Spinal lymphoma in a goat.

A 3-year-old Pygmy Wether was presented for chronic hindlimb paralysis. A neurological exam revealed nonambulatory paraplegia with absent deep pain nociception, lack of hindlimb withdrawal reflexes, and paraspinal pain on palpation with T3 to L3 neurolocalization. MRI of the lumbar spine revealed an extensive, dorsal to dorsolateral, severely compressive, heterogeneously contrast-enhancing extradural lesion of the lumbar spine with intervertebral foraminal extension into the surrounding paraspinal musculature. Vertebral bone marrow involvement was also noted in the L5 and L6 vertebrae. A diagnosis of lymphoma was obtained after cytological sampling. This is the first case report describing specific MRI findings (signal characteristics, enhancement pattern, and perilesional changes) in a goat with paraspinal lymphoma.

Ultrasonographic diagnosis of a lymphomatous lymph node presumptively infiltrating the ureter causing hydronephrosis in a 3-year-old dog.

A 3-year-old male neutered mixed breed dog was presented for chronic vomiting and diarrhea. Abdominal ultrasound revealed a large amorphous, heterogeneous mass within the left mid to caudal abdomen most consistent with medial iliac lymph node. It appeared to invade the left ureter and extend distally causing ureteral obstruction and hydronephrosis. Concurrent additional ultrasound findings were consistent with metastatic or multicentric neoplasia. Fine needle aspirates of the lymph node and spleen both confirmed large cell lymphoma. These findings present evidence of lymphoma invading directly from an organ into the ureter which has not previously been reported in dogs.

Echocardiographic and radiographic aortic remodeling in cats with confirmed systemic hypertension.

Systemic hypertension (SH) in cats may occur secondary to renal disease, hyperthyroidism, or idiopathic causes. Asymmetric dilation of the sinuses of Valsalva has been recognized in people with systemic hypertension as target organ damage (TOD). Aortic knob formation (lateral bowing of the aortic arch to proximal descending aorta on the posteroanterior/anteroposterior radiographic projection) is recognized as TOD in people due to SH. None of these changes have been reported in feline patients. The first objective of this retrospective case-controlled study was to compare echocardiographic changes in the aorta of 76 cats with systemic hypertension (SH) to those seen in 76 cats with normal blood pressure (NBP). Our second objective was to have blinded reviewers assess heart size and aortic shape and size from available thoracic radiographs of 49/76 cats with SH and 46/76 cats with NBP. A two-way unpaired t-test with significance set at alpha = 0.01 was used to evaluate aortic echocardiographic parameters. The mean of the aortic diameter and length of each aortic cusp was significantly larger in cats with SH than in cats with NBP. The aortic cusps were considered altered in size in 62 of 76 cats with SH, 12/62 ≥ with 0.5 mm, and 50/62 ≥ 1.0 mm. No significant difference in the vertebral heart score (VHS) was noted between groups. The aortic knob to lateral margin of the trachea in cats with SH had an area under the curve (AUC) of 0.74 (95% CI:0.61-0.87) with best cutoff of 1.12 cm with sensitivity of 81% and specificity of 69%.

An observational thoracic radiographic study of aortic remodeling in dogs with confirmed systemic hypertension.

Sustained systemic hypertension (SH) has been shown to cause target organ damage to various tissues in dogs and cats, including the aorta. Aortic dilatation occurs most commonly secondary to SH in people and develops prior to an aortic aneurysm. Our hypothesis was that blinded reviewers could be trained to recognize variable alterations of aortic shape and size on thoracic radiographs of canine patients with SH. A retrospective, observational, cross-sectional study was performed with three blinded reviewers evaluating thoracic radiographic images of 21 dogs with normal blood pressure compared to 145 dogs with system hypertension. Lateral radiographs showed variable aortic undulation and disproportionate enlargement of a portion of the aorta between the ascending and proximal descending aorta compared to the descending aorta just cranial to the diaphragm. On orthogonal projections, the aortic arch to proximal descending aorta bowed laterally similar to changes reported in people with the formation of an aortic "knob." After completing a training module, reviewers of the thoracic images had a 74% agreement with Fleiss' Kappa of 0.50 indicating moderate agreement recognizing SH changes to the thoracic aorta. The more experienced blinded reviewers had accuracies of 85% and 80% for identifying systemic hypertension, slightly better than the less experienced reviewer at 76%. The ratio of thoracic cavity width to aortic knob width was significantly different between the groups (median ratio 3.4 SH vs 4.1 normal). Evidence of target organ damage (TOD) to the thoracic aorta may prompt earlier recognition and treatment for systemic hypertension.

