Mycobacterium goodii infection in a dog with concurrent hyperadrenocorticism

Abstract A 9-year-old Boston terrier was diagnosed with multifocal, nodular panniculitis caused by an organism belonging to the Mycobacterium smegmatis group by histological evaluation and bacteriological identification. The mycobacterial species was identified by direct gene sequence analysis and confirmed to be Mycobacterium goodii. Treatment using doxycycline and ciprofloxacin was successfully implemented for the mycobacterial panniculitis over a period of 9 months. Concurrent pituitary-dependent hyperadrenocorticism (Cushing's disease) was also identified using routine diagnostic methods and mitotane therapy was implemented. There was follow-up for 14 months after cessation of antimicrobial therapy with no recurrence of mycobacterial infection. Although cutaneous infections are frequently recognized as complications of canine pituitary-dependent hyperadrenocorticism, concurrent mycobacterial panniculitis due to any rapidly growing mycobacterium has not previously been reported. This is the first confirmed case of mycobacterial panniculitis due to M. goodii infection in a dog and also the first of any rapidly growing mycobacterial infection in a dog with concurrent endogenous Cushing's disease.     

Paraganglioma,pituitary adenoma,and osteosarcoma in a dog

An 11‐year‐old neutered male Alaskan Malamute mixed‐breed dog was presented with a complaint of polyuria/polydipsia (PU/PD), weight loss, tachypnea, regurgitation, and a previous history of nontreated osteosarcoma of the right distal radius, diagnosed 21 months prior. On physical examination, an abdominal mass was palpated. The abdominal mass was aspirated and cytologically diagnosed as a neuroendocrine tumor, suspected to be a pheochromocytoma. Laboratory examination revealed a mild anemia and thrombocytopenia, markedly elevated ATP and ALP activities, and moderate hypercalcemia. A low‐dose dexamethasone suppression test and endogenous adrenocorticotropic hormone (ACTH) concentration were compatible with pituitary hyperadrenocorticism. On urinalysis, proteinuria was noted as well as a high urine metanephrine/creatinine ratio, consistent with a diagnosis of pheochromocytoma. The dog was treated with supportive care and euthanized 6 months later due to decreasing quality of life. On necropsy, an extra‐adrenal pheochromocytoma (paraganglioma) was diagnosed in the caudal abdomen, and a pituitary adenoma and an osteosarcoma of the right distal radius were confirmed.     

A case of chronic lymphocytic leukemia masked by Cushing’s disease in a dog

A 12-year-old, 3.5-kg, intact female dog was presented with polyuria, polydipsia, and a pendulous abdomen. Laboratory examinations showed elevated hepatobiliary enzyme levels and neutrophilic leukocytosis. The adrenocorticotropic hormone stimulation test confirmed hyperadrenocorticism (HAC). Trilostane therapy managed the clinical condition and cortisol concentration. However, lymphocytosis and nonregenerative anemia developed after HAC remission. Bone marrow aspiration analysis revealed a lymphoproliferative disorder with a clonal T-cell population. Accordingly, the patient was diagnosed with T-cell chronic lymphocytic leukemia (CLL) and concurrent HAC. Thereafter, chemotherapy was initiated, which improved the lymphocytosis. However, euthanasia was performed because of worsening quality of life at 45 weeks after the first presentation. These results suggested that CLL could be masked by excessive endogenous cortisol and discovered after HAC remission.     

Negative hepatic computed tomographic attenuation pattern in a dog with vacuolar hepatopathy and hepatic fat accumulation secondary to cushing's syndrome

This report describes an unusual computed tomographic (CT) hepatic pattern, characterized by negative attenuation values (from –19.59 to –28.85 Hounsfield Units, HU) in a canine patient with severe Cushing's syndrome. Attenuation values of the splenic parenchyma (63.26 HU) and abdominal fat (–118.34 HU) were within normal limits. The negative hepatic attenuation values allowed a CT diagnosis of severe hepatic fatty infiltration that was subsequently confirmed by tissue‐core biopsy and histopathological examination.     

Tertiary hypothyroidism in a dog

: A nine-year-old male entire Labrador was diagnosed with pituitary dependent hyperadrenocorticism. Following seven months of successful mitotane therapy, the dog presented with marked weight gain, seborrhoea and alopecia. Routine clinicopathological analyses revealed marked hypercholesterolaemia. Serum total and free thyroxine (T4) concentrations were below their respective reference ranges. Serum thyroid stimulating hormone (cTSH) concentration was within reference range. TSH and thyrotropin releasing hormone (TRH) response tests revealed adequate stimulation of total T4 in both, and cTSH in the latter test. Magnetic resonance imaging revealed a mass arising from the pituitary fossa, with suprasellar extension. A diagnosis of tertiary hypothyroidism was made. Following four weeks of levothyroxine therapy, circulating cholesterol concentration had declined, weight loss had ensued and dermatological abnormalities had improved. Euthanasia was performed four months later due to the development of neurological signs. A highly infiltrative pituitary adenoma, with effacement of the overlying hypothalamus was identified on post mortem examination. Tertiary hypothyroidism has not been previously reported in dogs.     

