Rabu, 18 November 2015
MAREK’S DISEASE
Penyakit Marek atau Marek?s Disease adalah jenis penyakit kanker unggas, salah satu penyakit limfoproliferatif yang paling umum pada unggas yang menyebabkan infiltrasi mononuklear dari satu atau lebih sel berikut: saraf perifer, kelenjar kelamin (gonad), iris (mata), otot, jeroan /isi perut (viscera), dan kulit. Beberapa nama lain Marek?k Disease adalah "range paralysis ", "neural lymphoma" and "skin leukosis".
Penyakit Marek atau Marek?s Disease (MD) sebagai penyakit limfomatous dan neuropatik biasanya terjadi pada ayam ternakan atau peliharaan dan tidak biasa pada kalkun dan burung puyuh.
Penyakit ini dinamai Marek ahli patologi Hungaria Jozsef Marek, yang pada tahun 1907 pertama kali mengumumkan pengamatannya mengenai penyakit lumpuh yang menyerang empat ayam. Marek ?s Disease telah menyebabkan kerugian ekonomi yang banyak bagi industri unggas di seluruh dunia selama bertahun-tahun.
Penyakit ini dinamai Marek ahli patologi Hungaria Jozsef Marek, yang pada tahun 1907 pertama kali mengumumkan pengamatannya mengenai penyakit lumpuh yang menyerang empat ayam. Marek ?s Disease telah menyebabkan kerugian ekonomi yang banyak bagi industri unggas di seluruh dunia selama bertahun-tahun.
Pada awal 1920-an wabah dengan tingkat kematian tinggi dan tingginya angka kejadian tumor visceral sudah terjadi di Amerika Serikat. Bila banyak kondisi lingkungan yang disukai (oleh virus MD) maka akan menimbulkan penyebaran yang cepat dan penyakit ini bisa segera ditemukan di seluruh dunia. (Fehler. F, 2001). Menurut de Boer dan Djaenudin kejadian penyakit Marek?s Disease di Indonesia adalah pada tahun 1949.
Marek's Disease merupakan infeksi virus Herpes pada ayam, jarang pada kalkun yang dekat atau erat berhubungan dengan ayam, terlihat di seluruh dunia. Dari tahun 1980-an dan 1990-an strain yang sangat virulen telah menjadi problem di Amerika Utara dan Eropa.
EPIDEMIOLOGI
Kejadian Penyakit
Kejadian Marek?s Disease di dunia adalah di: Azerbaijan 1994, Belize Januari 2011, Bulgaria 1998, Kroasia Juni 2005, Estonia 2004, Georgia 1991, Islandia 1998, Kenya Maret 2010, Latvia 2005, Oktober 2006, Libya 2009, Liechtenstein 2003, Malta 2007, Moldova Mei 2001, Norwegia 2004, Polandia Desember 2010, Portugal 2009, Serbia Desember 2010, Seychelles (hewan terdomestikasi Maret 2011, hewan liar 12 Desember 2009), Singapore 1999, Slovenia Maret 2007, Swedia 2009, Thailand November 2009, Tunisia November 2008, Ukraina Desember 2000, Venezuela 2002, Zambia (hewan terdomestikasi Juni 2011 , hewan liar Desember 2010).
Negara dengan Kejadian Marek?s Disease (menunjukkan gejala klinis) pada tahun 2011: Afghanistan, Argentina, Australia, Bangladesh, Brasil, Kanada, Chili, Cina Taipei, Kolombia, Kosta Rika, Kuba, Republik Dominika, Finlandia, Polinesia Prancis, Jerman, Hong Kong (SAR - RRC), Irlandia, Israel, Jepang, Korea (Rep), Lebanon, Madagaskar, Malaysia, Myanmar, Namibia, Nepal, Belanda, Selandia Baru, Pakistan, Reunion (Prancis), Sao Tome dan Principe, Sri Lanka, Suriname, Inggris, Amerika Serikat, Uruguay, Zimbabwe.
Kejadian Marek?s Disease terbatas pada zona tertentu /wilayah negara: Hongaria Juli - Desember 2011, Palestina Auton Territories Juli-Desember 2011, Spanyol bulan Juli - Desember 2011. ( oie )
Hospes /Inang
Marek?s Disease (MD) utamanya menyerang ayam komersial, namun demikian dapat juga menyerang unggas liar ataupun kalkun. Sering terjadi MD menyerang ayam umur 2-5 bulan (belum matang secara seksual), tetapi dapat juga menyerang ayam pada saat produksi telurnya naik.
Penularan
Virus Marek dapat ditularkan melalui udara dalam kandang ayam. Virus ini berada dalam bulu bulu, debu kandang ayam, kotoran /feces dan air liur. Unggas unggas yang terinfeksi membawa virus dalam darah mereka dan merupakan sumber infeksi bagi burung burung yang rentan.
Virus Marek dapat ditularkan secara kontak langsung dan tidak langsung antara burung. Penularan terutama melalui rute udara sebagaimana virus dilepaskan pada sel sel epitel folikel bulu, bulu, debu kandang ayam, kotoran /feces dan air liur. Virus ini memiliki daya tahan hidup yang lama dalam bulu sebagaimana virus telah diisolasi dari kandang yang telah dilakukan depopulasi sejak berbulan-bulan. Penularan melalui telur tidak signifikan.
Sumber Penyakit
Sumber penyakit Marek?s Disease adalah: Unggas yang terinfeksi, bulu, debu kandang ayam, feses, air liur.
ETIOLOGI
Klasifikasi Agen Penyebab Penyakit
Group: Group I (dsDNA), Ordo: Herpesvirales, Famili: Herpesviridae, Subfamili: Alphaherpesvirinae, Genus: Mardivirus, Spesies: Gallid herpesvirus 2 (GaHV-2).
Ketahanan Terhadap Tantangan Fisik Dan Kimia
1. Suhu: MDV (Marek?s Disease Virus) cepat tidak aktif ketika dibekukan dan dicairkan (Paul MC, 2004). Bulu bulu rontok dari ayam yang terinfeksi MDV dan disimpan dalam keadaan kering ditemukan memiliki tingkat penularan MDV yang signifikan. Setelah penyimpanan selama 3 minggu pada 37,5 C, selama 8 (tapi tidak 13) bulan pada suhu kamar (22-25 C) dan minimal 3 tahun pada suhu 4 C. Dengan kelembaban relatif disesuaikan sampai 80 %, virus yang menular tidak dapat pulih setelah 1 sampai 2 minggu pada 37,5 C.
2. pH: Virus Marek sensitif pada suasana asam dan basa, virus mati pada pH <6 dan> 8.
3. Desinfektan: Resisten /tahan terhadap beberapa disinfektan (amonium kuaterner dan fenol) (Paul MC, 2004). Beberapa larutan kimia disinfektan (klorin, senyawa amonium kuartener, yodium organik, asam cresylic, fenol sintetis, dan natrium hidroksida), mampu menghancurkan infektivitas bulu kering dalam jangka waktu pemberian 10 menit. Fumigasi gas Formaldehyde menghancurkan sebagian besar tapi tidak semua dari infektivitas, sementara air suling, deterjen (Tween-80 /merek), dan asam asetat glasial tidak berpengaruh signifikan terhadap infektivitas bulu.
