Spirocerca lupi infection in the dog: a review

Spirocercosis is a disease occurring predominantly in Canidae, caused by the nematode Spirocerca lupi. Typical clinical signs are regurgitation, vomiting and dyspnoea. The life-cycle involves an intermediate (coprophagous beetle) and a variety of paratenic hosts. Larvae follow a specific migratory route, penetrating the gastric mucosa of the host, migrating along arteries, maturing in the thoracic aorta before eventually moving to the caudal oesophagus. Here the worm lives in nodules and passes larvated eggs which can be detected using zinc sulphate faecal flotation. Histologically, the mature oesophageal nodule is composed mostly of actively dividing fibroblasts. Spirocerca lupi-associated oesophageal sarcomas may occur and damage to the aorta results in aneurysms. A pathognomonic lesion for spirocercosis is spondylitis of the thoracic vertebrae. Primary radiological lesions include an oesophageal mass, usually in the terminal oesophagus, spondylitis, and undulation of the aortic border. Contrast radiography and computed tomography are helpful additional emerging modalities. Oesophageal endoscopy has a greater diagnostic sensitivity than radiography. Endoscopic biopsies are not sensitive for detecting neoplastic transformation. Doramectin is the current drug of choice, effectively killing adult worms and decreasing egg shedding. Early diagnosis of infection is still a challenge and to date no ideal regimen for prophylaxis has been published.     

In vitro and in vivo bioactivity of recombinant canine hepatocyte growth factor

Hepatocyte growth factor (HGF) is crucial for the development and regeneration of the liver and offers a possible new therapeutic strategy for the treatment of canine liver disease. In this study, the in vitro and in vivo bioactivity of recombinant canine HGF (rcHGF) produced with a baculoviral expression system in insect cells was measured. In vitro rcHGF induced mitogenesis, motogenesis, and phosphorylated the HGF receptor c-MET and its downstream mediators PKB and ERK1/2 in two canine epithelial cell lines. After a partial hepatectomy (phx) in dogs, rcHGF increased phosphorylation of c-MET, PKB and ERK1/2. A moderate increase was seen with the cell cycle protein PCNA in rcHGF treated livers, but no HGF-induced increase in liver weight was seen 7 days after phx. Furthermore, rcHGF treated livers showed lower levels of the key mediator of apoptosis, caspase-3, at 7days after phx. It is concluded that rcHGF is a biologically active protein in vitro and in vivo and the baculoviral expression system supplies sufficient amounts of rcHGF for future clinical studies in dogs.     

Dermatographism in a horse,responsive to cetirizine treatment

Dermatographism is a common condition in man that occurs when pressure is applied to the skin and mast cells are triggered to release histamine, causing local urticarial lesions. This case report concerns a 4-year-old Quarter Horse gelding that was presented with pressure induced urticaria. Moderate pressure on the skin induced nonpruritic urticaria-like swelling after approximately 3–5 min, which lasted for approximately 2–3 h. Initial treatment with cyproheptadine gave an incomplete response and unacceptable sedation as a side effect. On the second generation antihistamine cetirizine (0.2 mg/kg bwt twice daily), dermatographism was no longer present and no side effects occurred. Treatment was continued for 4 months, with at least three attempts to discontinue therapy resulting in recurrence of lesions within 24 h. Lesions resolved each time within 24 h of recommencing therapy. Dermatographism did not recur after the horse was moved to another location despite discontinuation of therapy. This report describes a case of equine dermatographism responsive to cetirizine.     

Thymic hyperplasia causing right ventricular outflow tract compression following treatment for oesophageal rupture in an Arabian colt

True thymic hyperplasia has been reported sporadically in the human literature as an immunological rebound phenomenon following immunosuppressive treatment or disease. There are limited accounts in domestic species, mainly following vaccination, and thymic hyperplasia has not been a recognised condition in the horse to date. This report details a case of true thymic hyperplasia in a 10-week-old Arabian colt diagnosed by histopathology of core biopsy samples. The colt developed pulmonary stenosis caused by compression due to a space occupying lesion in the cranial mediastinum following a 3-month history of hospitalisation for treatment of traumatic oesophageal rupture with perioesophageal abscess formation. Diagnostic imaging of the cranial mediastinum was indicative of a thymic mass, and histopathology confirmed the mass was normal (hyperplastic) thymic tissue. The colt was treated with a tapering dose of corticosteroids, which led to involution of the hyperplastic tissue and resolution of pulmonary artery compression. Thymic hyperplasia may be an unrecognised sequela to chronic inflammation in horses and was only identified in this case when the size was sufficient to compress right cardiac outflow.