A 10-year-old castrated male Shih-tzu dog presented with a history of generalized demodicosis, refractory to conventional therapy with ivermectin and amitraz for a year. The patient was also diagnosed with concurrent deep pyoderma, Malassezia dermatitis, and otitis externa. Treatment with amoxicillin-clavulanate, antifungal drugs (itraconazole, miconazole), and milbemycin oxime resulted in a good response for 90 days. Approximately 4 months later, the first relapse of demodicosis occurred and the miticidal therapy was changed to ivermectin. Additional diagnostic tests were performed to investigate an underlying cause for the recurrence of demodicosis, and endocrinopathies and allergic dermatitis were excluded based on the results. Although ivermectin therapy was sustained for 440 days, a second relapse occurred and amitraz baths were added to the therapy. Despite this therapy, the demodicosis persisted, and the miticidal therapy was changed to oral fluralaner, which led to rapid resolution. Demodicosis did not recur again before death approximately 920 days after administration of oral fluralaner. This case report describes the complete resolution of refractory demodicosis using oral fluralaner in a dog.

A nine-year-old neutered male cat was presented with chronic cough and vomiting. Thoracic radiography showed regions of fatty opacity in the right caudoventral region. On positive contrast celiography, contrast agent did not move into thoracic cavity. Computed tomography revealed 7-mm diameter of defect at the right diaphragmatic crus and a 2-mm diameter defect at the left ventral diaphragmatic crus. Through the right diaphragmatic defect omental herniation was confirmed by the presence of contrast enhanced omental vessel running across the diaphragm. On exploratory thoracotomy, the omentum protruded into the thorax through the right diaphragmatic defect, and it contained a yellowish lipomatous mass. The protruded omentum containing a mass in the thorax was removed, and the right diaphragmatic defect was closed. Histopathologic examination revealed that the protruded omentum showed normal omental structure and the adipose mass showed lipoma surrounded by fibrous tissue. In conclusion, a thorough examination is necessary to confirm the origin of the mass located near the diaphragm.

A 12-year-old male American Cocker Spaniel was diagnosed with a type of chronic hepatits (CH) called cholangioheaptits. Routine supportive medication was administered to the patient, and ex vivo boosted immune cell (EBI-C) therapy was used for the treatment. A histopathologic examination of the liver 19 months later revealed that the cholangiohepatitis had progressed to cholangiocarcinoma. The medication and immune cell therapy was maintained. Two months after the new diagnosis, the patient's state worsened, and the dog died 635 days after the first visit. EBI-C therapy is a type of immunotherapy, where immune cells are isolated from the patient's peripheral blood mononuclear cells, expanded ex vivo, and then infused into the patient intravenously every two weeks. EBI-Cs (mean: 2.78 × 10⁸ cells) were obtained 38 times and infused every two weeks. Most EBI-C were T-lymphocytes (99.24% of total EBI cells). T-lymphocytes produce large interferon (IFN)-γ, and IFN-γ inhibits liver fibrosis in dogs with CH. Moreover, in bile duct cancer, an increase in T-lymphocytes correlates with decreasing tumor invasion and metastasis. Thus, we propose that EBI-C therapy is applicable as a new supportive therapy for canine liver disease if other treatments like drug medication, surgery, or radiation are unavailable.

A 10-year-old spayed female Maltese with a history of vomiting and lethargy was referred to the hospital. Physical examination revealed dehydration and severe pain following abdominal palpation. A large mass was observed in the cranial abdomen through radiography and ultrasonography. Laparotomy was performed to find the origin of the mass. The mass was about 8 cm originating from the cecum and subsequently removed. Histopathologic evaluation revealed that the cecal mass was suspected to be a mesenchymal-derived tumor. Through immunohistochemistry, the mass was diagnosed as a gastrointestinal stromal tumor (GIST) based on the c-kit expression. Given its recurrence, postoperative preventive therapy was initiated with masitinib mesylate, which is a tyrosine kinase inhibitor. The animal did not show any side effects during the medication period. After 6 months of therapy, it was well controlled without any recurrence. In this case, we introduced a novel postoperative management of GIST using masitinib mesylate.

An 11-years old spayed female Persian chinchilla cat presented with acute onset of blindness from bilateral retinal detachment and systemic hypertension. On physical examination, the cat was tachycardic (240 beats/min) with a systolic blood pressure of around 250 mmHg. Clinical findings, blood works, urinalysis, thyroid function test, radiography, echocardiogram, and ultrasonography were performed to rule out underlying diseases. Organ injury induced by systemic hypertension including bilateral retinal detachment and left ventricular hypertrophy were confirmed by ultrasound. Based on these results, it was diagnosed as feline idiopathic hypertension with target organ damage (TOD). The cat was treated with a combination therapy using high doses of amlodipine, telmisartan, and atenolol. After the treatment, its hypertension and TOD were improved. This case showed that appropriate therapeutic management can help prevent TOD associated with feline hypertension.

