Hypercalcaemia associated with chronic lymphocytic leukaemia in a Giant Schnauzer.

A 7-year-old male Giant Schnauzer was referred with a history of severe vomiting, lethargy, weight loss, polydipsia and polyuria. Detailed investigations revealed leucocytosis with a marked lymphocytosis, mild non-regenerative anaemia, thrombocytopenia, hypercalcaemia and azotaemia. Circulating lymphocytes were small and well-differentiated, and the same lymphoid population was present in bone marrow. Chronic lymphocyctic leukaemia with associated paraneoplastic hypercalcaemia was diagnosed. Immunohistochemical staining of a bone marrow biopsy revealed a neoplastic B-cell line expressing CD79. The dog responded to therapy with prednisolone and chlorambucil for a period of 8 months.     

Electrocorticogram disturbances detected in rats exposed from early stages of life to residual doses of lindane

Functional brain alterations induced by lindane were examined in Rat chronically exposed to low doses of lindane (1 and 2 μg L⁻¹ in drinking water) from conception. Histological and electrophysiological investigations were conducted at 14 weeks of age. Lindane did not induce histological changes. It did not significantly modify the sleep-wakefulness cycle and EEG did not show major alterations. The spectral EEG analysis, by recording cortical variations in both energy spectrum and energy levels of different frequency bands, showed an increase in the 11-15 Hz activity in both groups exposed to lindane. This activity was characterised by spindles well-depicted during slow wave sleep or associated with fast activity during wakefulness and theta activity in paradoxical sleep. These data suggest that chronic exposure to lindane doses as low as 1 μg L⁻¹ in drinking water could lead to central electrophysiological effects possibly involving GABA-benzodiazepine mechanisms.     

Association of hyponatremia and hyperglycemia with outcome in dogs with congestive heart failure

Objective: To evaluate plasma sodium and glucose concentrations in dogs with congestive heart failure (CHF) prior to treatment and evaluate the differences between survivors and non‐survivors. Design: Retrospective study. Animals: Fifty‐nine dogs with CHF prior to receiving cardiac medication. Interventions: None. Measurements and main results: The mean plasma sodium concentration in dogs with CHF was below the reference range (144–156 mmol/L) and significantly lower (P=0.009) in non‐survivors (141±6 mmol/L) compared with survivors (147±4 mmol/L). The mean plasma glucose concentration was above the reference range (76–117 mg/dL) and significantly higher (P=0.004) in non‐survivors (128±52 mg/dL) compared with survivors (100±13 mg/dL). Forty‐four percent of non‐survivors had concurrent low plasma sodium and high plasma glucose concentrations, whereas no survivors had both abnormalities (P<0.0001). Conclusions: Lower plasma sodium and higher plasma glucose are associated with a worse outcome in dogs with CHF.     

Platelet abnormalities and platelet-to-lymphocyte ratios in canine immunosuppressant-responsive and non-responsive enteropathy: A retrospective study in 41 dogs

Few studies have examined platelet alterations in dogs with chronic enteropathy. Our aim was to investigate platelet count (PLT), mean platelet volume (MPV), and platelet-to-lymphocyte ratio (PLR) in dogs diagnosed with immunosuppressant-responsive enteropathy (IRE). In this retrospective study of 41 dogs, data regarding signalment, canine chronic enteropathy clinical activity index (CCECAI), endoscopic and histopathological scores, PLT, MPV, PLR, total serum protein concentrations, albumin, and iron were collected. Clinical response and relapse were assessed with the evaluation of CCECAI over time. One month after starting therapy, dogs with >25% CCECAI reduction were considered responders. During a three-month CCECAI evaluation as part of a twelve-month follow-up, a CCECAI >3 together with a ≥2 unit increase in responder dogs was considered a relapse. PLT and PLR displayed significant negative correlation with MPV. MPV was positively correlated with total protein and albumin levels and negatively correlated with CCECAI. Three dogs were classified as non-responders, and 14 relapsed within 12 months. No differences were observed in PLT, MPV, or PLR between responding/non-responding and relapsing/non-relapsing groups. PLT, MPV, and PLR correlated with total protein, albumin, and CCECAI, confirming PLT as a potential marker, and suggesting MPV as a new marker of clinical efficacy against canine IRE.     

In-hospital development of an aorto-cardiac fistula in a Warmblood gelding with chronic renal disease

A 20-year-old Warmblood gelding presented for evaluation and treatment of ventral oedema and azotaemia of unknown aetiology. On presentation, a diastolic heart murmur was appreciated and echocardiography revealed moderate aortic insufficiency due to chronic degenerative valve disease. The horse was hospitalised and failed to respond to oral and i.v. fluids and diuretics. Following discontinuation of all fluid and diuretic therapy, the horse became acutely agitated and developed monomorphic ventricular tachycardia. The ventricular tachycardia spontaneously converted to normal sinus rhythm, however the heart murmur changed in timing to a right basilar continuous murmur and bounding jugular pulses were noted. Repeat echocardiogram revealed an aorto-cardiac fistula with dissection into the basilar interventricular septum and left-sided chamber volume overload that was not previously present. Attempts at stabilisation were unsuccessful and euthanasia was elected. Post-mortem examination confirmed chronic renal disease of unknown aetiology in addition to an aorto-cardiac fistula originating from the right sinus of Valsalva with subsequent dissection into the basilar interventricular septum.     

Fractionation of the reference inoculum of epizootic rabbit enteropathy in discontinuous sucrose gradient identifies aetiological agents in high density fractions

Epizootic rabbit enteropathy (ERE) is a major cause of economic loss in intensive rabbit production. Since its first recognition in 1997, much work has been done to determine the pathogenic mechanisms of the disease and to identify the aetiological agent(s). Unfortunately, the quest for aetiology has only met with limited success despite the ability to reproduce the syndrome by inoculation of intestinal contents from field cases. These intestinal inocula contain a huge number of microorganisms which could all be involved in the aetiology of ERE. To decrease the number of putative agents, the French reference inoculum TEC3 was fractionated on a discontinuous sucrose gradient so that seven fractions (supernatant, 10%, 20%, 30%, 40%, 50% and pellet) were obtained. Specific-pathogen-free rabbits were inoculated with three out of these seven fractions (supernatant, 30%, and pellet). The objectives were: (1) to characterise the seven fractions by bacteriological examination; (2) to verify whether the aetiological agent was present in the fractions by inoculation of rabbits; (3) to assign the aetiological agent of ERE to a morphological group of pathogens; (4) to identify a fraction which could replace the reference inoculum TEC3 in applications such as cell cultures or egg inoculation. The results strongly suggest that ERE is a bacterial disease and does not have a viral or parasitic aetiology.