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Biomedical subjects

B M Gray

Publications and source records attributed to B M Gray.

At least 55 records · Page 3Linked to original sources
PubMed1988

Role of adherence of Streptococcus pneumoniae in acute otitis media.

The adherence of Streptococcus pneumoniae to human nasopharyngeal epithelial cells was studied as a possible determinant in the development of acute otitis media (AOM). Pneumococcal isolates were obtained from the nasopharynx (NP) and middle ear fluid of infants followed from birth in a prospective study of pneumococcal carriage and infection. The adherence of 33 middle ear fluid isolates from 19 infants with AOM was compared with 143 strains recovered from NP cultures taken from each child both at the time of their acute infections and on other occasions. We studied 171 NP isolates from 29 "carrier" infants, who had no pneumococcal infections, for comparison. Adherence properties were not associated with any particular pneumococcal capsular types, nor were adherent strains more frequent among infants with AOM. There was no evidence to support the hypothesis that pneumococci associated with AOM have a special propensity for adherence. Adherence was a frequent characteristic of pneumococci recovered from the NP, especially in connection with upper respiratory tract infection, and may be required for the establishment of colonization but was not a property that discriminated between carriage strains and those causing AOM.

Bacterial Adhesion↗
PubMed1988

Hemodynamic responses of chronically instrumented piglets to bolus injections of group B streptococci.

Group B beta-hemolytic Streptotocci cause pulmonary hypertension when injected into animals and may precipitate the persistent pulmonary hypertension syndrome in infected human neonates. We used chronically instrumented piglets to study the effects of repeated injections of heat-killed group B Streptococcus (GBS) type III. Daily exposure to GBS was associated with a 2-fold or greater potentiation of pulmonary and systemic hypertensive responses after 1 wk. Throughout experimentation, pulmonary pressure changes were more marked than systemic changes. After establishing a dose-response relationship, we chose a control dose that produced intermediate hypertensive responses. We then evaluated the effects of antibody and various drugs on the hypertensive responses. Preincubation of organisms with rabbit antiserum containing type-specific antibody enhanced the responses. Beta endorphin blockade with naloxone had little or no effect; leukotriene synthesis inhibition also did not affect responses. Both indomethacin, a cyclooxygenase inhibitor, and dazmegrel, a specific thromboxane synthesis inhibitor, blocked the hypertensive responses to GBS. It appears that repeated doses of GBS potentiate the hypertensive responses, a process that we hypothesize may be mediated by development of type-specific antibody as type-specific antibody levels rose during potentiation. It is likely that thromboxane A2 is the effector of the pulmonary and systemic hypertensive responses to GBS injection, because thromboxane inhibition by dazmegrel was as effective as indomethacin in blocking these effects. Thromboxane synthesis blockade may prove useful in management of hemodynamic disturbances accompanying severe bacterial infections in humans.

Animals↗
PubMed1988

Specificity of monoclonal antibodies against group B streptococcus type II and inhibition of their binding by human secretions.

Mouse monoclonal antibodies against the type-specific polysaccharide antigen of type II group B Streptococcus may be divided into two general groups based on their antigen-binding properties. One group of antibodies binds to both intact and desialylated type II antigen and the binding can be inhibited by beta-galactopyranosides. The second group of antibodies react only with intact type II polysaccharide and are not inhibited by beta-galactopyranosides. The binding of antibodies of the first group can also be inhibited by carbohydrate components of normal human secretions that share structural similarities with the type II polysaccharide. The binding of antibodies of one specificity precluded the binding of antibodies of the other specificity, apparently by competing for binding sites within a combining area that includes both determinants.

Animals↗
PubMed1988

Inapparent Streptococcus pneumoniae type 35 infections in commercial rats and mice.

Streptococcus pneumoniae was isolated from specific-pathogen-free rodents in two rooms at a commercial breeding facility during vendor surveillance testing. In a survey of 274 animals from the two rooms over a period of 7 months, capsular serotype 35 S. pneumoniae was isolated from the upper respiratory tracts of 11% (9 of 82) of C57BL/6 mice in room A and 14% (10 of 72) of F344 rats in room B, but not from WKY rats, BALB/c mice or DBA/2 mice from room A. In both C57BL/6 mice and F344 rats, older rodents had higher colonization frequencies. Nasal lavage cultures gave the best results in identifying colonized rodents. No clinical illness or microscopic lesions were associated with pneumococcal colonization in rats or mice, and no other evidence of potential pathogen infection was found except for positive serologic tests for mouse rotavirus in mice. This is the first report of natural pneumococcal infection in mice, and the first report of type 35 S. pneumoniae infection in rodents. The findings support an earlier observation that pneumococcal infections in rat colonies tend to be monotypic and suggest that the same may be true in mice.

Animals↗
PubMed1987

Type-specific streptococcal antibodies in amniotic fluid.

