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Monday 28 March 2011

Perkembangan Pengendalian Penyakit AI

1. Perkembangan pengendalian AI di Indonesia sejak tahun 2004 s/d saat ini:

1) Situasi kasus AI, khususnya pada unggas pekarangan sejak 2004 mengalami peningkatan puncaknya pada tahun 2007 dan seterusnya tiap tahun mengalami penurunan hingga 2010. Namun demikian dalam setiap tahun terjadi peningkatan kasus pada bulan Januari s/d April selama musim hujan.

2) Selama ini dengan penerapan metode Participatory Disease Surveillance and Response (PDSR), yakni deteksi, lapor dan respon secara dini oleh Tim PDSR, sehingga kasus AI pada unggas pekarangan (sektor-4) dapat ditekan, baik jumlah maupun lokasi penyebarannya.

3) Sedangkan perkembangan kasus AI pada unggas komersial (sektor-1, 2, 3) dan rantai pasar unggas masih belum sepenuhnya berhasil dipantau pelaporannya.

4) Walaupun upaya pengendalian AI sudah cukup efektif dan tersistem pada sektor-4, namun tantangan masih sangat besar untuk memutus mata rantai penyebaran virus pada unggas komersial (sektor-1,2,3) dan rantai pemasaran unggas.

2. Langkah yang sudah dilakukan Pemerintah dalam menekan atau mengurangi penyebaran AI di Indonesia:

a. Guna mengantisipasi meningkatnya kasus AI di musim hujan dan agar dilakukan peningkatan kewaspadaan terhadap AI, maka Direktur Jenderal Peternakan dan Kesehatan Hewan telah menerbitkan Surat Edaran kepada Para Kepala Dinas Provinsi yang membidangi fungsi Peternakan dan Kesehatan Hewan se Indonesia, Nomor 20075 tanggal 20 Januari 2011.

b. Program pengendalian AI guna menekan atau mengurangi penyebaran AI di Indonesia, dilakukan per sektor secara ringkas dijelaskan sbb :

1) Pada Sektor-4 (unggas Pekarangan), antara lain:

a) Penerapan metode Participatory Disease Surveillance and Response (PDSR), yakni deteksi, lapor dan respon secara dini/cepat oleh Tim PDSR berbasis partisipasi masyarakat. Secara bertahap dikembangkan hingga saat ini pada 29 Provinsi di 350 Kab/Kota, sebanyak 2.250 petugas PDSR yang berbasis di tingkat Kab/Kota.

b) Setiap ada kematian mendadak unggas langsung lapor ke Tim PDSR dan dalam waktu kurang dari 24 jam dilakukan Uji Cepat (Rapid Test). Bila hasil positip, langsung dilaporkan melalui SMS Gateway dan dilakukan Respon berupa pemusnahan terbatas, disposal, disinfeksi, isolasi, penyuluhan. Dengan respon cepat tersebut, sehingga kasus penyakit AI dapat diisolir, diminimalisir penyebarannya.

2) Pada Sektor-3, antara lain :

a) Pelatihan “Cost Effective Biosecurity” atau Biosekuriti yang Efektif dan Ekonomis, dilakukan secara Training of Trainer atau pelatihan langsung kepada kelompok peternak
b) Penerapan Strategi Vaksinasi Tertarget melalui Pilot Proyek Intensifikasi Vaksinasi (InVak), di 10 Kabupaten tahun 2009 dan replikasi ke wilayah lain.
c) Program Veteriner Unggas Komersial (PVUK), guna meningkatkan pelayanan Dinas Kab kepada peternak ayam ras sektor-3 dengan pendekatan partisipatif, khususnya pelayanan biosekuriti, vaksinasi, manajemen kesehatan unggas, surveilans, dll.

3) Pada Sektor-1 dan 2, antara lain:

a) Percepatan pelaksanaan Audit Kompartementalisasi Bebas AI, khususnya ke Breeding Farm.
b) Mewujudkan program peningkatan kesehatan unggas nasional (P2KUN) sebagai wujud kemitraan antara Industri Perunggasan, Pemerintah dan Akademisi, dalam bentuk Komite Peningkatan Kesehatan Unggas Nasional.
c) Disamping itu juga perlu dirancang peraturan daerah yang mendukung jaminan kawasan perusahaan unggas pembibitan.

4) Pada mata rantai distribusi/pemasaran unggas, antara lain:
a) Melakukan surveilans pada Tempat Penampungan Unggas (TpnU), Tempat Pemotongan Unggas (TPU), Pasar Tradisional, untuk mengetahui prevalensi dan penelusuran sumber penularan virus AI. Diawali dengan Pilot Proyek di wilayah JABODETABEK.
b) Cleaning and Disinfection (C&D), kegiatan pembersihan dan disinfeksi pada kendaraan/alat transportasi, TpnU, TPU, Pasar Unggas. Diawali dengan Pilot Proyek di JABODETABEK.
c) Restrukturisasi Perunggasan, antara lain mendukung pelaksanaan PERDA No. 4 Th 2007 tentang relokasi TpnU dan TPU ke lokasi yang telah ditunjuk di Prov. DKI Jakarta.

3. Tugas dan fungsi UPPAI:

Berdasarkan Keputusan Menteri Pertanian bahwa Tugas dan Fungsi UPPAI adalah sebagai unit fungsional pada Direktorat Kesehatan Hewan – Ditjen. Peternakan dan Kesehatan Hewan, melaksanakan tugas membantu Direktur Kesehatan Hewan dalam operasionalisasi kebijakan pengendalian AI pada hewan secara nasional di Indonesia.

4. Yang dilakukan UPPAI dalam pengendalian penyakit AI:

a. Merumuskan bahan kebijakan dan Rencana Kerja Strategis Nasional (National Strategic Work Plan / NSWP) Pengendalian AI.

b. Mengkoordinasikan operasionalisasi berbagai Bantuan Luar Negeri agar sinergis dengan NSWP dan dapat mendukung/memperkuat program pengendalian AI dari pemerintah pusat dan pemerintah daerah provinsi dan kabupaten/kota.

c. Mengakomodasikan usulan rencana kerja operasional pengendalian AI di tingkat daerah ke dalam rencana kerja strategi nasional.

d. Mengupayakan terwujudnya koordinasi, kemitraan antara pemerintah dengan berbagai pihak terkait dalam pengendalian AI, antara lain : Industri perunggasan, asosiasi perunggasan, akademisi.

e. Memberikan sosialisasi dan advokasi kepada pemerintah daerah dalam penguatan kelembagaan, SDM kesehatan hewan, penganggaran dan sarana prasarana dalam program pengendalian AI di daerah.

f. Melakukan koordinasi operasional pengendalian AI dengan sektor terkait, terutama dengan jajaran Kementerian Kesehatan, Kementerian Dalam Negeri, Perguruan Tinggi, Lembaga Penelitian dan Industri/Asosiasi Perunggasan.

