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T Ramamurthy

Publications and source records attributed to T Ramamurthy.

At least 37 records · Page 2Linked to original sources

Shigellosis : challenges & management issues.

Infectious diseases kill about 11 million children each year while acute diarrhoeal diseases account for 3.1 million deaths in children under 5 yr of age, of which 6,00,000 deaths annually are contributed by shigellosis alone. Shigellosis, also known as acute bacillary dysentery, is characterized by the passage of loose stools mixed with blood and mucus and accompanied by fever, abdominal cramps and tenesmus. It may be associated with a number of complications of which haemolytic uraemic syndrome is the most serious. Shigellosis is caused by Shigella spp. which can be subdivided into four serogroups namely S.sonnei, S.boydii, S.flexneri and S.dysenteriae. Organisms as low as 10-100 in number can cause the disease. Shigellosis can occur in sporadic, epidemic and pandemic forms. Epidemics have been reported from Central American countries, Bangladesh, Sri Lanka, Maldives, Nepal, Bhutan, Myanmar and from the Indian subcontinent, Vellore, eastern India and Andaman and Nicobar islands. Plasmid profile of shigellae in Kolkata has shown a correlation between presence of smaller plasmids and shigellae serotypes- indicating epidemiological changes of the species. Diagnosis of shigellosis is essentially clinical. Laboratory diagnosis includes stool culture and polymerase chain reaction (PCR). Treatment includes use of an effective antibiotic, rehydration therapy (if there is dehydration) and appropriate feeding during and after an episode of shigellosis. Hand-washing is the single most important strategy for prevention of transmission of shigellosis from person to person. A safe and effective vaccine should be developed against the more important circulating strains i.e., S. dysenteriae type 1 and S. flexneri 2a.

Diagnosis, Differential↗

Environmental isolates of Citrobacter braakii that agglutinate with Escherichia coli O157 antiserum but do not possess the genes responsible for the biosynthesis of O157 somatic antigen.

While searching for Escherichia coli O157 in the aquatic environment of Calcutta using an immunodetection procedure, we fortuitously detected five strains of Citrobacter braakii, which cross-reacted with the commercially available O157 polyvalent antiserum. The five C. braakii isolates gave positive results when a sensitive dot-ELISA was performed with E. coli O157 monoclonal antibody. Further, the O157 monoclonal antibody recognized the bands of proteinase K treated whole cells of lipopolysaccharide of all the C. braakii isolates. Apart from weak reactions with two or three of the DNA probes, all the C. braakii strains did not hybridize with the other probes spanning the minimum region required for O157 O-antigen biosynthesis. These strains did not possess any of the virulence genes that are commonly found in the Shiga toxin-producing E. coli (STEC) specially the serotype O157: H7. Therefore, it appears that the serological cross-reaction between C. braakii and E. coli O157 antiserum is based on structural mimicry between the O-polysaccharide of C. braakii and E. coli O157.

Agglutination↗

Association of cytolethal distending toxin locus cdtB with enteropathogenic Escherichia coli isolated from patients with acute diarrhea in Calcutta, India.

Among Escherichia coli strains isolated from stool specimens from patients with acute diarrhea, 1.4% were found to harbor cdtB by use of enrichment cytolethal distending toxin (CDT) PCR. These isolates were identified as being enteropathogenic E. coli (EPEC). In a retrospective study using a probe hybridization assay, 6 of 138 EPEC strains were found to harbor the cdtB locus. cdtB-positive isolates mostly belong to the O86a and O127a serogroups, with the former being associated with higher expression of CDT. Pulsed-field gel electrophoresis profiles showed that the EPEC strains harboring cdtB strains are genetically diverse.

Acute Disease↗

Reemergence of epidemic Vibrio cholerae O139, Bangladesh.

During March and April 2002, a resurgence of Vibrio cholerae O139 occurred in Dhaka and adjoining areas of Bangladesh with an estimated 30,000 cases of cholera. Patients infected with O139 strains were much older than those infected with O1 strains (p<0.001). The reemerged O139 strains belong to a single ribotype corresponding to one of two ribotypes that caused the initial O139 outbreak in 1993. Unlike the strains of 1993, the recent strains are susceptible to trimethoprim, sulphamethoxazole, and streptomycin but resistant to nalidixic acid. The new O139 strains carry a copy of the Calcutta type CTX(Calc) prophage in addition to the CTX(ET) prophage carried by the previous strains. Thus, the O139 strains continue to evolve, and the adult population continues to be more susceptible to O139 cholera, which suggests a lack of adequate immunity against this serogroup. These findings emphasize the need for continuous monitoring of the new epidemic strains.

