Clinicopathologic findings of splenic marginal zone lymphoma with gallbladder involvement that progressed to diffuse large B-cell lymphoma in a dog.

A 12-year-old spayed female Dalmatian presented with acute vomiting and anorexia. The clinicopathological and imaging abnormalities included icterus, biliary obstruction, and multiple diffuse splenic hypoechogenic nodules. Cholecystectomy was performed to remove the obstruction, followed by liver biopsy and splenectomy. Histopathological and immunohistology evaluation of the spleen, liver, and gallbladder revealed splenic marginal zone lymphoma (MZL) with gallbladder and hepatic infiltration of neoplastic CD20/CD79α-positive cells. Moreover, we observed clonal rearrangements of the immunoglobulin heavy-chain (IgH) gene in all three tissues. The dog was in good condition without chemotherapy. However, there was progressive elevation of liver enzymes, which could be attributed to neoplastic hepatic infiltration. Chlorambucil and prednisolone were administered until day 108, when the liver enzyme levels normalized. On day 156, the dog developed diffuse large B-cell lymphoma (DLBCL) of the peripheral lymph nodes. Sequence analysis of the clonally rearranged IgH gene revealed that all neoplastic cells in the spleen, gallbladder, and liver at initial presentation, as well as lymph nodes on day 156, possessed the same sequence identity of the amplified IgH fragments. This demonstrated that all neoplastic cells were derived from the same B-lymphocyte clone. The DLBCL was considered to have transformed from the splenic MZL, with gallbladder involvement. In cases of splenic MZL, it is important to consider gallbladder involvement and transformation to DLBCL. Moreover, gallbladder lymphoma should be included in the differential diagnosis of dogs with gallbladder abnormalities. Further studies are warranted to investigate the prognosis of splenic MZL.

Focal cutaneous telangiectasia in a young dog of probable congenital origin.

BACKGROUND: Idiopathic cutaneous telangiectasia has been rarely described in the dog. OBJECTIVES: We present the first case of idiopathic focal cutaneous telangiectasia in a young dog of probable congenital origin. METHODS: An 18-month-old spayed female Maltese dog presented with demarcated erythema of the skin on the right thorax. The lesion consisted of scattered, florid, ramified macules with mild dermatrophia and desquamation. The lesion was examined with histopathology and immunohistochemistry using antibodies for alfa-SMA. RESULTS: Diascopy revealed a blanchable lesion. Tortuous capillary expansion was observed by dermoscopy. The histopathological examination revealed dilated but otherwise unremarkable capillaries in the superficial dermis compatible with cutaneous telangiectasia. The lesion was followed up over a 3-year period and had essentially remained stable. Other vascular anomalies displaying similarities with telangiectasia are discussed. CONCLUSIONS: In human vascular anomalies, this case would be presumably classified as 'telangiectasia' by the International Society for the Study of Vascular Anomalies. We propose that primary cutaneous telangiectasia should be included in the list of differential diagnoses for this type of lesions in dogs. We also suggest that dermoscopy would be a valuable tool for the identification of vascular anomalies in dogs.

Hepatosplenic lymphoma and visceral mast cell tumor in the liver of a dog with synchronous and multiple primary tumors.

