Anti-plakin and desmoglein autoantibodies in a dog with pemphigus vulgaris

Paraneoplastic pemphigus was suspected in a 14-year-old Labrador retriever because of mucocutaneous erosions, microscopic suprabasal acantholysis, and keratinocyte apoptosis. In this patient, circulating IgG autoantibodies recognized plakin (envoplakin, periplakin) and desmoglein (desmoglein-1 and -3) antigens. Necropsy, however, failed to confirm the concurrent existence of hematopoietic or solid neoplasia. The diagnosis of pemphigus vulgaris therefore was proposed. This study illustrates that such a combination of clinicopathologic lesions and plakin/desmoglein-specific autoantibodies is not restricted to canine paraneoplastic pemphigus but can also be detected in another form of suprabasal pemphigus.     

Pathogenesis of pemphigus vulgaris in dog and man - a review

Pemphigus vulgaris is a vesiculobullous disorder that predominantly involves the oral mucous membrane of the canine and human patients. The oral lesions are usually painful erosions and ulcers. This predilection for mucous membrane may reflect the smaller number of desmosomes in the oral epithelium as compared with the epidermis. The discovery of autoantibodies against the intercellular substance of stratified epithelium in patients with pemphigus vulgaris suggests that this disease represents an autoimmune disease. The exact role of these autoantibodies in the pathogenesis of pemphigus vulgaris is not clearly understood. The diagnosis is usually based on the presence of the characteristic flaccid bullae and erosions. Biopsy specimen taken from the edge of a fresh blister and adjacent epithelial layers is suitable for routine microscopic examination and direct immunofluorescence study. Combination of corticosteroids and immunosuppresive agents are used for treatment of this disease.     

Paraneoplastic pemphigus in a dog

This report presents a case of paraneoplastic pemphigus in a 7-year-old female Bouvier. The dog initially showed extensive oral ulcerations that exacerbated upon treatment with trimethoprim-sulfadiazine. Subsequently, the dog developed vesiculobullous and ulcerative lesions on the ear margins, the nose, periocular, and at the nail beds. Due to complete therapy resistance and a deteriorating general condition, the dog was euthanized. During post-mortem examination a thymic lymphoma was found. While an early biopsy of the oral cavity revealed features of erythema multiforme, skin lesions at necropsy were typical of pemphigus vulgaris. Indirect immunofluorescence of patient serum revealed an antikeratinocyte membrane pattern typical for pemphigus. The serum was also positive on bovine bladder epithelium. In a Western blot, autoantibodies to a 210 and a 190 kDa protein were detected.     

Suspected albuterol toxicosis in a dog

CASE DESCRIPTION: A 6-year-old male castrated Shetland Sheepdog was evaluated because of severe hypokalemia and progressive paresis. CLINICAL FINDINGS: Physical examination revealed fever, tachypnea, mydriasis, hyperemic mucous membranes, severe forelimb paresis, and hind limb paraplegia. The dog had superficial and deep pain sensation in all 4 limbs. Forelimb spinal reflexes were considered normal, but hind limb reflexes were normal to slightly hyperreflexive. The panniculus reflex was considered to be normal, and cranial nerve reflexes were intact. A CBC revealed mild leukocytosis and erythrocytosis, and serum biochemical analysis revealed severe hypokalemia. Thoracic and abdominal imaging did not reveal relevant findings. Blood pressure and ECG findings were within reference limits. Questioning of the owner revealed possible exposure to albuterol via ingestion of medication intended for the owner's horse. Results of serum testing via immunoassay were suggestive of albuterol toxicosis. TREATMENT AND OUTCOME: Treatment included IV administration of an electrolyte solution and supplemental potassium chloride. The rate of potassium chloride supplementation was slowly decreased as serum potassium concentration increased. No other medical intervention was required, and the dog made a rapid and complete recovery. CLINICAL RELEVANCE: Ingestion of albuterol can lead to profound physical and serum biochemical abnormalities. Appropriate historical information should be obtained to identify possible sources and routes of exposure to intoxicants. Albuterol-induced hypokalemia can be successfully managed medically.     

