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Biomedical subjects

D W Lawellin

Publications and source records attributed to D W Lawellin.

10 recordsLinked to original sources
PubMed1992

Paecilomyces lilacinus infection in a child with chronic granulomatous disease.

Chronic granulomatous disease (CGD) is a rare inherited disorder in which neutrophils do not appropriately generate cytotoxic superoxide anion, the respiratory burst, in response to invading bacteria or fungi as a part of normal host defence. We report the case of a child with CGD who had two abdominal wall abscesses caused by Paecilomyces lilacinus, an organism not previously known to cause infections in patients with CGD. The abdominal wall is a location that is rarely associated with Paecilomyces infections. Parenteral amphotericin B eradicated the infection in an immunocompromised child whereas this regimen has heretofore largely been unsuccessful in the treatment of this infection. Paecilomyces species and other fungi from immunocompromised hosts and thought to be laboratory contaminants, need to be carefully investigated for they may become pathogens in this clinical setting.

Abdominal Muscles↗
PubMed1991

A new proline aminopeptidase assay for diagnosis of bacterial vaginosis.

Bacterial vaginosis is one of the most common occurring vaginal conditions among women of reproductive age. A rapid and reliable laboratory test for diagnosis of bacterial vaginosis would be helpful in the clinical detection of this disease. Elevated proline aminopeptidase activity has been identified as a reliable marker enzyme for bacterial vaginosis. A proline aminopeptidase assay has been shown to predict accurately women with a clinical diagnosis of bacterial vaginosis. However, this assay has significant practical disadvantages, the most notable of which is the production of a carcinogenic end product, alpha-naphthylamine. We have developed a modified assay for this bacterial vaginosis marker enzyme with L-proline p-nitroanilide, a substrate that does not yield a carcinogenic end-product. The new proline aminopeptidase assay is a one-step test that is analyzed colorimetrically with microsomal leucine aminopeptidase used as a standard enzyme (linear from 3 to 125 mU per well). We have determined the activity of proline aminopeptidase in vaginal wet preparations from 57 patients with both assay methods. In addition, vaginal smears were examined with Gram's stain and analyzed for bacterial vaginosis with the Spiegel method. When compared with the Spiegel method, the two proline aminopeptidase assay methods were similar with respect to assay sensitivity (93%), specificity (91% to 93%), and the predictive value of a positive result (78% to 82%) or a negative result (97% to 98%). Vaginal wash samples also were assessed for proline aminopeptidase activity. Values for samples identified as bacterial vaginosis positive were significantly different (p less than 0.0001) from those that were negative according to the Spiegel analysis of Gram's stain: negative results, 66 +/- 41 mU/ml; positive results, 704 +/- 145 mU/ml. These findings indicate that this improved proline aminopeptidase assay will offer a rapid, sensitive, and objective laboratory method for the diagnosis of bacterial vaginosis.

Aminopeptidases↗
PubMed1990

Antibiotic inhibition of bacterially induced fetal membrane weakening.

A fetal membrane model was used to evaluate in vitro the efficacy of two antibiotics, erythromycin and clindamycin, in preventing bacterial protease-induced weakening of amniochorion. Standardized inocula of protease-producing bacteria (10(9) colony-forming units [cfu]/mL Staphylococcus aureus, incubated at 37C for 20 hours) reliably reduced fetal membrane structural integrity as reflected by bursting tension and work to rupture. Supraminimal inhibitory concentrations (supra-MICs) (erythromycin 0.23 microgram/mL; clindamycin 0.56 microgram/mL) and subminimal inhibitory concentrations (sub-MICs) (erythromycin 0.13 microgram/mL; clindamycin 0.06 microgram/mL) of both antibiotics prevented fetal membrane impairment due to test bacteria. Supra-MICs of both antibiotics prevented bacterial cell growth and release of protease. Sub-MICs of both antibiotics allowed bacterial cell growth of test microorganisms but inhibited protease release and subsequent fetal membrane damage. These findings suggest that inhibitory and even subinhibitory doses of antibiotics such as erythromycin and clindamycin may be effective in reducing the occurrence of premature rupture of membranes and subsequent preterm birth mediated by susceptible microorganisms.

Clindamycin↗
PubMed1989

Bacteria and inflammatory cells reduce chorioamniotic membrane integrity and tensile strength.

