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Biomedical subjects

P J Edelson

Publications and source records attributed to P J Edelson.

At least 19 recordsLinked to original sources
PubMed1992

Type b capsule inhibits ingestion of Haemophilus influenzae by murine macrophages: studies with isogenic encapsulated and unencapsulated strains.

Phagocytosis may be important in clearing Haemophilus influenzae from the bloodstream. To define the effect of type b capsule on phagocytosis, binding and ingestion by macrophages was measured for 5 isogenic sets of capsule-sufficient strains (clinical isolates and type b transformants of capsule-deficient mutants) and capsule-deficient mutants (strains lacking a 9-kb EcoRI fragment of chromosomal DNA associated with type b capsule expression). Capsule-sufficient strains were not bound in the absence of serum, whereas capsule-deficient strains were bound and ingested (1.8-5.1 organisms/macrophage; 59%-97% ingested). In the presence of nonimmune serum, capsule-sufficient strains were largely bound but not ingested (4.7-7.2 organisms/macrophage; 7%-21% ingested), whereas capsule-deficient strains were nearly all ingested (6.2-10.5 organisms/macrophage; 93%-97% ingested). Strains resisting ingestion caused persistent bacteremia 24 h after intravenous challenge in mice and were more likely than readily ingested strains to cause persistent bacteremia or death in infant rats. Thus, type b capsule inhibits ingestion by macrophages; resistance to ingestion may be an important virulence determinant of type b organisms.

Agglutination Tests↗
PubMed1992

Multiple methicillin-resistant Staphylococcus aureus strains as a cause for a single outbreak of severe disease in hospitalized neonates.

Methicillin-resistant Staphylococcus aureus (MRSA) is an important cause of nosocomial infection. Outbreaks of infection caused by these pathogens are generally considered to be traceable to introduction of single strains into a hospital population. A large outbreak of bacteremic disease that recently occurred in our neonatal intensive care unit (11 episodes in 10 patients) involved 9 low birth weight infants and was associated with serious infection (4 episodes of meningitis). To determine the role of a single point source in this outbreak, isolates were characterized based on phenotypic and genotypic analyses. Phenotypic analysis included assessing hemolytic activity, phage typing, antimicrobial susceptibility testing and methicillin resistance population analysis. Genotypic analysis included assessment of plasmid profiles, dot-blot hybridization, restriction enzyme fragment pattern analysis and hybridization analysis of chromosomal DNA using a panel of staphylococcal gene probes. This analysis established that at least two distinct strains of MRSA were responsible for disease during this outbreak. This experience demonstrates the potential for MRSA to cause severe disease in the neonatal intensive care unit and indicates that the epidemiology of MRSA outbreaks is more complex than the spread of a single strain of bacteria.

Cross Infection↗
PubMed1991

Medical care of the HIV-infected child.

Familiarity with the demographics of pediatric HIV disease and recognition of common and uncommon presentations of infection are keys to diagnosing the HIV-infected child. Subsequent management entails preventative care, including immunizations and nutritional support, as well as management of HIV-related complications.

Child, Preschool↗
PubMed1991

Pneumocystis carinii infections in HIV-infected children.

Since 1981, 1200 children with acquired immunodeficiency syndrome have been reported to the Centers for Disease Control. Among these children, Pneumocystis carinii has been the leading cause of serious morbidity and mortality. This review discusses the epidemiology, diagnosis, and treatment of P. carinii.

Acquired Immunodeficiency Syndrome↗
PubMed1991

The role of C3 in mediating binding and ingestion of group B streptococcus serotype III by murine macrophages.

