Case Studies

Thanks for the flowers! (Jennifer Kyes, DVM DACVECC)

Case Report

A 1.5 year male neutered cat presented to the hospital for declining appetite. He initially went to his regular veterinarian where blood work showed a severely elevated kidney values and a mild anemia. Upon meeting the owner and discussing Dexter’s history she mentioned that she does have a plant in the house that Dexter chews on chronically. The plant was named the Flamingo Flower (Anthurium sp). The Flamingo flower belongs to the oxalate-containing plant group.

A literature search was of limited value because it was seen in cattle, sheep, a koala and a guinea pig but it did indicated that it was indeed toxic to animals in both acute and chronic ingestions.

He was admitted to hospital and was started on therapy for kidney failure. An abdominal ultrasound was performed and both kidneys had signs consistent with an acute toxic insult. No other abnormalities were identified. His urine contained oxalate crystals.

He was treated in hospital for 7 days and he was discharged from hospital despite his kidney values not yet normal. At his first recheck appointment, 3 days after discharge, his kidney values had already started to increase. He was started on subcutaneous fluid therapy at home and a low protein diet. Over the next few months the renal values became progressively worse and he become so anemic that he received a unit of packed red blood cells.

Although he seemed a little brighter and showed an improved appetite on his next recheck his kidney values were still increasing.

Between June and July Dexter had several recheck appointments that showed increasing kidney values, periods of lethargy and in appetence and almost daily vomiting. A urine protein-creatinine ratio was performed. The results were 11.6 (normal is between 0-0.2uml./L).

On his last recheck he had not eaten in 4 days and had not urinated. He had developed peripheral edema (swelling) on all four legs and was euthanized due to end stage chronic kidney disease. His kidney was submitted for histopathology and confirmed the diagnosis of oxalate nephrosis causing chronic, progressive and fatal kidney disease.


Animals are generally discouraged from eating oxalate-containing plants as they taste bad and can cause ulcers to the mouth. In humans, it is reported that there is pain and numbness of the oral cavity and throat after ingestion. Vomiting was the most common symptom as seen in 24% of patients. In 17% of patients reported difficulty eating. Congestion and edema of the lips and mouth were seen in 70% of patients and drooling in 13%.

There are several reports of oxalate poisoning in animals including cattle, sheep, a koala and a guinea pig. Many animals had been grazing on oxalate-plants in the pasture. Affected animals developed low calcium levels causing a staggered gait, diarrhea and then became recumbent. Animals that suffered low calcium levels showed marked improvement after intravenous injection of calcium but still remained lethargic and anorexic. In acute toxicities you can see decreases in serum calcium resulting in low calcium levels. Animals can develop tremors and weakness leading to collapse and eventually death. Many animals died within two weeks of ingestion. Pathological evaluation revealed large quantities of calcium oxalate crystals in the kidneys causing kidney damage and lead to death through renal failure. A diagnosis of acute oxalate poisoning can be made based on the plant species consumed and the resultant hypocalcemia (low calcium) whereas chronic cases often have normal calcium levels but chronic kidney failure and calcium crystals in their urine.


Oxalate plants are readily available at florist shops and grocers. We need to inform the veterinary community and our clients as to the risks of oxalate plants in the household. Both the acute and chronic ingestion of these plants can result in life threatening illness either from acute hypocalcemia (low calcium) or chronic renal failure.




Flamigo Flower (Anthurium sp)


Well, now you have ticked me off! (Jennifer Kyes, DVM DACVECC)

Case Report

A 6-year-old female spayed Great Dane presented for lethargy and fever.

She was adopted by the owner through Great Dane rescue out of the United States several years ago but was unsure of the specific state.

Initial diagnostics included routine blood work that showed pancytopenia. Abdominal ultrasound showed hepato-splenomegaly. A bone marrow aspirate for the pancytopenia was normal. The pancytopenia resolved spontaneously shortly there after. She went to surgery for a splenectomy and liver biopsy. The biopsy report showed that both the liver and the spleen were normal and was discharged.

One month later she presented again for lethargy and fever. Routine blood work showed an anemia and elevated bilirubin. The CBC showed intracellular blood parasite, Babesia gibsoni (Figure 1).


