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

We recently reported the first case of accidental aspiration of polyacrylamide occurring in a 26-year-old man. The patient developed severe airway obstruction and parenchymal lung damage and died. Autopsy revealed numerous polyacrylamide particles in his lungs, as well as extensive bronchiolar and alveolar damage. Gas chromatographic and mass spectrometric assessment of the lung tissue failed to reveal polyacrylamide activity, although assessment of the suspending solvent of the polyacrylamide showed a pattern characteristic of an aliphatic hydrocarbon mixture with a prominent dodecane peak. This experimental study was performed to determine the nature and extent of damage to rat bronchial and alveolar epithelia following endotracheal instillation of polyacrylamide, hydrocarbon mixture (petroleum distillate), dodecane (C12H26), or normal saline. The rat lungs were examined grossly and microscopically 10 min and 24, 72, and 96 h after endotracheal instillation, following inflation and fixation with 10 percent buffered formaldehyde. Gross examination revealed congested, mottled visceral pleural surfaces in the rats treated with polyacrylamide and dodecane. There were no pleural exudates or effusions. Microscopically, vascular engorgement, bronchiolitis, and focal pneumonia were observed. Vascular engorgement was most pronounced at 72 to 96 h in rat lungs treated with polyacrylamide and dodecane and was moderate at 24 h in rats treated with petroleum distillate. Focal organizing pneumonia was marked at 96 h in rats treated with petroleum distillate, at 72 h in those treated with polyacrylamide, and at 24 h in those treated with dodecane. The saline-treated control animals showed no change. Our findings suggest that polyacrylamide, dodecane, and petroleum distillate are strong irritants to the airways. However, a direct obstructive/mechanical effect of the polyacrylamide upon the airway has not been excluded. Airway exposure to polyacrylamide may result in lung injury secondary to the polyacrylamide itself, its suspending agents, or both.
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PMID:Experimental polyacrylamide-induced acute injury in rat lung. 142 97

An acute haemorrhagic disease of rabbits was first reported in a southern province of China in 1984. It subsequently spread rapidly to South China and some parts of North China. The disease is characterized by an acute onset with fever, rapid respiration and sudden death. There is a high morbidity and mortality rate. The pathological changes are consistent with severe generalized circulatory dysfunction (hyperaemia, congestion and haemorrhage), marked degeneration of parenchymatous tissue, pronounced serous-haemorrhagic pneumonia and extensive disruption of reticulo-lymphoid tissue. The disease has been named rabbit viral haemorrhagic disease and it has been suggested that the aetiological agent is a picornavirus. A tissue-derived vaccine has been prepared by homogenizing the liver, lung, spleen and kidney of infected rabbits and inactivating with formaldehyde. This review summarizes the information on the aetiology, and epidemiology and clinical and pathological aspects of this new rabbit disease.
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PMID:Viral haemorrhagic disease in rabbits: a review. 255 Oct 93

To examine the characteristics of idiopathic BOOP and to compare them with those of organizing pneumonia (OP) with known causes, immunohistochemical examinations using monoclonal antibodies against T- and B-lymphocytes which are available for formaldehyde-fixed and paraffin-embedded sections, and polyclonal antibodies against human IgG, IgA and IgM, and bovine S-100 protein, were carried out, along with conventional histopathological examinations. Histopathological observations demonstrated that both of the 7 BOOP cases and 5 OP cases had polypoid masses of organizing tissue in the lumen of small airways, alveolar ducts, and some alveolar sacs, and infiltration of pulmonary interstitium by a large number of lymphocytes and moderate number of plasma cells, eosinophils and mast cells. Degree of bronchiolo-alveolitis was greater in idiopathic BOOP. Immunohistochemically, the majority of lymphocytes which had diffusely infiltrated into the interstitium were T-lymphocytes, the degree of which was higher in the cases of BOOP. On the other hand, B-lymphocytes were seen mainly in the lymphoid follicles. Furthermore, S-100 protein positive dendritic cells were noted in the lymphocyte rich interstitium in the all cases of both groups, and similarly between two groups. Immunoglobulin (Ig) positive plasma cells were also seen, but there was no evidence indicating the preferential increase of plasma cells which produce a particular class of Ig. These observations suggest that there might be some immunological mechanisms in the pathogenesis of BOOP in which T-lymphocytes, mast cells and eosinophils are involved.
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PMID:[Immunohistochemical study of idiopathic bronchiolitis obliterans organizing pneumonia]. 269 79

