Penyakit Sistem Syaraf Mamalia

Patologi Sistemik Veteriner

 1. BOVINE SONGIFORM
ENCEPHALOPATHY
• Bovine Spongiform Encephalopathy (BSE) atau yang biasa
disebut penyakit sapi gila merupakan penyakit yang dapat
ditemukan pada sapi, ditandai dengan gejala saraf dan biasanya
berakhir dengan kematian
• Disebabkan oleh prion yang merupakan molekul protein tanpa
asam inti
• Termasuk kedalam penyakit sub akut yakni transmissible
spongioform encephalopathy
• penyakit sapi gila (BSE) pertama kali ditemukan di Ingrris pada
tahun 1986
• BSE disebabkan karena sapi mengonsumsi meat bone milk
• Diagnosa BSE didasarkan pemeriksaan Histopatologi
(Wirata et al, 2013)
Mekanisme Penularan BSE
Penyebaran penyakit sapi gila melalui pemberian pakan
ternak yang mengandung MBM atau TDT dari ruminansia
yang terkontaminasi protein feed virus (PrP). Di saluran
pencernaan, sel-sel dendritik usus kecil melakukan PrPsc
ke organ limfoid sekunder (patch Payer), limpa, amandel,
dan timus, lalu mengekspresikannya ke sel T dan B, dan
kemudian mengangkut PrPsc ke sistem saraf tepi. Dan
sistem saraf pusat. Akumulasi PrPsc di otak dapat
menyebabkan perubahan patologis yang spesifik, yaitu:
degenerasi neuron, vakuolasi neuron secara
intrasitoplasma, tanpa inflamasi, astrosit mengalami
hipertrofi dan hiperplasia. Pada sapi yang menderita
penyakit sapi gila, patogen telah ditemukan di jaringan
otak, sumsum tulang belakang, retina, terminal ileum,
tonsil dan ganglia trigeminal (Wirata et al, 2013)
Gambaran Histopatologi
Definisi Histopatologi
• Secara histopatologi, lesi yang
disebut ensefalopati spongiform
akan ditemukan di otak.
Degenerasi vakuola neuronal,
hiperplasia glial, kematian neuronal
tanpa inflamasi, reaksi astrosit, dan
terkadang plak amiloid (Wirata et
al, 2013).
2. Meningitis pada Kitten

• Meningitis ditandai dengan peradangan pada meninges dengan

keterlibatan ruang subarachnoid. Penyakit radang sistem saraf
pusat (SSP) biasanya dibagi menjadi penyebab infeksi dan non
infeksi. Penyebab infeksi termasuk bakteri, jamur, protozoa,
parasit, rickettsiae dan virus
• Bakteri penyebab meningitis antara lain Staphylococcus aureus,
Staphylococcus epidermidis, Staphylococcus albus, P. multocida,
Actinomyces, dan Nocardia.
• pada study case kali ini meningitis disebabkan oleh Pasteurella
multocida
• Pada study case ini, anak kucing atau kitten digigit oleh anjing
yang mengakibatkan meningitis
(Ghaffari et al, 2008)
Gambaran Makroskopis

Pada pemeriksaan postmortem meninge di belahan kanan otak

besar menebal oleh selimut agar-agar keabu-abuan.
leptomeningitis purulen yang tersebar luas, melibatkan bagian
punggung dari belahan kanan (Ghaffari et al, 2008)
 Histopatologi

Studi histopatologi menunjukkan bahwa leptomeninges terdapat

sejumlah besar deposit fibrin dan neutrofil, dimana sedikit sel
mononuklear yang tersebar di antara mereka. Pembuluh darah
membengkak dengan sel darah merah, tetapi tidak ada
perdarahan yang diamati pada lesi Leptomeningitis
fibrinopurulen: akumulasi sel inflamasi, terutama neutrofil, dan
eksudat fibrinous di ruang subarachnoid (Ghaffari et al, 2008).
Mekanisme Infeksi
Dalam kasus yang disajikan, mekanisme infeksi seharusnya
inokulasi langsung bakteri ke dalam ruang subdural setelah
menembus luka gigitan anjing. Dalam hal ini, P. multocida
diisolasi dari kultur bakteri. Organisme Pasteurella secara
klinis signifikan pada banyak luka gigitan anjing dan kucing.
Organisme ini biasanya menghuni daerah hidung, gingiva dan
tonsil serta saluran pencernaan. Beberapa mekanisme telah
dijelaskan untuk terlibat dalam infeksi bakteri dari sistem saraf
pusat pada kucing dan anjing termasuk penyebaran
hematogen (emboli septik atau kolonisasi selaput lendir),
infeksi yang berdekatan dari struktur yang berdekatan (telinga
bagian dalam, pelat cribriform, sinus, mata dan tulang
belakang. ), inokulasi langsung (trauma, luka gigitan dan
pembedahan) dan migrasi benda asing atau parasit yang
menyimpang (Ghaffari et al, 2008)
3. Feline Cerebrovascular Disease

• Berbagai penyebab CVD iskemik pada kucing diidentifikasi

termasuk migrasi parasit cuterebra, migrasi cacing jantung,
iskemia terkait anestesi, telangiectasia intrakranial,
meningoensefalitis granulomatosa, dan eksperimental dan
defisiensi tiamin terkait makanan.
• Dalam sebagian kasus, penyebab kejadian serebrovaskular masih
belum ditentukan. Berbagai penyebab CVD iskemik pada kucing
diidentifikasi termasuk migrasi parasit cuterebra, migrasi cacing
jantung, iskemia terkait anestesi, telangiectasia intrakranial,
meningoensefalitis granulomatosa, dan eksperimental dan
defisiensi tiamin terkait makanan. acara tetap belum ditentukan.
• Kombinasi tanda klinis neurologis dan ekstraneurologis individu
dipengaruhi oleh jenis CVD, lokalisasi lesi intrakranial, dan
patologi yang mendasari.
(Altay et al, 2011)
Gambaran Makroskopis

Terdapat 2 Gambaran makros otak dari

kucing yang diduga mengalami defisiensi
tiamin. Nekrosis hemoragik di daerah gyrus
dentatus dan corpora geniculata (panah.
Pada kucing dengan CVD iskemik, jaringan
abnormal terlihat sangat jelas dan pada satu
kucing dengan infark merah perdarahan
petekie terlihat. Lesi makros terlihat jelas
pada satu kucing dengan hemoragi
intraparenkim. selain itu juga setelah
dilakukan postmortem diduga k u c in g
mengalami Ischemic polioencephalomalacia
(Altay et al, 2011).
Gambaran Makroskopis

Pada gambar yang diatas terjadi infrak parenkim.

sedangkan untuk gambar dibawahnya terjadi
hemoragi akut yang parah (bintang) dengan
nekrosis fibrinoid pada dinding pembuluh (panah)
di batang otak kucing. Perdarahan dapat terjadi
karena kerusakan pada endotel vaskular atau
ruptur pembuluh, terutama jika perfusi telah pulih
sebagian. Kerusakan endotel telah dikaitkan
dengan vaskulitis, angiopati amiloid (endapan
amiloid di dalam dinding pembuluh darah), atau
hipertensi (perubahan mikrovaskuler
arteriosklerotik) (Altay et al, 2011).
4. Distemper pada Anjing
• Penyakit distemper pada anjing merupakan penyakit viral yang
bersifat multisistemik diantaranya sistem pernafasan, pencernaan,
urinaria, saraf pusat dan sistem lainnya.
• Penyakit ini disebabkan oleh Virus Canine Distemper (VCD) family
virus morbili.
• Kerusakan sel otak yang terjadi pada infeksi canine distemper
adalah terjadinya demielinasi sistem saraf pusat yang disebabkan
oleh peradangan. Secara histopatologi, akibat pengaruh
peradangan pada area ini, otak akan menunjukkan peningkatan
sel glial yang diikuti dengan peningkatan kadar sitokin.

