Anti-basal ganglia antibodies and acute movement disorder following herpes zoster and streptococcal infections.

Anti-basal ganglia antibodies (ABGA) have been associated with poststreptococcal encephalitis similar to encephalitis lethargica (EL). We report two children with parainfectious encephalitis of similar phenotype and IgG ABGA. However, the associated pathogens in the two cases differed; beta-hemolytic streptococcus and herpes zoster. ABGA may not be specific to poststreptococcal encephalitis, but rather a surrogate marker of an inflammatory mediated movement disorder, which may respond to immunotherapy.     

Reliability and predictive value of salivary theophylline levels

The reliability and accuracy of salivary theophylline levels as a predictor of serum theophylline levels was investigated in 28 hospitalized chronic asthmatics, free of other chronic diseases, on continuous aminophylline infusion for greater than 24 hours. Twenty paired blood and saliva theophylline levels from 12 patients (group 1) were used to develop a formula for predicting serum theophylline levels from salivary levels. Twenty-one paired blood and saliva theophylline levels from 16 patients (group 2) were used to test the formula obtained. The formula predicted the serum theophylline concentration within 1.51 microgram/mL in 76% of the samples and within 1.88 microgram/mL in 100% of the samples. There was an excellent correlation between the predicted and actual serum theophylline concentrations, r = .93; thus under controlled conditions of steady-state pharmacokinetics in patients free of other diseases, salivary theophylline levels can be used to accurately predict serum levels.     

Participation of normal human immunoglobulins M, G, and A in opsonophagocytosis and intracellular killing of Bacteroides fragilis and Bacteroides thetaiotaomicron by human polymorphonuclear leukocytes.

Restoration of the ability of hypogammaglobulinemic serum to support opsonophagocytosis and intracellular killing of Bacteroides fragilis and Bacteroides thetaiotaomicron by human polymorphonuclear leukocytes was achieved by supplementation with normal human immunoglobulin M, but not with normal human immunoglobulin G. Polymorphonuclear leukocyte bactericidal activity in the presence of immunoglobulin A-deficient human serum was equivalent to that observed in the presence of normal human serum.     

Bacteroidaceae in Thromboembolic Disease: Effects of Cell Wall Components on Blood Coagulation In Vivo and In Vitro

The effects of Bacteroides sp., Fusobacterium mortiferum, Bacteroides fragilis, and Sphaerophorus necrophorus on various parameters of blood coagulation in vivo and in vitro were determined and compared to the coagulation effects of Escherichia coli and Salmonella minnesota, wild type and R595. Intravenous injection of washed cells, culture filtrate, lipopolysaccharide, or lipid A of the anaerobic gram-negative microorganisms into mice resulted in acceleration of coagulation. Lipopolysaccharide and lipid A of the anaerobic microorganisms had no apparent effect on circulating platelets in mice or rabbits and did not cause aggregation of human platelets in vitro. Washed cells, lipopolysaccharide, and lipid A of Bacteroides sp. and F. mortiferum also significantly accelerated the clotting time of recalcified platelet poor normal human plasma and C6-deficient rabbit plasma. Lipid A, but not lipopolysaccharide, of E. coli and washed cells of S. minnesota R595 accelerated coagulation by a similar mechanism. These results indicated that Bacteroides sp. and F. mortiferum can accelerate blood coagulation in vivo and in vitro by a mechanism which does not involve platelets or terminal components of complement.     

Activation of complement by opportunist pathogens and chemotypes of Salmonella minnesota.

Washed cells of Staphylococcus aureus, Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, and Salmonella minnesota chemotypes (S, Rb, and Re) were tested for their ability to activate the alternative complement pathway (ACP). Parameters of ACP activation were (i) conversion of C3 in 10 mM ethyleneglycol-bis-(beta-aminoethyl ether)-N,N1-tetraacetic acid-treated human serum supplemented with 2.5 mM MgCl2, (ii) lysis of glutathione-treated human erythrocytes in the presence of human serum, and (iii) C3 to C9 consumption in C4-deficient guinea pig serum. With the exception of S. minnesota Re and S. aureus, all of the strains were highly active in the test systems when compared with inulin. S. minnesota Re and S. aureus initiated C3 conversion in untreated human serum, suggesting that these microorganisms were capable of activating complement by a mechanism other than the ACP. These results provide direct evidence for ACP activation by opportunist gram-negative bacilli and refute the hypothesis that the lipid A moiety of the lipopolysaccharide cell wall is responsible for ACP activation.     

Temporal relationships among immunologic alterations in a guinea pig model of thermal injury

Temporal relationships among various humoral and cellular alterations of host defense mechanisms were investigated in a guinea pig model of thermal injury during three weeks after burning. Reduction in serum concentration of C3 and fixation of C3 on Pseudomonas aeruginosa, presence of activated C3 in plasma, and elevations in levels of 6-ketoprostaglandin F1 alpha and thromboxane B2 in wound fluid were observed at 3-6 hr after burning. These alterations were accompanied by reduction in intrinsic bactericidal activity of polymorphonuclear neutrophils (PMNs) against P. aeruginosa, suppression of bactericidal activity of PMNs by serum, and decreased blood clearance of P. aeruginosa. All parameters returned to normal values by seven to nine days after burning. Proliferative responses of splenic lymphocytes to T cell mitogens were depressed at four days after burning and were maximally reduced at eight days. These data support the concept that there is a continuum of immunologic alterations resulting from thermal injury and that consumption of complement and increase in arachidonic acid metabolism are early events.