911 resultados para VILLOUS PLACENTA


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Background: Monozygotic monochorionic triplet pregnancy with conjoined twins is a very rare condition and is associated with many complications. Case: In this study, we describe a monochorionic–diamniotic triplet pregnancy after in vitro fertilization with an intracytoplasmic sperm injection. At a gestational age of 6 weeks and 4 days of pregnancy one gestational sac was observed, and at a gestational age of 12 weeks and 2 days, triplets with conjoined twins were diagnosed. After consulting with the parents, they chose fetal reduction of the conjoined twins. Selective feticide was successfully performed by radiofrequency ablation at 16 weeks of pregnancy. Unfortunately, the day after the procedure, the membrane ruptured, and 1 week later, all fetuses and placenta were spontaneously aborted. Conclusion: Monochorionic triplet pregnancy with conjoined twins is very rare. These pregnancies are associated with very serious complications. Intra cytoplasmic sperm injection increases the rate of monozygotic twinning and conjoined twins. Counseling with parents before IVF is very important.

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Background: The most frequent viral diseases which can cause abortion in sheep are Blue tongue, Border disease virus, Cache Valley fever and Schmallenberg virus. The diagnosis of abortion, namely virus-induced represents a challenge to field clinicians, since clinical signs presented by the dam are discrete, non-specific and variable (Agerhom et al., 2015). On the other hand, while some foetuses reveal characteristic and visible malformations, others do not reveal any lesions. In face of it, definitive diagnosis requires an appropriate history collection, as well as sending fresh samples, namely abortion material, foetus, placenta and umbilical cord, to a specialty laboratory, to obtain a precise diagnosis. Objectives: The authors suggest a registration method of all mandatory data, in order to further assist the diagnosis of viral diseases at the laboratories, including the most frequent congenital malformations reported in sheep abortions. Methods: Abortion samples of suspected viral origin were collected and all data were registered, in worktables optimized for this purpose. Results: The authors document, using macroscopic figures lesions of malformations in abortions, emphasizing the frequency and the importance of documenting each case, proposing practical and effective worktables to assist the fieldwork. Conclusions: Field clinician’s awareness of the importance of early detection of viral diseases causing abortion outbreaks stimulates a proper data collection for each case of abortion, in order to contribute to a precise diagnosis and posterior consistent epidemiological studies, which may allow diminishing of economic losses.

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Salmonella are Gram-negative, intracellular food-borne pathogens that cause pregnancy complications. In pregnant mice, Salmonella enterica serovar Typhimurium (S.Tm) infection results in placental bacterial replication, inflammation, necrosis, and fetal loss by unknown mechanisms. Necroptosis, or programmed necrosis mediated by RIPK3 (receptor-interacting protein kinase 3), an inflammatory cell death pathway, is implicated in the pathogenesis of S.Tm in non-pregnant mice. This goal of this thesis was to investigate the role of necroptosis in the pathogenesis of S.Tm infection during mouse pregnancy. I hypothesized that elimination of the key necroptotic cell death protein RIPK3 would decrease placental inflammation and trophoblast cell death, and increase conceptus survival compared to controls. Mice expressing a functional Slc11a1 (encodes the natural resistance-associated macrophage protein 1, NRAMP1) gene with or without RIPK3 function (Ripk3-/-Slc11a1+/+ compared to Slc11a1+/+) were infected with 103 S.Tm by tail vein injection on gestational day (GD) 12. Mice were euthanized on GD 14 (48h post-infection) or GD 15 (72h post-infection) and implantation sites (IS) and maternal serum were harvested for analyses. In nearly all challenged mice (except one outlier), S.Tm were detected in most IS within a litter but there was limited immune cell infiltration, placental damage or cell death in Slc11a1 competent mice regardless of Ripk3 gene deletion. Maternal serum cytokine analyses confirmed lack of maternal immune responses to S.Tm infection. IS amongst the litter of a single dam (Ripk3-/-Slc11a1+/+ at 72h postinfection) displayed heavy but not universal placental S.Tm infection of decidual tissues and spongiotrophoblast, associated with elevated maternal serum pro-inflammatory cytokines. S.Tm infection of the fetal yolk sac (YS) was observed in 54.5% of IS from this dam. YS infection was confirmed in archival samples in mice expressing Ripk3 with intact Slc11a1 and in mice lacking functional Slc11a1. In Slc11a1 incompetent mice, S.Tm were detected in placental labyrinthine trophoblast. Based on the available data, this thesis suggests that Ripk3 and necroptosis have no significant roles in either promotion or prevention of progressive Salmonella infection during mouse pregnancy. It also provides pilot data that NRAMP1 controls placental localization and lethality due to YS infection.