(Fadilah et al, 2015)

Mekanisme penyakit
Virus penyebab penyakit canine distemper dapat
menyerang anjing dengan gejala klinis yang berbeda.
Penyakit ini sulit disembuhkan, sehingga jika tidak ditangani
secara dini, penyakit distemper anjing dapat mengakibatkan
kematian anjing. Distemper telah ditemukan hampir di
semua tempat di dunia. Anjing yang terinfeksi distemper
dapat mengalami gejala atau kerusakan pada mata, saluran
pernapasan, saluran pencernaan, saluran genitourinari,
sistem saraf, dan kulit. Anjing yang diserang biasanya
berumur kurang dari satu tahun, sehingga usianya masih
sangat muda, hal ini dikarenakan pada usia ini antibodi
maternal berkurang, tingkat stres tinggi akibat pertumbuhan,
dan penyakit lain yang menurunkan kondisi fisik. Iklim
berpengaruh besar terhadap terjadinya penyakit distemper
(Fadilah et al, 2015).
Patologi Anatomi
Secara patologi anatomi, anjing yang terinfeksi
distemper dapat menyebabkan berbagai infeksi
sistem. Gambaran klinis darah tepi anjing yang
terinfeksi virus ini awalnya mengarah pada
limfopenia, walaupun jumlah monosit / monosit
darah tepi meningkat setelah kadar subakut
sampai kronik. Dalam histopatologi, mungkin ada
perubahan ringan pada nekrosis, terutama folikel
jaringan limfoid, tempat hiperplasia limfoid dapat
ditemukan (Fadilah et al, 2015).
Perubahan Makroskopis
Lesi makros secara khas terjadi di otak kecil
(daerah meduler, materi putih folial, dan materi
putih subpial) dan tangkai serebelar (dengan
materi putih dan kadang-kadang keterlibatan
materi abu-abu pada pons). Lesi juga terjadi di
medula oblongata (terutama di daerah
subependymal dari ventrikel keempat), rostral
medullary vellum, serebrum (baik materi putih
maupun materi abu-abu), saraf optik, saluran
optik, sumsum tulang belakang, dan meninges
(Zachary et al, 2017).
 Histopatologi

Secara histopatologi, otak mengalami peningkatan infiltrasi sel-

sel glia yang diikuti dengan peningkatan kadar sitokin karena
pengaruh reaksi radang di daerah tersebut.Petunjuk tanda panah
menunjkukan adanya sel-sel radang; A tidak terjadi peradangan
(normal); B terjadi peradangan yang sedikit dan tidak menyebar;
C terjadi peradangan yang menyebar/multifokal (Fadilah et al,
2015).
5. Granulomatous
Meningoencephalitis
• Meningoensefalitis granulomatosa. Granulomatous
meningoencephalitis (GME) adalah salah satu dari dua ensefalitis
idiopatik penting pada anjing, yang kedua adalah ensefalitis
nekrotikans, yang ada dua varian.
• Meningoencephalitis granulomatosa paling sering terjadi pada
anjing ras kecil muda hingga paruh baya, termasuk pudel dan
berbagai ras terrier.
• Tanda-tanda klinis pada kasus dengan lesi otak bervariasi dan
termasuk perubahan perilaku dan berputar-putar. Lesi medula
spinalis dapat menyebabkan paresis dan ataksia
Perubahan Makroskopis
Granulomatous Meningoencephalitis, Bagian
Melintang Otak Tengah Hanya Rostral ke
Pons hewan anjing, mesencephalon bengkak,
berubah warna, sangat menyimpang, dan
lunak akibat peradangan granulomatosa
yang luas (panah), yang telah menggeser
garis tengah ke kanan. Saluran air
mesencephalic juga terkompresi dan
terdistorsi. Saat ini, lesi makros terdiri dari
abu-abu putih sampai merah, area luas di
dalam materi putih otak dan batang otak.
Lesi dapat memiliki batas yang tidak teratur
dan berbatas tegas dan konsistensi seperti
agar-agar atau kenyal atau tampak granular.
Ada dua pol a di stri busi penyaki t yang
berbeda, bentuk menyebar dan bentuk fokus.
Bentuk fokus paling sering terlihat di talamus
dan batang otak (Zachary, 2017).
Perubahan Histopathology

Terdapat akumulasi sel inflamasi

granulomatosa di ruang perivaskular.
Lapisan sel seperti itu meluas dari
waktu ke waktu dan menekan jaringan
saraf yang berdekatan, menghasilkan
degenerasi seperti Wallerian dari
akson mielin yang terkena dan atrofi
badan sel neuron yang terkena
(Zachary, 2017).
Histopatlogi
Secara histologis, penyakit ini menyebabkan manset perivaskular
berbeda yang hampir seluruhnya terdiri dari limfosit dan makrofag
dengan jumlah sel plasma dan neutrofil yang tersebar. Manset ini
hampir seluruhnya terbatas pada materi putih. Proporsi limfosit
dan makrofag dapat bervariasi dalam fokus yang terpengaruh.
Makrofag umumnya epiteloid, dan dalam kasus kronis terdapat
deposisi retikulin dan kolagen yang melimpah di daerah
perivaskular yang terkena (lihat Gambar 14-103, B). Lesi inflamasi
pada meningoensefalitis granulomatosa didominasi oleh limfosit
CD3 + dan akumulasi makrofag CD163 + perivaskular.
Pengamatan ini mengarah pada saran bahwa mekanisme yang
mendasari proses penyakit adalah hipersensitivitas tipe tertunda
yang dimediasi limfosit T dari penyakit autoimun spesifik organ.
Terlepas dari itu, penyebab meningoensefalitis granulomatosa
tetap membingungkan, dan berbagai upaya untuk secara
konsisten mengisolasi patogen dari anjing yang terkena telah
terbukti tidak membuahkan hasil (Zachary, 2017).
 Daftar Pustaka
Altay, U. M., Skerritt, G. C., Hilbe, M., Ehrensperger, F., & Steffen, F.
(2011). Feline Cerebrovascular Disease: Clinical and
Histopathologic Findings in 16 Cats. Journal of the American
Animal Hospital Association, 47(2), 89–97
Fadilah, M.F., Berata, I.K., Kardena, I,M. 2015. Studi Histopatologi
Limpa Anjing Penderita Distemper Dikaitkan Dengan
Sebaran Sel-Sel Radang Pada Otak Dan Paru.Buletin
Veteriner Udayana Volume 7 No. 2: 194-201
Ghafari, S.M., Dezfoulian, O.,and Moosakhani, F. Dog-bite induced
fatal meningitis in a kitten: a case report. Iranian Journal of
Veterinary Research, Shiraz University, Vol. 9, No. 4
Zachary, James. 2017. Pathologic Basis of Veterinary Disease. Louise,
Missouri ; Elsevier.
Wirata , I. K., Agus, J. U. G., Sudira, I.W., Widia ,I.K,, Fik,i I. K. 2013.
MONITORING PATOLOGI BOVINE SONGIFORM
ENCEPHALOPATHY (BSE) PADA RUMAH POTONG HEWAN
DI WILAYAH KERJA BBV DENPASAR TAHUN 2012. Buletin
Veteriner, BBVet Denpasar, Vol. XXV, No. 83.
 Buletin Veteriner, BBVet Denpasar, Vol. XXV, No. 83, Desember 2013 ISSN : 0854-901X Buletin Veteriner, BBVet Denpasar, Vol. XXV, No. 83, Desember 2013 ISSN : 0854-901X

