Use of IgG Avidity test in case definitions of toxoplasmosis in pregnancy.

A survey network for congenital toxoplasmosis (TOXO-NET) was set up in December 1996 in Piedmont (Italy). Participants were asked to classify the infections in pregnant mothers and newborns by the criteria of the European Network on Congenital Toxoplasmosis published by Lebech in 1996. Because the IgG Avidity test is largely employed as a 2nd level test in toxoplasmosis diagnosis and it could be helpful to date infection, the co-ordinators of TOXO-NET suggested including it in the "case definition" of "probable" infection and "unlikely" infection. 117 cases of toxoplasmosis in pregnancy divided into the risk categories under Lebech's criteria were re-examined using the "new" case definitions. 77 out of 117 (65.8%) Toxoplasma gondii infections during pregnancy could be defined with only one serum sample using the IgG Avidity test. The IgG Avidity test proved a useful method to classify the Toxoplasma gondii infections in pregnancy, especially when we had only one serum sample.

Potentiation of human polymorphonuclear leukocyte phagocytosis and intracellular bactericidal activity by amoxycillin/clavulanic acid.

The use of broad spectrum beta-lactamase inhibitors in association with beta-lactam agents provides one strategy to overcome the enzymatic resistance. Clavulanic acid is a potent inhibitor of a wide range of bacterial beta-lactamases and its potentiating effect on amoxycillin has been established both in vitro and in clinical trials. Since the efficacy of an antimicrobial agent in the therapy of infections depends on the interaction of bacteria, antibiotic and phagocytes, we investigated the effect of amoxycillin/clavulanic acid on the in vitro interaction between human polymorphonuclear cells (PMNs) and beta-lactamase producing strains of Klebsiella pneumoniae and Staphylococcus aureus. Clavulanic acid did not have any significant influence upon the PMN phagocytosis and killing against intracellular bacteria. Interestingly, the presence of the suicide inhibitor, with its beta-lactamase inhibitory properties, potentiated the activity of amoxycillin against the beta-lactamase producing strains of K. pneumoniae and S. aureus in such a manner that bacteria became significantly more susceptible to either phagocytosis or microbicidal activities of human phagocytes, compared to both the control and amoxycillin systems.

Effect of ticarcillin and ticarcillin/clavulanic acid on the in-vitro activity of human granulocytes against beta-lactamase-producing Klebsiella pneumoniae.

Clavulanic acid is an effective inhibitor of a broad range of clinically important beta-lactamases and its combination with some beta-lactam antibiotics such as ticarcillin has been shown to extend the inhibition spectrum of the beta-lactams. The activity of ticarcillin, both alone and in combination with clavulanic acid, upon PMN phagocytosis and bactericidal activity towards Klebsiella pneumoniae was investigated. The results indicate that a combination of ticarcillin with clavulanic acid is more active than ticarcillin alone against a beta-lactamase-producing strain of K. pneumoniae, and hence may significantly increase the bacterial vulnerability to phagocyte functions.

Genotoxicity assay of oil dispersants in bacteria (mutation, differential lethality, SOS DNA-repair) and yeast (mitotic crossing-over).

5 oil dispersants and a sample of paraffin were devoid of mutagenic activity in the Ames reversion test, with and without S9 mix, using 7 his- S. typhimurium strains (TA1535, TA1537, TA1538, TA97, TA98, TA100, TA102). However, 3 dispersants produced direct DNA damage in E. coli WP2, which was not repairable in repair-deficient strains (WP2uvrA, CM871, TM1080), as shown by two different DNA-repair test procedures. The uvrA excision-repair system was in all cases the most important mechanism involved in repairing the DNA damage produced by oil dispersants, while the combination of uvrA with other genetic defects (polA, recA, lexA) decreased the efficiency of the system. The observed genotoxic effects were considerably lowered in the presence of S9 mix containing liver S9 fractions from Aroclor-treated rats. The sample of oil dispersant yielding the most pronounced DNA damage in repair-deficient E. coli failed to induce gene sfiA in E. coli (strain PQ37), using the SOS chromotest, or mitotic crossing-over in Saccharomyces cerevisiae (strain D5). The direct toxicity of the oil dispersant to both bacterial and yeast cells was markedly decreased in the presence of rat-liver preparations. These two short-term tests were effective in detecting the genotoxicity of both direct-acting compounds (such as 4-nitroquinoline N-oxide and methyl methanesulfonate) and procarcinogens (such as cyclophosphamide, 2-aminoanthracene and 2-aminofluorene). Moreover, the SOS chromotest was successfully applied to discriminate the activity of chromium compounds as related to their valence (i.e. Cr(VI) genotoxic and Cr(III) inactive). Combination of oil dispersants with Cr(VI) compounds did not affect the direct mutagenicity to S. typhimurium (TA102) of a soluble salt (sodium dichromate) nor did it result in any release of a water-soluble salt (lead chromate), as also confirmed by analytical methods. On the other hand, exposure to sunlight tended to decrease, to a slow rate, the direct genotoxicity of an oil dispersant in the bacterial DNA-repair test.

Interaction between polycyclic aromatic hydrocarbons, crude oil and oil dispersants in the Salmonella mutagenesis assay.

Mutagenicity assays were carried out in the Salmonella/microsome test, using five S. typhimurium his(-) strains (TA1535, TA1537, TA1538, TA98 and TA100), both in the presence and absence of post-mitochondrial preparations from Aroclor-induced rat livers and suitable co-factors. Seven oil dispersants showed a wide range of toxicity towards the bacterial strains, without eliciting any mutagenic response at sub-lethal concentrations. One sample of crude oil and its dimethylsulphoxide (DMSO) extract were also negative, and no mutagenic effect could be detected by checking mixtures of crude oil with each of the seven dispersants tested. Two polycyclic aromatic hydrocarbons, benzo(a)pyrene (BP) and benz(a) anthracene (BA), which are generally considered to be the most documented carcinogenic components of crude oil, were mutagenic with a frameshift mechanism, requiring metabolic activation. BP mutagenicity was not affected by oil dispersants nor by seawater. Conversely, the mutagenicity of BP DMSO-solutions was abolished in the presence either of whole crude oil, of its DMSO extract, or of crude oil/dispersant mixtures. These losses of mutagenicity could be mainly ascribed to a mechanical trapping of BP by oil components.

Detection of animal viruses in coastal seawater and sediments.

Animal viruses, predominantly enteroviruses, were detected in shallow water at bottom depths and in clastic marine sediments. Viruses accumulated in sandy and slimy deposits of the sea bottom near the shore and could be easily released into water by means of simple mechanical shaking.