Development of effective programs for control of epidemic streptococcal infections.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to P G Quie.
Explore the source record for details and available documents.
To determine whether oxidative metabolic products of phagocytic cells are present in the middle ear during experimental pneumococcal otitis media, we measured the concentration of myeloperoxidase (MPO) in middle ear fluid (MEF) and the capacity of neutrophils isolated from MEF and peripheral blood to produce MPO and superoxide anion (O2-) after in vitro stimulation. Free MPO in MEF was significantly increased 24 and 48 h after either viable or nonviable pneumococci were inoculated into the middle ear. In vitro-stimulated production of MPO and O2- from middle ear neutrophils was significantly less than that from peripheral blood neutrophils 24 h after nonviable pneumococci were inoculated but similar to it after 48 h. Twenty-four hours after viable pneumococci were inoculated, middle ear neutrophils stimulated in vitro produced less MPO but the same amount of O2- as did blood neutrophils. Oxidative metabolic products, therefore, are released from phagocytic cells into the MEF during pneumococcal otitis media, and future studies will need to define the contribution of these products to acute and chronic middle ear tissue injury.
An encapsulated strain of Staphylococcus simulans was observed to be more resistant to phagocytosis by human granulocytes than was a nonencapsulated strain. Phagocytosis of the encapsulated strain was enhanced by antisera to S. simulans, but opsonic activity of antisera was removed by absorption with S. simulans capsular material. The encapsulated strain of S. simulans was also more invasive than the nonencapsulated S. simulans in vivo. More encapsulated than nonencapsulated S. simulans were found in heart blood when equal numbers of organisms were injected intraperitoneally into mice. Invasion of the bloodstreams of mice by encapsulated S. simulans was prevented by passive immunization (rabbit antiserum). Thus, the capsule of S. simulans inhibited phagocytosis in vitro and contributed to virulence in vivo.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Serious life-threatening neonatal infections with microbial species that are infrequently associated with infections in adults are related to the immature immune system of human newborn infants. The usually sterile intrauterine environment of the fetus is associated with a primed but inactive immune system at the time of birth. Sudden introduction into a complex microbial world stimulates the inflammatory system and an effective host defense rapidly develops. Defense mechanisms include innate phagocytic and complement systems, and specific adaptive immunity including antimicrobial antibodies. Fortunately, neonates have protective antibodies against many microbes at birth provided by their mothers via placental transfer of IgG. Specific antimicrobial antibody production by the newborn infant is delayed. Neutrophil numbers in the circulation are high in the normal neonate, but the bone marrow pool of cells is limited. Chemotactic responsiveness of circulating phagocytic cells is decreased in comparison with adult cells, although phagocytic and microbicidal activity of neonatal neutrophils and monocytes are normal. The newborn infant's lymphocyte system is relatively mature, and neonatal mononuclear cells have normal antigen-presenting and secretory function. T lymphocytes are present in normal numbers and although response of these cells to antigens is somewhat slower than in adult cells, a near normal response suggests intrauterine stimulation by maternally derived immunoregulators. B lymphocytes are also present in newborn human infants. However, maturation of B lymphocytes into antibody-producing plasma cells occurs gradually during the first weeks of life.(ABSTRACT TRUNCATED AT 250 WORDS)
Twelve of the 25 patients with chronic granulomatous disease treated at our institution between 1957 and 1987 were found to have urinary tract disorders. All 12 patients were male and 22 years of age or younger when chronic granulomatous disease was diagnosed. Six patients had hydroureteronephrosis in association with recurrent episodes of pyelonephritis, retroperitoneal lymphadenitis, and granuloma formation. The other six patients had genital lesions or dysuria. Among the six patients with hydroureteronephrosis, a nephrectomy was performed in two, ureterolysis was used to relieve obstruction in one, and hydroureteronephrosis resolved after antibiotic therapy alone in three. We conclude that complications involving the genitourinary system occur frequently in patients with chronic granulomatous disease. Periodic imaging of the urinary tract may detect asymptomatic hydroureteronephrosis or other treatable genitourinary abnormalities in these patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A collection of Streptococcus zooepidemicus strains from human and animal infections was examined for DNA banding patterns after nuclease digestion and agarose gel electrophoresis. The large variety of DNA fingerprints found revealed the complexity of the species but showed that isolates from clusters of outbreaks had identical prints. The results confirmed the specificity of bacteriocin and bacteriophage typing of S. zooepidemicus; the technique also gave useful profiles on untypable strains. Strains with common bacteriocin and biotyping patterns from sporadic infections could be differentiated by their DNA fingerprints. In several outbreaks and incidents, more than one strain of S. zooepidemicus were encountered, and the importance of carefully interpreting typing data is stressed. Chromosomal DNA fingerprinting is a very efficient technique for demonstrating differences between strains of S. zooepidemicus, and its use is recommended for future epidemiological studies of this infectious agent.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The human lung has an exquisitely effective and complex defense against infections. Mucus prevents attachment of bacteria to the epithelium, and those bacteria that cannot cross the mucus are cleared by exhalation or by the mucus-ciliary escalator. Alveolar macrophages dispatch microbes that reach the peripheral barriers of the lung. The pulmonary phagocytic system immobilizes, kills, and walls off invading bacteria. The phagocytic system, developed in bone marrow, includes alveolar macrophages, granulocytes, and monocytes. The phagocytic system is amplified by humoral factors, including inflammatory mediators, acute-phase reactants, and opsonins that allow rapid engulfment and killing of microbes. Highly mobile polymorphonuclear granulocytes reinforce the macrophages when invading organisms reach tissue. Sterility of the lower respiratory tract in the normal host is evidence that the defense systems of the lung are highly effective and potently bactericidal. The oxidative and nonoxidative microbicidal mechanisms of alveolar macrophages and granulocytes are lethal for most ordinary microbes. However, certain pathogens have means of preventing phagocytosis, and obligate intracellular species have evolved mechanisms of intracellular survival. Successful biologic détente between microbe and host is the usual situation in the normal human lung, but the relationship is unfortunately short-lived in patients with cystic fibrosis. Mucus is not an adequate barrier in these patients. Bacterial pathogens colonize respiratory tissue and, as a consequence, compromise lung function. Better understanding of local defenses in normal human lungs and of the defects in lung defenses in patients with cystic fibrosis should lead to methods that will provide these patients with successful defense against invading microbes.
