Transposition of flexor tendons on the hand.
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Biomedical subjects
Publications and source records attributed to J Jakubik.
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The primary sites of Aujeszky's disease virus (ADV) multiplication in intranasally (i.n.) infected pigs were found to be in the nasopharyngeal, tracheal and pulmonary regions. From the second day post infection (DPI) onward ADV invaded the central nervous system and other organs. The virus was isolated from the nasopharyngeal region for at least 2 weeks. In serum ADV was present with low levels from DPI 1 to DPI 7. In pigs vaccinated with an inactivated vaccine and then challenged the distribution of ADV was rather similar to that in non-vaccinated animals, in spite of the presence of neutralizing antibodies. The virus titres in the organs generally were lower than in non-vaccinated animals up to DPI 7. Thereafter, titre differences were no longer significant. Virus was isolated from the tonsils and the lungs for at least 2 weeks. Interferon production in vaccinated infected pigs was significantly lower than in non-vaccinated infected pigs. Though multiplication and dissemination of ADV occurred, vaccinated pigs did not show clinical symptoms of Aujeszky's disease. Traces of ADV were detected in a small percentage of white blood cells (WBC) of non-vaccinated infected pigs. ADV was isolated from the lymphocyte-enriched and polymorphnuclear leukocyte-enriched fractions, but not from the monocyte-enriched fractions, apparently on account of the small cell number. Multiplication of ADV was demonstrated in cultured WBC from some of the vaccinated and non-vaccinated infected animals.
A direct solid-phase radioimmunoassay (dRIA) was developed in order to demonstrate antibodies against Aujeszky's disease virus (ADV) in sera obtained from pigs and rabbits. In the presence of guinea-pig complement the above test is 160-fold to 1500-fold more sensitive than the neutralization test (NT) and 320-fold to 150 000-fold more sensitive than NT without complement. By means of dRIA ADV antibodies could be detected in swine sera obtained from an ADV-infected farm, which were found to be negative in the complement assisted NT. It is possible to test a single dilution of unknown serum by dRIA by comparing same with a standard curve and to make a statement regarding its ADV--specific binding capacity to 125I-labelled ADV antigen. The advantages of dRIA in comparison to the indirect RIA and the advantages and disadvantages with regard to ELISA were discussed.
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Neutralizing antibodies against ADV were transmitted from sows, vaccinated with inactivated ADV adjuvanted with DEAE dextran, to their offspring via colostrum. The suckling piglets were protected by colostral immunity against contact infection with ADV at week 1 p.p., however, they were not protected against i.n. infection (10(8) TCD50). At 2 and 3 weeks p.p. all the piglets were protected against both contact infection and i.n. infection. At 4 weeks p.p. 50 per cent of the litter were protected against i.n. infection, in spite of very low antibody titres (1:2--1:4). The colostral antibodies did not interfere with active antibody response when the piglets were vaccinated with the inactivated vaccine from 2 weeks p.p. onward. Lymphocytes from suckling piglets of a vaccinated sow showed in vitro reactivity (enhanced 3H-thymidine incorporation) against ADV and BHK antigen, both contained in the vaccine used for the immunization of the sow.
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The appearance of cell-mediated immunity was studied in Aujeszky diseased pigs with the aid of the in vitro stimulation of sensitized lymphocytes. The first cell-mediated immunity reaction of lymphocytes occurred 4 days after infection. From day 7 to 35, the latest day tested, the reactions were most marked with lymphocytes from lymph nodes and spleen, whereas blood and thymus lymphocytes reacted less frequently; bone marrow lymphocytes showed no response. Reinfection did not considerably enhance lymphocyte reactivity. Humoral immunity was demonstrated a few days later than cell-mediated immunity. Neutralizing antibodies were first detected at day 7, reaching optimal titers at day 14. Complement fixing antibodies were detected from day 14 onward. Reinfection caused a very weak booster effect only on neutralizing antibody production. The sensitivity of the neutralization test could be enhanced up to sixfold by the addition of fresh guinea pig complement. It is concluded that cell-mediated immunity influences the early stage of infection with Aujeszky disease virus when humoral immunity is not yet demonstrable or yet rather low. Lymph nodes and spleen are apparently of special importance for the appearance of ADV-reactive lymphocytes.
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