Feline megaesophagus is a rare disorder characterized by esophageal hypomotility and dilation, resulting in regurgitation, weight loss, and occasionally death. This report describes the clinical and paraclinical findings of generalized megaesophagus with a possible contribution of toxocariasis in a kitten. A 2-month-old female cat was referred with chief complaints of lethargy, hyporexia, dyspnea, and vomiting/regurgitation. Physical examination of the kitten revealed bradycardia, bradypnea, hypothermia, dehydration, and lung crackles. The most notable laboratory results were leukopenia with severe toxic changes in neutrophils. Radiographic findings were compatible with the diagnosis of generalized megaesophagus. Despite supportive measures, the kitten died the next day. Necropsy revealed diffuse esophageal dilation and Toxocara spp. roundworms in the stomach and duodenum. Histopathology showed an ascarid larva in the esophagus, necrosis and metaplasia in the pylorus, and absence of villi and Brunner's glands in the duodenum. Based on the morphological identification of the adult gastrointestinal nematodes, the final diagnosis was generalized megaesophagus of unspecified classification concurrent with toxocariasis. However, the exact cause of death could not be established. Although respiratory abnormalities raised suspicion of a pulmonary complication, pneumonia was not confirmed. We hypothesized that toxocariasis may have contributed to esophageal dysfunction in this kitten through potential mechanisms such as vomiting, gastrointestinal obstruction, or neurological involvement; however, these mechanisms could not be directly demonstrated. Therefore, parasitic diseases, including toxocariasis, may be considered among potential differential diagnoses or contributing conditions in young cats presenting with megaesophagus, particularly when concurrent gastrointestinal parasitism or related complications are identified. Further studies are required to clarify the possible relationship between toxocariasis and esophageal dysfunction.
Background Hepatic lymphoma is rarely characterized in mynah birds, and severe hepatomegaly in this group is often interpreted in relation to iron storage disease or other metabolic hepatopathies. Case Description This report describes hepatic B‐cell lymphoma in a 14‐year‐old common mynah ( Acridotheres tristis ) presented with lethargy, altered vocalization, poor body condition, ascites, dyspnea, chronic ataxia, and left‐leg lameness. Radiography revealed a large soft‐tissue opacity in the middle coelomic cavity, with caudodorsal displacement of the intestinal loops and compression of the thoracoabdominal air sacs. Ultrasonography identified a very large hepatic mass with granular and mixed echogenicity occupying most of the coelomic cavity. The bird was euthanized at the owner′s request because of the severity of the lesion and poor clinical condition. At necropsy, the liver was markedly enlarged, dark red to reddish‐brown, mottled and occupied most of the coelomic cavity. Histologically, the hepatic parenchyma was extensively replaced by densely packed mononuclear neoplastic cells, with effacement of hepatic cords and hepatocellular necrosis. No neoplastic infiltration was identified in the examined tissues, including spleen, kidney, intestine, lung, and heart; therefore, the liver was the only confirmed site of lymphoma among the examined tissues in this case. An immunohistochemical and histochemical panel including CD3, CD79 α /MB‐1, CD20, lysozyme, CD68, alpha‐1‐antitrypsin, toluidine blue, and Giemsa staining was applied to characterize the tumor lineage and exclude other round‐cell neoplasms. Neoplastic cells showed diffuse cytoplasmic immunoreactivity for CD79 α /MB‐1 and lacked evidence of T‐cell, monocyte/macrophage, or mast cell differentiation, supporting a diagnosis of hepatic B‐cell lymphoma. Conclusion This case highlights the need for tissue‐based diagnosis in mynah birds with marked hepatomegaly and demonstrates the value of integrating diagnostic imaging, histopathology, immunohistochemistry, and molecular testing in avian hepatic round‐cell tumors.
