Bursectomy

Abstract: Development of heterogeneity of immunoglobulin classes has been investigated in the chicken by studying the effects of antibody-mediated suppression of IgM synthesis. Treatment of 13-day embryos with purified goat antibodies to IgM resulted in the elimination of IgM-containing cells from the bursa of Fabricius of 16- and 19-day embryos. When combined with bursectomy at hatching, administration of anti-IgM in ovo suppressed the synthesis not only of IgM but also of IgG. A number of experimental birds lacked detectable circulating immunoglobulins, plasma cells, and germinal centers when killed at 10 weeks of age. Contrasting results were obtained when IgM synthesis was suppressed after bursectomy at hatching. Birds so treated produced little or no IgM but synthesized normal amounts of IgG. The results suggest that, within the bursal environment, IgG-producing cells arise exclusively from cells that previously synthesized IgM. A model for generation of antibody variability is presented.

Abstract: The highly virulent strain Cu-1 of infectious bursal disease virus caused 100% mortality in 4-week-old specific pathogen-free chickens. In contrast, chickens infected after bursectomy did not become sick and only showed some discrete and transient necrosis in lymphatic tissues. However, these chickens contained infectious virus and, subsequently, produced specific antibodies. The virus concentrations in the organs studied reached their maximum 2 days postinfection, but were about 1,000 times lower in non-bursectomized animals. It may be assumed that in bursectomized chickens the early events of infection are the same as in non-bursectomized ones. Virus is spread in varius organs, but due to the absence of a sufficient number of susceptible cells, virus multiplication is moderate and can be kept in check by the host defense mechanism. With the occurrence of circulating specific antibodies the virus can be rapidly eliminated. The studies particularly stress that the availability of a large number of highly susceptible cells is a crucial point in acute viral infections.

Abstract: Summary 1.Injection of 0.63 mg 19-nortestosterone into eggs prevents differentiation of the bursa Fabricii. Chickens resulting from such treatment were unable to produce precipitins when challenged with a single intravenous injection of BSA at 6 or 22 weeks of age. 2.Chickens surgically bursectomized at 1 and 2 weeks of age along with intact controls were challenged with BSA at 6 and 12 weeks of age. Antibody response of the bursectomized groups was significantly lower than the control group. The responses of age did not differ from one another. 3.Chickens bursectomized at 1, 5 and 10 weeks of age were injected with BSA at 22 weeks of age and were reinjected at 34 weeks of age. The response of chickens bursectomized at 1 week of age was significantly less than the control response, whereas bursectomy at 10 weeks of age had little or no effect on the response at 22 or 34 weeks of age. Bursectomy at 5 weeks appeared to decrease antibody production at 22 weeks but was without apparent effect at 34 weeks. 4.Surgical bursectomy had no effect on body weight. The hormonal injection of the incubating eggs produced birds weighing less than the controls and in generally poor health. Mortality in the hormone treated birds was high.

Abstract: The effects of cyclosporin A (CsA) treatment and hormonal bursectomy on Eimeria tenella infection of chickens were investigated to evaluate the role of humoral antibody and cell-mediated immunity (CMI) in the host protective immunity to an intestinal protozoan disease, coccidiosis. Hormonal bursectomy had no significant effect on the host response to E. tenella. CsA treatment had a differential effect on the course of disease depending on how CsA was given relative to infection. Daily administration of CsA for 7 days beginning 1 day before primary infection with E. tenella enhanced disease resistance, whereas a single dose of CsA given before primary infection enhanced disease susceptibility compared with that of untreated controls. Chickens treated with CsA during the primary infection were resistant to reinfection at 5 weeks post-primary infection. Treatment of chickens immune to E. tenella with CsA at the time of secondary infection abrogated their resistance to reinfection despite the presence of high levels of coccidia-specific secretory immunoglobulin A and serum immunoglobulin G. Splenic lymphocytes obtained after CsA treatment demonstrated a substantially depressed concanavalin A response, but not a depressed lipopolysaccharide response. Because CsA was not directly toxic to parasites in vivo when administered during the secondary infection, these results suggest that CsA interacts with the immune system to allow priming during the primary infection, while interfering with the effector function of CMI during the secondary infection. Taken together, present findings indicate that CMI plays a major role in host protective immunity to E. tenella.