Intravenous immune globulin: a cautionary note.
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Candidiasis↗
Biomedical subjects
A S Cross
Publications and source records attributed to A S Cross.
The importance of the K1 capsule in invasive infections caused by Escherichia coli.
We examined 534 clinical isolates of Escherichia coli for sensitivity to rough lipopolysaccharide-specific and K1-specific phages. Twenty-eight percent of bacteremic isolates were sensitive to rough-specific phages. Forty-two percent of these strains, against only 20% of bacteremic isolates insensitive to rough-specific phages, had K1 capsule (P less than 0.001). K1-positive strains were usually resistant to phagocytic killing, whereas strains lacking the K1 capsule were more likely to be killed regardless of capsular type. Eighty-two percent of strains were typable with O-specific, 57% with K-specific, and 74% with H-specific antisera. Sixty percent of E coli were agglutinated by only 10 O-specific antisera. K1 was the most common capsular type, followed by K5, K2, and K12, whereas four H antigens accounted for nearly half of the H-typable strains. We conclude that (1) the combination of rough-specific and K1-specific phage sensitivity defines functionally similar groups of bacteria and (2) a polyvalent vaccine against invasive E coli is possible given the relatively limited number of invasive O:K:H serotypes.
Adolescent↗
Human neutrophils increase expression of C3bi as well as C3b receptors upon activation.
We used monoclonal antibodies and flow cytometry to study the expression of the receptors for the complement fragments C3bi (CR3) and C3b (CR1) on human polymorphonuclear neutrophil leukocytes (PMN). Expression of both receptors was minimal on cells stained in anticoagulated whole blood incubated at 0 degree or 37 degrees C. PMN isolated with Percoll density gradients and held at 0 degree C also had only minimal expression of both receptors. With the isolated cells, however, a spontaneous increase in expression of both receptors occurred upon warming to 37 degrees C. This did not represent complete expression of either receptor since additional increments in surface expression could be induced upon stimulation with N-formyl-methionyl-leucyl-phenylalanine or Raji cell supernatant. The increases in complement receptor (CR) expression appeared to be specific since there were no changes in expression of the Fc gamma receptor or beta-2-microglobulin under any of these conditions. The increased CR expression seems to involve translocation from an intracellular pool since it is complete within minutes and is not blocked by puromycin or cycloheximide. These results demonstrate that both CR3 and CR1 expression increase rapidly upon activation of PMN and that isolated cells can be used to study this phenomenon, which may be a critical part of neutrophil function in vivo.
Antibodies, Monoclonal↗
Monoclonal antibody 2-2-B kills K1-positive Escherichia coli in conjunction with cord blood neutrophils and sera, but not with spinal fluid.
In conjunction with 400 ng/ml murine monoclonal antibody of the IgM class, cord neutrophils were able to kill K1-positive Escherichia coli in an in vitro opsonophagocytic assay. Neither adult nor cord neutrophils mediated bacterial killing in the absence of this monoclonal antibody. This bactericidal capacity was observed with eight of 11 (73%) but not all cord neutrophil samples, and under conditions of bacteria to neutrophil ratios as high as 15:1. Increasing the monoclonal antibody concentration up to 12 micrograms/ml paradoxically resulted in significantly lower amounts of bacterial killing. All 11 cord serum samples had sufficient complement activity to permit this monoclonal antibody to function; however, neonatal cerebrospinal fluid was not an effective complement source. We conclude that this monoclonal antibody may be a useful adjunct to conventional therapy of invasive disease caused by K1-positive E. coli; but it would have to work at the bacteremic phase of infection.
Adult↗
Lymphoblastoid cell supernatants increase expression of C3b receptors on human polymorphonuclear leucocytes: direct binding studies with 125I-C3b.
Human PMN incubated in culture supernatants of the Raji long-term human lymphoblastoid cell line showed increased rosette formation with sheep erythrocytes coated with C3b (EIgM C4b3b) but no change in rosette formation with IgG-coated erythrocytes. This suggested a specific increase in cell surface C3b receptors, which was further investigated using 125I-C3b for direct binding studies. The results confirmed that specific binding of 125I-C3b to PMN incubated in culture supernatants increased up to three- to four-fold over binding to PMN incubated in control media alone. Scatchard analysis revealed that the apparent Ka for supernatant-treated cells, 3.36 +/- 0.89 X 10(7) L/M did not differ from the Ka for cells incubated in control media, 3.76 +/- 0.75 X 10(7) L/M, suggesting an increase in a single class of C3b receptors. Kinetic studies revealed that the active factor was present within 24 hr of culture of the Raji cells, and that neutrophils incubated in culture supernatants increased their C3b receptors continuously for up to 4 hr, the longest interval tested. The effect of the culture supernatant was lost with dilution beyond eight- to 10-fold. The results suggest that culture supernatants of this long-term lymphoblastoid cell line contain soluble factors that induce increased expression of C3b receptors on PMN and may thus serve as a model for study of important physiologic effects of lymphocyte products on PMN in vivo.