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Malignant Catarrhal Fever (MCF), an often-lethal infectious disease, presents as a variable complex of lesions in susceptible ungulate species. The disease is caused by a -herpesvirus following transmission from an inapparent carrier host. Two major epidemiological forms exist: wildebeest-associated MCF (WA-MCF), in which the virus is transmitted to susceptible species by wildebeest calves less than approximately four months of age, and sheepassociated MCF (SA-MCF) in which the virus is spread by sheep (primarily adolescents). Due to the lack of an in-vitro propagation system for the causative agent of the more economically significant SA-MCF, and with the expectation that cross-protective immunity may be provided, vaccine development has focused on the more easily propagated alcelaphine herpesvirus-1 (AlHV-1) that causes WA-MCF. In 2008 a direct viral challenge trial showed that a novel vaccine, employing an attenuated AlHV-1 (atAlHV-1) `C5000 virus strain, protected British Friesian-Holstein (FH) cattle against an intranasal challenge with virulent AlHV-1 `C5000 virus. For cattle keeping people living near wildebeest calving areas in sub-Saharan Africa an effective vaccine would have value as it would release them from the costly annual disease avoidance strategy of having to move their herds away from the oncoming wildebeest. On the other hand, an effective vaccine will release herd owners from the need to avoid MCF, allowing them to graze their cattle alongside wildebeest on the highly nutritious pastures of the calving areas. As such conservationists have raised concerns that the development of a vaccine might lead to detrimental grazing competition. The principle objective of this study was to test the novel vaccine on Tanzanian shorthorn zebu cross cattle (SZC).We did this firstly using a natural challenge field trial (Chapter Two) which demonstrated that immunisation with the atAlHV-1 vaccine was well tolerated and induced an oro-nasopharyngeal AlHV-1-specific and -neutralising antibody response. This resulted in an immunity in SZC cattle that was partially protective and reduced naturally transmitted infection by 56%. We also demonstrated that non-fatal infections occurred with a much higher frequency than previously thought. Because the calculated efficacy of the vaccine was less than that seen in British FH cattle we wanted to determine whether host factors, particular to SZC cattle, had impacted the outcomes of the field trial. To do this we repeated the 2008 direct viral challenge trial using SZC cattle (Chapter Four). During this trial we also investigated whether the recombinant bacterial flagellin monomer (FliC), when used as an adjuvant, might improve the vaccine’s efficacy. The findings from this trial indicated that direct challenge with pathogenic AlHV-1 is effective at inducing MCF in SZC cattle and that FliC is not an appropriate adjuvant for this vaccine. Furthermore, with less control group cattle dying of MCF than expected we speculate that SZC cattle may have a degree of resistance to MCF that affords them protection from infection and developing fatal disease. In Chapter Three we investigated aspects of the epidemiology of MCF, specifically whether wildebeest placenta, long implicated by Maasai cattle owners as a source of MCF, might play a role in viral transmission. Additionally, through comparative sequence analysis, at two specific genes (A9.5 and ORF50) of wild-type and atAlHV-1, we investigated whether the `C5000 strain, the source of which was taken from Africa more than 40 years ago, was appropriate for vaccine development. The detection of AlHV-1 virus in approximately 50% of placentae indicated that infection can occur in-utero and that this tissue might play a role in disease transmission. And, despite describing three new alleles of the A9.5 gene (supporting previous evidence that this gene is polymorphic and encodes a secretory protein with interleukin-4 as the major homologue), the observation that the most frequently detected haplotypes, in both wild-type and attenuated AlHV-1, were identical suggests that AlHV-1 has a slow molecular clock and that the attenuated strain was appropriate for vaccine development. In Chapter Five we present the first quantitative assessment of the annual MCF avoidance costs that Maasai pastoralists incur. In particular we estimated that as a result of MCF avoidance 64% of the total daily milk yield during the MCF season was not available to be used by the 81% of the family unit remaining at the permanent boma. This represents an upper-bound loss of approximately 8% of a household0s annual