Solitary hepatic abscess: a delayed complication of neonatal bacteremia.
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Ampicillin↗
Biomedical subjects
C J Baker
Publications and source records attributed to C J Baker.
Type III group B Streptococcus: functional interaction with IgG subclass antibodies.
The functionally active IgG subclasses and the portion of the antibody molecule mediating opsonophagocytosis of type III, group B Streptococcus (III-GBS) have not previously been investigated. Serum from a healthy adult immunized with III-GBS vaccine was subjected to ion exchange chromatography, yielding 2,950 mg of IgG/dl and 1,440 micrograms of III-GBS-specific antibody/ml. Papain digestion for selective cleavage of IgG1 and IgG3 yielded an IgG2-rich pool that contained 31% of the initial IgG but 69% of the antibody to III-GBS. This pool retained opsonophagocytic activity of antibody to III-GBS at levels similar to that for the initial IgG pool. Analysis of F(ab')2 fragments of pepsin-digested IgG revealed that the level of alternative pathway-mediated opsonophagocytosis of III-GBS was similar to that mediating functional activity in the initial IgG preparation. Therefore, IgG2 is an active opsonin for III-GBS, but divalency appears to be required for alternative pathway-mediated opsonophagocytosis.
Antibodies, Bacterial↗
Unusual occurrence of an epidemic of type Ib/c group B streptococcal sepsis in a neonatal intensive care unit.
An epidemic of late-onset sepsis due to type Ib/c group B Streptococcus (Ib/c-GBS) occurred in a neonatal intensive care unit (NICU). During a seven-week period, five very low birth weight infants (index cases [ICs]) more than four weeks of age became bacteremic. Bacteriologic surveillance of neonates revealed persistent colonization in three ICs and identified three asymptomatic carriers (ACs). All ICs and one AC acquired Ib/c-GBS nosocomially, whereas the other two ACs were colonized at birth. Among nursery personnel, 39% carried GBS, but only two harbored Ib/c-GBS. Although phage typing of Ib/c-GBS isolates identified two patterns of susceptibility, we believe a single strain was involved in the epidemic, because the patterns overlapped and most isolates carried the same lysogenic phage. Analysis of events suggested infant-to-infant spread via the hands of personnel, but acquisition from the colonized staff was also possible. The control measures instituted prevented further spread of Ib/c-GBS in the NICU.
Anti-Bacterial Agents↗
Interaction of soluble fibronectin with group B streptococci.
Fibronectin binds to a variety of bacterial species, and we hypothesized that differential fibronectin binding might influence the invasive potential of group B streptococci (GBS). Human plasma fibronectin purified by a standard two-step chromatographic procedure was radiolabeled with 3H. Fifty GBS strains (invasive, colonizing, or bovine) representing serotypes Ia (10 strains), Ib (6 strains), Ia/c (6 strains), II (10 strains), III (11 strains), IV (1 strain), and nontypable (6 strains) were tested. No source or serotype variability was detected among GBS strains, and binding was uniformly less than 1.5% of available fibronectin. Lack of detectable binding occurred at both the log and stationary growth phases and persisted despite treatment with trypsin or neuraminidase or opsonization with immunoglobulin G containing high levels (greater than 40 micrograms/ml) of antibody specific for the Ia, II, or III GBS capsular polysaccharides. Incubation with GBS did not inhibit fibronectin binding to the Cowan 1 strain of Staphylococcus aureus. Strain COH 31-15, an isogenic, type III, capsule-deficient mutant of COH 31r/s, also failed to bind fibronectin. In contrast to other streptococci, GBS do not have readily detectable receptors for soluble fibronectin as part of their surface structures. If present, binding sites for soluble fibronectin are deep to surface structures, obscured from host defense systems, or require the presence of other factors to facilitate their recognition of fibronectin. The uniform ability of GBS to resist binding to soluble fibronectin could be a significant virulence factor in the pathogenesis of invasive infections of infants.
Chromatography, Affinity↗
A mouse model of chronic pulmonary infection with Pseudomonas aeruginosa and Pseudomonas cepacia.
