31 research outputs found

    Lights ands shadows on the molecular diagnosis of hepatitis C

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    The rational application of molecular biology to clinical diagnostic must take in consideration the economic demands, as the waste of sophisticated and expensive assays is of no use for the physician prescribing the assays and burdensome for the individual or the community paying them. Sometimes it is useless to apply to the molecular biology, and the information obtainable through serology answer our demands. This brief survey of the principal means available today for Hepatitis C diagnosis and monitoring, besides summarising the principles on which the different techniques are based, wants to underline the most noteworthy aspects of the different assays-from general indication to specific application to a single case- in the attempt to improve the efficacy of the test, which may be the right one at the right moment. There are qualitative and quantitative methods for viremia determination, which not always are alternative; on the contrary they must sometimes be complementary in order to obtain a complete clinical pattern. As a matter of fact the clinician should choose according to protocol susceptibility and considering what the expected viremia could be. The risk of false negatives is very dreadful for the clinician, as that of false positives (from contamination) is threatening for the laboratory, which must carry out more work than its capabilities consent. One must not misuse these diagnostic means, but they be used correctly in order not to transform an important service into a harmful inefficiency with unpleasant consequences both for the physician and the patient. Key words: HCV diagnosis, quantitation of viremia, HCV genotype, HCV quasispecies, HCV ISDR (Interferon Sensitivity Determining Region

    Brachyspira (Serpulina) pilosicoli of human origin interfere with the haemolytic activity and the growth of Clostridium perfringens alpha-toxin producer

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    Brachyspira (Serpulina) pilosicoli of human origin interfere with the growth of Clostridium perfringens alpha-toxin producer reducing the clostridial growth area and colonies number when bacteria were cultivated together in sheep blood agar plates. The growth inhibition of C. perfringens was only observed when B. (S.) pilosicoli grew 72-96 hours sooner than C. perfringens and after the inoculum of this latter the plates were anaerobically incubated for additional 48 hours. The phenomenon was observed at concentrations of B. (S.) pilosicoli ranging from 10(7) to 10(4) CFU/ml and at concentrations of C. perfringens ranging from 10(7) to 10(1) CFU/ml when the bacteria were 0-10 mm away from each other. When B. (S.) pilosicoli and C. perfringens were inoculated at the same time and when B. (S.) pilosicoli grew 24-48 hours sooner than C. perfringens, the clostridial growth inhibition was not appreciated and only a cooperative haemolysis was observed between the bacteria
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