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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections caused by Chlamydia pneumoniae were first described in 1985. The infection can cause common cold, sore throat, hoarseness, cough, headache, fatigue and sometimes influenza-like illness. Examination can indicate serous otitis media, sinusitis, laryngitis, bronchitis and pneumonia. The course can be long and relapsing. The recommended drugs for treatment are tetracycline or erythromycin for at least two weeks. Five verified cases are described in the article, four of them with symptoms from the upper respiratory tract only. It is concluded that Chlamydia pneumoniae is a not unusual cause of upper airway diseases. Up to now the diagnosis can best be verified by micro immunofluorescence. The authors call for a rapid and reliable test for use in physician's office. It is proposed that infections caused by Chlamydia pneumoniae be termed TWAR.
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PMID:[TWAR infection is a common diagnosis in outpatient clinics]. 157 35

Symptoms of infection in the elderly may be absent, vague or atypical. Infection should be suspected when an elderly patient presents with a decline in well-being or with non-specific symptoms such as falls, dizziness, confusion, anorexia or weakness. Common infections include bacterial pneumonia, urinary tract infection, intra-abdominal infections, gram-negative bacteremia and infection of decubitus ulcers. Antibiotic therapy is not recommended for asymptomatic bacteriuria or locally infected decubitus ulcers. Drug dosages should be adjusted for the age-associated decline in renal function and for hepatic or renal insufficiency. The trend in antibiotic therapy is evolving toward the use of third-generation cephalosporins instead of aminoglycosides to avoid the side effects of nephrotoxicity and ototoxicity. Pneumococcal, influenza and tetanus/diphtheria immunizations help prevent morbidity and mortality.
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PMID:Common infections in the elderly. 848 May 62

Our understanding of the host defense and pathogenesis of influenza has come from parallel studies in animal models and humans. Infection is initiated by deposition of influenza particles on either the upper respiratory tract epithelium or directly into the alveoli, with the former method having a lethal dose several orders of magnitude greater than the latter. The virus attaches to its cellular receptor by its hemagglutinin (HA); if this step is blocked by specific antibody, infection does not take place. The major role of antibody is in the prevention of disease. Even though serum antibody (primarily antihemagglutinin, but also antineuraminidase) has been known for decades to prevent viral pneumonia, it has only more recently been shown that passive administration of anti-influenza serum to virgin mice prevents pneumonia, but not rhinotracheitis. Further, intravenously administered anti-influenza IgA has been shown to be specifically transported into the nasal secretions and protect the murine nasopharynx against influenza infection. Whereas antibody is clearly required for protection against influenza, cytotoxic T-lymphocyte (CTL) activity is both necessary and sufficient for recovery from influenza. This was best shown in studies using nude (athymic) mice. Influenza-infected nude mice shed virus from their lungs indefinitely. Adoptive transfer of anti-influenza CTLs to influenza-infected nude mice will clear the virus from their lungs, whereas administration of anti-influenza antibody will lead to a cessation of viral shedding only as long as antibody is present. Influenza in aging presents a serious clinical problem. Recent studies suggest that the age-related decrease in anti-influenza CTL activity causes both prolonged viral shedding and increased viral spread through the respiratory tract.
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PMID:Influenza: pathogenesis and host defense. 160 66

Comparative studies on the local IgA, and circulating IgG subclass antibody responses of mice to A/Sichuan/2/87 (H3N2) influenza virus surface antigens administered with different carrier or delivery systems by the parenteral route, were carried out. The results obtained were compared with the responses observed following live influenza virus infection, and the protection afforded to these animals by these various preparations determined. Infection with live virus elicited early and high levels of protection against homologous virus challenge and this correlated with both local IgA and circulating IgG2a antibody levels. When incorporated into immunostimulating complexes (ISCOMS), A/Sichuan surface antigens promoted high levels of local IgA and circulating IgG1 antibody, and achieved a more rapid and more solid immunity against homologous virus challenge infection, than that elicited by the same surface antigens administered alone or together with Freund's complete adjuvant or alhydrogel.
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PMID:The IgA and subclass IgG responses and protection in mice immunised with influenza antigens administered as ISCOMS, with FCA, ALH or as infectious virus. 164 61

Infection by influenza virus is initiated by a cellular adhesion event that is mediated by the viral protein, hemagglutinin, which is exposed on the surface of the virion. Hemagglutinin recognizes and binds to cell surface sialic acid residues. Although each individual ligand binding interaction is weak, the high affinity of influenza virus for cells that bear sialic acid residues is thought to result from a multivalent attachment process involving many similar recognition events. To evaluate such binding we have synthesized three series of compounds, each containing two sialic acid residues separated by spacers of different length, and have tested them as ligands for influenza hemagglutinin. No increased binding to the bromelain-released hemagglutinin ectodomain was seen for any of the bivalent compounds as determined by 1H NMR titration. In contrast, however, a spacer length between sialic acid residues of approximately 55 A sharply increases the binding of these bidentate species to whole virus as determined by hemagglutination inhibition assays. The most effective compound containing glycines in the linking chain displayed 100-fold increased affinity for whole virus over the paradigm monovalent ligand, Neu5Ac alpha 2Me.
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PMID:Ligand recognition by influenza virus. The binding of bivalent sialosides. 174 43

