Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 8, Number 7—July 2002
Dispatch

First Outbreak of Dengue Hemorrhagic Fever, Bangladesh

Figures
Tables
Article Metrics
98
citations of this article
EID Journal Metrics on Scopus
Author affiliations: *ICDDR,B: Centre for Health and Population Research, Dhaka, Bangladesh; †Holy Family Hospital, Dhaka, Bangladesh; ‡The Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand;

Cite This Article

Abstract

During the first countrywide outbreak of dengue hemorrhagic fever in Bangladesh, we conducted surveillance for dengue at a hospital in Dhaka. Of 176 patients, primarily adults, found positive for dengue, 60.2% had dengue fever, 39.2% dengue hemorrhagic fever, and 0.6% dengue shock syndrome. The Dengue virus 3 serotype was detected in eight patients.

Dengue fever (DF) and dengue hemorrhagic fever (DHF) are caused by four antigenically distinct but related dengue virus (official name: Dengue virus [DENV]) serotypes transmitted primarily by Aedes aegypti (yellow fever mosquito). DHF, the severe form of the disease, is endemic and frequently intensifies into epidemics in Southeast Asia, resulting in frequent hospitalizations and deaths (1,2). Recently, dengue has emerged as a substantial global health problem with increased incidence in new countries and tropical areas (3,4). DF was documented in Bangladesh from the mid-1960s to the mid-1990s, but an outbreak of DHF has not been previously reported (5,6). During late June 2000, a 28-year-old patient was admitted to a hospital in Dhaka, Bangladesh, with hemorrhagic fever, ascites, pleural effusion, and thrombocytopenia. An enzyme-linked immunosorbent assay (ELISA) for anti-dengue antibodies confirmed the case as DHF (1). That summer, an outbreak of DF (>5,000 hospitalized cases reported) and DHF occurred in Dhaka and other major cities of Bangladesh (7).

The Study

We began surveillance for dengue among patients at a hospital in Dhaka during July 1–October 31, 2000. Clinical details of each patient were recorded on a standardized form; when indicated, chest radiographs and abdominal ultrasounds were done, in addition to hemoglobin, hematocrit, and total blood and platelet counts. Sera from all patients were tested by ELISA for anti-dengue and anti-Japanese encephalitis viral immunoglobulin (Ig)M and IgG (8). Paired sera were tested when available. Sera from 30 patients with fever of <6 days’ duration were also tested for serotype-specific dengue viral RNA by reverse transcription-polymerase chain reaction (RT-PCR) (9). Samples having >40 units of IgM or IgG antibodies were considered positive for dengue infection. A ration of IgM and IgG <1.8 defined a secondary infection and >1.8 a primary infection (8). DF, DHF, and dengue shock syndrome (DSS) were defined according to World Health Organization (WHO) criteria (1) and confirmed by positive IgM or IgG ELISA or RT-PCR. Statistical analysis was done by chi-square test.

Figure

Thumbnail of Age distribution of dengue cases, Bangladesh, 2000

Figure. Age distribution of dengue cases, Bangladesh, 2000

Of 336 suspected dengue patients, sera were available for 240 patients; 176 (73.3%) had confirmed dengue infection (168 by ELISA; 2 by RT-PCR; and 6 by both tests). RT-PCR detected dengue virus 3 serotype (DENV-3) in 8 (26.6%) of 30 patients tested. Both acute- and convalescent-phase sera were positive in 18 of 30 paired specimens available, and seroconversion occurred in 2 of the remaining 12 sera. All sera were negative for antibodies to Japanese encephalitis virus. Thirty-one (18%) cases were in children (<18 years of age). The highest proportion of cases occurred in persons 18–33 years of age (Figure). DF occurred most commonly (60.2%), followed by DHF (39.2%), and DSS (0.6%). Most (80%) patients reported to the hospital after 5 days of fever. Spontaneous bleeding occurred in 91% of patients with DHF, compared with 25% patients with DF (p<0.01). Frequent clinical features were fever (100%), headache (91%), myalgia/arthralgia (85%), vomiting (64%), macular rash (55%), bleeding (46%) (including melena [20%] and bleeding gums [11.6%]), thrombocytopenia (<100,000/mL, 56.7%), pleural effusion (12%), ascites (9%), and hepatomegaly (7.5%). Secondary infection was detected in 71% of 174 ELISA-positive cases, more commonly in patients with DHF than with DF (relative risk 2.14, p=0.002) (Table).

All but two adult patients recovered (case-fatality rate 1.14%). One DF patient died with severe hematemesis and melena; another DSS patient died within 2 hours of hospitalization.

Conclusions

Dengue causes more illness and death than any other arboviral infection in the world (4). This first outbreak highlights the geographic expansion of DHF in Bangladesh, where classic DF caused by multiple serotypes had been previously reported (5,6). The DHF outbreak started in late June 2000, peaked in September (during the rainy season), and subsided in the dry winter season in December 2000. While dengue affected all age groups, adults predominated in this hospital-monitored study. In Singapore, India, Malaysia, and Brazil, where dengue has been epidemic for several years, the mean age of dengue infection is increasing and adults are frequently infected, indicating an epidemiologic change in dengue infection in those locations (1,10).