Figure 1: Babesia gibsonia


Figure 2: Babesia canis


Etiology and Epidemiology

Canine babesiosis is a tick borne disease caused by a protozoan blood parasite. Babesiosis is characterized by a hemolytic anemia, fever and splenomegaly. Some infections are subclinical while others are life threatening.

There are more than 100 species of Babesia and the first documented case of canine babesiosis was in the United States in 1934. Each species of Babesia can vary in their biology, virulence and pathophysiology.

Ticks are the most important means of transmission for Babesia however some believe that non-vector transmission is the primary means for Babesia gibsoni.

Babesia canis (figure 2) is the most common species. Babesia canis is transmitted by the brown dog tick (Rhipicephalus sanguineus). Babesia gibsoni is transmitted by Haemaphysalis spp. and also by dog bites. Fighting breeds such as American Pit Bull Terriers have the highest incidence of B. gibsoni. There is also evidence of transplacental transmission.


The pathogenicity of Babesia is determined by the species but host factors and immunogenic response are also important. Infected erythrocytes are removed by the immune system. Dogs may develop anti-erythrocyte membrane antibodies against self-antigens and create an IMHA. Patients with splenctomies make the parasitemia and anemia more severe.

Dogs with Babesiosis often have non-specific signs that can wax and wane. They most commonly have uncomplicated babesiosis while others are subclinical carriers. Vomiting, anorexia, and weakness are often reported. Occasionally owners report jaundice, pale mucous membranes that are caused by the IMHA and associated bilirubinemia.

Clinical findings associated with B. gibsoni include thrombocytopenia, hemolytic anemia, leukopenia and pigmenturia.


There are 3 ways to identify Babesia sp; microscopic identification, serologic testing and nucleic acid based methods. Microscopic evaluation is limited and has poor sensitivity. It is not generally recommended as a stand-alone test. B gibsoni are single small intracellular organisms.

Serological testing is helpful in diagnosing Babesia infected dogs. Indirect fluorescent antibody testing is the most commonly used for detecting antibodies formed in infected dogs. A titre greater than or equal to 64 is indicative of exposure.

Molecular genetic detection is the most sensitive and specific. PCR assays are some 1300 fold more sensitive than light microscopy.


Our dane was started on Atovaquone and Azithromycin. These two drugs in combination are shown to be the most effective treatment for B. gibsoni. Dogs generally show improvement in 24-72 hours after initiating therapy however others can take up to a week to show improvement

Imidocarb dipropionate is an effective drug for B. canis. Imidocarb is not effective in clearing B gibsoni but might reduce morbidity and mortality. Atovaquone (13.3mg/kg orally every 8 hours) and Azithromycin (10mg/kg PO every 24 hours) were given for 10 days. Atovqauone is expensive and requires an emergency drug release application from the Canadian government for its use.

In summary, she was infected with B. gibsoni while in the United states where its prevalence is much higher than here in Canada. The vague clinical signs and the lack of B. gibsoni species seen on blood work prevented us from getting a diagnosis. After the splenectomy she was immunocompromised and the B gibsoni infection returned. The second time she presented the pathologist was able to visualize the B. gibsoni within the red blood cells. The pathologist was trained in Africa and quickly recognized this parasite.

She responded well to treatment and although she required a second course of therapy she made a full recovery and follow up evaluations were clear of B. gibsoni.

Waxing Lethargically


A 5 month old F Labrador-cross presented with a waxing history of lethargy and marked shifting forelimb lameness. On physical exam, the puppy was febrile (40.1C) and lethargic. Although she was not lame on any particular limb at presentation, she was reluctant to stand and ambulate. She demonstrated discomfort on palpation of the distal radii and tibiae. There was also firm swelling in these locations, which were warm to the touch. Otherwise she had excellent ROM in all her joints; there was no crepitus, effusion, swelling, pain or instabilities noted elsewhere on the limbs. Radiographs of the distal radii were performed (Figures 1 and 2; right distal radius).


