Migration-inhibition response of peripheral leukocytes to tuberculin in cats sensitized with viable Mycobacterium bovis (BCG).

Delayed hypersensitivity reactions to antigens injected intradermally are reported as not occurring in the cat. Cats infected with viable Mycobacterium bovis (BCG) organisms developed a transient migration-inhibition response of their leukocytes to tuberculin. The migration-inhibition response subsided in 6 weeks in spite of the persistance of viable BCG. Significant intradermal reactions to tuberculin 60 days after BCG injection did not occur. The response of the cat differs from that of many mammalian species in which strong in vivo and in vitro delayed hypersensitivity type reactions persist with mycobacterial infections. Despite the lack of continued measurable delayed hypersensitivity, the cat appears to have adequate resistance to mycobacterial infections.

Pathological changes in calves injected intradermally with Mycobacterium intracellulare serotype Davis and M. avium serotype 2.

Three strains of the M. intracellulare-M. avium complex were injected intradermally into 12 calves. M. intracellulare serotype Davis (M. avium complex serotype 8) was injected into five calves. One calf died with disseminated caseous granulomas at 79 days; three calves killed between 56 and 82 days after inoculation had widely disseminated caseous or caseous or caseocalcareous granulomas. One calf killed at 173 days had only encapsulated granulomas at the injection site and its regional lymph node. Two strains of M. avium serotype 2 (M. avium complex serotype 2) were injected intradermally into seven calves. Six had disseminated granulomas when killed 54-170 days after inoculation. One calf killed at 55 days had granulomas confined to the inoculation sites and their regional lymph nodes. Lesions induced by both M. avium serotype 2 and M. intracellulare serotype Davis were initially caseocalcareous granulomas which became encapsulated and nonprogressive after about 112 days. Two calves inoculated with similar doses of M. bovis and killed in extremis at 37 and 65 days after inoculation had disseminated progressive lesions without encapsulation.

Lesions and tuberculin sensitivity in calves inoculated with group III mycobacterial isolates from swine, pen soil, and cattle feed.

FIFTEEN calves, 7 to 11 months of age, were inoculated intradermally with group III mycobacteria ---6 isolates from swine, 1 isolate from cattle feed, and 2 isolates from soil of swine farrowing pens. Calves were tuberculin tested at 50 days and killed approximately 60 days after inoculation. Only 1 of the cultures, that of porcine origin (93c-0), produced any lesions. There were a caseo-calcareous granuloma 3mm in diameter in the regional lymph node (left prescapular) and a granuloma at the skin inoculation site. None of the 5 calves inoculated with soil- or feed-origin mycobacteria had any lesions. Three of the calves inoculated with porcine origin group III mycobacteria had suspicious or positive caudal fold reactions. Two of these had granulomas at the skin-inoculation sites and one had no lesions. The calf having lymph node and skin-inoculation site granulomas was negative. The 5 calves inoculated with feed- or soil-origin mycobacteria had negative caudal fold tuberculin tests.

Dithiothreitol-dependent antilisterial activity of lysates from normal macrophages exposed in vitro to culture fluids from spleen cells of BCG-immunized mice.

The effect of culture fluids from mouse lymphocytes on the antilisterial activity of normal macrophages in vitro was determined. Titers of lysates of macrophages incubated with or without culture fluids from lymphocytes from control mice had titers of 10 to 270 with or without a reducing agent, dithiothreitol. Lysates of macrophages after incubation with culture fluids of spleen lymphocytes from BCG-immunized mice had antilisterial titers with and without dithiothreitol of 197,000 and 810, respectively. This may indicate a dithiothreitol-dependent antilisterial system inherent in activated macrophages of cell-mediated immunity. Lysates of incubated spleen cells and their culture fluids also had slight antilisterial activity.

Delayed hypersensitivity and leucocyte migration inhibition in chickens with BCG or Marek's disease infection.

Production of Migration Inhibition Factor in vitro by lymphocytes from chickens with delayed hypersensitivity was examined. Chickens were sensitized with Bacille Calmette-Guerin (BCG) and others with Marek's Disease (MD) virus. Peripheral blood was used as a source of cells for in vitro radial migration inhibition. Using purified Band 24 antigen from Mycobacterium bovis and >>A<< antigen from MD virus, migration inhibition was demonstrated in BCG and MD sensitized chickens respectively, and not in controls. Results correlated well with intra-dermal skin reactions. Old Tuberculin and crude MD antigens inhibited radial migration of leucocytes from control chickens. The use of peripheral blood as a source of lymphocytes facilitates repeated sampling, both prior to and following sensitization. As a result, the role of the bursa and thymus in the induction and maintenance of delayed hypersensitivity can be studied in vitro. Furthermore, the role of cellular immunity and humoral antibodies as contributors to oncogenicity and/or protection in MD can be examined.

Electrophoretic and immunoelectrophoretic studies of sera from normal, tuberculous, and noninfected tuberculin-sensitive guinea pigs.

Dardas, T. J. (Michigan State University, East Lansing), and V. H. Mallmann. Electrophoretic and immunoelectrophoretic studies of sera from normal, tuberculous, and noninfected tuberculin-sensitive guinea pigs. J. Bacteriol. 92:76-81. 1966.-Normal guinea pig serum was separated into seven fractions by electrophoresis on cellulose acetate membranes. Thirty antigens were found by immunoelectrophoresis: albumin, 6 alpha(1) globulins, 11 alpha(2) globulins, 6 beta(1) globulins, 5 beta(2) globulins, and gamma globulin. Hyper-alpha(2)-globulinemia was detected in sera from guinea pigs 14 days after inoculation with viable virulent Mycobacterium bovis. An additional alpha(2) globulin, not demonstrable prior to infection, was detected concomitantly with the hyper-alpha(2)-globulinemia by immunoelectrophoresis. The additional alpha(2) globulin was tentatively named alpha(2)-T. It persisted until the death of the guinea pigs. Neither hyper-alpha-globulinemia nor the alpha(2)-T antigen was detected by cellulose acetate electrophoresis and immunoelectrophoresis of sera from guinea pigs sensitized with heat-killed M. bovis. Both changes were due to the disease, not to delayed sensitivity alone.