The precise magnitude of this countrywide outbreak is unknown; 5,575 hospitalized dengue cases were reported to the Ministry of Health in Bangladesh, with a case-fatality rate of 1.61% through mid-November 2000 (6). Most patients had DF, 25% with bleeding manifestations (a severe form of the illness) (1,4). WHO classification of dengue diseases is often not feasible in many countries because of lack of trained health professionals, adequate laboratories, and radiologic support. The facilities to detect DHF by using hematocrit (capillary method) and plasma leakage signs (chest radiograph or ultrasound) are not readily available in many tropical countries. Successful treatment of dengue depends on symptom recognition and careful fluid management (1). Thus, a simple classification scheme of dengue diseases based on symptoms and signs is needed to improve case management and reduce deaths.

DHF is believed to occur as a result of antibody-dependent enhancement of heterotypic-secondary dengue infections (1,4,11). Our findings support the role of sequential infection in the development of DHF. However, occurrence of DHF in some patients with primary infection suggests additional host and virologic factors.

In our study, DSS was a rare event, resulting in a lower case-fatality rate for dengue than reported elsewhere (7), likely representing hospitalization of less severe cases. We have insufficient data to comment on the virulence of the outbreak strain. High numbers of Ae. aegypti were identified throughout the city (Y. Wagatsuma, ICDDR,B; pers. comm.). Insecticide spraying, public health education (including community source reduction), and perhaps most importantly, the onset of the dry winter season may have contributed to ending this dengue outbreak in 2000.

Therapeutic strategies proposed by WHO have been widely circulated by the Bangladesh government, and physicians continue to gain experience in proper management of dengue. Ongoing surveillance, vector surveys, and epidemiologic studies to identify risk factors will provide key information for controlling dengue. Ultimately, a safe and effective vaccine will be needed to address this emerging problem in Bangladesh and elsewhere.

Dr. Mahbubur Rahman is a physician, clinical microbiologist, and molecular biologist in Laboratory Sciences Division, ICDDR,B: Centre for Health and Population Research, Bangladesh. His professional interests include infectious diseases, epidemiology, diagnosis, and management of emerging infectious diseases and antimicrobial resistance.

Top

Acknowledgments

We thank the Dengue Team of ICDDR, B and Timothy Endy and Duane Gubler for their assistance and guidance.

The work was supported by the U. S. Agency for International Development, Washington, DC, USA.

Top

References

  1. World Health Organization. Dengue haemorrhagic fever: diagnosis, treatment, prevention and control (2nd edition). Geneva: World Health Organization; 1997.
  2. Anuradha  S, Singh  NP, Rizvi  SN, Agarwal  SK, Gur  R, Mathur  MD. The 1996 outbreak of dengue hemorrhagic fever in Delhi, India. Southeast Asian J Trop Med Public Health. 1998;29:5036.PubMedGoogle Scholar
  3. Rigau-Perez  JG, Gubler  DJ, Vorndam  AV, Clark  GG. Dengue: literature review and case study of travelers from the United States, 1986–1994. J Travel Med. 1997;4:6571. DOIPubMedGoogle Scholar
  4. Gubler  DJ. The global pandemic of dengue/dengue haemorrhagic fever: current status and prospects for the future. Ann Acad Med Singapore. 1998;27:22734.PubMedGoogle Scholar
  5. Russell  PK, Buescher  EL, McCown  JM, Ordonez  J. Recovery of dengue viruses from patients during epidemics in Puerto Rico and East Pakistan. Am J Trop Med Hyg. 1966;15:5739.PubMedGoogle Scholar
  6. Amin  AAA, Hussain  AMZ, Murshed  M, Chowdhury  IA, Mannan  S, Chowdhuri  SA, Sero-diagnosis of dengue infections by haemagglutination inhibition test (HI) in suspected cases in Chittagong, Bangladesh. WHO Dengue Bull. 1999;23:348.
  7. Yunus  EB. Dengue outbreak 2000: the emerged issues. Bangladesh Med J (Khulna). 2000;33:467.
  8. Innis  BL, Nisalak  A, Nimmannitya  S, Kusalerdchariya  S, Chongswasdi  V, Suntayakorn  S, An enzyme-linked immunosorbent assay to characterize dengue infections where dengue and Japanese encephalitis co-circulate. Am J Trop Med Hyg. 1989;40:41827.PubMedGoogle Scholar
  9. Lanciotti  RS, Calisher  CH, Gubler  DJ, Chang  GJ, Vorndam  AV. Rapid detection and typing of dengue viruses from clinical samples by using reverse transcriptase-polymerase chain reaction. J Clin Microbiol. 1992;30:54551.PubMedGoogle Scholar
  10. Goh  KT. Changing epidemiology of dengue in Singapore. Lancet. 1995;346:1098. DOIPubMedGoogle Scholar
  11. Halsted  SB. Observations related to pathogenesis of dengue haemorrhagic fever. VI. Hypothesis and discussion. Yale J Biol Med. 1970;42:35060.PubMedGoogle Scholar

Top

Figure
Table

Top

Cite This Article

DOI: 10.3201/eid0807.010398

Table of Contents – Volume 8, Number 7—July 2002

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.

Top

Comments

Please use the form below to submit correspondence to the authors or contact them at the following address:

Mahbubur Rahman, Laboratory Sciences Division, ICDDR,B: Centre for Health and Population Research, GPO Box 128, Dhaka 1000, Bangladesh; fax: 880-2-8812529;

Send To

10000 character(s) remaining.

Top

Page created: July 16, 2010
Page updated: July 16, 2010
Page reviewed: July 16, 2010
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
file_external