Iron is an important factor for growth, virulence and immunogenicity of the species Pasteurella multocida. This has been demonstrated in numerous experiments with bacterial cultures in vitro and immunized and not immunized animals in vivo (mice, piglets, calves). Iron substrates or iron chelators affect in different manner the virulence of P. multocida in vivo, depending on chemical character of the given compounds, their dose, route and time of application, and also depending on the host. P. multocida has an up to time unknown iron transport system, which can acquire the essential iron from physiological substances, such as heme, ferritine, transferrine, lactoferrine etc. This conclusion results from in vitro experiments with growing cultures, with insertion of radioactive iron (Fe-59) from different sources, and with iron solubilization in neutral pH ranges. In the same way, the iron of iron dextran and low molecular iron compounds is available for P. multocida. Iron of unphysiological complexes, potassium ferrocyanide, and ferrocene is unavailable. On the other side such iron chelating agents as nitrilotriacetate, tirone, ferrocene, citrate, EDTA, and apotransferrine do not or only a little affect growth, and such chelators as alpha, alpha'-dipyridyle, phenanthroline and the microbial siderophores deferrioxamin B and enterobactin are inhibitory substances for multiplication of P. multocida. This substances also inhibit the insertion of Fe-59 into the bacterial cell. The conclusion is drawn that neither enterobactin nor deferrioxamine B as typical representatives of phenolate or hydroxamate siderophores take part in Fe-transport of P. multocida.

Intratracheal administration of 3H-labelled, 14C-labelled, 59Fe-labelled or 125J-Labelled Pasteurella multicida germs to mice resulted in more or less differentiated, nuclide-dependent, distributions of radioactivity in blood, spleen, liver, lung, kidney, and gastro-intestinal tract. All distributions were comparable to those following subcutaneous application. Elimination of antigen from lungs and other organs could be characterised by an e-function, once a certain level of distribution had been reached. Some of the antigen was persistent in the lung not less than 14 days. Extremely high activity concentration and persistence was recordable, following the use of 59Fe complete antigen. Phagocytosis of Pasteurella multicida germs through alveolar macrophages of the lung was secured by autoradiography. Most of the antigen seemed to be discharged from the lungs through the digestive tract. Antigen distributions recorded from immunised and non-immunised mice seemed to suggest that the fate of antigen applied was affected by the kind of immunisation. No difference in antigen distribution between non-immunised and subcutaneously immunised animals were recordable, following intratracheal antigen application, but is was clearly recordable, following intratracheal immunisation. Elimination of antigen from the lungs of intratracheally immunised animals was found to occur faster than it did from non-immunised animals.

One single injection of 50 mg/kg live weight cyclophosphamide or more to calves was followed by a latency of few days after which pneumonia or enteritis developed and caused death within one or two weeks. Cyclophosphamide application led to pronounced changes in the white blood count characterised, at the beginning, by rise of neutrophilic granulocytes and decline of lymphocates. Primary rise of granulocytes then was followed by almost complete disappearance of them. In those calves that survived the parameters of the white blood count were not restoredto normal until several weeks had elapsed. While an injection of 30 mg/kgcyclophosphamide usually was tolerated without any visible clinical reaction, it was also accompanied by the above pronounced changes in the white blood count. The activity of the reticulohistiocytary system, as recordable by means of ink and bacterial clearance, was not markedly affected by one single injection of 30mg/kg or 40 mg/kg cyclophosphamide. Calves with cyclophosphamide treatment exhibited unambigous humoral immune response, yet somewhat delayed or reduced in comparison to controls. While one single intravenous injectionof 30 mg/kg cyclophosphamide alone failed to trigger any clinical disease, it proved to be capable of rendering calves more susceptible to pneumonia pathogens. It, therefore, might be suitable for supporting experimental infection and thus facilitating the study of enzootic pneumonia of calf which usually is difficult to reproduce.

Studies were conducted with the view to elucidating the correlations between increased glucocorticosteroid levels in the blood and the defense potential of calf organism against infectious diseases. The test animals were exposed to several substances (ACTH, cortisol, colibacteria, coliendotoxin), and even one to two days of increased 11-OHKS values were followed by marked decline in phagocytosis activity of leucocytes. In addition, RHS function was considerably reduced, after ten to thirteen days of application had elapsed, since at that point the disappearance of intravenously applied bacteria from circulating blood of test animals took place at rates which were much lower than those recorded from untreated calves. Differentiated length of stress or action (four to thirteen days) was followed by conspicuous changes in the lymphatic tissue of calf organism, with severe involution of thymus and follicular atrophy of intestine-associated lymphatic tissue having been the major findings. The results seem to suggest that rise in adrenocortical hormone level under stress may reduce potential organic defense to infection.