Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006277 (bronchitis)
6,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A peritonitis caused by an ascending infection is a rare complication postpartum. A 37-year-old woman presented with a secondary peritonitis due to Streptococcus pneumoniae. The patient had given birth to a healthy boy 4 weeks before and showed no symptoms of a bronchitis on admission. An operation was performed after the patient developed an acute abdomen, showing a diffuse peritonitis. High vaginal swabs and blood cultures taken on admission were positive for S. pneumoniae as well as the specimen taken during the operation. Thus we concluded that this was a case of an ascending infection. After antibiotic therapy with penicillin the patient could be discharged 8 days after the operation.
Infection
PMID:Streptococcus pneumoniae peritonitis postpartum. 1078 99

Infectious bronchitis virus (IBV) is prevalent in all countries with an intensive poultry industry, with the incidence of infection approaching 100% in most locations. Vaccination is only partially successful due to the continual emergence of antigenic variants. At many sites, multiple antigenic types are simultaneously present, requiring the application of multiple vaccines. Although many countries share some common antigenic types, IBV strains within a geographic region are unique and distinct, examples are Europe, the United States of America and Australia. Measures to restrict the introduction of exotic IBV strains should therefore be considered. Infectious bronchitis has a significant economic impact; in broilers, production losses are due to poor weight gains, condemnation at processing and mortality, whilst in laying birds, losses are due to suboptimal egg production and downgrading of eggs. Chickens and commercially reared pheasants are the only natural hosts for IBV. Other species are not considered as reservoirs of IBV. The majority of IBV strains cause tracheal lesions and respiratory disease with low mortality due to secondary bacterial infections, primarily in broilers. Nephropathogenic strains, in addition to tracheal lesions, also induce prominent kidney lesions with mortality of up to 25% in broilers. Strains of both pathotypes infect adult birds and affect egg production and egg quality to a variable degree. Infected chicks are the major source of virus in the environment. Contaminated equipment and material are a potential source for indirect transmission over large distances. Virus is present in considerable titres in tracheal mucus and in faeces in the acute and recovery phases of disease, respectively. Virus spreads horizontally by aerosol (inhalation) or ingestion of faeces or contaminated feed or water. The virus is highly infectious. Clinical signs will develop in contact chicks within 36 h and in nearby sheds within one to two days. Infection is resolved within fourteen days with a rise in antibody titres. In a small number of chicks, latent infection is established with subsequent erratic shedding of virus for a prolonged period of time via both faeces and aerosol. Movement of live birds should be considered as a potential source for the introduction of IBV. Isolation and identification of IBV is needed for positive diagnosis. The preferred method of isolation is to passage a sample in embryonating specified-pathogen-free chicken eggs. Identification is either by monoclonal antibody based enzyme-linked immunosorbent assay (ELISA) or polymerase chain reaction. Virus neutralisation test in tracheal organ culture is the best method for antigenic typing. Continual use of live vaccines complicates diagnosis since no simple diagnostic tool can differentiate a field from a vaccine strain. Nucleotide sequencing of the S1 glycoprotein is the only method to discriminate between all IBV strains. Serology is also complicated by continual use of live vaccines. For surveillance purposes, ELISA is the method of choice, regardless of the antigenic type of IBV involved. The assay is used to monitor the response to vaccination, but field challenge can only be detected if flock antibody status is monitored continually. The antigenic type of a challenge strain involved cannot be ascertained by ELISA.
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PMID:Avian infectious bronchitis virus. 1093 76

Pulmonary infection with Pseudomonas aeruginosa in patients with cystic fibrosis (CF) causes a chronic destructive bronchitis. A xenograft model was used to study the susceptibility of the CF respiratory epithelium to P. aeruginosa strain PAK and the virulence of certain mutants. Despite an early trend toward increased susceptibility, colonization of CF xenografts (ID(95), 62 colony-forming units [cfu]) was not statistically different (P=.5) than in xenografts with normal respiratory cells (ID(95), 1.2x10(3) cfu). Infection severity in 12 CF xenografts (mean polymorphonuclear leukocyte [PMNL] density, 1.88x10(6)+/-1.75x10(6)/xenograft) was similar to that in 16 non-CF xenografts (3.19x10(6)+/-2.45x10(6) PMNL/xenograft; P=.38), despite slightly greater bacterial density in the CF xenografts (mean, 1.57+/-2.73x10(6) cfu/xenograft) versus xenografts with normal epithelium (mean, 1.03+/-1.3x10(6) cfu/xenograft). P. aeruginosa mutants pilA and fliF, but not rpoN, colonized normal respiratory xenografts, indicating that colonization and infection in this model depend on an uncharacterized RpoN-controlled gene. This model appears to be suitable for genetic study of P. aeruginosa virulence but not of the CF respiratory tract's unique susceptibility.
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PMID:Pseudomonas aeruginosa infection of respiratory epithelium in a cystic fibrosis xenograft model. 1123 9

