Monday, January 31, 2011
Please click here to see the Merrick FDA Alert.
Please click here to see the Horse Feed FDA Alert.
Novel gastroretentive controlled-release drug delivery system for amoxicillin therapy in veterinary medicine
Evaluation of orally administered famciclovir in cats experimentally infected with feline herpesvirus type-1
Sunday, January 9, 2011
Vet Clin Pathol. 2009 Mar;38(1):113-20.
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA.
Two young adult dogs with gastrointestinal signs were each found to have an intra-abdominal mass based on physical examination and diagnostic imaging. On exploratory laparotomy, small intestinal masses and mesenteric lymphadenopathy were found in both dogs; a liver mass was also found in dog 1. Cytologic and histologic examination of intestinal and liver masses and mesenteric lymph nodes revealed 2 distinct lymphoid cell populations: lymphoblasts and atypical Mott cells. With Romanowsky stains, the atypical Mott cells contained many discrete, clear to pale blue cytoplasmic inclusions consistent with Russell bodies that were positive by immunohistochemistry for IgM and CD79a in both dogs and for IgG in dog 2. The Mott cells and occasional lymphoblasts stained strongly positive with periodic acid-Schiff. Using flow cytometric immunophenotyping in dog 1, 60% of peripheral blood mononuclear cells and 85% of cells in an affected lymph node were positive for CD21, CD79a, IgM, and MCH II, indicative of B-cells. With electron microscopy, disorganized and dilated endoplasmic reticulum was seen in Mott cells in tumors from both dogs. Antigen receptor gene rearrangement analysis of lymph node and intestinal masses indicated a clonal B-cell population. Based on cell morphology, tissue involvement, and evidence for clonal B-cell proliferation, we diagnosed neoplasms involving Mott cells. To the authors' knowledge, this is the second report of Mott cell tumors or, more appropriately, B-cell lymphoma with Mott cell differentiation, in dogs. More complete characterization of this neoplasm requires further investigation of additional cases. This lymphoproliferative disease should be considered as a differential diagnosis for canine gastrointestinal tumors.
J Small Anim Pract. 2011 Jan;52(1):32-7
OBJECTIVE: To report clinical findings and outcome in dogs and cats undergoing choledochotomy or primary repair of extrahepatic biliary duct rupture.
METHODS: Retrospective study of dogs (n=7) and cats (n=2) that had choledochotomy or primary bile duct repair.
RESULTS: Extrahepatic biliary obstruction was confirmed at surgery in all cases. The underlying cause in four dogs and both cats was choledocholithiasis, two dogs had gall bladder mucocoeles with associated bile duct rupture, and one dog had inspissated bile obstructing the bile duct secondary to gall bladder carcinoid tumour. Three dogs and both cats had choledochotomies performed to relieve extrahepatic biliary obstruction, and four dogs with bile duct rupture underwent primary repair of the defect. One dog with a bile duct rupture was re-explored four days postoperatively and had suffered dehiscence of the repair; this rupture was re-repaired. All animals were discharged from the hospital, and did not have clinical recurrence of extrahepatic biliary obstruction.
CLINICAL SIGNIFICANCE: Choledochotomy and primary repair of extrahepatic biliary duct rupture were associated with low perioperative morbidity and no mortality in this small cohort of cases. These techniques are reasonable options either alone or in conjunction with other procedures when bile duct patency cannot be re-established by catheterisation or bile duct discontinuity exists.
CASE DESCRIPTION: A 19-year-old neutered male domestic shorthair cat was evaluated because of signs of urinary tract obstruction.
CLINICAL FINDINGS: Physical examination findings were consistent with urethral obstruction, and a mass could be palpated in the region of the bladder neck. Abdominal ultrasonography and thoracic radiography revealed a mass in the trigone of the urinary bladder and a solitary mass in the left caudal lung lobe. Cytologic examination of the urine sediment, samples obtained by means of traumatic urethral catheterization, and fine-needle aspirates of the bladder mass did not result in a diagnosis.
TREATMENT AND OUTCOME: A balloon-expandable metallic stent was placed in the proximal portion of the urethra to relieve the malignant obstruction. After stent placement, the cat had signs of urinary incontinence and detrusor atony, both of which resolved with medical treatment. The cat was euthanized 1 month after stent placement because of progressive azotemia. Histologic examination of necropsy samples revealed grade III urothelial carcinoma and papillary pulmonary adenocarcinoma.
CLINICAL RELEVANCE: Findings suggested that stent placement may be a viable palliative treatment in cats with malignant urinary obstruction.
A third-generation fluoroquinolone, pradofloxacin (PRA), is currently being developed to treat bacterial infections in dogs. The purpose of this study was to assess the clinical efficacy in 20 dogs affected with superficial and deep pyoderma. An initial aerobic skin culture was performed in dogs with superficial pyoderma; aerobic/anaerobic tissue culture was performed in dogs with deep pyoderma; and skin cytology and biopsies were obtained from all dogs. Pradofloxacin (approximately 3 mg/kg per os [PO]) was administered daily to all dogs. Clinical efficacy was recorded at 4 weeks for dogs with superficial pyoderma and at 3 and 6 weeks for dogs with deep pyoderma. At a mean dosage of 3.7 mg/kg PO once daily, PRA treatment resulted in an excellent to good clinical response within 3 to 6 weeks for all 20 dogs with superficial and deep pyoderma.
