Etiologies of Rhinovirus and Enterovirus Chest Infections
Primary Transmission Routes
Rhinoviruses and enteroviruses cause chest infections through airborne droplet transmission, direct contact with contaminated surfaces, and person-to-person spread via respiratory secretions. 1
Airborne droplet transmission occurs when infected individuals cough or sneeze, releasing virus-containing aerosols that can be inhaled by susceptible hosts. 1
Direct contact transmission happens through touching contaminated objects (utensils, towels, keyboards, toys, telephones) followed by self-inoculation via eyes, nose, or mouth. 1
Respiratory secretion contact represents a major route, as these viruses are eliminated at high titers in nasal and throat secretions. 1
Viral Species and Serotype Diversity
Over 200 viral types cause respiratory infections, with rhinoviruses accounting for 30–80% of common colds and representing the most frequent infectious agents worldwide. 1, 2
Rhinoviruses are classified into three species (RV-A, RV-B, RV-C), while respiratory enteroviruses belong to four species (EV-A, EV-B, EV-C, EV-D), comprising 108 serotypes total. 2, 3
EV-D68 has received particular attention after causing a large outbreak of severe respiratory illness in 2014, demonstrating the capacity of certain enterovirus strains to cause significant lower respiratory tract disease. 2
Pathophysiology of Lower Respiratory Tract Involvement
While traditionally considered upper respiratory pathogens, molecular diagnostic advances have revealed rhinovirus and enterovirus presence in the lower respiratory tract, establishing their role in pneumonia and bronchiolitis. 2, 3
These viruses cause cytokine release (IL-1, IL-6, IL-8) in the lower respiratory tract and bloodstream, which can trigger acute respiratory distress syndrome (ARDS), particularly in vulnerable populations. 4
Enteroviruses are considered the third leading etiological cause of bronchiolitis in infants aged 1–12 months, with CV-A16, EV-71, and EV-104 specifically implicated in severe or fatal pneumonia cases. 3
High-Risk Populations and Disease Severity Factors
Rhinovirus is a major trigger for asthma exacerbations in both children and adults, with experimental models showing it increases eosinophilic inflammation and airway hyperresponsiveness even in allergic non-asthmatic individuals. 1, 5
In hematopoietic stem cell transplant (HSCT) recipients, rhinoviruses are detected in up to 40% of symptomatic patients, with asymptomatic shedding occurring in 13% and prolonged shedding (>4 weeks) being common. 5
Lymphopenia (<500 cells/µL) in HSCT patients represents a specific risk factor for progression to lower respiratory tract disease from enteroviruses. 5
High viral load (≥10⁶ RNA copies/ml) in immunocompetent pediatric patients correlates with lower respiratory tract infections and wheezing, whereas medium-low viral loads (<10⁵ copies/ml) in immunocompromised adults may represent bystander detection rather than causative infection. 6
Environmental and Host Factors
Anatomic factors (decreased lung and airway size), genetic susceptibility, and cigarette smoke exposure determine individual responses to viral infection and disease severity. 1
Concomitant allergic processes may be required for certain respiratory viruses to induce airway hyperresponsiveness, as demonstrated in murine RSV models, though this relationship remains incompletely understood for rhinovirus and enterovirus. 1
Critical Clinical Pitfall
- Do not dismiss rhinovirus or enterovirus detection as mere colonization in immunocompromised patients with respiratory symptoms—these viruses can cause genuine lower respiratory tract disease with mortality rates approaching 10% in HSCT recipients who develop pneumonia, though this complication occurs in <10% of infected patients. 5