|Year : 2015 | Volume
| Issue : 5 | Page : 153-156
Chikungunya virus infection amongst the acute encephalitis syndrome cases in West Bengal, India
D Taraphdar1, BK Roy2, S Chatterjee1
1 ICMR Virus Unit, Department of Arbovirology, ID and BG Hospital Campus, Kolkata, India
2 Bangur Institute of Neurology, Kolkata, West Bengal, India
|Date of Submission||07-Feb-2014|
|Date of Acceptance||21-Aug-2014|
|Date of Web Publication||6-Feb-2015|
ICMR Virus Unit, Department of Arbovirology, ID and BG Hospital Campus, Kolkata
Source of Support: None, Conflict of Interest: None
Chikungunya virus (CHIKV) infection from the acute encephalitis syndrome cases is an uncommon form and has been observed in the year 2010-11 from West Bengal, India. The case-1 and case-2 had the acute encephalitis syndrome; case-3 was of acute disseminated encephalomyelitis whereas the case-4 had the symptoms of meningo-encephalopathy with bulbar involvement. We are reporting four cases with neurological complications involving central nervous system (CNS) due to CHIKV infection from this state for the first time. The virus has spread almost every districts of this state rapidly. At this stage, these cases are public health threat.
Keywords: AES cases, Chikungunya virus, India
|How to cite this article:|
Taraphdar D, Roy B K, Chatterjee S. Chikungunya virus infection amongst the acute encephalitis syndrome cases in West Bengal, India. Indian J Med Microbiol 2015;33, Suppl S1:153-6
|How to cite this URL:|
Taraphdar D, Roy B K, Chatterjee S. Chikungunya virus infection amongst the acute encephalitis syndrome cases in West Bengal, India. Indian J Med Microbiol [serial online] 2015 [cited 2020 Oct 26];33, Suppl S1:153-6. Available from: https://www.ijmm.org/text.asp?2015/33/5/153/150946
| ~ Introduction|| |
Chikungunya virus (CHIKV), is a mosquito-transmitted Alphavirus, belongs to family Togaviridae.  The virus was first isolated from Tanzania in 1952. In India, CHIKV was first isolated in Calcutta in 1963 and last reported from Maharashtra in 1973. , After that, the virus disappeared from this country.  In 2006, reports of large scale outbreaks of fever caused by CHIKV infection in several parts of India, including West Bengal have confirmed the re-emergence of this virus after more than three decades. 
CHIKV is normally responsible for an acute infection, characterised by high fever, poly-arthralgia, headache and rash.  Neurological complications due to CHIKV have been reported from several parts of India.  Although in West Bengal the virus had already affected many districts of the state, but to date, no such cases have been reported from this state as well as from Eastern part of India. For the first time we are reporting CHIKV infection amongst the referred acute encephalitic syndrome (AES) cases from this state as well as from Eastern India.
| ~ Case Reports|| |
On 20 th November, 2010, a 32-year-old female patient from the district of East Midnapore, West Bengal, India was admitted to Nilratan Sarkar Medical College and Hospital (NRSMCH), Kolkata with acute onset of high fever with chill and rigour for four days followed by one episode of generalised tonic clonic convulsion and prolonged unconsciousness. On examination, the patient was disoriented with positive melingeal signs (neck rigidity with positive signs). Haemodinamically the patient was stable. The cerebrospinal fluid (CSF) showed glucose 83 mg/dl, cell count 150/mm 3 (lymphocyte 92% and neutrophil 8%), protein 86 mg/dl and chloride 122 meq/L. At that time the random blood sugar was 160 mg/dl [Table 1].
|Table 1: Biochemical parameters of cerebrospinal fluid of four Chikungunya cases with CNS manifestation|
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On 23 rd November, 2010, the blood and the CSF sample of the patient were referred to ICMR Virus Unit, Kolkata for virological investigation, with informed consent. These were subjected to both enzyme linked immunosorbent assay (ELISA) and reverse transcriptase polymerase chain reaction (RT-PCR) test  for detecting the CHIKV infection. The CSF sample was positive by RT-PCR method [Figure 1] and IgM antibody against CHIKV was detected in blood sample by ELISA method [Table 2].
