In Print – Stephen Mehler, DVM, DACVS

January 9, 2011 Leave a comment

J Small Anim Pract. 2011 Jan;52(1):32-7

Choledochotomy and primary repair of extrahepatic biliary duct rupture in seven dogs and two cats.

Baker SG, Mayhew PD, Mehler SJ.


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.

In Print – Stephen Mehler, DVM, DACVS

January 9, 2011 Leave a comment

J Am Vet Med Assoc. 2009 Jan 15;234(2):236-9.

Use of a balloon-expandable metallic stent to relieve malignant urethral obstruction in a cat.

Newman RG, Mehler SJ, Kitchell BE, Beal MW.


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.

In Print – Ian Spiegel, VMD, MPH, DACVD

January 9, 2011 Leave a comment

J Am Anim Hosp Assoc. 2010 Sep-Oct;46(5):301-11.

Evaluation of the clinical efficacy of pradofloxacin tablets for the treatment of canine pyoderma.

Restrepo C, Ihrke PJ, White SD, Spiegel IB, Affolter VK.


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.

In Print – Eric Klaphake, DVM, DABVP (Avian), DACZS

January 9, 2011 Leave a comment

Vet Clin North Am Exot Anim Pract. 2010 Sep;13(3):375-92.

A fresh look at metabolic bone diseases in reptiles and amphibians.

Klaphake E.


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).

Dadone LI, Klaphake E, Garner MM, Schwahn D, Sigler L, Trupkiewicz JG, Myers G, Barrie MT.


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.

In Print – Jean-Yin Tan, DVM, DACVIM (Large Animal)

January 9, 2011 Leave a comment

Can Vet J. 2010 Sep;51(9):993-9.

Suspected systemic calcinosis and calciphylaxis in 5 horses.

Tan JY, Valberg SJ, Sebastian MM, Davis GD, Kelly JR, Goehring LS, Harland MM, Kuebelbeck KL, Waldridge BM, Newton JC, Reimer JM.


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.

Case Report – 5 Year Old FS Boxer with Severe Mast Cell Disease

January 8, 2011 Leave a comment

Zachary M. Wright DVM, DACVIM (oncology)


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 phyAlign Centersical 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.

An Update on EPM: The Latest in Diagnostics and Treatment

December 6, 2010 Leave a comment

Jean-Yin Tan, DVM, DACVIM Large Animal Internal Medicine


“My horse has been just a little off, Doc. I don’t really want to pay for a full-blown lameness or neuro exam or anything. Would you mind just taking a blood test for EPM while you’re here?”

If you’re a general equine practitioner, you’ve likely been asked a question like this in the middle of a routine vaccine visit, by a horse owner who’s been dabbling in reading a few of the latest horse publications and learning some catch phrases from her friends. Since you were hoping to just quickly knock off a few vaccines while on your way to 5 more lengthy calls that you have to cram into your afternoon, chances are you’ve been tempted to just pull the blood sample. After all, a full neurologic exam would take a lot of time and money, and that’s not what the owner wants to do, right?

It might be time to educate your client. The first rule of interpreting any diagnostic tests for EPM is that a clinical diagnosis of EPM must be made. In the absence of detectable neurologic deficits and elimination of other differential diagnoses, confirmation of exposure to Sarcocystis neurona via any number of diagnostic tests can mean very little.

Western Blot. Sensitivity is 80% and specificity 38% for testing of the serum of neurologic horses. That means it can be used to rule out EPM, but the low specificity means a large number of false positives, making the test inappropriate for diagnosing EPM. Cross-reaction may also occur with nonpathogenic Sarcocystis fayeri, which uses the horse as a natural intermediate host.

IFAT. The indirect immunofluorescent antibody test is a quantitative serologic test for EPM which provides actual titers and a likelihood ratio of the disease. Although sensitivity (83% for serum) is similar to that of the Western blot, specificity (97% for serum) is higher using the IFAT. Serum and CSF results have a moderately strong correlation. Furthermore, blood contamination of up to 104 RBCs/l does not affect CSF test results. The IFAT can also be used to detect EPM attributed to Neospora hughesii. There is however, cross-reaction with S. fayeri.

SAG-1 ELISA. The latest test is an ELISA that detects a specific surface antigen SAG-1 found on S. neurona merozoites. Although the low sensitivity and specificity (68% and 71% respectively) and geographical variation in presence of the surface antigen inhibits the commercially available SAG-1 ELISA from being a reliable diagnostic test, there is some potential for a more reliable SAG-2 ELISA in the future, especially given the lack of cross-reactivity with S. fayeri and N. hughesi.

So, what should I do? The Western Blot, IFAT, and SAG-1 ELISA are all different ways of detecting anti-S. neurona antibodies in serum or CSF. Currently, the IFAT offers the highest sensitivity and specificity. It is important, however, to take into consideration that cross-reaction with S. fayeri and vaccination can affect results.