Cell Line↗
A hospital-wide outbreak of septicemia due to a few strains of Staphylococcus aureus.
During a 6-month period at Walter Reed Army Hospital the monthly attack rate of Staphylococcus aureus bacteremia increased to 3.8 +/- 0.5 (mean +/- SEM) from 2.5 +/- 0.2 cases per 1,000 dispositions for the previous 48 months (P less than 0.05). A predominant phage pattern, designated S, was found in 12 (39%) of 31 bacteremic isolates typed and another strain, delta, was associated with four catheter-related infections. Two other strains also accounted for infections. Patients with isolates of the S phage pattern had a higher mortality (59%) than patients with non-S isolates (37%). Thirty-eight per cent of S. aureus carriers among hospital personnel harbored S or delta strains. Limitation of intravascular devices, strict handwashing, and the use of gloves were associated with a significant decrease in the incidence of S. aureus bacteremia to 1.9 +/- 0.5/1,000 dispositions over the next 6 months (P less than 0.05). S and delta strains were reduced to 20% of these isolates despite their persistence in 32% of staphylococcal carriers upon reculture of personnel. We conclude that S. aureus persists as an important pathogen in the hospitals, and that phage typing S. aureus isolates remains an important tool in hospital epidemiology. The presence of multiple S. aureus strains causing this outbreak and the extent of their dissemination among patients and personnel reported here emphasizes the need to reevaluate strategies of nosocomial staphylococcal control.
Clothing↗
Evaluation of immunotherapeutic approaches for the potential treatment of infections caused by K1-positive Escherichia coli.
Levels of antibody to the K1 polysaccharide capsule were examined in sera from patients naturally infected with K1-positive Escherichia coli, in sera from volunteers vaccinated with a group B meningococcal vaccine, in immune globulin prepared for intravenous use, and in a preparation of murine IgM monoclonal antibody to group B meningococci. In a phagocytic assay, the monoclonal antibody in mouse ascites fluid killed K1-positive E. coli to a final dilution of 1:250,000 (48 ng of antibody protein/ml); no killing was observed with any of the other antibody sources. This monoclonal antibody, which required human complement and exhibited a prozone when high concentrations of antibody (greater than 6 micrograms/ml) were used, killed all K1-positive strains but none of the K1-negative strains of E. coli tested. Levels of K1-binding antibody in the sera of vaccinated volunteers exceeded antibody levels resulting from natural infection or present in commercially prepared immunoglobulin and were less than those obtained in mouse ascites fluid containing the monoclonal antibody.
Antibodies, Bacterial↗
Progressive increase in antibiotic resistance of gram-negative bacterial isolates. Walter Reed Hospital, 1976 to 1980: specific analysis of gentamicin, tobramycin, and amikacin resistance.
During a five-year period at Walter Reed Army Hospital, Washington, DC, the frequency of aminoglycoside resistance among clinical bacterial isolates increased from less than 1% in 1976 to 13% of all isolates in later years. This resistance was seen among frequently isolated species of gram-negative bacilli isolated from patients throughout the hospital and from all anatomical sites, including blood. The incidence of gentamicin and amikacin resistance rose with increased administration of these antibiotics; however, the incidence of tobramycin resistance increased despite its minimal usage. From 1977 to 1978 and from 1979 to 1980, there was a decrease in the conjugal transmissibility of resistance to gentamicin and tobramycin. There was no detectable transmissible amikacin resistance. These findings suggest that high priority must be given to strategies that limit the emergence and dissemination of organisms resistant to these important antibiotics.
Amikacin↗
Sensitivity of K1-encapsulated Escherichia coli to killing by the bactericidal/permeability-increasing protein of rabbit and human neutrophils.
