Viral–bacterial co-infections in the respiratory tract

Abstract

Respiratory syncytial virus (RSV) is the most significant cause of paediatric acute respiratory infection (ARI). RSV and other respiratory viruses are commonly co-detected with potentially pathogenic bacteria, such as Streptococcus pneumoniae, in the upper airways of young children. While these bacteria are known to be carried asymptomatically, they are also capable of opportunistic infections. Interactions between RSV and S. pneumoniae have been demonstrated in both clinical and molecular studies. However, the clinical significance of these interactions remains debated, and the effect of clinically relevant strain variation in both virus and bacteria on these interactions is also unknown. This work aimed to better understand the role of S. pneumoniae colonisation during RSV infections. To determine the effect of RSV and S. pneumoniae co-detection on disease severity during ARI, molecular pathogen screening of nasopharyngeal samples was conducted in a cohort of young children under the age of two years presenting with ARI at the emergency department of the Royal Brisbane Children's Hospital, Australia. S. pneumoniae was co-detected in approximately 52% of RSV infections, and co-detection was associated with increased disease severity, suggesting that S. pneumoniae plays a pathogenic role in severe paediatric RSV infections. Having established a clinical role for S. pneumoniae during RSV infection, the dynamics of pneumococcal colonisation of the nasal cavity was investigated in the four weeks prior and subsequent to an RSV infection in a longitudinal birth cohort of Brisbane-based children. Approximately 33% of infants and young children with RSV infections were colonised by S. pneumoniae prior to the RSV detection, and strain characterisation of S. pneumoniae in the weeks immediately surrounding the viral infection suggested that any observed growth of S. pneumoniae during RSV infection arose from the pre-existing strain colonising the URT. In another 14% of RSV infections, S. pneumoniae was first detected during the virus infection, suggesting simultaneous acquisition of RSV and S. pneumoniae and possible co-transmission of the two pathogens. The results from the two paediatric cohorts suggested an interaction between RSV and S. pneumoniae that was advantageous to the bacteria. It was therefore hypothesised that the molecular mechanisms governing RSV and S. pneumoniae interactions might be pneumococcal strain-specific and stronger in strains frequently co-detected with RSV. Studies have shown that RSV can increase S. pneumoniae colonisation by enhancing pneumococcal adherence to airway epithelia, and virions iii can bind directly to the bacterium to form co-pathogen complexes. These interactions are in part mediated through the binding interactions between S. pneumoniae surface receptors and the RSV G surface glycoprotein. RSV G is highly variable, both antigenically and genetically, and is the main protein used to type RSV into subtypes A and B. The genetic variation of RSV G was characterised from nasopharyn...

Bacterial co‐infections with SARS‐CoV‐2

“…The mortality rate seems to be still growing mostly because of the rapid rate of aging in the human population. 41,42 Although viruses are commonly responsible for the development of acute upper and lower respiratory infections, in most cases patients may be infected by both bacterial and viral pathogens; however, the clinical manifestations at the early stages of the disease would not be nosologically distinguishable for physicians to differentially diagnose viral from a bacterial infection. 43 Recently, a group of respiratory emerging viruses has been identified, such as human coronavirus (HCoV), NL63, human bocavirus, influenza viruses' type H1N1 and H5N1, SARS, Middle East Respiratory Syndrome-related coronavirus (MERS), and Covid-19.…”

“…Commonly, viral infection can destroy histologically and functionally the respiratory tract of individuals upon viral spread. 42 Depending on the type of the virus, the histopathological outcomes could be relatively different from mild types to severe ones. These detrimental changes include altered mucus secretion, cell death, hyperplasia, decreased mucosal clearance, reduced oxygen exchange, and impaired surfactant secretion.…”

“…These detrimental changes include altered mucus secretion, cell death, hyperplasia, decreased mucosal clearance, reduced oxygen exchange, and impaired surfactant secretion. 42,77 Each of these effects is caused by various molecular mechanisms, depending on the virus, bacterial species, as well as the degree of the host immune reaction to either a bacterium or virus. 42 It has been noted that viral infections promote bacterial colonization of the airway through a variety of mechanisms.…”

MERS-CoV: Understanding the Latest Human Coronavirus Threat

“…Preceding or concurrent viral respiratory tract infections can predispose the host to secondary co-infections from other microorganism throughout the airway. The mechanisms by which viruses promote these superinfections are diverse and replete [63]. As yet, not much is known as to how MERS-CoV damages the airway and dysregulate the host immune responses which, in turn, supports the adherence and invasion of other pathogens into normally sterile sites within the respiratory tract.…”

Complement evasion by the human respiratory tract pathogens Haemophilus influenzae and Moraxella catarrhalis

“…Haemophilus influenzae and Moraxella catarrhalis are together with Streptococcus pneumoniae the most common pathogens found in the human respiratory tract. Preschool children carry these pathogens as commensals, and occasionally, also upon a simultaneous viral infection compromising the host's epithelial barrier, the polymicrobial dynamics will change and result in bacterial respiratory tract infections as exemplified by acute otitis media, rhinosinusitis, tracheitis or bronchitis/pneumonia [1,2]. In contrast to children, adults are less often colonized by H. influenzae and M. catarrhalis and, consequently, may be infected upon exposure, for example after contact with grandchildren carrying pathogens.…”