A 4 mo old male goldendoodle puppy was evaluated for chronic hematochezia with a history of recurrent rectal prolapse and tenesmus. A colo-colonic intussusception was diagnosed via abdominal imaging. Surgery was elected to reduce the intussusception, wherein a colonic mass was discovered. Colonic resection and anastomosis was performed, and the tissue were submitted for histopathological examination. The puppy was diagnosed with colonic hamartomatous ganglioneuromatosis based on the presence of markedly hyperplastic submucosal and myenteric plexi with infiltration and expansion of the mucosa and submucosa by Schwann cells and neuronal cell bodies. Ganglioneuromatosis is a rarely reported entity in the veterinary literature, and limited clinical follow up data is available for described cases. In humans, ganglioneuromatosis is associated with a PTEN genetic mutation, which confers increased susceptibility to the development of neoplasia of endocrine organs. Approximately 1 yr after the operation, this puppy appeared clinically normal with no abnormalities on repeated imaging. This case report describes the clinical presentation, surgical treatment, and histologic features of colonic hamartomatous ganglioneuromatosis with 1 yr postoperative clinical follow up data in a dog. Although uncommon, ganglioneuromatosis should be considered as a differential diagnosis list as a cause of gastrointestinal masses in puppies and young dogs.
Acquired myasthenia gravis (MG) in dogs can present with focal or generalized weakness and is diagnosed by the presence of circulating antibodies to the acetylcholine receptor. Megaesophagus is the most common focal form of MG. Although exacerbation of MG has been associated with the use of fluoroquinolones in humans, it has not been previously described in dogs. The medical records of 46 dogs diagnosed with MG based on acetylcholine receptor antibody testing from 1997 to 2021 were retrospectively evaluated to identify any dogs who demonstrated exacerbation of MG after the administration of a fluoroquinolone. Exacerbation of MG, from focal to generalized, occurred in a median of 4.5 days after initiation of fluoroquinolone therapy in six dogs. In addition, one dog with generalized MG and megaesophagus developed pyridostigmine resistance subsequent to fluoroquinolone therapy. Marked improvement in generalized weakness was reported 36 hr after discontinuation of fluoroquinolone therapy alone in one dog and in combination with pyridostigmine in two dogs. Fluoroquinolone therapy was never stopped in three dogs who were euthanized because of severe weakness and one dog who died of respiratory arrest.
A 4 yr old female neutered Labrador retriever was referred with a history of left hind-limb lameness and an acute, nonpainful, subcutaneous mass on the medial aspect of the left stifle. Stifle radiographs and fine needle aspirates of the soft tissue mass performed by the referring veterinarian confirmed the presence of predominantly highly granulated mast cells, consistent with a mast cell tumor. Computed tomography demonstrated a soft tissue mass centered on the left medial stifle, with associated joint effusion and polyostotic lytic lesions on the tibial plateau and distal patella. Ultrasound-guided aspirates of the liver, spleen, and popliteal lymph nodes were obtained to rule out further metastatic spread. Cytology of the joint fluid demonstrated a low number of well-differentiated mast cells. Surgical and oncological interventions were discussed, and full hind-limb amputation was elected. Histopathological analysis of the submitted tissues after amputation diagnosed a subcutaneous mast cell tumor with neoplastic cell infiltrate extending into sections of joint capsule and synovial membrane. Infiltration to the tibia and distal patella were suspected following the presence of mast cell clusters in both osteolytic lesions. No evidence of metastasis was identified in the popliteal lymph node. Postoperative monitoring of iliac lymph node size using ultrasound did not identify evidence of metastasis 12 mo postoperatively.
Otitis externa (OE) is a common disease in dogs, and topical medications are the preferred treatment. Compounded solutions of enrofloxacin are commonly used in practice to treat bacterial OE; however, the tolerability of different concentrations of this antibiotic in the ear canals of dogs has not been evaluated. The objective of this study is to determine if a higher concentration of enrofloxacin applied to the external ear canal is clinically tolerated in dogs with healthy ears. Sixteen client-owned dogs with bilateral healthy ears and no previous history of OE were enrolled. Injectable enrofloxacin 2.27% diluted with sterile sodium chloride in 1:1 (11.35 mg/mL) and 2:1 (15 mg/mL) ratios were applied into the dogs' right and left ears, respectively, q 12 hr for 14 days. Based on video otoscopic examination, clinical score for canine OE (OTIS3) results before application were ≤1 for all dogs. During the study and at the conclusion, all scores remained ≤2, which is considered normal. No cytologic inflammatory cells were seen in any of the dogs' ears throughout the study. Different concentrations of enrofloxacin solution applied topically were well tolerated by dogs with healthy ears and can be considered for the treatment of dogs with bacterial OE.
