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The AA. report the personal contributions and the recent findings of other investigators dealing with the toxic activities of Legionella pneumophila, the causative agent of Legionnaires' Disease. From the results of some tests (particularly Limulus endotoxin assay, pyrogenic reaction, skin Shwartzman reaction) there is an increasing evidence that Legionella pneumophila possesses some of the in vitro and in vivo biological properties associated with endotoxins of Gram negative bacteria, even if to a different of potency in different strains. However, the exact roles of an endotoxin and other bacterial products (e.g. haemolysins) as a pathogenetic mediators of the pathophysiological events of the disease remain to be determined.

In most recent papers some Authors have demonstrated that several bacteriocins are able to markedly inhibit the division of various neoplastic mammalian cell lines; also in vivo the inhibition of tumor growth or even regression relative to controls are statistically significant. Since such preparations are "crude" and it's possible that contaminating agents may represent a possible source of variability in the results, mostly in vivo; we have examined a preparation of Pyocin employed in this study for the possible endotoxin contamination using the Limulus assay. Such test was positive in triplicate and semiquantitative determination has shown and endotoxin amount of 5 to 10 microgram/ml. This level is, in vitro, not anough to give cytotoxic effect, but in vivo is able to influence experimental results. In addition, since some bacteriocins and enterotoxins are produced under exactly identical conditions, there is this a possibility that the enterotoxin are coproduced in these preparations and are causing some of the cytotoxic effects on experimental tumors. A more complete separation and purification of preparations will be required before definitive comments.

In a previous report it has been shown that enterotoxin preparations (cholera and E. Coli) able to activate adenylatecyclase system, abrogated platelet aggregation induced by ADP. In the present study the same experimental model has been applied to some purified filtrates from Salmonella typhimurium strains. Preparations from 986 and TLM (invasive strains causing also fluid secretion) interfere with platelet aggregation, while 1027 strain (invasive but not evoking fluid secretion) didn't show such effect. It has been argued, as Sandefur and Peterson have demonstrated with different experimental models, that the system of platelet aggregation induced by ADP is valid for some strains of Salmonella typhimurium, which act with a mechanism partially involving adenylatecyclase system (i.g. cholera-like).

The capacity of a strain of Mycoplasma pneumoniae to induce the production of procoagulant activity by human mononuclear cells is described. This finding could contribute to the understanding of the pathogenetic mechanism(s) involved in the thromboembolic complications often associated with fatal cases of Mycoplasma pneumoniae infection.

Some culture filtrates or enterotoxin preparations from enterobacteria that activate the adenylate cyclase system (vibrio cholerae, LT fraction from escherichia coli and klebsiella pneumoniae, shigella dysenteriae type 1) exibit an inhibiting effect on ADP-induced platelet aggregation, while other enterotoxin preparations not effective on adenylate cyclase system, don't interfere with this model. The A. propose the platelet aggregation as cellular assay to detect enterotoxin fractions effective upon adenylate cyclase system.

The in vitro effect of a virulent and a non virulent strain of Leptospira interrogans serotype icterohaemorrhagiae on human peripheral mononuclear cells was investigated. After addition of bacteria to citrated whole blood the production of mononuclear cell procoagulant activity (tissue factor) was observed. Indeed mononuclear cells isolated from whole blood-bacteria mixtures after prolonged incubation shortened the recalcification time of normal plasma. The virulent strain induced a significantly higher procoagulant activity than non virulent and this effect was dependent on the number of bacteria. The production of tissue factor, a potent trigger of blood clotting, by Leptospira icterohaemorrhagiae could help to understand the mechanism(s) responsible for the activation of intravascular coagulation sometimes associated with leptospirosis.

The A.A. have examined by Limulus endotoxin assay some LPS preparations from R. typhi, R. slovaka, C. burnetti phase I and II, as a demonstration of endotoxicity. All the preparations tested were able to gel the Limulus amoebocyte lysates, even if to a different degree of reactivity. The results add credibility to the hypothesis that LPS from Rickettsiaceae can represent at least in part the pathogenetic mediators of some manifestations described in Rickettsiosis; however, without endotoxin assay in the blood of patients, one cannot assume to this be true.

Administration of E. coli LPS prior to 3.5 mg/Kg dose of thiourea has been reported to protect rats against pulmonary edema and pleural effusion. However, LPS of Shigella sonnei (either in phase I or II) did not show any protective effect. These data might suggest a different mechanism of endotoxins on membranes.

Lipoglycans represent a special type of lipopoly-saccharide that differs in structure from the well-known gram-negative bacteria lipopolysaccharide. After briefly describing their most important characteristics, the authors take into consideration the in vitro interaction between lipoglycans from Acholeplasma granularum, Acholeplasma oculi, and Acholeplasma axanthum and human leukocytes in terms of production of procoagulant activity. The results obtained show that the examined lipoglycans possess, similarly to lipopolysaccharides, the capacity to induce the production of procoagulant activity, thromboplastin-like, from human mononuclear cells. However, the pathophysiological significance of this endotoxin-like activity remains to be established.

Protection against endotoxin challenge. The AA. have summarized shortly some experimental data dealing with trials of protection against endotoxin challenge pointing out, mostly, the effects of phosphate-containing compounds, as well as dextrane, anticoagulants, platelets, polymyxin B, and serum antiendotoxin and Lipid A antiserum. They have reported some experiments carried out by means of Limulus amebocyte lysate.