Abstract

Background : Chikungunya fever is an arboviral disease characterised by triad of fever, rash and polyarthralgia. Chikungunya virus (CHIKV) is transmitted to humans primarily via the bite of an infected Aedes species mosquito. The virus was first identified some 50 years back. The interest in the research of this disease increased after an important epidemiological outbreak in 2005 on the French metropolitan island of La Reunion and in India. In the last few years some of the unknown and varied manifestations of this arthropod borne alphavirus infection were brought into light. In fact, the name â€~chikungunya’ means â€~that which bends up’ in the Makonde language of East Africa and describes the severe arthritic pains of the disease.The clinical symptoms, in most affected individuals are high fever, severe myalgia and prolonged arthralgia, with occasional history of skin rash (petechiae). Neurologic complications were reported occasionally. Methods : Case Report: A 5-month-old infant presented with high grade fever and vomiting’s for 2 days, associated with irritability and 4 episodes of generalised tonic clonic seizures. Clinical examination revealed a toxic look, bulging AF, exaggerated reflexes. CNS and other system examination were normal. Child developed progressive respiratory failure despite escalating respiratory support requiring intubation and ventilation. Her blood reports including Hemogram, liver and renal function text and electrolytes were all within normal limits initially. Her CRP was elevated. Blood and urine cultures were sterile. Test for Dengue, Leptospira, Rickettsia, HSV, JE serologies, Widal test, Malaria were negative. CSF obtained on day 5 of illness showed 3mononuclear cells/mm3, sugar and protein level were 38 mg/ dl and 45.7 mg/dl respectively. Culture of CSF was negative for bacteria, fungi and mycobacteria. Result of a CSF PCR test for HSV DNA, Enterovirus RNA, VZV DNA, Neisseria meningitis DNA, Haemophilus species, Streptococcus pneumonia DNA, Cytomegalo virus DNA, Mycobacterium tuberculosis complex DNA were negative. During the stay in PICU the child developed rash on day 1 of illness which was maculopapular initially then vesicles appeared in perennial & peri-anal region which later spread to trunk and limbs. Subsequently the child had septic shock, DIC, with MODS (Transaminitis, AKI etc.). Inotropic support was optimised accordingly. Serum (MAC-IgM ELISA) collected 7 days after disease onset showed IgM antibodies to chikungunya virus. After initial antibiotic support, she was managed conservatively. She started showing progressive improvement, her inotropes were weaned and stopped, ventilator support was weaned and child was extubated successfully. Her rash subsided, sensorium and oral acceptance improved. At discharge, there were no neurological sequale noted. On follow up, after 3 months, child was asymptomatic. MRI Brain showed no detectable abnormalities. VEP and BERA were normal. Conclusion : This report highlights that, although rare, Chikungunyavirus may show neurotropism with very severe clinical presentation, including in young patients with unremarkable medical history in endemic regions. The virus can cause severe meningoencephalitis like our patient.

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