We wanted to determine the prevalence of pneumonias caused by Legionella species among patients on whom autopsies were performed in two medical centers in St Louis from January 1976 to June 1981. We screened formaldehyde-fixed deparaffinized lung tissue sections with microscopic evidence of pneumonia from 97 patients with use of the direct immunofluorescence antibody technique with a multivalent antilegionella conjugate containing antibodies to Legionella pneumophila serogroups 1 through 4 plus other Legionella species. One patient (1%) had disseminated L pneumophila serogroup 1 infection. We conclude that the prevalence of pneumonias caused by L pneumophila (serogroups 1 through 4), Legionella micdadei, Legionella bozemanii, Legionella dumoffii, or Legionella gormanii is low in the patients studied.
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PMID:Prevalence of pneumonias caused by Legionella species among patients on whom autopsies were performed. 634 38

The National Institute for Occupational Safety and Health (NIOSH) recommends that formaldehyde be considered a potential occupational carcinogen and that appropriate measures be taken to reduce worker exposure. It is a colorless, flammable gas with a strong pungent odor. It is an important industrial chemical of major commercial use and is found throughout the environment. Formaldehyde is usually manufactured by reacting methanol vapor and air over a catalyst, and is sold mainly as an aqueous solution. 1/2 of the formaldehyde produced is in turn used to produce synthetic resins which are primarily used as adhesives. Its widespread use is due to its high reactivity, colorlessness, purity in commercial form, and low cost. Various products made with or containing formaldehyde are listed in a table. NIOSH estimated that 1.6 million workers were exposed to formaldehyde in a 2-year period (1972-74), and of these workers, 57,000 workers were exposed for 4 or more hours/day. The occupational groups exposed to formaldehyde are listed in Appendix 1. It was recommended by NIOSH in 1976 that employee exposure to formaldehyde in the work environment be no greater than 1.2 mg/cubic meter of air (1 ppm) for any 30-minute sampling period. This was prior to knowledge about the carcinogenic potential which was first reported in October 8, 1979, based on laboratory animal studies. Formaldehyde was carcinogenic in rats exposed to 15 ppm for 6 hours/day, 5 days/week, for 16 months. Formaldehyde caused nasal cancer in these rats. Epidemiologic studies conducted to date do not permit a definitive evaluation of the carcinogenic risk to humans. However, a panel of scientists concluded that it would be wise to consider formaldehyde as posing a carcinogenic risk to humans. In addition, it has been known to be mutagenic. Other health effects include burning of the eyes, irritation to upper respiratory passages, pneumonitis, wheezing, productive cough, and dermatitis. NIOSH recommends that formaldehyde be handled in the workplace as a potential occupational carcinogen. Exposure to it should be decreased to reduce the probability of developing cancer. Appendices contain guidelines for minimizing worker exposure to formaldehyde, formaldehyde concentrations by industry, and a list of major formaldehyde manufacturers.
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PMID:Formaldehyde: evidence of carcinogenicity. 701 9