4. Ketahanan hidup: Virus bertahan untuk waktu yang lama (65 minggu) pada suhu lingkungan.
DIAGNOSA
Diagnosa berdasarkan pada sejarah, gejala klinis, distribusi lesi, usia hewan terinfeksi, ataupun dengan diagnosa laboratorium.
Penyakit ini memiliki berbagai manifestasi: a) Neurologis - Infiltrasi akut dari SSP (Sistim Syaraf Pusat) dan saraf yang mengakibatkan 'floppy broiler syndrome' dan kelumpuhan sementara, sebagaimana kelumpuhan kaki atau sayap dan lesi mata, b) Visceral - Tumor di hati, ovarium, otot, paru-paru, c) Cutaneous - Tumor folikel bulu.
Morbiditas adalah 10-50% dan Mortalitasnya hingga 100%. Kematian dalam sebuah kawanan yang terkena biasanya berlanjut pada tingkat sedang atau tinggi selama beberapa minggu. Infeksi Marek ?yang terlambat? biasanya dapat menimbulkan kematian sampai unggas berumur 40 minggu. Unggas yang terkena lebih rentan terhadap penyakit lain, baik parasit dan bakteri.
Gejala
Gejala klinis: penyakit Marek adalah jenis kanker unggas. Tumor pada saraf menyebabkan ketimpangan dan kelumpuhan. Tumor dapat terjadi pada mata dan menyebabkan pupil mata berbentuk tidak teratur dan kebutaan. Tumor hati, ginjal, limpa, gonad, pankreas, proventrikulus, paru-paru, otot, dan kulit dapat menyebabkan inkoordinasi, lemah, pucat, nafas lemah ataupun sesak, dan folikel bulu membesar. Pada tahap terminal, unggas kurus pucat, pial bersisik dan diare kehijauan. Penyakit Marek sangat mirip dengan Penyakit Limfoid Leukosis, tapi Marek biasanya terjadi pada ayam umur 12 sampai 25 minggu dan limfoid leukosis biasanya mulai terjadi pada unggas umur 16 minggu.
Gejala yang menonjol: 1. Kelumpuhan kaki, sayap dan leher; 2. Kehilangan berat badan; 3. Iris mata abu abu, pupil mata berbentuk tidak teratur; 4. Penglihatan berkurang; 5. Kulit di sekitar folikel bulu menonjol dan kasar.
Lesi
1. Penebalan urat saraf. Sering terlihat pembengkakan saraf perifer, khususnya saraf kaki dan sayap.
2. Foci (bintik) putih abu abu dari jaringan neoplastik dalam hati, limpa, ginjal, paru-paru, gonad, jantung, dan urat daging. Organ visceral mungkin berisi tumor mulai dari ukuran mikroskopis sampai ukuran cukup besar.
3. Mikroskopis - infiltrasi limfoid adalah polimorfik. Lesi tumor tersebut dapat dibingungkan dengan penyakit limfoid leukosis tanpa diagnosis laboratorium yang berkualitas.
(Paul McMullin 2004). (Anonimous, Miller Hatcheries. 2013).
Diagnosa Banding
- Avian Encephalomyelitis
- Erythroblastosis
- Genetic Grey Eye
- Histomoniasis
- Lymphoid leukosis
- Myeloblastosis
- Myelocytomatosis
- Newcastle Disease
- Ovarian Carcinoma
- Reticuloendotheliosis
- Riboflavin (vitamin B2) Deficiency
- Tuberculosis
Diagnosa Laboratorium
Sampel:
1. Bangkai; 2. Jaringan /organ segar dari ayam yang terinfeksi; 3. Darah; 4. Bulu; 5. Tumor.
Identifikasi Agen Penyakit:
a. Isolatsi virus:
Infeksi Virus Marek?s Diseases pada sekelompok ternak dapat dideteksi dengan mengisolasi virus dari jaringan ayam yang terinfeksi. Namun, sifat dasar mana-mana dari MDV yang harus dalam pertimbangan dan diagnosis MD harus didasarkan pada kombinasi dari isolasi MDV atau deteksi genom oleh polymerase chain reaction (PCR) dan penyakit klinis. Sumber yang umum digunakan adalah sel buffy coat dari sampel darah dengan heparin, atau suspensi sel limfoma atau sel limpa. Saat sampel ini dikumpulkan di lapangan, disarankan agar diangkut ke laboratorium dalam kondisi dingin. Sebagaimana MDV sangat terkait dengan sel, adalah penting bahwa suspensi sel ini mengandung sel-sel yang viabel. Suspensi sel diinokulasi ke dalam kultur monolayer sel ginjal ayam atau fibroblas embrio bebek (chicken embryo fibroblasts = CEF, kurang sensitif untuk isolasi virus primer). Virus serotipe 2 dan 3 lebih mudah diisolasi di CEF daripada di sel ginjal ayam. Biasanya 0,2 ml suspensi mengandung 106-107 sel hidup diinokulasi ke duplikat monolayers tumbuh di piring kultur sel plastik (diameter 60 mm). Kultur yang diinokulasi dan kultur tanpa inokulasi diinkubasi pada 38,5 C dalam inkubator lembab yang mengandung 5 % CO2. Sebagai alternatif, kultur vessel tertutup dapat digunakan. Media kultur diganti dalam interval 2 hari. Area efek sitopatik, disebut plak, muncul dalam waktu 3-5 hari dan bisa dihitung sekitar 7-10 hari.
Satu lagi, yang tidak biasa digunakan sumber dari MDV untuk tujuan diagnostik adalah tip bulu, yang mana cell-free MDV dapat diekstraksi. Tip sekitar 5 mm, atau saluran cincang kulit berisi tip bulu, yang disuspensikan dalam SPGA /EDTA (sucrose, phosphate, glutamate and albumin /ethylenediamine tetra-acetic acid) buffer untuk ekstraksi dan titrasi cell-free MDV (Calnek et al., 1970). Buffer dibuat sebagai berikut: 0,2180 M sukrosa (7,462 g); 0,0038 M monopotassium fosfat (0,052 g); 0,0072 M dipotassium fosfat (0,125 g); 0,0049 M L-monosodium glutamat (0,083 g); 1,0% bubuk bovine albumin (1.000 g); 0,2% EDTA (0,200 g), dan air suling (100 ml). Buffer disterilkan dengan filtrasi dan harus di sekitar pH 6,5.
Suspensi ini disonikasi dan kemudian disaring melalui 0,45 ?m filter membran untuk inokulasi selama diatas 24 jam drained monolayers sell ginjal ayam. Setelah absorbsi selama 40 menit, medium ditambahkan, dan kultur diinkubasi seperti di atas selama 7-10 hari.
