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Status Kerentanan Dan Mekanisme Resistensi Aedes aegypti Terhadap Insektisida Di Pelabuhan Dumai

Khairil Ardhi, Prof. dr. Tri Baskoro T Satoto, M.Sc., Ph.D; Dr. drh. Sitti Rahmah Umniyati, S

2024 | Tesis | S2 Ilmu Kedokteran Tropis

Latar belakang : Aedes aegypti adalah vektor penyakit arbovirus secara global. Pengendalian vektor bertujuan untuk mengurangi populasi vektor melalui intervensi pada tempat perkembangbiakan. Kepadatan vektor dan status kerentanan terhadap insektisida di Pelabuhan Dumai belum diketahui. Informasi ini akan mendukung pelaksanaan pengendalian vektor berbasis bukti.

Tujuan : Penelitian ini bertujuan untuk menilai kepadatan dan status kerentanan Ae. aegypti terhadap insektisida. Mekanisme resistensi juga dianalisi menggunakan uji biokimia dan molekuler.

Metode : Nyamuk dikumpulkan melalui survei larva dan ovitrap. Nyamuk dipelihara hingga dewasa dan diuji menggunakan uji kerentanan standar WHO. Uji biokimia dilakukan untuk lebih memahami mekanisme metabolik resistensi insektisida. Amplifikasi dengan PCR dilakukan untuk mendeteksi mutasi asam amino pada gen voltage-gated sodium channel (VGSC) dan gen Acetylcholinesterase-1 (AChE) dari nyamuk Ae. aegypti.

Hasil : Indeks entomologi berada di atas standar yang ditetapkan untuk pelabuhan oleh International Health Regulations tahun 2005. Resisten terhadap temefos ditemukan dengan nilai RR 9,75 hingga 11,75. Kematian Ae. aegypti kurang dari 90% diamati pada deltametrin 0,05?n permetrin 0,75%. Hasil uji biokimia menunjukkan bahwa aktivitas ?-esterase mengalami peningkatan. Mutasi V1016G/S989P (alel ganda) dan F1534C/V1016G/S989P (alel tiga) ditemukan pada Ae. aegypti. Sebaliknya, alel tipe liar G119 dari gen AChE ditemukan pada semua Ae. aegypti.

Kesimpulan : Tingkat infestasi Aedes spp yang tinggi menunjukkan risiko signifikan terhadap penularan penyakit arbovirus. Ae. aegypti sangat resisten terhadap temefos dan juga menunjukkan resisten terhadap piretroid. Mutasi pada gen AChE tidak ditemukan namun ditemukan mutasi pada gen VGSC.

Background : Aedes aegypti is the main vector of the arbovirus disease globally. Vector control is mainly based on reducing the vectors population through intervention, which target potential breeding sites. However, in Dumai International Seaport, little is known about this vector”s density and insecticide susceptibility status to support evidence-based implementation of control measures.

Objective : The present study aimed at asssessing the density and susceptibility status of Ae. aegypti  to various insecticides, and use biochemical and molecular assays to characterise resistance mechanism.

Method: Mosquito were collected in larval habitat surveys and through ovitraps. Mosquito reared to adult and tested using standar WHO susceptibility bioassays. Biochemical assays were conducted to further understand the metabolic mechanisms of insecticide resistance. Polymerase chain reaction (PCR) amplification conducted to detect amino acid mutations in paratype voltage gated sodium channel (VGSC) gene and Achetylcoline esterase-1 (AChE) gene of Ae. aegypti mosquitoes.

Result : All the entomological indices were above the critical level, prescribed for seaport by international health regulations Act, 2005. Resistance to temephos was observed, with RR values ranging from 9.75 to 11.75. Mortalities of Ae. aegypti were less than 90% observed against  deltamethrin 0,05% and permethrin 0,75%. The results of biochemical assays showed the presence of ?-esterase elevated activity. V1016G/S989P (double allele) and F1534C/V1016G/S989P (triple allele) mutations were found in Ae. aegypti. In contrast, G119 wild type allele of AChE gene was found from all Ae. Aegypti.

Conclusion : High infestations level observed indicate significant risk of Arboviruses disease.  Ae. aegypti is highly temephos resistant and also show of resistance againt pyrethroid. AChE gene mutation was not found. significant mutations were observed in the VGSC gene. 

Kata Kunci : Ae. aegypti, Pengendalian Vektor, Insektisida, Resistensi

  1. S2-2024-499992-abstract.pdf  
  2. S2-2024-499992-bibliography.pdf  
  3. S2-2024-499992-tableofcontent.pdf  
  4. S2-2024-499992-title.pdf