968 resultados para Chronic lymphoproliferative disorders. Immunophenotyping. Immune system lymphoma
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The hamster check pouch is an invagination of oral mucosa, characterized histologically as skin-like. In this paper we describe anatomical, histological and embriological features of the pouch and coment on the pouch as an immunologically privileged site since it lacks lymphatic drainage and has few Langerhans cells. We present the review from literature and our observations after inoculation in the pouch of mycobacteriae (BCG, Mycobacterium tuberculosis and Mycobacterium leprae) and a fungus (Paracoccidioides brasiliensis). Lesions in the pouch were granulomatous but smaller and long lasting; even granulomatous, the reaction was inefficient to control the proliferation of agents compared with inoculation in other sites, except for BCG. Appearance of immunity was also delayed or absent and, when it was detected, a sharp decrease in number of agents in pouch lesions was observed. These observations make the pouch an interesting site for the study of the role of immune system in infeccious diseases and in granuloma formation.
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Evaluation of TNF-alpha in patients with Kala-azar has drawn increasing interest due to its regulatory role on the immune system, in addition to its cachetizing activity. The objective of this study was to examine the association between plasma levels of TNF-alpha, measured by immunore-activity (ELISA) and bioactivity (cytotoxicity assay with L-929 cells), and clinical manifestations of visceral leishmaniasis. Plasma samples from 19 patients with Kala-azar were obtained before, during and at the end of antimonial therapy. TNF-alpha determinations was done by using the cytotoxicity assay (all patients) and the enzyme-linked immunoassay (ELISA - 14 patients). A discrepancy between results obtained by ELISA and cytotoxicity assay was observed. Levels of circulating TNF-alpha, assessed by ELISA, were higher in patients than in healthy controls, and declined significantly with improvement in clinical and laboratory parameters. Plasma levels before treatment were 124.7 ± 93.3 pg/ml (mean ± SD) and were higher than at the end of therapy 13.9 ± 25.1 pg/ml (mean ± SD) (p = 0.001). In contrast, plasma levels of TNF-alpha evaluated by cytotoxicity assay did not follow a predicted course during follow-up. Lysis, in this case, might be not totally attributed to TNF-alpha. The discrepancy might be attributed to the presence of factor(s) known to influence the release and activity of TNF-alpha.
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Parasitic diseases which during their course in the host switch the immune system from a T helper 1 to a T helper 2 response may be detrimental to the host, contributing to granuloma formation, eosinophilia, hyper-IgE, and increased susceptibility to bacterial and fungal infections. Patients and animals with acute schistosomiasis and hyper-IgE in their serum develop pyogenic liver abscess in the presence of bacteremia caused by Staphylococcus aureus. The Salmonella-S. mansoni association has also been well documented. The association of tropical pyomyositis (pyogenic muscle abscess) and pyogenic liver abscess with Toxocara infection has recently been described in the same context. In tropical countries that may be an interesting explanation for the great morbidity of bacterial diseases. If the association of parasitic infections and pyogenic abscesses and/or fungal diseases are confirmed, there will be a strong case in favor of universal treatment for parasitic diseases to prevent or decrease the morbidity of superinfection with bacteria and fungi.
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Listeria monocytogenes, etiological agent of severe human foodborne infection, uses sophisticated mechanisms of entry into host cytoplasm and manipulation of the cellular cytoskeleton, resulting in cell death. The host cells and bacteria interaction may result in cytokine production as Tumor Necrosis Factor (TNF) alpha. Hepatocytes have potential to produce pro-inflammatory cytokines as TNF-alpha when invaded by bacteria. In the present work we showed the behavior of hepatocytes invaded by L. monocytogenes by microscopic analysis, determination of TNF-alpha production by bioassay and analysis of the apoptosis through TUNEL technique. The presence of bacterium, in ratios that ranged from 5 to 50,000 bacteria per cell, induced the rupture of cellular monolayers. We observed the presence of internalized bacteria in the first hour of incubation by electronic microscopy. The levels of TNF-alpha increased from first hour of incubation to sixth hour, ranging from 0 to 3749 pg/mL. After seven and eight hours of incubation non-significant TNF-alpha levels decrease occurred, indicating possible saturation of cellular receptors. Thus, the quantity of TNF-alpha produced by hepatocytes was dependent of the incubation time, as well as of the proportion between bacteria and cells. The apoptosis rate increased in direct form with the incubation time (1 h to 8 + 24 h), ranging from 0 to 43%, as well as with the bacteria : cells ratio. These results show the ability of hepatocyte invasion by non-hemolytic L. monocytogenes, and the main consequences of this phenomenon were the release of TNF-alpha by hepatocytes and the induction of apoptosis. We speculate that hepatocytes use apoptosis induced by TNF-alpha for release bacteria to extracellular medium. This phenomenon may facilitate the bacteria destruction by the immune system.
