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Ureaplasma parvum or Mycoplasma hominis as Sole Pathogens Cause Chorioamnionitis, Preterm Delivery, and Fetal Pneumonia in Rhesus Macaques
Miles J. Novy, MD1*,
Lynn Duffy, MT2,
Michael K. Axthelm, DVM, PhD1,
Drew W. Sadowsky, PhD1,
Steven S. Witkin, PhD3,
Michael G. Gravett, MD4,
Gail H. Cassell, PhD5,
and
Kenneth B. Waites, MD2
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.
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Abstract |
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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 , 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
This version was published on January
5, 2009

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