g. Menyusun Roadmap menuju Indonesia bebas Avian Influenza tahun 2020:

1. Wilayah Risiko Rendah:
2011/2012: Maluku, Papua, Papua Barat, Nusatenggara Barat, Nusatenggara Timur, Gorontalo, Maluku Utara
2012: Kalimantan

2. Wilayah Proteksi Khusus : Bali

3. Wilayah Risiko Sedang :
2014 : Bangka Belitung, Kepulauan Riau
2015 : Sulawesi kecuali Sulawesi Selatan
2016 : Sumatera kecuali Lampung dan Sumatera Utara
2017 : Sulawesi Selatan sehingga seluruh Sulawesi bebas AI
2018 : Lampung dan Sumatera Utara sehingga seluruh Sumatera bebas AI

4. Wilayah Risiko Tinggi:
2020 : Pulau Jawa, sehingga Indonesia bebas AI

5. Capaian menjadi laporan resmi UPPAI hingga saat ini:

Capaian UPPAI yang telah berhasil dalam Program Pengendalian AI, antara lain khususnya telah dapat direalisasikannya sistem pelaporan cepat kasus AI, termasuk deteksi dan respon pengendalian AI secara dini, melalui penerapan metode PDSR, sehingga kasus AI telah dapat ditekan jumlah dan penyebarannya.

Pelaporan kasus AI pada unggas pekarangan (sektor-4) telah tersistematis baik melalui pengiriman form laporan tertulis maupun SMS Gateway secara cepat dari Tim PDSR di lapangan ke Koordinator LDCC di provinsi dan ke UPPAI Pusat.

Pola pelaporan SMS Gateway telah dimulai sejak September 2009. Data kasus AI dari SMS Gateway yang masuk setiap hari, direkapitulasi setiap akhir minggu dilaporkan oleh Dirjen. Peternakan dan Kesehatan Hewan kepada Menteri Pertanian. Data tersebut juga diberikan kepada Direktorat Penanggulangan Penyakit Bersumber Binatang (PPBB) – Kementerian Kesehatan guna antisipasi kewaspadaan penanganan kasus Flu Burung pada manusia, serta sebagai informasi resmi kepada semua pihak terkait.

6. Kendala yang dihadapi dalam upaya pengendalian penyakit AI di Indonesia, baik di pusat maupun daerah:

a. Kendala/Tantangan di Pusat:
1) Terbatasnya anggaran dari pemerintah Pusat (APBN), mengingat Program Pengendalian AI pada Kementerian Pertanian bukan lagi merupakan program strategis yang perlu didukung serius penganggarannya.
2) Semakin menurunnya dan akan segera berhentinya Bantuan Luar Negeri dalam waktu dekat, sehingga sangat diperlukan anggaran keberlanjutan dari pemerintah terhadap program yang sudah berjalan serta replikasi program ke wilayah baru.
3) Koordinasi antara para pejabat penentu kebijakan di pemerintah dengan para pihak pemangku kepentingan masih perlu terus ditingkatkan

b. Kendala/Tantangan di Daerah:
1) Belum adanya otoritas veteriner dan dokter hewan berwenang yang ditunjuk pemerintah daerah, yang sangat diperlukan untuk jalur hubungan teknis antara pusat dan daerah, khususnya pada dinas yang organisasinya heterogen dengan komoditas lainnya di luar peternakan.
2) Sebagian besar kab/kota masih belum menyediakan anggaran (APBD) pengendalian AI yang memadai, khususnya biaya operasional Tim PDSR dan LDCC.
3) Pengawasan lalu lintas unggas antar daerah maupun antar pulau masih belum efektif diberlakukan, disamping juga banyaknya lalu lintas unggas secara ilegal sehingga potensi risiko penyebaran virus AI antar daerah/antar pulau masih berisiko tinggi.


7. Program PDSR dan LDCC:

Program pengendalian AI menerapkan metode PDSR yang dioperasionalisasikan oleh Tim PDSR di tingkat Kab/kota dan dikoordinasikan oleh Koordinator LDCC di tingkat provinsi, sejak tahun 2005 difasilitasi oleh Bantuan Luar Negeri yang dikoordinasikan oleh FAO.

a. Pola hubungan fungsional antara pemerintah pusat (UPPAI Pusat) dengan pemerintah provinsi (LDCC/UPPAI Provinsi) dan Kab/kota (Tim PDSR) dalam program pengendalian AI, telah cukup efektif dilaksanakan khususnya guna menembus birokrasi otonomi daerah.

b. Beberapa (sekitar 11) provinsi dengan sebagian atau seluruh Kabupaten/Kota sejak Januari 2010 secara penuh telah dibiayai oleh APBD setempat.

c. Beberapa provinsi secara bertahap akan menurunkan sumber dana BLN dan digantikan oleh APBD setempat.

d. Metode PDSR diintegrasikan ke dalam Sistem Pelayanan Kesehatan Hewan Nasional (National Veterinary Services/NVS) yang berbasis pada Pusat Kesehatan Hewan (Puskeswan). Contohnya Saat ini metode PDSR telah mulai diterapkan pada program pemberantasan penyakit Rabies di Pulau Bali, dan pilot proyek di beberapa kab/kota lainnya.

8. Kasus AI akhir-akhir ini:

a. Berdasarkan laporan dari Tim PDSR yang diterima Pusat, bahwa benar secara umum terjadi peningkatan kasus AI khususnya pada unggas pekarangan (sektor-4) sejak bulan Januari, Februari dan Maret 2011.

b. Dari 17 provinsi yang terjadi kasus AI positip, sebanyak 5 provinsi dengan jumlah kasus tertinggi pada bulan Januari 2011 (Lampung, Jabar, DIY, Kaltim, Jatim), Februari 2011 (Lampung, Bengkulu, Jabar, Jateng, Jatim) dan bulan Maret 2011 (Sumbar, Riau, Lampung, Jambi, Jabar).

c. Disamping itu beberapa provinsi yang telah lama tidak terjadi kasus ternyata muncul kembali di tahun 2011 ini, antara lain provinsi, Bali, Kalimantan Timur.

9. Penyebab utama sampai saat ini kasus AI tetap muncul di berbagai daerah di Indonesia:

Berdasarkan analisa kajian, hasil penelusuran kasus AI yang terjadi meningkat akhir-akhir ini, adalah antara lain :

a) Pola tahunan sejak tahun 2006 s/d saat ini, kasus AI meningkat cukup tajam dilaporkan dan dideteksi positip AI terutama pada bulan Januari s/d April setiap tahunnya, hal tersebut berkaitan dengan datangnya musim penghujan, dimana kondisi tubuh unggas menurun, berbagai penyakit termasuk AI muncul dan meningkat.

b) Masih rendahnya kesadaran peternak ayam ras sektor-3 yang masih tetap menjual unggas sakit atau berisiko terinfeksi AI ke pedagang unggas atau masuk ke rantai pemasaran unggas, sehingga virus AI ikut menyebar dengan cepat ke berbagai wilayah dan berisiko menulari kembali peternakan ayam ras.

c) Potensi risiko penyebaran virus AI melalui aliran air mengikuti hulu sungai, terutama juga dampak setelah terjadi banjir. Hal tersebut diperkuat dengan sebagian masyarakat lebih memilih membuang bangkai ayam ke sungai daripada membakar dan menguburnya pada saat musim hujan.