income. Despite these considerable losses we concluded that, given an incidence of fatal MCF in cattle living in wildebeest calving areas of 5% to 10%, if herd owners were to stop trying to avoid MCF by allowing their cattle to graze alongside wildebeest, any gains made through increased availability of milk, improved body condition and reduced energy demands would be offset by an increase in MCF-incidence. With the development of an effective vaccine, however, this alternative strategy might become optimal. The overall conclusion we draw therefore is that, despite the substantial costs incurred each year avoiding MCF, the partial protection afforded by the novel vaccine strategy is not sufficient to warrant a wholesale change in disease avoidance strategy. Nonetheless, even the partial protection provided by this vaccine could be of value to protect animals that cannot be moved, for example where some of the herd remain at the boma to provide milk or where land-use changes make traditional disease avoidance difficult. Furthermore, the vaccine may offer a feasible solution to some of the current land-use challenges and conflicts, providing a degree of protection to valuable livestock where avoidance strategies are not possible, but with less risk of precipitating the potentially damaging environmental consequences, such as overgrazing of highly nutritious seasonal pastures, that might result if herd owners decide they no longer need to avoid wildebeest.

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During pregnancy, the maternal cardiovascular system undergoes major adaptation. One of these changes is a 40-50 % increase in circulating blood volume which requires a systemic remodelling of the vasculature in order to regulate maternal blood pressure and maximise blood supply to the developing placenta and fetus. These changes are broadly conserved between humans and rats making them an appropriate pre-clinical model in which to study the underlying mechanisms of pregnancy-dependent cardiovascular remodelling. Whilst women are normally protected against cardiovascular disease; pregnancy marks a period of time where women are susceptible to cardiovascular complications. Cardiovascular disease is the leading cause of maternal mortality in the United Kingdom; in particular hypertensive conditions are among the most common complications of pregnancy. One of the main underlying pathologies of these pregnancy complications is thought to be a failure of the maternal cardiovascular system to adapt. The remodelling of the uterine arteries, which directly supply the maternal-fetal interface, is paramount to a healthy pregnancy. Failure of the uterine arteries to remodel sufficiently can result in a number of obstetric complications such as preeclampsia, fetal growth restriction and spontaneous pregnancy loss. At present, it is poorly understood whether this deficient vascular response is due to a predisposition from existing maternal cardiovascular risk factors, the physiological changes that occur during pregnancy or a combination of both. Previous work in our group employed the stroke prone spontaneously hypertensive rat (SHRSP) as a model to investigate pregnancy-dependent remodelling of the uterine arteries. The SHRSP develops hypertension from 6 weeks of age and can be contrasted with the control strain, the Wistar Kyoto (WKY) rat. The phenotype of the SHRSP is therefore reflective of the clinical situation of maternal chronic hypertension during pregnancy. We showed that the SHRSP exhibited a deficient uterine artery remodelling response with respect to both structure and function accompanied by a reduction in litter size relative to the WKY at gestational day (GD) 18. A previous intervention study using nifedipine in the SHRSP achieved successful blood pressure reduction from 6 weeks of age and throughout pregnancy; however uterine artery remodelling and litter size at GD18 was not improved. We concluded that the abnormal uterine artery remodelling present in the SHRSP was independent of chronic hypertension. From these findings, we hypothesised that the SHRSP could be a novel model of spontaneously deficient uterine artery remodelling in response to pregnancy which was underpinned by other as yet unidentified cardiovascular risk factors. In Chapter 1 of this thesis, I have characterised the maternal, placental and fetal phenotype in pregnant (GD18) SHRSP and WKY. The pregnant SHRSP exhibit features of left ventricular hypertrophy in response to pregnancy and altered expression of maternal plasma biomarkers which have been previously associated with hypertension in human pregnancy. I developed a protocol for accurate