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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a multifactorial etiology. The primary aim of this study was to estimate HCV and HBV infection prevalence in a cohort of SLE and Cutaneous Lupus Erythematosus (CLE). We assessed the frequency of these infections in our cohort and the possible associations with disease clinical/laboratory features and disease activity status. The prevalence of chronic HBV infection was 2.2% in the CLE group, while no HBsAg positive patients were identified in the SLE group. Conversely, the prevalence of anti-HCV positive was 2.2% in the SLE group while no anti-HCV positive patients were identified in the CLE group. We found no significant association between anti-HBc positive status and clinical manifestations or disease activity status in either group of patients. Hemodialysis resulted significantly associated with anti-HBc positivity in SLE. In the present study, we found HBsAg positivity in CLE patients but not in the Systemic form (SLE); conversely, a similar prevalence of anti-HBc antibodies in both groups was observed. A possible protective role exerted by SLE in HBV infection may be hypothesized. A higher frequency of HCV infection in SLE compared to CLE suggests a possible involvement of HCV in some SLE-related clinical and immunological features.

We report the full-genome sequence of a Dengue serotype-1 virus (DENV-1) isolated from a traveller returning in July 2019 to Italy from Democratic Republic of Congo (DRC), which is currently affected by Ebola and measles outbreaks. The sequence shows high similarity with two 2013 strains isolated in Angola and China.

Background: Primary spinal infections are rare pathologies with an estimated incidence of 5% of all osteomyelitis. The diagnosis can be challenging and this might result in a late identification. The etiological diagnosis is the primary concern to determine the most appropriate treatment. The aim of this review article was to identify the importance of a methodological attitude toward accurate and prompt diagnosis using an algorithm to aid on spinal infection management. Methods: A search was done on spinal infection in some databases including PubMed, ISI Web of Knowledge, Google Scholar, Ebsco, Embasco, and Scopus. Results: Literature reveals that on the basis of a clinical suspicion, the diagnosis can be formulated with a rational use of physical, radiological, and microbiological examinations. Microbiological culture samples can be obtained by a percutaneous computed tomography-guided procedure or by an open surgical biopsy. When possible, the samples should be harvested before antibiotic treatment is started. Indications for surgical treatment include neurological deficits or sepsis, spine instability and/or deformity, presence of epidural abscess and failure of conservative treatment. Conclusion: A multidisciplinary approach involving both a spinal surgeon and an infectious disease specialist is necessary to better define the treatment strategy. Based on literature findings, a treatment algorithm for the diagnosis and management of primary spinal infections is proposed. © 2019 Medknow Publications. All rights reserved.

Objective We investigated the genetic diversity, molecular epidemiology and evolutionary dynamics of Staphylococcus aureus (SA) isolated from SLE patients by means of phylogenetic analysis. Methods Consecutive SLE patients (ACR 1997 criteria) were enrolled: clinical/laboratory data were collected and nasal swab for SA identification was performed. On the basis of the translation elongation factor (tuf) gene, a phylogenetic analysis was performed to investigate relationships and to assess significant clades. Selective pressure analysis was used to investigate the evolution of the SA tuf gene. The gene sequences from non-SLE individuals, downloaded from the GenBank database, were compared through phylogenetic analysis with the tuf gene from SLE patients. Results We enrolled 118 patients [M/F 10/108; median (interquartile range (IQR)) age 45.5 (13.2) years; median (IQR) disease duration 120 (144) months]. Twenty-four patients (20.3%) were SA carriers (SA+), three of them MRSA. SA+ SLE showed significantly higher SLEDAI-2k values [SA+: median (IQR) 2 (3.75); SA−: 0 (2); P = 0.04]. The phylogenetic analysis, restricted to 21 non-MRSA SA+, revealed a statistically supported larger clade (A, n = 17) and a smaller one (B, n = 4). Patients located in clade A showed a significantly higher prevalence of joint involvement (88.2%) in comparison with clade B (50.0%, P Conclusion We suggest a possible role of SA nasal carriage status in SLE disease activity. Moreover, our findings support the hypothesis that bacterial genetic variants may be associated with specific disease features.

