Sugunan Ap

Four cases of acute flaccid paralysis associated with chikungunya virus infection

The recent epidemic of chikungunya fever (2005-2006) in India has affected millions of people. The Andaman and Nicobar Islands, an archipelago situated in the Bay of Bengal 1200 km from peninsular India, also witnessed an outbreak of chikungunya fever starting in July 2006 which affected thousands of people. Chikungunya fever classically manifests as high fever, myalgia, arthralgia and arthritis and in a certain percentage of cases with maculopapular rashes. However, deviation from the classical clinical features of chikungunya fever was reported in the earlier and recent epidemics. During the recent epidemic in the Andaman and Nicobar Islands we came across ten cases of flaccid limb weakness following symptoms and signs suggestive of chikungunya fever. In four subjects we confirmed the diagnosis of chikungunya virus infection by serological method (IgM ELISA method). This is the case report of those four subjects.

Use of Fluorescent Amplified Fragment Length Polymorphism for Molecular Epidemiology of Leptospirosis in India

ABSTRACT Nineteen isolates of leptospires recovered from patients during three epidemics that occurred at different places and different times in the Andaman Islands and eight isolates from sporadic cases were characterized using serological and molecular genetic techniques. Group sera and monoclonal antibodies were used for antigenic characterization, whereas fluorescent amplified fragment length polymorphism (FAFLP) was used for genotyping. Of the 27 isolates, 19 were identified as belonging to serogroup Grippotyphosa, 3 belonged to serogroup Australis, 2 belonged to serogroup Icterohaemorrhagiae, and 1 each belonged to serogroups Hebdomadis, Canicola, and Sejroe. Analysis of FAFLP data grouped these 27 isolates into two main clusters of genotypes. One of the clusters, populated by 19 isolates, included 16 outbreak isolates. Seven of these 19 isolates belonged to serovar Ratnapura, 10 belonged to serovar Valbuzzi, and 1 each belonged to serovar Grippotyphosa and serovar Saxkoebing. Of the 27 patients from whom isolates were obtained, 9 had severe illness, and 6 of these 9 patients had pulmonary involvement, 1 had pulmonary and hepatorenal involvement, and the remaining 2 had hepatorenal involvement alone. Two patients out of the nine severe cases died subsequently. The isolates from sporadic cases showed great genetic diversity and were also diverse antigenically. Perhaps the strains belonging to a dominant genotype (the outbreak-associated cluster) possessed epidemic potential and higher virulence with a greater predilection to cause pulmonary complications than strains belonging to other genetic backgrounds.

Evaluation of Lepto Dri Dot as a rapid test for the diagnosis of leptospirosis

Lepto Dri Dot is a new card agglutination test developed by the Dutch Royal Tropical Institute for the rapid diagnosis of leptospirosis. We evaluated the test in field conditions in The Andaman Islands. Patients suspected of leptospirosis who attended three primary health centres were included in the study. The test results were compared with blood culture or microscopic agglutination tests on paired serum samples; 74 of 124 patients were diagnosed as having leptospirosis based on these criteria. Lepto Dri Dot had a sensitivity of 67.6% (50/74) and a specificity of 66.0% (33/50) during week 1. During weeks 2-4 the values increased to 85.5% (47/55) and 80% (40/50) respectively. An IgM ELISA was also performed on the serum samples for comparison and this was marginally less sensitive, but more specific, during the first week of illness. The positivity rates for the Dri Dot test during days 2-3, 4-5 and 6-7 were 53.1% (17/32), 75.0% (18/24) and 83.3% (15/18), respectively. The corresponding values for ELISA were 28.1% (9/32), 54% (13/24) and 77.8% (14/18). Both Dri Dot and ELISA showed good agreement with the standard diagnostic criteria after the first week of illness (kappa= 0.65 and 0.74, respectively). The overall concordance of the two tests was 89.5 % (kappa = 0.79). The test does not require special storage or sophisticated equipment and can be performed by relatively low skilled personnel.

