Summary In the winter of 1990/91 a new, economically devastating disease occured in european pig breeding herds, characterized by late‐term abortion, stillbirth and a high morbidity and mortality of suckling piglets. Because of the clinical picture the disease was named porcine epidemic and respiratory syndrome (PEARS). In this study investigations were carried out in tissues of uterus and placentae of late gestational sows (107 to 112 days of gestation) in three different groups of animals: group I = control animals (n=2) group II = naturally infected sows (n=12) from farms, where PEARS recently had been introduced; group III = sows (n=2), experimentally inoculated with placental homogenates from animals of group II. Both in naturally infected as well as in experimentally infected sows a multifocal, lymphohistiocytic vasculitis and perivascular cell infiltration was observed in the endometrium and maternal part of the placenta, but not in the fetal one. In the fetomaternal unit there were multifocal microseparations of the epithelial layers present. Transmission electron microscopically spherical or oval virus‐like particles of 45 to 75 nm in diameter were frequently found on the surface of endothelial cells of blood vessels in the maternal placenta, in a few cases in the intercellular channel system between uterine epithelial cells or on endothelial cells of capillaries in the fetal placenta. Serological results indicate, that an infection with Lelystad virus had occured in naturally and experimentally infected sows and that transplacental infection was present.

La insuficiencia del cérvix es una alteración del tejido cervical que impide mantener el embarazo hasta su término, provocando pérdidas fetales recurrentes en el segundo trimestre de embarazo. Se presenta un caso de incompetencia cervical, causante de tres abortos previos, el último pese a cerclaje vaginal; por tanto, se realiza cerclaje por vía abdominal, logrando un embarazo viable hasta las 35,6 semanas, que termina en cesárea por amenaza de parto pretérmino y ruptura prematura de membranas. Además, se expone una revisión de la literatura sobre el tratamiento de esta patología.

Rev Bras Ginecol Obstet 2016;38:369-372. Hypertensive disease of pregnancy, postpartum hemorrhage and infectious syndromes in pregnancy and puerperium are the leading causes of morbidity and mortality for pregnant women around the world. 1 Their frequency varies according to the country and accessibility to health care. 1 Hypertensive diseases, including preeclampsia, complicate 2-10% of all pregnancies. 1-3 In Latin America and the Caribbean, hypertensive disorders are responsible for at least 26% of maternal deaths. 3 Preeclampsia is a multifactorial disease caused by environmental factors that act over a genetic base, permitting the occurrence of this disorder. 4-12 Based on this premise, the risk factors considered for the development of this disease are: overweightness; obesity; nulliparity and multiparity; being at the extremes of reproductive life; vascular diseases, such as chronic hypertension; metabolic diseases, such as diabetes mellitus; collagen diseases, such as systemic lupus erythematosus; multiple pregnancies; maternal and paternal family history 12-14 (paternal imprinting expressed in the mother); pregnancy by assisted reproductive techniques; 12 micropolycystic ovary syndrome with insulin resistance; 15 severe anemia; 16 antiphospholipid syndrome; 17 and low-calcium diets consumed by people living at high altitudes. 18,19 The interaction of risk factors and multiple polymorphic genes induces the synthesis of several proteins with effects differing from their original function, leading to the impairment of placental perfusion and the consequent production of mediators that damage the endothelium. The main proteins and others factors involved are listed below. 7,8,20 Group I -vasoactive and vascular remodeling proteins: nitric oxide synthase; renin; type I and II angiotensin receptors; angiotensin converting enzyme; polycarboxypeptidase; endothelin-1; alpha and beta estrogen receptors; endoglin; tyrosine-kinase fms-like receptor-1; placental growth factor; and vascular endothelial growth factor. 20Group II -thrombophilia and hypofibrinolysis: methyltetrahydrofolate reductase; Leiden Factor V; prothrombin; fetal thrombophilia; plasminogen activator inhibitor-1; B3 integrin; and glycoprotein IIIA. 20Group III -oxidative stress, lipid metabolism, endothelial injury: epoxide hydrolase; glutathione transferase; superoxide dismutase; cytochrome P450 1A1; lipoprotein lipase; apolipoprotein E; and long-chain 3-hydroxyacylCoA dehydrogenase. 20Group IV -immunogenetic: human leukocyte antigen; interleukins 1 and 10; and tumor necrosis factor. 20 Physiologically, in order to promote vascular remodeling, the changes of the decidua also occur in the inner area of the myometrium. 21 An interaction of trophoblastic human leukocyte antigen (HLA) C, HLA-E, HLA-G with natural killer cells or dendritic cells or both is necessary for this event to occur. The presence of certain combinations of HLA-C and isoform types of immunoglobulin receptors bound to natural killer cells predispose to preeclampsia. [22][23][24]...

Objetivo: Determinar la prevalencia de uropatógenos, sensibilidad y resistencia antimicrobiana en la infección del tracto urinario que acuden al Hospital Básico Privado “Provida” del 1 de enero de 2014 al 31 de diciembre de 2016. Material y métodos: Se analizaron los resultados de 116 urocultivos de orina en mujeres no gestantes de todas las edades de 2014 a 2016, que fueron atendidas en el Hospital Básico Privado “Provida” de la cuidad de Latacunga, en Ecuador. El análisis de los datos obtenidos se realizó mediante estadística descriptiva. Resultados: De las 116 muestras, se aislaron: Escherichia coli (84,5%), Staphylococcus saprophyticus (8,6%) y Proteus spp. (6,9%). E. coli mostró sensibilidad a ceftriaxona en el 70 %, seguido de fosfomicina y gentamicina con el 62 y el 60%, respectivamente. La sensibilidad hallada para quinolonas fue del 40% y la ampicilina sulbactam alcanzó el 37%. Proteus spp. mostró sensibilidad del 75% para gentamicina y del 50% para quinolonas y cefuroxima. S. saprophyticus tuvo sensibilidad superior al 50% para gentamicina, ampicilina sulbactam, quinolonas y nitrofurantoína. Para E. coli la resistencia más alta registrada fue con ampicilina en el 86,5%, seguido de las quinolonas con una resistencia superior al 50%. La ampicilina asociada a inhibidor de betalactamasas, fosfomicina, cefalosporinas, nitrofurantoína y aminoglucósidos mostró resistencia inferior al 25%. Conclusión: El agente patógeno más prevalente en infecciones del tracto urinario (ITU) es E. coli (84,7%), porcentaje coincidente con lo reportado en la literatura nacional y mundial. Los antimicrobianos para este uropatógeno con mayor resistencia fueron ampicilina (86%), cirprofloxacina (55%) y norfloxacina (53%). Se podría tener en cuenta en el momento de administrar una terapéutica empírica, dato que debería ser corroborado con información de susceptibilidades de acuerdo con el contexto.

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