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Pediatrics · Chapter 12. Infectious and parasitic diseases

Acute respiratory viral infections (ARVI) in children

Infectiones virales systematis respiratorii acutae

Acute respiratory infections (ARIs) are a broad group of respiratory tract diseases classified in ICD-10 under categories J00–J06. The main feature of pathogens in this group is a pronounced tropism for epithelial cells of the respiratory tract, leading to inflammation, systemic intoxication, and the risk of bacterial complications.

Multietiological natureCaused by more than 200 different pathogens
At-risk groupThe peak incidence occurs in children aged 3 to 14 years
Reye's syndromeRisk of fatal encephalopathy when taking aspirin
Clinical coreTopical lesion, toxicosis, and secondary flora
3 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiological structure and epidemiology

Acute respiratory infections are characterized by a pronounced multietiological nature. Mixed (viral-bacterial, viral-mycoplasmal) and undifferentiated forms are frequently registered.

Main pathogen groups:

  • Viruses (dominant group): characterized by an enormous diversity of serotypes. They include influenza viruses (A, B, C), parainfluenza (5 types), rhinoviruses (over 114 types), adenoviruses (32 serotypes), and enteroviruses (60 serotypes). They also include coronaviruses (4 types), reoviruses, respiratory syncytial virus (RSV), metapneumovirus, bocavirus, and herpes simplex viruses.
  • Bacteria: most often act as secondary flora, but can also be primary pathogens (gram-positive cocci, meningococci, Haemophilus influenzae, Klebsiella, Legionella).
  • Atypical intracellular agents: chlamydiae (Chlamydophila pneumoniae, Chlamydia psittaci) and mycoplasmas (Mycoplasma pneumoniae, Mycoplasma hominis).

Children of all age groups fall ill, with an infected person serving as the source of infection. Maximum contagiousness is observed during the first week. The main transmission route is airborne (aerosol), less commonly contact-transmission. A sharp rise in incidence is associated with the start of attending preschool institutions and the cold season.

Pathogenesis of the disease

The portal of entry in the absolute majority of cases is the upper respiratory tract (less commonly the conjunctiva or gastrointestinal tract). All pathogens in this group are epitheliotropic.

Local reaction goes through several stages: adsorption of the virus on the cell, penetration into the cytoplasm, enzymatic disintegration of the envelope, and reproduction. As a result, dystrophy of the affected cells and local inflammation occur.

Next comes the stage of systemic effect. Viruses overcome the damaged barrier and enter the bloodstream. The circulation of viruses and epithelial breakdown products forms infectious toxicosis. The central nervous system and cardiovascular system become the main targets, and microcirculatory disorders develop. Due to the loss of the barrier function of the desquamated epithelium, favorable conditions are created for the addition of secondary bacterial flora.

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Topical diagnosis (viral tropism)

The basis for the clinical differentiation of ARVI is the affinity of the pathogen for specific structures of the respiratory tract:

  • Influenza: predominantly affects the lower respiratory tract (tracheitis, pneumonia develop).
  • Parainfluenza: selectively tropic to the larynx (laryngitis, pharyngitis).
  • RS infection: affects small bronchi and bronchioles (bronchiolitis, bronchospastic syndrome).
  • Rhinovirus: actively multiplies on the mucous membrane of the nasal cavity (pronounced rhinitis).
  • Adenovirus: has additional tropism for lymphoid tissue and the conjunctiva.

Severity assessment and therapeutic tactics

The degree of severity (mild, moderate, severe) is assessed by the severity of intoxication and the depth of motor disorders. The course may be smooth or complicated.

Treatment is built on the principle of a three-tier pyramid against the background of mandatory bed rest:

  1. Etiotropic therapy: prescribed in the early stages. For influenza A, neuraminidase inhibitors (oseltamivir, zanamivir) are used. For nonspecific ARIs, interferon preparations for a short course (5–7 days) or endogenous interferon inducers are used. Antibiotics are not routinely used; they are indicated only in case of a bacterial infection or the addition of secondary flora.
  2. Pathogenetic therapy: relief of the inflammatory cascade (combining treatment for mucosal edema, bronchospasm, and impaired mucociliary clearance). In severe forms, detoxification therapy is mandatory.
  3. Symptomatic therapy: plenty of warm fluids and adequate nutrition. Paracetamol and ibuprofen are permitted as antipyretics. Cough is relieved with mucolytics or expectorants, and nasal congestion with decongestants (xylometazoline, oxymetazoline).

Preventive measures

Specific prophylaxis for most ARIs (except influenza) has not been developed. The basis of control in the focus of infection is a strict sanitary and hygienic regimen. Mandatory measures include regular ventilation of premises, wet cleaning, and ultraviolet germicidal irradiation of the air.

How to memorize

PGRR: Parainfluenza — Larynx (Gortan'), Rhinovirus — Rhinitis, RSV — bronchioles (Respiratory Syncytium), Influenza — Deep (trachea).

Class and exam questions

Why is it strictly forbidden to give aspirin to children with ARVI?

The use of acetylsalicylic acid against the background of a viral infection in children is associated with a high risk of developing Reye's syndrome—an acute, severe hepatic encephalopathy.

Should antibiotics be prescribed immediately for high fever?

No. Antibacterial therapy is not used routinely. It is indicated exclusively for confirmed bacterial or atypical nature of the infection, as well as for the addition of bacterial complications.

What is the main pathogenetic mechanism for the development of complications in ARIs?

Destruction and death of the respiratory epithelium under the action of the virus lead to the loss of the barrier function of the mucosa, which opens the way for the addition of secondary bacterial flora.

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What else to study on this topic

  • Mechanisms of development of bronchospastic syndrome in RS infection
  • Differential diagnosis of influenza and adenoviral infection
  • Features of the clinical course of undifferentiated forms of ARI
  • Indications and regimens for the use of neuraminidase inhibitors

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