Seung-Gon Lee

Comparison of the pathogenicity in three different Korean canine parvovirus 2 (CPV-2) isolates

Canine parvovirus type 2 (CPV-2) is a major pathogen inducing acute hemorrhagic gastroenteritis in dogs. Despite the identification of numerous CPV-2 variants (from CPV-2a to CPV-2c), the pathogenic differences among the CPV-2 variants in dogs have not been evaluated. The aim of this study was to compare the pathogenicity of CPV-2 variants (CPV-2a-I, CPV-2a-V and CPV-2b) isolated mainly from Korea. We evaluated the pathogenicity of three different CPV-2 variants, by performing clinical, hematological, serological and histopathological examinations after experimentally inoculating three types of CPV-2 variants into young puppies. We found that the overall pathogenicity of the CPV-2a variants (CPV-2a-I and 2a-V) was severer compared to the CPV-2b variant. In addition, there was no significant difference in pathogenicity between the two CPV-2a variants. Our findings indicate that there are differences in the pathogenicity of CPV-2 variants in dogs, which may be useful to understand the different pathobiology of the CPV-2 variants.

Isolation, characterization and genetic analysis of canine GATA4 gene in a family of Doberman Pinschers with an atrial septal defect

GATA4 is expressed early in the developing heart where it plays a key role in regulating the expression of genes encoding myocardial contractile proteins. Gene mutations in the human GATA4 have been implicated in various congenital heart defects (CHD), including atrial septal defect (ASD). Although ASD is the third most common CHD in humans, it is generally rare in dogs and cats. There is also no obvious predilection for ASD in dogs and cats, based on sex or breed. However, among dogs, the incidence rate of ASD is relatively high in Samoyeds and Doberman Pinschers, where its inheritance and genetic aetiology are not well understood. In this study, we identified and investigated the genetic aetiology of an ASD affected family in a pure breed dog population. Although the GATA4 gene was screened, we did not find any mutations that would result in the alteration of the coding sequence and hence, the predicted GATA4 structure and function. Although the aetiology of ASD is multifactorial, our findings indicate that GATA4 may not be responsible for the ASD in the dogs used in this study. However, this does not eliminate GATA4 as a candidate for ASD in other dog breeds.

Prevalence of the endosymbiont Wolbachia in heartworms (Dirofilaria immitis)

Wolbachia are rickettsia-like, vertically transmitted, obligate intracellular bacteria that are associated with heartworms ( Dirofilaria immitis ) in small animals ([Werren and Jaenike 1995][1], [Stouthamer and others 1999][2]). Wolbachia has been found in the hypodermal lateral cords of male and

Percutaneous heartworm removal from dogs with severe heart worm (Dirofilaria immitis) infestation

Canine heart worm disease is often life-threatening due to its various complications, including right side heart failure, caval syndrome and pulmonary eosinophilic granulomatosis. Several preventive medications and melarsomine have been developed and they are very effective to control heartworm infestation. However, in a case of severe infestation, melarsomine therapy often results in an unfavorable outcome because of the severe immune reaction caused by rapid killing of the adult worm. Surgical removal and an interventional method using flexible alligator forceps have been well described in the literature. Despite the usefulness of mechanical removal using flexible alligator forceps, the methodology still needs to be upgraded for increasing the applicability for treating dogs with severe infestation. We describe herein a newly developed percutaneous removal method for heartworms and this was successfully applied to 4 dogs with severe heartworm infestation. The follow-up studies also showed favorable outcomes with no complications.

Genetic screening of the canine connexin 40 gene in dogs with inherited cardiac conduction defects.

Connexin 40 (Cx40) is a gap-junction protein expressed in the heart where it mediates the coordinated electrical activation of the atria and ventricular conduction tissues, facilitates cell-to-cell adhesion, and provides pathways for direct intercellular communication. Recent studies have shown that Cx40 null mice have cardiac conduction abnormalities with a very high incidence of cardiac malformations in heterozygous (18%) and homozygous (33%) animals, indicating that Cx40 plays a vital role in cardiomorphogenesis. Since several inherited cardiac conduction defects have also been found in dogs, we hypothesized that the clinical findings are genetically linked to a tissue-specific mutation or mutations in the canine Cx40 gene. We therefore screened the Cx40 gene in dogs with inherited cardiac conduction defects for mutations. In this study, we have identified three heterozygous base changes (C384G, C402T, C837T) in the dogs screened and determined them to be synonymous mutations. These mutations, however, have recently been found in an unrelated group of normal dogs.

Retrieval of an embolization coil accidentally dislodged in the descending aorta of a dog with a patent ductus arteriosus

A 3.5-year-old intact female miniature poodle (weighing 2.7 kg) was referred to the Veterinary Teaching Hospital at Kangwon National University, because of inadvertent aortic embolization, by an occlusion coil used for the closure of patent ductus arteriosus (PDA). The coil was found at the site of the branching renal arteries in the abdominal aorta. A foreign body forceps with a three-wire nail tip was used, with fluoroscopic guidance, to retrieve the coil. After the removal, the dog was treated with heparin to prevent thromboembolization.

Isolation, characterization and molecular screening of canine SLC26A2 (sulphate transporter) in German Shepherd dogs with hip dysplasia

The SLC26A2 gene codes for a sulphate transporter (the gene is also known as diastrophic dysplasia sulphate transporter gene; DTDST) and is a causative gene for human diastophic dysplasia due to undersulphation of proteoglycans in the cartilage matrix (Hastbacka et al. 1994). Several mutations in the SLC26A2 gene have been found in human diastrophic dysplasia (Hastbacka et al. 1994, 1996), achondrogenesis type IB (Superti-Furga 1994), and multiple epiphyseal dysplasia (Superti-Furga et al. 1999; Czarny-Ratajczak et al. 2001). Over 30 mutations in the SLC26A2 gene have been identified in human to date, including heterozygous single base deletions and splicing site mutations (Hastbacka et al. 1994, 1996; Superti-Furga et al. 1996, 1999; CzarnyRatajczak et al. 2001; Rossi and Superti-Furga 2001). Canine hip dysplasia is a developmental orthopedic disease in which an abnormal formation of the hip leads to looseness in the hip joints, causing cartilage damage (LaFond et al. 2002). Progressive arthritis can result, and when it does, it can be crippling. Hip dysplasia is not the same thing as arthritis in the hips, rather it is the most common cause of arthritis in the hips. Hip dysplasia is most common among larger breeds of dogs, especially German Shepherds, Rottweilers, Labrador Retrievers, Golden Retrievers, Mastiffs and Saint Bernards (Guilliard 2003). It is also seen in smaller breeds such as Cocker Spaniels and Springer Spaniels, as well as in mixed breeds (Guilliard 2003) Hip dysplasia is known to be transmitted genetically (Todhunter and Lust 2003), and recent genetic studies have found major genes for hip dysplasia in four Finnish dog populations (Maki et al. 2004), as well as quantitative trait loci (QTL) contributing to hip dysplasia in PortugueseWater Dogs (Chase et al. 2004). Further, the recent QTL mapping