retina en felinos
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Enfermedades de la retina Felina
11° Simposio Platense de Medicina Veterinaria
Pablo Sande, MV, PhD, DCLOVE p_sande@yahoo.com
www.veteoftalmo.com.ar
Esquema de la retina
Normal
Atrofia
Inflamación
Vaso
s Coro
ideo
sVa
sos
Ret
inia
nos
Retina Normal
Examen del fondo del ojo
Directo
PanopticoIndirecto
Métodos complementarios
!Guidelines for clinical electroretinography in the dog KRISTINA NARFSTRÖM1, BJÖRN EKESTEN2, SERGE G. ROSOLEN3,B ERNHARD M. SPIESS4, CHRISTINE L. PERCICOT5 and RON OFRI6, Documenta Ophthalmologica 105: 83–92, 2002.
ERG
Mixto
ConosPot. Osc.
Métodos complementariosRFG
RFG
ERG
Orác
ulo
Ecógrafo
Hereditarias
Nutricionales
Vasculares
Inflamatorias
Tóxicas
Degeneraciones Hereditarias, Atrofia progresiva de la Retina
# Ceguera progresiva, primero nocturna, luego diurna, desde periferia al centro
!- - - - - - - - - - - - - - - - - - - - - - !APR esta probada en el Gato Abisinio !Barnett y Carlise la describieron en
siameses !Rubin y Lipton la describieron en Persas !Buyukmichi en gatos mestizos
Functional Assessment of the Regional Distribution of Disease in a Cat Model of Hereditary Retinal Degeneration Mathias W. Seeliger1 and Kristina Narfstro¨m2
Atrofia progresiva de la Retina, Electrorretinografia
Nutricionales, Deficiencia de Taurina
# Aminoácido esencial en los felinos !# 10mg/kg de requerimiento diario !# Mayor concentración en retina y corazón !# Incluidos en los A. Balanceados
Imágenes angiograficas
Imágenes angiograficas
Pot. Oscilatorios
F. Blanco
Flicker
F. Azul
Electrorretinografia
# Las lesiones reflejadas en el ERG comienzan a
las 10 semanas !
# Las lesiones oftalmoscopicas
comienzan entre los 3 y 7 meses
!# La ceguera completa se
hace evidente 9 a 10 meses
Nutricionales, Deficiencia de Taurina
Vasculares, Retinopatia Hipertensiva
La hipertensión sistémica : !1. Primaria !2. Secundaria
#Insuficiencia renal
!# Hipertiroidismo
!# Patologías cardiacas
!# Diabetes mellitus
!# Anemias prolongadas
Ocular lesions associated with systemic hypertension in cats: 69 cases (1985-1998). Maggio F, DeFrancesco TC, Atkins CE, Pizzirani S, Gilger BC, Davidson MG. J Am Vet Med Assoc. 2000 Sep 1;217(5):695-702. Clinica Veterinaria Europa, Florence, Italy.
Sistólica: 160mmhg Diastólica: 100mmhg
Spontaneous feline hypertension: clinical and echocardiographic abnormalities, and survival rate. Chetboul V, Lefebvre HP, Pinhas C, Clerc B, Boussouf M, Pouchelon JL. J Vet Intern Med. 2003 Jan-Feb;17(1):89-95.
Hypertensive retinopathy and choroidopathy in a cat. Komáromy AM, Andrew SE, Denis HM, Brooks DE, Gelatt KN. Vet Ophthalmol. 2004 Jan-Feb;7(1):3-9.
Prevalencia de lesiones retinianas en gatos con hipertensión: 48%
!262 +/- 34 mmhg con retinopatía
!221 +/- 34 mmhg sin retinopatía
Vasculares, Retinopatia Hipertensiva
Imagenes angiograficas
Vasculares, Retinopatia Hipertensiva
# Daño vascular con perdida de plasma y células
!# Hemorragias en retina y vítreo,
desprendimientos de retina !
# Droga de elección: Amlodipina 0.625 a 1,25mg día
Vasculares, Retinopatia Hipertensiva
Signos en el Segmento Anterior
“Reconocer a los gatos en riesgo es importante a la hora de conservar la visión”
Inflamatorias, coroideoretinitis
# Focales
# Difusas
# Multifocales
Barrera Hemato-retiniana
BHO (Interna)
BHO (Externa)
identified rapid microglial process extension upon injection ofATP11. Fibrinogen is a novel molecular signal that can mediate asimilar response. ATP mediates microglial responses throughthe P2Y12 receptor44. As rapid microglial process extension isassociated with dramatic cytoskeletal rearrangements, presumablyinvolving activation of the Rho signaling pathway, cross-talk ofP2Y12 with integrin receptors might mediate the rapid microglialresponse induced by fibrinogen. Indeed, integrins are primarily
responsible for cytoskeletal rearrangements, and fibrinogeninduces Rho activation in microglia via CD11b/CD18 (ref. 27).ATP induces integrin-b1 expression in microglia through P2Y12receptor and integrin-b1 activation is involved in the directionalprocess extension by microglia in brain tissue45. Moreover, ATPincreases CD11b expression in microglia46 and eosinophils47.Future studies will determine the potential cross-talk betweenP2Y12 and microglial integrin receptors upon BBB disruption.
