Search PubMed⌕ Search

Biomedical subjects

C J Baker

Publications and source records attributed to C J Baker.

At least 199 records · Page 11Linked to original sources

Serological survey: immunity to vaccine preventable diseases among detainees at a Juvenile Hall facility.

Sera from 378 juveniles interned in a juvenile hall facility between February and March, 1978, were tested for antibody to polio viruses types 1, 2, and 3; diphtheria; tetanus; measles; and rubella. Only 57% of juveniles ages 11-18 years had neutralizing antibody greater than or equal to 1:8 to all three types of polio viruses. Juveniles most often lacked antibody to polio type 3. Over 92% of juveniles tested had a protective level of antitoxin (greater than or equal to .01 U/ml) to diphtheria and tetanus. Hemagglutination inhibition (HAI) antibody tests performed for measles and rubella revealed 87.5% and 81% with titers greater than or equal to 1:8 respectively. No major differences in immune status were found between those with a previously documented vaccination history and those without. Based on these data a uniform immunization policy was adopted for Los Angeles County's Juvenile Hall facilities.

Adolescent↗

Antibody-independent activation of C1 by type Ia group B streptococci.

A prototype fresh clinical isolate of type Ia group B streptococci (strain 515) can be opsonized by serum containing low levels of antibody. This opsonizing process can also occur in hypogammaglobulinemic serum, confirming its antibody independence, but it does require Ca++ ions and the second component of complement (C2). When formalin-fixed organisms are reacted with whole serum, C4 and C3 are cleaved. These data are strong evidence that this organism can directly activate C1 in the absence of antibody and that this activation leads to the formation of a classical C3 convertase (C4b2a), which cleaves C3. The observation that opsonization can occur in hypogammaglobulinemic serum suggests that complement alone, presumably the fixation of C3b, is sufficient for phagocytes to ingest this pathogen.

Complement Activation↗

Evaluation of Streptococcus pneumoniae type XIV opsonins by phagocytosis-associated chemiluminescence and a bactericidal assay.

The relative roles of serum factors required for opsonization of type XIV Streptococcus pneumoniae were investigated by means of luminol-enhanced chemiluminescence (CL), bactericidal, and immunofluorescence assays employing adult sera containing high (>1,000 ng of antibody nitrogen per ml) or low (<200 ng of antibody nitrogen per ml) antibody concentrations as determined by radioimmunoassay. Specific antibody concentration correlated directly with both total and heat-labile CL activity (P < 0.005) and with the bactericidal index (P < 0.05) at a serum concentration of 10%. The importance of specific antibody as an opsonin was confirmed by the abolition of CL activity and immunoglobulin immunofluorescence observed after absorption of heated sera with type XIV pneumococcal cells and by the dose response in CL and bactericidal activity observed with the addition of immunoglobulin G to hypogammaglobulinemic serum. A role for the classical complement pathway in opsonization was indicated by significantly greater CL integrals for high-antibody sera than for low-antibody sera depleted of factor D and by the bactericidal activity noted for untreated, but not magnesium ethylene glycol-bis(beta-aminoethyl ether)-N,N-tetraacetic acid-chelated low-antibody sera. The alternative pathway contributed more than half of the CL activity of both high- and low-antibody sera. However, after magnesium ethylene glycol-bis(beta-aminoethyl ether)-N,N-tetraacetic acid chelation, only sera with high antibody concentrations or agammaglobulinemic serum reconstituted with immunoglobulin G with high specific antibody levels supported significant bactericidal activity. Therefore, type-specific antibody and complement promote opsonization of type XIV S. pneumoniae, and this may occur via either complement pathway. These results suggest that CL is a suitable tool to delineate serum factors and their contribution to opsonization, but results must be related to other functional assays.

Antibodies, Bacterial↗

Enzyme-linked immunosorbent assay for measurement of antibody to type III group B streptococci.

