Listeriosis, a severe disease that results from exposure to the foodborne pathogen Listeria monocytogenes, is responsible for approximately 2500 illnesses and 500 deaths in the United States each year. Pregnant women are 20 times more likely to develop listeriosis than the general population, with adverse pregnancy outcomes that include spontaneous abortions, stillbirths, and neonatal meningitis. The objective of this study was to determine an infective dose that resulted in stillbirths and infectivity of selected tissues in pregnant guinea pigs. Pregnant guinea pigs were exposed orally on gestation day 35 to 10(4) to 10(8) L. monocytogenes CFU in sterile whipping cream. L. monocytogenes was recovered at 64, 73, 90, and 100% from the livers of animals infected with 10(5), 10(6), 10(7), and 10(8) CFU, respectively. In dams exposed to > or =10(6) CFU, L. monocytogenes was cultured from 50% of the spleen samples and 33% of the gallbladder samples. Eleven of 34 dams infected with > or =10(6) CFU delivered stillborn pups. L. monocytogenes was cultured from the placenta, liver, and brain tissue of all stillbirths. Dams that delivered nonviable fetuses after treatment with > or =10(7) L. monocytogenes CFU had fecal samples positive for L. monocytogenes at every collection posttreatment. On the basis of a log-logistic model, the dose that adversely affected 50% of the pregnancies was approximately 10(7) L. monocytogenes CFU compared with that estimated from a human outbreak of 106 CFU. Listeriosis in pregnant guinea pigs can result in stillbirths, and the overall disease is similar to that described in nonhuman primates and in humans.

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The ability of parents to cooperate in their children's treatment is not fixed, but is a potential that evolves in a clinical relationship. Such clinical work includes a hierarchy of limit-setting, ranging from education to legal intervention. The experience of an inpatient child psychosomatic service indicates that such limit-setting was relevant in more than 50% of cases, and served to enhance the alliance with parents and children.

The foodborne pathogen Listeria monocytogenes can cause infection in immunocompromised humans and in the fetuses of pregnant women. We have demonstrated that one group of genetically similar L. monocytogenes strains (random amplified polymorphic DNA [RAPD] type 9) dominate and persist in several independent fish processing plants. The purpose of the present study was to determine the virulence potential of one RAPD type 9 strain (La111), one human clinical strain (Scott A), and one monkey clinical strain (12443) in a pregnant guinea pig model. Animals were orally exposed to 10(8) CFU of L. monocytogenes in whipping cream on gestation day (GD) 36 and euthanized on GD 42, 45, or 56. Strains 12443 and Scott A were shed from treated animals for 20 days, whereas La111 was shed only in the first 10 days. Strains 12443 and Scott A were recovered from maternal liver, spleen, and gallbladder on all 3 days of euthanization, whereas La111 was recovered only at GD 45 and 56. Scott A was not isolated from any placentas or fetuses. For dams treated with 12443, 22% of the fetuses were positive for L. monocytogenes, and surprisingly, treatment of dams with La111 resulted in 56% infected fetuses. L. monocytogenes was isolated from 16 and 20% of placentas for 12443 and La111, respectively. The study demonstrates that a food processing plant persistent strain of L. monocytogenes is able to cross the fetoplacental barrier in pregnant guinea pigs. Furthermore, we demonstrate that although information can be gained from model virulence assays, assessment of the virulence potential of a strain may require more complex hosts.