[Downloaded free from http://www.ijmm.org on Saturday, June 13, 2015, IP: 61.16.135.116]
July-September 2015
455
Correspondence
CHIKV is a mosquito‑borne alphavirus which causes fever, rash and arthralgia. It affects all age groups of humans. In the past, life‑threatening complications were very rarely reported. However, during the recent worldwide outbreaks, there have been several reports of unusually severe complications and deaths.[2] Recently, neurologic involvement and deaths have been reported in Malaysia and Thailand.[3,4] Apart from typical clinical triad of high‑grade fever, arthralgia and vomiting in CHIK infection, we have observed a spectrum of neurological abnormalities in terms of altered mental functions, seizures, focal neurological deficit with abnormal CT scan of head and altered CSF biochemistry. The widely available and easily used tests are, however, serological tests in the initial few days of the illness. RT‑PCR can also be used for viral RNA detection and rapid diagnosis during viraemic phase.[5] Now it has become an important issue in domain of public health due to its rapid onset, its potential for epidemic and high morbidity. Typical history of CHIK infection, neurological complications associated with CNS abnormalities, supportive laboratory evidence C6/36 cell line showing typical cytopathic effect after inoculation with serum and CSF as well as findings of IgM antibodies against CHIK and positive serum, CSF and TCF with standard CHIK primers for RT‑PCR‑positive and sequencing results allow us to conclude this as the case of CHIK encephalitis. The present study indicates the fact that CHIKV infection is an important but unrecognized cause of febrile illness and emphasizes the need of surveillance for CHIKV disease using multiple diagnostic tests.
References 1. Yergolkar PN, Tandale BV, Arankalle VA, Sathe PS, Sudeep AB, Gandhe SS, et al. Chikungunya outbreaks caused by African genotype, India. Emerg Infect Dis 2006;12:1580‑3. 2. Robin S, Ramful D, Le Seach’ F, Jaffar‑Bandjee MC, Rigou G, Alessandri JL. Neurologic manifestations of pediatric chikungunya infection. J Child Neurol 2008;23:1028‑35. 3. Sam IC, Kamarulzaman A, Ong GS, Veriah RS, Ponnampalavanar S, Chen YF, AbuBakar S. Chikungunya virus‑associated death in Malaysia. Trop Biomed 2010;27:343‑7. 4. Chusri S, Siripaitoon P, Hirunpat S, Silpapojakul K. Case reports of neuro‑Chikungunya in southern Thailand. Am J Trop Med Hyg 2011;85:386‑9. 5. Grivard P, Le Roux K, Laurent P, Fianu A, Perrau J, Gigan J, et al. Molecular and serological diagnosis of Chikungunya virus infection. Pathol Biol (Paris) 2007;55:490‑4.
NJ Shaikh, *CG Raut, DP Sinha, MJ Manjunath National Institute of Virology (NJS, CGR, DPS, MJM), Bangalore Unit, RGICD Premises, 1st Main Someshwarnagar, Near NIMHANS, DRC Post, Bangalore - 560 029, India *Corresponding author (email: ) Received: 28-10-2014 Accepted: 20-01-2015 Access this article online Quick Response Code:
Website: www.ijmm.org PMID: ***
Acknowledgement
DOI: 10.4103/0255-0857.158600
We thank Director, National Institute of Virology, Pune for providing all the facilities to carry out the research work.
Study of virulence factors in association with antimicrobial resistance amongst urinary isolates of enterococci Dear Editor, Enterococci are increasingly being revealed as reservoirs of mobile genetic elements carrying resistance and virulence genes to other pathogens. We studied the prevalence of various virulence factors phenotypically and genotypically in association with drug resistance among the enterococcal isolates implicated in urinary tract infection (UTI). One hundred biochemically confirmed isolates of enterococci were tested for antimicrobial susceptibility by
Kirby Bauer disc diffusion test and respective screen agars for vancomycin (VRE) and high level gentamicin (HLGRE) as per standard.[1] Haemolysin and gelatinase production,[2] hemagglutination and biofilm formation[3] and presence of asa1 (aggregation substance), gelE (gelatinase), cylA (cytolysin), esp (enterococcal surface protein) and hyl (hyaluronidase) by multiplex polymerase chain reaction (PCR)[4] was studied. Presence of virulence factors and drug resistance was compared by Kruskal Wallis test and Mann U Whitney test (statistical package of social sciences, SPSS, version 15, Chicago, US).