MONITORING PATOLOGI BOVINE SONGIFORM ENCEPHALOPATHY

(BSE) PADA RUMAH POTONG HEWAN DI WILAYAH KERJA BBV
DENPASAR TAHUN 2012 PENDAHULUAN Wilayah kerja Balai Besar
Veteriner Denpasar meliputi
(Pathology Monitoring of Bovine Spongiform Encephalopathy (BSE) at the Bovine Spongiform Provinsi Bali, Nusa Tenggara
Slaughter House in the Working Area of Veterinary Center of Denpasar in Encephalopathy (BSE) atau yang Barat dan Nusa Tenggara Timur
2012) biasa disebut penyakit sapi gila merupakan daerah tujuan wisata
merupakan penyakit yang dapat yang banyak mengimpor daging
Wirata IK, Agus Joni U G, Sudira IW, Widia IK, Fiki Indra K. ditemukan pada sapi, ditandai sapi dari luar negeri untuk
dengan gejala saraf dan biasanya memenuhi kebutuhan hotel
Balai Besar Veteriner Denpasar berakhir dengan kematian. berbintang. Penggunaan limbah
ABSTRAK Penyebab BSE adalah prion, hotel sebagai pakan ternak
yakni molekul protein tanpa merupakan sumber potensial
Monitoring patologi Bovine Spongiform Encephalopathy (BSE) telah dilakukan di memiliki asam inti (DNA maupun
beberapa Rumah Potong Hewan (RPH) yang ada di Provinsi Bali, Nusa Tenggara Barat
kemunculan penyakit sapi gila
RNA). Masa inkubasi BSE (BSE).
(NTB) dan Nusa Tenggara Timur (NTT) oleh Balai Besar Veteriner Denpasar pada tahun
2012. Monitoring bertujuan untuk mendeteksi kemungkinan adanya agen penyakit BSE
berkisar antara 2,5 sampai 8
pada sampel otak sapi. Di Provinsi Bali diperoleh sebanyak 223 sampel otak. Di RPH tahun sehingga gejala klinis awal Disamping itu, intensifikasi
Mataram dan Kota Bima Provinsi NTB diperoleh sebanyak 62 sampel otak. Sedangkan BSE biasanya baru muncul pada pemeliharaan ternak oleh
dari RPH Borong, Kabupaten Manggarai Timur dan RPH Alok, Kabupaten Sikka, Provinsi sapi-sapi berumur diatas 2 tahun. masyarakat berdampak pada
NTT diperoleh sebanyak 23 sampel otak. Total sampel yang diperoleh pada saat peningkatan penggunaan
monitoring dilakukan adalah sebanyak 308 sampel otak sapi. Penyakit sapi gila (BSE) pertama konsentrat atau pakan jadi
Terhadap 308 sampel otak (medula oblongata) dilakukan pemeriksan
kali ditemukan di Inggris pada sebagai pakan ternak. Walaupun
histopatologi. Hasilnya, semua sampel otak tidak ada yang mengalami perubahan tahun 1986. Pada mulanya, BSE belum bisa dibuktikan bahwa
histopatologi ke arah penyakit BSE. Dapat disimpulkan bahwa dari hasil monitoring yang dikira hanya menyerang sapi, konsentrat atau pakan jadi untuk
dilakukan pada tahun 2012, tidak ditemukan kasus BSE pada ternak sapi yang dipotong tetapi kemudian BSE dianggap ternak ruminansia
di RPH wilayah kerja Balai Besar Veteriner Denpasar. berkaitan dengan penyakit pada mempergunakan MBM sebagai
Kata kunci: BSE, histopatologi, Monitoring. manusia. Penemuan kasus BSE bahan baku, akan tetapi tidak ada
menyebabkan kekhawatiran jaminan pula bahwa pakan /
terhadap keamanan konsentrat tersebut tidak
ABSTRACT
mengkonsumsi daging sapi di mempergunkan MBM hasil
sejumlah negara. importasi. Dengan situasi seperti
Pathology monitoring of Bovine Spongiform Encephalopathy (BSE) has been tersebut diatas dan dalam rangka
conducted by Veterinary Center of Denpasar in some Slaughterhouse (SH) in Bali, Nusa Indonesia sampai saat ini
Tenggara Barat (NTB) and Nusa Tenggara Timur (NTT) Provinces in 2012. The melaksanakan PERMENTAN
merupakan negara yang masih
monitoring’s aimed to detect the posibilities of presence of BSE agent in the cattle's brain Nomor. 367/Kpts/T
bebas dari kasus BSE. Untuk
samples. In Bali obtained as much as 223 brain samples. At the slaughterhouse Mataram N.530/12/2002, tentang
and Bima City which is the region of NTB province were obtained 62 brain samples.
mempertahankan kondisi
Pernyataan Negara Indonesia
While from slaughterhouse Borong, East Manggarai regency and slaughterhouse Alok, tersebut, pemerintah telah
Tetap Bebas Dari Penyakit
Sikka regency which is part of NTT province acquired brain samples as many as 23 mengambil langkah-langkah
samples. Total samples obtained at the time of the monitoring carried out are as much as Bovine Spongiform
strategis antara lain: penghentian
308 samples of brain cattles. Encephalopathy (BSE), maka
importasi hewan ruminansia dan
dipandang perlu untuk melakukan
Against 308 samples of brain (medulla oblongata) performed histopathological produknya yang berasal dari
kegiatan monitoring patologi
examination. And the result, there was no histopathological changes that leads to the negara tertular BSE, pelarangan
penyakit BSE di wilayah kerja
BSE in all brain samples. So that, it could be concluded that based on the results of the penggunaan tepung daging dan
monitoring conducted in 2012 there was no cases of BSE found in cattles that Balai Besar Veteriner Denpasar
tulang (TDT) atau meat bone
slaughtered in the slaughterhouse in the working area of Veterinary Center of Denpasar. secara teratur dan
meal (MBM) asal ruminansia
berkesinambungan.
sebagai pakan ternak ruminansia
Keywords: BSE, histopathology, Monitoring. serta melakukan surveilans dan
kajian resiko setiap tahun secara
berkelanjutan.

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Buletin Veteriner, BBVet Denpasar, Vol. XXV, No. 83, Desember 2013 ISSN : 0854-901X Buletin Veteriner, BBVet Denpasar, Vol. XXV, No. 83, Desember 2013 ISSN : 0854-901X

adalah berasal dari sapi yang PEMBAHASAN protein (PrP). Di dalam saluran
berumur 2 tahun keatas. Otak pencenaan, PrPsc oleh sel-sel
MATERI DAN METODE selanjutnya diberi pengawet Faktor Resiko dendritik usus halus disalurkan ke
formalin buffer netral 10%. organ limfoid skunder (Payer’s
BSE adalah anggota dari
patches), limpa, tonsil dan timus
kelompok penyakit yang dikenal
Materi sub akut yaitu transmissible untuk selanjutkan diekspresikan
spongiform encephalopathy ke sel T dan B (Huang and
Metode
Monitoring patologi BSE MacPherson, 2004).
(TSE) atau penyakit "prion". Ini
dilakukan dengan pengambilan Diagnosa BSE didasarkan pada mencakup juga "Creutzfeldt- PrPsc selanjutnya melalui
sampel otak sapi (Medula pemeriksaan histopatologi. Pada Jakob disease" (CJD) yang mekanisme retrograde transport
oblongata) di Rumah Potong kasus BSE, secara histopatologi menyerang manusia, "scrapie" menuju ke sistem saraf tepi dan
Hewan yang berada dibawah akan ditemukan lesi pada otak pada domba dan kambing, sistem saraf pusat. Akumulasi
pengawasan Pemerintah Daerah/ yang dikenal sebagai spongiform transmissible mink PrPsc pada otak menimbulkan lesi
Dinas Peternakan setempat yang encephalophaty. Terjadi encephalopathy (TME) dan yang spesifik yaitu: degenerasi neuron,
ada di wilayah kerja Balai Besar degenerasi vakuoler neuron, hanya ditemukan di Amerika vakuolisasi neuronal bersifat
Veteriner Denpasar. gliosis, kematian neuron tanpa Utara saja yaitu "chronic wasting intrasitoplasmik tanpa diikuti
Pengambilan sampel otak sapi diikuti reaksi radang (Debeer et disease" (CWD) pada wapiti adanya respon radang, sel-sel
dilakukan pada bagian obex dari al., 2002), reaksi astrosit dan (Cervus canadensis) dan astrosit mengalami hipertropi dan
Medula oblongata. Otak sapi kadang-kadang menimbulkan beberapa jenis rusa. Penyakit- hiperplasia (Scott et al., 1990;
yang diambil sebagai sampel plak amyloid. penyakit ini hanya dapat Williams and Young, 1993; Wells
dikonfirmasi secara pasca mati et al., 1994). Pada sapi menderita
(post mortem) dengan BSE agen penyakit banyak
pemeriksaan spesimen otak. ditemukan di jaringan otak, spinal
cord, retina, bagian distal ileum,
Upaya pengendalian penyakit
tonsil dan trigeminal ganglion.
dapat mengurangi risiko
terekspos BSE pada setiap Informasi yang berhasil diperoleh
spesies (termasuk manusia) pada saat kunjungan
dengan cara pengambilan sampel otak dari
mengkonsentrasikan upaya untuk instansi yang membidangi fungsi
mengeliminasi hewan-hewan peternakan dan kesehatan
yang secara klinis diduga tertular hewan di wilayah kabupaten/kota
BSE dari seluruh mata rantai Provinsi Bali, NTB dan NTT
makanan dan pakan ternak dan mengatakan bahwa tidak ada
menghancurkan material tertentu peternak sapi yang memberikan
yang berisiko (seperti jaringan pakan komersial pada ternak sapi
Gambar 1. tubuh hewan yang paling mereka. Pakan utama ternak
mungkin mengandung infeksi masyarakat adalah rumput dan
Sel neuron yang berisi vakuola-vakuola terang tanpa disertai adanya sel terutama jaringan SSP) dari kadang-kadang diberi dedak padi
radang pada otak sapi yang terinfeksi BSE. (HE 40x). (McGavin M.D., semua sapi diatas umur tertentu atau dedak gandum (polar). Sapi
2007). baik yang dipotong untuk yang dipotong di RPH tempat
konsumsi maupun yang tidak. kegiatan monitoring dilakukan
(Naipospos, 2010). Seperti rata-rata berumur diatas 2 tahun,
diketahui bahwa sumber utama yang dapat dilihat dari struktur
penularan BSE adalah melalui gigi hewan. Penentuan umur
pemberian pakan ternak yang hewan bisa dilakukan dengan
mengandung MBM atau TDT dari melihat struktur gigi hewan
ruminansia yang tercemar prion (gambar 1).