Chikungunya epidemic-related mortality.

Port Blair, the capital city of the Union Territory of Andaman and Nicobar Islands in the republic of India, witnessed an outbreak of chikungunya (CHIK) fever in 2006. Although no deaths attributable to CHIK fever were registered, thousands of people were affected. In view of evidence from other parts of the world indicating that CHIK fever does cause death we studied the mortality trend in Port Blair from 2002 to 2008 in order to verify if there was increased mortality during the CHIK fever epidemic. The expected number of monthly deaths in 2006 was calculated by multiplying the average monthly mortality rate from 2002 to 2008 (with the exception of 2006) with the monthly population in 2006. The results indicated that there was a significant increase in expected deaths during some months of 2006, which coincided with the peak in the CHIK fever epidemic in Port Blair.

Emergence of an Unusual Genotype of Rotavirus in Andaman and Nicobar Islands, India

Rotavirus is the most common cause of severe diarrhoea worldwide, affecting over 125 million young children every year in developing countries. The present study is a part of ongoing childhood diarrhoeal surveillance to determine the strain diversity of rotaviruses prevalent in Andaman and Nicobar Islands. From October 2010 to February 2012, 296 stool samples from children (age group 6–60 months) with gastroenteritis were obtained from different referral hospitals/primary health centres and community health centres in Andaman and Nicobar Islands. A total of 47 samples were found positive for GARV. Among these, 21 (44.7%) samples belong to G2P[4], 12 (25.5%) samples were G1P[8], 10 (21.2%) samples belong to G9P[4], 2 (4.3%) samples belong to G1P[4] and 2 (4.3%) samples had a mixed genotype. Rotavirus G2 genotype remains the most common genotype in these islands. The prevalence of G9 rotavirus reported in the present study is higher than that reported from mainland India. The results emphasize the role of the unusual serotype G9 as an epidemiologically important genotype and the need to include G9 specificity in a rotavirus vaccine.

Emergence of nalidixic acid-resistant Shigella sonnei in acute-diarrhea patients on Andaman and Nicobar Islands, India

