 24 (63%) in group 4. Groups 1, 2, and 4 consistently showed pneumonitis and splenitis. The pneumonitis of groups 1 and 2 was mild, predominantly interstitial, and mainly composed of macrophages; neither gross nor microscopic evidence of aspiration was seen. In group 1, 4 of 29 (14%) guinea pigs tested seroconverted to L. pneumophila compared with 0 of 7 (0%) in group 3 and 0 of 10 (0%) in group 5. In groups 1 and 2 combined, L. pneumophila was isolated from the lung of 5 of 57 (11%) guinea pigs and spleen of 5 of 47 (11%) guinea pigs compared with 0 of 14 guinea pigs in group 5. We conclude that viable L. pneumophila administered orally produces a self-limited febrile illness in guinea pigs.
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PMID:A self-limited febrile illness produced in guinea pigs associated with oral administration of Legionella pneumophila. 318 81

The clinical, pathomorphological and microbiological findings during meat inspection in 599 pigs with endocarditis at slaughter were studied. Clinical signs were observed in 41 per cent of the pigs on ante-mortem inspection. Lameness was the most common sign. However, this symptom is not very specific of endocarditis. This is also true of various other symptoms. Only dyspnoea and drowsiness were indicative of endocarditis to some extent, but occurred only sporadically. Extracardial lesions were observed in 66 per cent of the pigs with endocarditis on post-mortem inspection. Metastatic processes (infarction or inflammatory foci) were most frequently detected in the kidneys. These were highly specific of endocarditis. In addition, the following changes were observed in decreasing incidence: signs of sepsis (hyperplastic splenitis, petechiae and degradation of organs), inflammatory lesions of the joints and legs, metastatic pneumonia and inflammation of the tail. Bacteriological examination was positive in 62 per cent of the cases. Streptococci were the organisms most frequently isolated (36 per cent), followed by Corynebacterium pyogenes (19 per cent) and Erysipelothrix rhusiopathiae (14 per cent). The discussion is concerned with the significance of these bacteria to meat-consumers.
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PMID:[Endocarditis and meat inspection in slaughtering pigs. 1. Clinical, pathological and microbiological aspects]. 368 3

Based on autopsy findings in 301 adults who had died after intensive care, different patterns of single or multiple organ damage were identified. Signs of septicemia and/or exudative-to-fibrosing alveolitis (EFA) of the lungs, the prominent cause of the adult respiratory distress syndrome (ARDS), were recognized in 89 cases. Severe, progressive EFA, which appears to ensue mainly from continuing damage to alveolar walls, consequent fibroblast proliferation and so-called atelectatic induration (collapsed alveoli forming single thick septa), was registered only in individuals who had undergone long-term intensive care. The latter was necessitated in various severe conditions of which abdominal disease was the most important. Systemic disorders, such as hemorrhagic diathesis and multiple organ damage ("multiple organ failure"), showed a close correlation with septicemia. Infections with gram-negative bacteria appear to play a special role in such processes. Morphologically, these cases were characterized by multiple organ/system damage, e.g., in order of frequency, partial necrosis of renal proximal tubules, followed by signs of regeneration; jaundice; splenitis; lobular pneumonia; centrolobular-to-zonal liver necrosis, in part combined with cholestasis; petechial and/or extended hemorrhage; and others. This complex pattern contrasted strongly with findings in individuals who had been admitted to intensive care because of e.g. a cardiovascular incident: in this latter group (125 cases) intensive care was usually of short duration, progressive EFA was largely absent, signs of septicemia were exceptional, and multiple organ/system damage was rare. The group with polytraumatism (28 cases) exhibited a pattern of organ damage intermediate between (a) and (b).
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PMID:[Pathomorphologic findings following intensive therapy]. 372 1

Fatal Yersinia pseudotuberculosis infection was diagnosed in 3 bushbabies (Galago crassicaudatus) in a large prosimian colony. The clinical signs were diarrhea, dyspnea, hyperthermia, dehydration, and lethargy. Histologically, the disease was characterized by lesions of ulcerative enterocolitis, necrotizing hepatitis, splenitis, lymphadenitis, and nonsuppurative pneumonitis.
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PMID:Fatal Yersinia pseudotuberculosis infection in captive bushbabies. 700 3

Group B Beta Hemolytic streptococcal infection among newborn infants has recently grown in importance. The pathological changes in the early onset cases appear to be confined to the lung. In our patients, hyaline membranes with peripheral atelectasis was unusual, although fibrin deposited in areas without accompanying atelectasis may lead to confusion with hyaline membrane disease. The clinical features and pathologic changes caused by GBS had some differences from those due to other organisms giving rise to fatal pneumonia in the newborn. The lungs of GBS-infected babies in our autopsy series were not as heavy, had more alveolar fibrin deposition, but not more hyaline membrane disease than in nonstreptococcal cases. Alveolar inflammation was more marked in nonstreptococcal cases, but the GBS cases had more interstitial inflammation. Massive alveolar bacterial growth was more common in the GBS cases. Chronic thymic involution was less marked in the GBS cases, while acute splenitis was more common. Meningitis was present in four of our nonstreptococcal cases, but in none of the GBS cases. The clinical courses of GBS and nonstreptococcal fatal pneumonias differed. The mothers of infants with GBS infection were less febrile and ahd an increased frequency of prolonged rupture of the membranes, while the infants had a decreased duration of life, compared to those with nonstreptococcal sepsis.
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PMID:Group B beta hemolytic streptococcal sepsis in the newborn. 703 18

We have described the ultrastructural morphology of splenic and pulmonary exudates from guinea pigs infected intranasally and intraperitoneally by Legionella pneumophila. Legionella pneumophila produced pneumonia and splenitis by both routes of inoculation. The microbe was also disseminated to other organs. Within neutrophils, Legionella pneumophila typically displayed degenerating forms, suggesting that this intracellular environment is somewhat hostile to the bacterium. By contrast, macrophages tended to contain intact forms, located within organelles morphologically identical with rough endoplasmic reticulum. Some bacteria were replicating at this site. In macrophages containing greater than 25 microbes per section, Legionella pneumophila was usually dispersed within the cytoplasm outside of organelles, and many of the heavily infected macrophages exhibited ultrastructural features of injury. Neutrophils phagocytosed Legionella pneumophila, but we found no ultrastructural evidence of either ingestion of Legionella pneumophila by macrophages or of localization of the microbe to primary or secondary phagosomes of macrophages. Our findings support the contention that Legionella pneumophila is an intracellular parasite of macrophages. The homing of Legionella pneumophila to cytoplasmic organelles morphologically indistinguishable from rough endoplasmic reticulum has no bacteriologic parallel. It remains to be determined how Legionella pneumophila enters this organelle, whether this structure is, in fact, functional rough endoplasmic reticulum and whether this site is actively involved in replication of the bacterium. The animal models used herein seem suitable for further delineation of these questions.
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PMID:Electron microscopic examination of the inflammatory response to Legionella pneumophila in guinea pigs. 705 88


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