A 4-year-old female Coonhound presented for soft stools of two days. She became lethargic within the last 12 hours. On examination the only abnormalities noted was mild enlargement of the peripheral lymph nodes.

Fecal floatation showed Nanophyetus salmincola.  Treatment was initiated for Salmon Poisoning.

A dog ingesting raw fish infected with a fluke, Nanophyetus salmincola, typically causes salmon poisoning. Mostly salmonids, some non-salmonid fish, and the Pacific Giant Salamander can be infected with the fluke. Salmon poisoning can occur along the Washington coastlines, Oregon coastlines, and the Northern California coastlines, based on the snail (Oxytrema silicula) population that is used as the intermediate host by the fluke.

The fluke carries a rickettsia (Neorickettsia helminthoeca) that upon entering the host travels to the intestines and most lymph nodes causing inflammation at those sites. 

 The inflammation caused by the rickettsia causes clinical signs within 5 to 7 days after ingesting the infected fish. There is an initial fever that may resolve before presentation of other clinical signs. The inflammation may also cause: anorexia, acute weight loss, vomiting, and diarrhea. Enlarged lymph nodes can be seen as early as 5 days after ingestion. Death may occur within 7 to 10 days after the initial clinical signs.

The diagnosis can be made based on the dog’s history of exposure to raw fish or access to streams or lakes in the environment. A fecal floatation is performed to identify the fluke, Nanophyetus salmincola.  However the fluke is not present within the feces until 5 to 8 days post exposure, allowing false negatives to occur if performed early. Aspirating the enlarged lymph nodes, and identifying the rickettsia carried by the fluke within the lymphoid tissue confirms the diagnosis.

Treatment of salmon poisoning consists of supportive care and the elimination of the rickettsia and fluke from the system. Typically the patient is dehydrated from vomiting and diarrhea, requiring intravenous fluids to correct the fluid loss. Medication may be given to control the nausea and secondary inflammation to the large bowel. The rickettsia is eliminated by the administration of the drugs: doxycycline, tetracycline, oxytetracycline, or chloramphenicol. The fluke is eliminated by the administration of a dewormer, praziquantel. 

The prognosis of the pet depends on the severity of disease at the time of diagnosis. Most respond favorably to treatment when initiated. If left untreated the prognosis is poor.

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Sophie is a seven year-old spayed female Miniature Schnauzer. She presented with a complaint of increased thirst and frequency of urination. She had a great appetite, but seemed to be loosing weight.

On physical examination, it was found that Sophie had lost three pounds since her last visit 8 months ago. Despite weight loss, she was overweight. She also had small cataracts in both eyes.

Based on the history provided by the owner and findings on physical examination, a complete blood count, serum biochemical screen and urinalysis were performed. Abnormalities from the blood work included  hyperglycemia (increased blood sugar), hypercholesterolemia (high cholesterol), and mildly increased liver enzyme activity. The urinalysis showed glucosuria (sugar in the urine), and a moderate amount of bacteria. A urine culture was performed and was positive.

Sophie was diagnosed with diabetes mellitus and a secondary urinary tract infection. She was started on insulin injections twice a day and antibiotics. Her urinary tract infection has resolved, and her diabetes is well controlled.

Overview of Diabetes Mellitus in Dogs

Diabetes mellitus is an endocrine (hormone) condition in which a deficiency of insulin impairs the body’s ability to utilize sugar for energy. With low insulin levels, glucose (sugar) is not able to enter the cells of the body. Therefore, the level of glucose circulating in the bloodstream is too high. Disease occurs from these high glucose levels, as well as inadequate delivery of sugar to the tissues, and changes in metabolism.

Unlike humans, most dogs have type I diabetes. This means that there is inadequate production of insulin from the pancreas. It can occur secondary to chronic disease of the pancreas, but more often is a genetic predisposition that causes dysfunction.

Diabetes can affect dogs of any age, but is much more common between 7 and 9 years of age.  Females tend to be more prone to this disease. Breeds at increased risk include Australian terrier, Samoyed, Schnauzer, Bichon frise, Cairn terrier, Keeshond, Spitz, Fox Terrier and the Poodle.

Symptoms include increased thirst, increased frequency of urination, weight loss despite a good appetite, sudden blindness, lethargy and poor body condition.

Cataracts often cause blindness in diabetic dogs.

A diagnosis is made by detection of glucose in the urine and high levels of glucose in the blood.  Secondary urinary tract infections are common due to high levels of sugar in the urine. Urine culture is done routinely in a newly diagnosed diabetic patient.

A glucometer is used to measure blood glucose levels.

Treatment of diabetes mellitus is required for the life of the pet. Insulin injections need to be given on a daily basis. Most dogs need the injections every 12 hours. Dietary changes are an important part of treatment, as food high in fiber and low in fat help to regulate the blood sugar levels.