Menggunakan metode ini, MDV serotipe 1 dan 2 dapat diisolasi, bersama-sama dengan HVT (serotipe 3), bila merepresentasikan hasil vaksinasi. Dengan pengalaman, plak yang disebabkan oleh serotipe virus yang berbeda dapat dibedakan cukup akurat atas dasar saat penampilan, laju perkembangan, dan morfologi plak. Plak HVT muncul lebih awal dan lebih besar dari serotipe 1 plak, sedangkan serotipe 2 plak muncul kemudian dan lebih kecil dari serotipe 1 plak.
Plak MDV dan HVT dapat diidentifikasi sebagaimana tersebut dengan menggunakan antibodi spesifik yang dikumpulkan dalam ayam. Antibodi monoklonal dapat digunakan untuk membedakan serotipe.
b. Deteksi Antigen:
Sebuah variasi dari uji AGID digunakan untuk serologi (di bawah) dapat digunakan untuk mendeteksi antigen MDV dalam tip bulu sebagai indikasi infeksi oleh MDV. Slide kaca disiapkan dengan coating dari 0,7% agarosa (misalnya A37) dalam 8% sodium chloride, yang mengandung antiserum MDV. Tip bulu kecil yang diambil dari burung-burung yang akan diperiksa dan dimasukkan secara vertikal ke dalam agar-agar, dan slide dipertahankan seperti yang dijelaskan di bawah. Pengembangan zona radial presipitasi sekitar tips bulu menunjukkan keberadaan antigen MDV di bulu dan adanya infeksi pada burung.
c. Polymerase chain reaction (PCR):
Genom dari ketiga serotipe telah benar-benar disequensing. Uji PCR telah dikembangkan untuk diagnosis MD. Real-time PCR kuantitatif /Real-time quantitative PCR (qPCR) untuk mengukur salinan genom MDV juga telah digambarkan. Selain itu, tes PCR memungkinkan diferensiasi strain onkogenik dan non-onkogenik serotipe 1 MDV, dan strain vaksin MDV serotipe 2 dan 3 telah digambarkan. PCR juga dapat digunakan untuk menentukan jumlah /kuantitas bawaan virus dalam jaringan atau mendeteksi deferensiasi MDV dan HVT dalam darah atau tip bulu. (oie).
Tes /Uji Serologi:
Keberadaan antibodi terhadap MDV pada ayam yang tidak divaksinasi dari sekitar umur 4 minggu merupakan indikasi infeksi. Sebelum umur itu, antibodi tersebut dapat mengindikasikan penularan maternal antibodi melalui kuning telur dan bukti bukan infeksi aktif.
a. Agar gel immunodiffusion (AGID):
Tidak ada tes dipersyaratkan untuk perdagangan, tetapi uji agar gel immunodiffusion (AGID) paling umum digunakan untuk mendeteksi antibodi. Tes ini dilakukan dengan menggunakan slide kaca dicoating dengan 1 % agar dalam buffer fosfat salin yang mengandung 8 % natrium klorida. Sumur yang berdekatan diisi dengan antigen atau serum dan ini diinkubasi dalam suasana lembab pada suhu 37 C selama 24 jam agar difusi berlangsung; reaksi sera positip ditunjukkan dari identitas dengan diketahui serum positif dan antigen. Antigen yang digunakan dalam tes ini adalah tiap terpisahnya sel kultur jaringan MDV terinfeksi atau ekstrak tip bulu, atau kulit yang mengandung saluran bulu yang diperoleh dari ayam terinfeksi MDV. Kultur sel antigen disiapkan dengan mempropagasi MDV dalam sel ginjal ayam atau sel fibroblast embrio ayam. Bila efek sitopatik bertemu, sel-sel yang terlepas dari kultur vesel dan tersuspensi dalam media kultur atau phosphate buffered saline tanpa tryptose phosphate broth (kehadiran tryptose phosphate broth dapat menghasilkan garis precipitin non - spesifik pada konsentrasi sekitar 1 107 sel /ml. Suspensi ini kemudian membekukan - dicairkan tiga kali dan digunakan sebagai antigen.
Prosedur uji:
i) Buat larutan Difco Bactoagar 1% dalam 8% natrium klorida (sodium chloride) dengan membuat campuran dalam water bath panas.
ii) Sebuah slide mikroskop atau cawan Petri dapat digunakan dan agar dituangkan ke ketebalan 2-3 mm.
ii) Sebuah slide mikroskop atau cawan Petri dapat digunakan dan agar dituangkan ke ketebalan 2-3 mm.
iii) Potong lubang dalam agar menggunakan template dengan pusat sumur dan 6 sumur buat jarak pada jarak yang sama di sekitar pusat sumur. Diameter sumur harus sekitar 5,3 mm, dan sumur harus sekitar 2,4 mm terpisah. Sebuah template dengan pemotong tersedia secara komersial.
iv) Antigen ditempatkan tepat di tengah dan antiserum standar ditempatkan dalam sumur eksterior alternatif. Sampel serum yang akan diuji ditempatkan di sisa tiga sumur sehingga. Identitas garis kontinu terbentuk antara sampel yang tidak diketahui yang positif dan diketahui positif serum kontrol.
v) Inkubasikan slide selama 24 jam pada suhu 37 C dalam wadah lembab dan baca hasil diatas lampu di ruang yang gelap.
b. Uji lain:
Tes-tes lain untuk antibodi MDV meliputi tes antibodi fluorescent langsung dan tidak langsung. Ini menunjukkan kemampuan dari uji serum tes untuk mewarnai plak MDV dalam kultur sel (Silva et al, 1997;. Spencer & Calnek, 1970). Uji ini adalah kelompok spesifik dan lebih sensitif dibandingkan dengan pengujian AGID. Sebuah Uji netralisasi virus berkaitan dengan kemampuan serum untuk menetralkan properti pembentuk plak dari sel bebas MDV juga dapat digunakan. Namun, uji ini lebih cocok untuk tujuan penelitian dari pada untuk penggunaan diagnosa rutin. Enzyme-linked immunosorbent assay (ELISA) untuk mendeteksi antibodi MDV telah ada (Cheng et al, 1984;. Sharma, 1998; Zelnik et al, 2004.). Untuk mempersiapkan antigen untuk ELISA, sumur sumur piring microtitre dari 96 sumur dicoating dengan sel terinfeksi MDV. (oie).
PENCEGAHAN DAN PENANGGULANGAN
Pencegahan Dengan Sanitasi
Seleksi genetik: Dapatkan ayam yang tahan MD. Langkah pertama untuk mengelola penyakit ini adalah mengidentifikasi apakah virus yang terlihat dalam kawanan unggas kita dari beberapa kawanan yang tahan terhadap penyakit ini. Sebagaimana diketahui cara terbaik untuk mencegah penyakit Marek adalah dengan mengembangkan unggas yang secara alami resisten terhadap virus. Memperoleh kawanan unggas dan penggunaan pejantan yang tahan terhadap MD, karena ada tingkat kekuatan heritabilitas ketahanan genetik terhadap MD. Sebagai alternatif, mengikuti suatu wabah menggunakan jantan selamat yang kuat sebagaimana burung-burung ini telah menunjukkan resistensi terhadap MD. Mengembangkan kawanan unggas yang secara genetik resisten terhadap Penyakit Mareks adalah cara terbaik untuk menyembuhkan penyakit, tapi ingat langkah-langkah manajemen stres juga suatu keharusan!