Adolescent↗

Azithromycin in the treatment of cholera in children.

AIM: To evaluate the efficacy of azithromycin in the treatment of cholera in children. METHODS: A double-blind, randomized, controlled clinical trial on 80 children with acute watery diarrhoea and moderate to severe dehydration compared the efficacy of azithromycin and erythromycin in treating cholera. Data were analysed for 56 patients who were stool culture positive for Vibrio cholerae. In conjunction with rehydration therapy, 29 patients received azithromycin and 27 patients received erythromycin. Patients in the two treatment groups had comparable clinical and blood biochemical characteristics on admission. RESULTS: Patients who received azithromycin had significantly less stool output, shorter duration of diarrhoea and lower fluid intake compared with patients who received erythromycin. CONCLUSION: Azithromycin appears to be superior to erythromycin for treating cholera in children.

Anti-Bacterial Agents↗

Shiga toxin producing Escherichia coli infection: current progress & future challenges.

Shiga toxin producing Escherichia coli (STEC) is a newly emerged pathogen that has been the focus of immense international research effort driven by its recognition as a major cause of large scale epidemics and thousands of sporadic cases of gastrointestinal illness. It produces a severe bloody diarrhoea that is clinically distinct from other types of diarrhoeal diseases caused by other enteric pathogens. One of the most important areas of current exploration concerns how STEC enters our food chain, an investigational avenue that begins with the ecology of STEC in animals and in the environment. A variety of foods have been identified as vehicles of STEC-associated illness and this makes the organism one of the most serious threats to the food industry in recent years. The pathogenesis of STEC is multifactorial and involves several levels of interaction between the bacterium and the host. STEC strains carry a set of virulence genes that encode the factors for attachment to host cells, elaboration of effective molecules and production of two different types of Shiga toxins. These genes are found in the locus of enterocyte effacement (LEE), lamboid phages, and a large virulence associated plasmid. The publication of the complete genome sequence of Esch. coli O157:H7 chromosome offers a unique resource that will help to identify additional virulence genes, to develop better methods of strain detection and in the understanding of the evolution of Esch. coli through comparison with the genome of the non-pathogenic laboratory strain Esch. coli K-12. These research efforts in turn, should lead to development of new potent and cost effective anti-Stx therapies or vaccines and thereby major improvement in human health world-wide.

Animals↗

Incidence and molecular analysis of Vibrio cholerae associated with cholera outbreak subsequent to the super cyclone in Orissa, India.

An epidemiological study was carried out to find out the aetiological agent for diarrhoeal disorders in the cyclone and flood affected areas of Orissa, India. Rectal swabs collected from 107 hospitalized diarrhoea patients were bacteriologically analysed to isolate and identify the various enteropathogens. Detection of toxic genes among E. coli and V. cholerae was carried out by polymerase chain reaction (PCR) assay. Of the 107 rectal swabs analysed, 72.3% were positive for V. cholerae O1 Ogawa, 7.2% for V. cholerae O139, 1.2% for E. coli (EAggEC) and 1.2% for Shigella flexneri type 6. Using multiplex PCR assay it was found that all V. cholerae isolates were ctxA positive and El Tor biotype. Strains of V. cholerae O1 were observed to be resistant to nalidixic acid, furazolidone, streptomycin, co-trimoxazole and ampicillin. Except for nalidixic acid, the resistance pattern for O139 was identical to that of O1 strains. Representative strains of V. cholerae were further characterized by randomly amplified polymorphic DNA (RAPD) analysis and ribotyping. Both O1 and O139 V. cholerae strains exhibited the R3 pattern of ribotype and belonged to a similar pattern of RAPD compared with that of Calcutta strains. Early bacteriological and epidemiological investigations have revealed the dominance of V. cholerae O1 among the hospitalized patients in cyclone affected areas of Orissa. Drinking water scarcity and poor sanitation were thought to be responsible for these diarrhoeal outbreaks. Timely reporting and implementation of appropriate control measures could contain a vital epidemic in this area.

Cholera↗

Preferential association of the heat-stable enterotoxin gene (stn) with environmental strains of Vibrio cholerae belonging to the O14 serogroup.