An 11-year-old spayed female American Cocker Spaniel was presented with a 4-week history of anorexia and a 1-week history of abdominal distension. Clinicopathologic and imaging abnormalities included intra-abdominal hemorrhage, granular lymphocytes (GLs) in abdominal fluid smears, a splenic mass, and hepatomegaly with diffuse multiple hypoechogenic nodules. Based on the cytologic, histologic, and immunohistochemical evaluation of the spleen and liver, the diagnosis was hepatosplenic T-cell lymphoma (HSTCL) of GLs. Postoperatively, the dog was maintained in good condition with chemotherapy (ACNU [nimustine], L-asparaginase, and prednisolone). However, on day 85, ultrasound-guided fine-needle aspiration of the liver revealed a proliferation in neoplastic mast cells not associated with the GLs. The dog was diagnosed with a visceral mast cell tumor (MCT) originating from the liver. The chemotherapy was switched to vinblastine and toceranib. The dog remained in good condition until day 141 but died due to the progression of MCT on day 158. Liver cytology on day 155 showed no GLs, although HSTCL is thought to be resistant to chemotherapy. After the definitive diagnosis of HSTCL, we monitored this patient's response to chemotherapy with blood tests, including complete blood counts, ultrasound imaging, and cytologic aspirates of liver. Although canine HSTCL has a poor prognosis, the possibility of a new neoplasm, including visceral MCT, should be considered. Periodic liver cytology might be worthwhile in dogs receiving chemotherapy for HSTCL.

Clinicopathologic, immunohistochemical, and ultrastructural features of histiocytic sarcoma in a chinchilla (Chinchilla lanigera).

A 9-year-old intact female chinchilla (Chinchilla lanigera) was presented to a referring veterinarian due to small, multiple cervical nodules that had been rapidly increasing in size and number. Cytology of the nodules revealed sheets of pleomorphic round cells that were morphologically most compatible with histiocytic sarcoma. Histologically, the nodules were fairly demarcated, partially infiltrative, densely cellular neoplasm, and was composed of pleomorphic large round cells arranged in sheets. Special stains for bacteria (Gram stain and Ziehl-Neelsen stain) and fungi (periodic acid-Schiff stain) were all negative. On immunohistochemistry, the neoplastic cells showed strong cytoplasmic positivity for Iba-1 and CD204, but were negative for CD3 and CD20. Transmission electron microscopy failed to detect Birbeck's granules in the cytoplasm of the neoplastic histiocytes. The chinchilla received chemotherapy with lomustine but died spontaneously on day 62 despite treatment. Autopsy with histopathologic examination revealed disseminated histiocytic sarcoma involving the bone marrow, bronchial lymph nodes, nasal cavity, lung, heart, stomach, pancreas, pancreatic lymph nodes, liver, spleen, and kidney. To the best of our knowledge, this is the first report of disseminated histiocytic sarcoma in chinchillas.

Preoperative serum C-reactive protein concentration can be used to detect gallbladder rupture in dogs with gallbladder mucocele.

OBJECTIVE: To determine whether serum C-reactive protein (CRP) concentration could be used to detect gallbladder rupture (GBR) prior to surgery in dogs undergoing cholecystectomy for treatment of gallbladder mucocele (GBM). ANIMALS: 45 dogs that underwent cholecystectomy because of GBM at a companion animal referral hospital from 2017 to 2020. PROCEDURES: Electronic medical records were reviewed, and dogs were included if serum CRP concentration had been measured within 24 hours prior to cholecystectomy. Dogs were grouped as to whether the gallbladder was found to be ruptured or intact during surgery. Accuracy of using preoperative CRP concentration to predict GBR was compared with accuracy of abdominal ultrasonography and other preoperative blood tests. RESULTS: GBR was present in 15 dogs at the time of surgery. Median preoperative CRP concentration was significantly higher in dogs with GBR (15.1 mg/dL; interquartile range, 7.4 to 16.8 mg/dL) than in dogs with an intact gallbladder (2.65 mg/dL; interquartile range, 0.97 to 13.4 mg/dL). Sensitivity, specificity, and accuracy of using preoperative CRP concentration to predict GBR were 100%, 67%, and 78%, respectively. CLINICAL RELEVANCE: Measurement of preoperative CRP concentration provided excellent sensitivity and moderate specificity for detection of GBR in dogs undergoing cholecystectomy because of GBM. Accuracy of using preoperative CRP concentration for detection of GBR was not superior to the accuracy of preoperative abdominal ultrasonography. However, when CRP concentration was combined with results of ultrasonography, the sensitivity, specificity, and accuracy for detection of GBR were 100%, 93%, and 96%, respectively.

