432 Abstracts

NS4B, together with NS5 is capable of reducing cellularSTAT2 levels.

Discussion: These data provide further evidence of howdengue virus subverts the human innate immune responseand provide critical insights into disease pathogenesis.Th-ese data may enable us to engineer dengue viruses withenhanced sensitivity to IFNa, in order to generate saferand more cost-effective vaccine candidates

CHIKUNGUNYA VIRUS IS A CAUSE OFENCEPHALITIS IN CHILDREN IN BELLARY, INDIA

Penny Lewthwaite 1, Ashia Begum 2,M. Veerahsankar 2, R. Ravikumar 2, Anita Desai 3,Jane Osborne 4, Jenna Plank 4, Roger Hewson 4,V. Ravi 3, Nick Beeching 1, Tom Solomon 1

1University of Liverpool, Liverpool, United Kingdom2Vijayanagar Institute of Medical Sciences, Bellary,Karnataka, India3National Institute of Mental Health andNeurological Sciences, Bangalore, Karnataka, India4NADP, Health Protection Agency, Porton Down,United Kingdom

AbstractIntroduction: Chikungunya virus, a single stranded RNA

Alphavirus of the family Togaviridae, is transmitted tohumans by the bite of Aedes aegypti, Aedes albopictusand other mosquitoes. An epidemic starting in ReunionIslands in March 2005 spread to Southern India, affecting1.3 million people between Oct 2005 and Oct 2006. Theepidemic reached Bellary, Karnataka in southern India byDec 2005.

Methods: From Oct 2005 to Dec 2007, children admittedto the paediatric department of the Vijayanagar Institute ofMedical Sciences with an acute encephalitis syndrome wereprospectively studied. All children presenting to the paedi-atric ward were recruited if they had suspected CNS infec-tion or acute flaccid paralysis [and] fever or history of feverin the previous 2 weeks, together with one or more of thefollowing: meningism (neck stiffness), photophobia, severeheadache meriting lumbar puncture, altered mental state,reduced consciousness, convulsions, focal neurologicalsigns or acute flaccid paralysis.

Results: 243 patients have been recruited to date.Between April and Oct 2006, 8 children had positive plasmaPCR tests for Chikungunya RNA and are described in moredetail. Viral RNA was also detected by PCR in the CSF of 3of these 8. Mean age was 6 years, range 8 months to 11years, 5 were girls. 3 children had a rash at some stage intheir illness and one had conjunctivitis. Altered mentalstate was reported in 7, and 6 had a GCS of less than 15at admission. One had deafness, 3 had nausea and vomit-ing, and 3 had meningism. 7 had seizures, amongst whom4 had an episode of status epilepticus (seizure lastingmore than 30 minutes). 3 were aphasic during their illnessand 4 had extensor plantar reflexes. There were no fatali-ties. At discharge, 2 patients had ongoing aphasia. Theremaining 4 with a reduced GCS at admission had recoveredto full coma score. Sequencing information obtained from

the E1 envelope gene from plasma and CSF samplesconfirmed that the chikungunya genomes are of the EastAfrican lineage, which appears to have caused the moresevere epidemic form of illness, compared to the Asiangenotype which previously circulated in India.

Conclusions: Chikungunya virus causes encephalitis inchildren and may be found in the CSF. It can cause severeneurological disease sequelae although the extent to whichthese sequelae will persist is uncertain. Given frequenttravel between Asia and Europe and the potential forautochtonous transmission, as has occurred in Italy, weneed to be increasingly aware of global disease out-breaks.

A CASE OF HYPERCALCAEMIA IN THE RETURNINGTRAVELLER

Rebecca Lester, Samuel Douthwaite, Alec BoningtonDepartment of Infectious Diseases and TropicalMedicine (Monsall Unit), North Manchester GeneralHospital, Manchester, United Kingdom

AbstractA 51 year old Caucasian man with a history of alcohol

excess presented to our unit with a 2 month history offever, cough, worsening confusion and night sweats. Hissymptoms started on return from a trip to South East Asia.On examination, he had pyrexia, tachycardia, coarsecrackles in the right upper chest and abnormal neurology.His biochemistry revealed a significant hypercalcaemia of3.06mmol/L. CT Thorax showed right sided consolidationand hilar lymphadenopathy. The microbiologist at thereferring hospital had made a provisional diagnosis basedon a bronchial lavage. The patient received 6 months oftherapy during which time his symptoms and biochemicalabnormalities resolved. Extensive investigation and followup into the cause of the raised calcium revealed no obviousalternative cause. The hypercalcaemia resolved in parallelto treatment of the underlying infection.

UNUSUAL CAUSE OF A LARGE ULCER FROMTRAVELLING IN SOUTH AMERICA

Damian Mawer 1, Deborah Gascoyne-Binzi 2, HughMcGann 1

1St James’s University Teaching Hospital, Leeds,United Kingdom2Department of Microbiology, United Leeds TeachingHospitals NHS Trust, Leeds, United Kingdom

AbstractA 27 year old British man presented with a painless,

slowly enlarging ulcer on the lateral aspect of his left knee.The lesion had begun during a wildlife tour in the Pantanalregion of Brazil and the Southern Peruvian Amazon. Atpresentation it measured 11 x 6 cm and was characterisedby deeply undermined edges and a dense adherent eschar.It was debrided with larval therapy and then biopsied.Histology revealed numerous, atypical acid-alcohol fast