Faculty Bibliography

The immunogenic effect of inactivated hepatitis B vaccine (Merck Heptavax B) was evaluated in 202 seronegative healthy medical personnel. Three inoculations of vaccine were given at 1-month intervals. Of 116 vaccinees who received a 40-microgram dose, 39% had an anti-HBs response 1 month after the first dose, 88% 1 month after the second dose, and 99% 1 month after the third dose. Of 86 vaccinees who received a 20 microgram dose, 40% had an anti-HBs response 1 month after the first dose, 79% after the second dose, and 95% after the third dose. These results confirm the high immunogenic effect of a 20-microgram dose of vaccine

Rolling disease has been produced and studied in rats and mice, using the exotoxin of the A strain of Mycoplasma neurolyticum. The primary lesion of the brain consists of spongiform degeneration, associated with vesicle formation in the cortex and underlying white matter of the cerebral hemispheres, and in the molecular layer of the cerebellum. The brains of animals surviving 2 days or longer show extensive necrotizing lesions resembling ischemic necrosis, in both cerebral hemispheres. The brains of rats and mice with rolling disease become deeply stained by intraperitoneally injected trypan blue, indicating early disruption of the blood brain barrier. The toxin appears to be a thermolabile protein with a molecular weight exceeding 200,000. It is only active when injected by vein, and causes no disease when injected intracerebrally, intraperitoneally or subcutaneously, suggesting the existence of specific receptors within the vascular bed of the central nervous system. Protection is afforded by rabbit antibody against the toxin, but only when antibody is injected within less than 3 min after intravenous injection of toxin, indicating rapid fixation to receptors in the brain. The toxin is inactivated by incubation for 10 min at 37 degrees C with suspensions of the sedimentable component of normal brain. The inactivating factor in brain sediment is very thermostable, not affected by trypsin, and eliminated by treatment with periodate. Similar inactivation of toxin is demonstrable with water-soluble gangliosides of brain. A theoretical concept to explain the action of the toxin is proposed.

Turkey poults injected intravenously with suspensions of Mycoplasma gallisepticum develop a fatal neurologic disease associated with polyarteritis affecting almost exclusively the cerebral arteries. The incubation period depends on the dose of organisms. With high doses (10(10) to 10(11) mycoplasmas) the birds become ill and die within a few hours; with lower doses (10(6) to 10(8)) neurologic manifestations appear after 7 days. The rapid onset of neurologic signs after high doses indicates the presence of a toxin in the mycoplasma, but efforts to extract toxin from disrupted organisms or to demonstrate its presence in culture fluid free of mycoplasmas have been unsuccessful. The toxin appears to be associated only with living mycoplasmas. The toxic component of M. gallisepticum is inactivated by heating the organisms at 50 degrees C, disruption by repeated cycles of freezing and thawing, and exposure to specific antibody. Treatment of turkeys with gold thiomalate furnishes partial protection against the toxic effects of large doses of mycoplasmas, and protection against the development of cerebral arteritis. Treatment with tetracycline protects completely against both toxicity and arteritis, and, when delayed, restores diseased birds to a healthy state. Cortisone, methotrexate and 6-mercaptopurine have no effect on the course or outcome of the disease. Intracerebral injections of M. gallisepticum are less toxic and lethal than when the same dose was given by vein, indicating that the organism exerts its damaging action on blood vessels by way of the blood stream. The arterial lesions resemble those of serum sickness, except for their distribution, and are associated with glomerular inflammatory lesions. However, for various reasons discussed, it is considered more likely that they result from a direct toxic action of living mycoplasmas on the vessels concerned than from an immunologic mechanism.