Fish oil-induced yellow fat disease in rats. II. Enzyme histochemistry of adipose tissue

Adipose tissue in various stages of fish oil-induced yellow fat disease in the rat had the same acid phosphatase and 5-nucleotidase activity pattern as similar stages of the disorder in mink and pig. A weak acid phosphatase and 5-nucleotidase activity was seen in interstitial lipofuscin-laden macrophages in "stage M" yellow fat disease without fat cell degeneration. Activity of these macrophagic enzymes increased when there was fat cell degeneration ("stage S" and "stage E" yellow fat disease). This different phosphatase activity in the same cell type may result from phagocytosis of substrates with variable digestibility. Macrophages directly surrounding affected fat cells in steatitis areas ("stage S" and "stage E") had strong acid phosphatase and 5-nucleotidase activity. As in the pig, increased 5-nucleotidase activity was found in affected fat cells, which probably indicates plasma membrane damage. Increased nonspecific esterase activity occurred around affected fat cells. Only a small part of this esterase activity originated from inflammatory cells. This indicates that an increase of esterase activity in degenerating adipose tissue may be an endogeneous process in this tissue.     

Erwinia carotovora (Jones) Bergey et al. var. atroseptica (Hellmers et Dowson) Dye. Seed Tuber Infection Versus Symptom Expression in the Field1

Based on the time that symptoms of blackleg become evident in the field and the various ways of inoculation, it is concluded that the spread of symptom expression is due to the depth at which the bacteria penetrate into the interior of the tubers. Moreover, it is demonstrated that it is not the closed lenticels which prevent penetration, but the absence of a waterfilm in the intercellular spaces of the tuber tissue.     

Preliminary investigation of the causal agent(s) of a disease causing leaf curl of tobacco in South Africa

A high incidence (86%) of potyvirus infection was noted in tobacco plants exhibiting a form of leaf curl in South Africa. Despite leaf curl being reported in the literature to be of geminiviral aetiology, no geminiviruses were detected. Furthermore, no other virus particles were detected by virus purification, TEM and serology. Twelve species of dsRNA were consistently isolated from these tobacco plants, but were absent from other forms of leaf curl-affected and healthy tobacco. Aphid and mechanical inoculation demonstrated that the purified potyvirus(es) did not cause leaf curl symptoms, but rather mild mottle and mosaic symptoms in tobacco. Partial characterization of the potyvirus preparation showed a possible relationship to a South African strain of potato virus Y. Because potyvirus-inoculated plants did not manifest leaf curl symptoms, and because leaf curl symptoms were noted in some plants not infected with a potyvirus, it was concluded that the potyvirus is not involved in the leaf curl aetiology, but causes a latent infection, the symptoms of which are masked. The pattern of the dsRNA banding, induction of enations and lack of mechanical and seed transmission are common to plant reoviruses. The possibility of a phytoreovirus involvement in this form of leaf curl is currently being investigated. The results from this study suggest that tobacco leaf curl disease worldwide, with regard to geminiviruses, be re-evaluated.