Ultrasonographic features of gallbladder wall thickening in dogs with hypoalbuminemia.

Hypoalbuminemia has been considered as a cause of gallbladder wall thickening in humans and dogs. Recent study revealed that gallbladder wall thickening in dogs with hypoalbuminemia may not be associated with serum albumin/plasma levels within 48 h of ultrasound study. However, gallbladder wall edema may change within 48 h, and the ultrasonographic features of gallbladder wall thickening in dogs with hypoalbuminemia have not been reported. The purpose of this study is to describe the relationship between serum albumin levels within 24 h of ultrasound and gallbladder wall thickening, and to describe the ultrasonographic features of thickened gallbladder walls in dogs with hypoalbuminemia. 37 hypoalbuminemic dogs with gallbladder ultrasound images were retrospectively included. Ultrasound studies were reviewed, and gallbladder wall thickness, layering appearance, echogenicity, echotexture, distribution, evidence of gallbladder mucocele, and presence of peritoneal effusion were recorded. Additionally, serum albumin levels within 24 h of ultrasound study and the administerd sedation were recorded. The prevalence of gallbladder wall thickening in dogs with hypoalbuminemia was 13.5%. The 3-layer appearance of the gallbladder wall was observed in 4 dogs, and a single-layer gallbladder wall thickening in one dog. Diffuse thickening was observed in all 5 dogs. The serum albumin level of dogs with gallbladder wall thickening was not different (p = 0.14) from dogs without thickening. Gallbladder wall thickening was not common, occurring only with mild hypoalbuminemia, and was commonly associated with a 3-layer appearance and considered as gallbladder wall subserosal edema. Causes other than hypoalbuminemia may be responsible for thickening of the gallbladder wall in dogs with hypoalbuminemia.

Disseminated Halicephalobus gingivalis infection in a horse.

A 19-y-old American Saddlebred gelding was evaluated for epiphora of the right eye and generalized cachexia. Initial examination revealed anterior uveitis without ulceration, for which treatment was initiated. Despite the initial response to treatment, the signs progressively worsened to blindness. Histologic examination of the enucleated eye revealed granulomatous panuveitis and optic neuritis with intralesional nematode larvae identified as Halicephalobus gingivalis. Over time and despite anthelmintic treatment, blindness developed in the left eye along with neurologic signs, and the horse was euthanized. Disseminated halicephalobosis was diagnosed on postmortem examination, involving the heart, spleen, kidneys, oral cavity, tongue, left eye, lungs, CNS, adrenal glands, liver, and lymph nodes. Splenic involvement has not been reported previously, to our knowledge. Halicephalobosis is a sporadic parasitic disease that affects equids mostly and for which prognosis is poor despite aggressive systemic anthelmintic treatment. Parasitic granulomatous disease should be included as a differential diagnosis in equids with ocular or neurologic disease.

CT features of confirmed and presumed gastric wall edema in dogs.

Postcontrast computed tomographic (CT) characteristics of gastrointestinal (GI) wall edema in humans have been described as GI wall thickening with a thickened submucosal layer and thin enhanced inner and outer layers. Published studies describing CT features of gastric wall edema in dogs are currently lacking. The aim of this retrospective, case series was to describe CT features of gastric wall edema in a group of dogs. Medical records were searched for dogs with postcontrast abdominal CT scans and a diagnosis of gastric wall edema based on histopathology (group I) or CT characteristics consistent with those reported in humans (group II). Clinical diagnosis, mean serum albumin concentration, and histopathological diagnosis were recorded. The following CT characteristics were recorded: numbers of wall layers, attenuation and contrast enhancement, presence of blood vessels, locations, distribution, and thickness. Twelve dogs (3 in group I and 9 in group II) were included. The most common clinical finding was hypoalbuminemia. In group I, a well-defined three-layer appearance with a non-enhancing fluid-attenuating middle layer was observed in three dogs and thin blood vessels in the middle layer in two dogs. In group II, nine dogs had a three-layer appearance with a non-enhancing fluid-attenuating middle layer. Locations of gastric wall thickening were diffuse in two, focal concentric in six, and focal asymmetric in four dogs. Findings supported including gastric wall edema as a differential diagnosis for dogs with hypoalbuminemia and CT characteristics of a three-layer appearance in the gastric wall, with a non-enhancing fluid-attenuating middle layer and thin blood vessels.

Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

Malakoplakia in the Urinary Bladder of 4 Puppies.

