To better characterize the idiopathic hyperlipoproteinemia of Miniature Schnauzer dogs, the plasma lipoproteins of 20 Miniature Schnauzers (MS) and 11 dogs of other breeds (DOB) were evaluated by ultracentrifugation, electrophoresis, and biochemical tests. Seventeen M S were healthy; 3 had diabetes mellitus. Plasma from 6 of 17 healthy and all 3 diabetic M S was visibly lipemic. Lipemia was slight to marked in healthy lipemic MS, and marked in diabetic ones. All DOB had clear plasma; 8 were healthy and 3 had diabetes. All healthy lipemic MS and diabetic lipemic M S had hypertriglyceridemia associated with excess very low density lipoproteins. Chylomicronemia was present in 4 of 6 healthy lipemic M S and all 3 diabetic lipemic MS. Lipoproteins with ultracentrifugal and electrophoretic characteristics of normal low density lipoprotein were lacking in 4 of 6 healthy lipemic MS. The lipoprotein patterns of 4 of 11 healthy nonlipemic M S were characterized by mild hypertriglyceridemia associated with increased very low density lipoproteins and a lack of lipoproteins with characteristics of normal low density lipoproteins. Lipoprotein patterns of diabetic DOB closely resembled those of healthy DOB those of diabetic lipemic M S resembled those of markedly lipemic healthy lipemic MS. In conclusion, the hyperlipoproteinemia of Miniature Schnauzers is characterized by increased very low density lipoproteins with or without accompanying chylomicronemia; some affected dogs may have decreased low There is evidence that primary hyperlipoproteinemias occur in dogs, but these disorders have not been well characterized, and their etiologies have not been established."6 In one report, primary hyperlipoproteinemia was believed to be the cause of the persistent fasting lipemia of five Miniature Schnauzers. Serum from these dogs formed cream layers on refrigeration, indicating the presence of chylomicrons. Triglyceride concentrations were moderately to markedly increased, and cholesterol concentrations were moderately increased. Lipoprotein electrophoresis showed lipoproteins that stayed at the origin (expected behavior of chylomicrons), and greater amounts of beta and alpha-2 migrating lipoproteins than were seen in healthy dogs.5Several hereditary disorders that cause fasting hypertriglyceridemia occur in people, and many of these are characterized by chylomicronemia. The hyperlipoproteinemias that involve chylomicronemia are often associated with abdominal pain and/or pancreatitis, and dia- 253

Spirochetemia was diagnosed in 2 Siberian Huskies and a Rottweiler from the northwestern region of Texas between June 1999 and October 2001. Clinical findings were nonspecific; tick exposure was documented in 2 of the dogs. Hematologic abnormalities included anemia (n=2), neutrophilia (n=2, including 1 with a left shift), lymphopenia (n=3), eosinopenia (n=3), and thrombocytopenia (n=2). One anemic dog had a positive Coombs' test. In 1 dog, Western blot analysis of serum yielded multiple positive bands with B turicatae lysate, indicating the spirochetemia most likely was due to B turicatae infection. In 2 dogs, spirochetes were cultured from the blood and identified using DNA analysis as Borrelia turicatae; 1 of these dogs also was seropositive for Ehrlichia canis and B burgdorferi. In 2 cases, spirochetemia was more prominent in blood smears prepared immediately after sample collection than in smears prepared from EDTA blood. Two dogs recovered with doxycycline treatment; 1 dog declined clinically despite treatment and was euthanized. B turicatae is the agent of tick-borne (endemic) relapsing fever in humans and is distinct from B burgdorferi, the agent of Lyme disease; however, serologic cross-reactivity may occur. B turicatae is transmitted by the soft tick, Ornithodoros turicata, and infection should be considered in dogs with spirochetemia and possible exposure to the tick vector.

