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Background Extended-spectrum β-lactamases (ESBLs) are increasingly prevalent in Enterobacter spp., posing a challenge to the treatment of infections caused by this microorganism. The purpose of this retrospective study was to evaluate the prevalence, risk factors, and clinical outcomes of inpatients with bacteremia caused by ESBL and non ESBL-producing Enterobacter spp. in a tertiary hospital over the period 2004–2008. Methods The presence of bla CTX-M , bla TEM , bla SHV , and bla PER genes was detected by polymerase chain reaction (PCR) and nucleotide sequence analysis. Genetic similarity between strains was defined by pulsed-field gel electrophoresis (PFGE). Results Enterobacter spp. was identified in 205 of 4907 of the patients who had positive blood cultures during hospitalization. Of those cases, 41 (20%) were ESBL-producing Enterobacter spp. Nosocomial pneumonia was the main source of bacteremia caused by ESBL-producing Enterobacter spp. The presence of this microorganism was associated with longer hospital stays. The ESBL genes detected were: CTX-M-2 (23), CTX-M-59 (10), CTX-M-15 (1), SHV-12 (5), and PER-2 (2). While Enterobacter aerogenes strains showed mainly a clonal profile, Enterobacter cloacae strains were polyclonal. Conclusion Although no difference in clinical outcomes was observed between patients with infections by ESBL-producing and non-ESBL-producing strains, the detection of ESBL in Enterobacter spp. resulted in the change of antimicrobials in 75% of cases, having important implications in the decision-making regarding adequate antimicrobial therapy.

Extended-spectrum β-lactamases (ESBL) are plasmid-mediated enzymes that hydrolyze cephalosporins and monobactams. The lack of a standard method to detect ESBL in Enterobacter spp. has led to underestimating its frequency. The aim of this study was to evaluate ESBL detection in Enterobacter spp. By the double-disk synergy test (DDST) and combined disk test (CDT) assay using cefepime, cefotaxime, and ceftazime as substrates for ESBL, plus AmpC inhibitors in different associations. A total of 83 Enterobacter spp. ESBL and 31 non-ESBL Enterobacter spp. were tested, and a cutoff point ≥3 mm was defined using a receiver operating characteristic (ROC) curve for combined disc methods. All tests showed 100% specificity. The sensitivity was 89.2% for DDST and CDT without AmpC inibitor, 90.4% in the combined disc test in Mueller-Hinton agar containing phenylboronic acid (CDT-PBAA), and 94% in the combined disc test in Mueller-Hinton agar containing cloxacillin (CDT-CLXA). Cefepime was the best substrate, mainly when AmpC inhibitors were not used. However, superior results were achieved when all cephalosporins were evaluated together. In conclusion, to improve ESBL detection in Enterobacter spp., some modifications in phenotypic tests are needed, such as to reduce the distance between the discs to 20 mm in DDST, to use a cutoff point for ≥3 mm on the CDT, and to include a cefepime disk or an inhibitor of AmpC in all tests.

Clustering of autoimmune diseases is common and may be due to genetic background and exposition to environmental triggers.The aim is to carry out a laboratory and clinical study of the prevalence of gastrointestinal organ-specific autoantibodies in rheumatoid arthritis (RA) patients and their relatives.Serum samples of 156 RA patients, 200 relatives, and 100 healthy controls were studied for anti-smooth muscle antibody (ASMA), anti-mitochondrial (AMA), anti-parietal cell (APCA), anti-liver-kidney microsome (LKM), and anti-endomysium antibodies (IgA-EmA) by indirect immunofluorescence.A total of eight out of the 156 (5.1%) RA patients were positive for the autoantibodies (ASMA = 1; AMA = 2, APCA = 5). In the relative group, 12/200 (6%) had at least one positive autoantibody (ASMA = 1; AMA = 2, APCA = 7, IgA-EmA = 2). In the control group, two out of the 100 (2%) healthy controls were positive (ASMA = 1, APCA = 1). No statistical difference was found between RA patients, their relatives, and controls in relation to the frequency of autoantibodies evaluated.Although RA patients and their relatives have positivity of AMA, ASMA, and APCA without statistical difference in relation to healthy individuals, the findings may be of value for adequate clinical approach of these subjects.

Objectives. To evaluate the prevalence of anti-cyclic citrullinated peptide (anti-CCP) antibodies and RF in RA patients and their relatives from Southern Brazil. Methods. Anti-CCP2 and IgM-RF were evaluated in 156 RA patients and 200 relatives. Sera from 100 healthy unrelated individuals were used as control. The anti-CCP2 was detected by ELISA and the IgM-RF using the latex agglutination test. Results. We identified 117 anti-CCP2 (75%)-positive and 106 RF (67.9%)-positive patients. Anti-CCP2 was increased in relatives (5.5%; 11/200) when compared with unrelated individuals (1%; P = 0.050). Titre of anti-CCP2 in RA patients did not differ from relatives [140.4 (75.7) vs 115.6 (84.2) U, respectively; P = 0.30]. Positive relatives were younger than patients for anti-CCP2 (P = 0.0081), RF (P < 0.001) and both concomitantly (P = 0.012), and although there was no difference for anti-CCP2 positivity according to gender, increased RF positivity and concomitant anti-CCP2/RF were observed in the female relatives (P = 0.067 and 0.082, respectively). No difference regarding the relative degree of tobacco use in relatives was detected. Among the 11 anti-CCP2-positive relatives, 2 females had RA diagnosis established and 6 individuals presented with joint symptoms suggestive of RA. Conclusion. The results demonstrate a significant positivity of anti-CCP2 in relatives of RA patients from Brazil and reinforce the importance of serological tools to identify undiagnosed RA.

