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

Haemophilus influenzae type b is responsible for an estimated 15,000 to 20,000 cases of meningitis per year in the United States, mainly in children 2 months to 5 years old. The mortality rate from meningitis due to H influenzae type b infections ranges from 5% to 10%. Despite antibiotic treatment, up to 35% of survivors have permanent neurologic sequelae. In addition to meningitis, H. influenzae type b is responsible for other invasive infections, including epiglottitis, septicemia, cellulitis, septic arthritis, osteomyelitis, pneumonia, pericarditis, and otitis media; approximately 30,000 cases H influenzae diseases occur annually in the United States. The diseases peak in incidence between 6 and 12 months of age, with almost one half of the cases occurring before 1 year of age. About 75% of disease caused by H influenzae type b occurs in children younger than 24 months old. The incidence of disease is higher in children of certain groups, including blacks, Hispanics, Eskimos and Native Americans, young children attending day-care facilities, patients with asplenia or antibody-deficiency syndromes, and children of lower socioeconomic status. There is considerable evidence that antibody to the capsular polysaccharide (polyribosylribitol-phosphate [PRP] of H influenzae type b is protective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunogenicity of a new Haemophilus influenzae type b conjugate vaccine (meningococcal protein conjugate) (PedvaxHIB). 210 17

The hematological and clinicochemical profiles of healthy swine and swine with inflammatory processes were investigated. Blood was collected at slaughter and postmortem examination was performed to select healthy swine and swine with pleuritis, pneumonia or abscesses. In healthy swine, the values of several variables revealed significant differences between gilts, barrows and boars. This was caused predominantly by the values obtained for boars. Inflammatory processes altered the values of most variables investigated, particularly for erythrocyte sedimentation rate, hemoglobin and hematocrit, for the activity of alkaline phosphatase, and for concentrations of iron, phosphate, albumin and fibrinogen in plasma. Compared with healthy swine, differences were largest for swine with metastatic abscesses and swine with both abscesses and other pathological lesions; differences were less pronounced in swine with solitary abscesses and were minor in swine with pneumonia and swine with pleuritis. Porcine hematological and clinicochemical profiles reflect the degree of inflammation.
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PMID:Hematological and clinicochemical profiles of healthy swine and swine with inflammatory processes. 230 94

We previously demonstrated that pneumococcal extracts contain a highly specific inhibitor of human neutrophil elastase (HNE). We now show that the active inhibitor in these extracts is a high-molecular-weight, heat-stable substance that appears to be RNA, since inhibitory activity of pneumococcal extracts is decreased by incubation with ribonuclease but not by incubation with deoxyribonuclease or proteinase K. Moreover, metabolically labeled ([3H]uridine) pneumococcal RNA, isolated by phenol extraction followed by ethanol precipitation, strongly inhibits HNE. Pneumococcal capsular polysaccharide, although polyanionic, is only weakly inhibitory toward HNE and is not a major source of elastase-inhibitory activity in pneumococcal extracts. On the other hand, the capsule of Haemophilus influenzae type b contains polyribosylribitol phosphate. This highly charged polyanion possesses HNE-inhibitory activity, but only under special circumstances to be discussed below. Pneumococci (type I, type II smooth, type II rough) and H. influenzae (type b) all release HNE-inhibitory activity into their culture medium during growth. By contrast, Klebsiella pneumoniae and Staphylococcus aureus release little (if any) stable HNE-inhibitory activity during growth. We propose that some bacterial pneumonias may spare host tissue because polyanions released by the invading microorganisms (e.g. RNA from autolysing pneumococci) inhibit elastase released from inflammatory neutrophils and thereby modulate accompanying tissue proteolysis. Pneumonias caused by microorganisms that do not release stable polyanionic inhibitors of HNE (e.g., Staphylococcus and Klebsiella) may be correspondingly more injurious to the lung.
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PMID:Inhibition of human neutrophil elastase by bacterial polyanions. 244 47

