Leprosy in a mangabey monkey--naturally acquired infection.

Naturally acquired leprosy was detected in an otherwise normal "sooty" mangabey monkey (Cercocebus atys). This animal was imported from West Africa in 1975 and developed clinical symptoms of leprosy in 1979. Histopathologic findings were those of subpolar-lepromatous to borderline-lepromatous leprosy in the Ridley-Jopling classification. The disease was progressive, with crippling neuropathic deformities of the hands and feet. The disease regressed under specific therapy. The etiologic agent was identified as Mycobacterium leprae by the following criteria: invasion of nerves of host, staining properties, electron microscopic findings, noncultivable on mycobacteriologic media, DOPA-oxidase positive, lepromin reactivity, infection patterns in mice and armadillos, sensitivity to sulfone, and DNA homology. We believe the animal acquired the disease from a patient with active leprosy. The mangabey monkey offers promise as a primate model for leprosy, and adds a third reported species to animals with naturally acquired leprosy.

Depression of lymphocyte responses to mitogens in mangabeys with disseminated experimental leprosy.

Mononuclear cells from mangabey monkeys with disseminated experimental leprosy had increasingly severe depression of blastogenic responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen as the disease progressed. Blastogenic responses were not depressed in cells from mangabeys with more localized disease. Blastogenic responses of cells from normal mangabeys appeared to vary with a circannual rhythm. The demonstration of significant negative correlations between the blastogenic responses to mitogens and the percentages of OKT8+ cells suggested that the mangabey OKT8+ subset may contain cells with suppressor function. The depressed responses to mitogens by cells from monkeys with disseminated experimental leprosy were associated with relatively high percentages of OKT8+ cells. Polyclonal immunoglobulin plaque-forming cell responses to pokeweed mitogen were depressed in cells from experimentally infected mangabeys. The results indicated that defects in immune regulation may occur in experimental leprosy in mangabeys, similar in some respects to the defects that have been reported in human leprosy.

Cat-scratch disease. Bacteria in skin at the primary inoculation site.

Cat-scratch disease is a zoonotic infection characterized by a skin papule at the site of the scratch followed by regional lymphadenitis. Recently, small gram-negative pleomorphic bacilli were demonstrated in sections of lymph node from patients with the disease. We now report identical bacteria in the primary inoculation site of three patients with cat-scratch disease. Lymph nodes from two of these patients also contained the same bacilli. Identical bacteria in both skin and lymph nodes from these patients are further evidence that the bacilli are the cause of cat-scratch disease. In early infections, biopsy of the primary site of inoculation and demonstration of bacilli may replace excision and histologic examination of lymph node in establishing the diagnosis of cat-scratch disease.

Cat scratch disease: a bacterial infection.

Histopathologic examination of lymph nodes from 39 patients with clinical and pathological criteria for cat scratch disease revealed delicate pleomorphic Gram-negative bacilli in 34 of the 39 nodes. They were within the walls of capillaries in or near areas of follicular hyperplasia and within microabscesses. They were best seen with the Warthin-Starry silver impregnation stain. Organisms in lymph node sections exposed to convalescent serum from three patients and to immunoperoxidase stained equally well with all three samples. The organisms did not react with hyperimmune sera to Legionella pneumophila nor to several species of Rickettsia. These bacilli appear to be the causative agents of cat scratch disease.

Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.

The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5.

Possible humoral mechanism of 2450-MHz microwave-induced increase in complement receptor positive cells.

These studies indicate that the increase in the frequency of complement receptor-positive (CR+) spleen cells observed 6 days after a 30-min exposure to 2450-MHz microwaves is not the result of microwave-induced alterations of lymphocyte recirculation patterns, but is mediated by a soluble, humoral factor produced by cells within the spleen.

Biologic effects of microwave exposure. II. Studies on the mechanisms controlling susceptibility to microwave-induced increases in complement receptor-positive spleen cells.

In attempting to evaluate the mechanisms responsible for susceptibility to the inductive increase in splenic complement receptor-positive (CR+) cells following exposure to 2450-MHz microwaves, it was found that sensitivity to microwave-induced CR+ cell increases was under genetic control. In particular, evidence was accumulated suggesting that regulation was under the control of a gene or genes closely associated with but outside of the mouse major histocompatibility complex (H-2). All responsive strains of mice tested were of the H-2k haplotype, while mice of the H-2a, H-2b, H-2d and H-1i5 haplotypes were refractory to the microwave-induced increases in CR+ cells. By utilizing certain H-2k strains of mice that were genetically unable to respond to endotoxin, we were able to show that these strains of mice responded to microwaves, but not to endotoxin, by increasing CR+ cells. Microwave-induced increases in CR+ cells were not mimicked by the intraperitoneal injection of hydrocortisone. Athymic mice responded to microwave exposure, indicating that this event was not regulated by the T-cell population. Mice less than eight weeks old were found not to be susceptible to exposure to 2450-MHz microwaves. These studies indicate that microwaves do induce changes in the population of cells with specific cell-surface receptors, that susceptibility to these changes is under genetic control, and that it is unlikely that endotoxin, corticosteroids, or regulatory T cells play a significant role in the mechanisms regulating these increases.