A 10-year-old female spayed mixed breed dog was evaluated for diarrhea and vomiting. Diagnostic imaging demonstrated the presence of an intracardiac mass. A modified Seldinger technique was used to access the right jugular vein, and an endomyocardial biopsy forceps was introduced through a sheath to obtain several biopsies. Histopathology and immunohistochemistry demonstrated a paraganglioma. The dog underwent 1 fraction of radiotherapy and L-asparaginase chemotherapy and was discharged. The dog developed a pulmonary thromboembolism 2 days after radiotherapy and chemotherapy, and the owner elected humane euthanasia. Although long-term assessment of treatment response was unable to be performed, this novel diagnostic option could be considered for similar cases due to success in obtaining a histopathologic diagnosis, which is essential in developing a disease-specific treatment plan. This report also describes the use of radiotherapy for primary treatment of an intracardiac neoplasm, which can be a consideration in the future.

Objective: To document the clinical, radiographic, and histological characteristics of mandibular first molar teeth with developmental abnormalities previously attributed to dens invaginatus and enamel pearls in dogs. Materials and Methods: Affected mandibular first molar teeth from dogs were evaluated grossly and via intraoral radiography. Endodontically and/or periodontally compromised teeth were extracted and subjected to some combination of micro-computed tomography, histopathology, and immunohistochemistry with anti-amelogenin antibody. Results: Six dogs with developmental abnormalities of mandibular first molar teeth were identified, representing 11 affected teeth. The condition was bilateral in 5 dogs, while in 1 dog, only one mandibular first molar tooth was present. Patient weight ranged from 1.7 to 6 kg (median = 4.09 kg). On intraoral radiographs, root convergence or parallelism was noted in 6 of 11 teeth, and root dilaceration was noted in 3 of 11 teeth. Eight teeth required extraction due to periapical lucencies or periodontitis. On micro-CT, the abnormal teeth were characterized by the presence of abnormal, heterogenous hard tissue with beam attenuation characteristics midway between that of enamel and dentin. Enamel fissures were identified in 4 of 8 teeth, while ectopic radicular enamel was identified in 2 of 8 teeth. The abnormal tissue was traversed by channels measuring 20-40 µm in diameter. Channels communicated with the enamel fissures in 2/8 teeth, the furcation in 2/8 teeth and the pulp in 4/8 teeth. The abnormal tissue was frequently surrounded by disorganized dentin. Histologic features of enamel and dentin were absent from the abnormal tissue and immunohistochemistry to detect amelogenin in the abnormal tissue was negative in all samples. Conclusion: The dental abnormalities described here correspond to a previously unrecognized developmental abnormality involving the mandibular first molar teeth in dogs. The developmental origin of the abnormal tissue could not be ascertained, and further investigations are required to determine the mode of formation, origin of Ng et al. Mandibular Carnassial Tooth Malformations in 6 Dogs the abnormal tissue, and factors associated with development. These developmental abnormalities more closely resemble molar-incisor malformation, rather than dens invaginatus or enamel pearls as described in humans. The authors propose that affected mandibular first molar teeth simply be referred to as having carnassial tooth malformations.

OBJECTIVE To characterize the association between peritoneopericardial diaphragmatic hernia (PPDH) or congenital central diaphragmatic hernia (CCDH) and ductal plate malformations (DPMs) in dogs and cats. ANIMALS 18 dogs and 18 cats with PPDH or CCDH and 19 dogs and 18 cats without PPDH or CCDH. PROCEDURES Evaluation of clinical details verified PPDH or CCDH and survival times. Histologic features of nonherniated liver samples were used to categorize DPM. Immunohistochemical staining for cytokeratin-19 distinguished bile duct profiles per portal tract and for Ki-67–assessed cholangiocyte proliferation. Histologic features of herniated liver samples from PPDH or CCDH were compared with those of pathological controls (traumatic diaphragmatic hernia, n = 6; liver lobe torsion, 6; ischemic hepatopathy, 2). RESULTS DPM occurred in 13 of 18 dogs with the proliferative-like phenotype predominating and in 15 of 18 cats with evenly distributed proliferative-like and Caroli phenotypes. Congenital hepatic fibrosis DPM was noted in 3 dogs and 2 cats and renal DPM in 3 dogs and 3 cats. No signalment, clinical signs, or clinicopathologic features discriminated DPM. Kaplan Meier survival curves were similar in dogs and cats. Bile duct profiles per portal tract in dogs (median, 5.0; range, 1.4 to 100.8) and cats (6.6; 1.9 to 11.0) with congenital diaphragmatic hernias significantly exceeded those in healthy dogs (1.4; 1.2 to 1.6) and cats (2.3; 1.7 to 2.6). Animals with DPM lacked active cholangiocyte proliferation. Histologic features characterizing malformative bile duct profiles yet without biliary proliferation were preserved in herniated liver lobes in animals with DPM. CONCLUSIONS AND CLINICAL RELEVANCE DPM was strongly associated with PPDH and CCDH. Because DPM can impact health, awareness of its coexistence with PPDH or CCDH should prompt biopsy of nonherniated liver tissue during surgical correction of PPDH and CCDH.