Shigella infection has been occurring in both epidemic and sporadic forms on Andaman and Nicobar Islands in India (92 to 94°E longitude, 6 to 14°N latitude; Bay of Bengal). Although acute gastrointestinal infection clinically resembling shigellosis has been reported on the islands frequently, bacteriological surveillance was only started in 1994. The surveillance data showed that shigellosis is a common cause of bacterial diarrhea (1). Endemic infection is mainly due to Shigella flexneri 2a, whereas S. dysenteriae type 1 was responsible for the outbreaks that occurred among the general population and among the Andamanese tribe. The ampicillin- and co-trimoxazole-resistant pandemic strain of S. dysenteriae type 1 was first observed during an epidemic that occurred in 1986 (4). By 1994, 100% of the Shigella isolates had become ampicillin resistant and 80.6% had become co-trimoxazole resistant. All co-trimoxazole-resistant strains were also resistant to ampicillin. Nalidixic acid resistance was first observed among S. dysenteriae type 1 strains in 1995 (15.1%), and gentamicin resistance was first observed in 1996 (37%) (2). The proportions of different strains among the isolates have been showing considerable variability from year to year. During 1994 and 1995 to 1999 and 2000, a total of 15 S. sonnei strains were isolated from acute-diarrhea patients. All of the isolates were sensitive to nalidixic acid (Table ​(Table1).1). Since September 1999 to August 2000, a rural-community-based study was conducted to estimate the disease burden due to shigellosis. Three S. sonnei (phase I) isolates were recovered from patients who were identified in a follow-up study. The first isolate was sensitive to nalidixic acid, but two subsequent isolates were resistant. During 2001 and 2002, 106 samples from acute-diarrhea cases were processed. This yielded nine isolates (isolation rate, 8.49%). Seven were S. sonnei (phase I), one was S. flexneri 3a, and one was S. flexneri 4b. All seven of the S. sonnei isolates were resistant to nalidixic acid (30 μg/disk; HiMedia), ampicillin, and co-trimoxazole (the dates of isolation of the first and last reported isolates were 27.06.01 and 15.03.02, respectively), whereas the S. flexneri isolates were sensitive to nalidixic acid. The emergence of nalidixic acid-resistant S. sonnei has been observed since the last week of September 1999 (29.09.99) and has continued during the reported study period. The MIC of nalidixic acid was estimated by using both the E-test (AB Biodisk) and agar dilution (3) methods. It ranged from 24 to more than 96 μg/ml (mean, 40.88 ± 26.06 μg/ml) among the resistant strains. S. sonnei was also isolated in previous years (1, 2); however, those strains were sensitive to nalidixic acid. Besides nalidixic acid, ciprofloxacin and furazolidone are used in the treatment of bacillary dysentery in the hospital. Most of the S. sonnei isolates were isolated from children <5 years old admitted to G. B. Pant Hospital, the only referral hospital in Port Blair. The youngest child was 4 months old. They had fever, abdominal pain, and watery stools with mucus. TABLE 1. Nalidixic acid-resistant Shigella strains isolated from 1994 to 2002a During 2000 to 2001 and 2001 to 2002, S. flexneri 2a and S. dysenteriae type 1 were not isolated either from the community or from hospitalized patients. It appears that the multidrug-resistant S. sonnei strain is replacing the endemic S. flexneri 2a and epidemic S. dysenteriae type 1 strains as the predominant strain of Shigella in Port Blair. The patients who were infected with this strain of S. sonnei were from different parts of South Andaman, indicating a wide distribution of the strain in Andamans. A shift in the predominant Shigella strain, usually from S. flexneri 2a to S. dysenteriae type 1, precedes shigellosis epidemics. The present shift from S. flexneri 2a to S. sonnei may also be an early signal of an emerging important problem.

Tobacco use and nicotine dependency in a cross-sectional representative sample of 18,018 individuals in Andaman and Nicobar Islands, India

BackgroundData on prevalence, pattern of tobacco use, proportion of population dependent on nicotine and their determinants are important for developing and implementing tobacco control strategies. The aim of the study was to estimate the prevalence and determinants of tobacco use and nicotine dependency.MethodsA cross-sectional survey among a representative sample of 18,018 individuals in the age group of >=14 years was conducted in the Union Territory of Andaman and Nicobar Islands during 2007–09. A structured questionnaire, a modified version of an instrument which was used successfully in several multi-country epidemiological studies of the World Health Organisation, was used to survey individual socio-demographic details, known co-morbid conditions, tobacco use and alcohol use. Fagerström Test for Nicotine Dependence (FTND) was used to estimate nicotine dependence.ResultsThe response rate of our survey was 97% (18,018/18,554). Females (n = 8,888) were significantly younger than males (34.3 + 14.6 Vs 36.2 + 15.4 years). The prevalence of current tobacco use in any form was 48.9% (95% CI: 48.2–49.6). Tobacco chewing alone was prevalent in 40.9% (95% CI: 40.1–41.6) of the population. While one tenth of males (9.7%, 95% CI: 9.1–10.4) were nicotine dependent, it was only 3% (95% CI: 2.7–3.4) in females. Three fourth of the tobacco users initiated use of tobacco before reaching 21 years of age. Age, current use of alcohol, poor educational status, marital status, social groups, and co-morbidities were the main determinants of tobacco use and nicotine dependence in the population.ConclusionThe high prevalence of tobacco use especially the chewing form of tobacco in the Union Territory of Andaman and Nicobar Islands and the differences in prevalence and pattern of tobacco use and nicotine dependency observed across subgroups warrants implementation of culturally specific tobacco control activities in this population.

