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

Epizootiological observations were made on an outbreak of pneumococcal infection occurred in 14 inbred guinea pig colonies during January to October, 1981. Monthly incidences of diseased animals ranged from 16.6 to 0%, showing the highest rate in the first month of the occurrence. Affection rates were remarkably different according to guinea pig strains, being 75% in JY-1 but 0% in JYG and Strain 2. Affected animals showed ruffled fur, dry-dirty noses, emaciated abdomen and dyspnea, and some of them were resulted in death. At necropsy, the fibrinopurulent pneumonia, pleuropneumonia and pleuritis were found as the major pathological features, and in addition, the fibrinopurulent pericarditis and peritonitis with a large amount of exudate were also observed in some cases. Streptococcus pneumoniae was isolated from nearly all the affected organs, and also from the external nares and trachea. Isolation rate from the external nares was especially high, thus 97.1% of infected guinea pigs including healthy carriers were detected by cultivation of nasal swab samples. Carrier rates of healthy animals were gradually increased from 17.2% in April to 36.5% in October, but the organism was not detected from JYG strain at all. During the observation period, vaccination, advance of weaning age of animals and administration of high vitamin C dose were taken as preventive measures of the epizootic, but no remarkable effect was obtained. The same diseased conditions were successfully produced in Hartley guinea pigs by experimental nasal infection of a pneumococcal strain isolated from this epizootic.
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PMID:An epizootic of pneumococcal infection occurred in inbred guinea pig colonies. 685 18

Intranasal administration of an inoculum of 10(7) focus-forming units (FFU) of respiratory syncytial (RS) virus induced disease in BALB/c mice with signs of anorexia, cachexia, ruffled fur, and pneumonia. Mice displayed mild signs of illness on day 1 postinoculation (PI), followed by a transient recovery phase of 3 days. Disease rapidly reappeared on day 5 PI and worsened on subsequent days, with mortalities by day 7 PI. Mice inoculated with 5 x 10(6) FFU exhibited milder signs of disease, while those inoculated with 2 x 10(6) FFU and control mice given only Hep-2c cell suspension exhibited no noticeable signs of illness. High levels of bioactive tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected in both lungs and sera of mice inoculated with 10(7) FFU of virus. Peak levels of both cytokines were detected at day 1 PI but remained detectable throughout the 7 day period studied postinoculation. Cytokine levels were much lower or were undetectable in control mice. These results suggest that the macrophage is stimulated in vivo to produce inflammatory cytokines in response to RS virus infection.
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PMID:In vivo production of tumour necrosis factor-alpha and interleukin-6 in BALB/c mice inoculated intranasally with a high dose of respiratory syncytial virus. 804 22

Personnel at The Marine Mammal Center (The Center) treated 1,446 stranded marine mammals recovered from the central and northern California (USA) coast from 1984 through 1990, including California sea lions (Zalophus californianus), northern elephant seals (Mirounga angustirostris), Pacific harbor seals (Phoca vitulina richardsi), northern fur seals (Callorhinus ursinus), Steller sea lions (Eumetopias jubatus), and Guadalupe fur seals (Arctocephalus townsendi). The primary disease findings in stranded California sea lions were renal disease, renal disease complicated by severe verminous pneumonia, verminous pneumonia, seizures of unknown etiology, and renal disease complicated by severe pneumonia of unknown etiology. Stranded elephant seals included pups, yearlings with dermatological problems, and neonates. Most harbor seals admitted to The Center were underweight and premature pups. Stranded northern fur seals included animals with seizures of unknown etiology and emaciated pups. Stranded Steller sea lions included underweight pups and aged adult females with pneumonia. Two Guadalupe fur seals had hemorrhagic gastroenteritis. Incidental findings at the time of stranding among the six species included verminous pneumonia and pneumonia of unknown etiology, renal disease, internal parasitism, ophthalmologic problems, gastrointestinal disorders, otitis externa, and external wounds.
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PMID:Findings in pinnipeds stranded along the central and northern California coast, 1984-1990. 835 44

