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Am. J. Trop. Med. Hyg., 74(6), 2006, pp. 1067-1073
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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DIARRHEAL EPIDEMICS IN DHAKA, BANGLADESH, DURING THREE CONSECUTIVE FLOODS: 1988, 1998, AND 2004

BRIAN S. SCHWARTZ*, JASON B. HARRIS, ASHRAFUL I. KHAN, REGINA C. LAROCQUE, DAVID A. SACK, MOHAMMAD A. MALEK, ABU S.G. FARUQUE, FIRDAUSI QADRI, STEPHEN B. CALDERWOOD, STEPHEN P. LUBY, AND EDWARD T. RYAN
Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts; Department of Pediatrics, Harvard Medical School, Boston, Massachusetts; ICDDR,B: Centre for Health and Population Research, Dhaka, Bangladesh; Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts; Department of Medicine, Harvard Medical School, Boston, Massachusetts; Department of Immunology and Infectious Disease, Harvard School of Public Health, Boston, Massachusetts

We examined demographic, microbiologic, and clinical data from patients presenting during 1988, 1998, and 2004 flood-associated diarrheal epidemics at a diarrhea treatment hospital in Dhaka, Bangladesh. Compared with non-flood periods, individuals presenting during flood-associated epidemics were older, more severely dehydrated, and of lower socioeconomic status. During flood-associated epidemics, Vibrio cholerae was the most commonly identified cause of diarrhea, and the only diarrheal pathogen whose incidence proportionally increased in each epidemic compared with seasonally matched periods. Rotavirus was the second most frequently identified flood-associated pathogen, although the proportion of cases caused by rotavirus infection decreased during floods compared with matched periods. Other causes of diarrhea did not proportionally change, although more patients per day presented with enterotoxigenic Escherichia coli, Shigella, and Salmonella species–associated diarrhea during floods compared with matched periods. Our findings suggest that cholera is the predominant cause of flood-associated diarrheal epidemics in Dhaka, but that other organisms spread by the fecal-oral route also contribute.

Received November 5, 2005. Accepted for publication February 13, 2006.

Financial support: This work was supported by funding support from the ICDDR,B: Centre for Health and Population Research and NIH Grants K01-TW07144 (R.C.L.), U01-AI58935 (S.B.C.), and AI40725 (E.T.R.). J. H. is an NICHD fellow of the Pediatric Scientist Development Program (NICHD Grant K12-HD00850).

* Address correspondence to Brian S. Schwartz, UCSF–Mt. Zion Hospital, Box 1945, Room 532W, 1600 Divisadero Street, San Francisco, CA 94115. E-mail: bschwartz{at}medicine.ucsf.edu

Authors’ addresses: Brian Schwartz, UCSF–Mt. Zion Hospital, Box 1945, Room 532W, 1600 Divisadero Street, San Francisco, CA 94115, E-mail: bschwartz{at}medicine.ucsf.edu. Jason Harris, Regina LaRocque, Stephen Calderwood, and Edward Ryan, Division of Infectious Diseases, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, E-mail: jbharris{at}partner.org, rclarocque{at}partners.org, scalderwood{at}partner.org, etryan{at}partners.org. Ashraful Khan, David Sack, Mohammad Malek, Abu Faruque, Firdausi Qadri, and Stephen Luby, International Centre for Diarrhoeal Disease Research (ICDDRB), GPO Box 128, Mohakhali, Dhaka 1000, Bangladesh, E-mail: ashrafk{at}icddrb.org; dsack{at}icddrb.org, malekd05{at}yahoo.com, gfaruque{at}icddrb.org, sluby{at}icddrb.org.

Reprint requests: Brian Schwartz, UCSF–Mt. Zion Hospital, Box 1945, Room 532W, 1600 Divisadero Street, San Francisco, CA 94115, E-mail: bschwartz{at}medicine.ucsf.edu.




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