Molecular tracking of the lineage of strains of Vibrio cholerae O1 biotype El Tor associated with a cholera outbreak in Andaman and Nicobar Islands, India

A large outbreak of acute watery diarrhoea involving all age groups of mongoloid tribal aborigines occurred during October–November, 2002 in the Nancowry group of Andaman and Nicobar Islands in the Indian Ocean. Twenty‐one of the 67 stool samples from 67 patients were positive for toxigenic Vibrio cholerae O1, serotype Ogawa biotype El Tor, which showed striking similarity in its antibiogram with some of the strains of V. cholerae O1 Serotype Ogawa biotype El Tor isolated in Kolkata. The Nancowry and Kolkata isolates were compared with molecular tools involving random amplified polymorphic DNA (RAPD) fingerprinting, ribotyping and pulsed‐field gel electrophoresis (PFGE). RAPD fingerprinting and ribotyping techniques revealed that all the V. cholerae strains associated with the outbreak in these islands were clonal in nature and identical to a population of isolates obtained from Kolkata since 1993. PFGE could discriminate within these Kolkata isolates further and established that a particular subtype of this population reached the remote Nancowry islands and was responsible for the outbreak.

Changing patterns and widening of antibiotic resistance in Shigella spp. over a decade (2000-2011), Andaman Islands, India.

This study is a part of the surveillance study on childhood diarrhoea in the Andaman and Nicobar Islands; here we report the drug resistance pattern of recent isolates of Shigella spp. (2006-2011) obtained as part of that study and compare it with that of Shigella isolates obtained earlier during 2000-2005. During 2006-2011, stool samples from paediatric diarrhoea patients were collected and processed for isolation and identification of Shigella spp. Susceptibility to 22 antimicrobial drugs was tested and minimum inhibitory concentrations were determined for third-generation cephalosporins, quinolones, amoxicillin-clavulanic acid combinations and gentamicin. A wide spectrum of antibiotic resistance was observed in the Shigella strains obtained during 2006-2011. The proportions of resistant strains showed an increase from 2000-2005 to 2006-2011 in 20/22 antibiotics tested. The number of drug resistance patterns increased from 13 in 2000-2005 to 43 in 2006-2011. Resistance to newer generation fluoroquinolones, third-generation cephalosporins and augmentin, which was not observed during 2000-2005, appeared during 2006-2011. The frequency of resistance in Shigella isolates has increased substantially between 2000-2006 and 2006-2011, with a wide spectrum of resistance. At present, the option for antimicrobial therapy in shigellosis in Andaman is limited to a small number of drugs.

Emergence of Multidrug-Resistant Vibrio cholerae O1 Biotype El Tor in Port Blair, India

