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International Centre for Diarrhoeal Disease Research, Bangladesh

FacilityDhaka, Bangladesh
About: International Centre for Diarrhoeal Disease Research, Bangladesh is a facility organization based out in Dhaka, Bangladesh. It is known for research contribution in the topics: Population & Vibrio cholerae. The organization has 3103 authors who have published 5238 publications receiving 226880 citations. The organization is also known as: SEATO Cholera Research Laboratory & Bangladesh International Centre for Diarrhoeal Disease Research.


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Journal ArticleDOI
TL;DR: This study presents strong evidence for the first pandemicity in the history of V. parahaemolyticus and reports a novel toxRS-targeted PCR method that will be useful in epidemiological investigation of the cases associated with the current pandemic spread.
Abstract: Some strains of Vibrio parahaemolyticus, a marine bacterium, can cause gastroenteritis in humans through consumption of seafood. It was reported in the late 1960s that almost all clinical strains, but very few environmental strains, manifest Kanagawa phenomenon (KP), β-type hemolysis on Wagatsuma agar (8, 19). KP is caused by high-level production of thermostable direct hemolysin. Thermostable direct hemolysin is encoded by the tdh gene (13, 17), which was detected almost exclusively in clinical strains in an early study (11). The role of thermostable direct hemolysin in enterotoxigenicity was demonstrated by construction and examination of the tdh-deficient mutant of a KP-positive strain (10). Investigation of an outbreak in the Maldives in 1985 revealed that some clinical strains do not possess the tdh gene but carry the tdh-related hemolysin (trh) gene (14). The trh sequence was approximately 70% identical to the tdh sequence. There is much greater strain-to-strain divergence among trh sequences than among tdh sequences. The trh sequences in different strains, however, can be clustered into two groups represented by the trh1 and trh2 genes, which have 84% sequence identity (5). Strains possessing either the tdh gene, the trh gene, or both were shown to be strongly associated with gastroenteritis (5, 20). Surveillance for V. parahaemolyticus infection was initiated in January 1994 in Calcutta, India. A group of strains belonging to serovar O3:K6 and possessing the tdh gene but not the trh gene appeared suddenly in February 1996 and was shown to be responsible for the high incidence of V. parahaemolyticus infection since then in Calcutta (16). Serovar O3:K6 was not isolated before February 1996 in Calcutta. In addition, the O3:K6 strains isolated in Calcutta were shown to exhibit unique profiles in an arbitrarily primed PCR (AP-PCR) analysis (16). Strains belonging to the same group, i.e., O3:K6 strains possessing the tdh gene but not the trh gene and showing the unique AP-PCR profiles, were also detected among those isolated from travelers arriving in Japan from Southeast Asian countries from 1995 on (16). Thus, the Calcutta O3:K6 strains and the above strains from the travelers were considered to belong to a single clone (16). These results suggested that this unique clone, referred to below as a new O3:K6 clone, might have emerged recently and become prevalent not only in Calcutta, India, but also in other parts of the world. We examined this hypothesis, and we present evidence in this study for the first pandemicity in the history of V. parahaemolyticus. Clinical strains isolated over 22 years, starting from 1977, in a hospital in Bangladesh were available. The emergence of the new O3:K6 clone in 1996 but not earlier was demonstrated by examination of these strains. Next, we showed by AP-PCR analysis that the clinical strains of serovar O3:K6 isolated in six other countries, including the United States, from 1997 on belong to the same clone. We then developed a novel PCR method to identify the strains belonging to the new O3:K6 clone. We utilized the toxRS operon sequence to develop this PCR method. The toxR and toxS genes in the toxRS operon encode transmembrane proteins involved in the regulation of virulence-associated genes and are well conserved in the genus Vibrio (3, 7, 18; J. H. Rhee, S. E. Lee, S. Y. Kim, S. H. Shin, C. M. Kim, P. Y. Ryu, K. C. Leong, S. H. Choi, and S. S. Chung, Abstr. 98th Gen. Meet. Am. Soc. Microbiol., abstr. B-171, p. 84, 1998; V. Vuddhakul, T. Nakai, C. Matsumoto, T. Oh, T. Nishino, M. Nishibuchi, and J. Okuda, submitted for publication). We used the intraspecies variation of the toxRS sequence to develop a cluster-specific PCR method that allowed for confirmation of the clonality of the new O3:K6 strains. By using this PCR method in our investigation, we found emerging strains that were almost indistinguishable from the new O3:K6 clone, although the strains belonged to different serovars.

