DisplayTitle

Occurrence of a Severe Strain of Lisianthus necrosis virus in Imported Carnation Seedlings in Taiwan

In the 1995 to 1996 season, severe viral disease symptoms were observed on carnations (Dianthus caryophyllus [hybrid Kooij Echo kgr]) propagated from imported seedlings on farms in central Taiwan. Disease symptoms began on upper leaves as numerous yellow spots that enlarged and fused into large chlorotic patches and expanded to cover entire leaves, which eventually became necrotic. Electron microscopy of crude extracts, purified preparations, and ultrathin sections of diseased tissues revealed the presence of isometric particles ≈32 to 33 nm in diameter. Earlier, in the 1994 to 1995 season, a strain of Lisianthus necrosis virus (LNV-L) was identified in lisianthus (Eustoma russellianum (Don.) Griseb) in a nearby nursery propagating seedlings (1). Both the lisianthus and carnations were imported from Europe. Chlorotic leaves from carnations reacted strongly with antiserum prepared against LNV-L in tissue blot immunoassay. Extracts of diseased leaves also reacted positively to LNV-L antiserum in both immunodiffusion and doubleantibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) tests. Mouse monoclonal antibodies prepared against LNV-L reacted positively based on indirect ELISA with extracts of chlorotic carnation leaves. The capsid protein of the carnation virus (LNV-D) was ≈38 kDa in sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, similar to the LNV-L coat protein (1), and reacted with LNV-L antiserum in western blot analysis. LNV-D differs biologically from LNV-Japan and LNV-L isolates previously reported in Japan and Taiwan, respectively (1,2). In experiments, LNV-D has induced systemic infection in many hosts that are either nonhosts or local-lesion hosts for LNV-Japan or LNV-L. D. caryophyllus L. and D. chinensis L. are susceptible to systemic invasion by LNV-D but are nonhosts for LNV-Japan and LNV-L. D. barbatus L. is a systemic host for LNV-D but a nonhost for LNV-L and has not been tested as a host for LNV-Japan. Chenopodium amaranticolor Coste & Reyn. and C. quinoa Willd. are systemic hosts for LNV-D but are local-lesion hosts for both LNV-Japan and LNV-L. Capsicum annuum L. is a systemic host for LNV-D and LNV-L but is not susceptible to LNV-Japan. Lycopersicon esculentum Mill. is a systemic host for LNV-D, a local-lesion host for LNV-L, and a nonhost for LNV-Japan. All three isolates systemically infect E. russellianum, the only systemic host for all three isolates tested. The first reports of LNV in Japan and later in Taiwan were in lisianthus. To our knowledge, this is the first report of the natural occurrence of LNV in imported carnation seedlings in Taiwan. LNV infection in Taiwan was only noticed once in lisianthus (1994 to 1995 season) and once in carnation (1995 to 1996 season) in farms propagating imported seedlings. LNV is transmitted by Olpidium sp. (2). Olpidium-like structures were not observed in Taiwan in rootlets of diseased carnation and lisianthus nor were they isolated from soil around diseased plants. Surveys of LNV in the nurseries and nearby areas in subsequent years have not found a new case of infection. We believe that LNV disease is not endemic in Taiwan and that its occurrence in lisianthus and carnation are one-time incidents caused by the importation of infected seedlings or contaminated culture matrices associated with the seedlings.

References: (1) C. C. Chen et al. Plant Dis. 84:506, 2000. (2) M. Iwaki et al. Phytopathology 77:867, 1987.