10. Masih efektifkah program vaksinasi yang dilakukan peternak saat ini, khususnya yang masih menggunakan vaksin dari master seed lama:

Berdasarkan hasil kartografi OFFLU yang disampaikan pada pertemuan pada tanggal 17-18 November 2009 di Kementerian Pertanian serta 28-29 Oktober 2010 di Grand Kemang dan laporan kepada Pemerintah (Dirjenakeswan), bahwa virus AI yang ada di lapangan sudah bermutasi (Antigenic Drift) pada unggas komersial sehingga di beberapa daerah vaksin yang tersedia saat ini kurang protektif terhadap virus lapang. Namun demikian Program vaksinasi AI yang dilakukan peternak saat ini khususnya pada ayam buras intensif yang masih menggunakan vaksin dari master seed lama, pada daerah tertentu sebagian besar masih cukup protektif.

11. Kebijakan vaksinasi AI ke depan:

Seperti telah diketahui, dalam hal kebijakan vaksin AI di Indonesia, sejak tanggal 30 September 2009 Pemerintah telah menetapkan master seed yang digunakan sebagai vaksin dan challenge test (uji tantang) vaksin AI.

Adapun master seed tersebut adalah:
a. A/Chicken/West Java/PWT-WIJ/2006
b. A/Chicken/Pekalongan/BBVW-208/2007
c. A/Chicken/Garut/BBVW-223/2007
d. A/Chicken/West Java(Nagrak)/30/2007

Untuk challenge seed (seed tantang) baru untuk uji tantang vaksin dari master seed tersebut diatas adalah:

a. A/chicken/West Java Sbg/29/2007
b. A/chicken/West Java/SMI-PAT/2006

Sedangkan vaksin yang disarankan adalah vaksin yang homolog dan monovalen, karena untuk vaksin bivalen, kandungan antigen dari setiap seed virus harus sesuai dengan dosis monovalen. Disamping itu masih perlu dikaji data penelitian yang relevan untuk vaksin unggas yang mendukung penggunaan lebih dari 2 antigen dalam vaksin.

12. Peluang penggunaan vaksin reverse genetic:

Peluang penggunaan vaksin reverse genetic sangat terbuka, yaitu sesuai saran dari OIE, karena produksinya dapat dikelola (diproduksi) di BSL-2 sehingga menjadi lebih aman terhadap petugas dan lingkungan. Penggunaan vaksin reverse genetik ini telah dilakukan di beberapa Negara, contohnya negara China dan Mesir.

Namun demikian peraturan pembuatan dan peredarannya masih perlu melalui ketentuan peraturan dari Komisi Keamanan Hayati dan Keamanan Produk Hasil Rekayasa Genetika, bahwa produk reverse genetic vaksin AI oleh Komisi tersebut masih dikelompokkan dalam produk Rekayasa Genetika, sehingga masih memerlukan proses pengkajian yang cukup lama.

13. Program penataan pasar unggas hidup yang hingga saat ini masih diundur terus pelaksanaannya:

Pasar unggas / pasar tradisional merupakan sumber penularan penyakit AI, hal ini disebabkan oleh penjualan unggas yang berasal dari berbagai tempat dan berbagai jenis unggas seperti ayam (ayam kampung, broiler, layer afkir), itik, entok dan lainnya. Pemerintah melalui Surat Edaran Menteri Pertanian No. 283/TU.210/M/11/2006 tentang Restrukturisasi Perunggasan telah menghimbau kepada Gubernur Kepala daerah untuk melakukan upaya pembinaan, bimbingan dan pengawasan pemeliharaan unggas dan penanganan pasca panen melalui penataan di tempat penampungan dan tempat pemotongan unggas dengan harapan bahwa hanya karkas yang dijual di pasar.

Hal ini tidak mudah untuk dilakukan, perlu pembinaan dan sosialisasi pada masyarakat secara terus menerus mengingat masih banyak konsumen yang menghendaki pembelian unggas hidup di pasar dan dipotong di pasar juga untuk meyakini bahwa unggas yang dibeli berasal dari unggas sehat dan dipotong secara halal. Melalui penataan tempat penampungan dan pemotongan unggas secara berkesinambungan diharapkan pandangan masyarakat yang telah terbiasa membeli unggas hidup di pasar akan berubah dan percaya bahwa karkas yang dijual di pasar berasal dari tempat penampungan dan pemotongan unggas yang memenuhi kaidah biosekuriti dan persyaratan hygiene sanitasi.

14. Saran untuk peternak dan pelaku bisnis peternakan dalam meminimalisasi penyebaran dan penularan AI di Indonesia:

Peternak, pelaku bisnis peternakan dan pemerintah perlu meningkatkan koordinasi dan saling terbuka dalam situasi dan kondisi yang terjadi di masing-masing peternakan sehingga kejadian penyakit dapat dideteksi secara dini dan dapat ditangani secara cepat secara bersama sehingga penyebaran dan penularan penyakit dapat dicegah.

15. Himbauan:

a. Masyarakat agar terus meningkatkan kepeduliannya untuk segera melaporkan kepada Dinas yang membidangi fungsi kesehatan hewan/Tim PDSR bila menemui adanya kematian unggas mendadak miliknya atau disekitarnya, supaya dapat segera dilakukan deteksi, lapor dan respon secara dini/cepat guna mencegah penyebaran virus AI ke daerah lainnya dan mencegah penularannya ke manusia.

b. Masyarakat atau peternak unggas agar tidak menjual unggas yang sakit atau sekandang/di sekitar unggas sakit ke pedagang unggas atau pasar tradisional.

c. Masyarakat bila membutuhkan daging unggas agar membeli daging yang telah dipotong secara ASUH (Aman, Sehat, Utuh, Halal) dan menghindarkan membeli unggas yang masih hidup dari pasar tradisional.

d. Bila harus membeli unggas hidup sebagai bibit, maka harus diyakini dalam keadaan sehat dan dipisahkan (isolasi) terlebih dahulu selama 14 hari.

e. Peternakan ayam ras sector pembibitan, komersial skala besar, menengah dan kecil agar terus menerus meningkatkan tindakan pengendalian sesuai Prosedur Operasional Standar.

f. Pelaku usaha pada rantai pemasaran unggas (Tempat Penampungan Unggas, Tempat Pemotongan Unggas dan Pasar Tradisional) agar meningkatkan tindakan Biosekuriti, hygiene sanitasi untuk memperkecil risiko penularan dan memutus mata rantai penularan virus AI.

g. Masyarakat umum yang apabila menangani unggas hidup harus menggunakan Alat Pelindung Diri minimal dan menjaga Pola Hidup Bersih dan Sehat (PHBS) serta selalu mencuci tangan dengan sabun setelah kontak dengan unggas.

h. Bagi jajaran Petugas Dinas Yang membidangi fungsi kesehatan hewan, dan Laboratorium Veteriner agar terus meningkatkan kegiatan surveilans dan kajian dalam rangka program pengendalian AI.

i. Kepada Pemerintah Daerah dihimbau komitmen dan bantuannya untuk memimpin dan mengkoordinasikan tindakan pengendalian AI di daerah masing-masing.

j. Kepada media informasi dihimbau untuk turut mensosialisasikan program pengendalian AI dan memberikan informasi yang benar serta turut menjaga ketenteraman batin masyarakat.