a
b Healthy Pre-onset EAE Peak EAE
Pial macrophage
Fibrinogen
Axon
ROS
Microglia
Basal membrane
0
20
40
60
Cx3cr1GFP/+
Fib+/+
Cx3cr1GFP/+
Fib+/+
Cx3cr1GFP/+
Fib!390-396Α
Cx3cr1GFP/+
Fib!390-396Α
Clu
ster
s pe
r 0.5
mm
3 *Cx3cr1GFP/+Fib+/+ Cx3cr1GFP/+Fib!390-396A
Peak EAE
Cx3
cr1G
FP
/+ /
Rho
dam
ine
dext
ran
0
0.5
1
1.5
2
2.5 *
SM
I-32
(%
are
a)
SM
I-32
/D
AP
I
Figure 8 | Fibrinogen mediates perivascular microglial clustering and axonal damage via CD11b/CD18. (a) In vivo imaging of Cx3cr1GFP/þFibg390-396A
mice at the peak of EAE (n¼6) shows fewer perivascular clusters (top) and significantly less SMI-32 immunoreactivity (bottom) than in Cx3cr1GFP/þ
Fibþ /þ controls (n¼9). Correlated histology was performed in the same spinal cord areas in the mice that were previously imaged in vivo. Values aremean±s.e.m. *Po0.05 (Mann–Whitney test). Scale bars, top: 10mm; bottom: 50mm. (b) Schematic illustration and working model of the dynamicresponses of perivascular microglia and pial macrophages to BBB disruption and their contribution to axonal damage in neuroinflammatory disease. In thehealthy CNS, microglia are evenly distributed and stochastically extend and retract their processes. In EAE mice before the onset of neurological symptomsfibrinogen leaks in the CNS, triggering microglial process extension and cell body accumulation toward the vasculature. At the peak of disease, microglialclustering around the vasculature occurs almost exclusively in areas of fibrin deposition and is associated with axonal damage and release of ROS bymicroglia. Fibrinogen signaling via the CD11b/CD18 integrin receptor is required for the formation of perivascular clusters and the development of axonaldamage.
NATURE COMMUNICATIONS | DOI: 10.1038/ncomms2230 ARTICLE
NATURE COMMUNICATIONS | 3:1227 | DOI: 10.1038/ncomms2230 | www.nature.com/naturecommunications 11
& 2012 Macmillan Publishers Limited. All rights reserved.
identified rapid microglial process extension upon injection ofATP11. Fibrinogen is a novel molecular signal that can mediate asimilar response. ATP mediates microglial responses throughthe P2Y12 receptor44. As rapid microglial process extension isassociated with dramatic cytoskeletal rearrangements, presumablyinvolving activation of the Rho signaling pathway, cross-talk ofP2Y12 with integrin receptors might mediate the rapid microglialresponse induced by fibrinogen. Indeed, integrins are primarily
responsible for cytoskeletal rearrangements, and fibrinogeninduces Rho activation in microglia via CD11b/CD18 (ref. 27).ATP induces integrin-b1 expression in microglia through P2Y12receptor and integrin-b1 activation is involved in the directionalprocess extension by microglia in brain tissue45. Moreover, ATPincreases CD11b expression in microglia46 and eosinophils47.Future studies will determine the potential cross-talk betweenP2Y12 and microglial integrin receptors upon BBB disruption.
a
b Healthy Pre-onset EAE Peak EAE
Pial macrophage
Fibrinogen
Axon
ROS
Microglia
Basal membrane
0
20
40
60
Cx3cr1GFP/+
Fib+/+
Cx3cr1GFP/+
Fib+/+
Cx3cr1GFP/+
Fib!390-396Α
Cx3cr1GFP/+
Fib!390-396Α
Clu
ster
s pe
r 0.5
mm
3 *Cx3cr1GFP/+Fib+/+ Cx3cr1GFP/+Fib!390-396A
Peak EAE
Cx3
cr1G
FP
/+ /
Rho
dam
ine
dext
ran
0
0.5
1
1.5
2
2.5 *
SM
I-32
(%
are
a)
SM
I-32
/D
AP
I
Figure 8 | Fibrinogen mediates perivascular microglial clustering and axonal damage via CD11b/CD18. (a) In vivo imaging of Cx3cr1GFP/þFibg390-396A
mice at the peak of EAE (n¼6) shows fewer perivascular clusters (top) and significantly less SMI-32 immunoreactivity (bottom) than in Cx3cr1GFP/þ
Fibþ /þ controls (n¼9). Correlated histology was performed in the same spinal cord areas in the mice that were previously imaged in vivo. Values aremean±s.e.m. *Po0.05 (Mann–Whitney test). Scale bars, top: 10mm; bottom: 50mm. (b) Schematic illustration and working model of the dynamicresponses of perivascular microglia and pial macrophages to BBB disruption and their contribution to axonal damage in neuroinflammatory disease. In thehealthy CNS, microglia are evenly distributed and stochastically extend and retract their processes. In EAE mice before the onset of neurological symptomsfibrinogen leaks in the CNS, triggering microglial process extension and cell body accumulation toward the vasculature. At the peak of disease, microglialclustering around the vasculature occurs almost exclusively in areas of fibrin deposition and is associated with axonal damage and release of ROS bymicroglia. Fibrinogen signaling via the CD11b/CD18 integrin receptor is required for the formation of perivascular clusters and the development of axonaldamage.