Faktor stres terutama stres sosial dikenal mempercepat timbulnya Penyakit Mareks. Stres sosial adalah bentuk kecemasan yang dihasilkan oleh kepadatan populasi dalam kandang, sanitasi yang buruk, perkandangan yang tidak tepat, penyakit lain seperti cacing, koksidiosis, kutu dan tungau, atau pencampuran burung yang lebih tua dengan burung muda, yang mencegah burung muda dari istirahat makan atau minum pada dasarnya mencegah mereka untuk menjadi leluasa /senang. Manajemen stres adalah cara terbaik untuk mengontrol Mareks Disease pada ternak yang sebelumnya telah mengalami penyakit Mareks dari waktu ke waktu.
FAPP (filtered air positive pressure) ventilasi: Gunakan filter biologis untuk mencegah virus di udara.
Vaksinasi saja tidak akan mencegah penyakit Marek. Khusus untuk ternak komersial, penting untuk memiliki biosecurity yang baik untuk memastikan bahwa anak ayam yang divaksin akan mengembangkan kekebalan sebelum mereka mengalami tantangan berat dari virus. Misalnya, anak ayam harus dipelihara secara terpisah sehingga mereka bebas dari bulu yang terinfeksi dan debu burung yang lebih tua. Langkah-langkah kebersihan standar juga penting, termasuk kebersihan dan desinfeksi gudang dan peralatan dengan disinfektan yang efektif terhadap virus. Nutrisi yang baik dan pemeliharaan kebebasan dari penyakit lain dan parasit juga sangat penting. Praktek ini akan membantu menjaga kesehatan kawanan dan untuk memastikan bahwa burung memiliki ketahanan yang optimal terhadap infeksi Marek?s Disease.
Pengembangbiakan genetik dari ayam strain resisten, dikombinasikan dengan penggunaan vaksinasi dan kebersihan yang baik, juga dapat digunakan untuk membantu mengendalikan penyakit Marek.
Untuk Peternakan dengan masalah penyakit Marek yang serius, satu-satunya solusi adalah dengan depopulasi, bersihkan dan disinfeksi semua gudang dan peralatan, dan kosongkan kandang selama beberapa bulan. Kemudian ayam yang sudah divaksinasi dari penetasan yang terpercaya dapat dipakai sebagai pengganti.
Pengobatan Dan Pencegahan Secara Medis
Tidak ada pengobatan untuk penyakit Marek. Unggas yang sakit harus segera dimusnahkan dari kawanan dan musnahkan secara manusiawi. Unggas lain dalam kawanan yang mungkin terinfeksi pada tahap ini juga dimusnahkan, pengawasan yang ketat dari semua unggas adalah penting.
Vaksinasi adalah strategi utama untuk pencegahan dan pengendalian penyakit Marek. Kemanjuran vaksin dapat ditingkatkan, dengan sanitasi yang ketat untuk mengurangi atau menunda paparan dan oleh pemuliaan hewan untuk genetik yang resisten. Mungkin vaksin yang paling banyak digunakan terdiri dari virus herpes kalkun /turkey herpesvirus (HVT), yang telah terlihat dengan peningkatan pesat penggunaanya dalam beberapa tahun terakhir sebagai tulang punggung dalam vaksin rekombinan yang menampilkan penyisipan gen dari virus unggas lainnya, seperti virus Newcastle Disease, infeksi virus Bursal Disease, atau infeksi virus ILT (Infectious Laryngotracheitis ). Vaksin rekombinan menawarkan perlindungan terhadap kedua virus Marek?s Disease dan virus yang dimasukkan. Vaksin bivalen terdiri dari HVT dan strain SB - 1 atau 301B /1 dari Gallid herpesvirus 3 telah digunakan untuk memberikan perlindungan tambahan terhadap tantangan dengan isolat virus Marek?s disease yang virulent. Tampaknya vaksin komersial yang paling protektif yang tersedia saat ini CVI988/Rispens, virus Marek?s disease yang dilemahkan yang juga biasa dicampur dengan HVT pada saat vaksinasi. Karena vaksin diberikan pada penetasan dan membutuhkan 1-2 minggu untuk menghasilkan kekebalan yang efektif, paparan virus terhadap ayam harus diminimalkan selama beberapa hari pertama setelah menetas.
Vaksin juga efektif jika diberikan pada embrio pada hari ke-18 inkubasi. Dalam vaksinasi ovo sekarang dilakukan oleh teknologi otomatis dan secara luas digunakan untuk vaksinasi ayam broiler komersial, terutama karena biaya tenaga kerja berkurang dan presisi yang lebih besar dari pemberian vaksin.
Penanganan vaksin selama thawing dan pemulihan sangat penting untuk memastikan bahwa dosis yang diberikan tepat. Cell-associated vaccines umumnya lebih efektif daripada cell-free vaccines, karena mereka kurang dinetralkan oleh maternal antibodi. Dalam kondisi yang khas, kemanjuran atau efektifitas vaksin biasanya > 90 %. Sejak munculnya vaksinasi, kerugian dari penyakit Marek telah berkurang secara dramatis pada peternakan broiler dan layer. Namun, penyakit bisa menjadi masalah serius dalam kelompok tertentu atau wilayah geografis tertentu. Dari sekian banyak penyebab yang dikemukakan terjadinya kerugian yang berlebihan, paparan awal strain virus yang sangat virulen tampak menjadi salah satu penyebab yang paling penting.
***Penulis: drh. Giyono Trisnadi - dari berbagai sumber
English Version
MAREK?S DISEASE
Marek's disease (MD) is one of the most common lymphoproliferative diseases of chickens which causes mononuclear infiltration of one or more of the following cells: peripheral nerves, gonad, iris, muscle, viscera, and skin. MD has been called by several names including "range paralysis", "neural lymphoma" and "skin leukosis".
Marek's disease (MD) is a common lymphomatous and neuropathic disease of the domestic chicken and, less commonly, of turkey and quail. It is named after the Hungarian pathologist Jozsef Marek, who in 1907 first published his observations of a paralytic disease affecting four cocks. Marek?s disease have caused serious economic losses to the poultry industry worldwide for many years.
In the early 1920?s outbreaks with high mortality and high incidence of visceral tumors already occurred in USA. The environmental conditions described above favoured a rapid spread and the disease could soon be found all over the world. In Indonesia occurrence of Marek?s disease was in 1949, reported by de Boer and Djaenudin.
Marek's disease is a Herpes virus infection of chickens, and rarely turkeys in close association with chickens, seen worldwide. From the 1980s and 1990s highly virulent strains have become a problem in North America and Europe.