Aspergillus tracheobronchitis is an uncommon clinical form of invasive aspergillosis with fungal infection limited entirely or predominantly to the tracheobronchial tree. We report a case of Aspergillus fumigatus bronchitis, diagnosed by fiberoptic bronchoscopy, with fungal growth completely occluding the left main bronchus leading to lung collapse and acute respiratory failure in a 60-year-old male with erythroleukemia and profound granulocytopenia.
Infection 2001 Aug
PMID:Aspergillus bronchitis causing atelectasis and acute respiratory failure in an immunocompromised patient. 1154 91

The aim of this study was to present neurological complications of influenza infections. Infections caused by influenza viruses can be very serious and may lead even to death resulted from the post-infectious complications. The most often occurring complications are pneumonia, bronchitis, bronchiolitis, myocarditis and otitis media. The other group is neurological post-influenza complications, including dementia, epileptic disorders, cerebrovascular disease, febrile convulsions, toxic encephalopathy, encephalitis, meningitis, subarachnoid hemorrhages, lethargic encephalitis, psychosis or increase in the number of cases of Parkinson's disease. The first way of prevention of influenza is vaccination that results in healthy, social and economic benefits.
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PMID:[Neurological complication of influenza infections]. 1219 26

The 2 groups of human coronaviruses (HCoVs) represented by the prototype strains HCoV 229E and HCoV OC43 are mostly known as viruses responsible for common cold syndrome. HCoVs are difficult to detect, and epidemiological data are rare. From October 2000 through April 2001, we tested 1803 respiratory samples for HCoV by reverse-transcriptase polymerase chain reaction. From 8 February through 27 March 2001, HCoV OC43 was detected in samples obtained from 30 (6%) of 501 patients. The other viruses detected were respiratory syncytial virus (6.1%), parainfluenza virus 3 (1%), influenza virus A (7.8%), influenza virus B (7.2%), rhinovirus (6.4%), enterovirus (1%), and adenovirus (2%). Infection with HCoV OC43 was detected in patients of all age groups. The following clinical symptoms were noted: fever (in 59.8% of patients), general symptoms (in 30%), digestive problems (in 56.8%), rhinitis (in 36.6%), pharyngitis (in 30%), laryngitis (in 3.3%), otitis (in 13.3%), bronchitis (in 16.6%), bronchiolitis (in 10%), and pneumonia (in 6.6%). This study shows that an outbreak of HCoV OC43 respiratory infection was responsible for the lower respiratory tract symptoms observed in nearly one-third of patients identified by active surveillance for coronavirus infection.
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PMID:An outbreak of coronavirus OC43 respiratory infection in Normandy, France. 1268 10

A total of 136 children aged 5 years and under with respiratory tract diseases were examined for Chlamydophila pneumoniae infection. By means of the micro-immunofluorescence test, an acute infection was suggested in 37 (27.2%) of them. Infection was found in 23 (43.4%) of 53 children with bronchitis, seven (70.0%) of 10 with pharyngitis, and two (22.2%) of nine with pneumonia. C. pneumoniae DNA was detected in seven of 55 children by means of nasopharyngeal swabs, and serological evidence was present in all of seven. Five of them were suggested the acute infection and four of the five showed IgG titers increasing four times and over. By age distribution, five of the seven DNA-positive children were 1 year old, and the remaining two were 2 and 4 years old, respectively. The clinical findings of the seven DNA-positive children were characterized as indicative of bronchitis (n = 4), pharyngitis (n = 2), and pneumonia (n = 1). In Thailand, C. pneumoniae infection occurs frequently among children aged 5 years and under, and may cause pharyngitis, bronchitis, and sometimes pneumonia. However, it is suggested that C. pneumoniae infection is not a major cause of severe pneumonia among children in that age group.
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PMID:Chlamydophila pneumoniae infection among young children with respiratory diseases in Thailand. 1458 36