A mouse model of chronic pulmonary infection with either Pseudomonas aeruginosa or Pseudomonas cepacia was developed to compare bacteriologic and pathologic features of these infections. Experimental pneumonia was established in Swiss mice by transoral intratracheal inoculation of 10(3)-10(4) colony-forming units of mucoid P. aeruginosa or P. cepacia enmeshed in agarose beads. Unilateral infection with either strain was tolerated without morbidity. By 10 days postinoculation, the mean colony-forming units per infected lung was 3.8 X 10(5) for P. aeruginosa and 1.0 X 10(5) for P. cepacia. Bacterial counts remained stable through 21 days with no significant difference between organisms. Acute and chronic inflammatory histopathologic changes similar to many found in the lungs of cystic fibrosis patients were present in 95% of lung specimens. The changes occurred with both organisms but were more extensive with mucoid P. aeruginosa. This model represents an important tool for study of the contribution of complement, antibody, and adoptive transfer of T cell-mediated immunity to the pathogenesis of chronic pneumonia with Pseudomonas species, and represents the first successful model of chronic pulmonary infection with P. cepacia.
Animals↗
Group B streptococcal infection in newborns: prevention at last?
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Ampicillin↗
The role of complement and antibody in opsonophagocytosis of type II group B streptococci.
The role of complement and antibody in the opsonophagocytosis of type II group B streptococci (type II GBS) was defined with sera from healthy adults and two populations with theoretical susceptibility to type II GBS infection--neonates and insulin-dependent diabetics. Significant opsonophagocytosis (bactericidal index, greater than or equal to 90%) of five clinical isolates of type II GBS lacking components of protein antigen c was demonstrated by each of 12 adult sera, as well as by agammaglobulinemic serum, a result indicating that opsonophagocytosis can proceed by antibody-independent activation of the classic complement pathway. Strains containing components of protein antigen c were somewhat more resistant to opsonin-binding activity. Four of 10 neonatal sera and nine of 15 diabetic sera exhibited inefficient opsonophagocytosis. Some of the adult sera with either high or low concentrations of specific antibody to type II GBS promoted opsonophagocytosis via the alternative complement pathway, but this response was not observed with neonatal sera. The addition of sufficient amounts of specific antibody to type II GBS to neonatal and adult diabetic sera in vitro, however, promoted efficient opsonophagocytosis via the alternative pathway.
Adult↗
Transient Activation of Plasmalemma K Efflux and H Influx in Tobacco by a Pectate Lyase Isozyme from Erwinia chrysanthemi.
A purified pectate lyase isozyme derived from Erwinia chrysanthemi induced rapid net K(+) efflux and H(+) influx in suspension-cultured tobacco cells. Comparable fluxes of other ions (Na(+), Cl(-)) were not observed. The K(+) efflux/H(+) influx response began within 15 minutes after addition of enzyme to cell suspensions and continued for approximately 1 hour after which cells resumed the net H(+) efflux exhibited prior to enzyme treatment. The response was not prolonged by a second enzyme dose 1 hour after the first. The K(+)/H(+) response was characterized by saturation at low enzymic activity (2 x 10(-3) units per milliliter), and inhibition by the protonophore, carbonyl cyanide m-chlorophenylhydrazone, and was not associated with membrane leakiness caused by structural cell wall damage. The total K(+) loss and H(+) uptake induced by enzyme was one-fourth to one-third that induced by Pseudomonas syringae pv. pisi and did not reduce cell viability. These results indicate that pectate lyase induces a K(+) efflux/H(+) influx response in tobacco similar to but of shorter duration than that induced by P. syringae pv. pisi during the hypersensitive response. Pectate lyase or other cell wall degrading enzymes may therefore influence the induction of hypersensitivity.
Journal Article↗
Long-term sequelae of group B streptococcal meningitis in infants.