NATURE COMMUNICATIONS | DOI: 10.1038/ncomms2230 ARTICLE
NATURE COMMUNICATIONS | 3:1227 | DOI: 10.1038/ncomms2230 | www.nature.com/naturecommunications 11
& 2012 Macmillan Publishers Limited. All rights reserved.
F i g u re 8 | F i b r i no g e n m e d i at e s perivascular microglial clustering and axonal damage via CD11b/CD18
(b) Schematic illustration and working model of the dynamic responses of p e r i va s cu lar m i cro g l i a and p i al macrophages to BBB disruption and their contr ibution to axonal damage in neuroinflammatory disease. In the healthy CNS, microglia are evenly distributed and stochastically extend and retract their processes. In EAE mice before the onset of neurological symptoms fibrinogen leaks in the CNS, triggering microglial p roce s s ex tens ion and ce l l bo dy accumulation toward the vasculature. At the peak of disease, microglial clustering around the vasculature occurs almost exclusively in areas of fibrin deposition and is associated with axonal damage and release of ROS by microg l ia . Fibrinogen signaling via the CD11b/CD18 integrin receptor is required for the formation of perivascular clusters and the development of axonal damage.
# Fibrinogen-induced perivascular microglial clustering is required for the development of axonal damage in neuroinflammation
Dimitrios Davalos1, Jae Kyu Ryu1, Mario Merlini1, Kim M. Baeten1, Natacha Le Moan1,w, Mark A. Petersen1,2, Thomas J. Deerinck3,4, Dimitri S.
Smirnoff1, Catherine Bedard1, Hiroyuki Hakozaki4, Sara Gonias Murray1, Jennie B. Ling1, Hans Lassmann5, Jay L. Degen6, Mark H.
Ellisman3,4 & Katerina Akassoglou1,7
Inflamatorias, coroideoretinitis
NATURE COMMUNICATIONS
Causas mas frecuentes de Coriorretinitis
1. Infecciosas (Virales)
2. Micosis
3. Traumatismos !4. Neoplasias
PIF ViLeF ViF
Parasitaria
Vimos
un
Cripto
coco!!!
5.
ToxoplasmosisRaro!
Inflamatorias, Toxoplasmosis
Toxoplasma gondii (for a review, see Dubey, 2004). )
Inflamatorias, Criptococosis
Cryptococcus neoformans or Cryptococcus gattii (previously C. neoformans var gattii) (Wolf, 1989).
# Uveitis granulomatosa # Desprendimiento de retina # Neuritis optica
Inflamatorias, PIF
Inflamatorias, VIF
Inflamatorias, ViLeF
Toxicas, Secundarias a Quinolonas y algo mas……
Factores de Riesgo: !
# Edad del paciente ! # Renopatías , hepatopatías ! # Dosis, duración y vías de administración
# Retinal toxicity of liposome-incorporated and free ofloxacin after intravitreal injection in rabbit eyes. Wiechens B, Neumann D, Grammer JB, Pleyer U, Hedderich J, Duncker GI. Int Ophthalmol. 1998-1999;22(3):133-43.
# Fluoroquinolone-induced retinal degeneration in cats. Wiebe V, Hamilton P. J Am Vet Med Assoc. 2002 Dec 1;221(11):1568-71. Review
Quinolonas, Características Histopatólogicas
# Vacuolas citoplasmáticas !# Degeneración primaria de los conos !# Edema !# en la fase crónica ha y deg en e rac i ón c o m p l e t a d e l o s fotorreceptores
Quinolonas, Bases genéticas
(Ramirez et al., 2011)
# Alteración de la proteína ABCG2 de la Barrera Hemato-
Ocular !
# Acumulación de la Quinolona en la retina
!
# Formación de ROS y Daño retiniano
Electrorretinografía
Tóxicas, Secundarias a Quinolonas y algo mas……
# Griseofulvina
# Ivermectina
# Acetato de Megestrol
Degeneración súbita de fotorreceptores, supresión de la medula ósea y muerte (Rottman et al., 1991)
# signos neurológicos, ceguera c/an i socor ia , m idr ia s i s o m io s i s (Houston, 1985; Lewis et al., 1994).
# R e t i n i t i s h e m o r r á g i c a , Desprendimiento de retina (Bedford & Cotchin, 1983; Kunkle, 1984; Spiess et al., 1991)
Muchas Gracias!!!!
Pablo Sande, MV, PhD, DCLOVE p_sande@yahoo.com
www.veteoftalmo.com.ar
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