CLN2 neuronal ceroid lipofuscinosis is a hereditary lysosomal storage disease with primarily neurological signs that results from mutations in TPP1 which encodes the lysosomal enzyme tripeptidyl peptidase-1 (TPP1). Studies using a canine model for this disorder demonstrated that delivery of TPP1 enzyme to the cerebrospinal fluid (CSF) by intracerebroventricular administration of an AAV-TPP1 vector resulted in substantial delays in the onset and progression of neurological signs and prolongation of lifespan. We hypothesized that the treatment may not deliver therapeutic levels of this protein to tissues outside the central nervous system that also require TPP1 for normal lysosomal function. To test this hypothesis, dogs treated with CSF administration of AAV-TPP1 were evaluated for development of non-neuronal pathology. Affected treated dogs exhibited progressive cardiac pathology reflected by elevated plasma cardiac troponin-1, impaired cardiac function, and development of histopathological myocardial lesions. Progressive increases in plasma activity levels of alanine aminotransferase and creatine kinase indicated development of pathology in the liver and muscles. The treatment also did not prevent disease-related accumulation of lysosomal storage bodies in heart or liver. These studies indicate that optimal treatment outcomes for CLN2 disease may require delivery of TPP1 systemically as well as directly to the central nervous system.

A n 11-year-old Lipizzaner mare was referred for lethargy, abdominal distention, coughing, and weakness of 1 month's duration. The mare had been regularly dewormed and vaccinated against tetanus, influenza, and Eastern and Western equine encephalitis. Serum agar gel immunodiffusion assay for equine infectious anemia was negative. The mare was weak, lethargic, and mildly dehydrated. Abdominal distention was prominent (Fig 1), and borborygmi were absent. Mucous membranes were pale with a capillary refill time of 3.5 seconds. Heart (86 beats/min) and respiratory (40 breaths/min) rates were increased, and rectal temperature was 99.8uF. Body weight was 605 kg, but the mare was judged to be thin. Ventral abdominal subcutaneous edema was evident. Per rectum abdominal palpation identified a nongravid uterus. Moderate anemia (packed cell volume, 21%), mild lymphopenia, and hyperfibrinogenemia (0.5 g/dL; reference range, 0.1-0.4 g/dL) were present on the CBC. Serum biochemical analysis identified hypoglycemia (glucose, 47 mg/dL; reference range, 72-114 mg/dL), azotemia (BUN, 89 mg/dL; reference range, 8-27 mg/ dL; creatinine 5 8.8 mg/dL, reference range, 0.6-1.8 mg/dL), hyponatremia (sodium, 121 mmol/L; reference range, 132-144 mmol/L), hypochloremia (chloride, 86 mmol/L; reference range, 94-102 mmol/L), hyperka-lemia (potassium, 6.3 mmol/L; reference range, 2.7-4.9 mmol/L), hypoproteinemia (protein, 4.8 g/dL; reference range, 4.9-6.9 g/dL), hypoalbuminemia (albumin, 2.1 g/dL; reference range, 2.5-4.2 g/dL), hypocalcemia (calcium, 9.9 mg/dL; reference range, 10.7-13.4 mg/dL), hyperphosphatemia (inorganic phosphate, 13.9 mg/dL; reference range, 1.9-5.4 mg/dL), hypertriglyceridemia (triglyceride, 2,720 mg/dL; reference range, 4-44 mg/ dL), unconjugated hyperbilirubinemia (3.7 mg/dL; reference range, 0.1-1.9 mg/dL), and increased serum enzyme activities (CK, 3,147 U/L; reference range, 90-565 U/L; aspartate aminotransferase (AST), 2,268 U/L; reference range, 205-555 U/L; lactate dehydrogenase (LDH), 32,582 U/L; reference range, 520-1,480 U/L; gamma glutamyl transferase (GGT), 59 U/L; reference range, 12-45 U/L). Urinalysis indicated dilute urine (urine specific gravity [USG], 1.016) and hyaline casts (15 to 20 casts per low power field) were observed. The bladder was normal on endoscopic examination. Abdominal ultrasonography identified a large volume of anechoic abdominal fluid and revealed irregular cauliflower-like masses adherent to the abdominal wall at many locations, evidently fused to the peritoneum and characterized by mixed echogenicity (Fig 2). Other smaller masses were identified on the surface of the mesentery and adjacent to the dorsal aspect of the spleen. Abnormalities were not seen in the liver, kidneys, and intestines. Mild to moderate anechoic bilateral pleural effusion was observed. Abdominocentesis yielded a large volume of serosan-guineous peritoneal fluid (PF) characterized by a normal nucleated cell count (659 nucleated cells/mL), moderately increased protein concentration (3.2 g/dL), and a hematocrit...