Neonates at risk for fulminant type III, group B streptococcal (III GBS) infection are those who lack antibody to the capsular polysaccharide. A newly developed enzyme-linked immunosorbent assay (ELISA) was compared with a standard radioactive antigen-binding assay (RABA) for quantitation of III GBS antibody in human sera. Although there was a significant correlation between the ELISA and RABA (r = 0.81; P less than 0.001) in general, the ELISA detected antibody both to core and native antigens of III GBS, whereas the RABA detected antibody to native polysaccharide exclusively. The results of the two assays were discordant when sera which had only high native or core antibody (not both) were assessed. Although the ELISA was reproducible and required less than 1 microliter of serum, interpretation of data obtained by the assay should be viewed with caution since only antibody to native III GBS has been correlated with human immunity.

Adult↗

Antibody-independent classical pathway-mediated opsonophagocytosis of type Ia, group B streptococcus.

The opsonophagocytic requirements of human sera containing endogenous complement for a variety of type Ia, and group B streptococcal strains were defined. Significant reduction (>==90%) in colony-forming units was noted after a 40-min incubation for the highly encapsulated, mouse-passed prototype strain 090 by sera containing moderate to high concentrations of antibody to type Ia polysaccharide (mean, 16.5 mug/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 mug/ml). This absolute requirement for a critical amount of specific antibody in promoting opsonophagocytic killing of strain 090 was not found when 18 fresh clinical type Ia isolates were tested. In antibody-deficient and agammaglobulinemic sera, respectively, mean reductions in colony-forming units of 94 and 95% were seen for fresh clinical isolates, whereas strain 090 was not killed by polymorphonuclear leukocytes in the presence of these sera. All strains required a considerable amount of specific antibody for alternative pathway-mediated opsonophagocytosis. That opsonophagocytic killing of clinical type Ia isolates was mediated by the classical pathway in a nonantibody-dependent fashion was shown when MgEGTA chelation of agammaglobulinemic serum or use of serum deficient in C2 resulted in bacterial growth. The addition of C2 to C2-deficient serum restored bactericidal activity of this serum. These experiments indicate that substances other than the exposed surface of the type Ia capsular polysaccharide initiate classical pathway-mediated opsonophagocytosis of clinical isolates of type Ia, group B streptococci by human sera in the absence of immunoglobulin. Perhaps, a deficiency in classical complement pathway function is critical to the susceptibility of neonates to type Ia, group B streptococcal disease.

Animals↗

Subdural empyema: an unusual complication of meningococcal meningitis.

Subdural empyema rarely is associated with bacterial meningitis in infants, particularly when the etiologic agent is Neisseria meningitidis. We have described a 3-month-old infant in whom relapse of meningitis due to Meningococcus group C was accompanied by a right-sided subdural empyema. Full recovery followed appropriate antimicrobial therapy and closed drainage.

Brain Abscess↗

Nosocomial septicemia and meningitis in neonates.

The past decade brought with it both highly sophisticated neonatal intensive care with improved perinatal mortality rates, and increased risk for nosocomial septicemia and meningitis among survivors. Although most of these infections were caused by multiple antibiotic-resistant gram negative enteric bacteria, Staphylococcus aureus "outbreaks" appeared sporadically. Risk for nosocomial infection was related primarily to factors which enhance infant contact with these bacteria (crowding and high nurse to infant ratios, poor handwashing practices, contaminated life support equipment, antibiotic exposure and prolonged hospitalization) in combination with those poorly defined determinants of bacterial virulence and host defense. Control measures for the prevention or reduction of these infections are aimed at decreasing the neonate's contact with the "outbreak" strains--improvement in handwashing practices and equipment sterilization processes, cohorting of infants, establishment of appropriate nurse:infant ratios, and in certain instances, modification of antibiotic practices. Future efforts should be directed toward better definition of bacterial virulence, host susceptibility and preventive measures.

Bacterial Infections↗

Complications and sequelae of meningococcal infections in children.

