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

Three patients developed severe respiratory syncytial virus pneumonia after bone marrow autograft for acute leukaemia. Clinically, the disease presents as interstitial or bilateral alveolo-interstitial pneumonia with hypoxaemia. Signs of ENT infection (otitis media, sinusitis) are present in 30 percent of the cases. In all 3 patients, the syncytial virus was isolated by direct immunofluorescence in bronchoalveolar lavage fluid. In 2 patients the infection began soon after the autograft, in deeply aplastic subjects, and required intubation and assisted ventilation. These 2 patients died despite inhalation of aerosolized ribavirin combined, in one of them, with ribavirin injections. In the third patient the infection began some time after the autograft and responded well to ribavirin in aerosols. In these three cases the viral infection occurred in an epidemic and nosocomial context. The respiratory syncytial virus is usually transmitted by the hands. Owing to the severity of this infection with lung involvement in immunodepressed patients, specific prophylactic measures should be taken side by side with the conventional measures.
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PMID:[Severe respiratory syncytial virus pneumonia following bone marrow autograft. 3 cases]. 153 59

1. The major indication for tube feeding is the inability to ingest sufficient nutrients by mouth in the presence of a functioning gastrointestinal tract. 2. Diarrhea, a frequent complaint, may be due to a variety of factors, including medication side effects, bacterial contamination of formula, viral infection, low albumin, high osmolality of the formula, too rapid infusion rate, and fecal impaction. 3. Aspiration of the tube feeding resulting in pneumonia is a serious and potentially life-threatening complication seen more frequently in patients with altered mental status or the inability to protect their airway. 4. Key items in the nutritional assessment include body weight; weight loss; visceral protein estimation, eg, albumin; exercise tolerance; and muscle strength.
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PMID:Clinical considerations. Tube feeding in the elderly. 153 85

The severe fibrinonecrotic pneumonia associated with pneumonic pasteurellosis usually results from colonization of the lower respiratory tract by Pasteurella haemolytica biotype A, serotype 1(A1). Despite recent research efforts, the authors lack a detailed understanding of the interactions and host response to P. haemolytica in the respiratory tract. The authors hypothesize that management and environmental stress factors or viral infection alters the upper respiratory tract (URT) epithelium allowing P. haemolytica to colonize the epithelium. Once the URT is colonized, large numbers of organisms enter the lung where they interact with alveolar macrophages. Endotoxin, released from the bacteria, crosses the alveolar wall where it activates pulmonary intravascular macrophages, endothelium, neutrophils, lymphocytes, platelets, complement, and Hageman factor leading to complex interactions of cells and mediators. It is the progression of this inflammatory response with neutrophil influx that is ultimately responsible for the pulmonary injury. Leukotoxin is a major virulence factor of P. haemolytica that allows it to survive by destroying phagocytic cells. At subcytolytic concentrations it may also enhance the inflammatory response by activating cells to produce mediators and release reactive oxygen metabolites and proteases.
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PMID:Pasteurella haemolytica A1 and bovine respiratory disease: pathogenesis. 154 21

A prospective eight-month study was carried out in 50 children admitted to hospital for radiologically confirmed community-acquired pneumonia. A potential causative agent of infection was identified in 44 (88%) cases. Using virus isolation, virus antigen detection and enzyme immunoassay serology, respiratory virus infection was diagnosed in 30 (60%) patients. Antibody assays for seven bacteria and antigen detection from serum and urine for Streptococcus pneumoniae produced evidence of bacterial infection in 31 (62%) cases. Streptococcus pneumoniae (38%), respiratory syncytial virus (30%) and Mycoplasma pneumoniae (20%) were the most common causative agents. A mixed infection was diagnosed in 25 (50%) episodes. Nine patients failed to respond to antibiotics within 24 h after onset of treatment. Three of them had a pure viral infection, three a mixed viral-bacterial infection, two a Mycoplasma pneumoniae infection mixed with other bacteria and one a pure Mycoplasma pneumoniae infection. All three Mycoplasma pneumoniae infections were initially treated with penicillin.
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PMID:Pneumonia in childhood: etiology and response to antimicrobial therapy. 159 97