EPIDEMIOLOGY
Occurence
The last occurrence of Marek?s Diseases in the word: Azerbaijan 1994, Belize January 2011, Bulgaria 1998, Croatia June 2005, Estonia 2004, Georgia 1991, Iceland 1998, Kenya March 2010, Latvia 2005, October 2006, Libya 2009, Liechtenstein 2003, Malta 2007, Moldova May 2001, Norway 2004, Poland December 2010, Portugal 2009, Serbia December 2010, Seychelles (domestic March 2011, wild 12 December 2009), Singapore 1999, Slovenia March 2007, Sweden 2009, Thailand November 2009, Tunisia November 2008, Ukraine December 2000, Venezuela 2002, Zambia (domestic June 2011, wild December 2010).
Country with Occurence of Marek?s Disease (Demonstrated clinical disease) in year 2011: Afghanistan, Argentina, Australia, Bangladesh, Brazil, Canada, Chile, Chinese Taipei, Colombia, Costa Rica, Cuba, Dominican Republic, Finland, French Polynesia, Germany, Hong Kong (SAR - PRC), Ireland, Israel, Japan, Korea (Rep. of), Lebanon, Madagascar, Malaysia, Myanmar, Namibia, Nepal, Netherlands, New Zealand, Pakistan, Reunion (France), Sao Tome and Principe, Sri Lanka, Suriname, United Kingdom, United States of America, Uruguay, Zimbabwe.
Disease restricted to certain zone(s) / region(s) of the country: Hungary July - December 2011, Palestinian Auton. Territories July ? December 2011, Spain July - December 2011.(oie).
EPIDEMIOLOGY
Occurence
The last occurrence of Marek?s Diseases in the word: Azerbaijan 1994, Belize January 2011, Bulgaria 1998, Croatia June 2005, Estonia 2004, Georgia 1991, Iceland 1998, Kenya March 2010, Latvia 2005, October 2006, Libya 2009, Liechtenstein 2003, Malta 2007, Moldova May 2001, Norway 2004, Poland December 2010, Portugal 2009, Serbia December 2010, Seychelles (domestic March 2011, wild 12 December 2009), Singapore 1999, Slovenia March 2007, Sweden 2009, Thailand November 2009, Tunisia November 2008, Ukraine December 2000, Venezuela 2002, Zambia (domestic June 2011, wild December 2010).
Country with Occurence of Marek?s Disease (Demonstrated clinical disease) in year 2011: Afghanistan, Argentina, Australia, Bangladesh, Brazil, Canada, Chile, Chinese Taipei, Colombia, Costa Rica, Cuba, Dominican Republic, Finland, French Polynesia, Germany, Hong Kong (SAR - PRC), Ireland, Israel, Japan, Korea (Rep. of), Lebanon, Madagascar, Malaysia, Myanmar, Namibia, Nepal, Netherlands, New Zealand, Pakistan, Reunion (France), Sao Tome and Principe, Sri Lanka, Suriname, United Kingdom, United States of America, Uruguay, Zimbabwe.
Disease restricted to certain zone(s) / region(s) of the country: Hungary July - December 2011, Palestinian Auton. Territories July ? December 2011, Spain July - December 2011.(oie).
Hosts
Marek's disease is primarily a disease of commercial chickens, but it can also affect turkeys. MD often occurs in 2-5 month-old (sexually immature) chickens but can also occur after the onset of egg production.
Transmission
The Marek's virus is transmitted by air within the poultry house. It is in the feather dander, chicken house dust, feces and saliva. Infected birds carry the virus in their blood for life and are a source of infection for susceptible birds.
MDV can be transmitted by direct and indirect contact between birds. Transmission is primarily by airborne route as the virus is shed in epithelial cells of the feather follicle, dander, chicken house dust, feces and saliva. The virus has a long survival time in dander since viable virus has been isolated from houses that have been depopulated for many months. (Historically, prior to vaccine availability, control in broilers was based upon early brooding exposure to used broiler litter and dander, marketing survivors versus poorer results with the thoroughly cleaned and disinfected brooder houses). Transmission by egg has no significance (i.e., chicken hatched and reared in isolation will be free of MDV.
Sources of agent
Infected birds, feather, dander, chicken house dust, feces and saliva.
AETIOLOGY
Classification Of The Causative Agent
Group: Group I (dsDNA), Order: Herpesvirales, Family: Herpesviridae, Subfamily: Alphaherpesvirinae, Genus: Mardivirus, Species: Gallid herpesvirus 2 (GaHV-2).
Resistance To Physical And Chemical Action
1.Temperature: MDV (Marek?s Disease Virus) is inactivated rapidly when frozen and thawed (Paul MC, 2004). Feathers plucked from MDV infected chickens and stored in the dry state were found to have significant levels of infectious MDV. after storage for at least 3 weeks at 37.5C., for 8 (but not 13) months at room temperature 22?25C.) and for at least 3 years at 4C. With the relative humidity adjusted to 80%, infectious virus could not be recovered after 1 to 2 weeks at 37.5C.
2. pH: Virus sensitive at acids and alkalis, dies at pH < 6 and > 8.
3. Disinfectants: resistant to some disinfectants (quaternary ammonium and phenol) (Paul MC, 2004). Several chemical disinfectant solutions (chlorine, quaternary ammonium compound, organic iodine, cresylic acid, synthetic phenol, and sodium hydroxide), were able to destroy infectivity of dried feathers within a 10-minute treatment period. Formaldehyde gas fumigation destroyed most but not all of the infectivity, while distilled water, a detergent (Tween-80), and glacial acetic acid were without significant effect on the infectivity of the feathers.
4. Survival: The virus survives at ambient temperature for a long time (65 weeks) when cell associated.
DIAGNOSIS
3. Disinfectants: resistant to some disinfectants (quaternary ammonium and phenol) (Paul MC, 2004). Several chemical disinfectant solutions (chlorine, quaternary ammonium compound, organic iodine, cresylic acid, synthetic phenol, and sodium hydroxide), were able to destroy infectivity of dried feathers within a 10-minute treatment period. Formaldehyde gas fumigation destroyed most but not all of the infectivity, while distilled water, a detergent (Tween-80), and glacial acetic acid were without significant effect on the infectivity of the feathers.
4. Survival: The virus survives at ambient temperature for a long time (65 weeks) when cell associated.
DIAGNOSIS
History, clinical signs, distribution of lesions, age affected, histopathology.
The disease has various manifestations: a) Neurological - Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis, as well as more long-standing paralysis of legs or wings and eye lesions; b) Visceral - Tumours in heart, ovary, tests, muscles, lungs; c) Cutaneous - Tumours of feather follicles.
Morbidity is 10-50% and mortality up to 100%. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. In 'late' Marek's the mortality can extend to 40 weeks of age. Affected birds are more susceptible to other diseases, both parasitic and bacterial.