To understand how complement effects phagocytosis of type III group B streptococcus, we assessed the specific role of C3 in mediating binding and ingestion of these bacteria by macrophages. Phagocytosis of bacteria by resident mouse peritoneal macrophages was measured under conditions in which C3 deposition on bacteria was inhibited or after blockade of C3-ligands or of complement receptor type three (CR3) with specific antibodies. C3 depletion, incubation with F(ab')2 fragments of antibody to C3, or blockade of CR3 completely inhibited the binding of bacteria that was seen in the presence of nonimmune serum. Immune serum increased the number of associated organisms 6-fold compared to that seen with nonimmune serum. With this serum, 82% of organisms were ingested. C3 depletion or CR3 blockage had a modest effect, but this interaction could be ablated completely only after Fc receptors were blocked. Using varied concentrations of an IgG2a MAb against type III capsular antigen, it was possible to show that small amounts of antibody incapable of mediating bacterial binding by itself directed an interaction that also depended upon C3. Phagocytosis of group B streptococci by macrophages in the presence of little or no antibody requires complement and C3 opsonization specifically. C3-dependent binding may be important in determining mononuclear phagocyte-dependent clearance of these pathogens from blood, particularly in patients with little or no type-specific serum antibody.

Animals↗
PubMed1990

Role of complement in mouse macrophage binding of Haemophilus influenzae type b.

Previous in vivo studies demonstrated that clearance of encapsulated Haemophilus influenzae from blood is associated with the deposition of C3 on these bacteria and is independent of the later complement components (C5-C9). Since clearance of encapsulated bacteria is determined by phagocytosis of bacteria by fixed tissue macrophages, we studied the interaction of H. influenzae type b with macrophages in vitro. Organisms bound to macrophages in the presence of nonimmune serum. Binding was not evident in heat-treated serum or in serum from complement depleted animals and was inhibited by F(ab')2 fragments of antibody to C3 and by blockade of the macrophage complement receptor type 3. The majority of organisms bound in the presence of complement alone remained extracellular. Antibody in the form of convalescent serum or an IgG1 monoclonal to type b capsule did not increase the total number of organisms associated with macrophages, but did increase the number of organisms ingested. Furthermore, complement enhanced antibody-mediated ingestion. This in vitro study demonstrates that complement largely mediates binding of H. influenzae to macrophages. This binding may be critical in determining the early clearance of these bacteria from blood and may be an important mechanism of defense in the nonimmune, as well as the immune host.

Animals↗
PubMed1989

Resistance to serum bactericidal activity distinguishes Brazilian purpuric fever (BPF) case strains of Haemophilus influenzae biogroup aegyptius (H. aegyptius) from non-BPF strains. Brazilian Purpuric Fever Study Group.

We studied the ability of normal human serum to lyse H. influenzae biogroup aegyptius (H. aegyptius) isolates recovered from patients with Brazilian purpuric fever (BPF clone) or non-BPF clone strains. BPF clone isolates, although similar to non-BPF clone isolates with regard to the ability to fix C3 to their surfaces, could be distinguished from non-BPF clone strains by their resistance to lysis in vitro following incubation with normal adult human serum.

Blood Bactericidal Activity↗
PubMed1988

Complement-mediated early clearance of Haemophilus influenzae type b from blood is independent of serum lytic activity.

The role of complement-mediated serum lytic activity in the clearance of encapsulated Haemophilus influenzae type b was studied by comparing clearance of bacteria from blood in normal mice with that in congeneic C5-deficient animals and mice depleted of complement by using cobra-venom factor. The clearance of organisms from blood by C5-deficient and C5-sufficient normal animals was similar. C3 depletion and the inability to fix C3 to the surface of bacteria were, however, associated with impaired clearance of organisms during the first 24 h after intravenous bacterial challenge. These studies suggest that complement-mediated opsonization rather than bacteriolysis is important in determining early clearance of H. influenzae type b from the bloodstream.

Animals↗
PubMed1988

Anaerobic bacteremia in a neonatal intensive care unit: an eighteen-year experience.

