RSV+Parainfluenza = Paramyxoviridae (enveloped, negative-sense ssRNA, like measles/mumps). Adenovirus = DIFFERENT, non-enveloped dsDNA.
LEADING cause of infant/young child LOWER respiratory tract infection worldwide. Name = SYNCYTIA formation (infected cells fuse, multinucleated giant cells) — cytopathic mechanism (see General Virus Properties). Nearly all infected by age 2, but REINFECTION common lifelong (incomplete/non-durable immunity).
Clinical: BRONCHIOLITIS (wheezing, tachypnea, respiratory distress) = classic infant presentation, RSV = dominant cause. Older children/adults: milder cold-like reinfection. Severe disease: premature infants (smaller airways + reduced maternal Ab), cardiopulmonary disease infants, elderly/immunocompromised (increasingly recognized severe pneumonia cause, historically underappreciated vs flu).
Diagnosis: rapid antigen + PCR (nasopharyngeal). Treatment: supportive. Ribavirin = limited historical role, select severe cases. Prevention: Palivizumab (monoclonal Ab vs fusion protein) — passive season-long prophylaxis, high-risk infants. NEW: maternal RSV vaccination (pregnancy) + nirsevimab (long-acting monoclonal, infants) — mirrors pertussis maternal-vaccination strategy.
4 serotypes (1-4). Distinctive association: CROUP (laryngotracheobronchitis) — subglottic swelling → BARKING/SEAL-LIKE cough + INSPIRATORY STRIDOR. Young children (6mo-3yr peak), worse at night. “STEEPLE SIGN” on neck X-ray (subglottic narrowing). Type 1 = classic croup serotype. Also: bronchiolitis, pneumonia (infants), overlaps RSV clinically.
Diagnosis: antigen/PCR. Treatment: supportive mostly. Croup specifically: CORTICOSTEROIDS + nebulized EPINEPHRINE (severe, rapid temporary relief).
Non-enveloped dsDNA (classic example, see General Virus Properties; also common gene-therapy vector platform). BROAD disease range across organ systems — contrast RSV/parainfluenza’s respiratory confinement.
Clinical: Respiratory: pharyngitis, PHARYNGOCONJUNCTIVAL FEVER (pharyngitis+conjunctivitis+fever, “swimming pool conjunctivitis” outbreak pattern), pneumonia (military recruits/congregate settings). Non-respiratory: viral gastroenteritis (with rotavirus, see that topic), hemorrhagic cystitis (immunocompromised/transplant), disseminated disease (severe immunocompromise). Epidemic keratoconjunctivitis (more severe than simple conjunctivitis, corneal involvement) — see Ocular/Ear topic.
Diagnosis: PCR standard, antigen tests for specific syndromes. Treatment: supportive (self-limited, immunocompetent). Cidofovir: severe disseminated disease, immunocompromised.
| Virus | Family/genome | Classic association | Vulnerable group |
|---|---|---|---|
| RSV | Paramyxoviridae, (-)ssRNA | Bronchiolitis | Premature infants, elderly |
| Parainfluenza | Paramyxoviridae, (-)ssRNA | Croup (“steeple sign”) | Young children 6mo-3yr |
| Adenovirus | Non-enveloped dsDNA | Pharyngoconjunctival fever, broad disease | Congregate settings, immunocompromised |
RSV, parainfluenza, and adenovirus are grouped here as three genuinely common, largely self-limited respiratory viruses that together account for a large share of paediatric respiratory illness — RSV and parainfluenza both belong to Paramyxoviridae (sharing the family’s enveloped, negative-sense ssRNA, helical structure covered under General Properties of Viruses, and under Measles/Mumps), while adenovirus is a genuinely different, non-enveloped double-stranded DNA virus, notable as one of the few non-enveloped DNA viruses covered in this curriculum’s respiratory topics.
RSV is the leading cause of lower respiratory tract infection in infants and young children worldwide, and its name directly describes its defining cytopathic mechanism: infected respiratory epithelial cells fuse together into multinucleated giant cells (syncytia) — the same fusion-driven cytopathic effect mechanism covered generally under General Properties of Viruses’ discussion of cytocidal infection, here specifically responsible for the airway obstruction and inflammation that drive RSV’s characteristic clinical picture. Nearly all children have been infected at least once by age 2, but, genuinely notably, reinfection throughout life is common (immunity is incomplete and non-durable), meaning RSV causes disease across the age spectrum, not just in the initial childhood infection.