Diabetic pets require routine monitoring of blood glucose levels in response to administered insulin injections. They need frequent examination by the veterinarian, and blood and urine monitoring. With proper treatment and follow-up care, diabetic dogs can live a long life.

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An 8 year old female spayed Retriever mix presented with a history of exercise intolerance. On physical examination no abnormalities were found. Blood chemistries revealed hypercalcemia (elevated calcium levels). 

Hypercalcemia can be a result of: systemic fungal disease, bone resorptive diseases, spurious laboratory results, primary hyperparathyroidism, vitamin D toxicity, Addison’s disease, secondary to renal disease, or secondary to specific cancers.

The diagnosis in this case was primary hyperparathyroidism. The diagnosis was based on elevated parathyroid hormone (PTH) levels, elevated ionized calcium levels, no evidence of the cancerous tumors on physical examination or radiographs, and a solitary nodule on a right parathyroid gland found on ultrasound.

The parathyroid glands are four glands located with in the cervical neck adjacent to both the thyroid glands. The parathyroid glands release a hormone, PTH, to regulate ionized calcium levels within the body. 

Primary hyperparathyroidism is the excessive release of parathyroid hormone (PTH) from the parathyroid glands. The excessive PTH typically is a result of a benign adenoma (glandular tumor) on one or more parathyroid gland. Hyperparathyroidism is typically seen in older dogs and cats greater than 7 years of age. Keeshonds and Siamese appear to have a predisposition. Typically an incidental hypercalcemia (elevated calcium levels) is found on routine blood chemistries, with no other clinical signs. However the other clinical signs that may be found include:  lethargy, urinary incontinence, weakness, exercise intolerance, inappetence, shivering, muscle wasting, vomiting, constipation, stiffness, hematuria (blood in urine) from uroliths (bladder stones), polyuria (increased urination, and polydipsia (increased thirst).

Diagnosis of primary hyperparathyroidism starts with a physical examination and medical history to help rule out other differentials. A complete blood cell count (CBC) is found to be within normal limits. Blood chemistries show elevated calcium levels. Elevated kidney enzymes can be found in cases where the calcium has been elevated for a prolonged amount of time. An ionized calcium level is typically obtained to confirm the elevated calcium levels. The ionized calcium only measures the active form of calcium in circulation, whereas calcium levels found on routine blood chemistries measures inactive and active calcium within the body. Next the parathyroid hormone levels (PTH) and the parathyroid related protein levels (PTH-rP) are obtained to determine if a primary or secondary hyperparathyroidism is present. The PTH levels are elevated in primary hyperparathyroidism. An ultrasound of the parathyroid glands is performed to determine if a solitary nodule is present, which parathyroid gland the nodule is present on, and to ensure the margins of the nodule are defined to allow surgical resection.

The treatment of hyperparathyroidism consists of surgical removal of the enlarged parathyroid gland or ethanol ablation of the enlarged parathyroid gland via ultrasound. Ethanol ablation is about 70% effective, and may require a second treatment. The ablation requires a general anesthetic and the use ultrasound guidance to inject the ethanol into the affected parathyroid gland. Surgical excision (parathyroidectomy) tends to be more effective than the ethanol ablation. Prior to the surgery the patient may undergo fluid diuresis with intravenous fluids in conjunction with furosemide, prednisone, or pamidronate to lower the calcium levels within the patient. The abnormal tissue is submitted for histopathology post-operative to ensure a benign tumor was present.

Afterwards, with either treatment method the patient may develop hypoparathyroidism (low parathyroid levels and low calcium levels). The overactive parathyroid is being removed or destroyed, leaving the inactive parathyroid glands. The hypoparathyroidism may occur 1 to 7 days post-parathyroidectomy. The higher the calcium levels prior to surgery the increased likelihood the patient will develop hypoparathyroidism. Due to this, the patient is typically hospitalized for 5 to 7 days post-operatively to allow for monitoring of ionized calcium levels on a twice daily basis. If the patient should develop low ionized calcium levels or display clinical signs of hypoparathyroidism, treatment is initiated.  The clinical signs of hypoparathyroidism include: panting, nervousness, facial twitching, muscle twitching, ataxia, and/or seizures.

The treatment for hypoparathyroidism includes: oral vitamin D and calcium supplementation for long-term, and injection of calcium intravenously until clinical signs resolve for acute cases. The goal for treatment is to maintain calcium levels within the low to low-normal range without the patient experiencing clinical signs. This requires daily testing of ionized calcium levels until the calcium levels stabilize with treatment. Once the patient is stable the supplements are gradually withdrawn over 3 to 6 months while monitoring for reoccurrence of clinical signs and checking ionized calcium levels to determine if the atrophied parathyroid glands are becoming functional. There are some patients that will have to be maintained on vitamin D and calcium supplements for the lifetime.