The disease has various manifestations: a) Neurological - Acute infiltration of the CNS and nerves resulting in 'floppy broiler syndrome' and transient paralysis, as well as more long-standing paralysis of legs or wings and eye lesions; b) Visceral - Tumours in heart, ovary, tests, muscles, lungs; c) Cutaneous - Tumours of feather follicles.
Morbidity is 10-50% and mortality up to 100%. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. In 'late' Marek's the mortality can extend to 40 weeks of age. Affected birds are more susceptible to other diseases, both parasitic and bacterial.
Signs
Clinical signs: Marek's disease is a type of avian cancer. Tumors in nerves cause lameness and paralysis. Tumors can occur in the eyes and cause irregularly shaped pupils and blindness. Tumors of the liver, kidney, spleen, gonads, pancreas, proventriculus, lungs, muscles, and skin can cause incoordination, unthriftiness, paleness, weak labored breathing, and enlarged feather follicles. In terminal stages, the birds are emaciated with pale, scaly combs and greenish diarrhea. Marek's disease is very similar to Lymphoid Leukosis, but Marek's usually occurs in chickens 12 to 25 weeks of age and Lymphoid Leukosis usually starts at 16 weeks of age.
The main sign: 1. Paralysis of legs, wings and neck; 2. Loss of weight; 3. Grey iris or irregular pupil; 4. Vision impairment; 5. Skin around feather follicles raised and roughened.
Lesions
1. Grey-white foci of neoplastic tissue in liver, spleen, kidney, lung, gonads, heart, and skeletal muscle. The visceral organs may contain tumors ranging from microscopic size to fairly large.
2. Thickening of nerve trunks and loss of striation. Swelling of the peripheral nerves, particularly of the nerves of the leg and wing, is often noticeable. 3. Microscopically - lymphoid infiltration is polymorphic. Such tumor lesions may be confused with those of lymphoid leukosis without a qualified laboratory diagnosis.
Differential Diagnosis
- Avian Encephalomyelitis
- Erythroblastosis
- Genetic Grey Eye
- Histomoniasis
- Lymphoid leukosis
- Myeloblastosis
- Myelocytomatosis
- Newcastle Disease
- Ovarian Carcinoma
- Reticuloendotheliosis
- Riboflavin (Vitamine B2) Deficiency
- Tuberculosis
Samples:
1. Cadaver; 2. Fresh tissue organ from infected chicken; 3. Blood; 4. Feather pulp; 5. Tumors.
Identification Test Of The Agent:
a. Virus isolation:
Infection by MDV in a flock may be detected by isolating the virus from the tissues of infected chickens. However, the ubiquitous nature of MDV must be taken into consideration and the diagnosis of MD should be based on a combination of MDV isolation or detection of the genome by polymerase chain reaction (PCR) and clinical disease. Commonly used sources are buffy coat cells from heparinised blood samples, or suspensions of lymphoma cells or spleen cells. When these samples are collected in the field, it is suggested that they be transported to the laboratory under chilled conditions. As MDV is highly cell associated, it is essential that these cell suspensions contain viable cells. The cell suspensions are inoculated into monolayer cultures of chicken kidney cells or duck embryo fibroblasts (chicken embryo fibroblasts (CEF) are less sensitive for primary virus isolation). Serotype 2 and 3 viruses (see Section C.1.a) are more easily isolated in CEF than in chicken kidney cells. Usually a 0.2 ml suspension containing from 106 to 107 live cells is inoculated into duplicate monolayers grown in plastic cell culture dishes (60 mm in diameter). Inoculated and uninoculated control cultures are incubated at 38.5C in a humid incubator containing 5% CO2. Alternatively, closed culture vessels may be used. Culture medium is replaced at 2-day intervals. Areas of cytopathic effects, termed plaques, appear within 3?5 days and can be enumerated at about 7?10 days.
a. Virus isolation:
Infection by MDV in a flock may be detected by isolating the virus from the tissues of infected chickens. However, the ubiquitous nature of MDV must be taken into consideration and the diagnosis of MD should be based on a combination of MDV isolation or detection of the genome by polymerase chain reaction (PCR) and clinical disease. Commonly used sources are buffy coat cells from heparinised blood samples, or suspensions of lymphoma cells or spleen cells. When these samples are collected in the field, it is suggested that they be transported to the laboratory under chilled conditions. As MDV is highly cell associated, it is essential that these cell suspensions contain viable cells. The cell suspensions are inoculated into monolayer cultures of chicken kidney cells or duck embryo fibroblasts (chicken embryo fibroblasts (CEF) are less sensitive for primary virus isolation). Serotype 2 and 3 viruses (see Section C.1.a) are more easily isolated in CEF than in chicken kidney cells. Usually a 0.2 ml suspension containing from 106 to 107 live cells is inoculated into duplicate monolayers grown in plastic cell culture dishes (60 mm in diameter). Inoculated and uninoculated control cultures are incubated at 38.5C in a humid incubator containing 5% CO2. Alternatively, closed culture vessels may be used. Culture medium is replaced at 2-day intervals. Areas of cytopathic effects, termed plaques, appear within 3?5 days and can be enumerated at about 7?10 days.
Another, less commonly used source of MDV for diagnostic purposes is feather tips, from which cell-free MDV can be extracted. Tips about 5 mm long, or minced tracts of skin containing feather tips, are suspended in an SPGA/EDTA (sucrose, phosphate, glutamate and albumin/ethylenediamine tetra-acetic acid) buffer for extraction and titration of cell-free MDV (Calnek et al., 1970). The buffer is made as follows: 0.2180 M sucrose (7.462 g); 0.0038 M monopotassium phosphate (0.052 g); 0.0072 M dipotassium phosphate (0.125 g); 0.0049 M L-monosodium glutamate (0.083 g); 1.0% bovine albumin powder (1.000 g); 0.2% EDTA (0.200 g); and distilled water (100 ml). The buffer is sterilised by filtration and should be at approximately pH 6.5.
This suspension is sonicated and then filtered through a 0.45 ?m membrane filter for inoculation on to 24- hour-old drained chicken kidney cell monolayers. After absorption for 40 minutes, the medium is added, and cultures are incubated as above for 7?10 days.
Using these methods, MDV of serotypes 1 and 2 may be isolated, together with the HVT (serotype 3), if it is present as a result of vaccination. With experience, plaques caused by the different virus serotypes can be differentiated fairly accurately on the basis of time of appearance, rate of development, and plaque morphology. HVT plaques appear earlier and are larger than serotype 1 plaques, whereas serotype 2 plaques appear later and are smaller than serotype 1 plaques.
