MOLECULAR EPIDEMIOLOGY OF AVIAN POXVIRUS IN THE ORIENTAL TURTLE DOVE (STREPTOPELIA ORIENTALIS) AND THE BITING MIDGE (CULICOIDES ARAKAWAE) IN THE REPUBLIC OF KOREA.

A total of 600 wild birds were analyzed for the causes of mortality in the Republic of Korea (ROK) from 2011 to 2013. Avian poxvirus (APV) infections were identified as the primary cause of mortality in 39% (29/74) Oriental Turtle Doves (Streptopelia orientalis). At necropsy, all 29 S. orientalis birds, of which, 76% (22/29) were juveniles, had severe diphtheritic lesions in their oral and nasal cavities and on their eyelids, which were the lesions of APV that resulted in mortality. We detected APV infection by chorioallantoic membrane inoculation and molecular study of the partial region of the P4b gene. All isolates belonged to the same APV strain and were identical to strains isolated from several different pigeon species in South Africa. Phylogenetically, the APV strain identified in S. orientalis belonged to subclade A2, which includes isolates from several species of pigeons from different parts of the world, including the United Kingdom, Germany, India, Egypt, Hawaii, Georgia, Hungary, South Africa, Tanzania, and the ROK. This identity indicated that this diphtheritic APV strain may be a potential pathogen of other pigeon species in the ROK and neighboring countries throughout the range of S. orientalis. However, reticuloendotheliosis virus insertion into the APV genome was not detected by PCR in any of the 29 APV infections. An identical strain of APV observed in S. orientalis was also detected in Culicoides arakawae (biting midge), with annual peak populations corresponding to the presence of APV in S. orientalis. Culicoides arakawae may be a primary vector of APV in S. orientalis. Active surveillance of APVs in wild birds and C. arakawae is needed to better understand the epidemiology of APVs, host-vector relationships, and its ecological effects on S. orientalis in the ROK.

Pathology and molecular characterization of recent Leucocytozoon caulleryi cases in layer flocks.

Leucocytozoonosis was found in three layer farms in chickens with suspected fatty liver or fatty liver hemorrhagic syndrome in Korea between 2009 and 2011. These layer chicken flocks showed both mortality and decreased egg production for one or two weeks when they were between 59 and 82 weeks old. At the necropsy, the most prominent gross lesions were found in the liver, which was enlarged, had a fragile texture, exhibited yellowish discolorations, and had various hemorrhagic lesions. Tissue reactions associated with megaloschizonts specific for Leucocytozoon caulleryi were prominent upon microscopic examination of the liver without significant lipidosis. In addition, the ovaries and uterus were the most affected organs for Leucocytozoon caulleryi multiplication, which led to decreased egg productions. Molecular studies with formalin-fixed, paraffin-embedded tissues were performed in search of a partial region of the cytochrome b gene for hemosporidian parasites. Based on these results, the causal agent was determined to be closely related to Leucocytozoon caulleryi reported in Japan and Malaysia. In this study, we describe recently re-occurring leucocytozoonosis in layer chickens, which required histopathology for disease diagnosis. To prevent outbreaks and maintain chicken health and egg production, layer chickens need to be monitored for symptoms of leucocytozoonosis.