Deteksi Jalur Infeksi Bakteri Aeromonas hydrophila di Ikan Lele (Clarias spp.)

Abstract

Berbagai macam jenis ikan dapat terinfeksi Aeromonas hydrophila dan menyebabkan 80-100 % kematian dalam 1-2 minggu. Penelitian mengenai infeksi A. hydrophila telah banyak dilakukan untuk melihat patogenitas, manifestasi klinis dan perubahan histopatologi. Infeksi A. hydrophila melalui intramuscular menyebabkan kematian yang lebih tinggi dibandingkan infeksi melalui lingkungan, pakan dan intraperitoneal. Meski demikian belum banyak penelitian yang melaporkan jalur infeksi A. hydrophila. Penelitian ini bertujuan untuk menjelaskan jalur infeksi dan patogenesis A. hydrophila melalui infeksi buatan secara intramuscular di ikan lele (Clarias spp.) dengan mengevaluasi manifestasi klinis, histopatologi, jumlah A, hydrophila dan luas infeksi pada otot, kulit, insang, hati, limpa, dan ginjal. Hasil penelitian menunjukkan bahwa infeksi intramuscular A. hydrophila menyebabkan inflamasi dan hemoragi akibat peningkatan permeabilitas pembuluh darah dan menginduksi degenerasi serta nekrosis sel sehingga bakteri dapat masuk ke dalam sirkulasi darah kemudian menyebar dan menginfeksi epitel lamela insang, sitoplasma hepatosit hati, ellipsoid limpa, dan jaringan hematopoietik interstisial ginjal dalam waktu 3 jam pasca infeksi. Jumlah A. hydrophila di otot, kulit, insang, hati, limpa, dan ginjal tidak berbeda nyata namun pertumbuhan satu sel A. hydrophila menyebabkan pertambahan luas infeksi terbesar pada hati diikuti otot, kulit, limpa, ginjal kemudian insang. Puncak infeksi A. hydrophila terjadi pada 12-36 jam pasca infeksi.

Wide variety of fish can be infected by Aeromonas hydrophila and cause 80-100% of deaths within 1-2 weeks. Many studies has been done to define the pathogenicity, clinical signs and histopathological changes of A. hydrophila infection. Higher mortality rate occurs in intramuscular A. hydrophila infection compared to the environmental, oral and intraperitoneal infections. However, there is only a little number of studies have been reported about A. hydrophila infection pathway. This study aims to define the infection pathway and pathogenesis of A. hydrophila through intramuscular artificial infection in Clarias spp. by evaluating the clinical sign, histopathological changes, bacterial existence and the infection extent in muscle, skin, gills, liver, spleen, and kidney. The results showed that A hydrophila infection intramuscularly causes inflammation and hemorrhage due to increased permeability of blood vessels and induces cell degeneration and necrosis and resulting infiltrated A hydrophila in blood circulation then infect the epithelium of the gill lamella, cytoplasm of hepatic hepatocytes, spleen ellipsoid, and interstisial hematopoietic tissue of kidney within 3 hours post infection. The A. hydrophila amount in muscle, skin, gills, liver, spleen and kidney was not differ significantly but the accretion of a single cell A. hydrophila caused the largest expansion of infection area in the liver followed by muscle, skin, spleen, kidney and then gills. The highest infection occurs at 12-36 hours post infection.