Chemodectomas (aortic body tumors) are rare, slow-growing neoplasms arising from chemoreceptor tissue at the heart base in dogs, most frequently reported in brachycephalic breeds; to the authors' knowledge, their occurrence in nonbrachycephalic large breeds, such as the Alaskan Malamute, is uncommonly documented. An 8-year-old intact male Alaskan Malamute (body weight 44.8 kg) was referred with a history of lethargy, inappetence, exercise intolerance, and ascites. Echocardiography confirmed extensive pericardial effusion with cardiac tamponade and a multinodular, irregularly shaped heart-base mass invading the left atrium, right atrium, left auricle, and aortic root. The dog underwent two pericardiocentesis procedures, yielding 350 and 630 mL of serosanguinous fluid on Days 1 and 15, respectively. The dog died prior to the scheduled 1-week re-evaluation. Postmortem examination confirmed a multinodular, irregularly shaped, extensively invasive mass involving all cardiac chambers and the aortic root, with histopathological features morphologically consistent with chemodectoma. This case documents a fatal cardiac chemodectoma in an Alaskan Malamute, contributing to the limited literature on heart-base tumors in nonbrachycephalic large breeds, and emphasizes the importance of thorough echocardiographic evaluation, serial imaging in dogs with recurrent pericardial effusion, and counseling regarding a guarded-to-poor prognosis with extensive cardiac invasion.
A 4-year-old neutered male Labrador retriever presented with acute-onset nonweight-bearing lameness of the right forelimb following play activity. Physical examination revealed crepitus and pain on elbow flexion. Radiographic examination showed a linear lucency at the cranial margin of the medial coronoid process of the ulna (MCP), with sclerosis and periosteal new bone formation, consistent with degenerative joint disease secondary to elbow dysplasia (ED). Computed tomography (CT) identified two distinct fragments adjacent to the MCP. Arthroscopic partial coronoidectomy was performed with successful retrieval of both fragments. On histopathological examination, one fragment demonstrated chronic changes, consistent with dysplasia-related FMCP, whereas the other exhibited features consistent with acute trauma/fracture. The patient recovered well at 6-week postoperative evaluation. This is the first reported case of concurrent developmental FMCP and traumatic MCP fracture in the same limb in a canine patient, confirmed via multimodal imaging and histopathology. This report highlights the diagnostic role of CT imaging and histopathology in differentiating overlapping pathologies and raises the question whether underlying ED plays a role in secondary traumatic injuries in dogs.
Extensive postsurgical wounds remain a significant therapeutic challenge in small animal veterinary practice, particularly when reconstructive procedures fail and tissue viability is compromised. This report describes the successful management of a large postsurgical wound in an 8-year-old spayed mixed-breed female dog following wide-margin nodulectomy of a dorsal thoracic mass initially diagnosed cytologically as a suspected liposarcoma. Although primary closure using an H-plasty reconstructive technique was initially performed, progressive central necrosis developed at the surgical margins during the postoperative period. On postoperative Day 3 (POD 3), the wound exhibited tissue necrosis and serosanguineous exudation, necessitating management by second-intention healing. Following surgical debridement, the wound measured approximately 143 cm2 and was subsequently managed using a multimodal advanced wound care protocol based on the principles of the TIME framework, combined with tie-over dressing fixation, advanced wound dressings, fluorescence biomodulation, electrobioregulation, and topical regenerative therapies. Histopathological examination of the excised tissue ultimately revealed chronic-active pyogranulomatous panniculitis with abundant fibrosis, ruling out the initial suspicion of neoplasia. Progressive wound contraction, granulation tissue formation, and epithelialization were observed throughout the treatment period, with serial measurements demonstrating a reduction from 143 cm2 to complete closure over approximately 16 weeks. No evidence of local infection, recurrent tissue necrosis, wound dehiscence, or systemic complications was detected during follow-up. Complete wound healing was achieved with satisfactory functional and cosmetic outcomes, without the need for additional reconstructive surgery. This case highlights the potential clinical value of a multimodal, individualized approach to managing extensive, complicated wounds in dogs. It suggests that sequentially integrating the TIME framework, tie-over fixation, fluorescence biomodulation, and electrobioregulation may offer a useful therapeutic alternative when conventional reconstructive techniques are unsuccessful.