Cholera is a major disease in the developing world. The World Health Organization reported in 2006 that 236,896 cases of cholera occurred in 52 countries, a 79% increase over 2005.1 During the past decade, the dominance of the O1 Ogawa serotype of Vibrio cholerae and a quiescent period during the O139 era was observed.2 El Tor V. cholerae have replaced the classical biotype over the past few decades.3–5 Cycles of serotype shifting at intervals of 2–8 years have been reported.6 During the monsoon season, sporadic and small clusters of cases of cholera occur almost every year in Port Blair, India (Bhattgacharya DS and others, unpublished data). Two outbreaks of cholera have been reported from Andaman and Nicobar Islands. The first outbreak, which was caused by V. cholerae O1 Ogawa, occurred in Nancowry Islands in 2002.7 The second outbreak, which was caused by V. cholerae O1 Inaba, occurred in Port Blair and its suburbs in 2006.8 We report the emergence of multidrug-resistant V. cholerae O1 cholera in the Andaman Islands. This study was approved by the institutional ethical committee. During May–June 2010, there was an increase in diarrhea cases in Port Blair, the capital city of the Andaman and Nicobar Islands. Fecal samples were collected from persons with suspected cholera who were admitted to the G.B. Pant Hospital in Port Blair, the only referral hospital in the territory, and a private childcare hospital, and processed according to standard procedures for isolation and identification of V. cholerae. Written consent was obtained from the patients or guardians before collection of samples. The V. cholerae strains were serotyped by using polyvalent and monovalent antisera (Denka Seiken Co., Ltd., Tokyo, Japan). Susceptibility to different antimicrobial drugs was tested by using the disk diffusion technique according to Clinical and Laboratory Standards Institute (CLSI) (Wayne, PA) guidelines9 and commercially available antimicrobial drug disks (Hi-Media, Mumbai, India). The drugs tested were ampicillin (10 μg), carbenicillin (100 μg), imipenem (30 μg), amoxicillin-clavulanic acid (20/10 μg), cefixime (30 μg), cefuroxime (5 μg), cephalothin (30 μg), ceftriaxone (30 μg), cefotaxime (30 μg), ceftazidime (30 μg), tetracycline (30 μg), co-trimoxazole (20 μg), nalidixic acid (30 μg), ciprofloxacin (30 μg), norfloxacin (10 μg), ofloxacin (5 μg), gatifloxacin (5 μg), gentamicin (10 μg), amikacin (30 μg), nitrofurantoin (300 μg), azithromycin (30 μg), and chloramphenicol (30 μg). Escherichia coli strain ATCC 25922 was used as the quality control strain. The minimum inhibitory concentrations (MICs) of azithromycin, tetracycline, and ciprofloxacin were determined for all strains by using the Etest (AB Biodisk, Solna, Sweden) following CLSI procedures and interpretative standards for V. cholerae. Because there is no reference zone size for V. cholerae resistance to azithromycin, we considered a zone of inhibition ≥ 18 mm as the cut-off value to determine susceptibility, as followed in other studies on V. cholerae.10 All Vibrio cholerae O1 isolates were screened for virulence genes ctxA, tcpA (El Tor/Classical), toxR, toxS, toxRS, VPI, toxT, ace, zot, and tcpP by using a polymerase chain reaction–based detection technique.11 Random amplified polymorphic DNA fingerprinting was performed for all isolates by using an arbitrary primer M16 (5′-AAAGAAGGACTCAGCGACTGCG-3′).12 Reference strains of V. cholerae O139, V. cholerae O1 serotype Ogawa, and biotype El Tor were used as controls.13 A total of 62 stool samples were collected from patients with suspected cholera who came to or were admitted to the two hospitals in Port Blair. All patients were residents of South Andaman Island. Vibrio cholerae was isolated from 19 patients. Six (31.6%) isolates were V. cholerae Inaba, one (5.2%) was V. cholerae Ogawa, and 12 (63.2%) were non-agglutinating vibrios. The first confirmed case was detected on June 2, 2010, and the last confirmed case was detected on June 23, 2010. The last case-patient apparently had contracted the infection on another island, Little Andaman, and had symptoms develop while he was traveling to Port Blair. The isolate obtained from this patient was V. cholerae O1 Ogawa. No deaths caused by cholera were reported during the study period. None of the patients had any recent history of travel to mainland India or other islands, except the patient who contracted the infection on Little Andaman Island. Although the outbreak that occurred in the islands in 2002 was caused by V. cholerae O1 Ogawa resistant to ampicillin, nalidixic acid and co-trimoxazole, the outbreak of 2006 was caused by V. cholerae O1 Inaba that was resistant to nitrofurantoin, in addition to the above three