Jakarta, 25 Maret 2011
Sumber: Direktorat Kesehatan Hewan

Sunday 6 March 2011

ASEAN Biodiversity Outlook

While occupying only three per cent of the earth's surface, the ASEAN region boasts of globally significant terrestrial and marine biodiversity that include an astonishing 18 percent of all species assessed by the International Union for Conservation of Nature (IUCN). It has the most diverse coral reefs in the world and is home to the mega-diverse countries of Indonesia, Malaysia and the Philippines. The region also spans several unique bio-geographical units such as Indo-Burma, Malaysia, Sunda land, Wallacea, and the Central Pacific.

To protect this richness, the 10 ASEAN Member States, all Parties to the Convention on Biological Diversity (CBD), committed themselves in 2002 to the 2010 Biodiversity Target: "the achievement by 2010 of a significant reduction of the current rate of biodiversity loss at the global, regional and national levels as a contribution to poverty alleviation and to the benefit of all life on earth." This report, the ASEAN Biodiversity Outlook, confirms that the region, like the rest of the world, is increasingly losing biodiversity at an alarming rate within various ecosystems - forest, agro-ecosystems, peatlands, freshwater, mangroves, coral reefs and seagrass.

The region's biodiversity report card confirms the findings of the Third Global Biodiversity Outlook that the world failed to meet the target of significantly reducing biodiversity loss by 2010:

• The growing population's dependence on timber, fuel wood, and other forest products, as well as the conversion of forests into agricultural and industrial lands, are taking their toll on the region's forests. Already, Southeast Asian countries had lost a total of 555,587 square kilometers of forests between 1980 and 2007.

• While the ASEAN region is gifted with immense mangrove resources, it nonetheless suffers the highest rates of mangrove losses in the world. An area of 628 square kilometers of mangrove got stripped away each year throughout the last couple of decades. In 1980, the estimated regional total mangrove area was 63,850 square kilometers. As of 2005, this whittled down to 46,971 square kilometers for an aggregate decline of about 26 per cent within a 25-year period.

• There has been a general decline in coral reefs in the ASEAN region between 1994 and 2008. Although the region hosts the largest coral reef areas in the world, it also has the highest rate of loss, which today stands at 40 per cent.
• Bottom-trawling, extensive coastline destruction and modification, decline in coastal water quality, and human-induced development have endangered seagrass beds in the ASEAN region. Indonesia, the Philippines, Singapore and Thailand have each experienced from 30 up to 50 per cent losses of seagrass habitats, compounded by the fact that the loss figures for other Southeast Asian countries remain largely unknown.

The Outlook underscores that the drivers of biodiversity loss continue to intensify. The key drivers of biodiversity loss in the ASEAN region include ecosystems and habitat change, climate change, invasive alien species, over-exploitation (as a result of deforestation and land-use and water-use change, as well as wildlife hunting and trade for food), pollution and poverty.

In terms of addressing the drivers and threats to biodiversity loss, the ASEAN region remains slow in delivering progress, particularly in preventing invasive alien species, addressing the impact of biodiversity to species and ecosystems, and abating pollution and the exploitation of forests and wetlands. But the ASEAN region registered significant pockets of success stories. Progress has been made in expanding the coverage of terrestrial and marine protected areas.

The ASEAN Member States prioritized protecting major ecosystems and habitats through regional initiatives focusing on huge, biologically rich and critical ecosystems. Biodiversity corridors covering trans-boundary protected areas, for example, have been launched and initiated. Networks of protected areas such as the ASEAN Heritage Parks were given special attention. The countries also shored up efforts to further develop capacities and expand the network of wildlife law enforcers.

The Outlook for the ASEAN region is summarized as follows:

• Terrestrial ecosystems - The region's forest ecosystems and agro-ecosystems shall continue to play the crucial role of providing ecological stability to the ASEAN countries and globally.

Both, however, face numerous pressures. Addressing the pressures on these two ecosystems is critical for ASEAN. It will entail taking multiple measures that should be linked to enhancing the productivity from existing crop and pasture lands, reducing post-harvest losses, sustainable forest management and changing excessive and wasteful consumption.

• Inland water ecosystems - Inland water ecosystems in the ASEAN region are considered to be high value areas.

These cover wetlands, peatlands and freshwater bodies. Unfortunately, these ecosystem functions are often undervalued, consequently placing the rich biodiversity resources in these areas at imminent risk. As many of these areas are the initial frontiers for conversion for development expansion, there will be an increasing need for an integrated management of the ecosystems. By approaching the development of these areas in such a manner, the potential negative impacts from competing pressures can be minimized or averted.

• Marine and coastal ecosystems - Marine and coastal ecosystems are considered as one of the most valuable natural assets of the ASEAN region.

They, however, are faced with multiple pressures that may affect their ability to supply food, functional buffer zones for natural weather disturbances, and livelihood for communities. There is an urgent need to establish marine protected areas (MPAs) and MPA networks, as well as promulgate policies that allow marshes, mangroves and other coastal ecosystems to persist and even migrate inland to make these ecosystems more resilient to the impact of sea level rise, and thus help protect the vital services they provide.

The ASEAN region, as with the entire global community, has to move forward in collectively achieving the Biodiversity Target beyond 2010. Clearly, ASEAN Member States have to exert greater effort to inch their way toward achieving the biodiversity targets set for the region.

Ways forward have to be explored in order to successfully do this. There is a need to:
• Target efforts to critical areas and ecosystems
• Mainstream biodiversity in the national development process
• Connect biodiversity management with climate change efforts
• Take pride on the current efforts and building on them for designing future efforts
• Support efforts that will lead to the adoption of the access and benefit-sharing regime in the region.

The ASEAN Member States have already taken numerous steps in addressing biodiversity loss. The challenge is to push the envelop further, mindful that striking a balance between having a healthy life, secured livelihood and prosperity coupled with protected biodiversity resources and ecosystems is achievable if humans put their hearts into it.

