Mouse anti-Canine Heartworm Monoclonal antibody, clone D79H81

A 4 year-old, male Hungarian Vizsla dog which had never been abroad was referred with poor general condition, decrease in body weight, haematemesis and jaundice to the Central Clinic of Veterinary Science University, Budapest. After symptomatic treatment abdominal ultrasonography and diagnostic laparatomy were carried out. The dog was humanely euthanized two days later following owner's consent because of sudden worsening of clinical conditions. Two adult heartworms (Dirofilaria immitis) were found in the right ventricle partially coiling around the tricuspid valve. PCR on blood was positive for both D. immitis and Dirofilaria repens while only D. repens microfilariae were found by modified Knott's test and the serological test was negative for D. immitis antigens. This is the first, confirmed report of autochthonous canine heartworm infection in Hungary.

Background Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary arterial hypertension (PAH) in humans and can be classified in idiopathic, heritable, drug and radiation-induced, and associated with connective tissue disease or human immunodeficiency virus infection. Recently, biallelic mutations of the EIF2AK4 gene have been discovered as a cause for an autosomal recessive form of PVOD in humans. In dogs, PAH is poorly characterized and is generally considered to be idiopathic or secondary to (for example)congenital left-to right cardiovascular shunts or heartworm disease. However, recently, the pathologic features resembling human PVOD were retrospectively described in post-mortem lung samples of dogs presenting with respiratory distress and idiopathic pulmonary hypertension (PH), which suggests that PVOD contributes to an unknown percentage of cases with unexplained PH. In dogs, information on the clinical presentation of PVOD is scarce and the cause and pathogenesis of this disease is still unknown. Case presentationAn 11-year-old, intact male German Shepherd dog (GSD) was presented with a 2-day history of acute-onset dyspnea and generalized weakness. Physical examination, laboratory analysis, thoracic radiography, echocardiography, a computed tomography scan and an ante mortem lung biopsy demonstrated severe arterial hypoxemia and severe PH but were not diagnostic for a known disease syndrome. Based on the poor reaction to therapy with oxygen, sildenafil, pimobendan and dexamethasone the dog was euthanized. Histopathology of the lungs showed venous and arterial remodelling, segmental congestion of alveolar capillaries and foci of vascular changes similar to human pulmonary capillary hemangiomatosis, indicating that the dog suffered from PVOD. Whole genome sequencing analysis was performed on the case and a healthy GSD. Validation was performed by Sanger sequencing of five additional GSD's unknown for any form of respiratory stress and aged >= 10 years. No causal variants were found in the genes that are known to be involved in human PVOD and PAH. ConclusionsThis case report confirms that PVOD should be a diagnostic consideration in dogs presenting with dyspnea and unexplained PH. In the present case, no casual genetic mutations known to be involved in humans with PVOD and PAH were found.