Pathogen classification
Among the viruses causing diseases, two main classes are traditionally distinguished:
- Polioviruses — the causative agents of poliomyelitis.
- Non-polioviruses. This group is significantly broader and includes:
- Coxsackie A viruses (Coxsackie A): count 23 serotypes.
- Coxsackie B viruses (Coxsackie B): consist of 6 serotypes.
- ECHO viruses (from Enteric Cytopathogenic Human Orphans): include 29 serotypes. Notably, types 22 and 23 are now assigned to the genus Parechovirus.
- Unclassified enteroviruses: represented by 5 types (68 to 72).
Epidemiology and transmission
The sole source and reservoir of infection is an infected human (regardless of the disease form) or an asymptomatic carrier. The infection is transmitted through several routes:
- Contact: via direct contact or household items.
- Airborne: via droplet transmission.
- Vertical: from mother to fetus (transplacentally).
Natural susceptibility to the infection is extremely high, and the prior disease leaves unstable immunity that does not protect against reinfections. The incidence is predominantly sporadic, but local outbreaks are possible, especially in winter in childcare settings with poor sanitary and hygienic conditions and overcrowding.
Clinical manifestations and forms
The typical clinical form is characterized by a specific vesicular rash. The severity of the disease varies:
- Mild degree: sparse rash, temperature up to 37.5–38 °C, clean mucous membranes, almost no intoxication.
- Moderate degree: abundant rash all over the body, fever up to 39 °C, moderate intoxication.
- Severe degree: massive exanthema, hectic fever (above 39 °C), severe intoxication.
Atypical variants also occur: inapparent form (asymptomatic carriage) and abortive form (catarrhal signs, rhinitis, tonsillitis, and intoxication without specific features).
When neurological complications develop (e.g., viral meningitis), there is a prodromal period with catarrh and moderate headache, followed by an acute onset with pronounced generalized cerebral symptoms (severe headache, persistent vomiting), meningeal signs, and, in some cases, hemorrhagic rash.
Invasive diarrhea
Invasive diarrheas follow an inflammatory pattern. The pathogen (Shigella, Salmonella, Yersinia, Campylobacter, enteroinvasive and enterohemorrhagic strains of Escherichia coli) penetrates directly into the intestinal wall and multiplies intracellularly.
The released enterotoxins destroy cell membranes, leading to severe inflammation and necrosis of the mucosa, predominantly in the colon. Clinically, this manifests as frequent loose stools with pathological impurities such as mucus and blood, indicating tissue destruction.
Prevention
Non-specific prevention aims to break the mechanism of pathogen transmission and includes several levels:
- Individual: timely isolation of patients, strict adherence to hygiene by caregivers (handwashing, washing the breast before feeding).
- Organizational: maintaining a strict sanitary and epidemiological regime in hospitals and childcare facilities, disinfection in the focus of infection.
- Socio-sanitary: health education work, regular medical examinations of mandated groups (e.g., kindergarten staff), wellness activities.
For close contacts (children in groups, food industry workers), medical observation is established for 7 days with a single bacteriological screening.
Mnemonic for invasive diarrhea pathogens: Shigella, Salmonella, Yersinia, Campylobacter, EIEC/EHEC.
Class and exam questions
At what age does primary enteroviral infection most frequently occur?
In 80% of people, primary infection occurs in childhood, up to 13 years of age.
What is the main symptom distinguishing the typical form of enterovirus infection?
The main criterion of the typical form is the presence of a characteristic vesicular rash.
What happens at the cellular level during invasive diarrhea?
The pathogen penetrates the intestinal wall and multiplies inside cells (enterocytes and macrophages), while released toxins destroy cell membranes, causing necrosis.
Does lasting immunity develop after overcoming the infection?
No, post-infection immunity is unstable and does not protect against disease recurrences.
What else to study on this topic
- Pathogenesis of hemorrhagic syndrome development in severe forms
- Features of the clinical course of viral meningitis in early-age children
- Differential diagnosis of invasive and secretory diarrheas
- Mechanisms of action of enterotoxins (Shiga toxin, verotoxins)
- Principles of therapy and rehydration in moderate forms of AII
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