Veterinary clinical pathology最新文献

A 9-month-old female intact toy poodle and a 1-year-old female intact Labrador retriever mix presented to separate teaching hospitals for chronic histories of malaise and clinicopathologic evidence of hepatic dysfunction. The signalment and clinical histories of these dogs prompted consideration of a congenital portosystemic shunt as a primary differential. However, microscopic evaluation of peritoneal effusion, pleural effusion, and peripheral blood samples from the dogs revealed round to ovoid yeast organisms morphologically most compatible with Histoplasma capsulatum. Additional testing confirmed histoplasmosis in each case. The poodle underwent a computed tomography (CT) study, which showed hepatomegaly with a spleno-gonadal shunt, pancreatic and gastric wall edema, and marked peritoneal effusion, findings compatible with portal hypertension and secondary acquired shunt formation. The dog was later humanely euthanized due to clinical deterioration, and on necropsy hepatic histoplasmosis was verified, with additional affected tissues comprising lungs and spleen. The Labrador Retriever mix responded clinically and clinicopathologically to antifungal therapy, though no abdominal imaging was performed to definitively exclude the possibility of a congenital portosystemic shunt. In retrospect, several features were more compatible with histoplasmosis than portosystemic shunt in these cases, including hyperbilirubinemia, effusion, and hepatomegaly. These findings serve as a reminder of the need to interpret serum biochemical findings in the context of the totality of the clinicopathologic data and imaging findings, as well as the diagnostic value of microscopy in the evaluation of hematologic and body cavity fluid samples.

A 9-year-old dog was presented with weight loss, respiratory effort, and an enlarged abdomen. Imaging studies and exploratory surgery showed pulmonary and splenic masses and bi-cavitary effusion, later classified as hemorrhage. Cytology of the peritoneal and pleural fluids also revealed several microfilariae. Immunologic and molecular analyses confirmed Dirofilaria immitis infection and histopathology of the spleen indicated a cavernous endothelial proliferation with undefined etiology (hemangiosarcoma vs reaction to parasite infestation). The nematode larvae are speculated to have entered body cavities via erratic migration or via hemorrhage and visceral lesions to be related to parasitism. Nematode infection should be considered as a differential diagnosis for internal bleeding of undetermined origin.

A 9-year-old Arabian gelding was referred for a 4-day history of hyporexia and pigmenturia after a 2-hour trail ride with severe azotemia (creatinine 9.6 mg/dL, RI: 1.0–2.0; BUN 65 mg/dL, RI: 8–26) and increased muscle enzyme activities (AST 10 167 IU/L, RI: 148–420; Creatine kinase [CK] 22 266 IU/L, RI: 45–360) noted on day 2. Prior treatment included flunixin meglumine.

The horse appeared painful with diffuse muscle fasciculations, with no other exam abnormalities. A CBC revealed a mild leukocytosis (mild mature neutrophilia); the erythron and thrombon were unremarkable. Serum biochemistry demonstrated persistent azotemia (creatinine 13.5 mg/dL, RI: 0.8–1.5), increased CK (8471 U/L, RI: 186–760), high anion gap (27, RI: 10–19), hyponatremia (128 mmol/L, RI: 132–140), hypochloremia (80 mmol/L, RI: 95–103), hyperkalemia (5.2 mmol/L, RI: 2.6–4.7), hyperalbuminemia (3.4 g/dL, RI: 2.5–3.3), hyperglycemia (125 mg/dL, RI: 70–113) and hypercalcemia (14.4 mg/dL, RI: 11–13.4); free/ionized calcium was 1.53 mmol/L (RI: 1.09–1.67).

Cystoscopy revealed red filamentous material pooling in the urine (Figure 1A,B). The urine was isosthenuric (USG 1.010) and alkaline (pH 8.0) with 1+ protein and large blood. Unstained sediment contained 10–50 RBC/hpf, 10–20 WBC/hpf, many transitional epithelial cells, 0–5/lpf linear structures (Figure 1C), rare calcium carbonate crystals, and moderate mucus threads.