Type-specific antibodies against group B streptococcal and pneumococcal capsular antigens were measured in 68 amniotic fluid samples from healthy women between 16 and 20 weeks of pregnancy. Mean antibody levels ranged from 0.13 to 0.61 microgram/ml, with few samples having greater than 1 microgram/ml against any antigen. The role of antibodies in protection against intrauterine infection is discussed.

Adult↗
PubMed1987

Group B streptococcal carriage and disease: a 6-year prospective study.

A prospective study of group B streptococcal (GBS) carriage and disease was conducted over 6 years. Carriage rates at delivery for mothers and infants were 20% and 12%, respectively. Forty-five cases of GBS disease occurred in infants, 24 "early-onset" disease and 21 "late-onset" disease. The combined attack rate for early and late disease was 3.3 per 1000 live births over the 6 years. The rate of early-onset disease was highest in infants found to be heavily colonized at birth: 50 per 1000 live births. Twenty-three of 24 had evidence of intrauterine-acquired infection. All GBS serotypes were represented. Preterm delivery, prolonged labor, premature rupture of membranes, and maternal infection enhanced the risk of early disease. Septicemia was the predominant form of late-onset disease (15 of 21 cases); GBS type III accounted for 19 of 21 cases. Ten of 21 infants with late infections were colonized at birth with the GBS type that subsequently caused disease. Thus a maternal source of infection was identified in 34 of the 45 infants. These data reveal consistent year-to-year carriage and disease rates in the study population.

Anti-Bacterial Agents↗
PubMed1987

Thromboxane synthesis inhibition reverses group B Streptococcus-induced pulmonary hypertension.

Group B Streptococcus (GBS) sepsis in humans may cause the persistent pulmonary hypertension syndrome. Infusions of GBS in animals elevate pulmonary artery pressure (PAP) and resistance and are associated with elevated thromboxane levels. We investigated the hemodynamic effects of the specific thromboxane synthesis inhibitor, dazmegrel, in a piglet model of GBS-induced pulmonary hypertension. PAP rose from 22 +/- 6 to 42 +/- 11 (SD) mm Hg during infusion of heat-killed GBS; pulmonary vascular resistance increased from 1440 +/- 400 to 4000 +/- 1040 dyne X sec/cm5. No significant changes in cardiac output, mean arterial pressure, or left atrial pressure were noted. Treatment with 1 mg/kg of dazmegrel resulted in a rapid return of PAP and resistance to control values. No other hemodynamic effects of either bacteria or drug were observed despite continued infusion of GBS.

Animals↗
PubMed1987

Lack of correlation of in vitro adherence of Haemophilus influenzae to epithelial cells with frequent occurrence of otitis media.

The adherence to human epithelial cells, biotype and capsular type of 175 Haemophilus influenzae cultured from the upper respiratory tract were studied in a prospective study of children with recurrent otitis media. Forty-three children who had greater than 2 episodes of acute otitis media (AOM) during the first year of life were followed for at least 1 year. Cultures of the oropharynx were done periodically, and the middle ear fluid (MEF) was cultured at the time of AOM. H. influenzae was recovered from MEF in 44% of the 136 AOM episodes recorded. Thirty-one children had at least one episode of AOM caused by H. influenzae; the remaining 12 children, designated as "controls," had no otitis or had AOM caused by other organisms. The possible differences between carriage and infection strains were evaluated by comparison of MEF and oropharyngeal isolates, by pairwise comparison of MEF and oropharyngeal isolates and by pairwise comparison of multiple isolates from each host recovered at the time of AOM and during infection-free intervals. No significant differences in patterns of adherence, capsular type or biotype were found. The lack of correlation between these characteristics and infection suggests either that H. influenzae organisms have determinants of virulence yet to be defined or that variations in host susceptibility permit infection by the strain colonizing the upper respiratory tract. Adherence per se may be less important in the development of infection than in establishing and maintaining colonization within the host.

Acute Disease↗
PubMed1986

Quantitative levels of C-reactive protein in cerebrospinal fluid in patients with bacterial meningitis and other conditions.

We measured levels of C-reactive protein (CRP) in the cerebrospinal fluid in 145 children, using a solid-phase radioimmunoassay. The CRP levels in 49 patients with culture-proved bacterial meningitis ranged from 0 to 51,000 ng/ml (median 1460 ng/ml). In 33 patients with aseptic meningitis, values were much lower range 0 to 438 ng/ml; (median 17 ng/ml). In patients with CSF pleocytosis (greater than 10 WBC/microliter), CRP greater than 100 ng/ml was 95% accurate in identifying those with bacterial meningitis. However, a few patients with bacterial meningitis and little or no CSF pleocytosis had low levels of CRP at admission. Among the 63 patients with nonmeningitic conditions, those with bacterial infections frequently (10 of 13 had CRP greater than 100 ng/ml, whereas CRP elevations were infrequent (seven (18%) of 40) in patients with viral infections and other conditions. CRP diffuses into the CSF as readily as other proteins, but in bacterial meningitis the CSF/serum ratio of CRP was lower than that of albumin and IgG. The measurement of CRP in CSF is potentially a very useful diagnostic tool, but certain inherent limitations must be recognized, because some patients may fail to mount a prompt inflammatory response.