Eight-six children with meningococcal meningitis or bacteremia were evaluated prospectively between 1977 and 1979 to determine the incidence of complications and features predictive of their development. The majority (83%) of these infections were caused by serogroup B strains. Twenty-seven percent of survivors experienced one or more suppurative, allergic, or neurologic complications. Hearing loss, noted in 9% of children, occurred significantly more often in patients with admission leukocytosis or leukopenia, or with CSF leukocytosis greater than 10,000/mm3 than in those with an uncomplicated course (P less than 0.01). Ten percent of survivors developed allergic complications manifested as cutaneous vasculitis or arthritis with onset five to eight days after admission. Shock, purpuric skin lesions, and fever persisting longer than five days occurred significantly more often in these children than in those who developed hearing loss or those with an uncomplicated course (P less than 0.05). Resolution of allergic complications occurred within 14 days of their onset. Compared to Neisseria meningitidis groups A and C, group B strains appear to be intermediate in their potential for allergic complications associated with childhood infection.

Adolescent↗

Non-group D alpha-hemolytic streptococci: new neonatal pathogens.

Review of the bacteriologic records of a large city-county hospital from 1970 through 1980 has indicated a substantial increase in the frequency of isolation of non-group D alpha-hemolytic streptococci from blood and cerebrospinal fluid of neonates since 1978. These organisms accounted for 23% of all cases of neonatal septicemia and meningitis in 1980, and as a group were exceeded only by group B streptococci (28%) in prevalence. Most neonates (91.2%) had early-onset infection (mean age = 1.4 days); approximately one-third were premature (less than 36 weeks' gestation). Maternal obstetrical complications were common. Nearly 80% of the infants had signs or symptoms suggesting bacterial sepsis. Findings such as concomitant meningitis, shock, chest roentgenogram abnormalities, leukopenia, abnormal numbers of immature neutrophils, and death were infrequent when compared to those accompanying other invasive neonatal bacterial infections, suggesting that non-group D alpha-hemolytic streptococci may be less virulent for the neonate or that neonatal host defense mechanisms are more effective in containing the infection. Careful surveillance for these potential neonatal pathogens seems warranted.

Humans↗

Single oral-dose metronidazole therapy for trichomonas vaginitis in adolescents.

A group of 218 adolescent girls in a detention setting was treated for vaginal trichomoniasis with a single 2-g oral dose of metronidazole, a successful therapeutic approach in infected adults. This method of treatment has not been reported in teenagers. The initial diagnosis and posttreatment test for cure were based on a Gram stain of vaginal secretions. Administration of the medication and avoidance of reinfection were controlled. The test for cure was done 5 days after treatment. The cure rate under these conditions was 98%. Side effects were infrequent and minor. Our results suggest that single-dose therapy not only avoids the problem of patient compliance but is effective, safe, and less costly than a standard 7- or 10- day regimen.

Administration, Oral↗

Antagonism of ampicillin and chloramphenicol for meningeal isolates of group B streptococci.

The increasing prevalence of ampicillin-resistant Haemophilus influenzae type b has led to the recommendation that ampicillin and chloramphenicol be given as the initial therapy for suspected bacterial meningitis in infants and children. However, during the first 2 months of life, H. influenzae type b is a rare cause of meningitis, whereas group B streptococcus is the most frequently isolated agent. Since ampicillin and chloramphenicol have been shown to be antagonistic for other streptococci, an in vitro study of their effect on group B streptococci was performed. The effect of ampicillin and chloramphenicol, alone and in combination, on 18 meningeal isolates was determined for 2 different inocula of group B streptococci, using microtiter broth dilution and growth kinetic assays. Isoboles, fractional lethal concentration indices, or both indicated antagonism for all strains. Growth kinetic assays for two representative strains demonstrated inhibition of the early bactericidal activity of ampicillin by chloramphenicol. These findings of in vitro antagonism suggest that this combination may be contraindicated for the treatment of infants with group B streptococcal meningitis.

Ampicillin↗