dissection of the rat uteroplacental unit using qPCR probes specific for each layer. This allowed me to make an accurate and specific statement about gene expression in the SHRSP GD18 placenta; where oxidative stress related gene markers were increased in the vascular compartments. The majority of SHRSP placenta presented at GD18 with a blackened ring which encircled the tissue. Further investigation of the placenta using western blot for caspase 3 cleavage determined that this was likely due to increased cell death in the SHRSP placenta. The SHRSP also presented with a loss of one particular placental cell type at GD18: the glycogen cells. These cells could have been the target of cell death in the SHRSP placenta or were utilised early in pregnancy as a source of energy due to the deficient uterine artery blood supply. Blastocyst implantation was not altered but resorption rate was increased between SHRSP and WKY; indicating that the reduction in litter size in the SHRSP was primarily due to late (>GD14) pregnancy loss. Fetal growth was not restricted in SHRSP which led to the conclusion that SHRSP sacrifice part of their litter to deliver a smaller number of healthier pups. Activation of the immune system is a common pathway that has been implicated in the development of both hypertension and adverse pregnancy outcome. In Chapter 2, I proposed that this may be a mechanism of interest in SHRSP pregnancy and measured the pro-inflammatory cytokine, TNFα, as a marker of inflammation in pregnant SHRSP and WKY and in the placentas from these animals. TNFα was up-regulated in maternal plasma and urine from the GD18 SHRSP. In addition, TNFα release was increased from the GD18 SHRSP placenta as was the expression of the pro-inflammatory TNFα receptor 1 (Tnfr1). In order to investigate whether this excess TNFα was detrimental to SHRSP pregnancy, a vehicle-controlled intervention study using etanercept (a monoclonal antibody which works as a TNFα antagonist) was carried out. Etanercept treatment at GD0, 6, 12 and 18 resulted in an improvement in pregnancy outcome in the SHRSP with an increased litter size and reduced resorption rate. Furthermore, there was an improved uterine artery function in GD18 SHRSP treated with etanercept which was associated with an improved uterine artery blood flow over the course of gestation. In Chapter 3, I sought to identify the source of this detrimental excess of TNFα by designing a panel for maternal leukocytes in the blood and placenta at GD18. A population of CD3- CD161+ cells, which are defined as rat natural killer (NK) cells, were increased in number in the SHRSP. Intracellular flow cytometry also identified this cell type as a source of excess TNFα in blood and placenta from pregnant SHRSP. I then went on to evaluate the effects of etanercept treatment on these CD3- CD161+ cells and showed that etanercept reduced the expression of CD161 and the cytotoxic molecule, granzyme B, in the NK cells. Thus, etanercept limits the cytotoxicity and potential damaging effect of these NK cells in the SHRSP placenta. Analysing the urinary peptidome has clinical potential to identify novel pathways involved with disease and/or to develop biomarker panels to aid and stratify diagnosis. In Chapter 4, I utilised the SHRSP as a pre-clinical model to identify novel urinary peptides associated with hypertensive pregnancy. Firstly, a characterisation study was carried out in the kidney of the WKY and SHRSP. Urine samples from WKY and SHRSP taken at pre-pregnancy, mid-pregnancy (GD12) and late pregnancy (GD18) were used in the peptidomic screen. In order to capture peptides which were markers of hypertensive pregnancy from the urinary peptidomic data, I focussed on those that were only changed in a strain dependent manner at GD12 and 18 and not pre-pregnancy. Peptide fragments from the uromodulin protein were identified from this analysis to be increased in pregnant SHRSP relative to pregnant WKY. This increase in uromodulin was validated at the SHRSP kidney level using qPCR. Uromodulin has previously been identified to be a candidate molecule involved in systemic arterial hypertension but not in hypertensive pregnancy thus is a promising target for further study. In summary, we have characterised the SHRSP as the first model of maternal chronic hypertension during pregnancy and identified that inflammation mediated by TNFα and NK cells plays a key role in the pathology. The evidence presented in this thesis establishes the SHRSP as a pre-clinical model for pregnancy research and can be continued into clinical studies in pregnant women with chronic hypertension which remains an area of unmet research need.