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Case 1: A female spayed 8 year old Greyhound presented for weight loss, occasional vomiting, and diarrhea. On physical examination no abnormalities were noted.

Abdominal radiographs were taken. The abdominal radiographs (x-rays) revealed diffuse thickening of the small intestines. Fecal floatation was negative for internal parasites. A complete blood cell count (CBC) showed a mild anemia. The chemistry profile showed a hypoproteinemia (low protein levels). 

An abdominal ultrasound was performed. Abnormalities on the ultrasound were diffuse thickening of the intestines and enlargement of the mesenteric lymph nodes. The differentials for the ultrasound findings include:  inflammatory bowel disease (IBD), lymphosarcoma, and, lymphangectasia. 

Biopsies of the intestines were obtained via abdominal surgery. Histopathology of the intestinal biopsies showed moderate to severe infiltration of the intestinal mucosa with lymphocytes and plasma cells.     

The diagnosis in this case is inflammatory bowel disease (lymphocytic-plasmacytic enteritis). IBD is the most commonly encountered inflammatory disease of the small intestine in dogs and cats. The inflammatory disease is the immune systems response to food antigens in the intestinal tract. Infiltration of the intestinal mucosa with lymphocytes and plasma cells results in a malabsorptive syndrome, resulting in weight loss and diarrhea. Treatment consists of immunomodulation (suppression of the immune system) with medications in conjunction with dietary modification. The medications used may include: prednisone, metronidazole, azathioprine, cyclosporine, chlorambucil, and/or cyclophosphamide. The diet is changed to a restricted fat diet with a novel protein and carbohydrate source or a hypoallergenic diet with hydrolyzed proteins. The novel protein and carbohydrate are ones the immune system has not been exposed to in hope that the immune system will not recognize the diet as antigen. The hydrolyzed protein diet (ex Hill’s Z/D) processes the protein to a small size in order for the immune system to not respond to it as an antigen. In some cases cobalamine (a vitamin B) supplementation is given. Vitamin B is absorbed within the small intestine, however with malabsorptive disorders poor absorption of the vitamin occurs. Vitamin B promotes intestinal health. 

The medications are typically tapered one at a time every two to three weeks, usually starting with the prednisone. The goal is to taper the patient off of the medications or to the lowest dose necessary to control the clinical signs. Moderate to severe disease usually requires prolonged medical treatment. The dietary change is a lifetime treatment, and needs to be strictly followed to prevent disease relapses. Prognosis is typically good with medical treatment.

Case 2: A female spayed 8 year old Greyhound presented for weight loss, occasional vomiting, and diarrhea. On physical examination no abnormalities were noted.

Abdominal radiographs (x-rays) were taken. The abdominal radiographs revealed diffuse thickening of the small intestines. Fecal floatation was negative for internal parasites. A complete blood cell count (CBC) showed a mild anemia. The chemistry profile showed a hypoproteinemia (low protein levels).

An abdominal ultrasound was performed. Abnormalities on the ultrasound were diffuse thickening of the intestines and enlargement of the mesenteric lymph nodes. Adequate cytology of the mesenteric lymph nodes could not be obtained.

Biopsies of the intestines were obtained via abdominal surgery. Histopathology of the intestinal biopsies revealed a diagnosis of lymphosarcoma.

Lymphosarcoma (LSA) is one of the most common cancers seen in middle age to older dogs and cats. Lymphosarcoma is a proliferation of lymphocytes which can occur in any organ within the body. Lymphosarcoma is sensitive to chemotherapy, but usually not curable. Chemotherapy is used to put the cancer into remission (no presence of cancer) without decreasing the quality of life in the patient. The remission rate for cats is 65-75%, while the remission rate for dogs is 80-90%. Treatment consists of a multimodal chemotherapy regimen that may include some or all of the following drugs: prednisone, L-asparaginase, vincristine, cyclophosphamide, doxorubicin, and methotrexate. Radiation is typically not helpful with the treatment of lymphosarcoma. The survival rate without treatment is about one month; with the use of only prednisone is about two months. A multimodal protocol typically allows the patient to remain in remission for 4-9 months, before the protocol has to be repeated or a rescue protocol has to be used.  It is usually difficult to achieve a second remission. Overall with the use of a multimodal therapy the patient has about one year of survival. A poorer prognosis exists for the patients that present with hypercalcemia (high calcium levels), cancer in multiple organs or body cavities, and if a T-cell lymphosarcoma is present.

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Jack is a purebred Labrador retriever that presented to Kitsap Veterinary Hospital when he was six weeks old for vomiting after eating solid food. He was able to nurse without incident. Upon physical examination, Jack was underweight but otherwise healthy.

Jack was seen again at eight weeks of age for a similar complaint. No longer nursing, he vomited after every meal. Upon further questioning of the owner, it was determined that Jack was actually regurgitating undigested food. Physical examination revealed a soft, fluid-filled mass at the thoracic inlet (where the neck meets up with the chest). Wheezes were heard in his lungs, indicative of pneumonia.