We examined the interaction of viral pneumonitis with the respiratory effects of halothane/N2O anesthesia in six tracheostomized sheep. Ventilation-perfusion (VA/Q) distribution, pulmonary artery pressure (PAP), metabolic rate (VO2), and functional residual capacity (FRC) measurements were compared in awake and anesthetized animals before and 1 week after inoculation by tracheal instillation of ovine parainfluenza type-3 (PI-3) virus. Awake shunt (VA/Q less than 0.005) was 0.6 +/- 0.4% (+/- standard deviation [SD]) before, versus 3.9 +/- 2.0% after PI-3 infection (P less than 0.05). Awake arterial O2 tension (PaO2) was 139.9 +/- 14.0 mmHg before and 114.5 +/- 8.7 mmHg after infection (P less than 0.05). Mean PAP increased from 6.0 +/- 1.9 mmHg before to 11.5 +/- 1.6 mmHg after infection (P less than 0.05). Anesthesia shunt increased to 5.7 +/- 2.3% before and 11.2 +/- 3.4% after PI-3 (P less than 0.05 for the change from awake, and P less than 0.05 for a PI-3 anesthesia shunt difference). PAP was not significantly different from awake, either before or after infection. Anesthesia also produced an average 14.8 +/- 3.8% FRC reduction before and 17.4 +/- 6.4% reduction after infection (P less than 0.05 for FRC reduction with anesthesia, not significantly different for PI-3). Three of the six sheep developed shunt at higher FRCs after infection, both awake and during anesthesia; however, the average slope of the shunt/FRC response to anesthesia was unchanged, suggesting that this was not a neurogenic form of auto-PEEP. We therefore conclude that viral infection significantly enhanced the pulmonary effects of anesthesia.
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PMID:Effect of parainfluenza infection on gas exchange and FRC response to anesthesia in sheep. 204 87

The pathogenesis of parainfluenza 1 (Sendai) virus infection was compared among 25-day-old BN, F344, and LEW rats to identify a sensitive as well as a resistant inbred rat strain to Sendai virus-induced lung injury during early life. At 7 days after inoculation, BN rats had 65-fold higher (P less than .001) pulmonary viral titers and threefold higher (P less than .002) numbers of neutrophils in bronchoalveolar lavage fluid than did F344 rats. At 14 days after inoculation, when most virus-induced inflammation had been resolved, BN rats had a threefold greater (P less than .01) incidence of bronchioles with aggregates of lymphocytes and macrophages than did F344 rats. Control BN rats had higher numbers of bronchiolar eosinophils than did F344 or LEW rats. Although viral inoculation resulted in increased numbers of bronchiolar mast cells in all three strains at 14 days, bronchiolar mast cell density was greater (P less than .005) in virus-inoculated BN and LEW rats than in F344 rats. We conclude that BN rats are high responders and F344 rats are low responders to Sendai virus-induced bronchiolitis, pneumonia, and airway mastocytosis. These strain differences may be useful in elucidating important pathogenetic mechanisms in virus-induced airway injury and mastocytosis.
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PMID:Brown Norway rats are high responders to bronchiolitis, pneumonia, and bronchiolar mastocytosis induced by parainfluenza virus. 166 31

Pathomorphology of pneumonia induced by successive contamination of the Syrian hamsters with a pathogenic strain of Mycoplasma pneumoniae and an influenza virus A/PR8/34 as well as after contamination with an influenza virus against the background of a previous administration of the mycoplasma membrane fractions was studied. Mixed Mycoplasma-viral infection results in a tumor-like bronchiolar epithelium proliferation having a morphological similarity with bronchiolo-alveolar or acinar carcinoma, influenza virus infection against the background of a previous administration of protein fractions of mycoplasma membranes resulted in a chronization of pneumonia with development of several types of morphological changes: reversible tumour-like proliferation of the bronchiolo-alveolar epithelium, "inflammatory" pseudotumours and sarcoid-like granulomas.
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PMID:[Pathomorphology of chronization and outcomes of experimental mycoplasma-viral pneumonia]. 166 66