Source: ASEAN Center for Biodiversity

Thursday 3 March 2011

Feline chlamydophilosis

-->by AH Sparkes BVetMed PhD DipECVIM MRCVS *)

Introduction and classification

The life-cycle and classification of Chlamydiae have been reviewed by Caul & Sillis (1998). Chlamydiae are small (elementary bodies being 0.3 mikro meter diameter) RNA- and DNA-containing obligate intracellular prokaryote parasites. Elementary bodies (containing a cell wall like conventional bacteria) bind to and enter host cells and differentiate into larger (1.0 mikro meter diameter) reticulate bodies. Division occurs by binary fission within a membrane-bound vacuole, and there is differentiation back into elementary bodies prior to release of particles from the infected cell. Metabolically the Chlamydiae are distinct from free-living bacteria in that they require a source of ATP from their host.
Chlamydia currently form a single genus within the Eubacteria. The order Chlamydiales has a single family Chlamydiaceae containing this single genus. Four species of Chlamydia are recognised: C psittaci, C trachomatis, C pneumoniae and C pecorum. Antigenic differences are present within the Chamydia species leading to recognition of different strains. Within C psittaci at least five strains have been identified - avian, ovine abortion, ruminant non-abortion, feline and guinea pig and many of these strains appear to have developed a strong host-adaptation. Indeed recent genetic analysis suggests that some of these strains should be re-classified as separate species (see below).
Chlamydia trachomatis and C pneumoniae are recognised as human pathogens, whereas C pecorum is an animal (primarily ruminant) pathogen. Chlamydia psittaci is also an animal (mammalian and avian) pathogen with different strains having a predilection for different species. However, C psittaci is also recognised as a zoonotic agent, although its ability to infect humans clearly varies considerably depending on the strain involved.

Genetic analysis of Chlamydia psittaci strains

Overwhelming evidence exists to support the contention that the C psittaci strain that infects cats is distinct from other C psittaci isolates. There is only a single case report of suspected transmission of C psittaci from a non-feline species to a cat (Lipman et al 1994). In this report, C psittaci transmission from a Macaw to a cat was suggested, and the organism was isolated from both animals. However, the evidence provided was only circumstantial, as the chlamydial strains isolated could not be maintained in culture for further analysis.
In contrast, there is a wealth of literature to demonstrate the existence of different strains of C psittaci and to show that feline isolates form a distinct group. This evidence is based partly on the antigenic nature of isolates – gel electrophoresis of chlamydial polypeptides showed a profile for feline isolates distinct to those isolated from other species (McClenaghan et al 1991), and monoclonal antibodies to major outer membrane protein (MOMP) epitopes of feline C psittaci isolates did not to react with other C psittaci strains (ferret, guinea pig, mouse, cow, and sheep) or with C trachomatis (Kurodakitagawa et al 1993, Tsao & Magee 1994). However, these observations are also supported by numerous genetic studies.
In 1989, Fukushi & Hirai reported that feline C psittaci strains possessed considerable genetic variation to those isolated from a variety of other species (avian, human, ferret, sheep, cattle, and muskrat), based on DNA fingerprinting using restriction endonucleases, and southern blots using DNA probes. McClenaghan et al (1991) reported similar findings using restriction endonuclease analysis of chalmaydial DNA isolated from various species.
Random amplification of polymorphic DNA was used by Pudjiatmoko et al (1997a) to analyse feline, avian, ovine and guinea pig isolates of C psittaci. Using this technique, the authors demonstrated that feline isolates had a unique ‘fingerprint’ in comparison to isolates from other species, and that the six feline isolates studied appeared to form two distinct patterns.
Other studies (Sayada et al 1994, Sykes et al 1997) have amplified the ompA gene from feline and other (avian and guinea pig) isolates of C psittaci and used various restriction endonuclease analyses to compare the isolates. These studies also demonstrated that feline isolates had distinctly different patterns from avian and guinea pig isolates, and that all the feline isolates shared the same restriction pattern. The homogeneity of the feline isolates is interesting, as in the study by Sayada et al (1994), their feline isolates were collected from three different countries (France, UK and USA) over a 50 year period.
Restriction enzyme analysis and gene sequence analysis of 16S and/or 23S ribosomal RNA also yield patterns that identify feline isolates as a distinct C psittaci group (Meijer et al 1997, Everett & Andersen 1997, Pudjiatmoko et al 1997b).
These studies are all entirely consistent in suggesting that isolates of C psittaci that infect cats form a distinct and separate group. The lack of similarity between feline isolates and those from a variety of other species would suggest that cross-species transmission of this strain is extremely rare or, potentially, may not occur at all. The wealth of new information on the genetic analysis of chlamydial isolates has recently led to a new classification scheme being proposed for the order Chlamydiales (Everrett et al 1999). Under this proposal, the Chlamydiaceae form one of four families in the order (the others being Parachlamydiaceae, Simkaniaceae and an as yet unnamed family). The Chalmydiaceae are split into two genera under the new proposal – Chlamydia and Chlamydophila. The Chlamydia genus comprises three species - C suis, C murridarum and C trachomatis; while the Chlamydophila genus also comprises three species, all derived from the previous C. psittaci species: Ch abortus, Ch caviae, and Ch felis. This suggestion that they may form a separate species is further recognition of the distinct nature of feline isolates.

Feline infection with Chlamydophila felis

In both the UK and elsewhere, C felis has been established as a common feline pathogen. Baker first reported the isolation of C psittaci from cats in 1942, when it was described as an agent causing both upper and lower respiratory tract disease (‘feline pneumonitis’). Initially, the organism was thought to be responsible for most cases of acute upper respiratory tract infection in cats (Ott 1971, Studdert 1981). However, following further studies of the organism, and the subsequent isolation of feline herpesvirus and calicivirus and the recognition of their pathogenic role, it became clear that C psittaci (C felis) is primarily an ocular pathogen in cats (Cello 1971, Ott 1971, Hoover 1978, Studdert 1981) causing conjunctivitis as the primary clinical sign.
C. felis is now well established as an important and common cause of feline conjunctivitis worldwide (Cello 1971, Shewen et al 1978, Studdert et al 1981, Wills et al 1988, Danwitz & Rehman 1991, Pointin 1991, Beregi et al 1993, Nasise et al 1993, Gruffydd-Jones et al 1995, Gunn-Moore et al 1995). In the UK, a study of over 750 pet cats with conjunctivitis demonstrated chlamydophilosis infection in 30% of these (Wills et al 1988). This study also demonstrated that the highest prevalence of infection was in cats aged five weeks to nine months. More recently, a serological study of healthy pet cats in the UK demonstrated greater than 9% had been infected with C felis (Gunn-Moore et al 1995).
The conjunctival epithelium appears to be the chief target for Chlamydophila infection in cats. Experimental studies have demonstrated that the incubation period, from infection to the onset of clinical signs is typically 3-10 days with clinical signs characterised by the appearance of blepharospasm, chemosis, conjunctivitis, mucopurulent ocular discharge, regional lymphadenopathy and occasional sneezing and mild nasal discharge (Hoover et al 1978, Wills et al 1987. O’Dair et al 1994, Sparkes et al 1999).
C felis is an unusual organism and was initially classified as a virus, it is now, however, regarded as highly specialised intracellular bacteria. This is an important distinction as it means that unlike viruses Chlamydophila are susceptible to a limited number of antibacterial agents.