The minimum database findings were suggestive of inflammation/stress, dehydration, muscle injury, and renal injury/insufficiency. The presence of macroscopic urinary casts was striking and unique. In general, urinary casts are rare in herbivores due to alkalinuria.¹ Cellular and granular casts are abnormal and indicate acute renal tubular injury. Cellular casts are defined by their cell composition: epithelial casts indicate renal tubular degeneration or necrosis secondary to severe dehydration, ischemia/infarction, nephrotoxicity, or pigment nephropathy; leukocyte casts imply tubulointerstitial inflammation (eg, pyelonephritis); and erythrocyte casts indicate intrarenal hemorrhage.^1-3 Granular casts form from the degeneration of cellular casts. In this case, the granular-appearing casts were presumed to represent breakdown products/proteins from erythrocytes (hemoglobin) and muscle (myoglobin). Hemoglobin casts occur with intravascular hemolysis and renal hemorrhage, whereas myoglobin casts indicate severe muscle injury or necrosis.^{2, 3} These proteins can have a similar appearance on routine stains and can be delineated with Okajima stain (hemoglobin stains orange to orange-red) and myoglobin IHC (specific to myoglobin).

Endogenous injury from myoglobin or hemoglobin (pigment nephropathy) can result in renal tubular injury due to altered blood flow, cast formation, tubular obstruction, and oxidative injury.^1-3 Given the history of a trail ride

A 6-year-old spayed female Scottish Fold cat presented with lethargy and anorexia. A complete blood cell count indicated severe anemia and mild thrombocytopenia. Examination of peripheral blood smears revealed marked changes in the erythroid lineage, including the presence of basophilic stippling and Howell-Jolly bodies as well as an increase in nucleated erythrocytes, polychromatophils, ovalocytes, and schistocytes. Additionally, some erythrocytes contained a ring or figure-eight shaped structure known as a Cabot ring, which were especially observed in polychromatophilic erythrocytes. Hemolytic diseases (Mycoplasma infection and IMHA) were diagnostically excluded, and the cat was treated through prednisolone administration, whole blood transfusion, and administration of vitamins (K2 and B12); however, the anemia progressively worsened. Cabot rings were observed until Day 22 and subsequently disappeared as the number of nucleated RBCs increased, and the erythrocyte lineage shifted to immature population. On Day 42, peripheral blood examination revealed further left shifting and appearance of many rubriblasts. The patient died at home on Day 43. Necropsy revealed neoplastic cells infiltrating the bone marrow and other organs, which were immunopositive to CD71 which is an erythroid lineage marker. In humans, Cabot rings have been observed in megaloblastic anemia, lead poisoning, myelodysplastic syndrome, and myelofibrosis; further, they are thought to be related to stressed bone marrow and dyserythropoiesis. This is the first case report of a cat with Cabot rings, which are suggestive of defects in erythroid lineage production.

A 10-year-old neutered male Maltese dog was presented for an investigation of lymphocytosis. The dog was up-to-date on vaccinations and deworming. Physical examination did not reveal any significant abnormalities. A complete blood cell count (CBC) showed mild leukocytosis with moderate lymphocytosis, basophilia, and moderate neutropenia, but no significant left shift or toxic change. Serum biochemistry and urinalysis were unremarkable. All performed tests for infectious agents common in this geographical region were negative. No significant abnormalities were found on abdominal ultrasound examination. Multiparametric flow cytometry of peripheral blood showed a CD8⁺ T-cell lymphocytosis, and PCR for antigen receptor rearrangement revealed a clonal expansion of the T-cell receptor gamma chain genes. A clinical diagnosis of chronic lymphocytic leukemia (CLL) was made, and follow-up was recommended. On Day 48 post-presentation, the CBC showed mild non-regenerative anemia (NRA), moderate leucocytosis due to moderate to marked lymphocytosis, basophilia, and a marked increase in hyposegmented neutrophils with mild toxic change in the absence of neutrophilia or neutropenia. Treatment with chlorambucil and prednisolone was initiated. On Days 87 and 197 post-presentation, the CBC showed mild NRA, with progressively decreasing numbers of hyposegmented neutrophils. The dog remained without clinical signs. Basophilia and probable pseudo-Pelger–Huët anomaly were possibly secondary to CLL. To the authors' knowledge, this is the first report of these two hematologic conditions secondary to CLL in dogs. Recognition of a pseudo-Pelger–Huët anomaly is clinically relevant to avoid misinterpretation as a marked left shift due to severe inflammation and prevent unnecessary urgent therapeutic actions.