An 8-month-old female Lagotto Romagnolo dog was presented for a 1-month history of an initial severe reluctance to move, rapidly progressing to a marked stiff gait and progressive muscular weakness and evolving to tetraparesis, which persuaded the owner to request euthanasia. A primary muscle pathology was supported by necropsy and histopathological findings. Macroscopically, the muscles were moderately atrophic, except for the diaphragm and the neck muscles, which were markedly thickened. Histologically, all the skeletal muscles examined showed atrophy, hypertrophy, necrosis with calcification of the fibers, and mild fibrosis and inflammation. On immunohistochemistry, all three dystrophin domains and sarcoglycan proteins were absent. On Western blot analysis, no band was present for delta sarcoglycan. We sequenced the genome of the affected dog and compared the data to more than 900 control genomes of different dog breeds. Genetic analysis revealed a homozygous private protein-changing variant in the SGCD gene encoding delta- sarcoglycan in the affected dog. The variant was predicted to induce a SGCD:p.(Leu242Pro) change in the protein. In silico tools predicted the change to be deleterious. Other 770 Lagotto Romagnolo dogs were genotyped for the variant and all found to be homozygous wild type. Based on current knowledge of gene function in other mammalian species, including humans, hamsters, and dogs, we propose the SGCD missense variant as the causative variant of the observed form of muscular dystrophy in the index case. The absence of the variant allele in the Lagotto Romagnolo breeding population indicates a rare allele that has appeared recently.

Background: Skeletal dysplasia encompasses a heterogeneous group of genetic disorders characterized by an abnormal development of bones, joints, and cartilage. Two Chianina half-sibling calves from consanguineous mating with congenital skeletal malformations and cardiac abnormalities were identified. Hypothesis/Objectives: To characterize the disease phenotype, to evaluate its genetic cause, and to determine the prevalence of the deleterious alleles in the Chianina population. Animals: Two affected calves, their parents and 332 Chianina bulls. Methods: The affected animals underwent clinicopathological investigation. Whole-genome sequencing trio-approach and PCR-based assessment of the frequency of TDP-glucose 4,6-dehydratase (TGDS) and laminin subunit alpha 4 (LAMA4) alleles were performed. Results: The cases presented with retarded growth, poor nutritional status associated with muscular atrophy and angular deformities of the hindlimbs. Radiologic examination identified generalized osteopenia and shortening of the limb long bones. Necropsy showed osteochondrodysplastic limbs and dilatation of the heart right ventricle. On histological examination, the physeal cartilages were characterized by multifocal mild to moderate loss of the normal columnar arrangement of chondrocytes. Osteopenia also was observed. Genetic analysis identified a missense variant in TGDS and a splice-site variant in LAMA4, both of which were homozygous in the 2 cases. Parents were heterozygous and allele frequency in the Chianina population for the TGDS variant was 5% and for the LAMA4 variant was 2%. Conclusions and Clinical Importance: Genetic findings identified 2 potentially pathogenic alleles in TGDS and LAMA4, but no clear mode of inheritance could be determined.

Gastrointestinal nematode infections significantly impact equine health and welfare, with rising anthelmintic resistance demanding alternative control strategies. Emerging evidence suggests that parasitic nematodes harbour distinct microbiomes, potentially influencing host-parasite dynamics and parasite survival. This study aimed to characterize and compare the microbiomes of equine gastrointestinal nematodes and their hosts, focusing on differences in composition, diversity, and core microbiota structure across different intestinal sites, nematode subfamilies, and sexes. Faecal and nematode samples were collected from equids ( Equus caballus and Equus asinus ) at slaughterhouses. DNA was extracted, and the V3-V4 regions of the 16S rRNA gene were amplified and sequenced using the Illumina iSeq 100 platform. Bioinformatic analyses were performed with QIIME2 and MicrobiomeAnalyst, and statistical comparisons employed PERMANOVA, LEfSe, and alpha and beta diversity metrics. Nematodes exhibited a distinct microbiome dominated by Firmicutes, Proteobacteria, Bacteroidota, Verrucomicrobiota, and Actinobacteriota, differing significantly from the faecal microbiota. Alpha diversity analyses revealed lower richness in nematodes, while beta diversity indicated distinct community structures (p = 0.007). Microbial composition varied by gastrointestinal site, nematode subfamily, and sex. Proteobacteria were consistently enriched in nematodes, particularly in the caecum. Core microbiome analysis identified exclusive nematode-associated taxa such as Fusobacterium , Mesorhizobium , and Mycoplasma . Equine gastrointestinal nematodes harbour independent and structured microbiomes, distinct from those of their hosts. These findings underscore the ecological specialization of nematodes and highlight the potential of targeting parasite-associated microbiota for novel control strategies.