Antibiotic treatment was begun for pneumonia, and diagnostic tests were recommended to the owner.  Cervical (neck) and thoracic (chest) radiographs were obtained. Pneumonia was confirmed. Also, the trachea was displaced by a much dilated esophagus. A barium contrast radiograph showed that the dilation of the esophagus ended abruptly at the base of the heart. Contrast material entered the stomach in a small stream.

Based upon the findings on examination and radiographs, Jack is suspected to have a congenital malformation called Persistent Right Aortic Arch. This is a condition where a band of fibrous tissue entraps the esophagus as it passes over the heart base, causing strangulation. This leads to dilation of the esophagus in front of the entrapment, and precludes solid food from passing. Often, the food accumulates in the dilated pouch of the esophagus until it is regurgitated. Aspiration pneumonia is a common complication, as the regurgitated material is inhaled.

A Persistent Right Aortic Arch can be successfully treated surgically. The thoracic cavity is entered, and the fibrous band severed. In addition, a procedure is done to stretch the esophageal stricture. Following surgical intervention, a good prognosis is expected.

Jack is currently stable, but has intermittent bouts of aspiration pneumonia while awaiting his surgery.

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Mia a 12 year old female spayed German Shepherd-Rottweiler mix presented for a non-weight bearing lameness on the left front leg for three days duration. There was a previous history of osteoarthritis in the stifles (knees) and hips, along with biceps tendonitis (inflammation of the biceps tendon) in the left shoulder. There is no history of travel outside of Washington.

On physical examination Mia was painful on flexion and extension of the left shoulder. There was no pain on deep palpation of the humerus and scapula. The rest of the orthopedic examination was within normal limits.

Radiographs were taken of the left shoulder. The radiographs revealed a solitary lytic area present on the proximal-caudal humerus. Chest and abdominal radiographs were taken to check for metastases, no abnormalities were found. A complete blood cell count (CBC) and chemistry profile was within normal limits.

The differentials for solitary lytic bone lesions consist of: bone tumor (osteosarcoma, chondrosarcoma, synovial cell carcinoma, fibrosarcoma) and fungal infection (mycotic osteomyelitis).

The diagnosis in this case was osteosarcoma. Based on the breed, age, radiographic findings, and there being no travel history outside of Washington. Palliative treatment was chosen based on the age and presence of osteoarthritis in the other limbs. The treatment consisted of Rimadyl (anti-inflammatory) and Tramadol (synthetic opioid).

Osteosarcomas are the most common primary bone tumors in dogs, accounting for 80% of the cases. It is typically found in the long bones (proximal humerus, distal radius, distal femur, and the tibia) of middle age to older large breed dogs. Osteosarcomas have a characteristic appearance on radiographs. The radiographs have a moth-eaten appearance to the bone due to the tumor destroying bone and causing inflammation at the site. Typically osteosarcomas do not cross the joint space.  

A tentative diagnosis is made based on signalment, clinical signs, and radiographs. A definitive diagnosis can be made by performing a bone biopsy under anesthesia. This would help to differentiate neoplasia from fungal disease in patients with a history of travel to regions with endemic fungal disease. Bone biopsies must be taken from the center of the lesion. Based on the amount of reactive bone caused by the tumor it is difficult to obtain a diagnostic sample. The patient tends to be very painful after bone biopsies, and can be difficult to control the pain with medications. 

Osteosarcoma has a high incidence of metastasis to the lungs. Thoracic radiographs should be taken to look for metastatic lesions in the lung tissue. Typically only 10% of dogs have detectable lung lesions at diagnosis; however 90% of the cases have metastasis at the time of diagnosis. A CT scan can be performed under anesthesia to detect lung metastases fewer than 3mm in diameter. The presence of lung lesions carries a poor prognosis.

The treatment for osteosarcoma consists of amputation in conjunction with chemotherapy. Median survival with amputation and chemotherapy is 9 to 12 months, may be curative if there was no metastasis to the lungs. Amputation without chemotherapy has a median survival time of 3 to 4 months. One must take into consideration the dog’s quality of life to determine if amputation is an option. For the cases amputation is not an option palliative treatment is chosen focusing on pain control. The mean survival time with palliative treatment is 4 to 6 months. Pain control can be obtained using a combination of the following: 1. A NSAID (non-steroidal anti-inflammatory) in conjunction with an opioid, 2. Palliative radiation on an outpatient basis, 3. Use of bisphosphonates (Pamidronate) intravenously to slow bone lysis.

Osteosarcoma usually results in euthanasia of the patient when the pain is uncontrollable or a pathological fracture occurs at the primary tumor site due to the thinning and weakening of the bone from tumor lysis.