78 82
 RETROSPECTIVE STUDIES

TABLE 1B
Feline Cerebrovascular Disease: Clinical and Historical Complaints and Clinical Findings for Four Cats with Intracranial Hemorrhage

Histopathologic Findings in 16 Cats Clinical data

Sudden death
Number of cats
1
Lesion distribution (case numbers)
Cerebral and brainstem hemorrhage (15)
Seizures 2 Multifocal hemorrhage and perivascular meningitis (14); multifocal hemorrhage (16)
Ulrike Michal Altay, Dr.med.vet., DECVN, Geoff C. Skerritt, BVSc, MIBiol, CBiol, DECVN, FRCVS, Tetraparesis 1 Cerebral hemorrhage, concurrent mild meningitis (13)
Monika Hilbe, Dr.med.vet., DECVP, Felix Ehrensperger, Dr.med.vet., DECVP, Frank Steffen, Dr.med.vet., DECVN

infarction diagnosed. The cat made a full recovery. In case 12, the
lesion was not visible on CT. This cat’s hemorrhagic infarction was
ABSTRACT localized in the brainstem.
Sixteen cats with cerebrovascular disease confirmed via histology to be of nontraumatic and nonneoplastic origins are de- A full postmortem examination was performed on 15 cats
scribed. In addition, the anatomy of the arterial supply of the cat’s brain is reviewed. It is suggested that this unique arterial (Tables 2A, B, and Table 3). Gross lesions were visible in four of
design may influence the incidence of cerebrovascular accidents in this species. Of the 16 cats reviewed, seven cats had the 15 cats (Figure 2). In two of the cats with ischemic CVD,
ischemic infarctions, five had hemorrhagic infarctions, and four were diagnosed with intracranial hemorrhage. The median abnormal tissue was grossly visible and in one cat with red infarcts
age was 8 yr and 9.5 yr in cats with infarctions and intracranial hemorrhages, respectively. Clinical signs were severe, acute, petechial bleeding was seen. Gross lesions were obvious in one cat
consistent with the localization of the cerebrovascular lesion, and influenced by underlying pathology. Four cats with in- with intraparenchymal hemorrhage and changes found in the
farction showed lateralized neurologic signs. Four cats with infarctions were diagnosed with pulmonary disease antemortem histopathology are shown in Figures 3 and 4.
and three cats had hyperthyroidism. Cerebrospinal fluid analysis and computed tomography scans were available in two cats. Infarction and malacia were seen in the cerebral cortex of
None of the infarctions were grossly visible. All cats with hemorrhagic infarcts had severe liver pathology and nephritis was three of the 12 cats with an infarction, in the brainstem of five of
identified in four cats. Hypoxia was a feature in four cats and one cat suffered cardiac failure. In conclusion, the clinical the 12 cats with an infarction, in both the cerebral cortex and
picture is influenced by the type of cerebrovascular disease, the localization of the intracranial lesions, and any underlying brainstem in three of the 12 cats with an infarction, and in the basal
pathology. (J Am Anim Hosp Assoc 2011; 47:89–97. DOI 10.5326/JAAHA-MS-5480) nuclei of one cat with an infarction. All the red infarcts were
localized to the brainstem, whereas pale infarcts and malacia were
seen in the forebrain, brainstem, hippocampus, and basal nuclei.
Cases were graded as either large vessel disease (i.e., territorial
infarcts) or small vessel disease (i.e., lacunar infarcts). Of the
12 cats with an infarction, territorial infarcts were seen in three
cats, lacunar infarcts in seven cats, and global ischemia in two cats
(Table 3). Intraparenchymal hemorrhage was multifocal in two
cats and focal in two cats (Table 2B).
Extraneurologic clinical signs of CVD were correlated with the
following potentially predisposing conditions, which were con-
firmed by pathologic examination in 15 out of 16 cats: hyper-
thyroidism, heart disease, nephropathies, and hepatopathies.
Meningitis was a feature in five of these 16 cats. The inflammation
was mononuclear in case 6 and mixed cellular in cases 3 and 8. In
cases 13 and 14, the inflammation was seen to be attributed to
feline coronavirus on postmortem.
Concurrent diseases were noted on postmortem examination
in 14 of 16 cats (Tables 2A and B). All cats with red infarcts
(n¼5) showed severe liver pathology and two of these cats were

Introduction is the main supplying vessel in the dog, becomes obliterated in

Cerebrovascular disease (CVD) is currently topical in the veteri-
nary literature and much information has been recorded for the
dog. 1–4
Cerebellar infarcts have been described in two cats; how-
cats soon after birth. The maxillary artery supplies the arterial
TABLE 2A
circle by an anastomosing ramus, which includes a rete mirabile
(i.e., a network of fine arterioles). The arterial circle in the cat is Findings in 12 Cats with Infarction

ever, data on feline vascular encephalopathies are limited.5 Vas- not a closed ring because of the lack of a rostral communicating Lesion Case Lesion
distribution number* size Type Extraneurologic clinical signs Predisposing (bold) and concurrent diseases
cularization in the feline brain is different than in dogs rendering artery that is normally present in other species. Also, the direction
Cerebral Cortex 5 M Ischemic Dyspnea, lethargy, inappetence, vomitus, diarrhea, no Hypertrophic cardiomyopathy, acute cardiogenic
differences in lesion distribution feasible. The cerebral arterial of flow in the basilar artery is away from the arterial circle so that peripheral pulses, inability to jump, hypothermia lung edema
circle of Willis on the ventral surface of the brain collects blood maxillary blood from the external carotid arteries is distributed to 7 M Ischemic None reported None determined
from contributing arteries. The function of the arterial circle is to the entire brain, except for the caudal portion of the brainstem, 8 G Ischemic Inappetence, incontinence Mild meningitis
maintain a constant blood pressure in the end arteries.6 In the cat, which is supplied by the vertebral arteries (Figure 1).7–11 Brainstem 3 M Ischemic None reported Lymphoma (gastrointestinal), mild meningoencephalitis
9 M Red Icterus Hepatic lipidosis, pancreatic nodular hyperplasia
the arterial circle is supplied by anastomoses with the maxillary CVD refers to any abnormality in the brain resulting from
10 M Red Icterus, lethargy Hepatic lipidosis, pancreatitis
and pharyngeal arteries, which arise from the external carotid pathology of the supplying blood vessels. Insufficient blood supply
11 G Red Vocalization Hepatic lipidosis
artery. The proximal portion of the internal carotid artery, which leads to ischemia or infarction in which normal cellular function 12 M Red None reported Hepatitis, liver congestion, myocardial fibrosis,
mineralization of the mucosa of the stomach
Basal nuclei 6 G Ischemic None Hypoxia, lipidpneumonia (severe), nephritis,
hepatic lipidosis, focal meningoencephalitis
Multifocal 1 M Ischemic Dyspnea, fever (pyothorax) Hypoxia, pleuritis, mild thyroiditis
From the Department of Small Animals, Clinic of Small Animal CSF cerebrospinal fluid; CT computed tomography; CVD cerebrovascular
Surgery/Neurology (U.M.A., F.S.) and the Institute of Veterinary disease; MRI magnetic resonance imaging
2 M Ischemic Fever, lethargy, anorexia, cardiorespiratory Hypoxia (anesthesia related), mediastinitis
arrest during thoracocentesis (pyothorax)
Pathology (F.E., M.H.), Vetsuisse Faculty University of Zurich,
4 M Red Inappetence, weight loss Hyperthyroidism (functional adenoma), nephritis,
Zurich, Switzerland; and ChesterGates Referral Hospital, Chester, hepatic lipidosis, lafora bodies (intracerebral)
UK (U.M.A., G.S.).
* Case 8 had a brain biopsy with full recovery. All other cases, 1–7 and 9–12, had postmortem examinations.
Correspondence: ulrikemichal@yahoo.com (U.M.A.) G, grossly visible; M, microscopic

ª 2011 by American Animal Hospital Association JAAHA.ORG 89 92 JAAHA | 47:2 Mar/Apr 2011

Feline Cerebrovascular Disease

TABLE 2B
Morphologic Findings in Four Cats with Intracranial Hemorrhage and One Cat with Intraventricular Hemorrhage

Case Lesion
Lesion distribution number size Extraneurologic clinical signs Predisposing (bold) and concurrent disease
Right hemisphere 13 G Polyuria, polydipsia, inappetence, Meningitis (FIP)
weight loss
Multifocal 14 M Lethargy, anorexia, vocalization at night Meningitis (FIP), hyperthyroidism, hepatic lipidosis,
nephritis
16 M Ptyalism, vocalization, aggression, None determined
polyphagia
Brainstem (pons and medulla 15 M None reported Suffocation (in recovery from anesthesia for ocular
oblongata) surgery)

