[Disseminated protothecosis with ulcerative granulomatous colitis in a Rhodesian Ridgeback from Germany]. / Ulzerative granulomatöse Kolitis durch Prototheca spp. bei einem Rhodesian Ridgeback in Deutschland.

A 10-month-old male Rhodesian Ridgeback was presented to the Clinic of Small Animal Medicine, LMU, Germany, with a 6-month history of chronic diarrhea and hematochezia. The dog lived in Germany and had never traveled abroad. Complete blood count and serum biochemistry performed by the referring veterinarian revealed neutrophilia, hyperkalemia, and hyponatremia, with a basal cortisol of 4.3 µg/dl, which excluded hypoadrenocorticism. Since antibiotic treatment had not resulted in any improvement, a 2 week course of prednisolone administration had been initiated, leading to a marked deterioration of intestinal signs and a significant weight loss of 6 kg. At the time of referral, the patient was markedly emaciated, dehydrated, hypovolemic and had a rectal temperature of 39.6 °C. Abdominal ultrasound showed a thickened and irregular colonic wall. On colonoscopy, an irregular colonic mucosa with ulcerations was observed. Histopathologic examination revealed an ulcerative granulomatous colitis, and on Periodic acid-Schiff reaction (PAS) numerous organisms consistent with Prototheca spp. were identified. Prototheca zopfii infection was confirmed by culture and MALDI-TOF MS. In order to test for an underlying immunodeficiency, immunoglobulin levels in serum were determined. IgM was decreased, while IgG and IgA levels were within the reference interval. Due to deterioration of general condition, grave prognosis and costs of a treatment trial, the patient was euthanized one week later, and necropsy was performed. Prototheca spp. were detected on histopathologic examination in the lymphnodes, however not in the eyes or the central nervous system. Protothecosis should be considered an differential diagnosis in dogs with chronic diarrhea and ulcerative granulomatous colitis even in dogs living in Germany. Histopathologic examination of colonic biopsies with special stains such as PAS is recommended in every dog with signs of chronic large bowel disease in order to avoid missing this rare infectious disease.

Toxoplasma gondii-associated cholecystitis in a cat receiving immunosuppressive treatment.

A 9-year-old female neutered domestic shorthair cat diagnosed with immune-mediated thrombocytopenia that was treated with prednisolone and cyclosporine, was presented for anorexia, vomiting, increased liver enzymes, and hyperbilirubinemia. Abdominal ultrasound revealed a markedly thickened gallbladder and common bile duct wall. Bile cytology detected severe neutrophilic inflammation and protozoal zoites. Suspected Toxoplasma gondii infection was confirmed by real-time PCR of bile. The cat was treated with clindamycin and ursodeoxycholic acid for 6 weeks, recovered and remained stable for 2 years despite ongoing immunosuppressive treatment. Thereafter, the cat was presented with suspicion of intestinal lymphoma, and recurrence of toxoplasmosis was diagnosed. Following treatment with clindamycin and prednisolone over 4 weeks the cat was euthanized. This is the first report of Toxoplasma gondii zoites detected in bile fluid from a cat with cholecystitis. Pathogenesis of toxoplasmosis in cats is still not fully understood. Although immunosuppression can represent a relevant predisposing factor, other factors, such as virulence of the parasite and genetic polymorphism of the host, can also play an important role. Toxoplasmosis should be included as a differential diagnosis in cats developing clinical signs of an inflammatory disease while receiving immunosuppressive treatment.

[Diagnostic approach and management of hypercalcaemia in dogs exemplary of primary hyperparathyroidism]. / Diagnostische Aufarbeitung und Management der Hyperkalzämie des Hundes am Beispiel des primären Hyperparathyreoidismus.

Hypercalcaemia can be caused by many different diseases. This article summarizes the causes, pathophysiologic mechanisms and diagnostic procedures as well as treatment recommendations. The main focus is on hypercalcaemia in primary hyperparathyroidism (PH), complemented by a case report. An elevated total calcium level should generally be investigated and verified by measurement of ionized calcium concentration. The further diagnostic approach depends on the phosphate level. Tumour screening, measurement of parathormone and parathromone-related protein and sonography of parathyroid glands may be necessary. If the calcium-phosphate-product exceeds 60 mg/dl, there is a risk of tissue mineralisation and a rapid treatment of hypercalcaemia is required. For acute therapy, sodium chloride infusion, furosemide and glucocorticoids can be used. Glucocorticoids should only be given after strict indication and after a definite diagnosis. For long-term management, bisphosphates, particularly alendronate, are increasingly used successfully. Causal therapy of PH can be performed by parathyreoidectomy, heat ablation or ethanol ablation. Thereafter, particularly in cases of severe preoperative hypercalcaemia, hypocalcaemia can occur. Treatment is performed using vitamin D3 (calcitriol), which may also be given preoperatively in cases of severe hypercalcaemia. A concomitant oral calcium supplementation using calcium carbonate as medication of choice is contentious. Due to a potential relapse after successful excision of the affected parathyroid gland in PH, the serum calcium level should be monitored periodically.