A 7-year-old intact male Maltese dog was presented with firm, raised, erythematous, alopecic, and pruritic skin lesions on the right dorsal distal metatarsal region and the tail. The skin lesion started a year ago with a crust-like lesion on the right dorsal distal metatarsal region which gradually swelled as the patient continued to lick and chew without healing. Recently, similar lesions occurred on the tail. Based on the licking history and ruling out other diseases through skin examination, acral lick dermatitis (ALD) was diagnosed. Treatment included antidepressants, preventive antibiotics, topical corticosteroid, and wearing Elizabethan collar as a physical barrier. After three weeks, the lesion on the hind limb healed entirely. However, the tail lesion recurred as it was able to lick the tail again with a type of an E-collar. This case shows that it is essential to block the contact lesion and provide medical treatment until the lesion has been completely resolved for successful management of ALD.

A 4-year-old Thoroughbred mare was brought to the Korea Racing Authority Equine Hospital with heightened sensitivity to touch of the hindquarter, reluctance to step forward, frequent urination even during training, clitoral winking, tail swinging, tail lifting, and training difficulties due to being in constant heat. The trainer claimed that she was in heat and exhibited reduced performance. Physical and lameness examinations revealed no abnormality. Rectal palpation and transrectal ultrasonography revealed normal reproductive organs and estrus. As she exhibited typical estrous behavior without any other physical conditions, the mare was considered to express undesirable estrous behavior. An intrauterine glass ball was inserted into the mare on ovulation day. However, the estrous behaviors were reduced unsatisfactorily. Additionally, 1 mL of peanut oil was administered on the 10th day after the intrauterine device insertion. The mare returned to training and expressed no undesirable estrous behavior over 30 days after the peanut oil treatment. However, further follow-ups were not conduct as the mare was retired to a farm after a limb injury occurred during training. This is the first report of undesirable estrous behavior in a Thoroughbred mare under the rules of racing in Korea. It is recommended that equine clinicians in Korea consider peanut oil as a therapeutic agent to control mares' estrous behavior-related problems.

A seven-month-old castrated male Chihuahua weighing 1.6 kg presented with generalized tonic-clonic seizure following ingestion of isoniazid. Emergency treatment with three doses of diazepam (total 1.5 mg/kg, intravenous [IV]) and phenobarbital (15 mg/kg IV) was administered. The seizure stopped after administration of propofol (constant rate infusion [CRI]; 0.2 mg/kg/min). Blood analyses showed mildly increased serum blood glucose concentration, hyperkalemia, and hyperphosphatemia. On suspicion of isoniazid toxicity, activated charcoal (1 g/kg, orally), lipid emulsion (CRI; 9 mL/hr), and pyridoxine hydrochloride (70 mg/kg IV) were added to the treatment regimen. Twelve hours after presentation, the dog showed increased serum liver enzyme activities, serum blood urea nitrogen, and creatinine concentrations indicating hepatic and renal failure. Twenty-two hours after presentation, blood analysis still revealed increased liver enzyme activities, blood urea nitrogen, and creatinine concentrations with low blood glucose concentration. Twenty-six hours after presentation, the dog's vital signs deteriorated and the owner elected for the dog to be euthanized. This is the first report of the clinical course of isoniazid toxicosis in a dog in South Korea. Furthermore, to our best knowledge, this is the first report where secondary multiple organ failure was observed due to isoniazid toxicosis. Clinicians should be aware of the possibility of isoniazid toxicosis in dogs. Rapid initiation of treatment after clinical recognition is warranted in such cases.

A 10-year-old spayed female beagle referred to the Veterinary Teaching Hospital of Chungnam National University presented with acute diarrhea, depression, anorexia, and emaciation. The laboratory findings of the dog showed leukocytosis, high C-reactive protein, and low albumin levels. Fecal examinations revealed severe infection with Strongyloides (S.) stercoralis, with a high fecal score (6/7). Consequently, the dog was diagnosed with hyperinfection of S. stercoralis, and thus, was treated with fenbendazole and ivermectin after discontinuation of prednisolone treatment. The dog showed negative on the Fecal Dx^® Antigen Panel (IDEXX Laboratories Inc., Westbrook, ME, USA) after treatment, and clinical signs disappeared with normal stool consistency.