Captive tigers without clinical signs of disease tested positive for C felis. The PCR assay for C felis appeared to be more reliable than cytologic detection of piroplasms in tigers.

A n 11-year-old Lipizzaner mare was referred for lethargy, abdominal distention, coughing, and weakness of 1 month's duration. The mare had been regularly dewormed and vaccinated against tetanus, influenza, and Eastern and Western equine encephalitis. Serum agar gel immunodiffusion assay for equine infectious anemia was negative.The mare was weak, lethargic, and mildly dehydrated. Abdominal distention was prominent (Fig 1), and borborygmi were absent. Mucous membranes were pale with a capillary refill time of 3.5 seconds. Heart (86 beats/min) and respiratory (40 breaths/min) rates were increased, and rectal temperature was 99.8uF. Body weight was 605 kg, but the mare was judged to be thin. Ventral abdominal subcutaneous edema was evident. Per rectum abdominal palpation identified a nongravid uterus.Moderate anemia (packed cell volume, 21%), mild lymphopenia, and hyperfibrinogenemia (0.5 g/dL; reference range, 0.1-0.4 g/dL) were present on the CBC. Serum biochemical analysis identified hypoglycemia (glucose, 47 mg/dL; reference range, 72-114 mg/dL), azotemia (BUN, 89 mg/dL; reference range, 8-27 mg/ dL; creatinine 5 8.8 mg/dL, reference range, 0.6-1.8 mg/dL), hyponatremia (sodium, 121 mmol/L; reference range, 132-144 mmol/L), hypochloremia (chloride, 86 mmol/L; reference range, 94-102 mmol/L), hyperkalemia (potassium, 6.3 mmol/L; reference range, 2.7-4.9 mmol/L), hypoproteinemia (protein, 4.8 g/dL; reference range, 4.9-6.9 g/dL), hypoalbuminemia (albumin, 2.1 g/dL; reference range, 2.5-4.2 g/dL), hypocalcemia (calcium, 9.9 mg/dL; reference range, 10.7-13.4 mg/dL), hyperphosphatemia (inorganic phosphate, 13.9 mg/dL; reference range, 1.9-5.4 mg/dL), hypertriglyceridemia (triglyceride, 2,720 mg/dL; reference range, 4-44 mg/ dL), unconjugated hyperbilirubinemia (3.7 mg/dL; reference range, 0.1-1.9 mg/dL), and increased serum enzyme activities (CK, 3,147 U/L; reference range, 90-565 U/L; aspartate aminotransferase (AST), 2,268 U/L; reference range, 205-555 U/L; lactate dehydrogenase (LDH), 32,582 U/L; reference range, 520-1,480 U/L; gamma glutamyl transferase (GGT), 59 U/L; reference range, 12-45 U/L). Urinalysis indicated dilute urine (urine specific gravity [USG], 1.016) and hyaline casts (15 to 20 casts per low power field) were observed. The bladder was normal on endoscopic examination.Abdominal ultrasonography identified a large volume of anechoic abdominal fluid and revealed irregular cauliflower-like masses adherent to the abdominal wall at many locations, evidently fused to the peritoneum and characterized by mixed echogenicity (Fig 2). Other smaller masses were identified on the surface of the mesentery and adjacent to the dorsal aspect of the spleen. Abnormalities were not seen in the liver, kidneys, and intestines. Mild to moderate anechoic bilateral pleural effusion was observed.Abdominocentesis yielded a large volume of serosanguineous peritoneal fluid (PF) characterized by a normal nucleated cell count (659 nucleated cells/mL), moderately increased protein concentration (3.2 g/dL), and a hematocrit of 3%...

