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. 2003 Mar;71(3):1574-9.
doi: 10.1128/IAI.71.3.1574-1579.2003.

Nonhuman primate model for Listeria monocytogenes-induced stillbirths

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Nonhuman primate model for Listeria monocytogenes-induced stillbirths

Mary Alice Smith et al. Infect Immun. 2003 Mar.

Abstract

Listeria monocytogenes, isolated from outbreaks in either human or nonhuman primate populations, was administered orally at doses ranging from 10(6) to 10(10) CFU. Four of 10 treated animals delivered stillborn infants. L. monocytogenes was isolated from fetal tissue, and the pathology was consistent with L. monocytogenes infection as the cause of pregnancy loss. For all pregnancies resulting in stillbirths, L. monocytogenes was isolated from maternal feces, indicating that L. monocytogenes had survived and had probably colonized the gastrointestinal tract. Antibodies and antigen-specific lymphocyte proliferation against Listeria increased in animals that had stillbirths.

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Figures

FIG. 1.
FIG. 1.
Antigen-induced proliferation of peripheral blood lymphocytes. Proliferative response to heat-killed L. monocytogenes strain 12443 was measured by [3H]thymidine incorporation after 72 h of culture. Bars represent the mean responses ± standard errors of results for animals with normal pregnancy outcomes (filled bars; number of samples, 5) or stillbirths (empty bars; number of samples, 4). Proliferation responses were measured in samples collected immediately prior to infection and approximately 30 days after stillbirth or normal outcome of pregnancy. An asterisk indicates a result that is significantly different from the preinfection level at a P value of <0.05.

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