Pathogenesis and clinical signs

The conjunctival epithelium appears to be the chief target for Chlamydophila infection. The organism replicates in the cytoplasm of the epithelial cells, eventually causing the cell to rupture, liberating infectious elementary bodies which then infect other epithelial cells.
Although cats of any age can be infected, the disease is seen most frequently in kittens and young adults. In endemic colonies, as the kitten's maternally derived antibody levels (from the queen's colostrum) declines, they become vulnerable to infection at 5-12 weeks of age. Recurrent episodes of Chlamydophila conjunctivitis are not uncommon in cats particularly during times of stress.
The incubation period, from infection to the onset of clinical signs is 4-10 days. In the early stages of the disease there is a marked serous ocular discharge (watery eye), blepharospasm (blinking) and the conjunctivae are reddened and swollen (chemotic). Initially only one eye may be affected, but both eyes eventually become involved 5-12 days after signs are first noticed. With time the conjunctivae become more reddened (hyperaemic) and the ocular discharge often becomes mucopurulent as secondary bacterial invaders become involved. On rare occasions, when this occurs, the surface of the eye (cornea) may become ulcerated and lead to permanent damage to the eye. Mild nasal discharge and sneezing are occasionally seen as well as mild fever for several days during the initial stages of the disease. Apart from the conjunctival discomfort affected cats are generally well and usually continue to eat.
In untreated cats, clinical signs may resolve after three weeks to three months (Hoover et al 1978, Wills et al 1987. O’Dair et al 1994). However, cats may continue to excrete infective C felis beyond the time when clinical lesions have resolved (Hoover et al 1978, Wills et al 1987). In addition to isolation of the organism from oculo-nasal discharges, C felis can also be isolated from rectal swabs of some infected cats (Wills et al 1987, O’Dair et al 1994) and also vaginal swabs (Wills et al 1987), indicating that infection with the organism is not confined to the conjunctival mucosa. Chlamydophila organisms have also been described infecting the gastric mucosa of cats (Hargis et al 1983, Gaillard et al 1984) and experimental exposure of cats with organisms recovered from the gastric mucosa appeared to produce typical signs of C felis infection (Gaillard et al 1984). The significance of extra-ocular sites of infection with C felis has not been fully established in cats, but persistence of the organism at these sites may serve as a reservoir of infection (Gaillard et al 1984) and it has been suggested that genital infections may be associated with reproductive failure in cats (Wills et al 1987).
Cats may continue to excrete Chlamydophila for long periods (which can be in excess of 8 months) even though clinical signs appear to have resolved. On close examination of these cats a very low grade conjunctivitis is usually still present representing persistent infection rather than a true carrier status. In cases where there is a significant upper respiratory tract component (sneezing, coughing, nasal discharge) co-infection with one of the respiratory viruses is likely.

Diagnosis

Although Chlamydophila is the most common cause of contagious conjunctivitis in cats, it is not the only cause. In order to allow successful case management a positive diagnosis of chlamydophilosis needs to be made. A number of laboratory tests are available in order to help confirm the diagnosis:
1. Culture - this can be done by specialist laboratories. A firm conjunctival swab should be taken from the affected cat and placed in specially prepared transport media. Because the survival of Chlamydophila is poor outside of the host, the sample needs to arrive at the laboratory within 48 hours. Culture will establish a definite diagnosis in cats and is best done in cats that have been infected for less than 5-6 weeks and have not been treated with antibiotics. The use of topical local anaesthetic makes the procedure painless hence sedation is rarely necessary.
2. An ELISA test developed to look for Chlamydophila infection in people can be used to look for C felis in cats. The ELISA test can be carried out on a conjunctival swabs or conjunctival scrapings. Transport time is of less concern as the test will identify the Chlamydophila whether they are alive or dead. False positive results do occur, and the test is less reliable than isolation (culture) of the organism.
3. Antibodies titres to Chlamydophila can be evaluated, and demonstration of high titres in a group of cats indicates recent or current infection with Chlamydophila. This can be useful in colonies with chronic problems where few acute infections occur, or where the cats have been recently treated.
4. More recently specific and highly sensitive PCR-based assays have been developed for the detection of C felis. These assays are at least as sensitive as culture of the organism, and have the advantage that they do not have to rely on viable organisms being present in submitted samples
In individual cases of conjunctivitis there are numerous possible causes and a fairly extensive investigation may be required in order to establish a diagnosis. Reliable diagnosis is thus best achieved through isolation of the organism from conjunctivial swabs in cell culture (and its subsequent demonstration by immunofluorescence) or polymerase chain reaction (PCR) following DNA extraction from conjunctival swabs (McDonald et al 1998).

Treatment

Although several antibacterial agents may have some effect in relieving clinical signs of Chlamydophila conjunctivitis in cats, the relief is usually temporary, as only certain groups of antibacterial agent are really effective. The tetracyclines are generally considered the drugs of choice for all Chlamydophila infections (O’Dair et al 1994, Sparkes et al 1999). Systemic treatment is optimal for therapy, but additional topical therapy has also been recommended. However, in a recent study, we found no evidence of any specific benefit from the addition of topical therapy to systemic treatment, although it may presumably provide some local ‘soothing’ effect for the inflamed conjunctiva. Doxycycline (Ronaxan; Merial) has the advantage of only requiring once daily treatment, although it is more expensive than oxytetracycline.
If Chlamydophila is isolated from a cat colony, treatment should involve all the cats in the colony regardless of age or apparent infection. Antibiotic therapy should continue for at least 4-6 consecutive weeks or for at least two weeks after all clinical signs have subsided, whichever is the longer. The major drawback of using tetracyclines in kittens is the risk of causing discolouration of their permanent teeth. Tetracyclines should not be given to pregnant queens. Recent work suggests that systemic therapy is superior to topical therapy with tetracyclines for therapy of ocular signs and in addition, systemic therapy may have the advantage of eliminating infection at extra-ocular sites (Sparkes et al 1999).
An alternative to tetracycline therapy, which we have shown to be valuable in feline chlamydophilosisis the combination of amoxycillin and clavulnate. This requires a longer treatment period than tetracyclines, but does not carry the same risks for use in kittens.
Recently, azithromycin (a macrolide derivative with an extremely long tissue half life) has been suggested to be of value in the treatment of chlamydophilosis. However, although widely accepted as a treatment, and commonly recommended, especially among cat breeders, recent evidence based on controlled studies suggests that azithromycin is NOT effective against feline chlamydophilosis.

