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Reproductive Sciences
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Article

Ureaplasma parvum or Mycoplasma hominis as Sole Pathogens Cause Chorioamnionitis, Preterm Delivery, and Fetal Pneumonia in Rhesus Macaques

Miles J. Novy1*, Lynn Duffy2, Michael K. Axthelm1, Drew W. Sadowsky1, Steven S. Witkin3, Michael G. Gravett4, Gail H. Cassell5, and Kenneth B. Waites2

1 Oregon Health and Science University
2 University of Alabama at Birmingham
3 Weill Medical College of Cornell University
4 University of Washington, Seattle
5 Eli Lilly and Company

* To whom correspondence should be addressed. E-mail: novym{at}ohsu.edu.


   Abstract

The authors assess causal, cellular and inflammatory links between intraamniotic infection with Ureaplasma parvum or Mycoplasma hominis and preterm labor in a nonhuman primate model. Long-term catheterized rhesus monkeys received intraamniotic inoculations of clinical isolates of Ureaplasma parvum serovar 1, M hominis, media control or physiological saline. Genital mycoplasmas were quantified in amniotic fluid (AF) and documented in fetal tissues by culture and PCR. In association with elevated AF colony counts for U parvum or M hominis, there was a sequential upregulation of AF leukocytes, proinflammatory cytokines, prostaglandin E2 and F2{alpha}, metalloproteinase-9 and uterine activity (P < .05). Fetal membranes and lung were uniformly positive for both microorganisms; fetal blood and cerebrospinal fluid cultures and PCR were more often positive for M hominis than U parvum. Histopathologic findings of chorioamnionitis, a systemic fetal inflammatory response and pneumonitis worsen with duration of in utero infection. U parvum or M hominis, as sole pathogens, elicit a robust proinflammatory response which contributes to preterm labor and fetal lung injury.

First published on January 2, 2009, doi:10.1177/1933719108325508

Reproductive Sciences 2009;16:56.

A more recent version of this article appeared on January 1, 2009


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