MRI can accurately show many urinary tract anomalies in third-trimester fetuses. It may be a useful complementary tool in the assessment of bilateral urinary tract anomalies of fetuses, particularly in cases with inconclusive sonographic findings.

Pathogens may impair reproduction in association or not with congenital infections. We have investigated the effect of acute infection with Trypanosoma cruzi, the protozoan agent of Chagas' disease in Latin America, on reproduction of mice. Although mating of infected mice occurred at a normal rate, 80% of them did not become gravid. In the few gravid infected mice, implantation numbers were as in uninfected control mice, but 28% of fetuses resorbed. Such infertility and early fetal losses were significantly associated with high maternal parasitemia. The remaining fetuses presented with reduced weights and all died later in gestation or within 48 hours after birth. Several organs of these fetuses were infiltrated by polynuclear cells and presented ischemic necrosis but did not harbor T. cruzi parasites, discarding congenital infection as the cause of mortality. However, surprisingly, the deciduas were massively invaded by T. cruzi parasites, harboring 125-fold more amastigotes than the maternal heart or other placental tissues. Parasites were significantly more numerous in the placentas of dead fetuses. In addition, placentas contained inflammatory infiltrates and displayed ischemic necrosis, fibrin deposits, and vascular thromboses. These results show that acute T. cruzi infection totally impairs reproduction in mice through inducing infertility or fetal-neonatal losses in association with placental parasite invasion and ischemic necrosis. Besides direct effects of infection on placentas and fetuses, poor pregnancy outcome might arise from disturbances in the complex biological processes tightly regulated by hormones and cytokines involved in mammal reproduction.3-5 Indeed, proinflammatory/type 1 cytokines such as tumor necrosis factor-␣ and interferon-␥, produced at high levels in response to some pathogens, have been shown to be harmful for pregnancy. 6,7 Information on the effect of infection with T. cruzi (the protozoa agent of Latin American Chagas' disease) on pregnancy is scarce though, and according to the endemic area, such infection affects 3 to 51% of pregnant women from which 2 to 10% congenitally transmit the parasite. 8,9 Some studies suggest that Chagas' disease might cause abortion or prematurity, whereas others fail to show such a relation.9 -11 Studies in experimental infection might reinforce our knowledge of maternofetal interactions in T. cruzi infection. Infertility and fetal growth retardation, associated or not with congenital infection, have been reported in chronic infection of mice. 12,13 In acute experimental infection, placental infection has been reported without congenital transmission, 14 despite the high circulating level of parasites, known to release proinflammatory molecules 15,16 and the systemic production of cytokines potentially deleterious for pregnancy. 17,18 The aim of the present work was to gain more insight into the relation between acute T. cruzi infection and gestation in mice, by studying the reproductive capacity, the pregnancy outcome, and the histopathology of...

The course of infection, parasitic loads, and histopathology of cutaneous lesions, draining lymph node, spleen, and liver were compared in BALB/c and C57BL/6 mice over a period of 34 weeks after inoculation in footpad with promastigotes of a Leishmania mexicana reference strain. The results show that the primary footpad lesions first present a 12-week phase that develops similarly in both strains of mice. Thereafter, a cutaneous and visceral dissemination of L. mexicana parasites occurs in BALB/c mice; the latter experience an extensive breakdown of the lymphoid organ microarchitecture, whereas C57BL/6 mice succeed in eliminating the parasite infection from the lymph nodes but not from the primary cutaneous lesion, which does not heal. These results highlight marked differences between responses of key anatomical compartments controlling L. mexicana infection in BALB/c and C57BL/6 mice.

Sirs,It is not unusual for extra-genital neoplasms to metastasise to the female genital. However, the metastases are localised mainly in the ovary and vagina and rarely in the uterus. Metastasis of extra-genital tract neoplasms to an endometrial polyp has been described only twice; both cases concerned breast carcinomas, one of lobular type [1] and one of ductal type [7]. We would like to report the first observation of metastasis from an apocrine carcinoma of the breast to an endometrial tamoxifeninduced polyp.The patient was a 70-year-old woman who presented with a 1-month history of metrorrhagia. The patient had, 4 years previously, undergone total left breast mastectomy with ipsilateral axillary lymphadenectomy for an infiltrating apocrine breast carcinoma. The tumour was 20×10×10 mm in size with evidence of metastatic involvement of one axillary lymph node and was, therefore, reported as pT1cN1 in accordance with the 1997 International Union Against Cancer (UICC) staging of breast tumours. Complementary studies, including chest X-ray, hepatic ultrasonography and bone isotopic scan were all negative. Post-surgery treatment consisted of radiotherapy and tamoxifen therapy, although the tumour showed only focal and weak positivity for oestrogen receptors. Follow-up was uneventful for 4 years. However, 4 years later, the patient complained of recurrent metrorrhagia. She underwent hysteroscopy with curettage and abdominal ultrasound. The latter revealed a polypoid mass 1.5 cm in length appended to the uterine dome. Total abdominal hysterectomy with bilateral salpingooophorectomy was performed.Gross examination of the uterus confirmed the presence of a polypoid mass 1.5×1.0×0.5 cm in size attached to the uterine dome. Cervix, myometrium and annexes were grossly unremarkable. The microscopical features of the polyp were typical of those induced by tamoxifen therapy. They showed sparse, irregularly scattered, focally dilated glands, lined by either atrophic or proliferative epithelium. The stroma was diffusely fibrotic with thick-walled, dilated blood vessels. Clusters of large eosinophilic cells similar to those observed in the primary breast carcinoma with abundant granular cytoplasm, globoid nuclei and prominent nucleoli, were visible within the polyp stroma (Fig. 1). In addition, numerous vascular emboli from the same eosinophilic cells were also visible. Immunohistochemically, the tumour cells showed strong positivity for AE1 and AE3 cytokeratins, epithelial membrane antigen (EMA) and GCDFP-15 (Fig. 2). In contrast, oestrogen and progesterone receptors were negative. No other microscopic metastases were found in the adjacent endometrium, myometrium, ovaries, tubes or cervix.

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