Biological Characterization of a Less Virulent Taura Syndrome in Pacific White Shrimp Litopenaeus vannamei (Crustacea: Decapoda): Gross Signs, Histopathological Lesions, and Mortalities

Taura syndrome (TS) was first recognized in shrimp farms located near the mouth of the Taura River in the Gulf of Guayaquil, Ecuador in mid1992 (JimCnez 1992; Lightner et al. 1995), where the disease caused catastrophic losses with cumulative mortality rates from 60% to >90% of affected pond-cultured, juvenile Pacific white shrimp Litopenaeus vannamei (Perez Farfante and Kensley 1997). The geographic distribution of the disease now includes Ecuador, the adjacent region of Peru, the Pacific and Caribbean coast of Colombia, Honduras, Guatemala, El Salvador, northeast Brazil, Nicaragua, Belize, the states of Hawaii, Florida, and Texas in the USA, the Mexican states of Sonora, Sinaloa, Chiapas, and Guerrero, and recently Taiwan (Lightner 1996; Chien et al. 1999). The epizootiological and laboratory studies that followed its discovery and spread from Ecuador showed that Taura syndrome (TS) had a viral etiology in the American (L. vannamei, L. stylirostris, L. schmitti, L. setiferus, Farfuntepenaeus aztecus) and Asian (Penaeus monodon, Marsupenaeus japonicus, Fenneropenaeus chinensis) penaeid species naturally or experimentally infected by the virus. Litopenaeus vannamei was by far the most severely affected (Brock et al. 1995, 1997; Hasson et al. 1995, 1999b; Lightner 1996; Overstreet et al. 1997). Infectivity studies demonstrated that TS could be induced in specific-pathogen-free (SPF) L. vannamei. Shrimp started dying after being fed TSV-infected tissue between day 4 or 5, with mortalities of 80% (Brock et al. 1995). Test animals were also infected by intramuscular injection with crude homogenate and cell-free suspensions, from TSV-infected Ecuatorian L. vannamei, causing mortalities of 73% to 87% among treated groups. All moribund shrimp demonstrated moderate to severe pathognomonic TS lesions (Hasson et al. 1995), which consist of pyknotic and karyorrhectic nuclei and generally spherical cytoplasmic inclusions with multifocal areas of necrosis of the cuticular epithelium giving TS lesions a peppered or buckshot-riddled appearance (Brock et al. 1995; Lightner et al. 1995; Hasson et al. 1995; Lightner 1999). The hemispheric geographic distribution of TS indicates that the same virus or a closely related one is responsible for the TS epizootics that have occurred throughout America since 1992 (Hasson et al. 1999a). Ecuatorian and Hawaiian TS virus isolates were found to be identical in their biophysical, biochemical, and biological characteristics, and they were considered to be the same virus (Bonami et al. 1997). In early 1995, TSV was detected in wild adult L. vannamei collected from the offshore fishery of the southern Mexican state of Chiapas, near its border with Guatemala and near where TS had first appeared in