drugs. All V. cholerae isolates obtained during June 2010 also were resistant to ampicillin, nalidixic acid, co-trimoxazole, nitrofurantoin, tetracycline, cephalexin, and carbenicillin. Although four of the six V. cholerae Inaba isolates obtained during June 2010 were resistant to gentamicin, ciprofloxacin, amikacin, and azithromycin, only one isolate of V. cholerae Ogawa was resistant to amikacin and azithromycin. All isolates showed intermediate resistance to norfloxacin and ofloxacin by the disk diffusion method, with a MIC ranging from 0.125 to 1 μg/mL, respectively. The MICs of tetracycline and ciprofloxacin for strains resistant to these two drugs ranged from 16 to 32 μg/mL. The MICs of azithromycin for strains resistant to this drug ranged from 8 to 64 μg/mL (Table 1). Table 1 Antimicrobial drugs test results for Vibrio cholerae strains, Port Blair, India* A multiplex polymerase chain reaction showed that all V. cholerae O1 isolates had the virulence genes ctxA, tcpA (El Tor), toxR, toxS, toxRS, VPI, toxT, ace, zot, and tcpP. Random amplified polymorphic DNA RAPD analysis with primer M16 generated identical fingerprints for all the V. cholerae Inaba isolates, which were similar to fingerprints of V. cholerae O1 strains isolated during the outbreak of cholera in Port Blair in 2006. The fingerprinting profile of the sole V. cholerae Ogawa isolate, DS-597, was similar to that of V. cholerae O1 Ogawa strains isolated during 2002 outbreak. In the present study, all isolates showed multidrug resistance for 7–11 drugs. Three drug resistance patterns were observed among the seven V. cholerae isolates. Although multidrug resistance in V. cholerae isolates has been reported from elsewhere in India and neighboring countries,2,14–16 it has not been reported from Andaman and Nicobar Islands. It is likely that V. cholerae O1 Inaba has been circulating in the environment of South Andaman, probably in some non-pathogenic/non-cultivable form since the outbreak in 2006. The re-emergence after a quiescent period, when apparently no cholera occurred, might be caused by acquisition of virulence genes by non-pathogenic V. cholerae17,18 or by an increase in contamination of the environment by V. cholerae to a level adequate for successful transmission of infection. During the quiescent period, survival of V. cholerae in water bodies might have enabled dissipation of drug resistance to different serotypes or strains.14 During the last two outbreaks in 2002 and 2006 caused by V. cholerae O1 Ogawa and Inaba, respectively, all strains isolated were sensitive to tetracycline, gentamicin, amikacin, azithromycin, and cephalexin. Many of the V. cholerae strains isolated during the recent outbreak were resistant to these drugs. Ciprofloxacin and azithromycin resistance has already emerged in V. cholerae.19 Resistance to quinolones is generally associated with amino acid substitutions in portions of GyrA and ParC proteins, which are caused by mutations in the quinolone resistance–determining region.20 The presence of an integron, an integrative and conjugative element, and active efflux also adds to the factors conferring resistance to a wide range of antimicrobial drugs. Azithromycin resistance can be mediated by various mechanisms, including overexpression of efflux pumps, production of methylases, and mutations in the drug target, the 23S ribosomal RNA gene (A2059G). The mechanism of this high-level resistance could be novel or a combination of known mechanisms. However, the possibility of the strain being introduced into the environment of the islands by persons with undetected cholera who traveled to the islands from mainland India cannot be ruled out.14 Emergence of resistance to multiple drugs has been reported in other diarrheal pathogens in these islands.21 This finding is not unique because many investigations conducted in different areas have demonstrated an increase in the antimicrobial resistance spectrum among epidemically significant V. cholerae over time.20 Resistance to commonly used antimicrobial drugs is becoming a major public health concern because it complicates treatment and may result in longer hospital stays for patients. Spread of antimicrobial drug resistance has been recognized by the World Health Organization as an extremely serious problem. Vibrio cholerae possesses a number of mechanisms to evade the effects of antimicrobial drugs and a stage may come when the commonly used antimicrobial drugs are no longer effective.20 However, we are not yet stranded because strains are still sensitive to some of the newer quinolones and cephalosporins. Nonetheless, the expanding spectrum of drug resistance among these V. cholerae isolates is a cause for serious concern.