Clinical and clinicopathologic abnormalities in young dogs with acquired and congenital portosystemic shunts: 93 cases (2003-2008)

Objective-To determine whether clinical and clinicopathologic data could assist differentiation of congenital portosystemic shunts (CPSSs) from acquired portosystemic shunts (APSSs) in young dogs. Design-Retrospective case series. Animals-Dogs < 30 months of age with CPSSs (n = 62) or APSSs (31). Procedures-Medical records from 3 referral centers identified 31 dogs with APSSs and 62 dogs with CPSSs diagnosed from July 2003 to July 2008. Signalment, clinical signs, physical examination, and clinicopathological data were recorded, and statistical analyses were performed to determine differences between groups. Results-Univariable analysis showed APSS patients were older, heavier, and in poorer body condition, compared with CPSS patients. In CPSS patients, diarrhea was less prevalent, and neurologic signs were more prevalent. Ascites was more prevalent in APSS (Fisher exact test; OR, 50.2; 95% confidence interval [CI], 6.2 to 409.7), with no significant difference in albumin concentration between groups. The logistic regression model used to assess clinicopathological parameters showed lower Hct (OR, 1.42 × 10(-12); 95% CI, 1.42 × 10(-17) to 4.0 × 10(-6)), higher mean corpuscular volume (OR, 1.27; 95% CI, 1.08 to 1.50), and higher alanine aminotransferase concentrations (OR, 1.005; 95% CI, 1.001 to 1.009) were more likely in APSS patients. Conclusions and Clinical Relevance-Several clinicopathologic differences between dogs with congenital and acquired shunts were identified; however, assessed alone, these would be unlikely to enable differentiation between the 2 conditions. Awareness of the rarity of ascites in CPSS cases should prompt recognition of a likely diagnosis of APSS, allowing the veterinarian to target further diagnostics and counsel the owner appropriately.     

Correlation between blood and milk serum leptin in goats and growth of their offspring

Boer and Boer crossbred meat-type does were used in two experiments to determine whether goat milk serum contains leptin and to investigate possible correlations of milk and serum leptin in does and subsequent growth of their offspring. Blood and milk samples were collected within 2 h of kidding (d 0) from 20 (Exp. 1; spring) or 22 does (Exp. 2; the following fall). Blood milk samples were then collected again on d 0.5, 1, 3, 5, 7, 14, 21, 28, 35, 42, 49, and 56 (Exp. 1) or d 0.5, 1, 2, 3, 4, 5, 6, 7, 14, and 21 (Exp. 2). Body weights of kids were recorded on d 0, and BW of kids and does were recorded weekly beginning on d 7 (kids) or 21 (does), with BCS also recorded for does beginning on d 28 for Exp. 1 and on d 0.5, 1, 2, 3, 4, 5, 6, 7, 14, and 21 for Exp. 2. Leptin was detected in colostral milk and was influenced by days postpartum, decreasing (P < 0.001) over time with an average of 4.4 +/- 0.3 ng/mL (Exp. 1) and 18.1 +/- 1.0 ng/mL (Exp. 2) on d 0 compared with 1.0 +/- 0.3 ng/mL on d 56 (Exp. 1) and 2.9 +/- 0.2 ng/mL on d 21 (Exp. 2). Day postpartum and milk serum leptin were negatively correlated (P < 0.001) for Exp. 1 (r = -0.27) and Exp. 2 (r = -0.46). For Exp. 1 only, blood serum leptin tended (P = 0.09) to be influenced by day, with a weak positive correlation (r = 0.15; P < 0.02). Weak positive correlations (P < 0.01) were found between blood serum leptin and doe BCS (r = 0.42 in Exp. 1, and r = 0.13 in Exp. 2) and doe BW (r = 0.44 in Exp. 1, and r = 0.26 in Exp. 2), with the absence of a stronger relationship likely due in part to the short time period measured and the lack of significant changes in BCS and BW during that time. In conclusion, leptin was present in milk and blood serum of does, and blood serum leptin was weakly correlated with doe BW and BCS, but it was not related to kid BW. Therefore, further studies are needed to clarify the relationships involving milk and serum leptin in goats.     

Leptin concentrations in periparturient ewes and their subsequent offspring

Leptin is an adipocyte-derived hormone that suppresses feed intake and increases energy expenditure. Leptin is also involved in regulating body temperature. Thus, the presence of leptin in milk, which can be absorbed through the gut of neonates immediately after birth, may aid in the survival of neonates born in cold weather. Our objectives were to determine the temporal relationship between concentrations of leptin in postpartum ewe blood serum and ewe milk serum, and to determine whether ewe blood and milk serum leptin concentrations were correlated with concentrations of leptin in lamb blood serum in their off-spring. Approximately 1 wk before the expected date of lambing, blood samples, weights, and body condition scores (BCS; 0 to 5 scale) were collected from 27 mixed-parity ewes. Following parturition, ewe blood and milk samples were collected within 2 h of parturition (d 0), 12 h (d 0.5) and 24 h (d 1) after parturition, again on d 5, and weekly thereafter until d 47. Lambs were blood-sampled and weighed within 2 h of parturition (d 0), bled daily until d 5, and bled and weighed weekly thereafter to d 47. Prior to lambing, ewe blood serum leptin was positively correlated with congruent BCS (r2 = 0, 10, P = 0.06), but not weight (P = 0.14). Following parturition, ewe blood serum leptin was positively correlated with BCS, weight, and milk serum leptin (r2 = 0.14, P < 0.0001, r2 = 0.12, P < 0.0001, and r2 = 0.028, P = 0.04). Leptin in milk serum was correlated with ewe weight (r2=0.05, P = 0.007) but not ewe BCS (P = 0.7); however, concentrations of leptin in both ewe blood and milk serum varied with day of lactation (P = 0.0001), being maximal within 24 h of parturition and declining to nadir concentrations by d 5. Leptin in lamb serum was correlated with milk serum leptin, (r2 = -0.05; P = 0.001), but not ewe blood serum leptin (P = 0.5). Concentrations of leptin in lamb serum increased from birth to d 5 and declined thereafter to nadir concentrations by d 19. Elevated concentrations of leptin in milk during the early stages of lactation may provide a mechanism for thermoregulation, satiation, and homeostatic endocrine control in the neonate.     