|Figure 1: Result of agarose gel (1.5%) electrophoresis showing chikungunya specific band at 354 bp obtained following RNA extraction followed by RTPCR of the isolated RNA Lane L: 100 bp DNA Ladder; Lane S1-S8: Patients samples; Lane S1: Result of blood sample of case 2; Lane S2: Result of CSF sample of case 2; Lane S4: Result of CSF sample of case 1; Lane S7: Result of CSF sample of case 4; Lane C1: Positive control (CHIKV control strain); Lane C2: Negative (without template) control|
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|Table 2: Results of IgM ELISA and RTPCR in blood and CSF samples of chikungunya cases|
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The patient recovered slowly with conservative management and sensorium improved within 10 days and was discharged on 13 th December 2010.
A 50-year-old male patient from Bankura, West Bengal was admitted in Infectious Disease and Bengal General (ID and BG) Hospital, Kolkata on 23 rd November 2010 with a history of febrile illness, severe headache followed by disorientation for the last 4 days prior to admission. At the time of admission, the patient was totally unconscious, restless with macular eruptions all over the body, generalised lymphadenopathy and positive meningeal signs. CSF study revealed glucose 78.34 mg/dl, protein 135 mg/dl, cell count 92 (lymphocyte 80%). Blood sugar was 140 m/dl at that time [Table 1]. Blood and CSF sample of the patient was sent for virological investigations on the same day. Both blood and CSF samples were RT-PCR positive for CHIKV [Figure 1] and [Table 2].
On 28 th November, 2010, patient became stable although the headache continued. The patient was discharged from the hospital on 30 th November 2010. At time of discharge, patient had generalised weakness which started improving when he was examined subsequently in the hospital.
A non-diabetic, 29-years-old female patient was admitted to Nil Ratan Sircar Medical College and Hospital (NRSMCH), Kolkata on 24 th December 2010 with fever for seven days followed by vigorous rigour and chill. She had severe myalgias, headache followed by disorientation and neck rigidity. On admission, she had weakness in all four limbs which continued for 3 days. Initially, the weakness started at the lower limbs and then in upper limbs. The patient was semi-conscious, pulse rate was 80/min and blood pressure was 140/90 mm Hg. CNS examination revealed, diminished sensation up to upper chest level. The power in the lower limb was 1/5 and in upper limb, it was 4/5. Planter response was extensor bilaterally. The patient was treated with intravenous (IV) antibiotics, Methyl prednisolone 1 gm IV OD (Intravenous once per day) for 3 consecutive days. Investigation on 4 th January 2011 revealed that Malaria parasite was absent; haemoglobin and other routine parameters of peripheral blood were within normal range. CSF study showed glucose 66 mg/dl, protein 145 mg/dl, chloride 116.7 mEq/L. Random blood sugar level was 138 mg/dl [Table 1]. On the same day, virological investigations for CHIKV infection revealed that both blood and CSF samples were strongly reactive by ELISA method and negative by RT-PCR method [Figure 1], [Table 2]. MRI findings showed transverse myelitis, few hyper intense lesions (T2 and Flair lesion in supra and infra-tentorial white matter and in medulla which suggested the possibility of acute disseminated encephalomyelitis).
On 21 st January 2011, the patient was discharged from the hospital. The patient had significant clinical improvement at the time of discharge though, weakness of the lower limbs persisted (grade 3/5).
A non-hypertensive, non-diabetic and non-smoker 23-year-old male patient was admitted to the Seth Sukhlal Karnani Memorial (SSKM) hospital, Kolkata, India on 23 rd March, 2011 with a history of fever 3 days back followed by sudden onset tonic clonic movements of limbs and loss of consciousness, which lasted for about 24 hours. At the time of admission, he had speech problem with intractable hiccough and also had bulbar weakness. Examination on 25 th march, 2011, showed the involvement of right 7 th , 9 th , 10 th and 12 th cranial nerves with quadriparesis with increased deep tendon reflex and bilateral extensor plantar response. MRI findings suggested mild prominent cortical sulci. No focal lesion was seen in cerebral parenchyma. Signal changes were seen from right side of the medulla and also from right side of the cerebellum. Investigations showed normal haemogram and blood biochemistry. CSF study revealed cell count 15/mm 3 (all lymphocyte), ZN smear negative, sugar 93 mg/dl, protein 66 mg/dl, chloride 130 mEq/L and ADA 1.0U/L [Table 1]. Blood sugar level was 190 mg/dl at that time. On 30 th march, 2011 blood and CSF sample of the patient was referred to us for the detection of viral etiology. In blood sample IgM antibody against CHIKV was detected by ELISA method whereas viral RNA was detected in the CSF specimen [Figure 1] and [Table 2].
