Van Hellemond receives Merial Award.
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Animals↗
Biomedical subjects
T Schetters
Publications and source records attributed to T Schetters.
Vaccine development from a commercial point of view.
The development of a commercial vaccine comprises distinct stages. Initiation of a research project is triggered by demands from the market. If commercial and technical requirements are met, a feasibility study is carried out. Research is started, and aimed at formulating the product profile (what the product looks like). The product profile is subject to requirements set by the market (e.g. whether the product will fit into existing vaccination schedules) and very often technical aspects affect the product profile (e.g. whether the freeze-dried product is easy to reconstitute). Only after a cost-profit analysis is positive, the development phase is entered. During this phase, experiments are carried out to obtain registration. After the product has been registered it is ready for production and marketing. Only few vaccines for hemoparasitic diseases have reached the market. These comprise: attenuated parasites (Toxoplasma gondii, Eimeria species); killed vaccines (Anaplasma marginale) and subunit vaccines (Babesia canis). Factors relating to the product potential of these vaccines are discussed.
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[Is there a future for vaccines against gastrointestinal helminths?].
Vaccines against gastro-intestinal helminths have a large market potential, but they also generally have a narrow range of activity. This is a major drawback in the competition with the broad-spectrum anthelmintics and there is still a long way to go before molecular (recombinant) vaccines will appear on the market. Major problems are the induction of protective gut-mucosal immunity with subunit vaccines and the differences in genetic background within host populations, which largely determine the efficacy of vaccination. As yet the changes for vaccines against blood- and tissue parasites, comprising a number of veterinary important protozoa, seem to be better.
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Cerebral lesions in mice infected with Plasmodium berghei are the result of an immunopathological reaction.
Cerebral lesions in mice with Plasmodium berghei infections can be prevented by timely treatment with immune serum, by splenectomy, and by administration of dexamethasone. T cell deficient mice do not develop cerebral lesions. The results of these studies are compatible with the hypothesis that a pathological reaction is responsible for development of cerebral lesions in mice infected with P. berghei.
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Host diet in experimental rodent malaria: a variable which can compromise experimental design and interpretation.
Over the past few years several experienced groups studying malaria have encountered significant problems with their particular rodent malaria-host system. This has involved, in some cases, periods during which the recovery of cryopreserved parasite stocks and growth of bloodstream parasites was markedly inhibited and, in other cases, periods of drastically increased mortality rates. The common factor linking these incidents was that they coincided with alterations in the experimental animal diet used. The inhibition of growth of cryopreserved stabilates or bloodstream parasites was abolished by supplementation with p-aminobenzoic acid (PABA) or by changing the diet used. Although the suppressive effects of diets lacking PABA on parasite growth have been known for over 30 years, the variation of PABA levels in modern laboratory animal feed concentrates is not well recognized. We have not established the exact cause of increased mortality, but it has been overcome by changing the diet used. We are documenting our experiences with this potential variable to forewarn workers in other laboratories of possible problems inherent in the use of different diets.
4-Aminobenzoic Acid↗
A protective activity of physiological erythrophilic antibody in murine malaria infection and immunity.
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Selective depletion of immunoglobulin isotypes after decomplementation of mouse sera by heat treatment.
Inactivation of mouse serum by heat treatment (30 min at 56 degrees C) decreased antibody reactivity as shown by haemagglutination assays. This appeared to be due to loss of antibody since Ouchterlony analysis showed disappearance of antibody after heat treatment. By both isotype-specific ELISA and Ouchterlony analysis it was shown that mouse IgM, IgG2b and IgG3 are sensitive to heat treatment whereas IgG2a is relatively resistant. IgG1 is not sensitive to heat treatment. To avoid complement-dependent lysis in haemagglutination assays EDTA should be added to the serum samples.
Animals↗