Fifty-seven children ages 1 month to 12 years hospitalized because of community-acquired pneumonia were compared with age-matched controls who had acute asthma without pneumonia to test the value of rapid bacterial antigen detection and clinical and radiographic criteria for diagnosis of bacterial pneumonia. Bacterial pneumonia, defined on the basis of positive cultures of blood or pleural fluid, was diagnosed in 4 children (7%), 1 of whom also had viral pneumonia. Viral pneumonia, defined as a positive nasopharyngeal sample or positive serology, was diagnosed in 20 children (35%). Serum and concentrated urine were tested by latex agglutination (Wellcogen) for Haemophilus influenzae type b and pneumococcal antigens and by countercurrent immunoelectrophoresis for pneumococcal antigens. Pneumococcal antigen could not be detected in serum or urine from 3 children with culture-proved pneumococcal pneumonia, indicating poor sensitivity of the tests. In contrast apparent H. influenzae type b antigenuria was detected by latex agglutination in 4 of 40 children with pneumonia but also in 5 of 57 controls, and a sensitive enzyme-linked immunosorbent assay for polyribosyl ribitol (PRP) phosphate antigen showed that all 9 cases were false positives. The specificity of H. influenzae type b antigen detection was thus poor. Children with viral and bacterial pneumonia could not be distinguished by radiographic or clinical criteria (symptoms, fever) or by total or differential white blood cell counts, serum C-reactive protein or nasal or serum interferon levels. It is not possible to distinguish reliably childhood viral from bacterial pneumonia clinically or by rapid diagnostic tests.
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PMID:Problems in determining the etiology of community-acquired childhood pneumonia. 278 61

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 purpose of this investigation was to determine the relative roles of the humoral and cell-mediated immune responses in the resolution of chlamydial genital infection of mice and resistance to reinfection. To this end, female BALB/c mice were rendered B cell deficient by treatment with heterologous anti-immunoglobulin M (IgM) serum from birth. Controls were similarly treated with either normal serum or phosphate-buffered saline. Before inclusion in each experiment, anti-IgM-treated mice were screened for the absence of IgM in serum and for the presence of cell-mediated immune responses. In addition, spleen cells from anti-IgM-treated mice responded to concanavalin A and phytohemagglutinin but not to lipopolysaccharide. By these criteria, mice were designated B cell deficient. B-cell-deficient mice and controls were inoculated intravaginally with a suspension of mouse pneumonitis agent (MoPn), a Chlamydia trachomatis biovar. All B-cell-deficient mice resolved the infection. Additionally, no significant difference was seen in the course of the infection in B-cell-deficient mice when compared with controls. In contrast to control mice, B-cell-deficient mice displayed no detectable antibody responses to MoPn in serum or in genital secretions. However, both B-cell-deficient mice and controls developed delayed-type hypersensitivity and T-cell proliferative responses to MoPn. When challenged 53 days after primary infection, no significant difference was seen in the resistance of B-cell-deficient mice to reinfection when compared with that of the controls. These data indicate that cell-mediated immune mechanisms play an important role in the resolution of and resistance to chlamydial genital infection in this model.
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PMID:Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection. 325 86

We developed a modified double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) that detected relatively low concentrations of known Pneumocystis carinii antigen added to buffer or rat sera. Artificial immunization-derived polyclonal rabbit anti-P. carinii antibody was used on the solid phase to capture the antigen. Infection-derived (after P. carinii pneumonia) polyclonal rat anti-P. carinii antibody or a mixture of five murine monoclonal antibodies was used as the antigen detector antibody. Rabbit anti-rat immunoglobulin G antibody or goat anti-mouse immunoglobulin G antibody conjugated to alkaline phosphatase was used as the final antibody. After standardization and optimization of the various reactants in this ELISA system, approximately 53 ng of known P. carinii antigen per ml suspended in phosphate-buffered saline-Tween 20 buffer or 210 ng of antigen per ml suspended in normal rat serum diluted 1:4 could be detected. In addition, an indirect ELISA for P. carinii antibody measurement was developed, using as the antigen a soluble supernatant from a sonicated preparation of Percoll-purified whole cysts and trophozoites to coat the solid phase. Limited studies with sera from a small number of caesarian-obtained, barrier-sustained rats from Charles River Breeding Laboratories, Inc., and the National Institutes of Health and sera from normal and heavily infected rats indicated that the caesarian-obtained, barrier-sustained rats had negligible levels of antibody. The normal and heavily infected rats had variable antibody titers. A significantly high level of P. carinii antigenemia was detected in only 2 (11%) of 18 heavily infected rats. Extensive studies of the P. carinii pneumonia rat model with the ELISA did not reveal significant serum P. carinii antigenemia during the acute stage of infection. However, soluble P. carinii antigen was detected by the ELISA and Western blot assays in the supernatant of lavage fluid after centrifugation to sediment intact organisms. As expected, P. carinii antigens were detected by these assays in the lavage pellet recovered after centrifugation. In conclusion, the antigen assay used in this study detected P. carinii antigen in lung lavage but failed to detect P. carinii antigen in rat serum during the acute phase of infection.
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PMID:Pneumocystis carinii antigen detection in rat serum and lung lavage. 326 87