Clostridium piliforme, the agent of Tyzzer disease, has traditionally not been considered a major pathogen of cats. We queried the database of the Pathology Service of the Veterinary Medical Teaching Hospital, University of California–Davis, for kittens <6-mo-old autopsied between 2000–2021 that had colitis, hepatitis, and/or myocarditis; 37 cases met the search criteria. Sections of colon, liver, and heart from these 37 cats were stained with modified Steiner; 19 of 37 (51%) cases had intraepithelial, Steiner-positive rods compatible with C. piliforme in at least one organ, confirming Tyzzer disease. The affected age range was 7–42 d (median: 17.5 d). Eighteen were orphaned kittens. Colitis was the major lesion (18 of 19) followed by random hepatitis (11 of 19). Perianal dermatitis with intraepithelial stacked rods was seen in 2 of 19. Myocarditis was not evident in any of the cases. A PCR assay for C. piliforme on 10 selected cases using formalin-fixed, paraffin-embedded (FFPE) blocks was positive or suspected in colon (5 of 10), liver (5 of 10), and heart (1 of 10). The modified Steiner stain was more sensitive in the detection of bacteria than PCR on FFPE samples. Fifteen kittens had comorbidities. A weakened immune state caused by maternal, environmental, infectious, and/or nutritional causes is speculated to have contributed to disease onset. We found that Tyzzer disease is more common than previously believed in orphaned kittens and should be considered in kittens with colitis and/or hepatitis.

Background Canine visceral hemangiosarcoma (HSA) is a highly aggressive cancer of endothelial origin that closely resembles visceral angiosarcoma in humans, both clinically and histopathologically. Currently there is an unmet need for new diagnostics and therapies for both forms of this disease. The goal of this study was to utilize ChRO-seq and immunohistochemistry (IHC) to identify gene and protein expression signatures that may be important drivers of HSA progression. Methods Chromatin run-on sequencing (ChRO-seq) was performed on tissue isolated from 17 HSA samples and 4 normal splenic samples. Computational analysis was then used to identify differentially expressed genes and these factors were subjected to gene ontology analysis. Next, RT-PCR was performed on a subset of candidate genes to validate the ChRO-seq data. We then performed Masson’s trichrome, H&E, and IHC staining on these tissues to investigate morphological features of HSA tumor tissue as well as the expression patterns of several proteins identified in our ChRO-seq analysis. Results ChRO-seq analysis revealed over a thousand differentially expressed genes in HSA tissue compared with normal splenic tissue (FDR <0.005). Interestingly, the majority of genes overexpressed in HSA tumor tissue were associated with extracellular matrix (ECM) remodeling. This observation correlated well with our histological analysis, which found that HSA tumors contain a rich and complex collagen network. Additionally, we characterized the protein expression patterns of two highly overexpressed molecules identified in ChRO-seq analysis, podoplanin (PDPN) and laminin alpha 4 (LAMA4). We found that the expression of these two ECM-associated factors appeared to be largely limited to transformed endothelial cells within the HSA lesions. Conclusion Outcomes from this study suggest that ECM remodeling plays an important role in HSA progression. Additionally, our study identified two potential novel biomarkers of HSA, PDPN and LAMA4. Interestingly, given that function-blocking anti-PDPN antibodies have shown anti-tumor effects in mouse models of canine melanoma, our studies raise the possibility that these types of therapeutic strategies could potentially be developed for treating canine HSA.