Relationships Between Rhinitis Symptoms, Respiratory Viral Infections and Nasopharyngeal Colonization With Streptococcus pneumoniae, Haemophilus influenzae and Staphylococcus aureus in Children Attending Daycare

Rodrigues, Fernanda; Foster, Dona; Nicoli, Emily; Trotter, Caroline; Vipond, Barry; Muir, Peter; Gonçalves, Guilherme; Januário, Luís; Finn, Adam

doi:10.1097/inf.0b013e31827687fc

Cited by 74 publications

(86 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Staphylococcal pneumonia following influenza infection was responsible for a large proportion of the deaths in the 1919 pandemic; chickenpox predisposes to severe group A streptococcal pneumonia and infection at other sites; and, more recently, the role of viruses in altering the behaviour of biofilms during exacerbations has been the subject of research. Even the severity of a simple "cold" appears to be driven in large part by the load of potential pathogenic bacteria in the nose and nasopharynx rather than the simple presence of a respiratory virus [14], which, as noted earlier may be totally asymptomatic for most viruses. Studies using the conjugate pneumococcal vaccine in South Africa found reductions in admissions with apparent "viral-induced lower respiratory tract infection", further indicating the influence of bacteria on the impact of viruses [15].…”

Section: Identification Of Pathogens and Relationship To Disease And mentioning

confidence: 93%

“…Increasingly we are recognising that a microorganism must not only interact with the host and its defences, but must also compete and/or collaborate with other microorganisms. As noted by RODRIGUES et al [14], the Sino-Nasal Outcome Test score of a cold will be driven by host responses largely mediated by neutrophils (whose products not only drive symptoms but provide the colouration of the nasal discharge), and the magnitude of this response is likely to be driven by type of virus, viral load and presence of potentially pathogenic bacteria.…”

Section: Identification Of Pathogens and Relationship To Disease And mentioning

confidence: 99%

See 1 more Smart Citation

Paediatric respiratory infections

Everard

2016

Eur Respir Rev

View full text Add to dashboard Cite

Pulmonary infections remain a major cause of infant and child mortality worldwide and are responsible for a substantial burden of morbidity. During the 2015 European Respiratory Society International Congress in Amsterdam, some of the main findings from peer-reviewed articles addressing this topic that were published in the preceding 12 months were reviewed in a Paediatric Clinical Year in Review session. The following article highlights some of the insights provided by these articles into the complex interactions of the human host with the extensive and dynamic populations of microorganisms that call an individual "home". @ERSpublications A review of publications from the past year addressing acute life-threatening and chronic respiratory infections http://ow.ly/W4ahI

show abstract

Section: Identification Of Pathogens and Relationship To Disease And mentioning

confidence: 93%

Section: Identification Of Pathogens and Relationship To Disease And mentioning

confidence: 99%

Paediatric respiratory infections

Everard

2016

Eur Respir Rev

View full text Add to dashboard Cite

show abstract

“…Our group used this model to show that increased pneumococcal acquisition by initially uncolonized "contact" pups correlates with increased mucin production and bacterial shedding by colonized "index" pups with influenza A virus (IAV) coinfection (7). These responses among index pups were chiefly driven by the mucosal inflammatory response to IAV, which recapitulates the effects of respiratory viruses in children (6,12). Although most pneumococcal transmission in the human population may be seasonal, it is not generally associated with influenza coinfection (14).…”

mentioning

confidence: 99%

Infant Mouse Model for the Study of Shedding and Transmission during Streptococcus pneumoniae Monoinfection

et al. 2016

View full text Add to dashboard Cite

One of the least understood aspects of the bacterium Streptococcus pneumoniae (pneumococcus) is its transmission from host to host, the critical first step in both the carrier state and the disease state. To date, transmission models have depended on influenza A virus coinfection, which greatly enhances pneumococcal shedding to levels that allow acquisition by a new host. Here, we describe an infant mouse model that can be utilized to study pneumococcal colonization, shedding, and transmission during bacterial monoinfection. Using this model, we demonstrated that the level of bacterial shedding is highest in pups infected intranasally at age 4 days and peaks over the first 4 days postchallenge. Shedding results differed among isolates of five different pneumococcal types. Colonization density was found to be a major factor in the level of pneumococcal shedding and required expression of capsule. Transmission within a litter occurred when there was a high ratio of colonized "index" pups to uncolonized "contact" pups. Transmission was observed for each of the well-colonizing pneumococcal isolates, with the rate of transmission proportional to the level of shedding. This model can be used to examine bacterial and host factors that contribute to pneumococcal transmission without the effects of viral coinfection.T ransmission from one infected individual to another is necessary for most agents of infection. For Streptococcus pneumoniae (the pneumococcus), a leading opportunistic Gram-positive human pathogen, transmission occurs primarily from hosts colonized on the mucosal surfaces of their upper respiratory tract (the carrier state; 1). Bacterial acquisition and colonization of the mucosal surfaces of the nasopharynx by pneumococci are dynamic, transient processes which are generally asymptomatic and occur most commonly during early childhood. Under certain circumstances, however, pneumococci gain access to normally sterile environments within the host, resulting in diseases such as otitis media, pneumonia, sepsis, and meningitis. Acute respiratory infections associated with the pneumococcus represent a significant public health burden, with an estimated 14.5 million cases of serious pneumococcal disease worldwide (2). None of its many disease states, however, is thought to promote pneumococcal contagion (3).While bacterial and host factors contributing to the carrier state have been studied in the natural host and modeled in animals, there is relatively little mechanistic understanding of transmission (4). Person-to-person spread is thought to require close contact, such as within families or day care centers, either directly from nasal secretions or possibly via contact with contaminated surfaces (fomites; 3, 5). Therefore, one of the key steps in pneumococcal contagion involves the exit or shedding of the organism from the respiratory tract of a colonized individual.A factor known to enhance pneumococcal shedding is a concurrent or recent viral respiratory infection (6, 7). Increased rates of carriage associated ...

