Biomedical subjects

James L Smith

Publications and source records attributed to James L Smith.

20 records · Page 2Linked to original sources

PubMed2002

Campylobacter jejuni infection during pregnancy: long-term consequences of associated bacteremia, Guillain-Barré syndrome, and reactive arthritist.

Campylobacter jejuni infections are the main cause of foodborne gastroenteritis in the United States and other developed countries. Generally, C. jejuni infections are self-limiting and treatment is not necessary; however, infections caused by this organism can lead to potentially dangerous long-term consequences for some individuals. Bacteremia, Guillain-Barré syndrome (GBS; an acute flaccid paralytic disease), and reactive arthritis (ReA) are the most serious of the long-term consequences of C. jejuni infections. During pregnancy, foodborne infections may be hazardous to both the woman and the fetus. C. jejuni-induced bacteremia during pregnancy may lead to intrauterine infection of the fetus, abortion, stillbirth, or early neonatal death. Infection of a newborn by the mother during the birth process or shortly after birth may lead to neonatal enteritis, bacteremia, and/or meningitis. C. jejuni enteritis is the inducing antecedent infection in approximately 30% of cases of GBS. Thus, pregnant women infected with C. jejuni may contract GBS. GBS during pregnancy does not affect fetal or infant development and does not increase spontaneous abortion or fetal death; however, it may induce spontaneous delivery during the third trimester in severe cases. Reactive arthritis occurs in approximately 2% of C. jejuni enteritis cases and leads to the impaired movement of various joints. Pregnant women with C. jejuni-induced reactive arthritis can be expected to deliver a normal infant. A pregnant patient with GBS or ReA may be unable to care for a newborn infant because of the physical impairment induced by these diseases. Since C. jejuni infections put both fetuses and pregnant women at risk, pregnant women must take special care in food handling and preparation to prevent such infections.

Arthritis, Reactive↗

PubMedDate not supplied

The contribution of cytolethal distending toxin to bacterial pathogenesis.

Cytolethal distending toxin (CDT) is a bacterial toxin that initiates a eukaryotic cell cycle block at the G2 stage prior to mitosis. CDT is produced by a number of bacterial pathogens including: Campylobacter species, Escherichia coli, Salmonella enterica serovar Typhi, Shigella dystenteriae, enterohepatic Helicobacter species, Actinobacillus actinomycetemcomitans (the cause of aggressive periodontitis), and Haemophilus ducreyi (the cause of chancroid). The functional toxin is composed of three proteins; CdtB potentiates a cascade leading to cell cycle block, and CdtA and CdtC function as dimeric subunits, which bind CdtB and delivers it to the mammalian cell interior. Once inside the cell, CdtB enters the nucleus and exhibits a DNase I-like activity that results in DNA double-strand breaks. The eukaryotic cell responds to the DNA double-strand breaks by initiating a regulatory cascade that results in cell cycle arrest, cellular distension, and cell death. Mutations in CdtABC that cause any of the three subunits to lose function prevent the bacterial cell from inducing cytotoxicity. The result of CDT activity can differ somewhat depending on the eukaryotic cell types affected. Epithelial cells, endothelial cells, and keratinocytes undergo G2 cell cycle arrest, cellular distension, and death; fibroblasts undergo G1 and G2 arrest, cellular distension, and death; and immune cells undergo G2 arrest followed by apoptosis. CDT contributes to pathogenesis by inhibiting both cellular and humoral immunity via apoptosis of immune response cells, and by generating necrosis of epithelial-type cells and fibroblasts involved in the repair of lesions produced by pathogens resulting in slow healing and production of disease symptoms. Thus, CDT may function as a virulence factor in pathogens that produce the toxin.

Animals↗