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Sherwin Kabins, MD; Robert Keller, PhD; Ricki Peitchel, RT; Mir Akif Ali, MD

Arch Intern Med. 1976;136(1):100-101.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The herpes viruses of man, ie, Epstein-Barr virus, herpes simplex, varicella-zoster, and cytomegalovirus (CMV), have been incriminated as causes of acute idiopathic polyneuritis (Guillain-Barré syndrome).^1-4 The evidence for the causative role of CMV has been based on rising or elevated titers of complement-fixing antibodies, isolation of virus from urine or saliva, or both.^4-9 However, CMV has been recovered from urine and saliva of apparently healthy individuals.¹⁰ In addition, moderately elevated complement-fixation (CF) antibody titers can persist for years following a subclinical primary CMV infection. Therefore, previous evidence that associated CMV to acute idiopathic polyneuritis must be considered with some reservation.

We report a patient with acute idiopathic polyneuritis from whom CMV was isolated from the peripheral blood buffy coat (PBBC) shortly after the onset of neurologic symptoms. In addition, specific CMV-IgM antibodies were detected in the serum. Concomitant with the cessation of viremia, CMV first was recovered . . . [Full Text PDF of this Article]

Author Affiliations
From the departments of medicine and microbiology, Michael Reese Hospital and Medical Center, and the Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago.

Footnotes
Received for publication June 4, 1975; accepted July 15.

Reprint requests to Division of Infectious Diseases, Michael Reese Medical Center, 29th St and Ellis Ave, Chicago, IL 60616 (Dr Kabins).

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