Malakoplakia in humans most often affects the urinary bladder and is characterized by inflammation with von Hansemann-type macrophages, with or without Michaelis-Gutmann bodies, and is frequently associated with Escherichia coli infection. We describe the microscopic features of malakoplakia in the urinary bladder of 4 puppies. In all cases, the lamina propria of the urinary bladder was markedly expanded by sheets of large, round to polygonal macrophages with intracytoplasmic, periodic acid-Schiff-positive granules and granular inclusions, and rare Prussian blue-positive inclusions. Macrophages were positive for CD18 and Iba1. In 2 cases, Michaelis-Gutmann bodies were detected with hematoxylin and eosin stain and were best demonstrated with von Kossa stain. E. coli infection was confirmed in 2 cases with bacterial culture or polymerase chain reaction (PCR) and sequencing of the bacterial 16S ribosomal RNA gene. Transmission electron microscopy of one case demonstrated macrophages with abundant lysosomes, phagolysosomes, and rod-shaped bacteria. Microscopic features were similar to human cases of malakoplakia. In dogs, the light microscopic characteristics of malakoplakia closely resemble granular cell tumors and histiocytic ulcerative colitis.

Diagnosis of Collagen Type III Glomerulopathy Using Picrosirius Red and PASH/Masson's Trichrome Stain.

Canine collagen type III glomerulopathy (Col3GP) is a rare juvenile nephropathy in which irregular type III collagen fibrils and fibronectin accumulate in glomerular capillary walls and the mesangium. Necropsy findings were reviewed from 5 puppies diagnosed with Col3GP at 6 to 18 weeks of age. Histologically, with hematoxylin and eosin stain, the glomerular capillary walls and mesangium were diffusely and globally expanded by homogeneous pale eosinophilic material. Ultrastructurally, the subendothelial zone and mesangium were expanded by fibronectin and cross-banded collagen type III fibrils, diagnostic of Col3GP. Two additional stains were employed to identify the material within glomeruli as fibrillar collagen using light microscopy. In all 5 cases, the material was red with picrosirius red and birefringent under polarized light, and was blue with periodic acid-Schiff/hematoxylin/trichrome (PASH/TRI), thereby identifying it as fibrillar collagen. Based on these unique staining characteristics with picrosirius red and PASH/TRI, Col3GP may be reliably diagnosed with light microscopy alone.

Ultrasonographic features and prevalence of presumed gastric wall edema in dogs with hypoalbuminemia.

BACKGROUND: Ultrasonographic features of gastric wall edema have not been reported in dogs with hypoalbuminemia. OBJECTIVES: To describe the prevalence and ultrasonographic features of gastric wall thickening in dogs with hypoalbuminemia and analyze correlation with serum albumin concentrations. ANIMALS: Forty-two dogs with abdominal ultrasound and diagnosis of hypoalbuminemia (<2.3 g/dL). METHODS: Retrospective search in the medical records from 2018 to 2019 was performed. Ultrasound studies were reviewed and >5 mm were considered gastric wall thickening. The gastric wall changes such as thickness, layering appearance, echogenicity, echotexture, distribution of lesions, and presence of peritoneal effusion were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. Mean serum albumin concentration of dogs with and without gastric wall thickening was compared. RESULTS: Prevalence of gastric wall thickening in dogs with hypoalbuminemia was 21.4% (95% confidence intervals 7.4-35.4%). Mean gastric wall thickness was 10.0 ± 2.0 mm. Preserved mucosal layer and thickening of submucosal layer were observed in all 9 dogs. Five dogs had 3-layer appearance in thickened submucosal layer. Diffuse wall thickening was observed in 6 dogs. All 9 dogs had peritoneal effusion. Subsequent changes of gastric wall thickening were observed in 3 dogs (range 4-70 days). Gastric wall edema was confirmed histopathologically in 2 dogs via necropsy. There was no correlation between serum albumin concentration of the dogs and gastric wall thickness. CONCLUSIONS AND CLINICAL IMPORTANCE: Findings indicated that gastric wall edema is a common finding in dogs with hypoalbuminemia. However, serum albumin concentrations did not correlate with the gastric wall thickness.

Radiographic and computed tomographic appearance of caseous lymphadenitis in a goat.

A 2-year-old Boer doe was presented with respiratory distress and severe inspiratory dyspnea. Cervical and thoracic radiographs revealed a marked retropharyngeal soft tissue mass effect, several mineralized pharyngeal and retropharyngeal structures, and a pulmonary mass. Computed tomography (CT) revealed a severely enlarged right medial retropharyngeal lymph node, which caused laryngeal compression, leading to upper airway obstruction. Multiple cervical and thoracic lymph nodes, and the pulmonary mass had an irregular layered/laminated pattern of mineralization. Imaging findings were consistent with caseous lymphadenitis, and further confirmed with culture, necropsy, and histopathology. This is the first report of CT appearance of caseous lymphadenitis in a goat.