Figure 1: Lateral Radiograph: Right distal radius


Figure 2: DV Radiograph: Right distal radius



Hypertrophic Osteodystrophy (HOD)


HOD is a condition of young, typically large and giant breed dogs (Great Danes, Labradors, Irish Setters and Boxers). The grossly observable swellings of the distal radii and tibiae are characteristic for this condition. The etiology is unknown but has historically been associated with a vitamin C deficiency. This is no longer considered to be the case, but more recent studies indicated that it may be linked to the distemper virus. Radiographically there is typically a thin radiolucent line in the distal metaphysis of the affected bones. The radiolucent line becomes radiopaque with time. Extraperiosteal cuffing can also be appreciated in some cases. Treatment is symptomatic with NSAIDs and narcotics, as necessary. In severe cases, intravenous fluid administration is indicated. In most cases the clinical signs will disappear in 7-10 days, although relapse is possible. In severe cases, secondary angular limb deformities may occur.

Great Dane-lemma


A 6 year old female spayed Great Dane presented for lethargy, fever, anemia and elevated total bilirubin. She has a previously diagnosed pancytopenia three months prior that resolved without therapy. A complete blood count with pathologists review found this very interesting anomaly in the red blood cells (Figure 1).


Figure 1: Blood smear



Babesia gibsoni


Canine babesiosis is a tick borne disease (Figure 2) caused by a protozoan blood parasite. Both Babesia canis (Figure 3) and Babesia gibsoni (Figure 4) are found throughout the United States but are very rarely found in Canada. This patient was a rescue dog from the United States where the infection was likely acquired.

Grey hounds and pit bulls have a higher incidence of disease than other breeds of dogs. Babesia infections cause a wide variety of signs including anemia, splenomegaly, icterus, weight loss and fever.

Diagnosis is confirmed with blood smears and PCR (DNA testing) although there are several other tests available.

Treatment involves medications for a 10 day period but patients that are immunocompromised or have had a splenectomy are at increased risk for recurrence. To date, no drugs have been shown to eliminate B. gibsoni infections from dogs. Typically therapy has involved imidocarb diproprionate and/or diminazine aceturate. Recently, a combination of atovaquone and azithromycin was shown to either eliminate B. gibsoni infections or suppress the parasitemia below the limit of detection in the majority of treated dogs, and therefore shows promise.

Additional Figures

Figure 2: The brown dog tick can transmit Babesia gibsoni


Figure 2: Babesia canis


Figure 3: Babesia gibsoni


A Little Lame


A 3 year-old Golden Retriever presented with an acute RH lameness. Pelvic/RH radiographs were unremarkable and an ultrasound was performed.


Figure 1: Sagittal view of achilles tendon


Figure 2: Transverse view of achilles tendon



Torn right Achilles tendon


The Achilles tendon was repaired and a hybrid external fixation was used to maintain tarsal extension. Immediately post surgery the patient was given daily low level light laser therapy (LLLT) treatments for 5 days along the incision and around the area of the repair to decrease inflammation and aid in healing. The external fixator was removed after a period of 3 months and the patient was immediately referred for rehabilitation.

Upon assessment in rehab the patient was completely non-weight bearing on the right hind limb. There was considerable scar tissue around the achilles, mild to moderate atrophy of the hindlimb musculature and significantly decreased tarsal flexion.

Treatments in rehab have included:

  • Manual mobilizations of the talocrural joint to encourage tarsal flexion
  • Cross-friction massage and myofascial release techniques to break up adhesions and reorient tissue connective tissue fibres
  • Continued LLLT
  • Stretching of the right hind limb
  • Underwater treadmill, initially at slow speeds, to encourage weight bearing on the affected limb
  • Extensive home exercise program to strengthen, mobilize and stretch

After the patient’s initial treatment, weight bearing increased dramatically. Over the course of 3 months of in-house and at home treatment the patient is fully weight bearing and there is negligible atrophy of the hindlimb musculature. Talocrural flexion has dramatically improved and is well within a functional range.

The Chicken or the Egg?


A 1.5 year old male neutered Shih Tzu x Poodle mixed breed dog, presented to the neurology service for a cluster of 5-6 seizures within a 12 hour period before presentation. The seizures were increasingly frequent, with one episode every 30 min. Episodes lasted 30 sec each, were generalized tonic/clonic, with mouth foaming and urination. An MRI was performed.


