The Flat Coated Retriever is a breed at risk of development of histiocytic sarcoma (HS), but in contrast to the disseminated form of disease recognized in the Bernese Mountain Dog, most reports of HS in Flat Coated Retrievers describe a localized lesion affecting the musculature or fascia of limbs. The purpose of this study was to review data and material received though an ongoing Flat Coated Retriever tumor survey to better define the presentation of HS in the breed and to determine the utility of subclassification of tumors arising at different sites by histology and immunohistologic phenotyping. Data on 180 dogs bearing HS-like tumors were available for review, which showed that although the majority (101 lesions, 57%) were primary limb lesions, 47 dogs (26%) had visceral, mainly splenic lesions with no peripheral primary tumor. A detailed histologic and immunohistologic review of 20 limb tumors and 20 splenic tumors showed that 2 distinct phenotypic subtypes could be identified: a histiocytic subtype, most prevalent in the splenic tumors, and a histiocytic–spindle–pleomorphic subtype, mainly seen in the limb tumors. Despite their variable morphology, all tumors expressed major histocompatibility complex class II and the leukocyte antigen CD18, but only those tumors in the spleen consistently expressed CD11d. The majority of tumors also contained a mild to moderate infiltrate of T lymphocytes.

This study was designed to estimate the percentage of non-malignant skin tumours (papillomas) progressing to malignant squamous cell carcinomas (SCCs) in a carcinogenesis study using established transgenic mouse models. In our skin cancer model, we conditionally induced oncogenic point mutant alleles of p53 and k-ras in undifferentiated, basal cells of the epidermis. Upon activation of the transgenes through administration of tamoxifen, the vast majority of mice (> 80%) developed skin papillomas, yet primarily around the mouth. Since these tumours hindered the mice eating, they rapidly lost weight and needed to be culled before the papillomas progressed to SCCs. The mouth papillomas formed regardless of the route of application, including intraperitoneal injections, local application to the back skin, or subcutaneous insertion of a tamoxifen pellet. Implantation of a slow releasing tamoxifen pellet into 18 mice consistently led to papilloma formation, of which only one progressed to a malignant SCC. Thus, the challenges for skin carcinogenesis studies using this particular cancer mouse model are low conversion rates of papillomas to SCCs and high frequencies of mouth papilloma formation.

Introduction: Microglia and astrocytes are believed to play a central role in the pathogenesis of neuropathic pain (NeP). These glial cells are commonly identified by the expression of ionized calcium-binding adaptor molecule 1 (IBA1) for microglia and glial fibrillary acidic protein (GFAP) for astrocytes. Under pathological conditions, astrocytes and microglia undergo both morphological and transcriptional changes, which may promote shifts in functions that can have both protective and detrimental effects on the surrounding neuroparenchyma. Like humans, the dog breed Cavalier King Charles Spaniels (CKCSs) suffers from heritable syringomyelia (SM) which in both species is associated with NeP. Objectives: To investigate the potential role of IBA1 and GFAP-positive cells in the dorsal horn in CKCSs with SM and NeP. Methods: Using NanoString GeoMx technology, we conducted spatial transcriptomic analyses on spinal cord dorsal horns from CKCSs with SM and NeP. Results: Several differentially expressed genes were identified in dogs with SM and NeP. Cells positive for IBA1 showed upregulation of inflammatory genes as well as a downregulation of immune functions, while GFAP-positive cells indicated different states of reactivity. Pathway analyses indicated that the PI3K-Akt signaling pathway may be involved in the generation of NeP in CKCSs with SM. Conclusion: These findings provide new insights into the complex molecular changes in dorsal horn IBA1 and GFAP-rich areas in the presence of NeP and SM. The findings of this study serve as a foundation for future research that may facilitate new understandings of NeP mechanisms.

El objetivo del trabajo fue describir un caso de ataxia enzoótica en un Cervus elaphus (ciervo rojo) cautivo asociado a deficiencia de cobre, en el estado de Colima, México. En julio y octubre del 2018 dos hembras de ciervo rojo de 3 y 7 años manifestaron incoordinación con debilidad de los miembros posteriores y se estableció un diagnóstico anatomopatológico de ataxia progresiva. En septiembre del 2019 una hembra de 13 años manifestó signos nerviosos similares a los casos del 2018, por lo que se tomó una muestra de sangre para la medición sérica de cobre. Al animal se le aplicó eutanasia para su examen post mortem y se recolectaron muestras de tejido para histología, también se tomaron muestras de hígado, riñón, forraje y suelo para la medición de cobre y molibdeno. Las principales lesiones se encontraron microscópicamente en medula espinal, que mostró leucomalacia, desmielinización, cuerpos esferoides y cromatolisis neuronal. La concentración de cobre fue 2.7 en hígado, 4.67 en riñón y 0.08 en suero (mg/kg MS o ppm). La relación Cu:Mo para el suelo 1 fue Cu 8.48; Mo 3.00; Cu:Mo 2.83:1, suelo 2: Cu 9.10; Mo 3.00; Cu:Mo 3.03:1. Forraje 1: Cu 6.59; Mo 7.35; Cu:Mo 0.90:1; forraje 2: Cu 2.77; Mo 6.12 ± 0.61; Cu:Mo 0.45:1. Los signos clínicos, lesiones microscópicas y los niveles bajos de Cu en suero, hígado y forrajes son consistentes con ataxia enzoótica por deficiencia primaria de cobre. Hasta donde se conoce, este es el primer informe de ataxia enzoótica en un ciervo rojo cautivo en México.

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