Defaecation syncope and pulmonary thromboembolism in a cat

A 7-year-old male neutered domestic shorthair cat was referred for worsening gastrointestinal and haematologic abnormalities. Physical status deteriorated further despite intravenous crystalloids, blood transfusion and nutritional support. Cardiorespiratory signs developed and the cat died suddenly while straining to defaecate. Diffuse thrombosis, pulmonary thromboembolism, metastatic pancreatic carcinoma and histologic evidence of cardiomyopathy were present at necropsy. This is the first reported case of feline pulmonary thromboembolism associated with defaecation syncope. Predisposing factors for thrombotic disease in this case and aspects of human defaecation syncope are discussed. The risk of clot dislodgement by the Valsalva manoeuvre in patients with a thrombotic tendency is highlighted.     

Unconventional aqueous humor outflow of microspheres perfused into the equine eye

Normal drainage of aqueous humor from the anterior chamber of the equine eye occurred through conventional and unconventional routes. To determine the degree of uveoscleral outflow in the pony, 1- and 3-microns (diam) microspheres were perfused through the anterior chamber for 60 and 90 minutes. Two eyes were treated with pilocarpine before perfusion of spheres to observe any effect on outflow. Presence of spheres was detected by scanning electron microscopy and verified by light microscopy. By 60 minutes of the perfusion, 1- and 3-microns spheres thoroughly infiltrated the anterior uveal trabecular meshwork. The 3-microns spheres were notably excluded from the corneoscleral trabecular meshwork, whereas the 1-micron spheres packed into the corneoscleral trabecular meshwork and mixed with the angular aqueous plexus and intrascleral plexus vessels. After 90 minutes, 1- and 3-microns spheres penetrated the prominent supraciliary space and mixed with the suprachoroidea of the midchoroid. The 1-micron spheres infiltrated tissues more extensively than did the 3-microns spheres, packing into the anterior meshwork and supraciliary space and also moving as far posterior as the suprachoroidea of the peripapillary retina. Spheres also entered the iris, mostly at the root. Several 3-microns spheres moved into the interstitial spaces around axon bundles and vessels in the iris. The 1-micron spheres packed into these spaces in the iris root and were observed in the lumens of iris vessels. Single 1-micron spheres were observed in the lumens of choroidal vessels posteriorly. The present study supported evidence for uveoscleral and uveovortex flow in the horse and indicated that it may be more extensive than that in other species investigated (ie, the dog).     

An epidemiological investigation of an idiopathic myopathy in hunting dogs in New Zealand

AIM: To conduct an epidemiological investigation of an idiopathic myopathy, known as “Go Slow” (GSM), which was initially recognised in dogs used for pig hunting. A secondary aim was to describe the hunting activities, diet and health of dogs used for pig hunting in New Zealand.

METHODS: A retrospective cohort study was conducted between June 2014–June 2017. Cases of GSM in dogs were diagnosed by veterinarians using a combination of clinical history, physical examination findings, serum biochemistry and/or skeletal muscle histology. A telephone interview was conducted with the owner or primary veterinarian to provide information regarding the dog’s diet and exercise over the 7 days preceding the onset of clinical signs. In August 2015, a separate online survey of owners of dogs used for pig hunting was conducted to characterise the normal hunting activities, diet and health of these dogs.

RESULTS: A total of 86 cases of GSM were recruited, of which 58 (67%) were pig hunting dogs, 16 (19%) pet dogs and 12 (14%) working farm dogs. Cases were most commonly reported in the upper North Island, and 65 (76 (95% CI=67–85)%) were from the Northland region. Processed commercial dog food had been fed to 93 (95% CI=88–98)% of affected dogs. Ingestion of raw, frozen or cooked wild pig in the preceding week was reported for 76 (88 (95% CI=82–95)%) dogs with the myopathy. In the survey of owners of healthy pig hunting dogs, 203 eligible responses were received; pig hunting was reported to most commonly occur in Northland (20.2%), Waikato (22.3%) and Bay of Plenty (23.2%) regions. Commercial dog food was fed to 172 (85 (95% CI=80–90)%) of the dogs included in this survey, and 55 (27 (95% CI=20–33)%) had eaten wild pig in the preceding week. The most common reported health problem in pig hunting dogs was traumatic wounds.

CONCLUSIONS: Cases of GSM were most commonly recognised in dogs used for pig hunting, but also occurred in pet and working farm dogs. The disease was most frequently reported in the upper North Island of New Zealand and ingestion of wild pig was a consistent feature in cases of this myopathy.

CLINICAL RELEVANCE: To minimise the risk of dogs developing this myopathy, it would seem prudent to avoid feeding any tissues from wild pigs to dogs in areas where the disease is known to occur.     

Malignant neoplasia in four alpacas.

Malignant neoplasia in 4 alpacas was characterized by acute onset of clinical signs and rapidly deteriorating condition. Postmortem examination revealed metastatic or multicentric neoplasia in the abdominal organs of alpacas 1, 3, and 4 and an extensive thoracic mass in alpaca 2. Immunohistochemical stains supported a diagnosis of B-cell lymphosarcoma in alpacas 1-3 and a neuroendocrine neoplasm in alpaca 4.