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In order to determine the role of lysozyme, an antimicrobial peptide belonging to the innate immune system, against the dimorphic fungus Paracoccidioides brasiliensis, co-cultures of the MH-S murine alveolar macrophages cell line with P. brasiliensis conidia were done; assays to evaluate the effect of physiological and inflammatory concentrations of lysozyme directly on the fungus life cycle were also undertaken. We observed that TNF-α-activated macrophages significantly inhibited the conidia to yeast transition (p = 0.0043) and exerted an important fungicidal effect (p = 0.0044), killing 27% more fungal propagules in comparison with controls. Nonetheless, after adding a selective inhibitor of lysozyme, the fungicidal effect was reverted. When P. brasiliensis propagules were exposed directly to different concentrations of lysozyme, a dual effect was observed. Physiologic concentrations of the enzyme facilitated the conidia-to-yeast transition process (p < 0.05). On the contrary, inflammatory concentrations impaired the normal temperature-dependant fungal transition (p < 0.0001). When yeast cells were exposed to lysozyme, irrespective of concentration, the multiple-budding ability was badly impaired (p < 0.0001). In addition, ultra-structural changes such as subcellular degradation, fusion of lipid vacuoles, lamellar structures and interruption of the fibrilar layer were observed in lysozyme exposed conidia. These results suggest that lysozyme appears to exert a dual role as part of the anti-P. brasiliensis defense mechanisms.
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Visceral leishmaniasis is caused by protozoan parasites of the Leishmania donovani complex. During active disease in humans, high levels of IFN-γ and TNF-α detected in blood serum, and high expression of IFN-γ mRNA in samples of the lymphoid organs suggest that the immune system is highly activated. However, studies using peripheral blood mononuclear cells have found immunosuppression specific to Leishmania antigens; this poor immune response probably results from Leishmania antigen-engaged lymphocytes being trapped in the lymphoid organs. To allow the parasites to multiply, deactivating cytokines IL-10 and TGF-β may be acting on macrophages as well as anti-Leishmania antibodies that opsonize amastigotes and induce IL-10 production in macrophages. These high activation and deactivation processes are likely to occur mainly in the spleen and liver and can be confirmed through the examination of organ samples. However, an analysis of sequential data from studies of visceral leishmaniasis in hamsters suggests that factors outside of the immune system are responsible for the early inactivation of inducible nitric oxide synthase, which occurs before the expression of deactivating cytokines. In active visceral leishmaniasis, the immune system actively participates in non-lymphoid organ lesioning. While current views only consider immunocomplex deposition, macrophages, T cells, cytokines, and immunoglobulins by diverse mechanism also play important roles in the pathogenesis.
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In order to better understand the biology of Centrocestus formosanus in a definitive host model, mice of Swiss and AKR/J strains were experimentally infected with 100 metacercariae of the parasite. Fourteen days post-infection, the rodents were killed and adult trematodes were recovered from the small intestine. The percentage of parasite recovery from AKR/J mice (11.4%) was significantly higher than that from Swiss mice (5.3%). Moreover, trematodes recovered from the AKR/J strain were more developed and had greater fecundity. Peculiarities concerning the mice’s immune system could explain the difference in susceptibility and in worm development seen in the present study. The data obtained confirm that mice are susceptible to infection with C. formosanus and indicate that the AKR/J strain provides a more favorable environment for parasite development.
TUBERCULOSIS INFECTION MIGHT INCREASE THE RISK OF INVASIVE CANDIDIASIS IN AN IMMUNOCOMPETENT PATIENT
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Deep Candida infections commonly occur in immunosuppressed patients. A rare case of a multiple deep organ infection with Candida albicansand spinal tuberculosis was reported in a healthy young man. The 19-year-old man complained of month-long fever and lower back pain. He also had a history of scalded mouth syndrome. Coinfection with Mycobacterium tuberculosis and Candida albicans was diagnosed using the culture of aspirates from different regions. Symptoms improved considerably after antifungal and antituberculous therapy. This case illustrates that infection with tuberculosis might impair the host's immune system and increase the risk of invasive candidiasis in an immunocompetent patient.