A 7-year-old male neutered Boston Terrier, previously diagnosed with hyperadrenocorticism, was presented to the University of Missouri Veterinary Medical Teaching Hospital Neurology service for evaluation of a large pituitary mass revealed on computer tomography (CT) and progressively worsening clinical signs despite treatment. Upon arrival, the dog's vital parameters, including heart and respiratory rate and temperature, were within normal limits. The mucous membranes were dry. The neurologic examination revealed an inappropriate mentation, characterized by drowsiness, absent menace response bilaterally, postural reaction deficits limited to delayed hopping and proprioceptive positioning in the left pelvic limb, while gait was unremarkable and with no obvious ataxia, weakness or lameness, spinal reflexes were intact, and no hyperesthesia could be elicited upon paraspinal palpation. The dog's neuroanatomic diagnosis was bilateral forebrain lesion due to a pituitary macroadenoma and associated peritumoral edema. The CBC (Sysmex XT-2000iV; Sysmex America, Inc, Mundelein, IL, USA) was normal, except for a mild lymphopenia. The chemistry profile (Olympus AU400e; Beckman Coulter, Brea, CA, USA) revealed changes associated with hyperadrenocortism, including mildly increased GGT, ALT, and ALP activities. Additionally, marked hypernatremia, hyperchloridemia, and a mildly decreased corrected chloride concentration were found. Hypernatremia and hyperchloridemia were attributed to marked dehydration due to an altered mental state. The mildly decreased corrected chloride (corrected Cl = measured Cl 9 147/measured Na) suggesting a disproportionate decrease of chloride relative to sodium has been reported with hyperadrenocortism. 1 The increased endogenous ACTH concentration was supporting pituitary-dependent hyperadrenocortism. A transsphenoidal approach for hypophysectomy was taken to remove the mass. Intraoperative imprints were submitted for evaluation ( Figure 1). Figure 1. Imprints of an enlarged pituitary gland in a dog. Wright-Giemsa. 950 objective. A B

A 7-year-old female spayed Bulldog was presented to the University of Missouri Veterinary Medical Teaching Hospital for a 2-month history of progressive abdominal distension that was unresponsive to treatment for presumptive cardiac disease. On presentation, the dog was quiet, alert, and responsive. The vital parameters, including temperature, and heart and respiratory rates, were within normal limits. Physical examination revealed severe abdominal distention, symmetrical alopecia along the tail and dorsum, markedly enlarged mammary glands and vulva, and mucoid red-brown vulvar discharge. CBC and chemistry data revealed only mild abnormalities including mature neutrophilia, minimally regenerative anemia, hypoalbuminemia, and hyperglobulinemia. Thoracic radiographs revealed several soft tissue opacities in the lungs suggestive of metastatic disease. Therapeutic abdominocentesis was performed and approximately 1.5 L of serosanguinous fluid was removed. This fluid was submitted for evaluation and was classified as a modified transudate (2828 cells/lL, total protein 3.3 g/dL) with mild suppurative inflammation and moderate numbers of round, mildly pleomorphic cells most consistent with reactive mesothelial cells. An abdominal ultrasound examination revealed a multilobulated central abdominal mass that was too large to be measured. The organ of origin was not apparent. Fine-needle aspirates of the mass were submitted for cytologic evaluation (Figure 1). Figure 1. Aspirates of an intra-abdominal mass in a 7-year-old female spayed dog. Wright-Giemsa (A)920 objective. (B) 9100 objective. A B