Epidemiology and control

Chlamydophila felis is a labile organism (Cello 1971) and transmission between cats is thought to be primarily by direct contact. Although Chlamydophila can be present in vaginal fluid and faeces they are unlikely to be major sources of infection. The use of both inactivated and modified-live vaccines have been shown to be efficacious in controlling clinical disease (Wills et al 1987, Wasmoen et al 1992).
Once endemic in a colony, Chlamydophila can be very persistent and costly to eliminate. Not just in terms of the treatment, but also in the delays in being able to sell kittens and infertility in the queens. Natural immunity to the disease appears to be inefficient and recurrent episodes of the disease can occur in individual cats.
Control of endemic chlamydophilosisis best achieved using a combined approach. This should include:
i) Initial treatment of all cats with systemic antibiotics - doxycycline ideally
ii) Vaccination once the clinical signs have resolved. Both inactivated and modiified live Chlamydophila vaccines are available
iii) Management changes including kittening in isolation and then weaning the kittens at 4-5 weeks into isolation and good general hygiene.
iv) Vaccination of kittens or new adults before introduction into the colony.

Zoonotic risk

The zoonotic implications of feline chlamydophilosis

Human infection with Chlamydia psittaci

Chlamydiosis in humans has been reviewed by Wills (1986) and Caul & Sillis (1998). Avian chlamydiosis is recognised in at least 130 species of birds and transmission of infection from birds to man is well-established. Psittacines, turkeys, ducks, pigeons, chickens, pheasants and sea-birds have all been incriminated with disease in humans being referred to as psittacosis (where infection is derived from psittacines) or ornithosis (where infection is derived from non-psittacine birds). Transmission to humans is mainly through aerosolised organisms from dried faeces or plumage. Direct contact and bite wounds are also a possibility. Signs in man include ‘flu’-like symptoms (fever, anorexia, sore throat) and in more severe cases pneumonia. Diarrhoea, nausea, vomiting have been reported as have endocarditis, myocarditis, conjunctivitis and renal involvement.
In contrast to avian disease, there have been few well-documented cases of transmission of C psittaci infection from mammals to man although transmission from infected sheep is well established. Infection in pregnant sheep causes abortion, stillborn and weak lambs (enzootic abortion of ewes - EAE) and C psittaci is the major cause of ovine abortion in the UK. Transmission to humans has resulted in signs of disease similar to psittacosis including ‘flu’-like signs, pneumonia, conjunctivitis and abortion. Evidence for transmission from cattle and cats is controversial. Some evidence is simply based on serology which cannot reliably distinguish the origin of the strain.

Feline strains of Chlamydia psittaci causing human disease

Although feline C psittaci infections are commonly regarded as being potentially zoonotic, an extensive search of the literature has revealed only four case reports of suspected transmission from cats to humans.
  1. In 1969, Ostler et al reported a 21-year-old man who developed follicular conjunctivitis confined to the right eye. Chlamydia was isolated from conjunctival cultures and fluoresecent antibody tests for Chlamydia on conjunctival scrapings were postive. Complement fixing antibody titres also rose during the course of disease and no other pathogens were isolated. The man came from a boarding house where there were also 13 cats, and he reported close contact with a three-month-old kitten. Two weeks prior to the man’s illness, the cat was reported to have had a unilateral ocular discharge and subsequent conjunctival scrapings and nasal washings yielded Chlamydia organisms from the cat. Chlamydia was also isolated from another cat in the group that developed conjunctivitis two months later. Cultured Chlamydia from the human patient were inoculated into the eyes of four kittens, and conjunctivitis developed in these kittens with inclusion bodies seen on conjunctival scrapings. No other humans in the household exhibited evidence of infection, and the authors’ suggested that this may have been due to overwhelming infection in the patient that did develop disease.
  1. In 1978, Griffiths et al reported malaise, pyrexia and hepatosplenomegaly in a 38-year-old woman who had received a renal transplant two years earlier. Various diagnostic investigations were negative, but the woman developed a rising antibody titre to C psittaci. Antibodies were detected against both feline and avian strains. The woman was reported to have contact with birds at her local pet shop, but all had been asymptomatic. She also owned three cats but these also were asymptomatic. The authors concluded that the cats were the most likely source of infection, despite the fact that all of the cats proved to be seronegative for C psittaci antibodies. Cause and effect was therefore not established.
  1. In 1979, Regan et al reported on a 40-year-old man who developed endocarditis and secondary glomerulonephritis. An aetiological agent was not cultured from the patients blood, however antibodies were demonstrated to feline C psittaci (both IgM and IgG), which declined in magnitude as the patient responded to therapy (erythromycin). Although the patient reported close contact with cats, no investigations were performed on these cats, and antibody titres to other C psittaci strains were not reported.
  1. In 1987, Schmeer et al reported acute follicular conjunctivitis in a 25-year-old woman. C psittaci-specific IgM antibodies were detected in serum samples from the woman and her cat which was also showing signs of conjunctivitis. Other microbial investigations were negative, but C psittaci could not be isolated from either cat or patient (possibly due to prior antibiotic therapy). Transmission of infection from cat to human was suggested.
In two of these four reports (Griffiths et al 1978, Regan et al 1979) the evidence for transmission of C psittaci from cats to humans is weak. Only serological data was presented to support evidence of infection in the human patients, and the cats which were the proposed source of infection either showed no evidence of infection (Griffiths et al 1978) or were not investigated at all (Regan et al 1979). In contrast, the earlier report by Ostler et al (1969) does provide strong evidence of human C psittaci conjunctivits being acquired from a cat, and the report by Schmeer et al (1987) is also suggestive of this.

Summary and conclusions

The results of numerous studies of C psittaci isolates from a variety of different species are consistent in suggesting that feline isolates are distinct from those infecting other species. This provides very strong evidence that the feline strain is a very highly host-adapted and that if it infects other species this is a very rare event, and similarly other strains of C psittaci rarely, if ever, infect cats.
Although widely regarded as having zoonotic potential, only four case reports could be found suggesting transmission of C psittaci from cats to humans. Two of these reports must be regarded with some scepticism as the evidence reported in the papers was very weak. Nevertheless in the remaining two cases evidence was suggestive of human chlamydial conjunctivitis being acquired from a cat. In both these cases the human patient responded rapidly to therapy and no other adverse effects were reported.
While it is clearly prudent to advise caution when handing and medicating cats known to be infected with C psittaci it is clear that this common feline pathogen is extremely unlikely to be transmitted to humans. Indeed Wills (1986) reported no evidence of human disease in the course of investigating over 150 clinical cases of feline C psittaci infections.

