Outbreak of Chikungunya Virus Infection, Vanimo, Papua New Guinea

Paul F. Horwood

, Lisa J. Reimer, Rosheila Dagina, Melinda Susapu, Grace Bande, Michelle Katusele, Gussy Koimbu, Stella Jimmy, Berry Ropa, Peter M. Siba, and Boris I. Pavlin

Author affiliations: Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea (P.F. Horwood, G. Bande, P.M. Siba); Papua New Guinea Institute of Medical Research, Madang, Papua New Guinea (L.J. Reimer, M. Katusele, G. Koimbu); National Department of Health, Port Moresby, Papua New Guinea (R. Dagina, M. Susapu, B. Ropa); Vanimo General Hospital, Vanimo, Papua New Guinea (S. Jimmy); World Health Organization, Port Moresby (B.I. Pavlin)

Abstract

In June 2012, health authorities in Papua New Guinea detected an increase in febrile illnesses in Vanimo. Chikungunya virus of the Eastern/Central/Southern African genotype harboring the E1:A226V mutation was identified. This ongoing outbreak has spread to ≥8 other provinces and has had a harmful effect on public health.

Chikungunya virus (CHIKV) is a mosquito-transmitted virus of the family Togaviridae and genus Alphavirus. CHIKV can be classified into 3 distinct genotypes: Asian, Eastern/Central/Southern African (ECSA), and Western African. The usual vectors for CHIKV are Aedes aegypti mosquitoes; Ae. albopictus mosquitoes are a potential secondary vector. Human infection with CHIKV results in illness characterized by high fever, severe polyarthralgia, headache, maculopapular rash, fatigue, nausea, and vomiting. CHIKV has recently been responsible for explosive outbreaks of disease in the Indian Ocean region (1) and southern India (2).
Before June 2012, chikungunya had not been reported in Papua New Guinea. The recent increase in reported outbreaks of chikungunya in Papua New Guinea has coincided with the appearance of a variant strain of CHIKV that has a mutation from alanine to valine at amino acid position 226 in the envelope 1 (E1) glycoprotein gene. This mutation enables CHIKV strains to more efficiently replicate in the salivary gland of Ae. albopictus mosquitoes, thus enhancing the role of this vector in transmission of virus to susceptible human hosts (3). We report molecular detection, epidemiologic and entomologic investigations, and viral genetic characterization for an outbreak of chikungunya in Papua New Guinea.