Figures 1 A and B: MRI: Transverse and Fig 1B: Sagittal T2-weighted images of intracranial cystic structure (orange arrow). Cystic structure is seen as a dilated fluid-filled sac extending caudodorsally from the ventricular cisterna. The fluid is isointense with ventricular cerebrospinal fluid.


Figure 2: MRI: Transverse fluid attenuated inversion recovery sequence. Fluid in the cystic structure is hypointense to brain parenchyma and isointense to cerebrospinal fluid, indicating that the fluid in the cyst is cerebrospinal fluid.



Neurological Examination

  • Mental Status: BAR
  • Cranial Nerves:
    • Pupillary size normal and symmetrical
    • LR – responsive OU (direct and indirect)
    • Physiological nystagmus – present OU
    • Resting/positional nystagmus – absent OU
    • Menace response – OS: decreased to absent. OD: present
    • Palpebral reflex – present OU
    • Nasal septum response – present bilaterally
    • Facial symmetry – normal and symmetrical
    • Head tilt – none
  • Gait and Posture:
    • No gait deficits
    • Proprioceptive positioning – Right forelimb (+2); left forelimb (+1); Right hindlimb (+2); Left hindlimb (+1)
  • Spinal Reflexes: Adequate
  • Back Pain: None elicited

Cerebrospinal Fluid

No etiological agents or atypical cells were identified. Interpretation: No cytological abnormalities.

Magnetic Resonance Imaging

See Figures.


Quadrigeminal cyst (intracranial arachnoid cyst) and seizures

Magnetic Resonance Imaging

Adjacent to the third ventricle and continuously towards the fourth ventricle, there is an accumulation of fluid within the quadrigeminal cisterna. The fluid is hyperintense on T2-weight images. The fluid signal nulls on FLAIR images indicating accumulation of cerebrospinal fluid.


Quadrigeminal cyst. No other parenchymal abnormalities or contrast enhancing lesions.


  • Levetiracetam
  • Omeprazole
  • Phenobarbital


Intracranial arachnoid cyst (IAC), also known as quadrigeminal cyst, is a developmental brain disorder in which cerebrospinal fluid (CSF) accumulates in an additional pocket surrounded by arachnoid membrane, that forms during embryogenesis. It is a rare condition and the majority of dogs affected are small breed, brachycephalic breeds, the Shih Tzu being one of them. The most common clinical signs are seizures and cerebellovestibular dysfunction. Neck pain has also been reported. In humans, IACs are usually an incidental finding and literature suggests that may also be the same in dogs. As such, when IAC is found on imaging, other conditions that may cause similar clinical signs to the presenting complaint should be ruled out. In this particular case, neoplasia and meningoencephalitis were ruled out based on imaging and cerebrospinal fluid analysis.

For dogs that suffer from symptomatic IAC, medical therapy is usually successful initially but the response is often temporary. Successful surgical fenestration and cystoperitoneal shunting procedures have been described in literature for IAC dogs.

Seizures in this patient could be due to primary epilepsy or from the IAC. It would be difficult to differentiate the two scenarios with certainty. Response to therapy may provide some indication in the future.

A combination of antiepileptic drugs were used to control the seizures (Levetiracetam and Phenobarbital). In addition, Omeprazole, a proton pump inhibitor, was used to reduce production of cerebrospinal fluid to relieve symptomatic IAC.

She’s So (a)cute!


A 3.5 year old female spayed Boxer presented for evaluation of acute onset of severe head and neck pain while out for a walk. Proprioceptive positioning was delayed on the right side, but hopping was adequate. An MRI was performed (Figure 1).


Figure 1: MRI: Brain



Additional History

The Boxer initially presented for evaluation of pain, lethargy, and stiffness. Three months prior to presentation her owner had noticed her slowing down and she had been panting and sleeping more than usual. The patient had previously responded intermittently to Meloxicam 28kg dose PO q24h, Methocarbamol 500mg 1tab PO q12 and Tramadol 150mg tab ½ tab PO q8h.