“Doc, I read in a horse magazine about a medication called toltrazuril? Do you think we should try that on my horse? I think it’s supposed to work real well on EPM.”

It’s busy season and you haven’t had much of a chance to sit down, let alone read the latest in journals on equine neurologic disease. If you’ve never heard of toltrazuril, don’t panic. I’ve put together a brief synopsis of drugs used for EPM below.

Antiprotozoals. FDA approved options are: sulfadiazine/pyrimethamine, ponazuril, nitazoxanide, and diclazuril. In the studies cited, successful treatment is defined as improvement in neurological grade by at least 1 level or CSF testing becoming negative on Western blot.

Sulfadiazine/pyrimethamine (ReBalance). At 20mg/kg sulfadiazine and 1mg/kg pyrimethamine orally daily for 90 days, 62% of affected horses have successful outcomes. However, adverse effects from folic acid deficiency include bone marrow suppression (12%), GI disturbance, decreased spermatogenesis in stallions, and congenital defects in foals when used in pregnant mares.

Ponazuril (Marquis). At 5mg/kg orally daily for 28 days, this antiprotozoal drug is responsible for the successful treatment of 60% of horses and at double-dose, 65% of affected horses. There were no adverse effects in a study of 101 horses. However, possible side effects listed by the manufacturer include blisters, hives, diarrhea, colic, and a seizure.

Nitazoxanide (Navigator). Although no longer commercially available, this antiparasitic drug used at 50mg/kg orally daily for 28 days has been found to successfully treat 57% of horses. However, fatal enterocolitis, fever, anorexia, lethargy are noted side effects and affect up to 31% of horses.

Diclazuril. This FDA-approved but unmarketed antiprotozoal drug has been used as pellets at 1mg/kg orally daily for 28 days with a 67% success rate. Adverse reactions that may not necessarily be correlated with the drug include laminitis or decline in neurologic status.

Toltrazuril (Baycox 5%). An anti-coccidial drug used in other species, this drug is being reviewed by the FDA for use in horses for EPM. At 5mg/kg orally daily for 10 days, it has been found in limited studies to achieve excellent absorption into CSF with no adverse effects.

Antiinflammatories. Nonsteroidal antiinflammatory drugs can help decrease initial worsening of signs during treatment associated with inflammatory response to the parasite. Corticosteroids are not recommended but single doses may help curb inflammation and allow antiprotozoal drugs to work. Many veterinarians use DMSO as well. There have been no clinical trials to support or refute the use of Vitamin E and thiamine supplementation.

Immunostimulants. Some veterinarians have advocated the use of immunomodulation with drugs such as Prioponibacterium acnes, mycobacterial cell wall extracts, levamisole, and alpha-interferon. These could potentially affect T cell-mediated immunity and stimulate macrophages. However, without further investigation, theoretical immunopathologic effects on the CNS should also be considered.

What do I do if the horse relapses? It is theorized that 10% of horses relapse within 3 years of discontinuation of therapy. Treatment options include longer duration of therapy (off-label doubling of the standard period of treatment), using higher doses of ponazuril, combining ponazuril with sulfadiazine/pyrimethamine, using twice-weekly continuous therapy with sulfadiazine/pyrimethamine, and possibly using anthelmintic levamisole as an immunostimulant.

So…What should I treat with? Currently the only commercially available antiprotozoal with the least reported adverse effects is ponazuril. However, look for other options such as diclazuril or toltrazuril appearing on the market in the future. Although conservative use of antiinflammatories is widely accepted, the efficacy of treatments such as DMSO, thiamine, Vitamin E, and immunostimulants has not been specifically investigated but can be used at your discretion.

The new SAG-2 and SAG-4,3 assays for EPM which are now available. These have possible advantages over the previous available assays because:

-These surface antigens are those most commonly expressed by S. neurona strains
-Quantitative test
-Provide serum/CSF ratios
The disadvantage is that both CSF and blood samples need to be submitted to provide accurate information.

1. Daft B, Barr, BC, Gardner, IA, et al. Sensitivity and specificity of western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities. J Am Vet Med Assoc 2002;221:1007-1013.

2. Duarte P, Daft, BM, Conrad, PA, Packham, AE, Gardner, AE. Comparison of a serum indirect fluorescent antibody test with two Western blot tests for the diagnosis of equine protozoal myeloencephalitis. J Vet Diagn Invest 2003;15:8-13.

3. Duarte P, Daft, BM, Conrad, PA, et al. Evaluation and comparison of an indirect fluorescent antibody test for detection of antibodies to Sarcocystis neurona, using serum and cerebrospinal fluid of naturally and experimentally infected, and vaccinated horses. J Parasitol 2004;90:379-386.

4. Dubey J, Lindsay, DS, Saville, WJA, et al. A review of Sarcocystis neurona and equine protozoal myeloencephalitis (EPM). Vet Parasit 2001;95:89-131.

