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At least 1,189 records · Page 66Linked to original sources
PubMed2005

Frequency of detection of picornaviruses and seven other respiratory pathogens in infants.

BACKGROUND: Previous studies in which molecular-based techniques have been used to identify the causative pathogens of respiratory tract infection have investigated hospitalized children only. We report a prospective study designed to determine the frequency and clinical presentation of community-acquired respiratory illness in infancy associated with 8 common respiratory pathogens. METHODS: Eighty-eight infants were monitored through their first winter. With each respiratory illness, infants were examined, and a nasal lavage specimen was collected. Individual reverse transcription-polymerase chain reactions were performed to detect infection with picornaviruses (rhinoviruses and enteroviruses), coronaviruses (serotypes OC43 and 229E), adenoviruses, parainfluenza viruses 1-3, influenza viruses (types A and B), respiratory syncytial virus (RSV), Chlamydia pneumoniae and Mycoplasma pneumoniae. RESULTS: Picornaviruses were the most frequently detected pathogen identified in 46% (56 of 123) of episodes, followed by RSV (27%), parainfluenza viruses (13%) and coronaviruses (9%). Dual pathogen infections were identified in 20% of episodes, predominantly caused by picornaviruses together with either RSV or parainfluenza viruses. RSV infection was significantly associated with a diagnosis of bronchiolitis. No other associations were found between pathogen and clinical diagnosis. Dual infection did not predispose infants to a more severe clinical course. CONCLUSIONS: Picornaviruses are the predominant cause of community-acquired respiratory tract infection in the first year of life. Large prospective community-based studies will be needed to fully evaluate the contribution of picornaviruses, both in isolation and in combination with other respiratory pathogens, to the various clinical syndromes of respiratory infection observed during infancy.

Age Distribution↗
PubMedDate not supplied

[Role of parainfluenza varuses in etiology of acute respiratory infections in children (serological diagnosis)].

Serologic investigations carried out in 254 children admitted to a Clinic for Children for respiratory diseases, established a diagnosis of infection with parainfluenza virus in 19.2% of cases. The predominant age-group affected was 7--12 months and 0--6 months; the causative agent in most cases was parainfluenza type 3, followed by type 2 and then type 1. The role of parainfluenza viruses in the aetiology of laryngotracheobronchiectasis was confirmed, as well as their participation in the aetiology of pneumonia in infants. The results also showed the wide circulation of parainfluenza viruses in children and their outstanding contribution to respiratory diseases among hospitalized children within a period of four years.

Antibodies, Viral↗
PubMed1984

Alterations in pulmonary ultrastructure and morphometric parameters induced by parainfluenza (Sendai) virus in rats during postnatal growth.

The ultrastructural and morphometric effects of viral respiratory disease during postnatal lung growth were examined in weanling (22-day-old) and suckling (5-day-old) rats infected with parainfluenza Type 1 (Sendai) virus. Viral nucleocapsids and budding virions were identified by transmission electron microscopy in ciliated cells, mucous cells, and nonciliated bronchiolar epithelial cells of weanling rats at 5 days after inoculation and were associated with epithelial necrosis and erosion as well as hyperplasia of nonciliated bronchiolar epithelial cells. Interstitial pneumonia characterized in early stages by swelling and sloughing of Type 1 and Type 2 alveolar epithelial cells was also present at 5 and 7 days after inoculation. Lesions persisting at 30, 60, and 90 days after inoculation included multifocal connective tissue polyps in terminal bronchioles that partially obstructed bronchiolar lumens. Specific lung volume was greater (P less than 0.01) in weanling rats at 30 and 60 days following viral infection than in control rats, and specific alveolar surface area was 42% greater (P less than 0.01) in infected rats at 60 days after inoculation. Suckling rats infected during a phase of rapid postnatal lung growth at 5 days of age had 33% greater (P less than 0.02) specific alveolar surface area and 48% greater (P less than 0.001) mean terminal bronchiolar cross-sectional area when compared with control rats at 22 days of age. The results indicate that viral pulmonary infection during early life can induce acute and persistent alterations in pulmonary structure that could adversely affect lung function.

Animals↗
PubMed1999

Parainfluenza type 3 viral outbreak in a neonatal nursery.

An outbreak of parainfluenza virus type 3 infection that occurred in a special neonatal care unit is described. Birth weights of affected infants ranged from 1860 to 2080 g and gestational ages were between 28 and 32 weeks. Three infants presented with recurrent episodes of apnoea associated with oxygen desaturations on postnatal ages of 16 days, 26 days and 66 days respectively; upper respiratory tract infection symptoms such as coryza were absent in them. Two older infants who had oxygen dependent bronchopulmonary dysplasia presented with worsening of the respiratory status due to bronchiolitis at 5 and 6 months of age respectively. All infants required supplemental oxygen and assisted ventilatory support and there were no deaths. Parainfluenza virus type 3 was identified by direct antigen detection in 3 cases and was isolated in the other two. The outbreak was controlled by isolating the infected infants, use of gowns and strict hand washing. Nonporous surfaces contaminated with parainfluenza virus type 3 were cleansed with water and detergent. Viral respiratory infections should be considered in the differential diagnosis when growing premature infants present with recurrent apnoeic episodes and they may be severe enough to require assisted ventilatory support. The source of the outbreak was possibly a medical officer and a medical student who had an upper respiratory tract infection prior to the outbreak in the nursery. Medical and nursing staff with viral respiratory infections should avoid working in the nurseries until they are well.