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Despite its efficacy, including in the prevention of vertical transmission, the antiretroviral nevirapine is associated with severe idiosyncratic hepatotoxicity and skin rash. The mechanisms underlying nevirapine toxicity are not fully understood, but drug bioactivation to reactive metabolites capable of forming stable protein adducts is thought to be involved. This hypothesis is based on the paradigm that drug reactive metabolites have the potential to bind to self-proteins, which results in drug-modified proteins being perceived as foreign by the immune system. The aim of the present work was to identify hemoglobin adducts in HIV patients as biomarkers of nevirapine haptenation upon bioactivation. The ultimate goal is to develop diagnostic methods for predicting the onset of nevirapine-induced toxic reactions. All included subjects were adults on nevirapine-containing antiretroviral therapy for at least 1month. The protocol received prior approval from the Hospital Ethics Committees and patients gave their written informed consent. Nevirapine-derived adducts with the N-terminal valine of hemoglobin were analyzed by an established liquid chromatography-electrospray ionization-tandem mass spectrometry method and characterized on the basis of retention time and mass spectrometric fragmentation pattern by comparison with adduct standards prepared synthetically. The nevirapine adducts were detected in 12/13 patient samples, and quantified in 11/12 samples (2.580.8 fmol/g of hemoglobin). This work represents the first evidence of nevirapine-protein adduct formation in man and confirms the ability of nevirapine to modify self-proteins, thus providing clues to the molecular mechanisms underlying nevirapine toxicity. Moreover, the possibility of assessing nevirapine-protein adduct levels has the potential to become useful for predicting the onset of nevirapine-induced adverse reactions.
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SUMMARY Cerebral toxoplasmosis can be highly debilitating and occasionally fatal in persons with immune system deficiencies. In this study, we evaluated the Toxoplasma gondii-specific IgG subclass antibody response in 19 cerebrospinal fluid (CSF) samples from patients with cerebral toxoplasmosis who had a positive IgG anti-T. gondii ELISA standardized with a cyst antigen preparation. There were no significant differences between the rates of positivity and the antibody concentrations (arithmetic means of the ELISA absorbances, MEA) for IgG1 and IgG2, but the rates of positivity and MEA values for these two IgG subclasses were significantly higher than those for IgG3 and IgG4. The marked IgG2 response in CSF from patients with cerebral toxoplasmosis merits further investigation.
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Dissertation presented to obtain the Ph.D. degree in Biochemistry
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Dissertation presented to obtain the PhD degree in Biology
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RESUMO:Aterosclerose uma das principais causas de morbilidade e mortalidade no mundo ocidental. responsvel, direta ou indiretamente, pela maior percentagem de gastos com a sade na maioria dos pases europeus. A teoria lipdica da aterosclerose, que se baseia na dislipidemia como causa primria para a doena vascular tem algumas implicaes prticas importantes: permite a definio de linhas de orientao e protocolos simples e ainda estabelece alvos teraputicos que podem ser atingidos na maior parte dos casos com a atual interveno farmacolgica. A associao da aterosclerose com o sistema imunolgico (a teoria imunolgica), forneceu por sua vez novas formas de explorar os mecanismos envolvidos e abriu novas perspetivas para um conhecimento mais completo da doena. No entanto, levanta dificuldades evidentes no que diz respeito s possibilidades teraputicas. De todos os intervenientes no processo aterosclertico (bioqumicos, imunolgicos e anatmicos), as lipoprotenas de elevada densidade (HDL) so atualmente reconhecidas como um dos fatores mais importantes na aterognese. Isto baseado no reconhecimento das mltiplas propriedades anti-aterognicas das HDL como por exemplo: a anti-oxidante, a anti-inflamatria e a antitrombtica, bem como o seu importante papel na melhoraria da funo endotelial. Atualmente, consensual que as funes anti-aterognicas das HDL vo alm do seu papel no transporte reverso do colesterol (RCT) e a importncia das HDL no processo aterosclertico baseia-se no apenas no seu papel protetor impedindo a formao da placa de ateroma, mas tambm na estabilizao destas, prevenindo a sua ruptura e, consequentemente o evento trombtico. Como fundamentais no processo aterosclertico esto reconhecidos dois principais