The clinical picture of influenza A virus infections indicates that release of tumor necrosis factor-alpha (TNF-alpha) may be involved. In the present study we exposed the murine macrophage line PU5-1.8 to influenza A virus and observed a productive infection which was followed by subsequent cell death. Infection of macrophages was accompanied by TNF-alpha mRNA accumulation and TNF-alpha release. TNF-alpha production could only be induced by live virus whereas interferon release was also stimulated by inactivated virus. When virus-infected macrophages were exposed to low amounts of lipopolysaccharide (LPS; 1-10 ng/ml) TNF-alpha production was strongly potentiated. These data show that low LPS concentrations could readily trigger a high TNF-alpha release from influenza-A-virus-infected macrophages which could, at least partially, explain the serious complications of combined influenza A virus and bacterial infections.
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PMID:Influenza A virus infects macrophages and stimulates release of tumor necrosis factor-alpha. 188 18

This paper presents the epidemiological study of respiratory viral infections in Croatia from 1 September 1986 till 31 August 1987. A total of 527 patients with acute respiratory diseases were examined. Their nasopharyngeal secretion and/or throat swab were taken and the viruses were demonstrated by the method of direct viral diagnosis (isolation and rapid immunofluorescent detection). This 12-month study on acute respiratory infections in Croatia in 1986/1987 shows that viruses were the agents in 47.2% of these infections. Out of a total of 527 patients with acute respiratory disease, 177 patients had RSV (prevalence 33.6%), 40 adenovirus (prevalence 7.6%), 18 enterovirus (prevalence 3.4%), 12 parainfluenza (prevalence 2.3%), 8 herpes simplex virus (prevalence 1.3%) and 3 influenza virus (prevalence 0.6%) infection; (9 patients had mixed infections with two viruses). Viral etiology was proved in 44.0% of upper respiratory tract infections, 86.5% of bronchiolitis, 63.3% of pneumonia, 57.5% of bronchitis, and 33.3% of croup. The epidemical wave of RSV infections started in October 1986 and lasted for the next 7 and a half months with a peak in December 1986. Infections with parainfluenza occurred in November 1986 and subsided in March 1987 with a peak in December 1986. An epidemic of adenovirus occurred in two waves and lasted throughout 9 months. Enteroviruses caused infections during the fall and at the beginning of the winter 1986 but also again in the spring 1987.
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PMID:Epidemiological picture of respiratory viral infections in Croatia. 195 Jun 39

A total of 1,355 cases of tularemia observed between 1924 and 1987 in Japan were viewed on the basis of clinical manifestations and the results were compared with those in the United States. The incubation period varied from one day to over one month. In 75.5% of cases, the symptoms of illness appeared within seven days with the peak on the third day. A sudden onset of flu-like symptoms was generally observed, and 92% of cases was followed by regional lymph node swelling which mostly appeared in axillary and cubital regions. They were observed predominantly at the left rather than the right side. In contrast with the cases in the United States, the number of cases of ulceroglandular type in Japan was only one third of those of glandular type. None of the pleuropulmonary cases or fatal tularemia have been reported in Japan. The number of oropharyngeal cases has remarkably increased after World War II, and is still on the rise, presumably because of the change of dietary habits in Japan. All these characteristics of Japanese tularemia are assumed to be caused by low virulence of Japanese strains of Francisella tularensis.
Infection
PMID:Clinical manifestations of tularemia in Japan--analysis of 1,355 cases observed between 1924 and 1987. 201 2

The hemagglutinin (HA) and neuraminidase (NA) of influenza A viruses induce antibodies which augment the uptake of influenza A virus by antigen presenting cells via Fc receptor entry. Antibody-dependent enhancement of uptake of virus by cells was mediated by Fc receptors because F(ab')2 preparations of lgG mixed with virus did not enhance virus uptake. The enhanced infection was measured using a fluorescent focus assay and was confirmed by dot-blot hybridization analysis. A 25-fold increase in the number of cells containing influenza antigens was detected when virus was mixed with subneutralizing concentrations of immune serum to the homologous virus before adding to neuraminidase-treated cells. Infection was also augmented using reassortant viruses which shared only the HA or the NA of the virus used to induce antibodies. Specific antisera to purified HA or NA also enhanced virus uptake. These results indicate that both the HA and the NA induce antibodies that enhance uptake of virus by Fc receptor bearing cells. In addition we determined that the drift of neutralizing antigens occurred more quickly than the drift of infection-enhancing antigens during the evolution of virus strains of the H3 subtype. The increase in the number of antigen presenting cells as a result of uptake of virus complexed with cross-reactive enhancing antibodies may affect the T cell responses to influenza infection.
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PMID:Antibodies to HA and NA augment uptake of influenza A viruses into cells via Fc receptor entry. 202 64

Infection of seronegative Welsh mountain ponies was established by intranasal instillation or exposure to nebulised aerosol of egg grown H3N8 viruses. Pyrexia and coughing were noted following intranasal instillation and high titres of virus were recovered from the nasopharynx. Exposure to aerosol resulted in more severe clinical signs characterised by high temperatures, dyspnoea, anorexia and coughing; lower levels of virus were recovered from the nasopharynx. The severity of clinical signs and the kinetics of virus shedding were dose-related with the minimal infectious dose being 10(2)EID50/ml when ponies were exposed to aerosols produced by nebulisation of 20ml allantoic fluid. Full clinical signs only developed when ponies were exposed to a dose of 10(6)EID50/ml. It was concluded that exposure to nebulised aerosols of egg grown H3N8 viruses was a more reliable method of inducing clinical influenza than intranasal inoculation and would be more suitable for challenge studies.
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PMID:Experimental infection of ponies with equine influenza (H3N8) viruses by intranasal inoculation or exposure to aerosols. 215 88


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