FIP, feline infectious peritonitis

icteric. Overall, seven of 16 cats had liver disease on postmortem
examination. Chronic interstitial nephritis was a feature in three
of the 16 cats. Three cats had pathologic thyroid changes. Thyroid
adenoma was found in two of these cats and thyroiditis in one cat.
All three cats had confirmed positive results for thyroid disease.
Two cats were originally treated for pyothorax and pleuritis and
mediastinitis were identified on the postmortem examinations.
One of these cats suffered cardiorespiratory arrest during thor-
acocentesis and the other showed signs of dyspnea and hypoxia
prior to death. Ischemic polioencephalomalacia was diagnosed in
both of these cats postmortem. One cat died of cardiac failure (case
5). One cat with leukoencephalomalacia was found to have gas-
trointestinal lymphoma and mild meningoencephalitis (case 3).
The findings in cats with intracranial hemorrhage are sum-
marized in Table 2B. Meningitis was an intracranial finding in two
cats and changes in one of these two cats were associated with
feline coronavirus infection. Meningitis was a likely cause of the
hemorrhage in both cases. Case 15 suffocated during recovery
TABLE 3
Classification of Stroke
Case Appearance
1 Polioencephalomalacia
2 Polioencephalomalacia
3 Leucencephalomalacia
4 Multifocal malacias with hemosidering storage
5 Focal malacia and thrombi in small vessels
6 Focal malacia
7 Focal malacia
8 Focal malacia
9 Focal malacia
10 Multifocal malacias and extravasation of erythrocytes
11 Focal malacia and extravasation of erythrocytes, fibrinoid vessel degeneration
12 Focal malacia and extravasation of erythrocytes
from anesthesia for ocular surgery. No concurrent disease was
determined in case 16. FIGURE 3 Photomicrograph of rarefication and severe thinning
In the absence of concurrent abnormalities, cerebrovascular (stars) of the cortex due to an ischemic infarct. Hematoxylin and
lesions were cryptogenic in two of 16 cats. This includes the one cat eosin stain, original magnification 34.
that recovered fully after CT-guided biopsy.
FIGURE 2 Gross view of the brain from a cat with presumed
Discussion accident (Tables 1A and B) as reported elsewhere.5,14,15 Ischemic
thiamine deficiency. Hemorrhagic necrosis in the region of the gyrus
Information about cerebrovascular disease in cats is limited. The lesions were most commonly associated with seizures as the major
dentatus and the corpora geniculata are noted (arrows).
medical histories of 16 cats with cerebrovascular disease that neurologic sign. Case 7, with a focal cortical ischemic lesion,
were extracted from a computerized pathology database were presented with refractory seizures as the only clinical sign. In the
analyzed. One cat in which a CT-guided biopsy revealed an literature, only a few reports mention seizures as a clinical sign in
ischemic infarct was included in the study. The infarcts were the caudal brainstem is supplied by the vertebral arteries, and cats cats with CVD.23,24 Central vestibular signs were associated with
found to be hemorrhagic in five cats and ischemic in seven have a rete mirabile, a structure that is not present in dogs.9,10 brainstem involvement. Asymmetric neurologic signs were noted
cases. The other four cats suffered intraparenchymal hemor- Cerebellar infarcts in Cavalier King Charles spaniels have been in four of 12 cats with an infarction.
rhage. reported with increasing frequency, and recently, two cases of cats Extraneurologic clinical signs were seen in 10 of the 16 cats.
Publications describing the unique intracranial blood supply with cerebellar infarcts have also been reported.2,5 In the current They could be nonspecific or due to underlying disease as shown at
of the cat’s brain are sparse. In the cat, the blood supply of the study, a cerebellar infarct was not identified in any cat. Instead, the postmortem (Tables 2A and B). Inappetence was seen in three of
brain is from one main source: the external carotid artery. Only brainstem was affected in seven cats. An ischemic event during the 12 cats with infarction and icterus in two of the five cats with
anesthesia can cause neuronal cell loss; however, cells in the hemorrhagic infarcts. Cats with cerebrovascular disease may be
cerebellum are considered more resistant to ischemic insults.20 presented with neurologic signs or extraneurologic signs only.
Several diseases or factors have been associated with cere- Hypercoaguable states were proposed by several authors as
brovascular disease in cats: cuterebra parasitic migration, mi- a predisposing factor for CVD in humans and dogs.1,2,23 Tests for
Vessel size Type Localization grating heart worms, anesthesia-related ischemia, intracranial coagulation abnormalities were not carried out in the cats fea-
Global Ischemic Cerebrum, brainstem telangiectasia, granulomatous meningoencephalitis, and thiamine tured in this study and so coagulopathies could theoretically have
Global Ischemic Cerebrum, brainstem, hippocampus deficiency.14–23 Intracranial hemorrhage has been associated with been missed. In the literature, the clinical signs of feline coagu-
Lacunar Ischemic Brainstem primary and secondary hypertension, cerebral amyloid angiop- lopathies include hematuria, cutaneous hematomas, gingival
Lacunar Red Multifocal (brainstem, cerebrum) athy, and intracranial neoplasia.24–27 bleeding, epistaxis, or prolonged bleeding times.29–32 None of
Territorial Ischemic Cerebral cortex
Stroke is the sudden and abrupt onset of focal neurologic these signs were recorded for any of the cats in the current study;
Lacunar Ischemic Basal nuclei
6
Territorial Ischemic Cerebral cortex
deficits from an intracranial vascular event. Only one cat with however, liver disease (e.g., hepatic lipidosis) was the most
Territorial Ischemic Cerebrum (gray and white matter) underlying meningitis showed development of clinical signs over commonly cited cause of coagulation disorders.30,33 Indeed, seven
Lacunar Red Brainstem (lamina quadrigemina, pons) 1 mo, indicating that signs of cerebrovascular disease can be cats in the current study were diagnosed as having hepatic lip-
Lacunar Red Brainstem and midbrain 28
obscured by concurrent disease. idosis, hepatitis, or liver telangiectasia. Thus, a possible pre-
Lacunar Red Brainstem (corpus geniculatum laterale, pons) Neurologic signs, seen in six of the 16 cats included in this disposition for CVD cannot be ruled out, particularly in cats with
Lacunar Red Brainstem (medulla oblongata)
study, were consistent with the localization of the cerebrovascular hemorrhagic infarction (Tables 2A and B). In fact, kidney disease,

JAAHA.ORG 93 94 JAAHA | 47:2 Mar/Apr 2011

 CHAPTER 14  Nervous System 891

character—a dense infiltrate of lymphocytes, monocytes, and plasma
cells.
Gross lesions characteristically occur in the cerebellum (medul-
lary area, folial white matter, and subpial white matter) and cerebel-
lar peduncles (with both white matter and sometimes gray matter
involvement of the pons). Lesions also occur in medulla oblongata
(particularly in the subependymal area of the fourth ventricle),
rostral medullary vellum, cerebrum (both white matter and gray
matter), optic nerves, optic tracts, spinal cord, and meninges.
Microscopically, in addition to demyelination there is status
spongiosus, astrocytic hypertrophy and hyperplasia with focal and
variable syncytial cell formation, reduced numbers of oligodendrog-
lia, and variable neuronal degeneration (Fig. 14-97, A). Inclusion
bodies (cytoplasmic, nuclear, or both) are detectable, particularly in
astrocytes, which are important target cells for the distemper virus,
but also in ependymal cells and occasionally in neurons (Fig. 14-97,
B). The earliest evidence of myelin injury is a ballooning change
resulting from a split in the myelin sheath or more degenerative
changes, including axonal swelling. This lesion is also variably
A degeneration. Nuclear and cytoplasmic inclusions, positive for dis-
associated with astroglial and microglial proliferation. This initial
injury of the myelin sheath, which has been suggested to be a result
of perturbed astrocytic function after viral infection, is followed by
a progressive removal of compact myelin sheaths by phagocytic
microglial cells that infiltrate the myelin lamellae and variable
axonal necrosis.
A late stage of demyelination, which is a reflection of an affected
animal’s improved immune status, is more pronounced and is char-
acterized by nonsuppurative inflammation (perivascular cuffing,
leptomeningitis, and choroiditis) and also can be accompanied by
tissue degeneration and accumulation of gitter cells.
In addition to the dog, animals of the families Ailuridae (red
panda), Canidae (fox, wolf), Hyaenidae (hyena), Mustelidae (ferret,
mink), Procyonidae (raccoon, panda), Ursidae (bear), Viverridae
(civet, mongoose), and Felidae (exotic felids including lions, tigers,
and leopards) are susceptible to canine distemper viral infection.
Additionally, canine distemper has recently been reported in jave-
linas (collared peccaries) of the family Tayassuidae in the United
States.
Neurologic signs in all affected species include convulsions,
myoclonus, tremor, disturbances in voluntary movement, circling,
hyperesthesia, paralysis, and blindness.
Old-Dog Encephalitis.  Old-dog encephalitis is thought to arise
from long-term persistent infection of the CNS with a defective
form of CDV. This pathogenesis has been demonstrated in experi-
mental infections with the CDV. Although the virus has the same
general polypeptide composition and contains all of the major viral
proteins as the one causing conventional distemper, some differ-
ences among peptides have been reported. The mechanisms involved
in development of lesions are not known; however, they result in a
proliferation of nonsuppurative inflammatory cells.
Lesions are primarily in the cerebral hemispheres and brainstem.
Microscopic lesions are characterized primarily by demyelination
with disseminated, nonsuppurative encephalitis with variable,
sometimes prominent, lymphoplasmacytic perivascular cuffing,
microgliosis, astrogliosis, and variable leptomeningitis and neuronal
temper viral antigen, have been detected in neurons and astrocytes
in the cerebral cortex, thalamus, and brainstem but in contrast to
distemper, not in the cerebellum.
Old-dog encephalitis is a rare condition occurring in mature
adult dogs. Clinical signs include depression, circling, head pressing,
visual deficits, seizures, and muscle fasciculations.