Patient received full dose of methylprednisolone IV. On treatment, he showed improvement; hiccoughs were controlled. On 14 th April 2011, he was discharged with favourable conditions with oral steroid schedule. Examination of the patient on 4 th may 2011 did not show any meningeal signs, fever or trauma but was seen with tongue fasciculation and deviation to right side on protrusion.He had motor power of 4/5 in upper limbs and 5/5 in lower limbs with increased DTR and plantar was flexor bilaterally. The patient was referred to the department of neurology for further opinion.
In all cases, informed consent was taken. The study was duly approved by the joint ethical committee of ICMR (Indian Council of Medical Research) virus unit, Kolkata and NICED (National Institute of Cholera and Enteric Diseases), Kolkata, India
| ~ Discussion|| |
Normally infection due to CHIKV is a self-limiting illness. But large scale CHIKV infection with the involvement of CNS had been reported for the first time during La Re' union Island outbreak.  About 10% of the affected patients died. In India, the first large series of neurological complications like encephalitis, myopathy, neuropathy, myelopathy and myeloneuropathy due to CHIKV infection was reported from Maharashtra in 2006.  In the same year, altered level of consciousness, confusion, disorientation, drowsiness and delirium were observed amongst the hospitalised patients in Kota, India due to CHIKV infection.  About one third of the affected individuals showed the complications at the CNS levels and some of them were died also. Acute CNS infections in children with a febrile illness, altered mental status and seizures were observed at Bellary, India.  In Andaman and Nicobar Island, four cases of acute flaccid paralysis were reported due to CHIKV infection. 
In West Bengal, India, although the virus has become endemic in nature since its resurgence in the year 2006, but no Chikungunya case have yet been reported with neurological complications till 2010. These four cases were detected from the referred AES cases and showed the involvement of CHIKV in CNS manifestation from this state for the first time. All these cases were confirmed by ELISA and RT-PCR method.  In all four cases CSF report showed lymphocyte pleocytosis with moderately raised CSF protein (range 66-135 mg/dl) which indicated the cases of viral encephalitis. Here the case-1 and case-2 had the acute encephalitis syndrome; case-3 was the case of acute disseminated encephalomyelitis whereas the case-4 had the symptoms of meningo-encephalopathy with bulbar involvement. In the case-3, both the blood and CSF sample was RT-PCR negative. It may be explained by the fact that the viral RNA can be detected within the viremia stage which persisted in the blood and CSF from 2-10 days. But exclusively the sample of the third case was detected on eighteenth day of illness when the IgM antibody has already ushered in the blood and CSF and neutralised the viral particles. So it could not be detected by RT-PCR method.
The re-emerging CHIKV is of central-east African origin, replaced the previous Asian genotype from this country.  It is remain unclear whether the severity of the disease is due to the lack of immunity in the population or the changing of genotype. Detail study is required for this purpose.
| ~ Ethical Approval|| |
The study was duly approved by the joint ethical committee of ICMR (Indian Council of Medical Research) virus unit and NICED (National Institute of Cholera and Enteric Diseases), Kolkata, India.
| ~ Acknowledgement|| |
This work was supported by from the intramural funds of Indian Council of Medical Research, Government of India We express our sincere thanks to Dr. Sekhar Chakrabarti, Officer-In-Charge, ICMR Virus Unit, for allowing us to carry out the work. The enthusiastic help obtained from the physicians of District Hospitals in West Bengal, for providing us with the clinically suspected samples for this study, is gratefully acknowledged.
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[Table 1], [Table 2]