Survival of Rio Grande Wild Turkeys on the Edwards Plateau of Texas

Abstract: The southeastern portion of the Edwards Plateau of Texas, historically a stronghold of Rio Grande wild turkeys (Meleagris gallopavo intermedia), has seen a decline in turkey numbers since the 1970s. Because adult and juvenile survival are key parameters affecting turkey population dynamics, we used radiotagged individuals to compare Rio Grande wild turkey survival in areas of suspected decline versus stable portions of the Edwards Plateau during 2001–2003. Reproductive period (breeding or nonbreeding) had an impact on survival, but differences in age, sex, or region did not influence survival. Model averaged estimates of monthly survival were 0.97 (SE = 0.005) for nonbreeding periods and 0.96 (SE = 0.007) for breeding periods. Our results indicate juvenile and adult survival in the declining areas was similar to survival in the stable areas of the Edwards Plateau. This suggests causes of the decline might be associated with differences during other life-history stages, such as nest success or poult survival, although we cannot rule out the possibility juvenile or adult survival contributed to the decline in the past. This situation demonstrates why wildlife managers should be cognizant of the implications of initiating long-term monitoring programs after changes in population status occur, rather than initiating them in expectation of such changes.     

穇属颖果微形态及其系统学意义

在电子扫描显微镜下观察了穆属(Eleusine Gaertn.)9种植物颖果的微形态特征.结果表明,穆属颖果有卵形、披针形和矩圆形3种腹面形状,压扁方式有背腹压扁及两侧压扁,腹面形态有平腹面和凹腹面两种,胚比为0.29～0.58,种脐比为0.10～0.24,颖果纹饰有2种,包括疣突状一级纹饰和疣突规则排列构成的复合网状...     

Porcine reproductive and respiratory syndrome virus (PRRSV) infection spreads by cell-to-cell transfer in cultured MARC-145 cells, is dependent on an intact cytoskeleton, and is suppressed by drug-targeting of cell permissiveness to virus infection

Background

Porcine reproductive and respiratory syndrome virus (PRRSV) is the etiologic agent of PRRS, causing widespread chronic infections which are largely uncontrolled by currently available vaccines or other antiviral measures. Cultured monkey kidney (MARC-145) cells provide an important tool for the study of PRRSV replication. For the present study, flow cytometric and fluorescence antibody (FA) analyses of PRRSV infection of cultured MARC-145 cells were carried out in experiments designed to clarify viral dynamics and the mechanism of viral spread. The roles of viral permissiveness and the cytoskeleton in PRRSV infection and transmission were examined in conjunction with antiviral and cytotoxic drugs.

Results

Flow cytometric and FA analyses of PRRSV antigen expression revealed distinct primary and secondary phases of MARC-145 cell infection. PRRSV antigen was randomly expressed in a few percent of cells during the primary phase of infection (up to about 20–22 h p.i.), but the logarithmic infection phase (days 2–3 p.i.), was characterized by secondary spread to clusters of infected cells. The formation of secondary clusters of PRRSV-infected cells preceded the development of CPE in MARC-145 cells, and both primary and secondary PRRSV infection were inhibited by colchicine and cytochalasin D, demonstrating a critical role of the cytoskeleton in viral permissiveness as well as cell-to-cell transmission from a subpopulation of cells permissive for free virus to secondary targets. Cellular expression of actin also appeared to correlate with PRRSV resistance, suggesting a second role of the actin cytoskeleton as a potential barrier to cell-to-cell transmission. PRRSV infection and cell-to-cell transmission were efficiently suppressed by interferon-γ (IFN-γ), as well as the more-potent experimental antiviral agent AK-2.

Conclusion

The results demonstrate two distinct mechanisms of PRRSV infection: primary infection of a relatively small subpopulation of innately PRRSV-permissive cells, and secondary cell-to-cell transmission to contiguous cells which appear non-permissive to free virus. The results also indicate that an intact cytoskeleton is critical for PRRSV infection, and that viral permissiveness is a highly efficient drug target to control PRRSV infection. The data from this experimental system have important implications for the mechanisms of PRRSV persistence and pathology, as well as for a better understanding of arterivirus regulation.