Disseminated Rhodococcus equi in an Anglo-Nubian goat.

Disseminated Rhodococcus equi infection was diagnosed in an Anglo-Nubian goat presenting for non-weight bearing lameness of the right pelvic limb. Radiographs showed a moth-eaten osteolytic lesion in the proximal tibia suggestive of an aggressive bone lesion. Two pulmonary nodules were also present on thoracic radiographs. Initial antemortem cytology of the tibial lesion was suggestive of Rhodococcosis and the goat was sent to necropsy. Necropsy and bacterial culture confirmed the diagnosis of disseminated R. equi infection in the right tibia, lungs, and liver.

A case of hypercalcemia in a heifer presumably due to mammary carcinoma bovine hypercalcemia of malignancy.

Mammary carcinoma is rare in cattle with only a handful of cases found in the literature, and none have reported an associated hypercalcemia. An 8-year-old Holstein-Friesian heifer was presented to the Purdue University Veterinary Teaching Hospital's Large Animal Hospital with a 3-month history of lethargy. Laboratory abnormalities included ionized hypercalcemia and hypophosphatemia (2.28 mmol/L and 1.8 mg/dL, respectively). Physical examination revealed a mammary mass that was cytologically described as a suspected mammary carcinoma, which was later confirmed by histologic evaluation. On surgical removal of the mass, calcium initially decreased rapidly, and within a few days was within the RI, further supporting a diagnosis of hypercalcemia of malignancy in a heifer. However, attempts to confirm this using hormone profiles (parathyroid hormone [PTH], parathyroid hormone-related protein [PTHrp], and calcitriol) were inconclusive due to the lack of validated assays and RIs for cattle. Immunohistochemical staining for PTHrP showed scattered cytoplasmic staining among the neoplastic cells, suggesting PTHrP production by these cells.

Ultrasonographic features of presumed gastric wall edema in 14 dogs with pancreatitis.

BACKGROUND: Gastric wall edema has not been reported as a complication of acute pancreatitis in dogs. OBJECTIVE: To describe the ultrasonographic features of gastric wall thickening in dogs with acute pancreatitis. ANIMALS: Fourteen dogs with ultrasonographic evidence and clinical diagnosis of acute pancreatitis, with ultrasonographic evidence of increased gastric wall thickness (>5 mm). METHODS: A retrospective search in the medical records from 2014 to 2016 was performed to identify dogs that had ultrasonographic evidence of acute pancreatitis, that had increased thickness of the gastric wall and that were diagnosed with acute pancreatitis clinically. The gastric wall changes such as thickness, layering appearance, echogenicity, distribution of lesions, and perigastric changes were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. RESULTS: Mean gastric wall thickness was 9.9 ± 4.0 mm (SD). A complete loss of wall layering was observed in 2 dogs. Thickening of the submucosal layer was observed in 12 dogs, and 5 of them had concurrent muscularis layer thickening. The echogenicity of thickened submucosal layer was intermediate hyperechoic. Lacy appearances were present within the thickened submucosal layer in 7 dogs and in the muscularis layer of 1 dog. Thickening was focal in 12 dogs and adjacent to the diseased pancreas. Subsequent resolution of gastric wall thickening was observed in 3 dogs (range 3-28 days) via follow-up ultrasound. One dog underwent necropsy, and gastric wall edema was confirmed histopathologically. CONCLUSIONS AND CLINICAL IMPORTANCE: Findings indicated that gastric wall thickening presumably because of edema could be a complication of acute pancreatitis.

Role of Response-to-Diuretic in Predicting Prognosis in Discharged Heart Failure Patients After an Acute Decompensation.

BACKGROUND: The diuretic response has been shown to be a robust independent marker of cardiovascular outcomes in acute heart failure (ADHF) patients. The objectives of this clinical research, will aim are to: a) include diuresis in the formula for diuretic response (R-to-D); b) add to R-to-D the value of a pre-discharged determination of galectin-3 and BNP in predicting mid-term clinical outcome. METHODS: Consecutive patients discharged alive after an ADHF were enrolled. All patients underwent BNP and galectin-3, a 6 min walk test and an echocardiogram together with diuresis and body weight during diuretic administration. Death by any cause, cardiac transplantation and worsening HF requiring readmission to the hospital were considered cardiovascular events. RESULTS: 141 patients (98 males, age 73.8) were analysed (follow-up 17 months). During the follow-up 45 (31.9%) events were scheduled (19 cardiac deaths, 26 re-hospitalisation for HF). Patients who experienced CV-event had a worst renal function (p = 0.003), an higher BNP (p = 0.006) and galectin-3 (p = 0.008). At multivariate analysis, only R-to-D, galectin-3 and BNP showed a significant correlation with worst clinical prognosis (respectively p = 0.043; OR 6.01; p = 0.01; OR 8.9; p = 0.02 OR 10.38), independently of age and renal function. Kaplan-Meier curves depicted a powerful stratification using an R-to-D <1.2 kg/40 mg furosemide (log rank 10.96; p = 0.0009). Adding R-to-D<1.2 mg/40 mg furosemide to galectin-3>17.6 pg/mL and BNP>500 pg/mL the predictive value improved (log rank 23.59; p = 0.0001). CONCLUSION: Adding R-to-D to Gal-3 and BNP, a single pre-discharge strategy testing seemed to obtain a satisfactorily predictive value in alive HF patients discharged after an ADHF episode.

Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis.

Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and anti-angiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.

Role of galectin-3 and plasma B type-natriuretic peptide in predicting prognosis in discharged chronic heart failure patients.

Galectin-3 demonstrated to be a robust independent marker of cardiovascular mid-term (18-month) outcome in heart failure (HF) patients. The objective of this study was to analyze the value of a predischarged determination of plasma galectin-3 alone and with plasma brain natriuretic peptide (BNP) in predicting mid-term outcome in frequent-flyers (FF) HF (≥2 hospitalization for HF/year)/dead patients discharged after an acute decompensated HF (ADHF) episode.All FF chronic HF subjects discharged alive after an ADHF were enrolled. All patients underwent a determination of BNP and galectin-3, a 6-minute walk test, and an echocardiogram within 48 hours upon hospital discharge. Death by any cause, cardiac transplantation, and worsening HF requiring readmission to hospital were considered cardiovascular events.Eighty-three patients (67 males, age 73.2 ±â€Š8.6 years old) were analyzed (mean follow-up 11.6 ±â€Š5.2 months; range 4-22 months). During the follow-up 38 events (45.7%) were scheduled: (13 cardiac deaths, 35 rehospitalizations for ADHF). According to medical history, in 33 patients (39.8%) a definition of FF HF patients was performed (range 2-4 hospitalization/year). HF patients who suffered an event (FF or death) demonstrated more impaired ventricular function (P = 0.037), higher plasma BNP (P = 0.005), and Gal-3 at predischarge evaluation (P = 0.027). Choosing adequate cut-off points (BNP ≥ 500 pg/mL and Gal-3 ≥ 17.6 ng/mL), the Kaplan-Meier curves depicted the powerful stratification using BNP + Gal-3 in predicting clinical course at mid-term follow-up (log rank 5.65; P = 0.017).Adding Gal-3 to BNP, a single predischarge strategy testing seemed to obtain a satisfactorily predictive value in alive HF patients discharged after an ADHF episode.

Cardiolipin profiles as a potential biomarker of mitochondrial health in diet-induced obese mice subjected to exercise, diet-restriction and ephedrine treatment.

Cardiolipin (CL) is crucial for mitochondrial energy metabolism and structural integrity. Alterations in CL quantity or CL species have been associated with mitochondrial dysfunction in several pathological conditions and diseases, including mitochondrial dysfunction-related compound attrition and post-market withdrawal of promising drugs. Here we report alterations in the CL profiles in conjunction with morphology of soleus muscle (SM) and brown adipose tissue (BAT) in diet-induced obese (DIO) mice, subjected to ephedrine treatment (EPH: 200 mg kg(-1) day(-1) orally), treadmill exercise (EX: 10 meters per min, 1 h per day), or dietary restriction (DR: 25% less of mean food consumed by the EX group) for 7 days. Mice from the DR and EPH groups had a significant decrease in percent body weight and reduced fat mass compared with DIO controls. Morphologic alterations in the BAT included brown adipocytes with reduced cytoplasmic lipid droplets and increased cytoplasmic eosinophilia in the EX, DR and EPH groups. Increased cytoplasmic eosinophilia in the BAT was ultrastructurally manifested by increased mitochondrial cristae, fenestration of mitochondrial cristae, increased electron density of mitochondrial matrix, and increased complexity of shape and elongation of mitochondria. Mitochondrial ultrastructural alterations in the SM of the EX and DR groups included increased mitochondrial cristae, cup-shaped mitochondria and mitochondrial degeneration. All four CL species (tri-linoleoyl-mono-docosahexaenoyl, tetralinoleoyl, tri-linoleoyl-mono-oleoyl, and di-linoleoyl-di-oleoyl) were increased in the BAT of the DR and EPH groups and in the SM of the EPH and EX groups. In conclusion, cardiolipin profiling supported standard methods for assessing mitochondrial biogenesis and health, and may serve as a potential marker of mitochondrial dysfunction in preclinical toxicity studies.