Echocardiographic changes in the shape and size of the aortic cusps in dogs with confirmed systemic hypertension.

Systemic hypertension (SH) in dogs typically occurs secondary to renal disease, diabetes mellitus, hyperadrenocorticism, malignant adrenal tumors, or various medications. Echocardiography performed on people with SH has shown asymmetric dilation of the sinuses at the level of the aortic valves, previously undescribed in canine patients. The objective of this retrospective case-control study was to determine if there was a difference in size and shape of the aortic cusps at the level of the sinus of Valsalva in dogs with SH compared to dogs with normal blood pressure. We reviewed echocardiographic findings in 74 dogs with SH and 37 dogs with normal blood pressure (NBP), defined as less than 150 mmHg. Systemic hypertension was classified as mild (150-159 mm Hg), moderate (160-179 mm Hg), or severe (greater than 180 mm Hg). There was a significant difference (P < .001) in the mean size of the aorta cusps at the level of the sinuses in 67 of 74 dogs with SH and none of 37 dogs with NBP. Of the 74 dogs with SH, 70 had left ventricular hypertrophy (18 asymmetric, 15 concentric, and 37 eccentric). Additionally, there was aortic root dilatation in 15 dogs, aortic insufficiency in 21, mitral regurgitation in 50, and left atrial enlargement in 71. The standard deviation of the three cusp measurements between the dogs with SH and dogs with NBP had a sensitivity of 92% and specificity of 97% for diagnosis of SH. Asymmetric size of the aortic cusps on echocardiography is therefore a reliable indicator of SH in dogs.

Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension.

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross-sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta-caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta-caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.

Mucopolysaccharidosis-like phenotype in feline Sandhoff disease and partial correction after AAV gene therapy.

Sandhoff disease (SD) is a fatal neurodegenerative disease caused by a mutation in the enzyme ß-N-acetylhexosaminidase. Children with infantile onset SD develop seizures, loss of motor tone and swallowing problems, eventually reaching a vegetative state with death typically by 4years of age. Other symptoms include vertebral gibbus and cardiac abnormalities strikingly similar to those of the mucopolysaccharidoses. Isolated fibroblasts from SD patients have impaired catabolism of glycosaminoglycans (GAGs). To evaluate mucopolysaccharidosis-like features of the feline SD model, we utilized radiography, MRI, echocardiography, histopathology and GAG quantification of both central nervous system and peripheral tissues/fluids. The feline SD model exhibits cardiac valvular and structural abnormalities, skeletal changes and spinal cord compression that are consistent with accumulation of GAGs, but are much less prominent than the severe neurologic disease that defines the humane endpoint (4.5±0.5months). Sixteen weeks after intracranial AAV gene therapy, GAG storage was cleared in the SD cat cerebral cortex and liver, but not in the heart, lung, skeletal muscle, kidney, spleen, pancreas, small intestine, skin, or urine. GAG storage worsens with time and therefore may become a significant source of pathology in humans whose lives are substantially lengthened by gene therapy or other novel treatments for the primary, neurologic disease.

Ultrasonographic evaluation of adrenal gland size compared to body weight in normal dogs.

