Pneumococcal immune adherence to human erythrocytes.

BACKGROUND: Human red blood cells bind various C3b-coated microorganisms via their C3b/CR1 receptor, a phenomenon referred to as immune adherence. The aim of the present study was to measure pneumococcal adherence to human red blood cells by flow cytometry and to study kinetic aspects of this binding. MATERIAL AND METHODS: We quantified pneumococcal adherence to human erythrocytes by FACS analysis and tested the involvement of antibodies and complement activation in this process. RESULTS: Pneumococci are able to bind to human red blood cells in the presence of human serum. Coating with C3b/C4b appeared obligatory for pneumococcal adherence to red blood cells. The ligand on erythrocytes was confirmed to be complement receptor 1. Kinetic studies showed that innate (mannose-binding lectin) and specific immune factors (IgG antibodies) contributed to the binding of C3b-coated pneumococci to human erythrocytes. After initial binding, serum-derived factor I was found to induce bacterial detachment from the erythrocyte. CONCLUSIONS: Pneumococci are able to adhere to red blood cells. Both the classical and lectin complement pathways are important for optimal C3b-coating of pneumococci for immune adherence. Bound pneumococci are detached from red blood cells by factor I. These findings are in line with the hypothesis of immune adherence in which human erythrocytes are able to bind pneumococci and target the bacteria to the reticulo-endothelial system in the spleen.

Complications of percutaneous endoscopic gastrostomy with or without concomitant antireflux surgery in 96 children.

BACKGROUND/PURPOSE: A study was conducted of the complications of percutaneous endoscopic gastrostomy (PEG) with or without antireflux surgery (ARS). METHODS: A retrospective review was conducted of all patients, receiving a PEG in the period January 1993 through December 1997. Patients' characteristics including underlying disease, indications, results of preoperative screening, and complications were recorded. PEG placement was performed with the Seldinger technique and, in some cases, under laparoscopic control. In the event of a pathologic pH study during preoperative screening, laparoscopic antireflux surgery (ARS) was added. RESULTS: Mean age was 5 years and 10 months. The majority of the children were mentally retarded. The main indications for PEG were vomiting, food refusal, inability to swallow, and aspiration. Fifty-nine patients had PEG without ARS. Nineteen of these patients had concomitant laparoscopy. Thirty-seven patients had PEG with ARS. One patient died postoperatively of gastric leakage. PEG-related complications occurred in 31% of the patients. There was a significant higher incidence of complications in the group of patients that underwent ARS together with PEG compared with PEG placement without ARS. Roughly half of the complications were peristomal infection related to the use of T-fasteners and the other half gastroduodenal obstruction caused by the balloon of the gastrostomy catheter, both preventable complications. Preoperative vomiting without a positive pH-study disappeared in most cases after PEG placement. Although the pH study normalized in 34 of 37 patients after concomitant ARS, vomiting persisted in 7 of 17 patients. PEG improved the nutritional status in 75% of the children. CONCLUSIONS: PEG improved the nutritional status in the majority of the children. However, PEG placement can lead to a considerable amount of complications, especially when combined with ARS. ARS together with PEG is successful in treating GER but does not necessarily cure preexistent vomiting. PEG alone cures vomiting in 80% of the patients and rarely leads to vomiting. There seems no good reason for combining PEG with ARS. Only if symptoms progress after PEG, ARS should be considered. Caretakers and patients should be well informed before placement.

Respiratory viral infection predisposing for bacterial disease: a concise review.

Although bacterial superinfection in viral respiratory disease is a clinically well documented phenomenon, the pathogenic mechanisms are still poorly understood. Recent studies have revealed some of the mechanisms involved. Physical damage to respiratory cells as a result of viral infection may lead to opportunistic adherence of bacteria. Enhanced bacterial adherence by specific mechanisms has been documented for respiratory cells infected with influenza A virus, respiratory syncytial virus and adenovirus in both in vitro and in vivo models. To date, results of various experimental studies indicate that different mechanisms for increased bacterial adherence induced by viruses are operating for specific viral-bacterial combinations. In the present review, a number of key findings obtained during the past two decades is presented and discussed.