show abstract

“…These secretions promote bacterial growth (3), and inflammation is important for bacterial transmission in a viral coinfection model (4). Human studies have demonstrated that higher bacterial burdens are correlated with a more profound rhinitis (5); however, as a result of this inflammatory response, colonization is normally cleared by the host's immune system within several weeks (6).…”

mentioning

confidence: 99%

Sensing of Interleukin-1 Cytokines during Streptococcus pneumoniae Colonization Contributes to Macrophage Recruitment and Bacterial Clearance

2015

View full text Add to dashboard Cite

Streptococcus pneumoniae (the pneumococcus), a leading cause of bacterial disease, is most commonly carried in the human nasopharynx. Colonization induces inflammation that promotes the organism's growth and transmission. This inflammatory response is dependent on intracellular sensing of bacterial components that access the cytosolic compartment via the pneumococcal pore-forming toxin pneumolysin. In vitro, cytosolic access results in cell death that includes release of the proinflammatory cytokine interleukin-1␤ (IL-1␤). IL-1 family cytokines, including IL-1␤, are secreted upon activation of inflammasomes, although the role of this activation in the host immune response to pneumococcal carriage is unknown. Using a murine model of pneumococcal nasopharyngeal colonization, we show that mice deficient in the interleukin-1 receptor type 1 (Il1r1 ؊/؊ ) have reduced numbers of neutrophils early after infection, fewer macrophages later in carriage, and prolonged bacterial colonization. Moreover, intranasal administration of Il-1␤ promoted clearance. Macrophages are the effectors of clearance, and characterization of macrophage chemokines in colonized mice revealed that Il1r1 ؊/؊ mice have lower expression of the C-C motif chemokine ligand 6 (CCL6), correlating with reduced macrophage recruitment to the nasopharynx. IL-1 family cytokines are known to promote adaptive immunity; however, we observed no difference in the development of humoral or cellular immunity to pneumococcal colonization between wild-type and Il1r1 ؊/؊ mice. Our findings show that sensing of IL-1 cytokines during colonization promotes inflammation without immunity, which may ultimately benefit the pneumococcus. Streptococcus pneumoniae (the pneumococcus) is an opportunistic bacterial pathogen that is responsible for over 1 million deaths annually, mostly in children under the age of 5 years (1). The pneumococcus serially colonizes the mucosal surfaces of the human upper respiratory tract, and carriage of the organism provides the reservoir for all pneumococcal disease (2). Colonization induces airway inflammation that is characterized by a suppurative rhinitis and increased mucus secretion. These secretions promote bacterial growth (3), and inflammation is important for bacterial transmission in a viral coinfection model (4). Human studies have demonstrated that higher bacterial burdens are correlated with a more profound rhinitis (5); however, as a result of this inflammatory response, colonization is normally cleared by the host's immune system within several weeks (6).A well-defined murine model of pneumococcal colonization (7) has elucidated bacterial and host factors that are critical to immune recognition of the pneumococcus, which drives the eventual resolution of the carrier state. Although early colonization triggers the recruitment of neutrophils, these are ineffective at resolving the infection. Clearance of pneumococci from the upper airway over a period of weeks requires a sustained presence of macrophages in the nasopharynx (8). Althou...

show abstract

Relationships Between Rhinitis Symptoms, Respiratory Viral Infections and Nasopharyngeal Colonization With Streptococcus pneumoniae, Haemophilus influenzae and Staphylococcus aureus in Children Attending Daycare

Cited by 74 publications

References 37 publications

Paediatric respiratory infections

Paediatric respiratory infections

Infant Mouse Model for the Study of Shedding and Transmission during Streptococcus pneumoniae Monoinfection

Sensing of Interleukin-1 Cytokines during Streptococcus pneumoniae Colonization Contributes to Macrophage Recruitment and Bacterial Clearance

Contact Info

Product

Resources

About