Bacteria and the inflammatory response they engender are implicated in the pathophysiology of premature rupture of fetal membranes and preterm birth. We tested the hypothesis that bacteria and polymorphonuclear neutrophils may have both separate and combined effects in weakening the amniochorionic membrane, and thus predispose to premature rupture of membranes. We examined how three parameters of membrane integrity (bursting tension, work to rupture, and elasticity) were affected by standardized preparations (10(9) cfu/mL) of group B streptococci or Staphylococcus aureus in the presence or absence of purified human neutrophils (32 x 10(6)/mL). In addition, effects of purified human neutrophil elastase were evaluated. Exposure to either group B streptococcus or S aureus decreased membrane strength, elasticity, and work to rupture. Only activated neutrophils had significant effects on membrane strength. Membrane exposure to S aureus plus neutrophils led to an additive weakening of fetal membranes. On the other hand, group B streptococci did not interact with neutrophils to yield a significant further weakening of the membranes. Elastase (150 U/mL) also weakened the membrane. The results were correlated with measures of protease (Azocoll and ninhydrin assays) and peroxidase (dimethoxybenzidine) activity. Our findings support the concept that human neutrophils and their constituent enzymes may act in concert with bacteria and their protease(s) in weakening amniochorion, and may possibly predispose to premature rupture of membranes in some women. These observations require clinical correlations.

Endopeptidases↗
PubMed1987

Influence of focal growth conditions on the pathogenesis of toxic shock syndrome.

Patients with toxic shock syndrome (TSS) had sequestered focal sites colonized or infected with Staphylococcus aureus significantly more frequently than did patients with scalded skin syndrome. Growth conditions within the infected foci of four patients with TSS included nearly physiological levels of pH, pO2, pCO2, protein, calcium, and magnesium. Two strains of S. aureus had typical TSS phenotypes (production of TSS toxin-1 [TSST-1] and protease), which were optimally expressed in vitro under conditions similar to those documented in vivo (6% CO2, pH 7.0, aerobic, high levels of protein). Altering any one of these growth factors significantly decreased production of TSST-1. In protein-containing media, depletion of divalent cations had a less-profound effect on organism growth and TSST-1 production. The unique in vivo environment in patients with non-menstrual TSS is similar to conditions associated with tampon use during menstruation. Growth conditions may play an important role in the expression of S. aureus phenotype and the pathogenesis of TSS.

Bacterial Toxins↗
PubMed1984

Phenotypic distinctiveness of Staphylococcus aureus strains associated with toxic shock syndrome.

Twenty Staphylococcus aureus strains from patients with toxic shock syndrome (TSS) and 20 from control patients (non-TSS) with infection but no clinical evidence of TSS were compared phenotypically in a collaborative, blinded, randomized study. TSS strains were significantly (P less than 0.05) more likely than non-TSS strains to produce various previously described but related toxic shock-associated proteins (pyrogenic exotoxin C, enterotoxin F, and TSS marker protein), as well as differing in other distinctive phenotypic characteristics, such as hemolysis, bacteriocin susceptibility, arsenate resistance, pigment production, and casein proteolysis. TSS strains were significantly less likely to carry plasmids than control strains. A combination of two variables--proteolysis and toxic shock-associated protein production--statistically accounted for all other phenotypic variations between TSS and non-TSS strains. Only proteolysis covaried with all other significant variables, suggesting a primary role in the phenotypic distinctiveness of TSS S. aureus strains and possibly in the pathogenesis of TSS.

Bacterial Proteins↗
PubMed1977

Enzyme-linked immunosorbent analysis for aflatoxin B1.

An enzyme-linked immunosorbent analysis (ELISA) permitted the detection of less than 10 pg of aflatoxin B1 per ml. The antitoxin was most specific for aflatoxins B1 and B2alpha, and least specific for aflatoxin G1.

Aflatoxins↗
PubMedDate not supplied

Alteration of proteins reacting with antibody to toxic shock syndrome toxin 1 by endogenous proteases of Staphylococcus aureus.

Many cases of toxic shock syndrome (TSS) have been associated with Staphylococcus aureus strains that produce in vitro a 22,000-dalton protein called toxic shock syndrome toxin 1 (TSST-1). TSST-1 has been shown to be linked phenotypically to the production of the type II (thiol) staphylococcal protease; however, some strains clearly associated with TSS do not produce TSST-1. With the use of a variety of antibodies to TSST-1, representatives of both TSST-1-positive and TSST-1-negative TSS-associated strains were shown to produce proteins of 32,000, 53,000, and 76,000 daltons that cross-reacted with TSST-1 but that did not appear to be TSST-1 aggregates or to be protein A. TSST-1-negative strains were significantly (P less than .05) more likely than TSST-1-producing strains to produce the type I protease and less likely to produce the type II protease. In vitro the type I (serine) protease digests purified TSST-1. When combinations of type II and type III protease chemical inhibitors were used, the production of the high-molecular-weight cross-reacting proteins during in vitro growth could be selectively enhanced. Since the infected foci (e.g., abscess, vagina) associated with TSS may contain natural protease inhibitors, it is possible that such TSST-1 cross-reacting proteins may be expressed in vivo or that levels of TSST-1 may be increased by an inhibitor of the serine protease.

Animals↗