DETEKSI RESISTENSI INSEKTISIDA SINTETIK PIRETROID PADA Aedes aegypti (L.) STRAIN PALEMBANG MENGGUNAKAN TEKNIK POLYMERASE CHAIN REACTION

Abstract. Aedes aegypti is a vector of several pathogens including dengue fever/dengue hemorrhagic fever virus. Five hundred thousand dengue haemorrhagic fever new cases occur every year throughout the world. Vector control is an effective way to break the transmission; unfortunately constant insecticide ultimately caused resistance. Insecticides resistance in Ae.aegypti was first discovered on trichloroetane diphenyl dichloro (DDT), followed by temephos and synthetic pyrethroid. Three detection ways according to WHO procedure are bioassay, biochemistry and molecular. The biochemical detection that conducted previously in Palembang were turned out negative, nevertheless incidence rate has not yet decreased. Molecular detection is needed to determine the mechanisms of insecticide resistance. Molecular detection can detect gene mutations in the metabolic enzyme and target site insecticides, such as the voltage gated sodium channel (VGSC). The purpose of research was to identify the Val1016Ile and Val1016Gly point mutation in the VGSC gene of Ae.aegypti in Palembang. Population were all 3rd and 4th instar larvae of Ae.aegypti derived from breeding eggs obtained from villages of Bukit Kecil, Ilir timur I and Sukarami sub distric. Identification took place in BBLK Palembang while molecular test took place both in BBLK Palembang and Clinical Microbiology Department of Muhammad Hoesin Hospital Palembang. Results showed that there has been Val1016Ile point mutation and there is no Val1016Gly point mutation of voltage gated sodium channel gene. It can be concluded that there has been Val1016Ile point mutation in the voltage gated sodium channel gene of Ae.aegypti as the marker of synthetic pyrethroid insecticides resistance in Palembang Keywords: Aedes aegypti, synthethic pyrehtroid resistance, point mutation VGSC, target site, Val1016Ile Abstrak. Aedes aegypti merupakan vektor dari berbagai patogen, termasuk diantaranya virus dengue fever. Sebanyak 500 ribu kasus baru demam berdarah dengue (DBD) terjadi tiap tahunnya di seluruh dunia. Pengendalian nyamuk vektor merupakan cara efektif memutus rantai penularan DBD. Namun penggunaan satu jenis insektisida secara intensif dalam waktu lama terbukti menyebabkan resistensi. Resistensi Ae.aegypti terhadap insektisida awalnya terjadi pada dichloro diphenyl trichloroetane (DDT), lalu terhadap temefos kemudian sintetik piretroid. Tiga cara mendeteksi resistensi sintetik piretroid menurut WHO yaitu bioassay, biokimia dan molekuler. Deteksi biokimia yang pernah dilakukan di Palembang menunjukkan hasil negatif, tetapi kenyataan incidence rate DBD belum turun. Penelitian lebih lanjut menggunakan deteksi molekuler diperlukan untuk mengetahui mekanisme resistensi insektisida. Deteksi molekuler dapat mendeteksi mutasi pada gen enzim metabolisme dan gen target site insektisida, semisal pada voltage gated sodium channel (VGSC). Penelitian ini dilakukan untuk mengidentifikasi mutasi titik gen VGSC Val1016Ile dan Val1016Gly Aedes aegypti. Desain penelitian ini adalah berupa deskriptif laboratoris dengan uji molekuler. Populasi adalah seluruh larva instar III-IV Ae. aegypti yang berasal dari pembiakan telur yang diperoleh dari kelurahan-kelurahan di Kecamatan Bukit Kecil, Sukarami dan Ilir Timur I kota Palembang. Identifikasi larva dilakukan di Balai Besar Laboratorium Kesehatan (BBLK) Palembang dan uji molekuler dilakukan di Departemen Mikrobiologi Klinik Rumah Sakit Muhammad Hoesin Palembang dan BBLK Palembang. Hasil penelitian menunjukkan terjadi mutasi titik Val1016Ile serta tidak terjadi mutasi titik Val1016Gly gen VGSC. Disimpulkan terjadi mutasi titik Val1016Ile gen VGSC Ae.aegypti sebagai penanda resistensi yang bersifat target site atas sintetik piretroid di Palembang. Kata Kunci: Aedes aegypti, resistensi insektisida, mutasi titik, target site, Val1016Il