375 citations

Journal ArticleDOI
TL;DR: The global burden of shigella and ETEC diarrhoea according to age, sex, geography, and year from 1990 to 2016 is analyzed to assess the health burden of bacterial diarrhoeal pathogens globally.
Abstract: Summary Background Shigella and enterotoxigenic Escherichia coli (ETEC) are bacterial pathogens that are frequently associated with diarrhoeal disease, and are a significant cause of mortality and morbidity worldwide. The Global Burden of Diseases, Injuries, and Risk Factors study 2016 (GBD 2016) is a systematic, scientific effort to quantify the morbidity and mortality due to over 300 causes of death and disability. We aimed to analyse the global burden of shigella and ETEC diarrhoea according to age, sex, geography, and year from 1990 to 2016. Methods We modelled shigella and ETEC-related mortality using a Bayesian hierarchical modelling platform that evaluates a wide range of covariates and model types on the basis of vital registration and verbal autopsy data. We used a compartmental meta-regression tool to model the incidence of shigella and ETEC, which enforces an association between incidence, prevalence, and remission on the basis of scientific literature, population representative surveys, and health-care data. We calculated 95% uncertainty intervals (UIs) for the point estimates. Findings Shigella was the second leading cause of diarrhoeal mortality in 2016 among all ages, accounting for 212 438 deaths (95% UI 136 979–326 913) and about 13·2% (9·2–17·4) of all diarrhoea deaths. Shigella was responsible for 63 713 deaths (41 191–93 611) among children younger than 5 years and was frequently associated with diarrhoea across all adult age groups, increasing in elderly people, with broad geographical distribution. ETEC was the eighth leading cause of diarrhoea mortality in 2016 among all age groups, accounting for 51 186 deaths (26 757–83 064) and about 3·2% (1·8–4·7) of diarrhoea deaths. ETEC was responsible for about 4·2% (2·2–6·8) of diarrhoea deaths in children younger than 5 years. Interpretation The health burden of bacterial diarrhoeal pathogens is difficult to estimate. Despite existing prevention and treatment options, they remain a major cause of morbidity and mortality globally. Additional emphasis by public health officials is needed on a reduction in disease due to shigella and ETEC to reduce disease burden. Funding Bill & Melinda Gates Foundation.

375 citations

Journal ArticleDOI
TL;DR: Effective deployment of this filtration procedure in 65 villages of rural Bangladesh yielded a 48% reduction in cholera (P < 0.005) compared with the control.
Abstract: Based on results of ecological studies demonstrating that Vibrio cholerae, the etiological agent of epidemic cholera, is commensal to zooplankton, notably copepods, a simple filtration procedure was developed whereby zooplankton, most phytoplankton, and particulates >20 μm were removed from water before use. Effective deployment of this filtration procedure, from September 1999 through July 2002 in 65 villages of rural Bangladesh, of which the total population for the entire study comprised ≈133,000 individuals, yielded a 48% reduction in cholera (P < 0.005) compared with the control.

353 citations

Journal ArticleDOI
TL;DR: Sixteen interrelated SNP subtypes were defined by genotyping both extant and extinct strains of M. leprae from around the world and showed a strong geographical association that reflects the migration patterns of early humans and trade routes, with the Silk Road linking Europe to China having contributed to the spread of leprosy.
Abstract: Reductive evolution and massive pseudogene formation have shaped the 3.31-Mb genome of Mycobacterium leprae, an unculturable obligate pathogen that causes leprosy in humans. The complete genome sequence of M. leprae strain Br4923 from Brazil was obtained by conventional methods (6x coverage), and Illumina resequencing technology was used to obtain the sequences of strains Thai53 (38x coverage) and NHDP63 (46x coverage) from Thailand and the United States, respectively. Whole-genome comparisons with the previously sequenced TN strain from India revealed that the four strains share 99.995% sequence identity and differ only in 215 polymorphic sites, mainly SNPs, and by 5 pseudogenes. Sixteen interrelated SNP subtypes were defined by genotyping both extant and extinct strains of M. leprae from around the world. The 16 SNP subtypes showed a strong geographical association that reflects the migration patterns of early humans and trade routes, with the Silk Road linking Europe to China having contributed to the spread of leprosy.

349 citations


Authors

Showing all 3121 results

NameH-indexPapersCitations
Stanley Falkow13434962461
Myron M. Levine12378960865
Roger I. Glass11647449151
Robert F. Breiman10547343927
Harry B. Greenberg10043334941
Barbara J. Stoll10039042107
Andrew M. Prentice9955046628
Robert H. Gilman9690343750
Robert E. Black9220156887
Johan Ärnlöv9138690490
Juan Jesus Carrero8952266970
John D. Clemens8950628981
William A. Petri8550726906
Toshifumi Hibi8280828674
David A. Sack8043723320
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20235
202234
2021494
2020414
2019391
2018334