Background: In humans, there is a growing body of evidence that neoangiogenesis is crucial for tumour growth and progression in urothelial carcinomas (UC) which also typically exhibit overactivation of the RAS‐MAPK pathway. In canine UC (cUC), the same pathway has been aberrantly activated due to V595E BRAF variant and BRAF inhibitors has been evaluated as more effective treatment. However, BRAF inhibition is hampered in humans by rapidly occurring of chemoresistance. Targeting angiogenesis has been speculated to increase the effectiveness of BRAF inhibitors and to delay the development of chemoresistance.Objectives: This study aimed to investigate the level of angiogenic markers in urine samples of UC affected dogs (n = 15) in comparison to an unmatched control group (n = 16) along with the clinical, morphological and molecular features.Methods: In urine, both vascular endothelial growth factor (VEGF) concentration, using an ELISA assay, and MMP2 and 9 activities, using the zymographic assay, were measured. BRAF analysis was carried out using a digital PCR method.Results: Urinary VEGF concentration (mean pg/g_uCrea 6.9 ± 27.7 vs. 1074 ± 1797, p < 0.01) and MMP activity (mean 6.8 × 10⁶ ± 9.2 × 10⁶ vs. 2.5 × 10⁷ ± 2.3 × 10⁷, p < 0.05) were higher in affected dogs than in healthy controls. Urinary active MMP9 was significantly correlated with T3 stage, it was absent in dogs with undetectable VEGF and it correlated well with urinary VEGF concentration. In this cohort, 10/10 UC affected dogs exhibited the V595E BRAF variation.Conclusion: The findings are consistent with the presence of overactive neoangiogenesis in cUC. Urinary active MMP9 may be suitable for use as tumour progression biomarker. The addition of angiogenesis targeting may be rationale for novel therapeutic strategies.

Rumenitis is an inflammatory condition of the rumen, typically seen in adult cattle managed on high-energy diets. In calves, it is uncommon and often linked to ruminal drinking due to esophageal groove dysfunction. Early diagnosis is challenging due to nonspecific clinical signs. A one-month-old male Limousin calf was presented with persistent non-fetid fluid regurgitation, rhythmic mastication, inappetence, and progressive neurological signs. Clinical examination revealed signs of dehydration and neurological dysfunction. Laboratory evaluation demonstrated metabolic acidosis (pH 7.16), hyperkalemia, and elevated serum urea. Endoscopy identified diffuse mucosal hyperemia, erosions, and fluid accumulation in the rumen. Symptomatic and supportive therapy was initiated; however, the calf died spontaneously. Necropsy was therefore performed, and rumen samples were collected for histological and microbiological investigations. Histopathological analysis confirmed acute suppurative rumenitis. The microbiological culture of rumen and reticulum samples yielded mixed bacterial flora, including Escherichia coli and Proteus mirabilis. The fungal culture isolated Penicillium spp., Mucoraceae, Geotrichium spp., and Aspergillus fumigatus. This case details the value of integrating clinical examination, blood gas analysis, endoscopy, histopathology, and microbiology in diagnosing rumenitis in young calves. Although Limousin calves are not considered predisposed, management and feeding practices may play a critical role in disease onset. Rumenitis should be considered in calves presenting persistent regurgitation and neurological signs. Early, minimally invasive diagnostics such as endoscopy can improve diagnostic accuracy and inform timely clinical decision-making.