Neurological Examination

  • Mental Status: BAR
  • Cranial Nerves: NAF
  • Gait and Posture: Ambulates well without assistance. Proprioceptive positioning delayed on right side, but hopping is adequate
  • Spinal Reflexes: Right thoracic limb flexor is harder to elicit
  • Back Pain: NAF, good cervical range of motion


In the lateral right hemisphere, affecting the frontal, parietal and temporal lobes, there is a well-demarcated 2x2x2.5cm lesion with patchy enhancement on post gadolinium T1 weighted images. The mass abuts the calvarial wall and displaces brain parenchyma medially with leftward deviation of the falx cerebri, the mass does not have broad-based contact with the calvarium, suggestive of intra-axial rather than extra-axial origin. Conclusions: mass lesion in right cerebral hemisphere, suspicious for glioma, with surrounding vasogenic edema.

Surgical Biopsy of Brain

Fleshy spindle cells which form whorls. Some of the whorls surround vascular structures giving the appearance of a hemangiopericytoma. The tumor cells have oval to elongated nuclei often with a distinct nucleolus. Cell margins are indistinct. The mitotic rate is low (1-3 mitoses PHPF). There is a marked, mainly lymphocytic, inflammatory reaction at the margins of the tumor. Hemorrhage and fibrino-cellullar exudate are also evident at the margins.


Angioblastic meningioma

Follow Up

6 months later after radiation therapy (cyber knife): There is a resolution of mass effect and right cerebral lesion identified on previous MRI (Figure 2). No pathological contrast enhancement was identified after gadolinium injection.

Additional Figures

Figure 2: MRI: Brain 6 months post radiation therapy



The patient was referred to Yonkers, New York for a type of radiation treatment called Cyberknife therapy. This type of advanced treatment uses both MRI and CT scan to precisely target the brain tumor with little radiation delivered to the surrounding normal structures. This precision allows high doses of radiation to be delivered in just one to three treatments.


Definitive or curative intent treatments for brain tumors in dogs include surgery and/or radiation therapy. Best results are seen when surgery is followed by radiation therapy, since wide surgical margins are not possible in this location and microscopic disease is often left behind leading to eventual local recurrence and a median reported survival time of 7-12 months. Radiation therapy is either delivered in small daily (Monday through Friday) doses over 4 weeks (fractionated radiotherapy) or as 1-3 large doses via a very precise machine that uses both MRI and CT scan to target the tumor (gamma knife, cyberknife or stereotactic radiosurgery). Fractionated radiation therapy is available at OVC via a cobalt unit or in the U.S. with more advanced linear accelerators. The more advanced machinery for stereotactic or cyberknife treatment is only available at some locations in the US, the closest being a private practice in Yonkers, NY. With radiation therapy, either as the sole treatment or in conjunction with surgical debulking, median survival times ranging from 1 to 3 years are reported.

The palliative benefits of corticosteroids and anti-seizure drugs can benefit dogs with brain tumors. These medications are not affecting the actual tumor cells, but are decreasing peri-tumoral edema and inflammation (steroids) and decreasing the seizure threshold. They do not affect the growth of the tumor, which eventually could lead to more seizures or development of other neurologic clinical signs. The median survival times reported with these medications ranges from 1 to 4 months. Chemotherapy is an area of interest for prolonging survival in dogs receiving palliative care or as an adjuvant to surgery or radiation therapy. The chemotherapy may act to stabilize the tumor and prevent or slow the growth, therefore delaying the time to when the tumor causes quality-of-life affecting symptoms.

Hydroxyurea is one chemotherapy drug that has been investigated in both human and canine meningioma. It tends to be well tolerated by most dogs. Potential side effects include gastrointestinal upset, anemia, immunosuppression, methemoglobinemia, hair loss, and sloughing of the toenails. Therefore, complete blood counts are recommended 2 weeks after starting and then monthly after that. An abstract has been presented which showed a benefit in overall survival in canine meningioma patients receiving hydroxyurea compared to symptomatic therapy (steroids and anti-seizure medications) alone, with a median survival time of 7-8 months.