The long-term outcome and admission features predictive of outcome were determined for 61 patients with group B streptococcal meningitis treated between 1974 and 1979. Infection was rapidly fatal in 13 patients (21%). Among the 48 survivors, 38 (79%) 3 years of age or older were available for comprehensive evaluation. Excluding five who had died before age 3 years, the mean age at evaluation was 6.0 years (range 3.3 to 9.0 years). Among survivors, 11 (29%) had severe neurologic sequelae, eight (21%) had mild to moderate deficits, and 19 (50%) were functioning normally. Analysis of predictive features revealed a significant risk of death or severe impairment among infants who at hospital admission were comatose or semicomatose, had decreased perfusion, total peripheral WBC less than 5,000/mm3, absolute neutrophil count less than 1000/mm3, and CSF protein greater than 300 mg/dl (P less than or equal to 0.05). These data indicate that, although mortality from group B streptococcal meningitis has declined, approximately half of the survivors of acute infection have some degree of morbidity when evaluated at ages permitting the detection of language delay and borderline or mild mental retardation.
Cognition Disorders↗
Immune globulin for intravenous use: enhancement of in vitro opsonophagocytic activity of neonatal serum.
Neonates born with less-than-protective levels of transplacentally derived specific antibody are at risk for the development of disease due to type III, group B Streptococcus (III-GBS). The effect of immune serum globulin modified for intravenous use (MISG) on in vitro opsonophagocytosis of III-GBS was evaluated. Cord blood was obtained from 13 healthy, full-term neonates, and bactericidal activity for III-GBS was measured. Before the addition of MISG, one of three serum specimens with moderate levels of antibody to III-GBS, and eight of 10 specimens with low antibody levels demonstrated no bactericidal activity. The mean bactericidal index increased from 27.1% before the addition of MISG to 96.5% with MISG added in a volume equal to that of serum. The effect of MISG on opsonophagocytosis decreased with its dilution in buffer, and no effect was shown at dilutions greater than or equal to 1:4. Thus, MISG can substantially increase in vitro opsonophagocytosis of III-GBS in sera from newborns.
Antibodies, Bacterial↗
Single-dose pharmacokinetics of imipenem-cilastatin in neonates.
The single-dose pharmacokinetics of imipenem (N-formimidoyl thienamycin), a beta-lactam antibiotic, used in combination with cilastatin, a renal dehydropeptidase I inhibitor, were evaluated in 10 neonates 1 to 8 days of age. The imipenem-cilastatin combination was given intravenously over a 15-min period at a dose of 15 or 25 mg/kg. Drug concentrations in serum, urine, and cerebrospinal fluid (when available) were determined by high-pressure liquid chromatography, and plasma disposition of the drugs was described by a two-compartment open model. The mean peak plasma levels of imipenem 30 min postinfusion were 55.4 and 27.2 micrograms/ml, and the mean t1/2 beta values were 2.1 and 1.8 h at doses of 25 and 15 mg/kg, respectively. The calculated volume of distribution was 0.41 liters/kg. In two patients from whom cerebrospinal fluid was obtained 1.5 h postinfusion, imipenem levels were 5.6 and 1.1 micrograms/ml at doses of 25 and 15 mg/kg, respectively, representing 10 and 4% of the 1-h serum levels. No side effects attributable to a single dose of imipenem-cilastatin were noted.
Chromatography, High Pressure Liquid↗
Cell structure and antigenic composition of GBS.
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Animals↗
The role of complement in opsonization of GBS.
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Adult↗
Vaccination as a measure for prevention of neonatal GBS infection.
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Adult↗
Moxalactam therapy for neonatal meningitis due to gram-negative enteric bacilli. A prospective controlled evaluation.
Moxalactam and ampicillin sodium therapy were compared with amikacin sulfate and ampicillin therapy for meningitis due to gram-negative enteric bacilli in 63 infants enrolled in the Third Neonatal Meningitis Cooperative Study. The population characteristics and causative organisms were comparable for the two treatment groups. Cultures of CSF were positive for approximately three days in both study groups. Case-fatality rates were 23% and 15% for moxalactam-treated infants and ampicillin- and amikacin-treated infants, respectively. Developmental or neurological abnormalities were found in about 40% of survivors, and the rates were comparable for both treatment groups. Computed tomograms in 44 infants were interpreted as normal in 13 (30%); hydrocephalus, abscesses, and low-density areas were the most frequent abnormalities. We conclude that moxalactam is a suitable alternative for treatment of meningitis due to gram-negative enteric bacilli.