The accepted cut-off value for adrenal gland maximum diameter of 0.74 cm to distinguish adrenal gland enlargement in dogs regardless of body weight may not be appropriate for small to medium breed dogs. The purpose of the current retrospective study was to examine adrenal gland dimensions as a function of body weight in healthy dogs in three weight categories (< 10 kg, 10-30 kg, and > 30 kg) representing small, medium, and large breeds, respectively, to establish greater confidence in determining if adrenal gland size is abnormal. The measurements of length (sagittal plane), cranial and caudal pole thickness (sagittal and transverse planes), and caudal pole width (transverse plane) of both adrenal glands were obtained ultrasonographically in clinically healthy dogs (n = 45) with 15 dogs in each weight group. Findings support our hypothesis that adrenal gland size correlates with body weight in normal dogs, and more precise reference intervals should be created for adrenal gland size by categorizing dogs as small, medium, or large breed. The caudal pole thickness of either adrenal gland in a sagittal plane was the best dimension for evaluating adrenal gland size based on low variability, ease, and reliability in measurement.

Ultrasound dilution cardiac output and echocardiography findings in anesthetized mature alpacas (Vicugna pacos) during normotension, hypotension and hypertension.

Alpacas (Vicugna pacos) have physiologic adaptations to live at high altitude. These adaptations may result in unexpected responses to changes in cardiac performance and blood pressure during general anesthesia. There are few studies evaluating cardiovascular variables in anesthetized alpacas. The purpose of this study was to report cardiovascular performance in anesthetized mature alpacas during normotension, hypotension, and hypertension using ultrasound dilution and echocardiography. Six adult alpacas, 3 females and 3 castrated males, weighing 62.6 to 88.7 kg were anesthetized and maintained with isoflurane and placed in right lateral recumbency. Each alpaca underwent ultrasound dilution and echocardiography measurements during three cardiovascular phases, normotension, hypotension via increased isoflurane concentration, and hypertension via phenylephrine infusion. Variables were analyzed with a Friedman test and a post hoc Dunn's test when significant. A p < 0.05 was used for significance. Cardiac output, cardiac index, systemic vascular resistance, stroke volume, total ejection fraction, left ventricular internal diameter during diastole, and total stroke volume indexed to body weight were greater for hypertension compared to hypotension. Total ejection fraction, stroke volume, and left ventricular ejection time were greater for hypertions compared to normotension. There was no difference between ultrasound dilution and echocardiography determined cardiac output measurements within each cardiovascular phase. Phenylephrine appeared to have increased ventricular performance and/or increased preload in anesthetized, mature alpacas. For detecting change in cardiovascular status in anesthetized alpacas, ultrasound dilution and echocardiography may be useful.

Case report: Intraneural perineurioma in dogs: a case series and brief literature review.

Intraneural perineurioma is an exceptionally rare neoplasm in animals. This case study comprises a series of three cases and a brief literature review focusing on canine intraneural perineurioma. The pathological and immunohistochemical findings are documented, revealing that canine intraneural perineurioma frequently affects adult dogs aged between 3 and 10 years old, with a male predominance. Clinical signs associated with intraneural perineurioma in dogs include spinal pain, lameness, and paresis, resulting from the involvement of spinal nerve roots of the pelvic limbs, brachial plexus, or distal part of the median nerve. Most neoplasms had characteristic pseudo-onion bulb patterns on histopathology. Neoplastic perineurial cells, in most cases, expressed laminin and claudin-1, and NF200 consistently highlighted the central axon. While the immunohistochemical (IHC) profile of intraneural perineurioma in veterinary medicine remains incompletely characterized, the available IHC data from all reported cases suggest that a combination of laminin and claudin-1 immunomarkers, along with distinctive histological features, can assist in establishing a definitive diagnosis of intraneural perineurioma.

Case report: Tunneling foreign body in the metatarsal bones of a dog.

A 2-year-old male intact goldendoodle presented for intermittent lameness, persistent draining tracts, and radiographic identified boney lytic lesions involving the metatarsal region, which had persisted for approximately 8 months before presentation to our referral hospital. Radiographic and computed tomography (CT) images suggested a tubular structure encircling and tunneling through the right metatarsal bones. Exploratory surgery confirmed a circumferential rubber band foreign body, with lytic boney tunneling within the metatarsal bones. CT provided vital information to assist in the surgical planning for this patient with a chronic tunneling foreign body.

Multimodal treatment of recurrent sinonasal cryptococcal granulomas in a horse.