Hemorrhagic diathesis and bone marrow aplasia secondary to lomustine overdose in a dog

A 9‐year‐old mixed breed 13 kg spayed female dog was presented for evaluation of two masses in the right abdominal mammary gland region. Surgery was conducted to excise the masses. A grade I complex mammary gland carcinoma and high grade (grade III) mast cell tumor with an inguinal lymph node metastasis were diagnosed. Forty‐seven days after the surgical procedure, the mast cell tumor relapsed, and neoadjuvant treatment with lomustine (81 mg/m²) was prescribed. Thirteen days from initiation of lomustine therapy, the dog was re‐presented to the hospital with bloody diarrhea, hematemesis, epistaxis, an elevated rectal temperature, depression, severe dehydration, and marked dyspnea. The CBC showed severe thrombocytopenia and leukopenia. According to the owner, lomustine (45mg per os [PO]) was mistakenly administered daily for 10 consecutive days (total dose, 810 mg/m²). The dog died and a necropsy was performed. The main gross lesions consisted of severe multifocal hemorrhages in multiple organs, especially in the digestive system. Histopathologic evaluation revealed disseminated hemorrhages, as well as marked bone marrow aplasia. This report describes the clinical, hematologic, gross, and histologic findings in a fatal case of lomustine overdose in a dog.     

Acute polyneuromyopathy with respiratory failure secondary to monensin intoxication in a dog

Objective

To describe a successfully managed case of polyneuropathy and respiratory failure secondary to presumed monensin intoxication.

Case Summary

A 9‐month‐old Australian Shepherd was evaluated for progressive generalized weakness and respiratory distress. Several days preceding presentation, the dog was seen playing with a monensin capsule, and had free access to a barn where the product was stored and where chewed capsules were subsequently found. The dog was presented with flaccid tetraparesis, hyperthermia, and severe respiratory distress. Bloodwork and urinalysis revealed marked increase in serum creatine kinase concentration and presumed myoglobinuria. Cardiac troponin I level was markedly increased. Management included mechanical ventilation for 5 days, fluid‐therapy, active cooling, antimicrobial therapy, analgesia, gastroprotectants, antiemetics, enteral feedings, continuous nursing care, and physiotherapy. Intravenous lipid rescue therapy was administered with lack of improvement in respiratory function and muscle strength. The patient completely recovered and was discharged after 12 days of hospitalization.

New or Unique Information Provided

Monensin intoxication should be considered in the differential diagnosis of acute polyneuromyopathy and respiratory failure in dogs with access to this compound. Respiratory failure secondary to monensin intoxication does not necessarily carry a poor prognosis if mechanical ventilation can be provided as a bridge until return of respiratory function is achieved.     

Pneumothorax in a dog with a pulmonary abscess and suspected infective endocarditis.

Nontraumatic pneumothorax was diagnosed in a dog with a pulmonary abscess and evidence of infectious endocarditis, including fever, mitral murmur, and vegetative lesion of mitral valve leaflets. Pneumothorax persisted after 4 days of continuous thoracic drainage. At exploratory thoracotomy, the diaphragmatic lung lobe was identified as the source of air leakage and was excised. Results of culturing of blood and lung tissue for aerobic and anaerobic bacteria were negative. Antibiotics were administered because of suspected bacterial endocarditis. Pneumothorax and fever resolved after surgical and medical treatments.     

Canine hypophysectomy using a ventral paramedian approach

OBJECTIVE: To evaluate the degree of pituitary exposure, completeness of hypophysectomy, and perioperative morbidity associated with an alternative paramedian surgical approach and excisional technique for the canine pituitary gland. STUDY DESIGN: Experimental imaging, surgical, and endocrinologic study. ANIMAL POPULATION: Nine healthy, purpose-bred Beagle dogs. METHODS: Surgical landmarks for the pituitary were determined by computed tomography (CT), and then using a ventral paramedian approach medial to the rami of the mandible, the pituitary was exposed and removed en bloc by manipulation and ultrasonic aspiration. Efficacy of the procedure was evaluated using endocrinologic and pathologic observation. RESULTS: CT images allowed the precise location of surgical landmarks for hypophysectomy. Statistically significant decreases in secretion of all measured pituitary hormones except adrenocorticotropic hormone (ACTH) occurred after hypophysectomy. Despite the absence of gross evidence of residual pituitary tissue, immunohistochemical staining revealed residual pituitary cells in the sella turcica of most dogs. CONCLUSION: CT imaging and a paramedian approach facilitated surgical access to the pituitary gland by a transoral technique; however, use of an ultrasonic aspirator removed all visible pituitary glands but left cellular remnants capable of ACTH secretion in the sella turcica. CLINICAL RELEVANCE: Although this technique did not result in complete hypophysectomy, clinical use in dogs with pituitary-dependent hyperadrenocorticism is warranted because the goal is not complete hypophysectomy but removal of a pituitary tumor.     

CISTERNOGRAPHY COMBINED WITH LINEAR TOMOGRAPHY FOR VISUALIZATION OF PITUITARY LESIONS IN DOGS WITH PITUITARY-DEPENDENT HYPERADRENOCORTICISM

Cisternography combined with sagittal linear tomography was performed in eight dogs with pituitary-dependent hyperadrenocorticism, in search of pituitary lesions. In one dog with a pituitary microadenoma, the dimensions of the pituitary gland were within normal limits. In six dogs the pituitary gland was enlarged. In the remaining dog the pituitary gland was also enlarged, but could not be measured due to absence of contrast medium in the cisternae around the pituitary gland. In these seven dogs large pituitary tumors were found at autopsy. With linear tomography the height of the pituitary gland could only be measured in the dog with the microadenoma. In all other dogs compression of the subarachnoid space at the dorsal aspect of the pituitary gland interfered with the assessment of the height of the pituitary lesion, and therefore with the assessment of the presence and extent of compression of the hypothalamus. It is concluded that cisternography combined with linear tomography provides information about the size of the pituitary gland and the presence of suprasellar expansion, although the present technique does not allow an assessment of the severity of the suprasellar expansion.