B Welsh corgi, and Great Pyrenees). Based on its prevalence in
Figure 14-97  Canine Distemper, Dog. A, Acute polioencephalomyelitis.
Hippocampus. Note the necrotic neurons (arrows) and edema of the dentate
gyrus. Low numbers of mononuclear inflammatory cells are present. H&E
stain. B, Inclusion bodies, brain, midbrain periventricular white matter, dog.
Distinct acidophilic (red) intranuclear inclusion bodies (arrows) are present
in astrocytes and some gemistocytes. Similar inclusions can be observed in
the cytoplasm of epithelial cells throughout the body (bladder epithelium,
respiratory epithelium, gastric epithelium). H&E stain. (A courtesy Dr. W.
Haschek-Hock, College of Veterinary Medicine, University of Illinois.
B courtesy Dr. M.D. McGavin, College of Veterinary Medicine, University
of Tennessee.)
Degenerative Diseases
Metabolic
Aging-Related Degenerative Myelopathy (German Shepherd
Myelopathy).  A degenerative myelopathy is most commonly seen
in the German shepherd, but a similar condition has been described
in other predominatly large canine breeds (Belgium shepherd, Old
English sheepdog, Rhodesian ridgeback, Weimaraner, Pembroke
German shepherds, it has been suggested that there is a genetic
“aging” predisposition in this breed. Altered suppressor lymphocyte
activity has been noted in affected dogs, but the relevance to the
CNS disease is unknown. Some investigators have reported low
vitamin E concentrations and suggested oxidative stress injury;
others have found elevated concentrations of acetylcholinesterase
in CSF. The cause of this disorder remains to be discovered.
Gross lesions in the CNS are not present in dogs with age-related
degenerative myelopathy; however, atrophy of caudal axial and
appendicular muscles occurs. Microscopic lesions are most notable
in the thoracic spinal cord and can be diffuse or multifocal. Dorsal

894 SECTION II  Pathology of Organ Systems

Topographically, gross lesions are consistently observed in the the thalamus and brainstem. Histologically, this disease causes
midthoracic segments, with extension to the midcervical and mid- distinct perivascular cuffs composed almost entirely of lymphocytes
lumbar segments in the most severe cases. Gross lesions include and macrophages with scattered numbers of plasma cells and neu-
softening and cavitation of the affected segments. Lesions are bilat- trophils. These cuffs are almost entirely restricted to the white
eral and symmetric regardless of the region affected. In the thoracic matter. The proportion of lymphocytes and macrophages can vary
segments the ventral funiculi are most severely affected, although in affected foci. Macrophages are commonly epithelioid, and in
lesions can be found circumferentially around the spinal cord white chronic cases there is abundant deposition of reticulin and collagen
matter. In the cervical and lumbar segments, the lesions tend to be in the affected perivascular regions (see Fig. 14-103, B). The inflam-
focused either in the dorsal or ventral horns. Histologically, in severe matory lesion in granulomatous meningoencephalitis is predomi-
lesions there is destruction of white matter, with an influx of mac- nantly CD3+ lymphocytes and perivascular accumulations of
rophages accompanied by myelin degradation, glial cell loss, and CD163+ macrophages. This observation has led to the suggestion
vascular proliferation. The gray matter and the fasciculus proprius that the underlying mechanism of the disease process is a T
are typically spared in this disease. Neuronal cell bodies in spinal lymphocyte–mediated delayed-type hypersensitivity of an organ-
cord gray matter and ventral spinal nerve rootlets are similarly specific autoimmune disease. Regardless, the cause of granulomatous
unaffected. meningoencephalitis has remained enigmatic, and various attempts
Clinical signs begin between 3 and 13 months of age and progress to consistently isolate pathogens from affected dogs have proved
rapidly to paraplegia or tetraplegia within 1 to 3 weeks. fruitless.
Leptomeningeal Fibrosis.  Aging dogs have varying degrees of
leptomeningeal fibrosis involving the recesses of the cerebral sulci
(Fig. 14-102). This lesion is not present in the leptomeninges cover-
ing the outermost surfaces of the gyri. This latter feature can be
useful in differentiating meningeal fibrosis from suppurative menin-
gitis. In cases of suppurative meningitis, exudate accumulates over
the entire surface of the gyri.
Granulomatous Meningoencephalitis.  Granulomatous menin-
goencephalitis (GME) is one of two important idiopathic encepha-
litides of the dog, the second one being necrotizing encephalitis, of
which there are two variants (see later). Granulomatous meningo-
encephalitis occurs most commonly in young to middle-aged small
breed dogs, including poodles and various terrier breeds. No sex
predilection is known, although some studies are skewed slightly
toward female. Clinical signs in cases with brain lesions are variable
and include behavioral changes and circling. Spinal cord lesions can
result in paresis and ataxia. A
When present, gross lesions consist of gray-white to red, expan-
sive areas within the white matter of the brain and brainstem
(Fig. 14-103, A). Lesions can have irregular, well-defined margins
and a gelatinous or rubbery consistency or appear granular. There
are two different distribution patterns of the disease, a disseminated
form and a focal form. The focal form is most commonly seen in

Figure 14-102  Meningeal Fibrosis, Leptomeninges (Pia-Arachnoid
Mater), Dog. In old dogs the leptomeninges can have areas of fibrosis (white
areas around blood vessels in sulci), particularly in the sulci. This lesion must
not be confused with acute leptomeningitis and accumulation of exudate in
the leptomeninges and subarachnoid space. In the latter the exudate extends
into the sulci and also covers the gyri (see Fig. 14-43, A). (Courtesy College
of Veterinary Medicine, University of Illinois.)
B
Figure 14-103  Granulomatous Meningoencephalitis, Transverse
Section of Midbrain Just Rostral to the Pons, Dog. A, The mes-
encephalon is swollen, discolored, markedly distorted, and soft as the result
of extensive granulomatous inflammation (arrows), which has displaced the
midline to the right. The mesencephalic aqueduct is also compressed and
distorted. B, Note the accumulation of granulomatous inflammatory cells in
the perivascular space. Such layers of cells expand over time and compress
adjacent neural tissue, resulting in Wallerian-like degeneration of affected
myelinated axons and atrophy of affected neuron cell bodies. H&E.
(A courtesy Dr. J. Edwards, College of Veterinary Medicine, Texas A&M
University; and Dr. J. King, College of Veterinary Medicine, Cornell Uni-
versity. B courtesy Dr. J.F. Zachary, College of Veterinary Medicine, Univer-
sity of Illinois.)
Buletin Veteriner Udayana Volume 7 No. 2: 194-201 Buletin Veteriner Udayana Fadilah et al.
p-ISSN: 2085-2495; e-ISSN: 2477-2712 Agustus 2015