CASE DESCRIPTION: A 7-year-old 509-kg (1,120-lb) Tennessee Walking Horse mare was evaluated because of bilateral mucosanguinous nasal discharge, intermittent right-sided epistaxis, and worsening dyspnea of 9 months' duration. CLINICAL FINDINGS: Multiple masses in the nasopharynx were detected via endoscopic and radiographic examinations. Cytologic and histologic examinations of biopsy specimens of 1 mass revealed round yeasts with thick nonstaining capsules and occasional narrow-based budding that resembled cryptococcal organisms. TREATMENT AND OUTCOME: Oral administration of fluconazole and organic ethylenediamine dihydriodide and intermittent intralesional injections with fluconazole, amphotericin B, and formalin resulted in resolution of lesions for a period of 2.5 years. The horse then developed exophthalmos, recurring clinical signs, and extensive nasopharyngeal masses. The masses were surgically debulked via a large frontonasal bone flap, and the horse was treated with IV injections of amphotericin B and long-term oral administration of fluconazole. Clinical signs did not recur in the following 2-year period. A presumptive diagnosis of cryptococcosis was made following cytologic and histologic evaluations of the masses; results of serologic analysis and fungal culture confirmed infection with Cryptococcus neoformans. CLINICAL RELEVANCE: Cryptococcal infection of the upper respiratory tract in horses has previously been described as a uniformly fatal disease. As this case report illustrates, medical and surgical treatment of sinonasal cryptococcal granulomas in horses may be successful, but the importance of long-term follow-up and the potential for disease recrudescence should be considered. As efficacious antifungal agents become less expensive, their increased use will likely decrease mortality rates in horses with fungal infections.

Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats.

Mast cells have diverse roles throughout the body as evidenced by their heterogeneous nature. In the heart, cardiac mast cells have been implicated in left ventricular (LV) remodeling in response to elevated myocardial stress. Accordingly, the purpose of this study was to use mast cell deficient rats (Ws/Ws) to delineate the interaction between cardiac mast cell activation and LV remodeling. LV matrix metalloproteinase (MMP) activity, fibrillar collagen, TNF-alpha levels, and LV diameter were compared in Ws/Ws and wild type (WT) rats subjected to 5 d (n=3/group) and 8 weeks (n=4/group) of aortocaval fistula-induced volume overload. In contrast to attenuation of myocardial remodeling in the Ws/Ws group: 1) MMP-2 activity was significantly increased in the WT group at 5 days; 2) there was marked degradation of the extracellular collagen matrix in WT at 5 days and 8 weeks; 3) the percent increase in LV diameter from baseline was significantly greater in WT at 2, 4, 6, and 8 weeks post-fistula; and 4) myocardial TNF-alpha levels were markedly elevated in the WT group at 5 days post-fistula. These results underscore the importance of cardiac mast cells in mediating MMP activation, collagen degradation and LV dilatation and suggest that mast cell-derived TNF-alpha plays a role in early myocardial remodeling.

Defective intracellular Ca2+ homeostasis contributes to myocyte dysfunction during ventricular remodelling induced by chronic volume overload in rats.

1. Previous studies have demonstrated progressive ventricular hypertrophy, dilatation and contractile depression in response to chronic volume overload. Whether this decompensation was related to intrinsic myocyte dysfunction was not clear. The present study evaluated ventricular myocyte function at critical times during the progression of ventricular remodelling induced by volume overload. 2. Chronic volume overload was induced with an infrarenal aortocaval fistula in rats. Myocyte contraction and intracellular Ca(2+) concentrations ([Ca(2+)](i)) were evaluated using a fura-2 fluorescence and edge detection system. Protein levels of sarcoplasmic reticulum (SR) Ca(2+) transporters were determined by western blots. Progressive ventricular dilatation developed following creation of the fistula. Although myocyte function in 5 week fistula rats was comparable to that of the control group, myocytes from rats 10 weeks post-fistula demonstrated significant depression of cell shortening and peak [Ca(2+)](i). Application of isoproterenol (0.1 micromol/L) was not able to compensate for the functional deficiency in myocytes from 10 week fistula rats. Caffeine (10 mmol/L) induced SR Ca(2+) release, as well as protein expression of SR Ca(2+)-ATPase, and ryanodine receptors were reduced in myocytes obtained from the same group of 10 week fistula rats. 3. These data indicate that the transition to heart failure secondary to chronic volume overload is related to depressed myocyte contractility secondary to altered intracellular Ca(2+) homeostasis.

