This family includes two groups: Enteroviruses and Rhinoviruses.
Three antigenic types (1, 2, and 3) are determined based on outer capsid proteins.
PVR (human poliovirus receptor) is a cell surface protein that plays an important role in cell-mediated immune response. Virus progeny are released after lysis of the host cell.
Pathogenesis: Once it enters the human body, it multiplies in the epithelial and lymphoid tissues of the gastrointestinal tract. It causes a viraemia, during which it multiplies in cells of the reticuloendothelial system and reaches the brain and spinal cord, where it multiplies in neurons. It can also spread retrogradely to the CNS along nerve axons. It preferentially multiplies in the anterior horn cell motor neurons of the spinal cord. Lysis of cells during release of progeny virions causes loss of motor neurons and consequent flaccid paralysis.
[Quick question - What kind of paralysis is seen in UMN lesions?]
Clinical features: Poliovirus can cause four types of infections as follows.
Laboratory diagnosis of polio: Virus can be isolated from feces and throat early in the infection. Electron microscopy can demonstrate virus in samples. Cell culture shows rounding up of cells and eosinophilic, intranuclear inclusions. A rise in antibody titres shown by neutralization test and CFT can be used.
There are two types: Coxsackie A and Coxsackie B. Both groups cause different diseases.
Insulin-dependent diabetes mellitus has been correlated with Coxsackie B infections.
Clinical features: Several clinical syndromes are caused by Coxsackie viruses. Aseptic meningitis with fever, chills, headache, irritability, etc. is seen with both types (more with B). Encephalitis, flaccid polio-like paralysis, and Guillain Barre Syndrome (type A) can occur. Myopericarditis with cardiomegaly, friction rub, cardiac failure, and dyspnea can be seen.
Hand foot mouth disease (HFMD) : Seen in children. It starts with fever and sore throat, followed by blisters that later become painful ulcers on the hands, feet, legs, and buttocks. The rash involves the palms and feet. Seen in Coxsackie A.
Herpangina: Caused by Coxsackie A. Sore ulcers and blisters are seen on the posterior oropharynx, with fever, sore throat, odynophagia, and dysphagia. Differentiate from HFMD by the location of blisters.
Epidemic pleurodynia with chest muscle pain and spasms (type B) and epidemic hemorrhagic conjunctivitis are other diseases caused.
[Do you remember the other viral cause of hemorrhagic conjunctivitis?].
Laboratory diagnosis of Coxsackie virus infections: Diagnosis is made by isolation of virus in cell culture or suckling mice, PCR for viral RNA in CSF, and a rise in antibody titre by neutralization tests.
ECHO stands for enteric cytopathic human orphan virus. They are transmitted by the feco-oral route. There are 34 serotypes. They primarily infect the gastrointestinal tract.
They cause common cold, aseptic meningitis, encephalitis, gastroenteritis, hemorrhagic conjunctivitis, fever, and rash. Laboratory diagnosis is made by culture and antibody detection by neutralization tests.
All Enteroviruses discovered after 1969 are named numerically (e.g., Enterovirus 70 and so on). The specific diseases caused by them are as follows.
Rhinovirus is the most common cause of the common cold. It has more than 100 serotypes. It replicates preferentially at lower temperatures of 33 degrees C, which relates to the common cold (the nose is cooler than the rest of the body). It is readily killed by gastric acid.
ICAM 1 is the cell surface receptor for Rhinovirus.
Common cold presents as rhinorrhea, headache, and sore throat. Fever is typically absent unless there is a secondary bacterial infection like sinusitis or otitis media.
Laboratory diagnosis is made by isolation in tissue culture. Serological tests are not useful due to the occurrence of multiple serotypes.
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