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We report a widespread Usutu virus outbreak in birds in the Netherlands. Viral presence had been detected through targeted surveillance as early as April 2016 and increased mortality in common blackbirds and captive great grey owls was noticed from August 2016 onwards. Usutu virus infection was confirmed by post-mortem examination and RT-PCR. Extensive Usutu virus activity in the Netherlands in 2016 underlines the need to monitor mosquito activity and mosquito-borne infections in 2017 and beyond.

Laboratory examination revealed hypohalaemia (1.6 mmol/1; reference range 3.4-5.7 mmo1/1) and echocardiographic findings seemed to be compatible with hypertrophic cardiomyopathy. Potassium suppletion, first intravenously and then orally, and treatment with the (13-blocking agent atenolol (Tenormin®, Zeneca;6.25 mg once daily) and acetylsalicylic acid (40 mg twice daily) resulted in good recovery. On 29 June, 3 weeks after stopping potassium suppletion and atenolol, the cat was presented to the owner's veterinarian for weakness in the hind legs. The cat was not lethargic and was eating and drinking normally. The history of cardiomyopathy raised the possibility of complicating thromboembolism. A saddle thrombus at the distal aortic trifurcation was considered unlikely because the femoral pulses were easily palpated and the footpads of the hind legs were warm and pink. The previous treatment was resumed but the dose of acetylsalicylic acid was lowered to twice weekly 25 mg. The cat did well on this regimen but the plasma concentrations of potassium remained low. When potassium gluconate (Tumil Ke, Aesculaap by, Boxtel, NL) was given orally in a dose of 2 mmol four times daily, the plasma potassium concentration remained s 2.2 mmo1/1. On 1 September the cat collapsed again, even though the potassium supplementation had been increased to 2 mmol six times daily for 2 weeks. In addition to muscular weakness, there was mydriasis, restlessness, and panting. Potassium concentrations in plasma ranged from 1.9 to 2.1 mmo1/1. An angiotensin-converting enzyme inhibitor (once daily 1 mg enalapril, Enalfor®, Mycofarm) was added to the treatment. The cat recovered but the plasma potassium concentration remained at the same low level. Hyperadrenocorticism was excluded as the cause of the muscular weakness by the finding that the basal urinary corticoid/creatinine ratio (average on two consecutive days: 24 x 10-6) was below the upper limit of the reference range (37 x 10-6) (11) and the urinary corticoid/creatinine ratio was readily suppressed (to 3.0 x 10-6 ) following three oral doses of 0.5 mg dexamethasone. A possible relation to hyperthyroidism (21) was excluded by the finding of a normal plasma thyroxine concentration (29 nmi51/1).Between the episodes of muscular weakness the cat's condition and behaviour were unremarkable but in search of an explanation for the persistent hypokalaemia the cat was referred to the Utrecht University Clinic for Companion Animals in September 1998. HYPERALDOSTERONISM IN A CAT WITH METASTASISED ADRENOCORTICAL TUMOURA.Rijnberk1,6, G. Voorhout2, H.S. Kooistra1, R.J.M. van der Waarden3, F.J. van Sluijs1, J. Uzer4, P. Boer5, and W.H. Boer5 Vet Quart 2001; 23: 38-43 Accepted for publication: January 10, 2000. SUMMARYIn a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and ...

Abstract. The hepatic progenitor compartment is of vital importance in liver regeneration when hepatocellular replication is impaired, as it occurs in acute fulminant hepatitis or severe liver fibrosis. It consists of resident progenitor cells in the normal liver, and ductular reaction and intermediate hepatobiliary cells in diseased livers. An histologic and immunohistochemical study was conducted to demonstrate putative hepatic progenitor cells in the normal liver (n 5 5) and in a range of hepatic diseases (n 5 13) in the cat. Formalin-fixed, paraffin-embedded specimens were stained with HE, the van Gieson stain, and the reticulin stain according to Gordon and Sweet, and immunohistochemically stained for cytokeratin-7 (CK7), human hepatocyte marker 1 (Hepar1), and multidrug resistancebinding protein-2/ATP binding cassette C2 (MRP2). The normal feline liver contains a liver progenitor cell morphologically similar to humans and dogs, which resides in the canal of Hering. In acute and chronic feline liver diseases a ductular reaction is present, whether in the parenchyma or in a portal or septal location. The putative progenitor cells could easily be demonstrated by staining for CK7, whereas they were generally negative for Hepar1 and MRP2. In a parenchymal ductular reaction mitotic figures and cells with an intermediate hepatobiliary phenotype could be demonstrated. This is the first account of hepatic progenitor cells in feline liver.

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