Clinicopathologic Findings of Spontaneous Leukemia in 9 Pet African Hedgehogs (Atelerix Albiventris).

Previous reports of leukemia in hedgehogs are limited. We describe clinicopathologic features of leukemia in 9 hedgehogs, including eosinophilic leukemia (n = 3) and acute leukemia/leukemic phase of lymphoma (n = 6). All 3 hedgehogs with eosinophilic leukemia were older than 2 years of age; in contrast, 4 of 6 cases of acute leukemia/lymphoma were <2 years old. Hedgehogs presented for non-specific clinical signs of anorexia and lethargy. On hematologic testing, hedgehogs with eosinophilic leukemia had a marked leukocytosis, consisting mostly of eosinophilic precursors with fewer mature eosinophils, whereas there were 43-97% immature cells (blasts) in the blood of hedgehogs with acute leukemia/lymphoma. Anemia (n = 6) and/or thrombocytopenia (n = 6) were concurrent findings. Increased liver enzyme activities (alanine aminotransferase, alkaline phosphatase) and hypoalbuminemia were the common findings on biochemical panels. All cases of eosinophilic leukemia and 4 cases of acute leukemia/lymphoma died shortly after diagnosis (median 7 days, range 0-41 days), whereas 2 cases of acute leukemia/lymphoma lived for 94 or 101 days. Postmortem examination in 5 cases (1 eosinophilic leukemia, 4 acute leukemia/lymphoma) showed bone marrow infiltrates, confirming eosinophilic leukemia and acute leukemia in 1 and 3 cases, and bone marrow necrosis in 1 animal with acute leukemia/lymphoma. Immunohistochemical staining of bone marrow sections confirmed a T-cell acute leukemia in 1 case. Several hedgehogs had concurrent carcinomas. Hedgehogs suffer from eosinophilic leukemia and acute leukemia/lymphoma. However, classification of acute leukemia by lineage was not possible due to lack of hedgehog cross-reactive or species-specific reagents.

Acute leukemia in six horses (1990-2012).

Acute leukemia is rare in horses. Herein we describe historical, clinicopathologic, and postmortem findings in 6 horses with acute leukemia. Medical records of horses with >20% bone marrow blasts and cytochemical or immunophenotyping results were reviewed. Affected horses were 2-8 y of age and of different breeds and sex. Horses were presented acutely with nonspecific signs (e.g., fever, lethargy). Characteristic hemogram findings were bi- or pancytopenia with low blast numbers. Histologic examination revealed extramedullary infiltrates, especially in lymph nodes, spleen, kidney, liver, and lungs. Leukemias were classified as B-cell ( n = 3) and acute myeloid leukemia (AML) ( n = 3). Tumors in 4 cases expressed multiple lineage markers, which complicated classification. Acute leukemia should be suspected in horses with moderate-to-severe bi- or pancytopenia. Blood smears should be reviewed for neoplastic cells, and bone marrow examination is required for diagnosis. Leukemia classification is best achieved using combined morphologic, cytochemical, and immunophenotyping results.

Imaging diagnosis--Neuronal ceroid lipofuscinosis with a chronic subdural hematoma.

A subdural hematoma was found to accompany neuronal ceroid lipofuscinosis in an 11-month-old Dachshund. Results from clinical, magnetic resonance (MR) imaging, histopathologic, ultrastructural, and molecular assessments are described. The dog had a 3-month history of progressive neurologic signs. In MR images, there was severe asymmetric cerebral atrophy with a subdural hematoma. Histopathologically, there was autofluorescent, periodic acid-Schiff-positive lipopigment in neurons and transmission electron microscopy confirmed a typical curvilinear profile of the storage bodies. We hypothesize that rapid brain atrophy contributed to the subdural hematoma formation, a complication not described previously in dogs with neuronal lipofuscinosis.