conjuntos de eventos: um caracterizado por alteraes no metabolismo das lipoprotenas que resultam em lipoprotenas pr-inflamatrias e pr-oxidantes que interagem com os componentes celulares da parede arterial e que conduzem formao da placa de ateroma; o outro evento a resposta imunolgica desencadeada contra um novo conjunto de antignios que por sua vez leva produo de citoquinas pr-inflamatrias. Dada a complexidade da HDL e das suas mltiplas funes estas lipoprotenas tornaram-se um potencial alvo para a resposta auto-imune, e cujas consequncias podem explicar algumas das associaes identificados em estudos clnicos e epidemiolgicos. Contudo esta interao entre o sistema imunolgico e HDL nunca foi exaustivamente estudada. Portanto, pomos a hiptese de que em condies oxidativas e pr-inflamatrias, um aumento do antignio (HDL) conduz a um consequente acrscimo na produo de anticorpos anti-HDL (aHDL) responsveis pela alterao quantitativa e / ou qualitativa das HDL. O conceito de que estes anticorpos podem contribuir tanto para a evoluo a longo prazo do processo aterosclertico, como para o desencadeamento de eventos clnicos pode tambm explicar a heterogeneidade encontrada em cada doente e nos grandes estudos clnicos, no que diz respeito aos fatores de risco e outcomes clnicos. Para alm disso, a confirmao desta hiptese pode permitir explicar porque que as intervenes teraputicas atualmente em desenvolvimento para aumentar os nveis de HDL, no conseguem mostrar a to esperada reduo do risco vascular. O objetivo geral desta tese foi identificar e caracterizar a resposta humoral contra os componentes da HDL, e avaliar possveis mecanismos que possam contribuir para a modificao das propriedades anti-aterognicas das HDL. Para alcanar este objetivo investigou-se: 1) A presena de anticorpos aHDL em doentes com lpus eritematoso sistmico (SLE) e em doentes com manifestaes clnicas de aterosclerose, como os doentes com doena arterial coronria (CAD), acidente vascular cerebral isqumico (IS) e diabetes tipo 2; 2) Os principais alvos antignicos dentro do complexo das HDL e a associao entre os ttulos de anticorpos aHDL e diferentes caractersticas clnicas destas doenas; 3) As modificaes das funes normais associadas s HDL, em particular da funo anti-oxidante e anti-inflamatria; 4) A atividade biolgica dos anticorpos aHDL isolados do soro de doentes atravs de um conjunto de experincias in vitro de inibio da atividade da paraoxonase 1 (PON1) e da expresso de molculas de adeso em culturas de clulas endoteliais. Para tal foi necessrio estabelecer um mtodo de isolamento dos anticorpos. Os anticorpos aHDL isolados do soro de doentes foram utilizados de forma a identificar as potenciais alteraes dos sistemas celulares utilizados; 5) O efeito de frmacos usados no tratamento das dislipidemias, em particular o cido nicotnico e as estatinas, na variao dos ttulos de anticorpos aHDL atravs de ensaios clnicos randomizados, controlados com placebo e em dupla ocultao. Os mtodos utilizados neste trabalho incluram: tcnicas imunolgicas (como por exemplo, enzyme-linked immunoabsorbent assay - ELISA, ensaio imunoturbidimetrico e cromatografia de imuno-afinidade) tcnicas bioqumicas (tais como a quantificao de atividade enzimtica por espectrofotometria e por luminescncia), experincias com cultura de clulas e citometria de fluxo. Os nossos resultados mostram que: 1) A presena de anticorpos aHDL, e mais especificamente anticorpos contra alguns do seus principais componentes como a apolipoprotena A-I (ApoA-I, principal apolipoprotena presente nas HDL) e a PON1 (o enzima que mais contribui para a propriedade anti-oxidante das HDL), quer em doentes com doenas auto-imunes, como o SLE, quer em doentes com manifestaes clnicas de aterosclerose, como CAD, IS e diabetes tipo 2. Os doentes apresentaram ttulos de anticorpos IgG aHDL, aApoA-I e aPON1 significativamente mais elevados do que controlos saudveis com a mesma idade e sexo. 2) A correlao positiva estatisticamente significativa entre os ttulos de aHDL e aApoA-I e aPON1 sugere que estes sejam dois dos principais alvos antignicos dentro do complexo das HDL. Os anticorpos encontrados nestes doentes esto associados com a diminuio da atividade da PON1 e a uma reduo da capacidade anti-oxidante total (TAC) do soro, um aumento dos biomarcadores de disfuno endotelial (como por exemplo dos metabolitos do xido ntrico - NO2- e NO3-, as molculas de adeso vascular e intracelular - VCAM-1 e ICAM-1 e os nveis de 3-nitrotirosina). Nos doentes com SLE os ttulos destes esto associados a um aumento do dano cardiovascular e atividade global da doena avaliados pelas escalas SLICC/ACR DI e BILAG score, respetivamente. Enquanto que nos doentes com diabetes tipo 2 estes anticorpos esto associados com um aumento dos nveis de glicemia em jejum (FGP) e hemoglobina glicada (HbA1c). 