Mycoplasma pneumoniae is an intracellular pathogen, devoid of cell wall, able to invade airway epithelial cells. Infection may either remain asymptomatic or induce bronchitis and pneumonia. M. pneumoniae is the first-ranking aetiological agent of community-acquired pneumonias in children over five years of age. Clinical features are usually mild, but this should not preclude the initiation of a treatment, in order to avoid serious sequelae such as impairment of pulmonary gas exchange capacity. In children at high-risk of asthma, infection with M. pneumoniae can induce exacerbation. A survey was performed in children admitted to hospital Saint-Vincent-de-Paul (Paris) for an episode of severe asthma exacerbation with persistent hypoxemia. Mycoplasma infection was identified in 26% of children with a history of asthma and 50% of those for whom the exacerbation was the presenting manifestation of the disease. Furthermore, if the Mycoplasma infection was atypical, asthma exacerbation recurred within one month. M. pneumoniae should be considered not only as a preeminent agent of respiratory infection in children, but also as a triggering factor in exacerbation and even inception of asthma. As a consequence, it is mandatory to carefully search for and actively treat Mycoplasma infection in children.
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PMID:[Mycoplasma pneumoniae, community-acquired pneumonia and asthma]. 1589 45

Related to its potential vulnerability the respiratory tract has a very complex and effective defence apparatus. The interaction between these defence mechanisms and certain characteristics of aetiological agents results in a pattern in which initial infections by these agents tend to occur at specific sites in the tract. Infections in which the primary portal of entry is in the upper respiratory tract include Bordetella bronchiseptica and Haemophilus spp in pigs; Pasteurella spp in cattle, sheep, pigs; Mycoplasma spp in cattle, sheep, pigs and poultry; equine herpesvirus 1 in horses; infectious bovine rhinotracheitis in cattle; parainfluenza 3 in cattle and sheep; infectious laryngo-tracheitis and infectious bronchitis in poultry; feline viral rhinotracheitis and calicivirus in cats; Aujeszky's disease virus and swine influenza in pigs; and equine influenza in horses. Infections in which the primary portal of entry is in the lower respiratory tract include Aspergillus fumigatus in poultry and mammals, respiratory syncytial virus in cattle, distemper virus in dogs and adenovirus in cattle and dogs. A fuller understanding of the interactions between an agent and the host at the point of entry would make it much easier to develop effective vaccines and therapeutic agents.
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PMID:Mechanisms of infection in the respiratory tract. 1603 Aug 6

Chlamydia pneumoniae causes a range of respiratory infections including bronchitis, pharyngitis and pneumonia. Infection has also been implicated in exacerbation/initiation of asthma and chronic obstructive pulmonary disease (COPD) and may play a role in atherosclerosis and Alzheimer's disease. We have used a mouse model of Chlamydia respiratory infection to determine the effectiveness of intranasal (IN) and transcutaneous immunization (TCI) to prevent Chlamydia lung infection. Female BALB/c mice were immunized with chlamydial major outer membrane protein (MOMP) mixed with cholera toxin and CpG oligodeoxynucleotide adjuvants by either the IN or TCI routes. Serum and bronchoalveolar lavage (BAL) were collected for antibody analysis. Mononuclear cells from lung-draining lymph nodes were stimulated in vitro with MOMP and cytokine mRNA production determined by real time PCR. Animals were challenged with live Chlamydia and weighed daily following challenge. At day 10 (the peak of infection) animals were sacrificed and the numbers of recoverable Chlamydia in lungs determined by real time PCR. MOMP-specific antibody-secreting cells in lung tissues were also determined at day 10 post-infection. Both IN and TCI protected animals against weight loss compared to non-immunized controls with both immunized groups gaining weight by day 10-post challenge while controls had lost 6% of body weight. Both immunization protocols induced MOMP-specific IgG in serum and BAL while only IN immunization induced MOMP-specific IgA in BAL. Both immunization routes resulted in high numbers of MOMP-specific antibody-secreting cells in lung tissues (IN>TCI). Following in vitro re-stimulation of lung-draining lymph node cells with MOMP; IFNgamma mRNA increased 20-fold in cells from IN immunized animals (compared to non-immunized controls) while IFNgamma levels increased 6- to 7-fold in TCI animals. Ten days post challenge non-immunized animals had >7,000 IFU in their lungs, IN immunized animals <50 IFU and TCI immunized animals <1,500 IFU. Thus, both intranasal and transcutaneous immunization protected mice against respiratory challenge with Chlamydia. The best protection was obtained following IN immunization and correlated with IFNgamma production by mononuclear cells in lung-draining LN and MOMP-specific IgA in BAL.
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PMID:Comparison of intranasal and transcutaneous immunization for induction of protective immunity against Chlamydia muridarum respiratory tract infection. 1615 55


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