THE JOURNAL OF INFECTIOUS DISEASES. VOL. 154, NO.3. SEPTEMBER 1986 © 1986 by The University of Chicago. All rights reserved. 0022-1899/86/5403-0001$01.00 The Role of Parvovirus B19 in Aplastic Crisis and Erythema Infectiosum (Fifth Disease) Terence Chorba, Peter Coccia, Robert C. Holman, Peter Tattersall, Larry J. Anderson, Jon Sudman, Neal S. Young, Elizabeth Kurczynski, Ulla M. Saarinen, Robyn Moir, Dale N. Lawrence, Janine M. Jason, and Bruce Evatt From the Division of Host Factors and the Division of Viral Diseases, Center for Infectious Diseases, and the Division of Field Services, Epidemiology Program Office.Centers for Disease Control, Public Health Service, U. S. Department of Health and Human Services, Atlanta, Georgia; Case Western Reserve University, and the Kaiser Foundation Hospital, Cleveland, Ohio; Yale University, New Haven, Connecticut; and the National Heart, Lung, and Blood Insitute, National Institutes of Health, Public Health Service, U. S. Department of Human Services, Bethesda, Maryland In 1984, simultaneous outbreaks of aplastic crisis and erythema infectiosum occurred in northeastern Ohio. Sera were analyzed from 26 patients with aplastic crisis: 24 had IgM specific for parvovirus B19, five had Bl9-like particles by electron microscopy, and 13 had DNA from B19; no sera from 33 controls had evidence of recent infection with B19 (P< .0001). DNA from B19was also detected in specimens of throat gargle and urine from two patients with aplastic crisis. Sera from 36 of 51 children with erythema infectio- sum had Bl9-specific IgM, compared with serum from one of 42 susceptible controls (P < .0001). DNA from B19 was detected in sera from only two of 51 patients who had erythema infectiosum. The secondary attack rates among susceptible contacts decreased with age (overall total, 49.6070). Differential rates of asymptomatic infection were observed among black (68.8070) and white (20.0070) household members (P = .003). These were the first identifiedsimultaneous outbreaks of aplastic crisis and erythema infectiosum. Their occurrence provided an opportunity to study the epidemiology and spectrum of B19infection with geographically and temporally matched comparison groups; our results support the hypothesis that infection with parvovirus causes these two clinical entities. An infectious cause for acquired pure red cell apla- sia (aplastic crisis) in patients with chronic hemo- lytic anemias has long been suspected because of community epidemics [1] and family clusters [2-6] of aplastic crises, and because aplastic episodes usu- Received for publication 6 January 1986, and in revised form 9 April 1986. This work was presented in part at the 26th annual meeting of the American Society of Hematology, held in Miami on 4-7 December 1984. The use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U. S. Department of Health and Human Services. This work was supported in part by grant AI-21118 from the National Institute of Allergy and Infectious Diseases (to P. T.). We thank Dr. B. Chukwumah and many other physicians and personnel of Case Western Reserve University, the Ohio State Health Department, the Cuyahoga County District Board of Health, and the Cleveland Health Department; T. Jones, J. Betros, S.Porterfield, A. Schwartz, J. Kelly, D. Williams, K. Coats, H. Hritz, and Drs. F. Silver, E. Danish, C. Krill, J. Kastelic, C. Rasch, J. Pecorak, D. Worthington, L. Sripada, B. Cameron, and V. D. Morledge for assistance in the epidemiological investigation; Dr. 383 ally occur only once in a lifetime [1]. Erythema in- fectiosum (EI) has also been thought to have a sin- gle infectious cause [7], but numerous attempts to isolate an agent from patients with naturally occur- ring EI have failed. In 1981, infection with human parvovirus B19 was first associated with aplastic crisis [1], and in 1983, infection with B19 or similar par- vovirus was associated with EI [8]. Numerous other case reports and studies have also associated recent B19 infection with aplastic crisis [1, 9-19] or EI [8, 18-23]. E. Palmer for electron microscopy; Dr. S. Cotmore for hybrid- ization studies; C. Tsou and Drs. H. Wulff and J. Stewart for serological analyses; J. Moore for erythropoiesis inhibition as- says; C. Ivey, R. Odum, and D. Kotlovker for data preparation and programming assistance; D. Donovan, M. Parvin, C. Beck, D. Arinson, J. Davis, and S. Price for specimen collection and management; A. Navin, L. Grabbe, D. Collier, and Drs. A. Friede and R. Gunn for critical review of this manuscript. Please address requests for reprints to Dr. Terence Chorba, Division of Host Factors, 1600 Clifton Road, 1-1407, Atlanta, Georgia 30333. at IDSA member on October 5, 2015 http://jid.oxfordjournals.org/ Downloaded from