This article describes studies of two unrelated patients, ages 5.5 and 26 years, with leukocyte granulation abnormalities similar to those in the Chediak-Higashi syndrome. Both patients presented with neurologic manifestations characterized by psychomotor impairment, but neither had any evidence of oculocutaneous albinism, photophobia, or increased susceptibility to pyogenic infection. The leukocytes were studied for cytochemical, ultrastructural, ultrastructural cytochemical, and functional characteristics. Abnormal granules were present in neutrophils, eosinophils, basophils, monocytes, and lymphocytes; in the neutrophil series the abnormalities involved both the azurophilic and specific granules. On ultrastructural examination, the abnormal granules in the neutrophils were found to result from fusion of both peroxidase-positive and peroxidase-negative granules. Large numbers of normal granules were also present. The abnormal large granules in the eosinophils and basophils were the result of fusion of normal granules. The neutrophil function studies showed normal chemotaxis, chemiluminescence, bactericidal activity, and nitro-blue tetrazolium reduction. The normal neutrophil function studies were paralleled by the clinical histories in that neither patient had a history of severe infectious episodes.
Explore the source record for details and available documents.
We measured the luminol- and lucigenin-enhanced chemiluminescent response of human polymorphonuclear leukocytes (PMN) stimulated by various strains of Streptococcus pneumoniae and Haemophilus influenzae. In the absence of opsonin, phagocytosis of either bacterial species elicited good PMN response when the bacteria were adhered to a surface but minimal PMN response when they were in suspension. When 10% pooled human serum was used as a source of opsonin, a moderate to excellent chemiluminescent PMN response was elicited during phagocytosis of opsonized bacteria both in suspension and adhered to surface. We conclude that opsonin significantly enhances PMN chemiluminescence when a suspension-type assay is used and that opsonin-independent mechanisms play a significant role in the chemiluminescent response of PMN during phagocytosis of adherent bacteria.
The interaction of Staphylococcus epidermidis slime with human neutrophils (PMN) was examined by using isolated slime and allowing bacteria to elaborate slime and other extracellular products in situ. S. epidermidis slime was found to contain a chemoattractant. Incubation of PMN with 50 micrograms or more of slime per ml inhibited subsequent chemotaxis of the PMN to n-formyl-methionyl-leucyl-phenylalanine by 27% and to zymosan-activated serum by 44 to 67% with increasing slime concentrations. S. epidermidis slime stimulated little degranulation of untreated PMN. After pretreatment of PMN with 5 micrograms of cytochalasin b per ml, slime predominantly induced release of specific granule contents (33.8% lactoferrin release by 250 micrograms of slime per ml versus 10% myeloperoxidase release by 250 micrograms of slime per ml). By a surface phagocytosis assay, PMN uptake of radiolabeled S. epidermidis which were incubated for 18 h on a plastic surface for slime expression was less than that for S. epidermidis adhered to the plastic for 2 h or grown in unsupplemented nutrient broth. These results suggest that S. epidermidis slime interaction with PMN may be potentially detrimental to host defense and may contribute to the ability of this organism to persist on surfaces of foreign bodies in the vascular or central nervous system.
We examined the chemiluminescence response of peripheral blood monocytes from patients with cystic fibrosis (CF) and their asymptomatic parental carriers of the CF gene to three different types of stimulation. We found that monocytes from both patients and carriers have increased luminol-dependent chemiluminescence in the first 25 min after stimulation by adherence to glass. These results are consistent with the hypothesis that monocytes from both CF heterozygotes and homozygotes respond to adhesion with increased oxygen radical formation. The increased adherence-induced monocyte chemiluminescence of the parental carriers did not vary with age or length of exposure of the parents to a child with CF. Also, repeated exposure to medications and respiratory secretions of CF patients was not associated with an increase in adherence-induced monocyte chemiluminescence of their nonbiologically related caretakers. Thus, this observed increase in chemiluminescence is not simply secondary to the medications or respiratory dysfunction seen in the patients with CF. Patients with other types of obstructive lung disease did not show increased adherence-induced monocyte chemiluminescence. We conclude that increased early phase adherence-induced monocyte chemiluminescence occurs in patients with cystic fibrosis and the obligate carriers of the CF gene independent of environmental influences.