MDV and HVT plaques may be identified as such using specific antibodies raised in chickens. Monoclonal antibodies may be used to differentiate serotypes.
b. Antigen detection:
A variation of the AGID test used for serology (see below) may be used to detect MDV antigen in feather tips as an indication of infection by MDV. Glass slides are prepared with a coating of 0.7% agarose (e.g. A37) in 8% sodium chloride, containing MDV antiserum. Tips of small feathers are taken from the birds to be examined and are inserted vertically into the agar, and the slides are maintained as described below. The development of radial zones of precipitation around the feather tips denotes the presence in the feather of MDV antigen and hence of infection in the bird.
c. Polymerase chain reaction (PCR):
Genomes of all three serotypes have been completely sequenced (Afonso et al., 2001; Lee et al., 2000). PCR tests have been developed for the diagnosis MD. Real-time quantitative PCR (qPCR) to quantify MDV genome copies has also been described (Abdul-Careem et al., 2006; Baigent et al., 2005; Islam et al., 2004). In addition, PCR tests that enable differentiation of oncogenic and non-oncogenic strains of serotype 1 MDV, and of MDV vaccine strains of serotypes 2 and 3 (Becker et al., 1992; Bumstead et al., 1997; Handberg et al., 2001; Silva, 1992; Zhu et al., 1992) have been described. PCR may also be used to quantitate virus load in tissues (Baigent et al., 2005; Bumstead et al., 1997; Burgess & Davison, 1999; Reddy et al., 2000) or differentially detect MDV and HVT in the blood or feather tips (Baigent et al., 2005; Davidson & Borenshtain, 2002). (oie).
Serological Tests:
This suspension is sonicated and then filtered through a 0.45 ?m membrane filter for inoculation on to 24- hour-old drained chicken kidney cell monolayers. After absorption for 40 minutes, the medium is added, and cultures are incubated as above for 7?10 days.
Using these methods, MDV of serotypes 1 and 2 may be isolated, together with the HVT (serotype 3), if it is present as a result of vaccination. With experience, plaques caused by the different virus serotypes can be differentiated fairly accurately on the basis of time of appearance, rate of development, and plaque morphology. HVT plaques appear earlier and are larger than serotype 1 plaques, whereas serotype 2 plaques appear later and are smaller than serotype 1 plaques.
MDV and HVT plaques may be identified as such using specific antibodies raised in chickens. Monoclonal antibodies may be used to differentiate serotypes.
b. Antigen detection:
A variation of the AGID test used for serology (see below) may be used to detect MDV antigen in feather tips as an indication of infection by MDV. Glass slides are prepared with a coating of 0.7% agarose (e.g. A37) in 8% sodium chloride, containing MDV antiserum. Tips of small feathers are taken from the birds to be examined and are inserted vertically into the agar, and the slides are maintained as described below. The development of radial zones of precipitation around the feather tips denotes the presence in the feather of MDV antigen and hence of infection in the bird.
c. Polymerase chain reaction (PCR):
Genomes of all three serotypes have been completely sequenced (Afonso et al., 2001; Lee et al., 2000). PCR tests have been developed for the diagnosis MD. Real-time quantitative PCR (qPCR) to quantify MDV genome copies has also been described (Abdul-Careem et al., 2006; Baigent et al., 2005; Islam et al., 2004). In addition, PCR tests that enable differentiation of oncogenic and non-oncogenic strains of serotype 1 MDV, and of MDV vaccine strains of serotypes 2 and 3 (Becker et al., 1992; Bumstead et al., 1997; Handberg et al., 2001; Silva, 1992; Zhu et al., 1992) have been described. PCR may also be used to quantitate virus load in tissues (Baigent et al., 2005; Bumstead et al., 1997; Burgess & Davison, 1999; Reddy et al., 2000) or differentially detect MDV and HVT in the blood or feather tips (Baigent et al., 2005; Davidson & Borenshtain, 2002). (oie).
Serological Tests:
The presence of antibodies to MDV in non-vaccinated chickens from about 4 weeks of age is an indication of infection. Before that age, such antibodies may represent maternal transmission of antibody via the yolk and are not evidence of active infection.
a. Agar gel immunodiffusion:
a. Agar gel immunodiffusion:
There is no prescribed test for trade, but the agar gel immunodiffusion (AGID) test is employed most commonly to detect antibody. The test is conducted using glass slides coated with 1% agar in phosphate buffered saline containing 8% sodium chloride. Adjacent wells are filled with antigen or serum and these are incubated in a humid atmosphere at 37C for 24 hours for diffusion to take place; positive sera show reactions of identity with known positive serum and antigen. The antigen used in this test is either disrupted MDV-infected tissue culture cells or an extract of feather tips, or skin containing feather tracts obtained from MDV-infected chickens. The cell culture antigen is prepared by propagating MDV in chicken kidney cells or chicken embryo fibroblast cells. When cytopathic effect is confluent, the cells are detached from the culture vessel and suspended in culture medium or phosphate buffered saline without tryptose phosphate broth (presence of tryptose phosphate broth may produce non-specific precipitin lines) at a concentration of about 1 107 cells/ml. This suspension is then freeze?thawed three times and used as antigen.
Test procedure:
i) Make a 1% solution of Difco Bactoagar in 8% sodium chloride by standing the mixture in a boiling water bath.
ii) Either a microscope slide or a Petri dish can be used and the agar is poured to a thickness of 2?3 mm.
iii) Cut holes in the agar using a template with a centre well and 6 wells spaced at equal distance around the centre well. The diameter of wells should be approximately 5.3 mm, and the wells should be about 2.4 mm apart. A template with cutters is commercially available.
iv) The antigen is placed in the centre well and the standard antiserum is placed in alternate exterior wells. Serum samples to be tested are placed in the remaining three wells so that .a continuous line of identity is formed between an unknown sample that is positive and the known positive control sera.
v) Incubate the slide for 24 hours at 37C in a humid container and read the results over a lamp in a darkened room.
b. Other tests:
Other tests for MDV antibody include the direct and indirect fluorescent antibody test. These demonstrate the ability of a test serum to stain MDV plaques in cell cultures (Silva et al., 1997; Spencer & Calnek, 1970). These tests are group specific and more sensitive than the AGID test. A virus neutralisation test for the ability of a serum to neutralise the plaque-forming property of cell-free MDV can also be employed. However, this test is more suitable for research purposes than for routine diagnostic use. Enzyme-linked immunosorbent assays (ELISA) for detecting MDV antibodies are available (Cheng et al., 1984; Sharma, 1998; Zelnik et al., 2004). To prepare antigen for the ELISA, wells of a 96-well microtitre plate are coated with MDV-infected cells. (oie).
Test procedure:
i) Make a 1% solution of Difco Bactoagar in 8% sodium chloride by standing the mixture in a boiling water bath.
ii) Either a microscope slide or a Petri dish can be used and the agar is poured to a thickness of 2?3 mm.
iii) Cut holes in the agar using a template with a centre well and 6 wells spaced at equal distance around the centre well. The diameter of wells should be approximately 5.3 mm, and the wells should be about 2.4 mm apart. A template with cutters is commercially available.
iv) The antigen is placed in the centre well and the standard antiserum is placed in alternate exterior wells. Serum samples to be tested are placed in the remaining three wells so that .a continuous line of identity is formed between an unknown sample that is positive and the known positive control sera.
v) Incubate the slide for 24 hours at 37C in a humid container and read the results over a lamp in a darkened room.
b. Other tests:
Other tests for MDV antibody include the direct and indirect fluorescent antibody test. These demonstrate the ability of a test serum to stain MDV plaques in cell cultures (Silva et al., 1997; Spencer & Calnek, 1970). These tests are group specific and more sensitive than the AGID test. A virus neutralisation test for the ability of a serum to neutralise the plaque-forming property of cell-free MDV can also be employed. However, this test is more suitable for research purposes than for routine diagnostic use. Enzyme-linked immunosorbent assays (ELISA) for detecting MDV antibodies are available (Cheng et al., 1984; Sharma, 1998; Zelnik et al., 2004). To prepare antigen for the ELISA, wells of a 96-well microtitre plate are coated with MDV-infected cells. (oie).