We report a case of Rhodococcus equi cavitary pneumonia in a 37-year-old patient with occult HIV infection. Because of his good immune status, the patient was given oral erythromycin and rifampin which rapidly resolved the infection. This modality of treatment may be sufficient in HIV-positive selected patients fur the resolution of Rhodococcus equi pneumonia.
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PMID:Rhodococcus equi pneumonia in a patient with occult HIV infection: successful therapy. 917 24

We report the case of a 48-year-old man with asthma and pulmonary eosinophilia. He presented with coughing, dyspnea, and wheezing that began 6 months after he began keeping a rabbit in his house. He was referred to our department for further examination of pulmonary infiltrative shadows. An inhalation test with rabbit-fur antigen induced both immediate and late asthmatic responses. In addition, infiltrative shadows appeared in the right segments 2, 8, and 9 on chest CT films after the antigen inhalation. Examination of fluid obtained by bronchoalveolar lavage from the right S9 showed an increase in the fraction of eosinophils. Examination of a specimen obtained by transbronchial lung biopsy from those segments revealed infiltration of inflammatory cells into the alveolar septa and alveolar spaces, which was consistent with eosinophilic pneumonia. Our diagnosis was asthma and pulmonary eosinophilia due to rabbit-fur antigen.
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PMID:[Pulmonary infiltration with eosinophilia due to rabbit-fur antigen: diagnosis by allergen inhalation test]. 921 74

Q-Fever is a worldwide zoonosis caused by Coxiella burnetti. C. burnetti is an obligate intracellular parasite. It lives in phagolysosome of the host cell. By its infection of the sensitive persons develops the acute noncharacteristic disease, which passes noncharacteristically, with the appearance of higher temperature, headache, fever, weakness of the organism or by the appearance of symptoms of the undifferentiated infection of the upper parties of the respiratory system. In the course of the infection is being developed the intersticial pneumonia, what is the reason of the infected hospitalization. Most often get sick the sheep, cows and goats, what showed also on our examined sample. In most animals the symptoms of this bacterial infection are not present, pass unobviously, and get turned out during their gravidity. The most important carriers of the causes of this disease on the domestic or wild animals are artropodes, in which within the kind is possible also the transvatial and transstadial transfer. The wild animals transfer the disease at the domestic ones, and people most often are infected by contact with these animals, their consuming of meat or milk or by contact with their secretions. Though, the most important way of getting infected of people is aerosol contaminated by the carrier as these bacteria for a long get kept in the contaminated dust, wool, animal skin, fur, straw and the excretions of the infected animals. In the illusorilly healthy and pregnant animals the bacteria are to be found in the fertile water, chorions, and placenta, that is C. burnetti becomes the cause of the premature birth or abortion in these animals. In this way comes to the bacterial contamination of the environment of the animal itself. The diagnosis of Q.-Fever is complement fixation test, indirect immunofluorescence assay (IFT) and enzyme immunoassay (EIA).
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PMID:Q-fever, human and animal morbidity in some regions of Bosnia and Herzegovina, in 2000. 1237 56

We recently described the discovery, genome, clinical features, genotypes and evolution of a novel and global human respiratory virus named human coronavirus HKU1 (HCoV-HKU1) which is not yet culturable. We expressed a C-terminal FLAG-tagged CoV-HKU1 spike (S) protein by the Semliki Forest Virus (SFV) system and investigated its maturation profile. Pulse chase labeling revealed that S-FLAG was expressed as high-mannose N-glycans of monomers and trimers. It was predominantly cleaved into subdomains S1 and S2 during maturation. S1 was secreted into the medium. Immunofluorescence analysis visualized S along the secretory pathway from endoplasmic reticulum to plasma membrane. Cleavage of S and release of HCoV-HKU1 S pseudotyped virus were inhibited by furin or furin-like enzyme inhibitors. The cell-based expressed full-length S-FLAG could be recognized by the convalescent serum obtained from a patient with HCoV-HKU1 pneumonia. The data suggest that the native form of HCoV-HKU1 spike expressed in our system can be used in developing serological diagnostic assay and in understanding the role of S in the viral life cycle.
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PMID:Spike protein, S, of human coronavirus HKU1: role in viral life cycle and application in antibody detection. 1884 44