Studi Histopatologi Limpa Anjing Penderita Distemper Dikaitkan PENDAHULUAN
Dengan Sebaran Sel-Sel Radang Pada Otak Dan Paru
Distemper adalah salah satu penyakit
(HISTOPHATOLOGICAL STUDY OF SPLEEN ON DOGS INFECTED WITH virus menular yang dapat menyerang
DISTEMPER ASSOCIATED TO INFLAMATION IN THE BRAIN AND LUNGS) anjing. Penyakit distemper disebabkan
oleh virus dari genus Morbillivirus,
Muhamad Furkan Fadilah¹, I Ketut Berata2, I Made Kardena2* famili Paramyxoviridae dan mempunyai
1
Mahasiswa Fakultas Kedokteran Hewan Universitas Udayana hubungan dekat dengan virus measles
2
Laboratorium Patologi Veteriner Universitas Udayana dan Rinderpest (Frisk et al., 1999;
Jl. PB. Sudirman Denpasar-Bali Mochizuki et al., 1999; Rudd et al.,
*Email: adenbali@yahoo.com 2006). Virus distemper dapat menyerang
hewan dari famili Canidae, Mustelidae,
ABSTRAK dan Procyonidae (Headley dan Graca,
2000). Penyakit tersebut telah dilaporkan
Penelitian ini bertujuan untuk mengetahui adanya sebaran sel radang berdasarkan tingkat kejadiannya pada mamalia air seperti
keparahan penyakit pada anjing distemper ditinjau dari tingkat peradangan pada organ limpa, otak anjing laut (Kennedy et al., 2000) dan
dan paru. Sampel yang digunakan 20 sampel yang diambil dari organ limpa, otak, dan paru dari anjing liar di Afrika (Bildt et al., 2002;
anjing penderita distemper. Organ-organ tersebut diproses dalam pembuatan preparat histopatologi Spenser dan Burroughs, 1992). Walaupun
dengan teknik paraffin embedded block dan diwarnai dengan Harris Hematoksilin-Eosin. Preparat kucing dan babi dilaporkan dapat
histopatologi diperiksa berdasarkan lesi peradangan pada limpa, otak dan paru. Hasil pemeriksaan diinfeksi secara eksperimental, tetapi
pada limpa, otak dan paru menunjukkan adanya lesi berupa sel-sel limfoid yang bervariasi pada dianggap tidak penting dalam penyebaran
masing-masing organ tersebut. Dari 20 sampel yang diperiksa sesuai dengan derajat peradangan penyakit distemper anjing (Headley dan
diperoleh data, sembilan sampel (45%) limpa mengalami peradangan ringan, tujuh sampel (35%) Graca, 2000).
peradangan sedang, dan empat sampel (20%) peradangan berat. Pada otak tiga sampel (15%) tidak
Virus penyebab penyakit distemper
mengalami peradangan, 12 sampel (60%) peradangan ringan, lima sampel (25%) peradangan
sedang, dan tidak teramati adanya peradangan berat. Paru enam sampel (30%) peradangan ringan, ini dapat menyerang anjing dengan gejala
11 sampel (55%) peradangan sedang, dan tiga sampel (15%) peradangan berat. Dapat disimpulkan klinis yang bervariasi. Penyakit ini sangat
peradangan secara mikroskopis dapat diamati terjadi pada limpa, otak dan paru dari anjing yang sulit untuk disembuhkan sehingga jika
terinfeksi virus canine distemper. tidak ditangani secara dini, penyakit
distemper dapat menyebabkan kematian
Kata kunci: histopatologi, distemper, limpa, otak, paru pada anjing. Penyakit distemper
ditemukan hampir di seluruh dunia
ABSTRACT (Timoney et al., 1992). Anjing yang
terinfeksi penyakit distemper dapat
This study aim was to determine the distribution of inflammatory cells in canine distemper in menimbulkan gejala atau lesi pada mata,
terms of the level of inflammation in the spleen, brain and lungs. The sample used 20 infected dogs saluran respirasi, gastrointestinal,
wihich from the spleens, brains, and lungs of the dogs were collected. These organs were processed urogenital, sistem saraf, dan kulit
for histophatological observation using harris hematoxilyn-eosyn stain. The inflammation of the (Koutinas et al., 2004, Siegmund dan
organs examined by using binocular microscope with 200X magnification. the results showed that
Frases, 2008). Anjing yang diserang pada
inflammation was observed in the spleens: 9 samples (45%) showed the presence of lymphoid
cells that experienced a mild inflammation 7 (35%) moderate inflammation, and 4 (20%) severe umumnya berumur muda yaitu kurang
inflammation in brain, 3 samples (15%) did not show observe inflammation, 12 (60%) mild, 5 dari satu tahun, hal ini terjadi karena pada
(25%) moderate inflammation, and not observed any severe inflammation in brain, pulmonary: 6 umur ini terjadi penurunan antibodi
(30%) mild inflammation, 11 (55%) moderate inflammation, and 3 (15%) severe inflammation. It maternal, tingkat stress yang tinggi
can be concluded that the inflammation was observed microscopically in the spleen, brain and lung karena masa pertumbuhan, dan serangan
in the dog that infected with canine distemper virus penyakit lain yang menurunkan kondisi
tubuh (Suartha et al., 2008). Iklim sangat
Keywords: histopathology, distemper, spleen, brain, lungs berpengaruh terhadap terjadinya penyakit
distemper (Uzunova dan Koleva, 2005).
Secara patologi anatomi, anjing yang
terinfeksi penyakit distemper dapat
menyebabkan infeksi multi-sistemik.
Gambaran klinis darah perifer dari anjing
yang terinfeksi virus ini mula-mula
mengakibatkan terjadinya lymphopenia,
walaupun pada tingkat sub akut sampai
kronis diikuti dengan meningkatnya
jumlah monosit/peripheral blood
mononuclear cells (Nielsen et al., 2009).
Secara histopatologi dapat terjadi
perubahan ringan sampai nekrosis
terutama folikel jaringan limfoid, dimana
dapat ditemukan proliferasi limfoid.
Secara histopatologi, paru-paru dari
hewan yang terinfeksi penyakit distemper
akan tampak mengalami peradangan.
Pneumonia interstitialis akan teramati
pada paru-paru yang diikuti dengan
banyak infiltrasi sel-sel radang. Bila
berlangsung kronis, reaksi peradangan
akan meluas sampai ke bagian alveoli.
Apabila terjadi infeksi sekunder terutama
terinfeksi oleh bakteri pyogenes,
peradangan dengan eksudat purulen dapat
juga terjadi pada organ ini (Chvala et al.,
2007).
Kerusakan sel-sel otak yang terjadi
pada infeksi penyakit distemper anjing
dikarenakan reaksi demyelinisasi pada
saraf pusat akibat reaksi radang. Secara
histopatologi, otak akan tampak terjadi
peningkatan sel-sel glia yang diikuti
dengan peningkatan kadar sitokin karena
pengaruh reaksi radang pada daerah
tersebut (Stein et al, 2008).
METODE PENELITIAN
Materi Penelitian
Materi yang dipergunakan dalam
penelitian adalah kasus distemper pada
anjing yang masuk ke Laboratorium
Patologi Veteriner dan telah dikonfirmasi
dengan uji PCR (Polymerase Chain
Reaction) di Laboratorium Virologi,
Fakultas Kedokteran Hewan Universitas
Udayana. Data kasus yang diambil adalah
data dari tahun 2009 sampai tahun 2013,
berupa preparat histopatologi jaringan
limpa, otak, dan paru.

194 195

Buletin Veteriner Udayana Volume 7 No. 2: 194-201 Buletin Veteriner Udayana Fadilah et al.
p-ISSN: 2085-2495; e-ISSN: 2477-2712 Agustus 2015

Dari total 20 sampel yang diperiksa
pada limpa terdapat sembilan sampel
yang mengalami peradangan ringan,
tujuh sampel mengalami peradangan
sedang, dan empat sampel mengalami
peradangan berat. Pada otak terdapat tiga
sampel yang tidak mengalami
peradangan, 12 sampel mengalami
peradangan ringan, lima sampel
mengalami peradangan sedang dan tidak
terjadi peradangan berat. Pada paru enam
sampel mengalami peradangan ringan, 11
sampel mengalami peradangan sedang
dan tiga sampel yang mengalami
peradangan berat. Pada limpa tampak
terjadi peradangan yang hampir
menyeluruh bahkan terdapat empat
sampel yang mengalami peradangan
berat karena limpa merupakan organ
yang berperan penting pada infeksi virus.
Selain mengalami peradangan, limpa juga
akan mengalami perubahan berupa
proliferasi limfoid (Liang et al., 2007).
Gambaran tingkat peradangan pada
limpa, otak, dan paru dapat dilihat pada
Gambar 2, 3 dan 4
Gambar 3. Histopatologi otak anjing penderita distemper dengan pewarnaan HE (200X);
tanda panah menunjkukan adanya sel-sel radang; A tidak terjadi peradangan (normal); B
terjadi peradangan yang sedikit dan tidak menyebar; C terjadi peradangan yang
menyebar/multifokal.