Aims: Down syndrome (DS) patients present several immunological disturbances, with high rates of infections, malignancies and autoimmune phenomena. The present study aims to evaluate the prevalence of autoantibodies in children and adolescents with DS that are not usually investigated, and to establish possible clinical and laboratory associations. Methods: One hundred and fifty Caucasoid DS patients from southern Brazil (93M, 57F; median age 4 years) and 105 healthy children (58M, 47F; median age 8 years) were evaluated for the presence of anti-mitochondrial (AMA), smooth-muscle (SMA), liver-kidney microsomal (LKM), nuclear (ANA), gastric parietal cell (GPC) and neutrophil cytoplasmic (ANCA) antibodies, by indirect immunofluorescence, and rheumatoid factor (RF), by turbidimetry. Results: Forty-three DS patients (28.6%) showed positivity to at least one autoantibody, in comparison with eight of the controls (7.6%; P

O sistema complemento e parte fundamental da imunidade inata e contribui na remocao de complexos imunes e na ativacao de processos inflamatorios. Essas proteinas representam um meio rapido e eficiente de protecao do hospedeiro contra microorganismos invasores. Associacoes entre complemento e doencas sao observadas em situacoes de deficiencia do complemento, anormalidades na regulacao do complemento e nas inflamacoes. Ativacao impropria ou excessiva do complemento pode levar a consequencias lesivas em virtude da grave destruicao tecidual inflamatoria. Evidencias clinicas e experimentais ressaltam o papel do complemento na patogenese de inumeras doencas inflamatorias, que incluem nao apenas doencas por imune-complexos e auto-imunes, como tambem falencia de orgaos subsequentes a sepse, traumas multiplos e queimaduras. O polimorfismo genetico tem sido descrito para diversos componentes de membrana, proteinas soluveis de controle e receptores do sistema complemento. Atualmente, o polimorfismo dos componentes do complemento pode ser estudado usualmente, tanto pela pesquisa fenotipica das variantes proteicas (fenotipagem) como pela caracterizacao genomica do DNA (genotipagem), e tem contribuido para o entendimento da patogenese de diferentes enfermidades. Doencas imunologicamente mediadas estao associadas as variantes alotipicas do complemento, em particular lupus eritematoso sistemico, artrite reumatoide, esclerose multipla, doenca celiaca, deficiencia de IgA e IgG4, entre outras. A presente revisao tem por objetivo dar uma visao dos conhecimentos atuais na area da genetica do complemento, bem como da participacao desse sistema na patogenia de diferentes doencas.

Purpose This study proposes to assess MBL serum concentrations in HPV positive women that developed high risk preinvasive lesions, CIN III. Materials and methods A total of 90 consecutive women (mean age 32.2 years, range 18–45 years) with CIN III lesions confirmed by cone biopsy were enrolled as cases at the gynecology cancer department of the Erasto Gaertner Hospital, a center of reference for cancer treatment in Southern Brazil. All the patients were HPV positive. In addition, 81 healthy women, voluntary blood donors, were enrolled as healthy control subjects (mean age 33.3 years, range 14–71 years) with no evidence of HPV infection, tested by hybrid capture, or CIN lesions, from the same geographic area. Results The median concentration of MBL in the cases was 912 ng/ml (IQR: 100–5820 ng/ml) and in the controls was 1207.3 ng/ml (IQR 100–4320.6 ng/ml). No statistically significant difference was observed between cases and controls. Conclusion This study reports data on MBL serum concentrations in HPV infected women for the first time. The analysis of our findings did not show a statistically significant difference between MBL serum concentrations in HPV women that developed CIN III lesions and healthy controls.