PREVENTION AND CONTROL
Sanitary Prophylaxis
Genetic selection: MD resistant chicks are obtained.
The first step to managing this disease is to identify whether the virus is present in your family of birds as some families are resistant to the disease - as the best way to prevent Marek's Disease is to develop a family of birds that is naturally resistant against the virus. Acquire families of birds and use sires that are resistant to MD, because there is strong level of heritability for genetic resistance against MD. Alternatively, following an outbreak use strong male survivors as these birds have shown a resistance to MD. Developing a family of birds that is genetically resistant to Mareks Disease is by far the best way to cure the disease ? but remember stress management measures are also a must!
Stress factors especially social stress is known to precipitate Mareks Disease ? Social stress is any form of anxiety produced by overcrowding, poor sanitation, improper housing, other illnesses like worms, coccidiosis, lice and mites - or mixing older birds with young birds - that prevent the young birds from resting eating or drinking ? basically preventing them for being happy. Stress management is the best way to control Mareks Diseasein flocks that have previously experience Mareks diseases from time to time.
FAPP (filtered air positive pressure) ventilation: Biological filters to keep out airborne viruses are used.
Vaccination alone will not prevent Marek's disease. Particularly for commercial flocks, it is important to have good biosecurity to ensure that vaccinated chicks will develop immunity before they are subjected to a severe challenge of virus. For example, chicks need to be reared separately so that they are free from the infected fluff and dust of older birds. Standard hygiene measures are also important, including a thorough clean-out and disinfection of sheds and equipment between batches of chicks with a disinfectant effective against viruses. Good nutrition and maintenance of freedom from other diseases and parasites are also very important. These practices will help maintain the flock?s health and to ensure that the birds have optimum resistance against Marek?s disease infection.
The breeding of genetically resistant strains of chickens, combined with the use of vaccination and good hygiene, can also be used to help control Marek?s disease.
For flocks with a serious Marek?s disease problem, the only solution is to depopulate, clean and disinfect all sheds and equipment, and spell for several months. Vaccinated chicks from a reputable hatchery would then need to be sought as replacements.
Medical Prophylaxis
There is no treatment for Marek?s disease. Diseased birds should be promptly removed from the flock and humanely destroyed. Other birds in the flock are likely to be infected at this stage also, so close monitoring of all birds is important.
Vaccination is the central strategy for the prevention and control of Marek's disease. The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay exposure and by breeding for genetic resistance. Probably the most widely used vaccine consists of turkey herpesvirus (HVT), which has seen rapidly increased use in recent years as a backbone in recombinant vaccines featuring the insertion of genes from other poultry viruses, such as Newcastle disease virus (see Newcastle Disease and Other Paramyxovirus Infections), infectious bursal disease virus (see Infectious Bursal Disease), or infectious laryngotracheitis virus (see Infectious Laryngotracheitis). These recombinant vaccines offer protection against both Marek's disease virus and the inserted virus. Bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 have been used to provide additional protection against challenge with virulentMarek's disease virus isolates. The most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek's disease virus strain that is also commonly mixed with HVT at vaccination. Because vaccines are administered at hatching and require 1?2 wk to produce an effective immunity, exposure of chickens to virus should be minimized during the first few days after hatching.
Vaccines are also effective when administered to embryos at the 18th day of incubation. In ovo vaccination is now performed by automated technology and is widely used for vaccination of commercial broiler chickens, mainly because of reduced labor costs and greater precision of vaccine administration.
Proper handling of vaccine during thawing and reconstitution is crucial to ensure that adequate doses are administered. Cell-associated vaccines are generally more effective than cell-free vaccines, because they are neutralized less by maternal antibodies. Under typical conditions, vaccine efficacy is usually >90%. Since the advent of vaccination, losses from Marek's disease have been reduced dramatically in broiler and layer flocks. However, disease may become a serious problem in individual flocks or in selected geographic areas (eg, the Delmarva broiler industry). Of the many causes proposed for these excessive losses, early exposure to very virulent virus strains appears to be among the most important.
The breeding of genetically resistant strains of chickens, combined with the use of vaccination and good hygiene, can also be used to help control Marek?s disease.
For flocks with a serious Marek?s disease problem, the only solution is to depopulate, clean and disinfect all sheds and equipment, and spell for several months. Vaccinated chicks from a reputable hatchery would then need to be sought as replacements.
Medical Prophylaxis
There is no treatment for Marek?s disease. Diseased birds should be promptly removed from the flock and humanely destroyed. Other birds in the flock are likely to be infected at this stage also, so close monitoring of all birds is important.
Vaccination is the central strategy for the prevention and control of Marek's disease. The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay exposure and by breeding for genetic resistance. Probably the most widely used vaccine consists of turkey herpesvirus (HVT), which has seen rapidly increased use in recent years as a backbone in recombinant vaccines featuring the insertion of genes from other poultry viruses, such as Newcastle disease virus (see Newcastle Disease and Other Paramyxovirus Infections), infectious bursal disease virus (see Infectious Bursal Disease), or infectious laryngotracheitis virus (see Infectious Laryngotracheitis). These recombinant vaccines offer protection against both Marek's disease virus and the inserted virus. Bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 have been used to provide additional protection against challenge with virulentMarek's disease virus isolates. The most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek's disease virus strain that is also commonly mixed with HVT at vaccination. Because vaccines are administered at hatching and require 1?2 wk to produce an effective immunity, exposure of chickens to virus should be minimized during the first few days after hatching.
Vaccines are also effective when administered to embryos at the 18th day of incubation. In ovo vaccination is now performed by automated technology and is widely used for vaccination of commercial broiler chickens, mainly because of reduced labor costs and greater precision of vaccine administration.
Proper handling of vaccine during thawing and reconstitution is crucial to ensure that adequate doses are administered. Cell-associated vaccines are generally more effective than cell-free vaccines, because they are neutralized less by maternal antibodies. Under typical conditions, vaccine efficacy is usually >90%. Since the advent of vaccination, losses from Marek's disease have been reduced dramatically in broiler and layer flocks. However, disease may become a serious problem in individual flocks or in selected geographic areas (eg, the Delmarva broiler industry). Of the many causes proposed for these excessive losses, early exposure to very virulent virus strains appears to be among the most important.
*** By: Giyono Trisnadi, DVM - from many references
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