Streptococcus suis serotype 2 is a zoonotic Gram-positive bacterium responsible for arthritis, meningitis, pneumonia and septicemia in swine and humans. Little information about the regulation of iron on its gene expression had been reported. In this study, 63 S. suis genes upregulated under an iron-restricted condition were identified using selective capture of transcribed sequences (SCUTS) technique: 23 genes involved in metabolism, 22 genes responsible for the replication and genetic information proceeding of the bacteria, eight genes relative to the construction of the cell wall, five ATP-binding cassette transporters, four transcriptional regulators and one uncharacterized gene conserved among streptococcal species. To adapt to the stress, S. suis modulated its physiological activities, which were validated by the upregulation of RelA (a crucial enzyme in stringent response), ArcA (a component of the arginine deiminase system catalyzing the conversion of arginine to ornithine) and CpdB (a cell surface protein that is a substrate of sortase A). All of them were reported to be virulence factors in S. suis or other bacteria. Besides, together with the results of quantitative reverse transcriptase PCR, we found that several homologous genes (fur, fhuGBDA operons) associated with iron uptake as reported in other bacteria were also upregulated under an iron-restricted condition in S. suis.
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PMID:Identification of Streptococcus suis genes preferentially expressed under iron starvation by selective capture of transcribed sequences. 1919 74

The tremendous success of Staphylococcus aureus as a pathogen is due to the controlled expression of a diverse array of virulence factors. The effects of host environments on the expression of virulence factors and the mechanisms by which S. aureus adapts to colonize distinct host tissues are largely unknown. Vertebrates have evolved to sequester nutrient iron from invading bacteria, and iron availability is a signal that alerts pathogenic microorganisms when they enter the hostile host environment. Consistent with this, we report here that S. aureus senses alterations in the iron status via the ferric uptake regulator (Fur) and alters the abundance of a large number of virulence factors. These Fur-mediated changes protect S. aureus against killing by neutrophils, and Fur is required for full staphylococcal virulence in a murine model of infection. A potential mechanistic explanation for the impact of Fur on virulence is provided by the observation that Fur coordinates the reciprocal expression of cytolysins and a subset of immunomodulatory proteins. More specifically, S. aureus lacking fur exhibits decreased expression of immunomodulatory proteins and increased expression of cytolysins. These findings reveal that Fur is involved in initiating a regulatory program that organizes the expression of virulence factors during the pathogenesis of S. aureus pneumonia.
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PMID:Staphylococcus aureus fur regulates the expression of virulence factors that contribute to the pathogenesis of pneumonia. 2010 Aug 57

The present study aimed to investigate polypoid colonic metastases from gastric stump carcinoma by performing a retrospective analysis of the clinical data of a patient with such a diagnosis, and by discussing other previous case studies from the literature. The patient of the present study was an 80-year-old male who had undergone a gastrectomy 48 years previously for a benign perforated gastric ulcer. A colonoscopy revealed >10 multiple polypoid lesions of 6-10 mm in diameter distributed throughout the entire colon, except in the rectum. Each lesion had either erosion or a depression at the top and several were covered with a white fur-like substance. Biopsy specimens excised from the stomach showed a poorly-differentiated adenocarcinoma with diffuse signet ring cells, and a colonoscopy-guided biopsy revealed a signet ring cell adenocarcinoma. The patient was referred to the Oncology unit (Beijing Shijitan Hospital, Beijing, China) for assessment and chemotherapy treatment, which was initiated with 1,000 mg Xeloda orally administered twice a day for two-week courses every three weeks. The patient succumbed to upper gastrointestinal hemorrhage and pneumonia after three months. Gastric or gastric stump carcinoma may metastasize to the colon presenting as solitary or multiple colonic polyps. Thus, it is important to consider this diagnosis as such colon metastases may mimic solitary or multiple colonic polyps, which are commonly observed. A differential diagnosis is required in this complicated situation.
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PMID:Polypoid colonic metastases from gastric stump carcinoma: A case report. 2512 Jun 69


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