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Part 1 of the study aims to: evaluate NGF and VEGF levels obtained at parturition from mare, foal and umbilical cord vein plasma, as well as in amniotic fluid; evaluate NGF and VEGF content in plasma of healthy foals during the first 72 h of life; evaluate NGF and VEGF levels at parturition in relation to selected mares’ and foals’ clinical parameters; evaluate the relationship between the two trophic factors and thyroid hormone levels in the first 72 h of life; assess mRNA expression of NGF, VEGF and BDNF and their cell surface receptors in the placenta. Part 2 aims to clinically characterize a population of foals spontaneously affected by Neonatal Encephalopathy (NE), and then to: evaluate NGF and VEGF levels in plasma samples obtained in the affected population at parturition from mare’s jugular vein, umbilical cord vein and foal’s jugular vein, as well as in amniotic fluid; evaluate NGF and VEGF content in plasma of foals affected by NE during the first 72 h of life/hospitalization; evaluate NGF and VEGF levels at birth/admission in relation to selected mares’ and foals’ clinical parameters; evaluate the relationship between the two trophic factors and thyroid hormone levels in the first 72 h of life/hospitalization; assess the mRNA expression of NGF, VEGF and BDNF, and their cell surface receptors, in the placenta of mares that delivered affected foals. The close relationship between the two trophic factors in foal plasma over time and their fine expression in placental tissues under physiological conditions appear to be key regulators of fetal development and adaptation. Their less pronounced decrease in compromised foals compared to healthy ones, their relationship with thyroid hormones over time, and the reduced expression of NGF and BDNF in placental tissues, could be key regulators in the mechanisms of NE.

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O objeto começa explicando que o puerpério é o período que inicia logo após a expulsão total da placenta e das membranas ovulares e se estende até o retorno das condições normais pré-gravídicas, durando em torno de seis a oito semanas ou mais, dependendo da duração da lactação. Lembra que as unidades de saúde devem desenvolver práticas educativas e de assistência que promovam o aleitamento materno. Convida a revisitar conteúdos acerca dos fenômenos regressivos do puerpério (involução uterina e loqueação), fenômeno progressivo (lactação) e também sobre as modificações locais e sistêmicas, decorrentes da gestação e recuperação do parto, e tempo de recuperação e cuidados no puerpério. Destaca que as Equipes de Saúde da Família devem conhecer as políticas públicas e a situação nacional e local da prevalência e da duração do aleitamento materno, além de estar devidamente capacitados para o manejo clínico da amamentação. Finaliza lembrando que o Ministério da Saúde tem publicado materiais abordando as diferentes dimensões dessa prática, todos podendo ser localizados na biblioteca virtual do MS e faz uma recapitulação da Rede Amamenta Brasil. Unidade 5 do módulo 6 que compõe o Curso de Especialização em Saúde da Família.