Suspected congenital hyperinsulinism in a Shiba Inu dog

A 3-month-old male intact Shiba Inu dog was evaluated for a seizure disorder initially deemed idiopathic in origin. Seizure frequency remained unchanged despite therapeutic serum phenobarbital concentration and use of levetiracetam. The dog was documented to be markedly hypoglycemic during a seizure episode on reevaluation at 6 months of age. Serum insulin concentrations during hypoglycemia were 41 U/μL (reference range, 10-29 U/μL). The dog was transitioned to 4 times per day feeding, diazoxide was started at 3.5 mg/kg PO q8h, and antiepileptic drugs were discontinued. No clinically relevant abnormalities were identified on bicavitary arterial and venous phase contrast computed tomographic imaging. The dog remained seizure-free and clinically normal at 3 years of age while receiving 5.5 mg/kg diazoxide PO q12h and twice daily feeding. Seizures later occurred approximately twice per year and after exertion, with or without vomiting of a diazoxide dose. Blood glucose curves and interstitial glucose monitoring were used to titrate diazoxide dose and dosing interval. Congenital hyperinsulinism is well recognized in people but has not been reported in veterinary medicine.     

Suspected hypothyroid-associated neuropathy in a female rottweiler dog

A 7-year-old, 46-kg spayed female rottweiler dog was presented with sudden onset of disorientation, bilateral convergent strabismus, and enophthalmos. Diagnostic workup revealed hypothyroid-associated cranial neuropathy. Symptoms abated considerably upon treatment with levothyroxine-sodium (T4) at an initial dose of 800 μg/kg body weight (BW), PO, q12h, which was reduced 3 days later to 600 μg/kg BW, q12h due to severe agitation and panting. Two weeks later the dosage of the levothyroxine-sodium (T4) was reduced to 400 μg/kg BW in the morning and 600 μg/kg BW in the evening. Eight weeks after the initial presentation, the dog had recovered with only mild convergent strabismus in the right eye. This is the first case report of suspected hypothyroid-associated neuropathy resulting in these symptoms.     

Suspected drug-induced destructive cholangitis in a young dog

A nine-month-old miniature doberman was referred for the evaluation of chronic icterus. History and clinical and histopathological findings were supportive of a diagnosis of drug-induced destructive cholangitis. The main histopathological findings were canalicular, centrilobular cholestasis and ductopenia with moderate inflammatory infiltrate. The dog had received three types of treatment for demodicosis before the onset of jaundice. Amoxicillin-clavulanate, amitraz, milbemycin oxime or an interaction between two of the three drugs may have been responsible for the destructive cholangitis.     

Paraneoplastic pemphigus in a dog with splenic sarcoma

Paraneoplastic pemphigus (PNP) is an autoimmune blistering skin disease of humans that consists of characteristic skin lesions associated with concurrent neoplasia. In this study we provide histologic and serologic evidence to support a diagnosis of PNP in a dog with splenic sarcoma. Skin lesions consisted of widespread erosions involving haired skin, mucocutaneous junctions, and oral mucosa. Microscopic examination of skin and mucosae revealed lesions consistent with both pemphigus vulgaris and erythema multiforme. Immunoprecipitation confirmed that circulating IgG autoantibodies from this patient recognized five distinct antigens, presumed to represent epidermal plakins. Clinical, histopathologic, and immunologic findings in this patient were similar to those observed in human patients with PNP. The splenic neoplasia in this dog was diagnosed as a phenotypically variable spindle cell sarcoma. To date, only one other dog has been reported with PNP. This is the second reported case of canine PNP and the first patient in whom skin lesions were identified in association with splenic neoplasia.     

Suspected immune-mediated megakaryocytic hypoplasia or aplasia in a dog

Megakaryocytic hypoplasia or aplasia causing thrombocytopenia was diagnosed in a 3-year-old Miniature Poodle with scleral hemorrhage, melena, ecchymoses, and blood-loss anemia. Immunosuppressive, cytotoxic, and lithium carbonate therapy resulted in successful correction of the dog's disease. It is important to recognize megakaryocytic hypoplasia or aplasia as the cause of thrombocytopenia, since the response to therapy will be slower when there is stem cell injury.     

Suspected primary hyperparathyroidism in the dog

Abstract

Extract

Primary hyperparathyroidism is the term given to a group of primary pathological conditions of the parathyroid gland which result in the excessive production of parathyroid hormone. It was first described as a disease entity in man by Barr et al. (1929 Barr, D. P., Bulger, H. A. and Dixon, H. H. 1929. Hyperparathyroidism. J. Amer. med. Ass., 92: 951–952.  [Google Scholar]) who grouped under this heading a series of conditions that had hitherto been described as osteomalacia, multiple cystic tumours of the bone, or parathyroid tumours.