3) Aps se ter estabelecido um mtodo de isolamento dos anticorpos que permite isolar quantidades significativas de anticorpos do soro de doentes sem perder a sua especificidade, foi identificada a capacidade dos anticorpos isolados do soro de doentes inibirem de uma forma dependente da concentrao a atividade da PON1 at um mximo de 70% no caso dos doentes com SLE e ente 7-52% no caso dos anticorpos isolados de doentes com CAD e IS. 4) O efeito anti-inflamatrio das HDL na inibio da produo de VCAM-1 induzida por citoquinas (como o TNF-) foi revertido em mais de 80% pelos anticorpos aHDL isolados do soro de doentes. 5) A angiogenesis induzida por HDL atravs do aumento do fator de crescimento do endotlio vascular (VEGF) foi anulada em 65% pelos anticorpos aHDL isolados do soro de doentes. 6) Os atuais agentes farmacolgicos disponveis para aumentar as concentraes de HDL-C esto associados a um aumento dos ttulos de anticorpos.-------- ABSTRACTAtherosclerosis is the major cause of morbidity and mortality in the western world. It is also responsible, directly or indirectly, for the highest percentage of health costs in most European countries. Despite the use of new technologies for the diagnosis of vascular disease and regardless of the major advances in treatment, the atherosclerosis-related clinical burden is still raising. The lipid theory of atherogenesis, which identifies dyslipidemia as the primary cause of this vascular disease has some important practical implications: it allows the definition of simple guidelines and establishes therapeutic targets which can be generally met with current pharmacologic intervention. The association between atherosclerosis an the immune system (the immune concept) has in turn provided new ways of exploring the mechanisms involved in this condition and has opened new perspectives in the understanding of the disease. However, it raises obvious difficulties when it comes to treatment options. Of all the players (biochemical, immunological and anatomical) involved in this matter, high-density lipoproteins (HDL) are currently recognised as one of the most important factors in atherogenesis. This is based on the recognition of HDL's multiple anti-atherogenic properties: anti-oxidant, anti-inflammatory and antithrombotic, as well as its capacity to improve endothelial function. Nowadays, it is widely recognized that the anti-atherogenic functions of HDL go beyond reverse cholesterol transport (RCT), and the importance of HDL is based not just on its ability to reduce atheroma formation but also on its ability to stabilise plaques, therefore preventing their rupture and ultimately thrombosis. Two main set of events have been recognised as fundamental in atherogenesis: one, characterized by lipoprotein metabolism alterations, resulting in pro-inflammatory and pro-oxidative lipoproteins, which interact with the normal cellular elements of the arterial wall leading to atheroma formation; the other, the immune cellular response towards new sets of antigens which lead to the production of pro-inflammatory cytokines. Given to HDL complexity and multiple functions this lipoprotein has became a potential target for an auto-immune response, the consequences of which may explain some of the association identified in epidemiological and clinical studies, though the interaction between the immune system and HDL has never been thoroughly addressed. Therefore, we hypothesized that under oxidative and pro-inflammatory conditions, the increase in the antigen (HDL) would lead to a consequent increase in the production of anti-HDL (aHDL) antibodies be responsible for quantitative and/or qualitative changes of HDL. The concept that these antibodies may contribute either to the long-term evolution of atherosclerosis or to the triggering of clinical events may also explain the heterogeneity found in individual patients and in large cohorts regarding risk factors and clinical outcomes. Moreover this may be a major breakthrough in understanding why therapeutic interventions that increase HDL levels, failed to show the anticipated reduction in vascular risk. The overall aims of this thesis were to identified and characterize the humoral response towards HDL components and to evaluate the possible mechanisms that may contribute to the modifications of the anti-atherogenic properties of HDL. To achieve this objective we investigated: 1) the presence of aHDL antibodies in patients with systemic lupus erythematosus (SLE) and in patients with atherosclerosis-related clinical events, such as coronary artery disease (CAD), ischemic stroke (IS) and type 2 diabetes; 2) the association between the titres of aHDL antibodies and different clinical features of these diseases; 3) the modifications of the