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Durante a gravidez, é importante garantir a saúde do binômio mãe e feto, para isso quanto mais precoce for confirmado a gravidez deve ser iniciado o acompanhamento, pré-natal. Após o parto, é mantido o acompanhamento da mãe, período esse chamado de puerpério. O puerpério vai desde a dequitação da placenta até o momento que os órgãos da mãe retornam para o seu período prégravídico. Este trabalho tem por objetivo melhorar a assistência pré-natal e puerpério na UBS dos Guarapes, Natal/RN. Trabalhamos da seguinte forma: visita as puérperas tanto pela enfermeira quanto pela médica, ACS e técnica de enfermagem. O atendimento das grávidas tanto pela médica quanto pela enfermeira. Na assistência pré-natal foram solicitados os exames sorológicos, prescrito ácido fólico e sulfato ferroso, aferição de pressão, medição da altura uterina e pesagem. As gestantes receberam orientações através de palestras sobre importância do prénatal, aleitamento materno, higienização e saúde bucal, parto e puerpério, doenças sexuais. No puerpério fizemos as visitas domiciliares para acompanhar a recuperação das puérperas, orientar sobre os cuidados com o recém-nascido e lembrar a consulta de 42 dias pós-parto. Foram realizados os exames das mamas, ginecológico e do abdômen nas puérperas. Os problemas enfrentados na UBS foram a falta de água e materiais que impossibilitaram a realização do exame de citopatologia oncótica e o tratamento odontológico adequado na unidade. Os resultados que tivemos com a intervenção foi uma maior capacitação dos profissionais trabalhando em equipe e compartilhando conhecimento de forma multidisciplinar. No terceiro mês do projeto, foi observado um maior numero de grávidas que iniciaram o pré-natal no primeiro trimestres; todas as grávidas passaram pelo menos na primeira consulta com o dentista. O índice de faltosas foram zero. A intervenção também contribuiu para aproximar a comunidade da UBS, as grávidas se sentiam a vontade para tirar suas dúvidas, participar das palestras e não faltaram as consultas. A ficha espelho anexada ao prontuário, as palestras semanais foram incorporadas a rotina da unidade.

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Período pós-parto ou puerpério se inicia após a dequitação da placenta,é o intervalo entre o parto e a volta do corpo da mulher ao estado anterior à gestação. Ajustes fisiológicos e psicológicos começam a surgir nesse período. Nesse sentido o objetivo de estudo se definiu como: O absenteísmo das puérperas á consulta de enfermagem no puerpério em uma Unidade De Saúde da Família. Esta situação problema se definiu: O que faz com que as puérperas não compareça as consultas de puerpério? A partir desta problemática surgiram as seguintes situações norteadoras: Qual a importância da consulta puerperal? Que ações a enfermagem vem desenvolvendo para resolver essa questão, em relação ao absenteísmo, na consulta puerperal? Definimos como objetivo geral: abordar os motivos pelos quais as puérperas não procuram a consulta em uma Unidade de Saúde da Família justifica-se e relava-se esta pesquisa no momento em que a humanização da atenção a saúde é um processo continuo e demanda reflexão permanente sobre os atos e condutas. Busca o acolhimento em todos os níveis de assistência, com orientação sobre os problemas apresentados e possíveis soluções assegurando-lhe a participação nos processos de decisão em todos os momentos de atendimento e tratamentos necessários. No tratamento dos dados coletados obtivemos quatro áreas temáticas que foram discutidas a luz do referencial teórico.concluiu-se que:o trabalho buscou identificar as causas do absenteísmo d mulher na consulta puerperal e teve como resultado a falta de orientação por parte dos profissionais de saúde á clientela especifica foco desta pesquisa.

