Background/Objectives: Rabbit farming in Romania is increasingly important for providing high-quality meat, yet productivity is frequently threatened by enteric diseases, particularly in young animals. Among bacterial etiologies, Clostridioides difficile (C. difficile) has emerged as a significant gastrointestinal pathogen, with findings suggestive of systemic dissemination and public health implications. This study aimed to investigate a fatal case of C. difficile infection in a farmed rabbit and to characterize the pathogen's microbiological, toxigenic, and antimicrobial profile. Methods: An 11-month-old male German Giant Spotted rabbit presenting acute diarrhea, anorexia, and rapid deterioration after unsupervised administration of enrofloxacin and sulfaquinoxaline was submitted postmortem. Necropsy was performed, and samples from cecum, colon, liver, spleen, mesenteric lymph nodes, lungs, and femoral bone marrow were collected. Microbiological analysis included selective culture on CCFA medium, ELISA for toxin A and B detection, MALDI-TOF MS identification, PCR confirmation, and antimicrobial susceptibility testing with the VITEK 2 system. Histopathological examination was conducted on intestinal and parenchymal tissues. Results: Necropsy revealed severe congestion and necrosis of the cecal and colonic mucosa, hepatomegaly, splenic congestion, and petechial hemorrhages. C. difficile was isolated from intestinal sites, confirmed as toxigenic by ELISA and PCR. Histopathology showed necrotizing colitis with epithelial desquamation, fibrin deposition, and heterophilic infiltration. The strain exhibited resistance to clindamycin, ampicillin, and tetracycline, with susceptibility to vancomycin, linezolid, and tigecycline. Conclusions: This case demonstrates that C. difficile can cause severe disease in rabbits, particularly following antimicrobial-induced dysbiosis. The findings underscore the importance of prudent antibiotic use, monitoring of toxigenic strains in rabbit populations, and implementation of preventive strategies to mitigate health risks in both animals and potentially humans.

Schistosomiasis remains a major neglected tropical disease, affecting approximately 600 million individuals worldwide and accounting for nearly 500,000 deaths annually. The principal causative species-Schistosoma haematobium, S. mansoni, and S. japonicum-drive significant morbidity through hepatomegaly, splenomegaly, and progressive hepatic fibrosis. Praziquantel (PZQ) remains the cornerstone of treatment; however, its limited efficacy against immature worms and eggs, combined with concerns over emerging drug resistance, underscores the urgent need for novel therapeutic alternatives. This study investigated the anti-schistosomal potential of green-synthesized zinc oxide (ZnO) nanoparticles (NPs) in a murine model of S. mansoni infection, benchmarked against PZQ. ZnO NPs were fabricated using ginger extract via an eco-friendly green synthesis approach. Fifty male BALB/c mice were randomly assigned to five groups (n=10): normal control, infected untreated control, infected treated with PZQ alone, infected treated with ZnO NPs alone, and infected treated with a PZQ-ZnO NP combination. Parasitological, histopathological, and fibrosis assessments were subsequently performed. All treatment groups demonstrated significant reductions in worm burden and tissue egg counts relative to infected untreated controls. Histopathological examination of untreated infected mice revealed extensive chronic granulomatous inflammation, concentric perioval fibrosis, fibroblast proliferation, hepatocellular necrosis, hydropic degeneration, marked collagen deposition, and portal-to-portal fibrous bridging. Treated groups, by contrast, exhibited marked hepatic improvement characterized by reduced granuloma size, diminished fibrosis, and decreased collagen deposition. Collectively, these findings indicate that green-synthesized ZnO NPs possess promising anti-schistosomal and antifibrotic properties, warranting further investigation as a potential adjunct or alternative therapeutic strategy for schistosomiasis management.