Gambar 2. Histopatologi limpa anjing penderita distemper, dengan pewarnaan HE (200X);

tanda panah menunjukkan adanya sel-sel radang. A terjadi peradangan yang padat, namun
belum ada bentuk mikrolimfoma; B terjadi peradangan ringan yang ditandai dengan
tampaknya pulpa putih dan pulpa merah; C terjadi peradangan yang banyak/padat sampai
berbentuk mikrolimfoma. Gambar 4. Histopatologi paru anjing penderita distemper dengan pewarnaan HE (200X);
tanda panah menunjukkan adanya sel-sel radang; A terdapat sel-sel radang sedikit/lokal
Kategori peradangan berat pada Penyebab terjadinya peradangan yang menginfiltrasi paru tetapi tersebar (multifokal); B terdapat sel radang sedikit/lokal
limpa ditemukan empat dari 20 sampel pada otak adalah adanya kerusakan sel- meninfiltrasi paru; C Terjadi peradangan padat sampai mengalami difusa, sehingga alveoli
organ (20 %), paru-paru tiga organ (15 sel otak yang terjadi pada infeksi pada paru semakin menipis.
%) dan pada otak tidak terjadi penyakit distemper anjing. Kerusakan
peradangan berat. Hasil ini sel-sel otak tersebut menimbulkan reaksi Secara mikroskopis, paru-paru dari menimbulkan peradangan dengan eksudat
menyimpulkan bahwa hubungan tingkat demyelinisasi pada syaraf pusat akibat hewan yang terinfeksi akan tampak purulen (Chvala et al, 2007).
keparahan pada limpa lebih terkait reaksi radang yang terjadi di otak yang mengalami peradangan. Pneumonia
langsung dengan paru, bahkan ada tiga terinfeksi virus. interstitialis akan teramati pada paru-paru SIMPULAN DAN SARAN
organ (15 %) pada otak tidak ada Secara histopatologi, otak yang diikuti dengan banyak infiltrasi sel-
peradangan. Peradangan akut akan terjadi mengalami peningkatan infiltrasi sel-sel sel radang. Bila berlangsung kronis, Simpulan
pada paru dan limpa, namun pada otak glia yang diikuti dengan peningkatan reaksi peradangan akan meluas sampai ke Berdasarkan hasil penelitian dapat
sulit terjadi kronis karena barrier otak kadar sitokin karena pengaruh reaksi bagian alveoli. Kejadian penyakit akan disimpulkan bahwa variasi peradangan
yang sulit ditembus virus dalam waktu radang di daerah tersebut (Stein et la., bertambah parah jika diikuti dengan pada limpa tidak berkaitan langsung
yang singkat. 2008). infeksi sekunder. Anjing penderita dengan peradangan pada otak tetapi
distemper sering mengalami infeksi variasi peradangan pada limpa berkaitan
sekunder oleh bakteri pyogenes, dengan dengan peradangan pada paru.
198 199
Iranian Journal of Veterinary Research, Shiraz University, Vol. 9, No. 4, Ser. No. 25, 2008 Iranian Journal of Veterinary Research, Shiraz University, Vol. 9, No. 4, Ser. No. 25, 2008

Scientific Report Thoracic and abdominal radiographs showed

no significant abnormality. The cat received
intravenous cefazolin (25 mg/kg) and Ringer
Dog-bite induced fatal meningitis in a kitten: solution (10 ml/kg/h). Approximately one
a case report hour after admission, the cat developed
severe apnoea and asystole.
Selk Ghaffari, M.1*; Dezfoulian, O.2 and Moosakhani, F.1 Cardiorespiratory resuscitation was
unsuccessful and the animal died. At
1
Department of Clinical Sciences, Faculty of Veterinary Medicine, Karaj Branch, Islamic Azad University, postmortem examination the meninge of the
Karaj, Iran; 2Department of Pathobiology, College of Veterinary Medicine, Lorestan University, Lorestan, right hemisphere of cerebrum was thickened
Khorramabad, Iran by a grayish gelatinous blanket (Fig. 1). This
cloudy material was feature of the
* Fig. 2: Fibrinopurulent leptomeningitis:
Correspondence: M. Selk Ghaffari, Department of Clinical Sciences, Faculty of Veterinary Medicine, concentrated pus, which also covered the
Karaj Branch, Islamic Azad University, Karaj, Iran. E-mail: selkghaffari@gmail.com internal surface of the skull (endosteum accumulation of inflammatory cells,
predominantly neutrophils, and fibrinous
membrane). For microbiological
(Received 20 Aug 2007; revised version 12 Nov 2007; accepted 8 Jan 2008) exudates in subarachnoid spaces, (H&E,
examination, a sample of purulent exudates ×100)
was taken by sterile cotton-tipped swab and
Summary inoculated on both blood and MacConkey of suppurative cells was observed in the
Bacterial infection of the brain is relatively rare in dogs and cats. A cat at approximately three months of agars. The plates were incubated aerobically parenchyma of the brain.
age was admitted to the clinic with a history of dog bite seven days before admission. On clinical at 37°C for 48 h. Gram staining of colonial
presentation, the cat was unconscious and in lateral recumbency. One hour after admission, the cat developed material revealed small, Gram-negative rods Discussion
severe apnoea and asystole. Cardiorespiratory resuscitation was unsuccessful and the animal died. Necropsy and coccobacilles. On the basis of colony,
and histopathological examination revealed a purulent meningitis. A sample of purulent exudates was cellular morphology and biochemical In the presented case, the mechanism of
submitted for microbiological examination. Pasteurella multocida was isolated from bacterial culture. Due to properties, the isolate was identified as P. infection was supposed to be direct
the history of dog biting, direct inoculation of P. multocida into the subdural space following penetrating multocida. Tissue samples were fixed in inoculation of bacteria into the subdural
dog-bite wounds was suggested to be the cause of meningitis and death of the kitten. This report highlights 10% formalin, routinely embedded in space following penetrating dog-bite
the importance of antibiotic therapy in bite wounds to reduce such fatal complications.
paraffin and cut into 4 µm sections which wounds. In this case, P. multocida was
Key words: Meningitis, Cat, Pasteurella multocida were stained with haematoxylin and eosin. isolated from bacterial culture. Pasteurella
Histopathological study showed that the organisms are clinically significant in many
Introduction kitten following the dog bite. leptomeninge was invaded by large amount dog- and cat-bite wounds. These organisms
of fibrin deposits and neutrophils, which normally inhabit the nasal, gingival and
Meningitis and encephalitis refer to Case history scant of mononuclear cells scattered among tonsillar regions and gastrointestinal tract of
inflammatory conditions of the meninges them (Fig. 2). Blood vessels were engorged approximately 12 to 92% of dogs and 52 to
and brain parenchyma. Meningitis is A male, stray cat at approximately three with RBC(s), but no haemorrhage was 99% of cats as well as many other animals
characterized by inflammation of the months of age was admitted to the clinic observed in the lesion. (Weiss et al., 1998; Green and Goldstein,
meninges with involvement of subarachnoid with a history of dog bite seven days before The surface of pia matter was intact and 2006). The most common consequence of P.
space. Inflammatory diseases of central admission. The history indicated that the firmly attached to the adjacent outer layers multocida infection is a local cellulitis,
nervous system (CNS) are usually divided treatment included the application of topical of the brain, also no evidence of infiltration although serious systemic diseases may
into infectious and non-infectious causes. povidine-iodine on the bite wounds by the occur (e.g., meningitis, empyema,
Infectious causes include bacteria, fungi, owner. Two days before admission, the cat pneumonia, peritonitis, osteoarticular
protozoa, parasites, rickettsiae and viruses showed two episodes of grand mal seizures; infections, endocarditis and septicaemia)
(Wingfiled, 1997). Bacterial infection of the furthermore, cervical rigidity, lethargy and (Kimura et al., 2004). Several mechanisms
brain is relatively rare in dogs and cats progressive abnormal mental status was have been described to be involved in
(Munana, 2004). observed by the owner. On clinical bacterial infections of the central nervous
The true incidence of dogs and cats bite presentation, the cat was unconscious and in system in cats and dogs which included
wounds is unknown, but dog-bite wounds lateral recumbency. Physical examination haematogenous spread (septic emboli or
were responsible for 15% of canine revealed several bite wounds in the neck and mucous membrane colonization), contiguous
admissions to an emergency service in one forearms. Rectal temperature showed infection from adjacent structures (inner
study (Holt and Griffin, 2000; Scheepens et hypothermia (36°C). Cardiac auscultation ears, cribriform plate, sinuses, eyes and
al., 2006). Cats are not as frequently bitten revealed bradycardia (90 beats/min). No vertebrae), direct inoculation (trauma, bite
as dogs, and victims are often younger than heart murmur or obvious arrhythmia was wound and surgery) and migration of
the mean age of cats in the overall hospital detected. Fig. 1: A widespread purulent leptomenin- foreign bodies or aberrant parasites (Braund,
population (Shamir et al., 2000). This report Complete blood count indicated gitis, involve the dorsal portion of the right 2003).
describes a case of fatal meningitis in a neutrophilic leukocytosis with left shift. hemisphere In our case, bradycardia, hypothermia,

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