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A Sífilis e a Sífilis Congênita tem sido um sério problema de saúde pública no nosso país. O Ministério da Saúde estima que de 3 a 4% das gestantes no país sejam portadoras do agente causador da Sífilis, o que pode ter como consequência a contaminação do feto através da placenta. A necessidade constante de vigilância e melhora da qualidade da assistência pré-natal devem ser os norteadores da assistência que culminará com a redução da Incidência da Sífilis Congênita para 1 caso para cada 1.000 nascidos vivos, conforme preconizado pelo Ministério da Saúde. Introdução: A sífilis segundo Ministério da Saúde é uma doença infectocontagiosa sistêmica, de evolução crônica. A sífilis congênita é a infecção do feto pelo Treponema Pallidum, transmitida pela via placentária em qualquer momento da gestação ou estágio clínico da doença em gestante não tratada ou inadequadamente tratada. Objetivo: Discorrer sobre aspectos científicos, epidemiológicos, preventivos, diagnóstico e de tratamentos relativos à Sífilis e da Sífilis Congênita. O percurso metodológico: Este estudo caracterizou-se por ser uma revisão bibliográfica de natureza exploratória, descritiva e método qualitativo, constituído de levantamento bibliográfico exploratório, ensejando pesquisa científica. Foram utilizados artigos publicados nos sites da Biblioteca Virtual de Saúde, Base de dados: Lilacs, SciELO, Bireme etc, livros que tratam do tema, além de Manuais do Ministério da Saúde. Foram utilizadas publicações do ano 2000 até 2010. Descritores: Sífilis, Sífilis Congênita, Prevenção e Controle, Vigilância Epidemiológica. Conclusão: Existe uma subnotificação da Sífilis em gestantes no país o que leva a crer que pela ausência do diagnóstico nas mães ou mesmo quando há diagnóstico, muitas delas não são adequadamente tratadas levando então ao grande número de nascimento de crianças com Sífilis Congênita.

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A toxoplasmose tem importância médica de destaque na gravidez devido ao risco de infecção fetal. Em geral, a doença congênita é oligossintomática e a chance de transmissão aumenta com o avançar da gravidez, quando o impacto da infecção no feto é menor, mas pode evoluir com sequelas tardias, como cegueira, surdez, retardo mental e psicomotor. Se adquirida no início da gestação a doença pode ser devastadora, acarretando desde abortos a óbitos fetais, causados principalmente por graves lesões inflamatórias na placenta e no sistema nervoso central (SNC). A população que faz parte da área de abrangência da unidade de saúde PSF4 - Unidade Básica de Saúde da Família Bolívar José Santana (Canápolis - MG) possui condições econômicas, em sua média, desfavoráveis, e é observada, de forma geral, uma necessidade de abordagem das gestantes quanto a sua vulnerabilidade em relação à toxoplasmose. A cidade de Canápolis não possui informações que possibilitem quantificar ou descrever estatisticamente este processo. Assim, a susceptibilidade das gestantes em relação ao Toxoplasma gondii mostra-se um problema relevante através da observação ativa e contínua na rotina da UBS. Este projeto visa elaborar um plano de intervenção visando interromper atitudes de risco entre gestantes susceptíveis a Toxoplasmose. O projeto foi desenvolvido baseado na observação diária da unidade, discussão com a equipe de saúde e anotações do motivo que levavam as gestantes a procurarem a unidade de saúde, entre os meses de abril e julho de 2015 no município de Canápolis. Foi também realizado levantamento bibliográfico de artigos científicos, livros e textos indexados sobre o tema a partir dos descritores: toxoplasmose congênita, saúde coletiva, gestante, saúde da mulher, susceptibilidade. Para a elaboração do plano de intervenção foi utilizado o Método do Planejamento Estratégico Situacional (PES). Concluiu-se que o plano de ação viabilizou a execução de ações preventivas para a Toxoplasmose Congênita e, por conseguinte, todas as sequelas e implicações que a doença traz para o concepto e a família.