Bronchiolitis — wheezing, tachypnoea, and respiratory distress from small-airway inflammation and obstruction — is the classic, defining presentation in infants specifically, and RSV is the dominant identifiable cause of this age-specific syndrome. In older children and healthy adults, reinfection typically causes a milder, common-cold-like illness. Severe disease concentrates in specific vulnerable groups: premature infants (whose airways are anatomically smaller and more easily obstructed, and whose passively transferred maternal antibody protection is itself reduced by preterm birth), infants with underlying cardiopulmonary disease, and the elderly/immunocompromised (where RSV is an increasingly recognized, genuinely significant cause of severe pneumonia, historically under-appreciated relative to influenza in this population).
Rapid antigen tests and PCR on a nasopharyngeal specimen are standard diagnostic methods. Treatment is supportive; ribavirin has a limited, largely historical role reserved for select severe cases. Palivizumab — a monoclonal antibody against the RSV fusion protein — provides passive, season-long prophylaxis for high-risk infants (premature infants, those with significant cardiopulmonary disease), a genuinely notable example of monoclonal-antibody-based passive immunoprophylaxis distinct from the polyclonal immunoglobulin preparations covered under Vaccines and Immunoprophylaxis. Maternal RSV vaccination during pregnancy and a newer long-acting monoclonal antibody (nirsevimab) for infants represent genuinely recent additions to RSV prevention, mirroring the maternal-vaccination strategy already established for pertussis (see that topic) in providing passive protection during the vulnerable early-infancy window.
Parainfluenza viruses (four serotypes, 1–4) cause a spectrum of paediatric respiratory illness, with the single most clinically distinctive association being croup (laryngotracheobronchitis) — subglottic airway inflammation and swelling producing the disease’s hallmark barking (seal-like) cough and inspiratory stridor, typically in young children (peak incidence around 6 months to 3 years), worse at night, and, genuinely usefully, often demonstrating the characteristic “steeple sign” (subglottic narrowing) on a frontal neck X-ray when imaging is performed — parainfluenza type 1 is the classic, most frequently implicated serotype for croup specifically. Beyond croup, parainfluenza also causes bronchiolitis and pneumonia, particularly in infants, with a clinical picture that can overlap substantially with RSV.
Diagnosis is by antigen testing or PCR where clinically warranted; most cases are managed supportively without specific antiviral treatment. Croup specifically is managed with corticosteroids (reducing airway inflammation) and, for more severe presentations, nebulized epinephrine (providing rapid, if temporary, symptomatic relief of airway obstruction).
Adenovirus, a non-enveloped dsDNA virus (covered structurally under General Properties of Viruses as a classic example of a non-enveloped DNA virus, and under Antigen-Antibody Reactions/immunology topics as a common gene-therapy/vector-platform virus given its stability and well-characterized biology), is genuinely notable for causing an unusually broad range of clinical syndromes across multiple organ systems, well beyond the respiratory tract alone — a real point of contrast with RSV and parainfluenza, which stay comparatively confined to respiratory disease.
Respiratory: pharyngitis, and, in a genuinely distinctive combined presentation, pharyngoconjunctival fever (pharyngitis plus conjunctivitis plus fever together, sometimes in outbreak settings linked to shared swimming pools — “swimming pool conjunctivitis” is a recognized epidemiological pattern for adenoviral conjunctivitis specifically), plus pneumonia, particularly in military recruits and other close-contact congregate settings where specific adenovirus serotypes cause recognized outbreaks. Non-respiratory: adenovirus is also a significant cause of viral gastroenteritis in children (covered alongside rotavirus under Viral Gastroenteritis), haemorrhagic cystitis (particularly in immunocompromised/transplant patients), and, in severely immunocompromised hosts, disseminated disease. Epidemic keratoconjunctivitis — a more severe ocular presentation than simple conjunctivitis, with corneal involvement — is covered in more depth under Ocular and Ear Infections given its ophthalmological significance.
PCR is the standard diagnostic method across the various clinical presentations; antigen testing is also available for specific syndromes (e.g. rapid conjunctivitis or gastroenteritis antigen tests). Treatment is generally supportive, since adenovirus infection in an immunocompetent host is typically self-limited regardless of which organ system is affected; cidofovir has a role specifically in severe, disseminated disease in immunocompromised patients, where the infection can be genuinely life-threatening rather than self-limited.
| Virus | Family/genome | Classic association | Key vulnerable group |
|---|---|---|---|
| RSV | Paramyxoviridae, (–)ssRNA | Bronchiolitis | Premature infants, elderly |
| Parainfluenza | Paramyxoviridae, (–)ssRNA | Croup (“steeple sign”) | Young children (6mo-3yr) |
| Adenovirus | Non-enveloped dsDNA | Pharyngoconjunctival fever, broad multi-organ disease | Congregate settings (military), immunocompromised |
Personal revision notes, mnemonics and reminders.