The presence of K1 capsular polysaccharides increases the resistance of Escherichia coli to killing by serum and phagocytosis by polymorphonuclear leukocytes (PMNs). To determine whether K1 capsule impedes the action of intracellular bactericidal systems of PMNs, we compared the sensitivity of several K1-encapsulated and non-encapsulated strains of E. coli to killing by the bactericidal/permeability-increasing protein (BPI) isolated from rabbit and human PMNs. BPI appears to be the principal bactericidal agent of PMNs toward E. coli and other gram-negative bacteria (Weiss et al., J. Clin. Invest. 69:959-970, 1982). The presence of K1 capsule was monitored by sensitivity to K1-specific bacteriophages. The non-encapsulated strains used represent both random bacteremic isolates and non-encapsulated derivatives of K1-encapsulated strains obtained by selection for resistance to K1-specific phages. We found little or no difference in the sensitivity of K1-encapsulated and non-encapsulated E. coli to killing by neutralized acid extracts of rabbit PMNs. Bacterial killing by these crude fractions can be attributed to the action of BPI because: (i) bacterial killing was blocked by immune (anti-BPI) immunoglobulin but not by preimmune immunoglobulin and (ii) comparison of the dose-response curves of bacterial killing by crude extracts and by purified BPI showed that the bactericidal activity of crude fractions corresponded closely to the BPI content. Human and rabbit BPIs exhibited similar bactericidal potency toward K1-encapsulated E. coli; i.e., <5 mug of either protein killed >90% of 2.5 x 10(7) bacteria. Thus, the potent bactericidal action of BPI toward E. coli is not impeded by K1 capsule, suggesting that the virulence of K1-encapsulated E. coli is a consequence of extracellular survival but not of resistance to intracellular killing.
Animals↗
Role of respiratory assistance devices in endemic nosocomial pneumonia.
The role of respiratory assistance devices and techniques in the acquisition of endemic hospital-associated pneumonia was prospectively studied in 13,086 patients over 11 months. Of these, 914 (7 percent) had a respiratory assistance device for at least 24 hours. Cultures of respirator effluent air and nebulizer fluid (taken after 24 hours), tracheostomy sites and irrigating solutions and respirometers were obtained in the 144 of 914 patients who had a respiratory assistance device for at least 72 hours. There were 108 episodes of hospital-associated pneumonia in 107 patients (0.82 percent incidence). Gram-negative organisms were associated with 70 percent of these episodes and Strep. pneumoniae with 5 percent. The risk of hospital-associated pneumonia was 0.3 percent in patients without a respiratory assistance device (35 percent of total hospital-associated pneumonia) versus (1.3 percent with endotracheal tubes and respirators (11 percent of hospital-associated pneumonia), 25 percent with tracheostomy (12 percent of hospital-associated pneumonia) and 66 percent in patients with tracheostomy and a respirator (9 percent of hospital-associated pneumonia). No case of hospital-associated pneumonia occurred in patients on respirators less than 24 hours, but the risk of hospital-associated pneumonia increased significantly after the fifth day of therapy. None of the 63 cultures of nebulizer fluid was positive. Although positive cultures of respiratory effluent, tracheal suction fluid or respirometer were not predictive of the acquisition of hospital-associated pneumonia, nine of 107 patients acquired this infection after a previously positive culture of a respiratory assistance device, and in five instances with the same organism. Since contaminated respiratory assistance devices are rarely a direct cause of hospital-associated pneumonia, routine in-use monitoring of respiratory assistance devices does not appear warranted.
Cross Infection↗
Production of exoenzyme S by clinical isolates of Pseudomonas aeruginosa.
Exoenzyme S differs from toxin A and diphtheria toxin in that it does not adenosine diphosphate (ADP)-ribosylate elongation factor-2, but rather catalyzes the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide to a number of different proteins in extracts of eucaryotic cells. Polyoma-transformed BHK-21 cells were isolated which were resistant to diphtheria toxin and toxin A. Extracts from these cells are ADP-ribosylated by exoenzyme S but not toxin A or diphtheria toxin, providing an assay which distinguishes between S and A activities. A total of 124 clinical isolates of P. aeruginosa were analyzed for production of toxin A and exoenzyme S. Exoenzyme S production was detected in 38% of the strains, whereas 80% of the strains produced toxin A.
ADP Ribose Transferases↗
Evidence for the role of toxin A in the pathogenesis of infection with Pseudomonas aeruginosa in humans.