Pneumocystis carinii, an extracellular parasite thriving in the lungs of immunosuppressed mammals, is a major cause of death in AIDS patients in the USA. As a prelude to growth, the parasite adheres mostly to type I pneumocytes lining the alveolar spaces. The mechanism of adherence remains unknown, largely because of difficulties in isolating type I pneumocytes and maintaining them in vitro. As a first step to understand P. carinii adherence to its natural substrate, we developed an in situ method to directly study parasite binding to lung alveolar cells. We used formaldehyde-fixed paraffin-embedded sections of normal rat lung as substrate for adhesion. As in its binding to the lungs in vivo, P. carinii adhered preferentially to type I pneumocytes. Adherence was saturable, time and dose dependent, and selectively blocked by glycoconjugates, in particular bovine submaxillary mucin, fetuin, and asialofetuin, suggesting that it may be mediated by a lectin type of interaction. Further, IgG of rats with P. carinii pneumonia inhibited adherence, suggesting that it may react with parasite ligands involved in the recognition of type I cell receptors. Our results demonstrate the usefulness of the in situ model for studying the mechanisms of P. carinii adherence to alveolar cells. In addition, this method may be valuable for identifying neutralizing antibodies and drugs potentially useful for controlling the infection in vivo.
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PMID:A novel in situ model to study Pneumocystis carinii adhesion to lung alveolar epithelial cells. 750 75

Nanoemulsion, a water-in-oil formulation stabilized by small amounts of surfactant, is non-toxic to mucous membranes and produces biocidal activity against enveloped viruses. We evaluated nanoemulsion as an adjuvant for mucosal influenza vaccines. Mice (C3H/HeNHsd strain) were vaccinated intranasally with 5 x 10(5) plaque forming units (pfu) of influenza A virus (Ann Arbor/6/60 strain) and a nanoemulsion mixture. The mice were challenged on day 21 after immunization with an intranasal lethal dose of 2 x 10(5) pfu of virus. Animals vaccinated with the influenza A/nanoemulsion mixture were completely protected against infection, while animals vaccinated with either formaldehyde-killed virus or nanoemulsion alone developed viral pneumonitis and died by day 6 after the challenge. Mice vaccinated with virus/nanoemulsion mixture had rapid cytokine responses followed by high levels of specific anti-influenza immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies. Specificity of the immune response was confirmed by assessment of the proliferation and cytokine production in splenocytes. This paper demonstrates that nanoemulsion can be employed as a non-toxic mucosal adjuvant for influenza virus vaccine.
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PMID:Development of immune response that protects mice from viral pneumonitis after a single intranasal immunization with influenza A virus and nanoemulsion. 1292 14

This article summarizes our previously achieved and published results. The method for the determination of bacterial volatile fatty acid patterns (VFA) in clinical samples was elaborated. It employs gas chromatography (GC), solvent extraction or head-space solid phase microextraction (SPME). This method was validated by analyses of reference bacterial strains. After cultivation in defined media, aerobic and facultative anaerobic bacteria provided profiles with a low or none acid content, while anaerobic bacteria provided characteristic but medium-dependent profiles with a higher acid content. This method was used for the analyses of clinical samples of total 375 blood cultures, 205 suppurative and apyogenous exudates, and 210 bronchoalveolar lavages (BALs). These analyses enabled within 30 minutes the detection of microbes, probably non-sporulating anaerobes not found by false-negative cultivation, in 11.2% of blood cultures, in 20.0% of exudates, and in 9.0 to 20.0% of BALs. Using the mass spectrometry (MS) methods, a number of other components with unclear diagnostic importance were found in BAL samples, in particular hydrogen cyanide, methanol, ethanol, hexanol, acetone, cyclohexanone, acetonitrile, formaldehyde, acetaldehyde, ethyl acetate, and other esters. Cyclohexanone, occurring mainly in BALs of patients with pneumonia, undergoing intensive care, may originate as a residual solvent from the plastic parts of the ventilation apparatus.
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PMID:Chromatographic analysis in bacteriologic diagnostics of blood cultures, exudates, and bronchoalveolar lavages. 1631 66