Amikacin↗
Characterization of freeze-thaw induced ultrastructural damage to endothelial cells in vitro.
The pathophysiology of endothelial cells is important to a variety of vascular conditions including coagulation and hemostasis resulting from clinical frostbite. Use of an in vitro model system demonstrated that when bovine endothelial cells were frozen at 1 degrees C or 20 degrees C/min and thawed immediately (20 degrees C/min), a variety of ultrastructural alterations occurred. Membranous structures were most extensively damaged, with mitochondria the most sensitive organelle. Low amplitude mitochondrial swelling, first evident at 0 degrees C, progressed to high amplitude swelling by -10 degrees C (frozen). In addition, the rough endoplasmic reticulum was dilated and formed large vesicles with a homogeneous matrix. Nuclear changes first occurred at -15 degrees C. These included separation and distortion of the nuclear membrane, changes in chromatin distribution, and disruption of the nucleolus. Scanning electron microscopy revealed perforated plasma membranes in some cells at -10 degrees C (frozen) and in most cells by -20 degrees C. Cultures frozen at 20 degrees C/min revealed mostly the same ultrastructural damage noted at 1 degrees C/min except a higher percentage of cells exhibited alterations. Data from the recovery index and lactic dehydrogenase (LDH) release correlated well with observed ultrastructural changes. Early swelling of mitochondria and dilation of rough endoplasmic reticulum was not lethal in the absence of freezing. Increased swelling in cytoplasmic organelles coupled with nuclear alterations at -15 degrees C resulted in a decreased survival rate and release of significant quantities of LDH by -20 degrees C. No unique morphological changes were temperature specific, but the total number of cells that displayed alterations increased as temperature decreased.
Animals↗
Potentiation of virulence by group B streptococcal polysaccharides.
The ability of group B streptococcal (GBS) capsular polysaccharides to potentiate virulence was examined. Incubation of soluble type Ia or III polysaccharide in hypogammaglobulinemic human serum inhibited classical complement-dependent opsonophagocytic killing of type Ia strain 515. When functional complement components were measured, C1 activity increased in sera with added polysaccharide whereas C4 activity decreased 80%-90%. Incubation of purified C1 with type Ia polysaccharide inhibited lysis of EAC4 cells in a C1 transfer assay. In a mouse lethality model, tail-vein injection of 50 micrograms of type Ia or III polysaccharide decreased the 50% lethal dose (LD50) from 3.2 X 10(6) to 2.2 X 10(5). Total hemolytic complement levels in mice immediately after polysaccharide injection were increased over levels in control mice, but this difference was not seen 30 min later. The LD50 in mice depleted of C3 (with cobra venom factor) was 6 X 10(5) and simultaneous injection of polysaccharide did not further lower the LD50.
Animals↗
Immune response of infants and children to disseminated infections with Neisseria meningitidis.
Acute- and convalescent-phase sera from 34 children and 10 young adults were studied to determine if, at what age, and to which antigens of Neisseria meningitidis they respond during disseminated disease. Seven children older than two years of age who were infected with group C or Y strains developed significant increases in both binding and bactericidal antibody. Children infected with group B strains infrequently (eight [31%] of 26) had measurable increases in serum antibody to this capsular polysaccharide; response was meager when it did occur, was unrelated to age, and was considerably poorer than that of young adults, of whom 80% responded. Convalescent-phase sera from all children contained bactericidal antibody. Binding capacity for group B polysaccharide accounted for only 35% of the bactericidal activity in convalescent-phase sera of children infected with group B strains. Bactericidal antibody in the sera of children who did not respond to capsular polysaccharides was often to a lipooligosaccharide antigen.
Adult↗