Toxigenic Vibrio cholerae O1 and O139 serogroups have the capacity of causing epidemic and pandemic cholera but are infrequently found in the environment. The other serogroups are abundant in aquatic environments but do not possess the virulence genes necessary for causing the disease. Of the 559 environmental strains of V. cholerae, collected during different periods from environmental samples in Calcutta, 9 (1.6%) harboured the heat-stable enterotoxin gene (stn). Six of the 9 strains belonged to the O14 serogroup. Thus, V. cholerae strains carrying the stn gene revealed preferential association with the O14 serogroup. Three of the six strains harboured the tcpA gene of the E1 Tor type, which is an unusual feature among environmental V. cholerae strains. A strain that possessed the E1 Tor type tcpA also had the CTX prophage. Pulsed field gel electrophoresis (PFGE) revealed that the stn gene positive O14 strains of V. cholerae were not clonal.

Animals↗

Antibiotic resistance, virulence gene, and molecular profiles of Shiga toxin-producing Escherichia coli isolates from diverse sources in Calcutta, India.

Antibiotic resistance, virulence gene, and molecular profiles of Shiga toxin-producing Escherichia coli (STEC) non-O157 strains isolated from human stool samples, cow stool samples, and beef samples over a period of 2 years in Calcutta, India, were determined. Resistance to one or more antibiotics was observed in 49.2% of the STEC strains, with some of the strains exhibiting multidrug resistance. The dominant combinations of virulence genes present in the strains studied were stx(1) and stx(2) (44.5% of strains) and stx(1), stx(2), and hlyA (enterohemorrhagic E. coli hemolysin gene) (19% of strains). Only 6.4% of the STEC strains harbored eae. The diversity of STEC strains from various sources was assessed by random amplification of polymorphic DNA (RAPD). STEC strains that gave identical or nearly similar DNA fingerprints in RAPD-PCR and had similar virulence genotypes were further characterized by pulsed-field gel electrophoresis (PFGE). Identical RAPD and PFGE profiles were observed in four sets of strains, with each set comprising two strains. There was no match in the RAPD and PFGE profiles between strains of STEC isolated from cows and those isolated from humans. It appears that the clones present in bovine sources are not transmitted to humans in the Calcutta setting although these strains showed evolutionary relatedness. Maybe for this reason, STEC has still not become a major problem in India.

Animals↗

Escalating association of Vibrio cholerae O139 with cholera outbreaks in India.

Between December 1999 and December 2000, teams from the National Institute of Cholera and Enteric Diseases, Calcutta, India, examined eight outbreaks of cholera, which occurred in different parts of the country distant from each other. In two of these outbreaks each, only V. cholerae O1 biotype ElTor or V. cholerae O139 could be isolated, while in the remaining four outbreaks, both O1 and O139 were isolated. The interesting feature is the escalating association of V. cholerae O139 with outbreaks of cholera; two of the most recent outbreaks, one in Calcutta and one in Orissa, were caused exclusively by O139. The O139 strains from the six different outbreaks were genotypically closely related. These trends indicate a shift in the outbreak propensity of V. cholerae O139.

Bacterial Typing Techniques↗

Decreasing trend in the occurrence of Salmonella enterica serotype Typhi amongst hospitalised children in Kolkata, India during 1990-2000.

In a prospective hospital based surveillance, 1454 children clinically diagnosed as typhoid fever were enrolled during the period between 1990 to 2000. Of them 336 (23.1%) children were positive for Salmonella enterica serotype Typhi by blood culture. A declining trend of hospitalization and identification of the pathogen was observed from 1992 to 2000 as compared to 1990-1991. A declining trend of resistance to the commonly used anti-typhoid drugs was seen in the S. enterica serotype Typhi isolates. Recently in 2000, nine strains were detected as ciprofloxacin resistant. Misuse and overuse of ciprofloxacin for the treatment of typhoid fever influenced the development of ciprofloxacin resistant strains of S. enterica serotype Typhi in and around Kolkata.

Child↗

A localised outbreak of Vibrio cholerae O139 in Kolkata, West Bengal.

