Enteroviral infection

Graves, P.M., etal. Prospective study of enteroviral infections and development of beta-cell autoimmunity. Diabetes autoimmunity study in the young (DAISY), Diabetes Res. Clin. 

Differential Diagnosis With single cases, rather than clearly epidemic cases, the illness could be confused with Guillain-Barre syndrome, myasthenia gravis, or tick paralysis. Other possible considerations may include enteroviral infections, as well as nerve agent and atropine poisoning. 

Chow, L.H., Beisel, K.W., and McManus, B.M. (1992). Enteroviral infection of mice with severe combined immunodeficiency. Evidence for direct viral pathogenesis of myocardial injury. Lab Invest 66, 24-31. 

Enteroviral Infection, especially hand, foot, and mouth disease... 

Rotbart HA. Enteroviral infections of the central nervous system. Clin Infect Dis. 1995 20(4) 971-981. 

Picornavimses are small, nonenveloped RNA vimses. Members of this family include rhino- and enteroviruses, which are responsible for a variety of human diseases (viral respiratory infection, viral meningitis, myocarditis, pericarditis, encephalitis, chronic meningoencephalitis, herpangina, otitis media, neonatal enteroviral disease, and acute exacerbations of asthma). 

There are important differences between mice and men and between enteroviral paralytic illness and rhinoviral upper respiratory tract infections. 

Hamilton MS, Jackson MA, Abel. Clinical utility of polymerase chain reaction testing for enteroviral meningitis, Pediatr Infect Dis J 1999 18 533-8. 

Marshall GS, Hauck MA, Buck G, Rabalais GP. Potential cost savings through rapid diagnosis of enteroviral meningitis. Pediatr Infect Dis f 1997 16 1086-7. 

Glimaker M. Enteroviral meningitis Diagnostic methods and aspects on the distinction from bacterial meningitis. Scand J Infect Dis Suppl 1992 85 1-64. 

Sawyer MH, Holland D, Aintablian N, et al. Diagnosis of enteroviral central nervous system infection by polymerase chain reaction during a large community outbreak. Pediatr Infect Dis J 1994 13 177-182. 

The feature common to the cytotoxic effects brought on by nonreplicating influenza virus, poxvirus, and defective-interfering vesicular stomatitis virus is the high multiplicity of infection required. This has led to the assumption that the toxic effect is caused by one or more components of the parental input virion, most likely protein in origin. However, Cordell-Stewart and Taylor (1971, 1973) have provided evidence that the double-stranded viral RNA isolated from cells infected with bovine enterovirus causes a rapid cytopathic effect as determined by trypan-blue uptake or Cr release from affected Ehrlich ascites tumor cells or L1210 cells toxic effects are reduced or do not occur in cells exposed to single-stranded or heat-denatured double-stranded viral RNA and the toxic effect of bovine enteroviral double-stranded RNA is not abolished by inhibitors of protein synthesis such as puromycin or cycloheximide. 

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