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1.
Prev Vet Med ; 214: 105908, 2023 May.
Artículo en Inglés | MEDLINE | ID: mdl-37004500

RESUMEN

Babesiosis and ehrlichiosis are the most clinically significant tick-borne infections in dogs. Although epidemiological investigations of these diseases have been performed in some Asian regions, little data is available in Hong Kong, where competent vector tick species are endemic. The objectives of this study were to determine the molecular prevalence of Ehrlichia canis and Babesia species (B. canis, B. gibsoni, B. vogeli) in owned dogs suspected of tick-borne infection in Hong Kong and to identify risk factors associated with B. gibsoni infection. Electronic records from the Veterinary Diagnostic Laboratory of City University of Hong Kong were searched to identify canine blood samples submitted for molecular testing of these pathogens by real time PCR between March 2018 and May 2021. Electronic patient records from the affiliated veterinary hospital were searched to identify a subset of tested dogs to investigate the potential risk factors for B. gibsoni infection using logistic regression models. Among 1508 tested dogs for all four pathogens of interest, Babesia spp. were detected in 435 (28.8%) and E. canis in 112 (7.4%). Babesia gibsoni was detected in 408 dogs while B. vogeli was detected in 27 dogs. Babesia canis was not detected in any dog. Co-infections of different combinations of B. gibsoni, B. vogeli and E. canis were present in 25 dogs. In multivariable logistic regression, mixed breed dogs were more likely to be infected with B. gibsoni than purebreds (P = 0.005), while dogs > 10 years of age were less likely to be infected than younger dogs (P = 0.019). Hematological abnormalities significantly associated with B. gibsoni infection included thrombocytopenia, neutropenia, or pancytopenia. Babesiosis caused by B. gibsoni is a common infection in owned dogs suspected of tick-borne infection in Hong Kong. The risk factors reported should be considered in diagnosing dogs suspected of infection with this agent. Furthermore, consideration for testing for B. gibsoni infection should be given if the results of a complete blood count show thrombocytopenia even in the absence of anemia, neutropenia or pancytopenia.


Asunto(s)
Babesia , Babesiosis , Enfermedades de los Perros , Neutropenia , Pancitopenia , Enfermedades por Picaduras de Garrapatas , Perros , Animales , Babesiosis/epidemiología , Ehrlichia , Prevalencia , Pancitopenia/veterinaria , Hong Kong/epidemiología , Enfermedades por Picaduras de Garrapatas/epidemiología , Enfermedades por Picaduras de Garrapatas/veterinaria , Factores de Riesgo , Neutropenia/veterinaria , Enfermedades de los Perros/epidemiología , Enfermedades de los Perros/diagnóstico
2.
Am J Pathol ; 187(10): 2208-2221, 2017 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-28739342

RESUMEN

Current treatments for choroidal neovascularization, a major cause of blindness for patients with age-related macular degeneration, treat symptoms but not the underlying causes of the disease. Inflammation has been strongly implicated in the pathogenesis of choroidal neovascularization. We examined the inflammatory role of Toll-like receptor 2 (TLR2) in age-related macular degeneration. TLR2 was robustly expressed by the retinal pigment epithelium in mouse and human eyes, both normal and with macular degeneration/choroidal neovascularization. Nuclear localization of NF-κB, a major downstream target of TLR2 signaling, was detected in the retinal pigment epithelium of human eyes, particularly in eyes with advanced stages of age-related macular degeneration. TLR2 antagonism effectively suppressed initiation and growth of spontaneous choroidal neovascularization in a mouse model, and the combination of anti-TLR2 and antivascular endothelial growth factor receptor 2 yielded an additive therapeutic effect on both area and number of spontaneous choroidal neovascularization lesions. Finally, in primary human fetal retinal pigment epithelium cells, ligand binding to TLR2 induced robust expression of proinflammatory cytokines, and end products of lipid oxidation had a synergistic effect on TLR2 activation. Our data illustrate a functional role for TLR2 in the pathogenesis of choroidal neovascularization, likely by promoting inflammation of the retinal pigment epithelium, and validate TLR2 as a novel therapeutic target for reducing choroidal neovascularization.


Asunto(s)
Neovascularización Coroidal/patología , Inflamación/patología , Degeneración Macular/patología , Epitelio Pigmentado de la Retina/metabolismo , Epitelio Pigmentado de la Retina/patología , Receptor Toll-Like 2/metabolismo , Anciano , Anciano de 80 o más Años , Animales , Anticuerpos Neutralizantes/farmacología , Núcleo Celular/efectos de los fármacos , Núcleo Celular/metabolismo , Núcleo Celular/efectos de la radiación , Chlamydia/efectos de los fármacos , Chlamydia/efectos de la radiación , Neovascularización Coroidal/complicaciones , Neovascularización Coroidal/metabolismo , Citocinas/metabolismo , Dipéptidos/farmacología , Rayos gamma , Regulación de la Expresión Génica/efectos de los fármacos , Regulación de la Expresión Génica/efectos de la radiación , Humanos , Inflamación/complicaciones , Inflamación/genética , Lípidos/química , Macrófagos/efectos de los fármacos , Macrófagos/metabolismo , Macrófagos/patología , Degeneración Macular/complicaciones , Degeneración Macular/metabolismo , Masculino , Ratones Endogámicos C57BL , FN-kappa B/metabolismo , Oxidación-Reducción , Transporte de Proteínas/efectos de los fármacos , Transporte de Proteínas/efectos de la radiación
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