References

Baker JA (1942) A new feline pneumonia virus. Science 96:475-476
Beregi A, Lakatos B, Magdus M, et al (1993) Diagnosis of chlamydiosis in cats in Hungary and a survey on the incidence of the infection. Magyar Allatorvosok Lapja 48:137-140
Caul EO, Sillis M (1998) Chlamydiosis. In: Textbook of the Zoonoses. SR Palmer, L Soulsby, DIH Simpson (eds) Oxford University Press, Oxford. pp.53-65
Cello RM (1971) Microbial and immunological aspects of feline pneumonitis. Journal of the American Veterinary Medical Association 158,932-938
Danwitz BRV, Rehman SU (1991) Studies of the prevalence of chlamydial infection in cats. Tierarztliche Umschau 46:313
Everett KDE, Andersen AA (1997) The ribosomal intergenic spacer and domain I of the 23S rRNA gene are phylogenetic markers for Chlamydia spp. International Journal of Systematic Bacteriology 47:461-473
Everett KDE, Bush RM, Andersen AA (1999) Amended description of the order Chlamydiales, proposal of Parachlamydiaceae fam. Nov. and Simkaniacease fam. Nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the identification of organisms. International Journal of Systematic Bacteriology 49:415-440
Fukushi H, Hirai K (1989) Genetic diversity of avian and mammalian Chlamydia psittaci strains and relation to host origin. Journal of Bacteriology 171:2850-2855
Gaillard ET, Hargis AM, Prieur DJ, et al (1984) Pathogenesis of feline gastric chlamydial infection. American Journal of Veterinary Research 45:2314-2321
Griffiths PD, Lechler RI, Treharne JD (1978) Unusual chlamydial infection in a human renal allograft recipient. British Medical Journal II;1264-1265
Gruffydd-Jones TJ, Jones BR, Hodge H, et al (1995) Chlamydial infection in cats in New Zealand. New Zealand Veterinary Journal 43:201-203
Gunn-Moore DA, Werrett G, Harbour DA, et al (1995) Prevalence of Chlamydia psittaci antibodies in healthy pet cats in Britain. Veterinary Record 136:366-367
Hargis AM, Prieur DJ, Gaillard ET (1983) Chlamydial infection of the gastric mucosa in 12 cats. Veterinary Pathology 20:170-178
Hoover EA, Kahn DE, Langloss JM (1978) Experimentally induced feline chlamydial infection (feline pneumonitis). American Journal of Veterinary Research 39:541-547
Kurodakitagawa Y, Suzukimuramatsu C, Yamaguchi T, et al (1993) Antigenic analysis of Chlamydia pecorum and mammalian Chlamydia psittaci by use of monocloinal antibodies to the major outer membrane protein and a 56-kd to 64-kd protein. American Journal of Veterinary Research 54:709-712
Lipman NS, Yan LL, Murphy JC (1994) Probable transmission of Chlamydia psittaci from a Macaw to a cat. Journal of the American Veterinary Medical Association 204:1479-1480
McClenaghan M, Inglis NF, Herring AJ (1991) Comparison of isolates of Chlamydia psittaci of ovine, avian and feline origin by analysis of polypeptide profiles from purified elementary bodies. Veterinary Microbiology 26:269-278
McDonald M, Willett BJ, Jarrett O, et al (1998) A comparison of DNA amplification, isolation and serology for the detection of Chlamydia psittaci infection in cats. Veterinary Record 143,97-101
Meijer A, Kwakkel GJH, deVries A, et al (1997) Species identification of Chlamydia isolates by analysing restriction fragment length polymorphism of the 16S-23S rRNA spacer region. Journal of Clinical Microbiology 35:1179-1183
Nasisse MP, Guy JS, Stevens JB, et al (1993) Clinical and laboratory findings in chronic conjunctivitis in cats – 91 cases (1983-1991). Journal of the American Veterinary Medical Association 203:834-837
O’Dair HA, Hopper CD, Gruffydd-Jones TJ (1994) Clinical aspects of Chlamydia psittaci infection in cats infected with feline immunodeficiency virus. Veterinary Record 134:365-368
Ostler HB, Schachter J, Dawson CR (1969) Acute follicular conjunctivitis of epizootic origin - feline pneumonitis. Archives of Ophthalmology 82;587-591
Ott RL (1971) Comments on feline pneumonitis. Journal of the American Veterinary Medical Association 158:939-941
Pointin AM, Nicholls JM, Neville S, et al (1991) Chlamydia infection among breeding catteries in South-Australia. Australian Veterinary Journal 21:58-63
Pudjiatmoko, Fukushi H, Ochiai Y, et al (1997a) Diversity of feline Chlamydia psittaci revealed by random amplification of polymorphic DNA. Veterinary Microbiology 54:73-83
Pudjiatmoko, Fukushi H, Ochiai Y, et al (1997b) Phylogenetic analysis of the genus Chlamydia based on 16S rRNA gene sequences. International Journal of Systematic Bacteriology 47:425-431
Regan RJ, Dathan JR, Treharne JD (1979) Infective endocarditis with glomerulonephritis associated with cat chlamydia (C. psittaci) infection. British Heart Journal 42:349-352
Sayada C, Andersen A, Rodriguez P, et al (1994) Homogeneity of the major outer membrane protein of feline Chlamydia psittaci. Research in Veterinary Science 56;116-118
Schmeer N, Jahn GJ, Bialasiewicz AA, Weber AA (1987) The cat as a possible infection source for Chlamydia psittaci keratoconjunctivitis in humans. Tierarztl Prax 15:201-204
Shewen PE, Povey RC, Wilson MR (1978) Feline chlamydial infection. Canadian Veterinary Journal 19,289-292
Sparkes AH, Caney SMA, Sturgess CP, et al (1999) Topical and systemic therapy for the treatment of experimental feline chlamydiosis. Journal of Feline Medicine and Surgery 1:31-35
Studdert MJ, Studdert VP, Wirth HJ (1981) Isolation of Chlamydia psittaci from cats with conjunctivitis. Australian Veterinary Journal 57:515-517
Sykes JE, Studdert VP, Anderson G, et al (1997) Comparison of Chlamydia psittaci from cats with upper respiratory tract disease by polymerase chain reaction anaysis of the ompA gene. Veterinary Record 140:310-313
Tsao YC, Magee WE (1994) Monoclonal antibody to a major membrane protein of feline Chlamydia psittaci: antibody specificity and anti-idiotype antibody production. Veterinary Microbiology 42:1-13
Wasmoen T, Chu HJ, Chavez L, et al (1992) Demonstration of a one-year duration of immunity for an inactivated feline Chlamydia psittaci vaccine. Feline Practice 20:13-16
Wills JM (1986) Chlamydia zoonoses. Journal of Small Animal Practice 27:717-723
Wills JM, Gruffydd-Jones TJ, Richmond SJ, et al (1987) Effect of vaccination on feline Chlamydia psittaci infection. Infection and Immunity 55:2653-2657
Wills JM, Howard PE, Gruffydd-Jones TJ, et al (1988) Prevalence of Chlamydia psittaci in different cat populations in Britain. Journal of Small Animal Practice 29,327-339
Zhang DJ, Fan H, McClarty G, Brunham RC (1995) Identification of the Chlamydia trachomatis RecA-encoding gene. Infection and Immunity 63:676-680

*) The Feline Unit
Centre for Small Animal Studies
Animal Health Trust
Lanwades Park
Kentford, Suffolk,
UK