A case report of an unusual formaldehyde exposure that had happened accidentally is described. A 54-year-old male ingested 10% formaldehyde and inhaled while vomiting and he developed cough, dyspnea and wheezing with prevalent ronci and bilateral infiltrates on chest x-ray (cxr). His pulmonary symptoms and FEV1 responded well to systemic corticosteroids and nebulised salbutamol given for the possible diagnosis of hypersensitivity and/or chemical pneumonitis, and infiltrates were cleared. Two weeks after the incident, he had massive haemoptysis, fever, leucocytes, prevalent crackles, bronchospasm, and new infiltrates on CXR. After an antibiotic and steroid therapy, his symptoms and crackles relieved, radiographic infiltrates were regressed. Delayed type hypersensitivity to formaldehyde patch test was appropriate with late-onset symptoms. This is a first case of pneumonitis as well as asthma different from the occupational exposure to formaldehyde. This data suggests direct and indirect effects of formaldehyde in healthy human airways.
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PMID:An unusual form of formaldehyde-induced lung disease. 1759 75

THE RESULTS OF THIS INVESTIGATION MAY BE SUMMARIZED AS FOLLOWS: 1. The inhalation of formaldehyde gas in even small quantities is followed by bronchitis and pneumonia. Pneumonia is due to the inhalation of the gas and not to secondary infection. 2. Formalin belongs to that rare group of poisons which are capable of producing death suddenly when swallowed. 3. The introduction of formalin into the stomach is followed by the production of a gastritis which varies greatly in character. The duodenum and upper jejunum may also be involved in the inflammatory process. 4. Intraperitoneal injections of formalin cause peritonitis of a fibrino-haemorrhagic character. A definite reaction is obtained when very dilute formalin (1-1000) is employed. In the peritoneal cavity formalin exercises a destructive action upon all organs (pancreas, liver, peritoneal fat, Fallopian tubes, etc.) with which it comes in contact and causes inflammation in these organs. 5. The lethal dose of formalin when injected intraperitoneally into guinea pigs is approximately 2 cc. of 1-1000 formalin for each 100 grm. of body weight. 6. The injection of formalin into the lungs is followed by pneumonia and bronchitis. 7. The inflammation which follows subcutaneous injections of formalin is characterized by intense exudation. 8. The injection of formalin into the muscles produces myositis. 9. The injection of formalin into the anterior chamber of the eye causes the accumulation of an exudate containing leucocytes and fibrin. When formalin is dropped into the conjunctival sac iritis follows and may be severe enough to destroy the eye. 10. Formalin in whatever way introduced into the body is absorbed, and is then capable of producing lesions in the parenchymatous organs. 11. Changes in the liver after absorption of formalin consist of mild or severe grade of cloudy swelling accompanied by vacuolation of the protoplasm, changes in the nuclei and leucocytic infiltration. Focal necrosis may result. Similar changes follow the inhalation of formaldehyde. 12. The injection of formalin or the inhalation of the vapors of formaldehyde produces cloudy swelling of the parenchyma of the kidney. Focal necrosis may result. 13. Pneumonia and bronchitis are found in all animals after the injection of formalin. 14. The leucocytic infiltration which follows the introduction of formalin into an organ has these general characteristics: The eosinophiles are the first leucocytes to appear; these are followed by the other polynuclear leucocytes; last appear the large and small mononuclear leucocytes. Similar phenomena occur in the trachea, bronchi and lungs of animals subjected to formaldehyde inhalations. 15. Formalin is, directly or indirectly, chemiotactic for leucocytes. The tissues which are not infiltrated with leucocytes after the injection of formalin are those which have been so injured by the chemical that an inflammatory reaction is impossible. 16. Animals subjected to chronic poisoning with formalin administered by intraperitoneal injection develop fibrinous peritonitis, associated with marked eosinophilia. The changes in the kidneys and liver consist of cloudy swelling, fatty degeneration, focal necrosis and leucocytic infiltration.
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PMID:THE TOXIC EFFECTS OF FORMALDEHYDE AND FORMALIN. 1986 82


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