A review of anaerobic bacteremia in the Neonatal Intensive Care Unit identified 29 episodes of clinically significant bacteremia occurring over the past 18 years. This experience suggested that certain clinical settings were associated with specific anaerobic infections. Although Gram-positive and Gram-negative anaerobes were isolated with similar frequency, 8 of 12 infants bacteremic within the first 48 hours of life were infected with Gram-positive, penicillin G-susceptible organisms whereas 11 of 17 infants older than 2 days were bacteremic with Gram-negative, penicillin G-resistant anaerobes. Eleven of 17 infants with anaerobic bacteremia associated with necrotizing enterocolitis were bacteremic with Gram-negative anaerobes. Five of 6 infants with anaerobic bacteremia associated with chorioamnionitis were bacteremic with Gram-positive anaerobes. These observations should be considered in making decisions regarding empiric therapy for the newborn at highest risk for anaerobic bacteremia.

Anti-Bacterial Agents↗
PubMed1988

Neonatal Staphylococcus epidermidis right-sided endocarditis: description of five catheterized infants.

Coagulase-negative staphylococci are important causes of bacteremia and focal infections in infants hospitalized in neonatal intensive care units. The medical records and echocardiograms of 58 newborns with persistent Staphylococcus epidermidis bacteremia who were hospitalized in the neonatal intensive care unit at The New York Hospital during the past 5 1/2 years were reviewed, and five infants were identified as having S epidermidis right-sided infective endocarditis. These episodes were associated with placement of umbilical venous catheters in the right atrium, slow resolution of bacteremia, and persistent thrombocytopenia. This experience suggests the role of endocardial trauma resulting from the placement of umbilical venous catheters in the pathogenesis of endocarditis. The increasing importance of coagulase-negative staphylococci as a cause of bacteremia in the newborn may explain the emergence of S epidermidis as an important cause of infective endocarditis in the neonatal intensive care unit. These cases underscore the potential severity of S epidermidis infection in the premature newborn.

Catheterization↗
PubMed1987

Leishmania promastigotes are recognized by the macrophage receptor for advanced glycosylation endproducts.

In this paper we demonstrate the involvement of the macrophage receptor for advanced glycosylation endproducts (AGE) in the phagocytosis of Leishmania major promastigotes. Blocking of this receptor with the ligand, AGE-BSA, leads to a 50% decrease in phagocytosis relative to controls, and a comparable decrease in the respiratory burst. The inhibition of phagocytosis by AGE-BSA was specific to leishmania. The binding of zymosan or C3bi-RBC and the phagocytosis of IgG-RBC or latex beads was not affected by the presence of AGE-BSA. Blocking of both the AGE receptor and CR3 decreases leishmania binding by nearly 90%, and reduces the respiratory burst by 80%, indicating that the two receptors account for the bulk of L. tropica promastigote recognition and uptake by the macrophage.

Animals↗
PubMed1985

The mouse macrophage receptor for C3bi (CR3) is a major mechanism in the phagocytosis of Leishmania promastigotes.

We examined the role of the macrophage receptor for C3bi, the CR3, in the phagocytosis of Leishmania major promastigotes and report that M1/70, a monoclonal antibody to the CR3, inhibited the binding of leishmania to macrophages both when the assays were performed in the presence of normal serum and in its absence. In serum, leishmania activate complement and fix C3. Fixation and subsequent cleavage to C3bi occurs rapidly, and by as early as 5 min both forms of the molecule can be identified on the parasites' surface. Complement fixation results in an enhanced phagocytosis of leishmania promastigotes by mouse macrophages. In the case of L. major, 63% of this serum-enhanced binding is inhibitable by M1/70. Binding assays were also performed in the absence of serum with the use of thoroughly washed promastigotes. The addition of M1/70 inhibited binding under these conditions by 54%. Two other rat monoclonal antibodies directed against different antigens on the macrophage plasma membrane did not inhibit binding. M1/70 did not inhibit the binding of promastigotes to rat bone marrow cells, nor did it inhibit IgG-SRBC binding to mouse peritoneal macrophages. These data indicate that the inhibition observed in the presence of M1/70 was specific for the CR3 and that the macrophage receptor for C3bi plays a major role in the phagocytosis of Leishmania major promastigotes, even in the absence of serum.

Animals↗