INTRODUÇÃO: A artrite reumatoide (AR) é uma doença autoimune inflamatória e crônica que afeta aproximadamente 1% da população adulta mundial. A doença caracteriza-se pela inflamação do tecido sinovial de múltiplas articulações, levando a destruição tecidual, dor, deformidades e redução na qualidade de vida do paciente. Sua etiologia é complexa e em grande parte desconhecida, porém estudos demonstram a influência de fatores genéticos e ambientais em sua patogênese. Devido à forte influência genética, familiares de pacientes com AR formam um grupo de risco para o desenvolvimento da doença, principalmente em sua forma mais grave. Apesar de seu elevado potencial incapacitante, o curso da AR pode ser modificado por meio do diagnóstico precoce e do manejo adequado do paciente. No entanto, o diagnóstico precoce da AR é ainda bastante difícil diante da heterogeneidade das manifestações clínicas da doença, o que acaba retardando a implantação terapêutica. O tratamento da AR baseia-se no uso de anti-inflamatórios não esteroidais (AINEs), corticosteroides, drogas antirreumáticas modificadoras do curso da doença (DMARD) e agentes imunobiológicos. Além da terapia medicamentosa, também são adotadas medidas como educação do paciente e terapias psico-ocupacionais. Atualmente, estudos têm se voltado à identificação de fatores preditores de doença mais grave, como autoanticorpos como fator reumatoide (FR) e anticorpo antipeptídio cíclico citrulinado (anti-CCP), que constituem importantes marcadores imunológicos de diagnóstico e prognóstico da AR. DISCUSSÃO E CONCLUSÃO: Apesar dos significativos avanços tanto no entendimento como no diagnóstico e no tratamento da AR, ainda persistem inúmeros desafios a serem superados. INTRODUCTION: Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, which affects approximately 1% of the world's adult population. It is characterized by the inflammation of synovial tissue from multiple articulations, leading to tissue destruction, pain, deformities and reduced quality of life. RA etiology is complex and largely unknown, although studies support the influence of genetic and environmental factors on its pathogenesis. Due to its major genetic component, relatives from RA patients are part of the risk group, mainly as to the development of the most severe forms. In spite of its high disability risk, RA development can be affected through early diagnosis and adequate therapy. Nonetheless, its early diagnosis is still very demanding due to the heterogeneity of its clinical presentations, which delays therapeutic approach. RA treatment includes non-steroidal anti-inflammatory drugs, corticosteroids, disease-modifying antirheumatic drugs (DMARD), and immunobiologic agents. Furthermore, raising patient's awareness and developing psyco/occupational therapies are also part of the therapeutic approach. Currently, several studies focus on the identification of predictive factors for severe RA such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) autoantibodies, which are major immunological diagnostic and prognostic markers for RA. DISCUSSION AND CONCLUSION: Despite the fact that there has been substantial progress in the investigation, diagnosis and treatment of RA, there are still several challenges to be overcome.

The aim of the present study was to perform a screening for rheumatoid factor (RF) and anti-nuclear antibody in Kaingang, Guarani and Mestizos individuals from Mangueirinha Reservation, State of Paraná, Brazil, and associate it with demographic and clinical data. Serum samples from 321 aborigines (125 male and 196 female; 4-86 years old) and 180 non-Indians healthy individuals were analysed (62 male and 118 female; 2-81 years old). Antinuclear antibody (ANA) was tested by indirect immunofluorescence, and RF by agglutination in latex and turbidimetry. RF was higher in Kaingang when compared to Guarani (P = 0.009), Mestizos (P = 0.061) and non-Indians (P = 0.010). A significant increase of RF was observed in Kaingang women versus Kaingang men (P = 0.002) and, among the women, in Kaingang when compared to Mestizos and Guarani (Por= 0.008). The positivity for ANA did not show significant differences between the groups. Clinical evaluation of RF positive individuals (n = 6) confirmed rheumatoid arthritis in two Kaingang Indians. Other two individuals (RF positive) will be under medical observation, as well as two Mestizos. The differences observed among the investigated groups, suggest the influence of genetic and hormonal factors in the development of auto antibodies in these populations.

Celiac disease is the most common intestinal disorder of caucasian populations and presents a prevalence of 8% to 18% between the relatives of patients. The anti-endomysial (IgA-EmA) and anti-tissue transglutaminase antibodies (IgA-tTG) have represented an important non invasive and sensitivity method of screening and diagnosis of celiac disease in risk groups and populations.To investigate the prevalence of IgA-EmA and IgA-tTG antibodies in relatives of celiac patients and verify the degree of concordance between them.One hundred and seventy seven relatives of celiac patients (76(feminino); 101(masculino); 2-79 years) and 93 healthy individuals were evaluated (34(feminino); 59(masculino); 2-71 years). IgA-EmA were detected by indirect immunofluorescence, with human umbilical cord as substrate, while anti-IgA-tTG titers were measured by enzyme-linked immunosorbent assay (ELISA), using commercial kit.Total positivity to antibodies in relatives of celiac patients was of 21% (37/177), and showed significant difference compared to control group (0%; 0/93). Twelve percent (21/177) of celiac disease relatives were positive to IgA-EmA, 13.56% (24/177) to IgA-tTG, and 4.52% (8/177) to both assays simultaneously. The concordance between both methods was 83.6% (148/177) and the discordance was 16.4% (29/177), with a positive and significant correlation (r = 0.435). Among the concordant results, 79.1% (140/177) were negative and 4.52% (8/177) were positive to both antibodies. Among the discordant results, 7.34% (13/177) were positive to IgA-EmA and negative to IgA-tTG, while 9.04% (16/177) were negative to IgA- EmA and positive to IgA-tTG.Although the high positivity to IgA-EmA and IgA-tTG emphasizes the importance of the serological screening in relatives of celiac patients, the discordances detected in this study showed that the use of only one method can lead to false negative results. Consequently these relatives will not be submitted to intestinal biopsy to confirm the diagnosis of celiac disease, and to the correct and earlier treatment.