www.ijmm.org
[Downloaded free from http://www.ijmm.org on Saturday, June 13, 2015, IP: 61.16.135.116]
456
Indian Journal of Medical Microbiology
Figure 1: Different virulent genes amongst the enterococcal isolates detected by multiplex PCR
Of the total, 46 isolates were E. faecalis and 54 E. faecium, of which 70% (32 E. faecalis and 38 E. faecium) were HLGRE and 7% (1 E. faecalis and 6 E. faecium) were VRE. Haemolysin and gelatinase production, haemagglutination and biofilm formation was seen in 29%, 17%, 39% 34%, respectively. Virulence factors were more in E. faecalis (P > 0.05). asa1 and gelE were the most prevalent virulence genes [Figure 1]. None harboured all the virulent genes and 10 isolates did not show any virulence factors. Majority of the strong biofilm producers possessed either asa1 or gelE gene. On statistical analysis, decreasing expression and possession of virulence genes was seen with increasing drug resistance (P
July-September 2015
455
Correspondence
CHIKV is a mosquito‑borne alphavirus which causes fever, rash and arthralgia. It affects all age groups of humans. In the past, life‑threatening complications were very rarely reported. However, during the recent worldwide outbreaks, there have been several reports of unusually severe complications and deaths.[2] Recently, neurologic involvement and deaths have been reported in Malaysia and Thailand.[3,4] Apart from typical clinical triad of high‑grade fever, arthralgia and vomiting in CHIK infection, we have observed a spectrum of neurological abnormalities in terms of altered mental functions, seizures, focal neurological deficit with abnormal CT scan of head and altered CSF biochemistry. The widely available and easily used tests are, however, serological tests in the initial few days of the illness. RT‑PCR can also be used for viral RNA detection and rapid diagnosis during viraemic phase.[5] Now it has become an important issue in domain of public health due to its rapid onset, its potential for epidemic and high morbidity. Typical history of CHIK infection, neurological complications associated with CNS abnormalities, supportive laboratory evidence C6/36 cell line showing typical cytopathic effect after inoculation with serum and CSF as well as findings of IgM antibodies against CHIK and positive serum, CSF and TCF with standard CHIK primers for RT‑PCR‑positive and sequencing results allow us to conclude this as the case of CHIK encephalitis. The present study indicates the fact that CHIKV infection is an important but unrecognized cause of febrile illness and emphasizes the need of surveillance for CHIKV disease using multiple diagnostic tests.
References 1. Yergolkar PN, Tandale BV, Arankalle VA, Sathe PS, Sudeep AB, Gandhe SS, et al. Chikungunya outbreaks caused by African genotype, India. Emerg Infect Dis 2006;12:1580‑3. 2. Robin S, Ramful D, Le Seach’ F, Jaffar‑Bandjee MC, Rigou G, Alessandri JL. Neurologic manifestations of pediatric chikungunya infection. J Child Neurol 2008;23:1028‑35. 3. Sam IC, Kamarulzaman A, Ong GS, Veriah RS, Ponnampalavanar S, Chen YF, AbuBakar S. Chikungunya virus‑associated death in Malaysia. Trop Biomed 2010;27:343‑7. 4. Chusri S, Siripaitoon P, Hirunpat S, Silpapojakul K. Case reports of neuro‑Chikungunya in southern Thailand. Am J Trop Med Hyg 2011;85:386‑9. 5. Grivard P, Le Roux K, Laurent P, Fianu A, Perrau J, Gigan J, et al. Molecular and serological diagnosis of Chikungunya virus infection. Pathol Biol (Paris) 2007;55:490‑4.
NJ Shaikh, *CG Raut, DP Sinha, MJ Manjunath National Institute of Virology (NJS, CGR, DPS, MJM), Bangalore Unit, RGICD Premises, 1st Main Someshwarnagar, Near NIMHANS, DRC Post, Bangalore - 560 029, India *Corresponding author (email: ) Received: 28-10-2014 Accepted: 20-01-2015 Access this article online Quick Response Code:
Website: www.ijmm.org PMID: ***
Acknowledgement
DOI: 10.4103/0255-0857.158600
We thank Director, National Institute of Virology, Pune for providing all the facilities to carry out the research work.
Study of virulence factors in association with antimicrobial resistance amongst urinary isolates of enterococci Dear Editor, Enterococci are increasingly being revealed as reservoirs of mobile genetic elements carrying resistance and virulence genes to other pathogens. We studied the prevalence of various virulence factors phenotypically and genotypically in association with drug resistance among the enterococcal isolates implicated in urinary tract infection (UTI). One hundred biochemically confirmed isolates of enterococci were tested for antimicrobial susceptibility by
Kirby Bauer disc diffusion test and respective screen agars for vancomycin (VRE) and high level gentamicin (HLGRE) as per standard.[1] Haemolysin and gelatinase production,[2] hemagglutination and biofilm formation[3] and presence of asa1 (aggregation substance), gelE (gelatinase), cylA (cytolysin), esp (enterococcal surface protein) and hyl (hyaluronidase) by multiplex polymerase chain reaction (PCR)[4] was studied. Presence of virulence factors and drug resistance was compared by Kruskal Wallis test and Mann U Whitney test (statistical package of social sciences, SPSS, version 15, Chicago, US).
www.ijmm.org
[Downloaded free from http://www.ijmm.org on Saturday, June 13, 2015, IP: 61.16.135.116]
456
Indian Journal of Medical Microbiology
Figure 1: Different virulent genes amongst the enterococcal isolates detected by multiplex PCR
Of the total, 46 isolates were E. faecalis and 54 E. faecium, of which 70% (32 E. faecalis and 38 E. faecium) were HLGRE and 7% (1 E. faecalis and 6 E. faecium) were VRE. Haemolysin and gelatinase production, haemagglutination and biofilm formation was seen in 29%, 17%, 39% 34%, respectively. Virulence factors were more in E. faecalis (P > 0.05). asa1 and gelE were the most prevalent virulence genes [Figure 1]. None harboured all the virulent genes and 10 isolates did not show any virulence factors. Majority of the strong biofilm producers possessed either asa1 or gelE gene. On statistical analysis, decreasing expression and possession of virulence genes was seen with increasing drug resistance (P