Core Binding Factor Acute Myeloid Leukemia (CBF-AML), defined by RUNX1::RUNX1T1 or CBFB::MYH11 fusions, represents a biologically favorable AML subtype. The Indian data-especially under WHO 2022 criteria-are limited. This study analyzed the demographic, morphological, and immunophenotypic spectrum of CBF-AML in a large North Indian cohort, focusing on pediatric-adult differences, low-blast presentations, and immunophenotypic signatures.An ambispective study (2017-2024) of 196 genetically confirmed CBF-AML cases included clinical, hematopathological, and flow cytometric evaluation. Statistical comparisons were performed using appropriate tests. CBF-AML constituted 16.4% of all AML cases, more frequent in pediatric (44.2%) than adults (11.1%). RUNX1::RUNX1T1 accounted for 85.7% and CBFB::MYH11 for 14.3%. Age-stratified analysis showed higher rates of lymphadenopathy, hepatomegaly, and splenomegaly in CBFB::MYH11 patients aged 41-60 years (p < 0.05). Extramedullary disease occurred in 11.2%. Sixteen patients (8.2%) had <20% marrow blasts, often mimicking myelodysplastic/myeloproliferative neoplasms (MDS/MPN), underscoring the need for molecular testing irrespective of blast count. Morphologically, CBFB::MYH11 was associated with myelomonocytic features and eosinophilia; RUNX1::RUNX1T1 showed dysgranulopoiesis and long slender Auer rods. Immunophenotyping revealed CD123 and CD86 overexpression in CBFB::MYH11 (90% and 83.3%, respectively) besides higher expression of monocytic markers. RUNX1::RUNX1T1 showed frequent CD19, CD22, and CD56 expression. Survival analysis limited to a small treated subset (n = 30), revealed complete remission rate of 76.7% following induction, with median overall and relapse-free survival of 408 and 215 days, respectively. This largest single-center Indian series of CBF-AML in the WHO 2022 era highlights subtype-specific clinicopathological patterns, reaffirms classic morphology, and emphasizes routine molecular testing, particularly in low-blast or atypical presentations. Overexpression of CD123 and CD86 in CBFB::MYH11 may have diagnostic and therapeutic relevance.

Desmoplastic small round cell tumor (DSRCT) is a rare and highly aggressive malignancy predominantly affecting young male patients, typically originating from the abdomen or pelvis, with a poor prognosis. Since the first description as a distinct clinical entity in 1989, approximately 850 cases have been reported in the literature. All cases share the chromosomal translocation t(11;22)(p13;q12), leading to the formation of the EWSR1-WT1 fusion gene. DSRCT characteristically arises in the abdomen or pelvis and carries a poor prognosis despite multimodal therapy. We report a rare and extensive case of abdominopelvic DSRCT with liver and peritoneal metastases in a 17-year-old Moroccan male, who presented with a progressive abdominal mass, pain, and hepatomegaly. The diagnosis was initially challenging due to the non-specific clinical presentation. The final diagnosis was established through liver biopsy and immunohistochemical analysis. The patient is currently undergoing treatment with a multidrug chemotherapy regimen.

Mucolipidosis II (MLII) is a severe lysosomal disorder caused by loss of GlcNAc-1-phosphotransferase activity, leading to defective mannose-6-phosphate (M6P) tagging and subsequently misrouting of M6P-dependent lysosomal hydrolases, and progressive multi-organ pathology. We generated a Gnptab p.R364X knock-in mouse model of MLII, which recapitulated the biochemical, skeletal, visceral, and neurological features of human MLII. Proteomic analysis of lysosomes isolated from MLII fibroblasts by LysoIP showed depletion or decrease of M6P-dependent hydrolases, upregulation of M6P-independent enzymes, and increased abundance of lysosomal membrane proteins. Zoledronic acid treatment increased both M6P-dependent and M6P-independent luminal hydrolases, and reduced glycosaminoglycan storage in MLII skin fibroblasts. Besides skeletal density improvement, Zoledronic acid, administered from 4 to 24 weeks to MLII mice, ameliorated multiple system manifestations, including articular cartilage degeneration, motor impairment, hepatomegaly, along with decreased urinary heparan sulfate and brain neuroinflammation. Our findings demonstrate that zoledronic acid ameliorates multiple system pathologies in MLII mice, which may be mediated, at least in part, through partial restoration of M6P-dependent proteins within lysosomes.

Massive splenomegaly refers to a marked and clinically significant enlargement of the spleen beyond normal limits. Although uncommon, it is clinically significant because it may be associated with hematologic, infectious, infiltrative, malignant, or portal hypertensive disorders. Chronic hemolytic anemias are a recognized cause of marked splenic enlargement due to persistent erythrocyte destruction and reticuloendothelial hyperplasia. Ongoing hemolysis also increases bilirubin production, predisposing patients to pigment gallstone formation and biliary tract disease. We report the case of a 29-year-old male who presented with jaundice and imaging findings consistent with choledocholithiasis. His medical history was notable for chronic hemolytic anemia and recurrent episodes of jaundice. Magnetic resonance cholangiopancreatography confirmed common bile duct stones and marked splenomegaly. The patient underwent exploratory laparotomy with splenectomy and common bile duct exploration followed by choledochoduodenal anastomosis. Intraoperatively, a massively enlarged spleen and hepatomegaly were identified. Significant bleeding from the splenic pedicle required vascular control and a blood transfusion. The postoperative course was favorable, with progressive reduction in bilirubin levels and no evidence of further complications. Histopathological examination demonstrated a congestive spleen with extensive hemorrhagic areas. This case highlights the importance of a multidisciplinary approach in the evaluation and management of massive splenomegaly and illustrates that timely surgical treatment can achieve satisfactory outcomes in selected patients.