anti-atherogenic properties of HDL; 4) the biologic effect of aHDL antibodies isolated from serum of patients on the anti-oxidant and anti-inflammatory properties of HDL; 5) the effect of different pharmacologic treatments for dyslipidemia on the prevalence and activity of aHDL antibodies. The methodologies used in this work included immunologic-related techniques (e.g. enzyme-linked immunoabsorbent assay ELISA, immunoturbidimetric immunoassay and immunoaffinity chromatography), biochemical techniques (enzymatic assays with quantification by spectrophotometry and luminescence methods), cell culture experiments and flow cytometry. Our results indicate that: 1) The titres of IgG aHDL, anti-apolipoprotein A-I (aApoA-I) and anti-paraoxonase 1 (aPON1) antibodies were higher in patients with SLE, CAD, IS and type 2 diabetes when compared with age and sex matched healthy controls. 2) The antibodies found in these patients were associated with decreased PON1 activity, (the enzyme responsible for most of the anti-oxidant effect of HDL), reduced total anti-oxidant capacity (TAC) of serum and increased biomarkers of endothelial dysfunction (nitric oxide metabolites, adhesion molecules, nitrotyrosine). In patients with SLE the antibody titres were associated with an increase in disease-related cardiovascular damage and activity whereas in patients with type 2 diabetes they were directly related with the fasting glucose plasma (FGP) levels and the glycosylated haemoglobin (HbA1c). 3) The antibodies isolated from serum of our patients, directly inhibited HDL-associated PON1 activity in a dose dependent way ranging from 7 to 52%. 4) The anti-inflammatory effect of HDL, measured by the percentage of inhibition of the cytokine-induced production of vascular adhesion molecules (VCAM-1), was reduced in more than 80% by aHDL antibodies isolated from our patients. 5) The HDL-induced angiogenesis by increasing vascular endothelial growth factor (VEGF) levels was abrogated in 65% by the antibodies isolated from serum of patients. 6) The current available pharmacologic agents for increasing HDL-C concentrations were associated with an increase in the titres of IgG aApoA-I antibodies. This increase was higher in the extended release niacin when compared to statins probably due to their dampening effect on oxidative stress. In conclusion, aHDL antibodies are present in different pathologic conditions. aHDL antibodies represent a family of self-reacting immunoglobulins, of which ApoA-I and PON1 might be the most relevant targets. These antibodies are biologically active, interfering with the HDL anti-oxidant and anti-inflammatory properties and, consequently, with the atherosclerotic process. The pathogenic potential of these antibodies may lead to the identification of a new biomarker for vascular disease, whilst presenting itself as a novel target for a different treatment approach which may redefine the treatment strategies and clinical trials design for HDL interventions in the future.
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RESUMO - O gnero Listeria contm oito espcies (L. monocytogenes, L. ivanovii, L. innocua, L. seeligeri, L. welshimeri, L. grayi, L. marthii, e a L. rocoutiae), das quais duas so patognicas. L. monocytogenes patognica para humanos e animais; L. ivanovii primeiramente infecta animais e raramente causa doenas em humanos. A Listeria monocytogenes uma bactria patognica Gram-positiva facultativa intracelular, ubqua na natureza. Nos ltimos anos o nmero de casos de listeriose tem vindo a aumentar. Pode causar uma doena rara e grave chamada listeriose, especialmente nas mulheres grvidas, nos idosos ou em indivduos com o sistema imunitrio debilitado, de maneira espordica ou em forma surtos. Realizou-se um estudo observacional, descritivo com o objectivo de se fazer a descrio e a caracterizao do surto de listeriose ocorrido na regio de Lisboa e Vale do Tejo entre 2009-2011. O perodo de maior nmero de casos diagnosticados de listeriose ocorreu entre o ms de Abril e Agosto de 2010. Mas a janela temporal em que ocorreu o surto estendeu-se de Maro de 2009 a Janeiro de 2012. Ocorreram 51 casos de internamento com diagnstico de listeriose, dos quais 25 casos foram confirmados, pela tcnica de PFGE, pertencer mesma estirpe I, sorotipo 4b e pulsotipo 070 e 0101. Na maioria dos casos eram do sexo feminino, com uma mdia de 57,14 anos de idade e com residncia na regio de Lisboa e Vale do Tejo. Em 96,08% dos doentes internados com listeriose apresentavam factores de predisposio, comorbilidade e /ou imunossupresso. A bacteriemia foi a manifestao clnica mais frequente, seguida da meningite. A letalidade da listeriose foi de 15,69%.
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Dissertation presented to obtain the Ph.D degree in Biology.