Eye Spy


A 7 year old spayed female Lab presented for evaluation of a 2-week history of coughing. She had a history of enucleation 2 month prior for an ocular mass that was diagnosed as an iridiociliary carcinoma. Radiographs revealed multifocal pulmonary masses (figure 1) and cytology was obtained by ultrasound-guided fine needle aspiration (figure 2).


Figure 1: Thoracic Radiograph: Multifocal pulmonary masses


Figure 2: Fine Needle Aspirate: pulmonary mass


Metastatic melanoma


Cytology was diagnostic for metastatic melanoma. The most common site for malignant melanoma in the dog is the oral cavity. Complete oral examination did not reveal any lesions, and physical examination did not reveal any suspicious cutaneous lesions. Review of the histopathology report from the enucleated eye showed that the diagnosis was based on very few cells and that the majority of the tumor was found to be necrotic. The most likely explanation is that the eye mass was a malignant melanoma that was not diagnosed due to the high degree of tumor necrosis.

The majority of canine intraocular melanomas arise from the iris or ciliary body and are classified as benign. Tumors classified as malignant on histopathology have a modest metastatic rate reported at ~25% in one study. When metastasis does develop, it is typically only a few months after surgery and the prognosis is guarded. Radiographs had not been taken at the time of enucleation, because the histopathology came back with a diagnosis of iridiociliary carcinoma, and the metastatic risk was considered very low. Treatment options for metastatic melanoma include immunotherapy with the Canine Melanoma Vaccine, chemotherapy, and antiangiogenic therapy.

Feeling Crusty


Jasmine is a 5 year old, FS, Himalayan cross that presented with severe pinnal and facial crusting dermatitis (Figure 1) and purulent paronychia (Figure 2) unresponsive to antibiotic therapy. The owners reported that Jasmine was lethargic and partially inappetant. Impression cytology from beneath a newly formed crust was performed (Figure 3).


Figure 1: Severe pinnal dermatitis


Figure 2: Purulent paronychia


Figure 3: Impression cytology



Pemphigus foliaceus


Pemphigus foliaceus is the most common autoimmune dermatitis in cats. Age of onset is highly variable but the highest incidence occurs between 2-5 years of age. Lesions in cats initially appear on the head including the pinna and paws, especially at claw folds. The classic lesion is a pustular eruption. Pustules are often fragile and therefore transient. Cats typically present with crusts or erosions on the skin and purulent paronychia affecting multiple digits. An impression smear showing neutrophils and acantholytic keratinocytes suggests pemphigus foliaceus, however skin biopsies of pustules or newly formed crusts are required to confirm the diagnosis.


Immunosuppressant doses of corticosteroids (prednisolone or dexamethasone) in combination with antibiotics for secondary bacterial infection are the initial therapy. Combination immunomodulatory therapy with steroids and chlorambucil may be required in recalcitrant cases. Therapy is typically life long but some feline patients can be slowly weaned off medications and remain in remission.

Pustular Puzzle


A 3.5 year-old MN Giant Schnauzer presented with a diffuse alopecic pustular dermatitis (Figure 1). The dog was previously diagnosed with immune-mediated hemolytic anemia, and is currently receiving prednisone, azathioprine and cyclosporine. On it’s skin scraping you see something unexpected (Figure 2).


Figure 1: Alopecic pustular dermatitis lesion


Figure 2: Skin scrape of lesion



Cutaneous toxoplasmosis


Cutaneous protozoosis was diagnosed on this skin scraping cytology. Postmortem examination revealed additional protozoa within cutaneous, cardiac, pancreatic, and pulmonary tissues. Further testing of the protozoa indicated that it divided by endodyogeny, had the morphology of Toxoplasma gondii (T. gondii) tachyzoites, and stained positively with T. gondii polyclonal antibodies but not with antibodies to Neospora caninum or Sarcocystis neurona, confirming the diagnosis of cutaneous and disseminated toxoplasmosis.

Immune-mediated hemolytic anemia had been diagnosed 45 days previously. At the time of presentation, the dog was receiving prednisone, azathioprine, and cyclosporine. Immunosuppression may have predisposed this dog to disseminated toxoplasmosis, which is an uncommon presentation of toxoplasmosis.


This case was published in the Journal of the American Animal Hospital Association, 2005;41:198-202 (pdf copy).