It has been reported that hypertriglyceridemia can partially mediate between diabetes mellitus (DM) and pancreatitis in dogs, implying that another mediator, such as chronic hyperglycemia, might exist. Therefore, this study aimed to evaluate the relationship between hyperglycemia and serum canine pancreatic lipase immunoreactivity (cPLI) concentration in diabetic dogs. This retrospective cohort study included 26 client-owned diabetic dogs, divided according to their serum fructosamine levels (<500 μmol/L = well-controlled DM group; ≥500 μmol/L = untreated or poorly controlled DM group). Five of the 26 DM dogs (19.2%) had serum cPLI concentrations consistent with pancreatitis, among which two showed ultrasonographic evidence of pancreatitis without clinical signs. The serum cPLI concentrations (median [interquartile range]) were significantly higher in the untreated or poorly controlled group (520 μg/L [179.76-1000 μg/L]) than in the well-controlled group (77 μg/L [32.22-244.6 μg/L], P = 0.0147). The serum fructosamine concentration was positively correlated with the serum cPLI concentration (r = 0.4816; P = 0.0127). Multivariate analysis revealed serum triglyceride and fructosamine concentrations were associated with the serum cPLI concentration. In conclusion, this study suggests that chronic hyperglycemia may induce pancreatic inflammation in diabetic dogs; however, the clinical significance of increased cPLI concentration is unknown.
Lipoma of the liver has not been reported in dogs. An 8 yr old spayed female Great Dane was referred for diagnostic workup of abdominal distention. Computed tomography showed fat-attenuating masses with negative attenuation values (variable between -60 to -40 Hounsfield units) and minimal contrast uptake within the left cranial abdomen. Left lateral and right medial liver lobectomies were performed to remove two liver masses. Histopathology showed large lipomas arising from within the hepatic parenchyma. Immunohistochemistry for smooth muscle actin was negative, consistent with true lipomas. The dog was euthanized 8 mo later because of causes likely unrelated to the liver lipoma. This is the first case report of lipoma in the liver of a dog. The purpose of this case report and brief literature review is to provide evidence that surgical excision of fat-attenuating masses within the liver that are consistent with lipoma using immunohistochemistry can be curative.
Canine mast cell tumors (MCTs) have highly variable clinical behavior, and predicting outcomes in individual dogs remains challenging. Many studies combine dogs with varying tumor grades, clinical stage, or treatments, confounding those results. The purpose of this retrospective study was to determine outcome and prognostic factors in a specific subset of dogs with high-grade, stage 2, cutaneous MCTs treated with adequate local control via surgery with or without radiation therapy and adjuvant cytotoxic chemotherapy. Seventeen dogs met the inclusion criteria, and the median survival time was 259 days. Development of local recurrence, tumor location, and presence of ulceration were all associated with shorter survival times. Tumor size, mitotic count, chemotherapy protocol, lymph node classification, and radiation therapy were not significantly associated with outcome. In this study, a specific population of dogs characterized by high-grade MCTs with local lymph node metastasis who received aggressive local and systemic therapy had a median survival of about 8.5 mo. Dogs with ulcerated tumors, recurrent tumors, or tumors located on the head had a worse outcome despite aggressive therapy. These results may serve as a basis of comparison for future research exploring alternative treatment combinations in this specific population of dogs.
An 11 yr old female French bulldog was presented for acute onset of seizures and a 2 wk history of disorientation. On physical examination, a nodular mass at the fourth mammary gland level was observed. Neurological evaluation showed obtundation and compulsive behavior. Brain MRI study did not reveal any abnormalities. Cerebrospinal fluid (CSF) collected from the cerebellomedullary cistern showed a marked increase of total nucleated cell count (400 cells/μL). Cytological evaluation identified the presence of a monomorphic round cell population characterized by large cell bodies, a single eccentrical located nucleus with high nuclear:cytoplasmatic ratio, and marked atypia with anisocytosis, anisokaryosis, and multiple nucleoli. Leptomeningeal carcinomatosis (LC) was suspected. The dog was euthanatized for worsening of clinical signs. Post-mortem examination identified an anaplastic mammary carcinoma in the nodular mammary mass. Infiltration by neoplastic cells exhibiting the same morphological features was detected along leptomeninges of the telencephalon and cerebellum associated with cortical and subcortical parenchymal micrometastases. To our knowledge, this is the first case of LC in a dog detected by CSF evaluation but without any MRI abnormalities. This finding emphasizes the usefulness of CSF cytology in patients with suspected LC even in the absence of any MRI identifiable lesions.
A 1 yr old, 1.7 kg, spayed female Chihuahua was presented for respiratory distress and an enlarged cardiac silhouette as seen on thoracic radiographs. Echocardiogram revealed pericardial effusion and cardiac tamponade. Computed tomography revealed marked pleural and pericardial effusion, thickening of the pericardium caudally, and a mass along the mediastinum. Pericardial fluid obtained via pericardiocentesis showed suppurative inflammation with mixed anaerobic bacteria isolated on culture. Subtotal pericardiectomy and partial lung lobectomy was performed to treat septic pericarditis. Postoperative echocardiogram showed increased right-sided pressures consistent with constrictive epicarditis, and 10 days after surgery, the dog was re-presented for right-sided heart failure. An epicardectomy was performed. A definitive source of infection was not identified, although a penetrating foreign body (e.g., grass awn) was suspected. The dog recovered and 10 yr follow up revealed no evidence of constrictive pathology on echocardiogram. This case report demonstrates the successful treatment of septic pericarditis and constrictive epicarditis via subtotal pericardiectomy and epicardiectomy.