Adolescent↗
PubMed1986

Influence of prostaglandin D2 on hemodynamic effects of group B streptococcus in neonatal lambs.

Infusions of group B streptococci cause pulmonary hypertension in several neonatal animal models. A continuous infusion of prostaglandin D2 reduced the magnitude of this pulmonary hypertensive response; indomethacin completely blocked the response. Prostaglandin D2 or cyclooxygenase inhibitors may be important therapeutic agents for infants with group B streptococcal sepsis who manifest pulmonary hypertension.

Animals↗
PubMed1986

Type-specific antibody prevents platelet aggregation induced by group B streptococci type III.

Group B streptococci (GBS) type III organisms readily induced platelet aggregation and serotonin release in human platelet-rich plasma (PRP). In a system using a GBS/platelet ratio of 1.5, aggregation occurred after 2 to 9 minutes (maximum aggregation, 73% +/- 11%). Serotonin release began within the first minute, reaching 40% before aggregation was detected. Maximum release was 65% +/- 9%. The addition of type-specific rabbit antisera inhibited aggregation and release in a dose-dependent fashion, whereas rabbit antisera against GBS type II and a pneumococcus type 14 and 19 had no effect. To test the activity of different isotypes, monoclonal antibodies against the sialic acid determinant of the GBS type III antigens were used. IgG, IgM, and IgA antibodies were all effective in blocking aggregation and serotonin release. Although the significance of this phenomenon is not clear, it may represent a protective function of antibody that is not directly related to opsonization and phagocytosis.

Adult↗
PubMed1985

Penicillin-intermediate pneumococci in a children's hospital.

During the three-year period from 1981 to 1984, all clinical isolates of Streptococcus pneumoniae were screened for resistance to penicillin in the clinical bacteriology laboratory at The Children's Hospital of Alabama, Birmingham. Twenty-eight of 828 isolates were presumed resistant by disk diffusion testing with 1-microgram oxacillin disks (zone diameter, less than 20 mm). Seventeen of the 28 (61%) were found to be intermediately sensitive to penicillin by a conventional agar dilution method. Penicillin-intermediate strains had a minimal inhibitory concentration of 0.125 to 0.5 mg/L; no penicillin-resistant (minimal inhibitory concentration, greater than 1 mg/L) strains were encountered. The prevalence of penicillin-intermediate strains was thus 17 of 828 isolates, or 2.1%. These strains were also examined for susceptibility to ampicillin, vancomycin, cefotaxime, and chloramphenicol. We present the clinical features of 17 patients with disease due to penicillin-intermediate pneumococci.

Alabama↗
PubMed1985

Myoglobin levels in mothers and neonates.

Myoglobin levels were measured in 70 maternal and 74 cord sera drawn immediately after delivery. The mean cord myoglobin was 28 ng/ml. Myoglobin levels increased with birthweight, and black infants tended to have slightly higher levels than white babies. Myoglobin levels were not elevated in babies with fetal distress (evidenced by abnormal monitor tracings or meconium staining) compared to babies with no distress. Maternal myoglobin (18 +/- 15.3 ng/ml) was about 10 ng/ml lower than cord levels and there was little correlation between the two. Mothers differed among themselves only with respect to complications of labor and delivery. Those with complications had significantly higher myoglobin levels (29 +/- 24.1 ng/ml) than mothers without difficulties (15 +/- 10.0 ng/ml, P less than 0.05). The fetal myoglobin level was relatively independent of the mother's. While high or potentially toxic myoglobin levels were not observed in this study, it appears that the fetus may be protected by the placental barrier.

Apgar Score↗
PubMed1985

Seroepidemiological studies of group B Streptococcus type II.

In the course of prospective epidemiological studies of group B streptococcal (GBS) colonization and infection, we surveyed 401 paired maternal and cord sera (obtained at delivery) and 23 sera from patients with systemic type II infection for IgG antibody to GBS type II. Type II carriers were more likely to have antibody (greater than 2 micrograms/ml) than were those carrying other GBS types, whereas noncolonized patients were the least likely to have antibody. The overall prevalence of levels of antibody greater than 2 micrograms/ml was estimated to be approximately 6%, on the basis of assay results of the 401 maternal-cord pairs and adjusted for known-colonization status for the entire population of 8,928 deliveries that occurred during the study period. The majority of patients with infection had antibody levels less than 2 micrograms/ml. Five patients, however, had antibody present at levels ranging from 2.7 to 5.8 micrograms/ml. These findings suggest that "antibody deficiency" was widespread and was not by itself a useful determinant of risk for disease caused by GBS type II.

Antibodies, Bacterial↗