BACKGROUND & OBJECTIVES: An explosive outbreak of diarrhoeal disease which occurred in the Baishnabghata, Patuli area of Kolkata Municipal Corporation during September 28 to October 12, 2000, was investigated by a team from the National Institute of Cholera and Enteric Diseases, Kolkata, to identify the causative agent and determine the antimicrobial susceptibility pattern. METHODS: Clinical and epidemiological data were collected from domiciliary cases and also from patients attending two medical camps that had been set up for the purpose. Stool and water samples were collected for isolation of diarrhoeagenic pathogens. RESULTS: A total of 710 cases of diarrhoea occurred with an attack rate of 7.1 per cent; majority were adults. All 6 faecal samples and 2 water samples collected, were positive for Vibrio cholerae O139. The strains were uniformly (100%) susceptible to the commonly used drugs for cholera such as tetracycline, norfloxacin, ciprofloxacin, co-trimoxazole and nalidixic acid but resistant (100%) to furazolidone and ampicillin. INTERPRETATION & CONCLUSION: This is the first localised outbreak of V. cholerae O139 in Kolkata since the devastating epidemic in 1992. Extensive chlorination of all water sources resulted in a dramatic decline of the outbreak. The appearance of resistance in V. cholerae O139 to furazolidone is a matter of great concern since this drug is used for the treatment of cholera in children and pregnant women.

Cholera↗

Comparison of antibiogram, virulence genes, ribotypes and DNA fingerprints of Vibrio cholerae of matching serogroups isolated from hospitalised diarrhoea cases and from the environment during 1997-1998 in Calcutta, India.

This study identified 17 matching serogroups of Vibrio cholerae belonging to serogroups other than O1 and O139 isolated from human cases and from the environment during a concurrent clinical and environmental study conducted in Calcutta, a cholera endemic area. Isolates within these matching serogroups were compared by various phenotypic and genotypic traits to determine if the environment was the source of the organisms associated with the disease. Clinical strains of V. cholerae were resistant to a greater number of drugs and exhibited multi-drug resistance compared with their environmental counterparts. Except for the presence of the genes for the El Tor haemolysin and the regulatory element ToxR in most of the strains of V. cholerae examined, non-O1, non-O139 V. cholerae strains lacked most of the other known virulence traits associated with toxigenic V. cholerae O1 or O139. Restriction fragment-length polymorphism of virulence-associated genes, ribotypes and DNA fingerprints of strains of matched serogroups showed considerable diversity, although some gene polymorphisms and ribotypes of a few strains of different serogroups were similar. It is concluded that despite sharing the same serogroup, environmental and clinical isolates were genetically heterogeneous and were of different lineages.

Blotting, Southern↗

Concomitant infection of enterotoxigenic Escherichia coli in an outbreak of cholera caused by Vibrio cholerae O1 and O139 in Ahmedabad, India.

In Ahmedabad, a major city in the state of Gujarat, India, an outbreak of acute secretory diarrhea caused by Vibrio cholerae O1 Ogawa El Tor, V. cholerae O139, and multiple serotypes of enterotoxigenic Escherichia coli (ETEC) occurred in January 2000. All of the representative V. cholerae O1 and O139 isolates examined harbored the ctxA gene (encoding the A subunit of cholera toxin) and the El Tor variant of the tcpA gene (encoding toxin-coregulated pilus). ETEC isolates of different serotypes were positive for the elt gene, encoding heat-labile enterotoxin. To further understand the molecular characteristics of the pathogens, representative isolates were examined by ribotyping and pulsed-field gel electrophoresis (PFGE). Ribotyping showed that the isolates of V. cholerae O1 Ogawa exhibited a pattern identical to that of the prevailing clone of O1 in areas where cholera is endemic in India, and all of the O139 isolates were identical to the BII clone of V. cholerae O139. PFGE of the representative O1 Ogawa isolates exhibited an identical pattern, comparable to the H pattern of the new clone of O1 reported in Calcutta, India. PFGE analysis of the V. cholerae O139 isolates showed identical patterns, but these differed from the PFGE patterns of O139 isolates reported during 1992 to 1997 in Calcutta. ETEC isolates showed genetic heterogeneity among isolates belonging to the same serotype, although the identical PFGE pattern was also observed among ETEC isolates of different serotypes. Antibiograms of the isolates were unusual, because all of the O139 isolates were resistant to nalidixic acid. Likewise, all of the E. coli isolates showed resistance to ciprofloxacin, norfloxacin, and nalidixic acid. This is a unique outbreak, and we believe that it is the first in which V. cholerae and ETEC were concomitantly involved.

Anti-Bacterial Agents↗