5. Furr M, McKenzie, H, Saville, WJA, et al. Prophylactic administration of ponazuril reduces clinical signs and delays seroconversion in horses challenged with Sarcocystis neurona. J Paristol 2006;92:637-643.

6. Granstrom D, Howe, D, Bentz, B, et al. Current treatments for equine protozoal myeloencephalitis. Equine Disease Quarterly 2007;16.

7. Hoane J, Morrow, JK, Saville WJ, et al. Enzyme-linked immunosorbent assays for detection of equine antibodies specific to Sarcocystis neurona surface antigens. Clin Diagn Lab Immunol 2005;12:1050-1056.

8. Johnson A. Evidence-based review of diagnosis and treatment of Sarcocystis neurona infection (Equine Protozoal Myeloencephalitis). AAEP 2009.

9. MacKay R. Equine essentials – equine protozoal myeloencephalitis: Managing relapses. Veterinary Technician 2008;29.

10. Reed S, Saville, WJ, Schneider, RK. Neurologic disease: Current topics in-depth. AAEP 2003.

11. Saville W, Dubey, JP, Oglesbee, MJ, et al. Experimental infection of ponies with Sarcocystis fayeri and differentiation from Sarcocystis neurona infections in horses. J Parasitol 2004;90:1487-1491.

Categories: EPM, Equine, Neurology, Tan

Blue Buffalo Dog Food Recall

October 11, 2010 Leave a comment

Meet Dr. Jean-Yin Tan

April 30, 2010 Leave a comment

Dr. Tan graduated from Cornell University in 2005. She went on to complete an internship at Mid-Atlantic Equine Medical Center in NJ and a large animal internal medicine residency at the University of Minnesota. She spent a year at UC Davis completing an Equine Primary Care fellowship and is now working in New Jersey. Dr. Tan has publications in journals including the American Journal of Veterinary Research and the Canadian Veterinary Journal and has spoken at various local conferences as well as ACVIM Forum. Her interests include neonatology, respiratory disease, and gastroenterology. She has experience with all large animals as well as horses!

Case Spotlight – Young Anemic Cat

April 20, 2010 Leave a comment

“Teddy” – 1 and ½ year old MN DSH –
Cindy Stubbs, DVM, DACVIM (Small Animal Internal Medicine)

Owner reports lethargic, not as playful as normal, appetite decreased. PCR panel pending.
Cat one of three from a litter raised by owner. Littermates still in same household and are clinically normal with normal blood work. This pet reported to be quieter than the rest.

Never tested for FeLV/FIV. Was exposed to a FeLV positive cat in same house but separated.
No fever.
Inside only cat.
On Revolution for flea control. No history of exposure to fleas and ticks.

Pet looks fine on exam – normal weight and appearance. No overt abnormalities.

Blood work shows significant anemia with little to no regeneration. Path review still pending.

Anemia – suspect infectious disease as underlying cause (Feline Leukemia virus most likely), immune-disease also a consideration. Could have had an infectious disease that sparked an immune component to anemia.

(1) Check FeLV/FIV status on peripheral blood of this cat and other cats in the household.

(2) If negative, consider bone marrow aspirate or core biopsy. Perform CBC at time of bone marrow sampling so lab can compare. Perform Feline Leukemia IFA or PCR on the bone marrow sample (National Veterinary Labs recommended).

(3) Consider empirical treatment with doxycycline 5 mg/kg every 12 hours or 10 mg/kg once daily (follow with food or water to prevent esophageal issues) and/or prednisolone 5-10 mg/cat daily. Prednisolone preferred in feline patients as it is the active form of prednisone. Cats can make the conversion of prednisone to prednisolone in their liver but it is not reliable.

(4) Based on exam, pet has been anemic for some time and has adjusted to the anemia. A blood transfusion is not indicated at this time.

Follow Up
Follow-up telephone discussion: “Teddy” tested positive for both FeLV and FIV. The littermates were negative. Since the owner wishes to keep all the cats together, it will be important to stress the need for continued vaccination for FeLV and advise owner of the efficacy of the vaccines.

I recommend treatment for “Teddy” consist of doxycycline 10 mg/kg once daily for 3 weeks and possibly prednisolone 5 mg daily for 3 weeks. Reassess the PCV after that period of time to determine if there is a response to therapy. If the red blood cell count improves, the medications may have to be continued long term to maintain the PCV.

Pet should be handled as an immunosuppressed patient, with every cough or sneeze treated in a more aggressive manner. His long-term prognosis is quite guarded especially with the development of the apparent non-regenerative anemia. However, if the anemia does improve there is a chance he might do well for a longer period of time.

Anti-viral therapy has been met with questionable efficacy and I do not routinely recommend their use.

Categories: Anemia, FeLV, FIV, Stubbs