Lumpy skin disease is an infectious viral disease of cattle, which often occurs in epizootic form. The disease is characterized by the eruption of nodules in the skin, which may cover the whole of the animal's body. Systemic effects include pyrexia, anorexia, dysgalactia and pneumonia; lesions are often found in the mouth and upper respiratory tract. The severity of the disease varies considerably between breeds and strains of cattle. Many cattle suffer severe emaciation and loss of production for several months. The skin lesions cause permanent damage to the hides. The mode of transmission of the disease has not been clearly established. Contact infections do not readily occur and the evidence from the epizootiology strongly suggests that insect vectors are involved. The disease has been confined to sub-Saharan Africa, until it recently appeared in epizootic form in Egypt and in Israel. Transmission occurs in a wide variety of biotypes, from semi-desert to temperate grasslands and irrigated land. It has the potential to extend its range further.
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PMID:Lumpy skin disease, an African capripox virus disease of cattle. 177 92

Bacterial tracheitis (BT) was found in 10 of 748 children (1.3%) admitted with croup during 1983-1990. 9.9% of all the 748 croup cases seen (74) were admitted to the pediatric intensive care unit (PICU) and 16 of the 74 required intubation. 10 of those intubated (62.5%) were found to have BT and had typical features of croup, including inspiratory stridor, hoarseness and cough. Airway obstruction resulted mainly from accumulated tracheal pus. After endotracheal intubation all required frequent suctioning of thick purulent secretions. In 2 children causative microorganisms were cultured from the blood, and in all 10 from the tracheal pus. All children were given antibiotic therapy but a 7 month-old girl died of secondary complications (respiratory syncytial virus infection, pneumonia and adult respiratory distress syndrome). The others recovered and were discharged from the PICU within 3-14 days. BT should be suspected when tracheal intubation is required in croup. In such cases close monitoring in a PICU and frequent tracheal suctioning after intubation is necessary; antibiotic therapy should be considered.
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PMID:[Bacterial tracheitis in children]. 178 11

K virus, a murine papovavirus, produces a lethal pneumonia in newborn mice. Animals surviving acute illness develop a persistent infection which reactivates under conditions of immunosuppression. The present study was conducted to identify the cell populations which support persistent K virus infection and to determine the cell populations in which this persistent infection is reactivated during immunosuppression. Mice inoculated by the oral route with 100 50% newborn mouse lethal doses (LD50) of K virus at 14 days of age were followed over a period of 7 months. The distribution of infection was studied by virus assay, immunohistochemistry, and in situ nucleic acid hybridization methods. Viral replication during the acute phase of infection was confined to pulmonary and systemic vascular endothelial cells, as well as to scattered, apparently lymphoid cells within spleens. Beginning 2 months after inoculation, however, specific hybridization for K virus nucleic acids was detected in rare renal tubular epithelial cells, and by 6 months after inoculation renal tubular epithelial cells represented the major site of viral persistence. Positive cells were frequently present in groups of two or more, and a minority of positive cells also expressed viral capsid (V) antigen. Immunosuppression with cyclophosphamide resulted in reactivation of infection, with highest titers of virus being detected in kidneys and with increased numbers of renal tubular epithelial cells expressing viral capsid antigen. Capsid antigen was also detected in rare endothelial cells in kidneys, livers and lungs of these immunosuppressed mice. Although K virus behaves as an endotheliotrope during acute infection, the major site of K virus persistence and reactivation, the renal tubular epithelial cell, is similar to that involved during persistent infection by polyoma virus in mice, SV40 virus in monkeys, and BK and JC viruses in man. The observation that persistently infected renal tubular epithelial cells occur in groups of two or more and occasionally express capsid antigen suggests that virus may persist as a productive infection which is confined by antiviral antibody but maintains itself by cell-to-cell-spread. The present study represents the first instance in which the cell populations which support infection by a member of the polyomavirus subgroup in its natural host have been defined during acute, persistent, and reactivated infection.
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PMID:The major site of murine K papovavirus persistence and reactivation is the renal tubular epithelium. 181 76


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