phenylephrine-hydrochloride and Immunologic-Deficiency-Syndromes

Topics: Biomarkers; Cystic Fibrosis; Diagnosis, Differential; Diagnostic Imaging; Humans; Immunologic Deficiency Syndromes; Mucociliary Clearance; Nasal Cavity; Nose; Pressure; Pulmonary Ventilation; Rhinitis; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; Sinusitis; Smell; Sound

Mice with the scid mutation are highly susceptible to Mycoplasma pulmonis infection and develop a disseminated disease. In order to study the contribution of humoral immunity to the immune response, M. pulmonis was inoculated intranasally to X-linked immunodeficient (xid) mice. Severe combined immunodeficient (scid) and immunocompetent CBA mice were used as controls. The mice were killed and necropsied at day 30 or 37 post-infection. Samples from the nose, lungs and joints were taken for bacteriological and histological examination. Rhinitis was observed in all mouse strains. Chronic purulent bronchopneumonia was diagnosed in some of the CBA mice. Xid mice did not show severe lung lesions, despite the presence of numerous mycoplasma organisms in the lungs, in contrast to immunocompetent mice, which developed lung pathology. Scid mice showed less signs of pneumonia, but unlike in xid and CBA mice, there was spread of mycoplasmas from the respiratory tract and severe pathological changes in the joints. Our results indicate that B and/or T lymphocytes protect against dissemination of M. pulmonis from the airways. Innate immune reactions and/or bacterial virulence factors seem to contribute to the development of joint lesions, whereas IgG3 and IgM antibodies might be involved in lung pathology.

Topics: Animals; Disease Susceptibility; Genetic Linkage; Immunologic Deficiency Syndromes; Lung; Male; Mice; Mice, Inbred CBA; Mice, SCID; Mycoplasma Infections; Nose; X Chromosome

Beige mice show increased susceptibility to intranasal infection with organisms of the Mycobacterium avium complex (MAC) compared with their immunocompetent congenics, C57BL/6 mice. This increased susceptibility was clear 2 weeks postinfection, before the activation of the specific immune response. T lymphocytes from 4-week infected beige mice, cultured in vitro, produced amounts of gamma interferon similar to those found in cells from C57BL/6 mice. Macrophage activation, as judged by NO production and lysis of the macrophage target P815, occurred in the lungs of beige mice. Despite the inability of bone marrow-derived NK cells from beige mice to lyse NK-susceptible YAC-1 cells, their gamma interferon production was normal. Monoclonal antibody to NK1.1 was used to deplete C57BL/10 mice of lytic activity against YAC-1 cells without exacerbating infection between 2 and 6 weeks of observation, making it unlikely that any deficiency in NK cells was the cause of susceptibility in beige mice. There was a striking influx of neutrophils in the lungs of beige mice compared with C57BL/6. More than half of the MAC organisms appeared associated with the neutrophils of beige mice, while in C57BL/6 mice, most MAC organisms were associated with cells of macrophage/monocyte morphology. Injection of monoclonal antibody specific for neutrophils failed to eliminate those cells from the lungs of beige mice. However, in C57BL/6 mice, neutrophil numbers were reduced by 95% without exacerbating the infection. We conclude that, although neutrophils are not essential to the relative resistance of C57BL/6 mice, the known deficiencies in both neutrophils and macrophages account for the susceptibility of beige mice.

Topics: Animals; Immunologic Deficiency Syndromes; Interferon-gamma; Killer Cells, Natural; Macrophages; Male; Mice; Mice, Inbred C57BL; Mycobacterium avium; Neutrophils; Nose; Pneumonia; Tuberculosis

Topics: Child; Cytokines; Female; Humans; Immunologic Deficiency Syndromes; In Vitro Techniques; Interferon-gamma; Mitogens; Mycobacterium Infections; Necrosis; Nose; Opportunistic Infections; Recombinant Proteins; Skin Ulcer; T-Lymphocytes

A laminar airflow room was used to provide a low-pathogen environment for a child with lymphopenic immune deficiency transplanted with paternal bone marrow. Comparison of flora from the patient, personnel, and the environment indicated that no colonization with exogenous organisms occurred in the patient during the 45-day period of study. The number of organisms recovered from the laminar airflow room was exceedingly small. Conventional hospital isolation rooms contained more bacteria and fungi than the laminar airflow room, even when strict aseptic procedures were followed in the former. Patients with lymphopenic immune deficiency and agranulocytosis admitted to conventional isolation rooms were colonized with exogenous organisms within 1 week. Each developed infection with these strains, and one patient died. Laminar airflow isolation seems at present the best means to prevent exogenous infection during hospitalization of patients with lymphopenic and other severe immune-deficiency diseases and may be essential when bone marrow transplantation is performed to treat their immunological defect.

Topics: Air Microbiology; Bacteria; Bacteriological Techniques; Bacteriophage Typing; Bone Marrow Transplantation; Cross Infection; Equipment and Supplies, Hospital; Feces; Humans; Immunologic Deficiency Syndromes; Infant; Intensive Care Units; Lymphopenia; Male; Methods; Nose; Perineum; Personnel, Hospital; Pharynx; Serotyping; Statistics as Topic; Transplantation, Homologous; Ventilation