Metabolic bone diseases (MBDs) are a common presenting complaint in reptiles and amphibians to veterinarians; however, understanding of the causes and diagnostic and treatment options is often extrapolated from human or other mammalian medicine models. Although the roles of UV-B, calcium, phosphorus, and cholecalciferol are better understood in some MBDs, there remain many X factors that are not. Likewise, quantitative diagnosis of MBDs has been difficult not only in terms of staging a disease but also regarding whether or not a condition is present. Treatment options also present challenges in corrective husbandry and diet modifications, medication/modality selection, and dosing/regimen parameters.
J Zoo Wildl Med. 2010 Sep;41(3):538-41.
Pituitary cystadenoma, enterolipidosis, and cutaneous mycosis in an Everglades ratsnake (Elaphe obsoleta rossalleni).
An 11-yr-old captive-born male Everglades ratsnake (Elaphe obsoleta rosalleni) presented with dysecdysis, hyperkeratosis, and inappetance. Two skin biopsies demonstrated a diffuse hyperkeratosis with both a bacterial and fungal epidermitis. Fusarium oxysporum was cultured from both biopsies and considered an opportunistic infection rather than a primary pathogen. Medical management was unsuccessful, and the snake was euthanized. Histologic findings included a pituitary cystadenoma arising from the pars intermedia, severe intestinal lipidosis, generalized epidermal hyperkeratosis, and lesions consistent with sepsis. It is hypothesized that endocrine derangements from the pituitary tumor may have caused the skin and intestinal lesions.
Five horses were presented with signs of myopathy along with systemic malaise, hyperfibrinogenemia, hyperphosphatemia, and an elevated calcium phosphorus product (Ca*P). Postmortem findings were consistent with systemic calcinosis, a syndrome of calcium deposition in the tissue of organs including lungs, kidneys, muscle, and heart that has not been previously described in horses.
Saturday, January 8, 2011
Maddi originally presented to my oncology service with a 6 month history of a mass on the right flank. The mass was eventually completely excised by the referring veterinarian and diagnosed as a grade II mast cell tumor. Maddi did very well post-operatively. 1 month prior to the oncology referral, the owner noticed multiple skin growths on her forehead and inner thighs. Every day had resulted in more noticeable masses and progression of the original tumors. At the time of presentation, Maddi was on routine hydroxyzine and Tramadol for discomfort.
T- 102.6 HR- 110 RR-panting Wt- 57.8lbs.
Maddi was bright and alert. Her heart and lungs ausculted within normal limits. Her abdomen was soft and non painful. All of her peripheral lymph nodes palpated within normal limits. She had approximately 300 dermal masses throughout her entire body (see photos). The lesions were red, raised, and of varying sizes. The remainder of her physical exam was unremarkable.
Cytology of multiple, randomly picked masses were all consistent with well granulated mast cell tumors.
The treatment of choice for all mast cell disease is surgical removal with wide (2cm) surgical margins. However, in Maddi’s presentation, the number of masses was so extensive that surgical removal was unrealistic. Thus, Maddi’s disease should be treated as a systemic illness since the entirety of her skin is involved.
The standard chemotherapy options for stage III or IV mast cell disease is a combination of vinblastine, lomustine and prednisone. However, the recent advancement of tyrosine kinase inhibitors (TKI) as a treatment for mast cell tumors has just recently landed on the veterinary market. C-kit (CD117) is a tyrosine kinase receptor (TKR) that is both mutated and over-expressed in many canine mast cell tumors. Some laboratories (Michigan State University) can evaluate histopathologic samples for these mutations and over expressions. These changes in c-kit will lead to increase cell cycle replication and more aggressive mast cell tumors.
Palladia (Pfizer) is the first veterinary approved tyrosine kinase inhibitor for the treatment of canine cancers. While it blocks a variety of different TKR, it is specifically created to block c-kit and thus has its greatest efficacy against canine mast cell disease.
Due to financial restraints, additional diagnostics (including c-kit evaluation and routine mast cell tumor staging) could not be performed and the owner elected to try the more experimental Palladia therapy instead of conventional chemotherapy.
Maddi was started on 3.0mg/kg of Palladia every other day. She was also started on standard dosages of Benadryl and Pepcid AC. Due to significant gastrointestinal toxicity associated with Palladia, it is recommended to put all naïve patients on daily sucralfate as well.
Maddi presented for a recheck exam 7 days after initiation of therapy. No Palladia toxicity was reported by the owner. Her physical exam noted dramatic reduction in most of her masses (see photos). The remainder of her physical exam was unremarkable.
She had a mild neutropenia (2000) on a CBC
which is anticipated with Palladia therapy. Treatment was continued at the previously prescribed frequencies and dosages.
Maddi again presented for a recheck exam 3 weeks later. There was still no clinical signs associated Palladia toxicity. On physical exam, her masses had almost completely resolved. However, in areas where masses were no longer palpated, Maddi had developed depigmentation in the areas of previous mast cell tumors. Her neutropenia remained but was stable.
Maddi continued to do well on the Palladia treatment protocol for another 3 months. At that time, her masses developed a resistance to the treatment and progressed rapidly causing significant pruritus and a general decline in overall quality of life. At that time, the owners elected for humane euthanasia.