RESPIRATORY INFECTIONS IN CYSTIC FIBROSIS PATIENTS CAUSED BY VIRUS, CHLAMYDIA AND MYCOPLASMA–POSSIBLE SYNERGISM WITH PSEUDOMONAS AERUGINOSA

Abstract

116 cystic fibrosis patients were observed, by monthly examinations over an eight-month period, to investigate the importance of non-bacterial respiratory infections (NBI) in exacerbations of the respiratory disease. Sputum was examined for bacteria, and serum investigated for antibody response against virus, mycoplasma and chlamydia and for antibodies against Pseudomonas aeruginosa. During this period each patient had, on an average, 2.9 exacerbations of which 76% were associated with bacteria, most frequently P. aeruginosa (51%), and 20% with NBI, although bacteria were also present in most of these cases. No etiology was established in 18% of the exacerbations. The NBI were caused by respiratory syncytial virus (RSV) (9%), parainfluenza virus (5%), influenza virus (3.6%), adenovirus (2.4%), mycoplasma (0.6%) and chlamydia (0.6%). The incidence of exacerbations was higher in patients with chronic P. aeruginosa infections. RSV infections were more common in patients who developed chronic P. aeruginosa infection during the study period, and RSV infections were frequently associated with a rise of P. aeruginosa antibodies in patients who harboured these bacteria. The important role of NBI as mediators of onset of chronic P. aeruginosa infections in cystic fibrosis patients is suggested.

Twenty-Five-Year Outbreak of Pseudomonas aeruginosa Infecting Individuals with Cystic Fibrosis: Identification of the Prairie Epidemic Strain

“…This is largely owing to the fact that the majority of studies are prospective in nature and thus unable to determine when the initial transmission event occurred (13,17,28,(36)(37)(38)(39). Critically, the bulk of transmission studies are concentrated in the pediatric patient age group (17,28,36,(38)(39)(40)(41)(42). Our study provides an important longitudinal perspective to studies of transmissible P. aeruginosa infection in adult populations.…”

Rhinovirus Disrupts the Barrier Function of Polarized Airway Epithelial Cells

“…The coinfection of viruses and bacteria have been recognized in several respiratory diseases including pneumonia, otitis media (1-3), chronic obstructive pulmonary disease (COPD) (4-7) and cystic fibrosis (CF) (8)(9)(10)(11). Viruses predispose the host to bacterial infection by various mechanisms including destruction of the respiratory epithelium, modulation of innate defenses, and alteration of cell membranes, which in turn facilitates bacterial adherence.…”

Viral Respiratory Tract Infections in Cystic Fibrosis

“…RSV represents 9-58% of all reported viral infection in CF, with the highest incidence in young children (Armstrong, Grimwood et al 1998). It is possible that RSV precipitates in the initial infection by P. aeruginosa of the CF airway (Petersen, Hoiby et al 1981), the proposed mechanism of which will be discussed later. A new subtype of human rhinovirus was recently identified, rhinovirus C, and was shown by de Almeida et al (de Almeida, Zerbinati et al 2010) that it is significantly associated with respiratory exacerbations in children with CF (Odd ratio-1.213).…”

“…Influenza A and B take 12-27%, but in one small study, it comprised of 77% of positive samples (Hordvik, Konig et al 1989). PIV are found in lower frequencies with only one study showing a detection rate of 43% from positive samples (Petersen, Hoiby et al 1981). Metapneumovirus has recently been detected in www.intechopen.com nasopharyngeal aspirates taken from hospitalised children and infants with respiratory tract infections who had signs and symptoms similar to those of RSV infection (van den Hoogen, de Jong et al 2001).…”

“…Early studies looking at respiratory viruses in CF relied on repeated serological testing, either alone (Petersen, Hoiby et al 1981) or in combination with viral cultures for viral detection (Wang, Prober et al 1984;Ramsey, Gore et al 1989;Pribble, Black et al 1990;Armstrong, Grimwood et al 1998;Hiatt, Grace et al 1999). These methods are relatively insensitive and more recent studies have utilised PCR based methodologies (Smyth, Smyth et al 1995;Collinson, Nicholson et al 1996;Punch, Syrmis et al 2004;Olesen, Nielsen et al 2006;).…”