Beta1-adrenergic receptor blockade attenuates angiotensin II-mediated catecholamine release into the cardiac interstitium in mitral regurgitation.

BACKGROUND: This study tested the hypothesis that beta1-adrenoreceptor blockade modulates the angiotensin II (Ang II)-evoked neural release of norepinephrine (NE) and epinephrine (Epi) into the cardiac interstitial fluid (ISF) space in experimentally induced mitral regurgitation (MR) in the dog. METHODS AND RESULTS: Normal dogs (n=8) were compared with dogs with MR of 2 (n=8) and 4 (n=6) weeks' duration and with dogs with MR treated with beta1-receptor blockade (RB; extended-release metoprolol succinate, 100 mg QD; MR+beta1-RB) that was started 24 hours after MR induction for 2 (n=6) and 4 weeks (n=8). Left ventricular end-diastolic dimension increased 20% as plasma Ang II levels increased >5-fold in both MR and MR+beta1-RB dogs at 2 and 4 weeks. Ang II infusion into the left atrium produced increases in ISF NE and Epi in normal dogs, which were further increased in 2- and 4-week MR dogs but were restored to normal in 4-week MR+beta1-RB dogs. Ang II infusion produced 4-fold increases in circulating NE and Epi in 2- and 4-week MR dogs that returned to normal in 4-week+beta1-RB dogs. Left ventricular angiotensin-converting enzyme activity and ISF Ang II were increased in 4-week MR dogs but were decreased in 4-week MR+beta1-RB dogs. CONCLUSIONS: beta1-RB decreases renin-angiotensin system sympathostimulation and activation by attenuating the Ang II-mediated NE and Epi release into the cardiac ISF and circulation and by decreasing left ventricular angiotensin-converting enzyme expression in the early phases of volume overload.

Beta1-adrenoceptor blockade mitigates excessive norepinephrine release into cardiac interstitium in mitral regurgitation in dog.

Mitral regurgitation (MR) is associated with increased neuronal release of norepinephrine (NE) and epinephrine (EP) into myocardial interstitial fluid (ISF) that may be necessary in sustaining left ventricular (LV) function via activation of cardiomyocyte beta-adrenergic receptors (ARs). However, activation of neuronal beta-ARs on cardiac neurons may lead to further catecholamine release, with an attendant risk of functional deterioration. We hypothesize that a beneficial effect of beta-AR blockade may therefore mitigate excessive catecholamine release from cardiac adrenergic neurons in dogs with MR. We measured the effects of chronic beta-receptor blockade (beta-RB) on ISF NE and EP release using in vivo microdialysis in open-chest anesthetized dogs after 4 wk of MR with or without extended release of metoprolol succinate (100 mg/day) as well as in control dogs. Fractional shortening increased by 30% in both MR and MR + beta-RB dogs after 4 wk of MR. In MR + beta-RB dogs, stellate-stimulated heart rate change was attenuated compared with control and MR dogs, whereas peak change of LV pressure over time (+dP/dt) increased equally in all groups. Stellate-stimulated ISF NE increased fivefold over baseline in MR versus twofold in control dogs (< 0.05), but the NE release was significantly attenuated in MR + beta-RB dogs. In contrast, stellate-stimulated increases in ISF EP did not differ in control, MR, and MR + beta-RB dogs. This study demonstrates that beta-RB attenuates ISF NE release from cardiac neurons and that the LV functional response to MR is not dependent on an excess increase in ISF NE. Thus beta1-RB may exert a beneficial effect by attenuating untoward effects of excessive sympathetic efferent neural NE release while sustaining early LV functional adaptation to MR.