Between January 1984 and December 1985, 183 adult patients, subsequently shown to have pneumococcal bacteraemia, were admitted. Of these infections, nine were caused by penicillin-resistant strains, and three of these were resistant to other antibiotics. The organisms from 150 patients were serotyped/grouped. The primary site of infection was lung in 90 per cent of patients. Among the patients with pneumonia, those with serovar 3 strains accounted for most intensive care unit admissions, most cases requiring inotropic drugs, and mechanical ventilation and had the highest complication rate and mortality. Findings which predicted the need for intensive care included higher age, elevated concentrations of serum urea, creatinine, and phosphate and lower levels of total serum protein, albumin and calcium. Twenty-four patients died of whom 23 had pneumonia. The case fatality rate among all of the patients admitted to the intensive care unit was 60 per cent and among those not admitted to the unit, 9.2 per cent. Of the patients who died, 41.7 per cent did so within the first five days of admission. The prophylactic use of polyvalent pneumococcal vaccine in industrial workers from low socio-economic groups should be carefully considered.
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PMID:Pneumococcal bacteraemia in adults in a low socio-economic urban population. 327 83

The purpose of this investigation was to determine the role of the humoral immune response in the production of arthritis in mice immunized with the chlamydial agent of mouse pneumonitis (MoPn) (Chlamydia trachomatis biovar). Mice were made B cell deficient (BCD) by treatment with rabbit antiserum to murine IgM. Control mice included animals treated similarly with normal rabbit serum or phosphate-buffered saline. Male mice were immunized with MoPn inactivated with ultraviolet irradiation while female mice were immunized by genital tract infection with viable chlamydiae. Arthritis was elicited in all mice by intra-articular inoculation of inactivated MoPn. When knee joints were examined for pathologic changes at varying times after challenge, a marked enhancement of the arthritis was observed in both male and female BCD mice when compared with controls at all time points. These data indicated that the humoral immune response is not essential for the production of arthritic disease in this model but may have some role in the modulation of the process in immunologically intact animals. Persistence of chlamydial antigen in joint tissue of BCD mice suggested that antibody may play a role in the elimination of antigen, thus decreasing the stimulus for the development of cell-mediated immunologic injury. Regulatory role for T suppressor cells cannot be ruled out however, because B cell deficient mice have been shown to lack certain T suppressor cell subsets.
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PMID:Antibody-mediated modulation of arthritis induced by Chlamydia. 340 Jul 79

Virus replication is described, and the clinical trials and indications for amantadine, rimantadine, vidarabine, vidarabine phosphate, acyclovir, ribavirin, and other promising antiviral agents are reviewed. Amantadine and rimantadine are useful for the treatment and prophylaxis of viral influenza A infections. Vidarabine is a second-line agent and is effective for the treatment of herpes simplex encephalitis, neonatal herpes simplex types 1 and 2, and varicella-zoster infections. Vidarabine phosphate (also known as vidarabine monophosphate) has a similar spectrum of activity and can be administered in smaller volumes than vidarabine. Acyclovir has demonstrated clinical efficacy for chickenpox, shingles (herpes zoster), genital herpes, and other herpes simplex infections. Acyclovir is also useful for the suppression of herpes infections. Systemically administered ribavirin is indicated for the treatment of Lassa fever. Aerosol ribavirin is effective for the treatment of respiratory syncytial virus pneumonia in children and infants and influenza A infections in adults. Only acyclovir, amantadine, ribavirin, and vidarabine are used in clinical practice. Vidarabine phosphate and investigational agents such as rimantadine, ganciclovir (DHPG, BW B759U), phosphonoformate, and bromovinyl-deoxyuridine (BVDU) need further investigation.
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PMID:Recent advances in antiviral therapy. 354 44


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