Antigens, Viral↗
PubMed1996

Parainfluenza-3-virus infection enhances allergic sensitization in the guinea-pig.

BACKGROUND: Viral respiratory tract infections have been previously considered to be associated with induction of allergic sensitization. OBJECTIVE AND METHODS: In order to investigate this relationship in an animal model, guinea-pigs were inoculated intranasally with Parainfluenza-3-(PI-3) virus (n = 16) or virus-free culture medium (controls, n = 12), sensitized at day 4 with inhaled ovalbumin (OA) and challenged 3 weeks later with inhaled OA using specific bronchial provocation testing with body plethysmographic measurement of compressed air (CA). Furthermore, specific anti-OA-IgG1-antibodies in serum before challenge were determined by enzyme linked immunosorbent assay (ELISA). For investigation of airway epithelium permeability horseradish peroxidase (HRP) was inhaled at day 4 after inoculation by six animals, and HRP serum concentrations were determined by a direct ELISA 30 min after inhalation. RESULTS: PI-3 infected animals were found to be significantly more sensitized to OA compared with controls, with higher CA values (P < 0.001) on specific bronchial provocation and with increased specific anti-OA-IgG1 titers. Serum-HRP concentrations were about 20 times higher in the infected animals compared with controls. PI-3 infected and sham-infected animals had comparable bronchial reactions on specific provocation with OA when sensitized systemically. CONCLUSIONS: We conclude that viral respiratory tract infection with PI-3 virus enhances inhalative allergic sensitization in the guinea-pig. Increased mucosal permeability to antigens may be an important pathophysiological mechanism.

Adjuvants, Immunologic↗
PubMed1982

Antiviral activity of sodium 5-aminosulfonyl-2,4-dichlorobenzoate (M12325).

Sodium 5-aminosulfonyl-2,4-dichlorobenzoate (M12325) was evaluated for antiviral activity in tissue culture and infected mice. At concentrations ranging from 2.5 to 75.8 micrograms/ml, M12325 inhibited the cytopathic effects of 10 mean tissue culture infective doses of influenza virus A/WSN, A/FM, A/Kumamoto, and B/Great Lakes; parainfluenza virus; rhinovirus; echovirus; respiratory syncytial virus; and vesicular stomatitis virus. Concentrations up to 150 micrograms/ml did not inhibit the cytopathic effects of herpes simplex virus, vaccinia virus, or adenovirus. Concentrations up to 3,160 micrograms/ml did not inhibit the growth of MDCK, Vero, or HEL cells in culture. Single oral doses of M12325, ranging from 10 to 300 mg/kg, administered 1 h before and 1 h after challenge, reduced mortality in mice inoculated intranasally with influenza A/WSN virus. Twice daily oral doses for 14 days effected significant reductions in the mortality of mice infected intranasally with influenza A/WSN, A/FM, A/Kumamoto, and B/Great Lakes, and parainfluenza virus, but they were not effective in mice infected with herpes simplex virus. Multiple doses of 10 and 30 mg/kg, administered intraperitoneally, reduced lung consolidation and virus titer. M12325 was well tolerated in multiple doses up to 1 g/kg orally. These observations support the conclusions that M12325 has a broad spectrum of activity against RNA viruses in vitro and in vivo, selective toxicity, and a large margin of safety.

Amantadine↗
PubMed1977

Interactions between calf alveolar macrophages and parainfluenza-3 virus.

Cells washed from the lungs of freshly killed calves (lung wash cells; LWC) were cytotoxic for calf kidney (CK) target cells infected with parainfluenzavirus type 3 (Pi-3) when assayed by chromium release. LWC collected from 25 calves, including two gnotobiotic animals that had not previously been infected with Pi-3, were all cytotoxic, giving a specific chromium release between 11 and 50%. Cytotoxicity was detected at ratios of LWC to target cell as low as 5:1. The cytotoxic reaction required viable LWC, was inhibited by Pi-3 antiserum, and was not the result of virus-induced damage to the target cells. The cytotoxic cells in the LWC population were identified as alveolar macrophages from observations on glass adherence, phagocytic activity, killing by silica and fine-structural appearance. When LWC were added to CK cells or organ cultures of bovine trachea infected with Pi-3, the yield of virus was reduced for the first 2 to 3 days. However, subsequently, Pi-3 virus replicated in the LWC. Infection of LWC with Pi-3 virus reduced their cytotoxic activity. The significance of these interactions between alveolar macrophages and Pi-3 virus is discussed.

Animals↗