OBJECTIVE: To evaluate the validity of the IgG avidity test in the serodiagnosis of acute T. gondii infection; to verify the maturation of IgG avidity during the course of infection; to observe whether the kinetics of IgG maturation could be affected by antibiotic treatment. METHODS: Serial serum samples, collected in three Italian hospitals (Perugia, Treviso and Bologna), from untreated and antibiotic-treated patients with primary toxoplasmic infection, were assayed for IgG avidity, and IgM and IgA positivity. Single serum samples from patients at different stages of infection were assayed for IgG avidity and the results were correlated to the likely stage of infection. RESULTS: The IgG avidity value increased from 3.5% in the first month to 38.7% 1 year from the onset of infection. Antibiotic-treated patients showed significantly different values of IgG avidity at 2 and 4 months after the onset of infection. In single serum samples the IgG avidity values correlated with the likely stage of infection. CONCLUSIONS: The IgG avidity test was confirmed as a useful tool in the serodiagnosis of acute T. gondii infection and could be predictive of the stage of infection. Antibiotic treatment may affect the kinetics of the maturation of IgG avidity.
Accumulation of stable RNA and production of guanosine polyphosphates (ppGpp and pppGpp) were studied during amino acid starvation in four species of halobacteria. In two of the four species, stable RNA was under stringent control, whereas one of the remaining two species was relaxed and the other gave an intermediate phenotype. The stringent reaction was reversed by anisomycin, an effect analogous to the chloroamphenicol-induced reversal of stringency in the eubacteria. During the stringent response, neither ppGpp nor pppGpp accumulation took place during starvation. In both growing and starved cells a very low basal level of the two polyphosphates appeared to be present. In the stringent species the intracellular concentration of GTP did not diminish but actually increased during the course of the stringent response. These data demonstrate that (i) wild-type halobacteria can have either the stringent or the relaxed phenotype (all wild-type eubacteria tested have been shown to be stringent); (ii) stringency in the halobacteria is dependent on the deaminoacylation of tRNA, as in the eubacteria; and (iii) in the halobacteria, ppGpp is not an effector of stringent control over stable-RNA synthesis.
The stringent halobacterial strain Haloferax volcanii was subjected to a set of physiological conditions different from amino acid starvation that are known to cause production of guanosine polyphosphates [(p)pp Gpp] in eubacteria via the relA-independent (spoT) pathway. The conditions used were temperature upshift, treatment with cyanide, and total starvation. Under none of these conditions were detectable levels of (p)ppGpp observed. This result, in conjunction with our previous finding that (p)ppGpp synthesis does not occur under amino acid starvation, leads to the conclusion that in halobacteria both growth rate control and stringency are probably governed by mechanisms that operate in the absence of ppGpp. During exponential growth, a low level of phosphorylated compounds with electrophoretic mobilities similar, but not identical, to that of (p)ppGpp were observed. The intracellular concentration of these compounds increased considerably during the stationary phase of growth and with all of the treatments used. The compounds were identified as short-chain polyphosphates identical to those found under similar conditions in Saccharomyces cerevisiae.In 1969, Cashel and Gallant reported that wild-type Escherichia coli is capable of producing two unusual compounds originally named magic spots I and II and later identified as guanosine tetra-and pentaphosphates, respectively [collectively referred to as (p)ppGpp] (3). These guanosine nucleotides are generated in a relA-dependent manner by the relA gene product, (p)ppGpp synthetase I, and in a relA-independent manner by the spoT gene product, the SpoT enzyme, which is also implicated in (p)ppGpp degradation. Kinetic studies have shown that pppGpp is formed from GTP, that ppGpp is derived from pppGpp, and that pppGpp inhibits its own synthesis (12).In eubacteria, the rate of stable RNA synthesis at different growth rates is subject to a control mechanism that is distinct from that of other cellular molecules (growth rate control of RNA synthesis). An inverse correlation between the ppGpp concentration, produced in this case by the relA-independent pathway, and the rate of stable RNA synthesis was observed at a wide range of different growth rates (5), which suggested that ppGpp could act as an effector molecule negatively regulating stable RNA synthesis in growth rate control. The isolation by Xiao et al. (21) of relA spoT mutants unable to produce ppGpp permitted Gaal and Gourse (8) to show that ppGpp either is not the mediator or does not act alone, since growth rate control is normal in the double mutants. Hernandez and Bremer have recently shown that in wild-type E. coli, three factors increase with the growth rate: RNA polymerase concentration, RNA polymerase activity, and the distribution of active RNA polymerase between stable and mRNA genes. In an E. coli⌬relA⌬spoT mutant that does not produce ppGpp, RNA polymerase synthesis and activity increase with the growth rate but the distribution of active RNA polymerase between stable and mRNA genes does not. This...
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