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Sugarcane yields have been severely reduced by white leaf and grassy shoot phytoplasma diseases in many parts of Asia. Australian sugarcane crops are not known to be affected by these diseases, but plant pathogenic phytoplasmas found in other introduced and native grasses in northern Australia could pose a serious threat to the Australian sugarcane industry. To further evaluate this threat, leaves from plants of 20 grass species, with and without symptoms, were collected during field surveys in northern Australia and tested to determine whether phytoplasmas were present and whether symptoms were reliable indicators of phytoplasma presence. Molecular tools were used to detect and characterize phytoplasmas. Four different phytoplasmas were found in seven grass species known to grow near healthy sugarcane crops. All the phytoplasmas were closely related to sugarcane white leaf phytoplasma (SCWL), one of the phytoplasmas that causes disease in sugarcane in Asia. Four of the host plant species and two of the phytoplasmas were new records. The relationship between symptoms and phytoplasma presence was poor. Because some plants with symptoms tested negative for phytoplasmas, a series of surveys was carried out in which flowers, leaves, roots and stems of two known host plant species, Whiteochloa cymbiformis and Sorghum stipoideum, were tested separately on nine occasions during two wet seasons. This was done to investigate the distribution of phytoplasmas within plants over time. Results showed that spatial and temporal variation of phytoplasmas occurred in these two host plant species. Hence, evaluation of disease distribution within a region requires repeated testing of all plant parts from plants without symptoms, as well as those with symptoms. To date, there is no report of a vector capable of transmitting to Australian sugarcane the phytoplasmas found in grasses in this study. If one is present, or occurs in the future, then native and introduced grasses could constitute a large reservoir of phytoplasma for vectors to draw on. This work provides an early warning for the sugarcane industry that the potential for infection exists.  相似文献   
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To determine the effect of swine hepatitis E virus (HEV) infection on pregnant gilts, their fetuses, and offspring, 12 gilts were intravenously inoculated with swine HEV. Six gilts, who were not inoculated, served as controls. All inoculated gilts became actively infected and shed HEV in feces, but vertical transmission was not detected in the fetuses. There was no evidence of clinical disease in the gilts or their offspring. Mild multifocal lymphohistiocytic hepatitis was observed in 4 of 12 inoculated gilts. There was no significant effect of swine HEV on fetal size, fetal viability, or offspring birth weight or weight gain. The offspring acquired anti-HEV colostral antibodies but remained seronegative after the antibodies waned by 71 days of age. Swine HEV infection induced subclinical hepatitis in pregnant gilts, but had no effect on the gilts' reproductive performance, or the fetuses or offspring. Fulminant hepatitis associated with HEV infection was not reproduced in gilts.  相似文献   
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Eight calves were fed from the fourth to the twentieth week of age a milk powder diet containing 40 mg lead acetate per kg dry substance. This is twice the lead concentration legally permitted. In average, each animal has daily taken up 0.834 mg lead per kg body weight. Eight calves were used as controls. The animals gained the usual fattening weights and did not show clinical symptoms. Beginning with week 14, increased levels of blood urea were encountered in the animals which received lead in their diet. Morphologically, severe renal lesions were found in these calves. The kidneys were increased in weight, pale and of firm consistency. Histologically, fibrosis and periglomerular interstitial non-purulent nephritis were found. Light- and electronmicroscopically, numerous intranuclear inclusion-bodies typical for lead poisoning were demonstrated in epithelial cells of proximal tubules. The results show, that daily uptake of less than 1 mg lead per kg body weight must be considered as a toxic dose for calves, and not 5-7 mg as stated in literature.  相似文献   
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