Coxsackie virus

Role in the structure of infections and GI involvement

Enteropathogenic viruses dominate the global structure of infectious diarrheas. Their role decreases with age, yet remains clinically significant. Coxsackie viruses belong to the viral etiologic group of acute intestinal infections (AII), alongside rotaviruses, noroviruses, and adenoviruses.

In addition to classic intestinal syndrome, the infection frequently causes nonspecific febrile states in young children. A key feature of Coxsackie viruses is their tropism for glandular tissue. In pediatric gastroenterology, they are recognized as a significant infectious factor in the development of acute pancreatitis (this same etiological group includes mumps virus, staphylococci, and Shigella).

Oropharyngeal lesions: herpetic angina (herpangina)

Group A Coxsackie viruses are specific causative agents of herpangina, which is most typical for young children (under 3 years of age).

• Clinical presentation: characteristic small vesicles appear on the tonsils and palatine arches. The local process often co-occurs with herpetic stomatitis. The eruptions resolve without a trace within 3–4 days.
• Laboratory diagnostics: a complete blood count (CBC) shows a typical "viral shift" — mild leukopenia accompanied by relative lymphocytosis.
• Differential diagnosis: herpangina must be distinguished from other acute tonsillopharyngitis cases. For instance, common ARVI features prominent catarrhal syndrome (rhinitis, cough), infectious mononucleosis presents with systemic involvement (lymphadenopathy, hepatosplenomegaly), and oropharyngeal candidiasis features white curdy patches.

Exanthem and neurological complications

Infection caused by Coxsackie viruses is frequently accompanied by skin rashes and central nervous system involvement.

1. Enteroviral exanthem: the rash is characterized by marked polymorphism. Consequently, the clinical picture must be carefully differentiated from scarlet fever-like exanthems, as well as classic childhood infections — measles and rubella.
2. Aseptic meningitis: Group B Coxsackie viruses (alongside echoviruses) account for 80–90% of enteroviral aseptic meningitis cases in children. The disease exhibits distinct summer-autumn seasonality. Meningeal symptoms may develop in parallel with oropharyngeal lesions, and the etiology is confirmed in the presence of an epidemiological outbreak.

Role in the development of juvenile dermatomyositis

Coxsackie viruses (types A and B) and other picornaviruses are considered major infectious triggers of juvenile dermatomyositis (JDM), a severe diffuse connective tissue disease. Specifically, an association between dermatomyositis and the Coxsackie A9 serotype has been proven.

The pathology manifests when the virus acts on a genetically predisposed organism (carrying histocompatibility antigens HLA-B8, HLA-B14, HLA-DR3). The pathogenesis of virus-induced muscle injury involves three parallel mechanisms:

• Direct cytotoxic effect of the virus on myofibrils.
• Immune attack by T-lymphocytes and macrophages against viral antigens fixed on the surface of muscle fibers.
• Antigenic mimicry: due to structural homology between viral proteins and host tissues, autoantibodies are produced that begin to attack the macroorganism's own cells.

In addition to JDM, modern medicine actively discusses the triggering role of enteroviruses in the development of type 1 diabetes mellitus, encephalitis, and Guillain-Barré syndrome.

Class and exam questions

What else to study on this topic

• Differential diagnosis of scarlet fever-like exanthems in children.
• Pathogenesis and morphological features of juvenile dermatomyositis.
• Etiological classification of acute intestinal infections.
• Clinical and laboratory diagnostics of viral and bacterial tonsillopharyngitis.
• Causes and classification of acute pancreatitis in pediatrics.

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