Levels of antibody to toxin A of Pseudomonas aeruginosa were determined by a solid-phase radioimmunoassay. Mean (+/- SEM) peak levels of IgG in 24 normal soldiers were 2.6 +/- 0.5 microgram/ml, white mean peak levels in 12 patients colonized with and 13 patients infected in sites other than the blood with toxin A-producing strains were 16.7 +/- 7.0 and 17.1 +/- 4.4 microgram/ml, respectively. Levels of IgG were determined in 52 patients with pseudomonas bacteremia, and those surviving and those dying of bacteremia due to toxin A-producing strains had mean peak levels of 25.8 +/- 5.5 and 4.6 +/- 2.0 microgram/ml, respectively. The antitoxin response in sequential bacteremic sera began shortly after onset of bacteremia and decreased gradually, but antitoxin could be recalled promptly upon reinfection with Pseudomonas. Death from pseudomonas bacteremia was significantly associated with infection by a toxin A-producing strain, presence of underlying disease, hypotension, and antitoxin level of < 2 microgram/ml.
Adult↗
Stimulation of polymorphonuclear leukocyte bactericidal activity by supernatants of activated human mononuclear cells.
Supernatants of phytohemagglutinin-activated human mononuclear cells stimulated polymorphonuclear leukocyte (PMN) activity against the gram-negative organism Serratia marcescens. In the absence of serum opsonins, when control PMN could not impede bacterial growth, stimulated PMN averaged more than 0.6-log kill of the original bacterial inoculum. In the presence of optimal amounts of serum opsonins, when control PMN were significantly bactericidal, stimulated PMN killed, on the average, at least 0.6 log more of bacteria. Stimulation was not found when PMN were preincubated with supernatants for 1 h or less. The data strongly suggested that the action of the PMN stimulating factor was independent of and different from classically described serum opsonins. PMN stimulating activity may be an additional lymphokine-mediated immune defense mechanism enabling hosts to kill invading microorganisms.
Antibodies↗
Septicemia and chronic hemodialysis.
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Anti-Bacterial Agents↗
Infective endocarditis and access site infections in patients on hemodialysis.
Infective endocarditis has been a subtle and very often lethal complication of hemodialysis. Thirty-five episodes have been described to date. Antecedent infections, particularly those involving the access site, access manipulation, and dental work appear to predispose to IE. Once IE is acquired, factors associated with mortality are involvement of two or more valves, infection caused by enterococci, antecedent infection, steroid therapy, infection in the first year post-access insertion and patient age over 46. The incidence of access infection with the arteriovenous fistula is significantly less than that associated with the arteriovenous cannula. Staphylococci are the most common organisms in access infections and in IE. Gram-negative bacilli and particularly Pseudomonas aeruginosa are a frequent cause of access infection but an unusual cause of IE. Access removal may be madatory in the successful management of IE in patients on hemodialysis.
Adult↗
Comparison of phlebitis produced by cephapirin and cephalothin.
In a single-blinded study involving 120 patients neither the incidence nor severity of phlebitis observed with cephapirin and cephalothin was significantly different.
Adult↗
Pulmonary mechanics after uncomplicated influenza A infection.
Pulmonary mechanics were evaluated in 13 nonsmoking adults with acute, uncomplicated influenza A/Port Chalmers/73(H3N2) virus infection. Subjects had no evidence of lower respiratory tract involvement on physical examination. Viral and/or scrologic evidence of influenza infection was established for all subjects. Physiologic measurements included forced expiratory rates by spirometry and total pulmonary resistance (RT) measured at 3, 5, 7, and 9 cycles per sec by the oscillometric technique. Subjects were studied at time of acute illness and at 1, 3, and 5 weeks thereafter. Spirometric measurements were initially normal in all subjects and did not change significantly throughout the study. Elevated RT measured at 3 cycles per sec and an abnormal degree of frequency dependence of RT, determined by comparing RT at 3 cycles per sec to RT at 9 cycles per sec, were initially present in 10 of 13 subjects. All 7 of these subjects initially abnormal who were tested 7 days after the onset of illness had abnormal frequency dependence. At 3 weeks, 7 of the 10 subjects initially abnormal continued to have frequency dependence of RT. All but 2 subjects reverted to normal levels by 5 weeks. Frequency dependence of RT indicates that acute influenza infection produces uneven time constants in the airways. A generalized increase in peripheral airway resistance or localized compliance changes could account for these abnormalities. Because these abnormalities persisted well beyond the period of clinical illness, these data imply that asymptomatic mechanical dysfunction of the lungs is a frequent sequela to acute influenza A virus infection. RT measured by the oscillometric method was a suitable noninvasive method for detecting abnormal airway time constants in these subjects with acute upper respiratory diseases.
Adult↗
Fevers of unknown origin.
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Fever of Unknown Origin↗