Objectives: Transmitted drug resistance (TDR) and HIV-1 genetic diversity may affect treatment efficacy and clinical outcomes. Here we describe the circulating viral subtypes and estimate the prevalence of drug resistance among antiretroviral therapy (ART)-naïve patients attending Sapienza University Hospital (Rome, Italy) from 2006–2017. Methods: Genotypic resistance testing (GRT) was performed on 668 ART-naïve patients for integrase (n = 52), protease and reverse transcriptase (n = 668) sequences. Results: Twenty-one different HIV-1 subtypes and circulating recombinant forms (CRFs) were identified. Subtype B was the most common (67.1%), followed by CRF02_AG (8.4%), and subtypes C and F (both 6.0%). A significantly increase in the proportion of non-B strains (P < 0.001) and the rate of non-Italian patients was observed over time. The overall prevalence of TDR was 9.4% (NRTI, 4.2%; NNRTI, 5.8%; and PI, 1.0%) and was higher in subtype B strains. Transmitted INSTI mutations (Q148H and G140S) responsible for high-level resistance to raltegravir and elvitegravir and intermediate resistance to dolutegravir and bictegravir were found, for the first time, in two individuals. Minor or accessory INSTI mutations were detected in 17.3% of patients. No significant decrease in the prevalence of TDR was documented over time. Conclusion: The significant increase in non-B subtypes suggests that the molecular epidemiology of HIV-1 is changing. Detection of a major INSTI mutation in two ART-naïve patients highlights the importance of performing GRT before commencing treatment. This finding and the lack of a significant reduction in TDRs underline the importance of continuous surveillance of resistance mutations.

Implant related infection is one of the most frequent complications in orthopaedic and trauma surgery. Local antibiotic treatment strategies are becoming part of the prevention and treatment methodology for this fearful complication. To date, there are two coatings available on the market, both with a polylactic acid base. Current evidence supports the use of these types of coatings in the prophylaxis of periprosthetic infections and fracture-related infections. However, their therapeutic use has been less investigated. The purpose of this article is to summarise recent evidence relating to the clinical application of antibacterial hydrogels and coatings in orthopaedic and traumatology surgery and indicating which future applications may benefit from it.

Background Blastocystis is one of the most common intestinal protozoa in human faecal samples with uncertain impact on public health. Studies on the prevalence of Blastocystis in HIV-positive patients are limited and dated. Methods A cross-sectional study was carried out involving 156 HIV-positive patients to evaluate the prevalence of Blastocystis-subtypes by molecular amplification and sequencing the small subunit rRNA gene (SSU rDNA), to identify the risk factors for its transmission, to examine the relationship between the presence of the protist and gastrointestinal disorders. Furthermore, the evaluation of the faecal calprotectin by immunoassay from a sample of subjects was performed to evaluate the gut inflammation in Blastocystis-carriers. Results Blastocystis-subtypes ST1, ST2, ST3, ST4 were identified in 39 HIV-positive patients (25%). No correlation was found between the presence of the protist and virological or epidemiological risk factors. Blastocystis was more frequently detected in homosexual subjects (p = 0.037) infected by other enteric protozoa (p = 0.0001) and with flatulence (p = 0.024). No significant differences in calprotectin level was found between Blastocystis-carriers and free ones. Conclusions Blastocystis is quite common in HIV-positive patients on ART showing in examined patients 25% prevalence. Homosexual behaviour may represent a risk factor for its transmission, while CD4 count and viremia didn’t correlate with the presence of the protist. The pathogenetic role of Blastocystis remains unclear and no gut inflammation status was detected in Blastocystis-carriers. The only symptom associated with Blastocystis was the flatulence, evidencing a link between the presence of the protist and the composition and stability of gut microbiota.

Background:Infective factors play a central role in autoimmune diseases pathogenesis. It is possible to speculate that the host genotype could interact with genetic background of infective agents. We previously evaluated a large SLE cohort, observing the association between theS. Aureus(SA) carriage status and presence of a more active disease in terms of autoantibodies positivity.Objectives:We evaluated epidemiological, molecular characterization, genetic diversity and evolution of SA isolated from SLE patients by means of phylogenetic analysis.Methods:Consecutive SLE patients (ACR 1997 criteria) were enrolled: clinical/laboratory data were collected and nasal swab for SA identification was performed. On the basis of translation elongation factor (tuf) gene, a phylogenetic analysis was performed to investigate phylogenetic relationships and to assess significant clades in patients with persistent carriage status (nasal swab positive in two consecutive evaluation, performed 1 week apart). The first dataset was composed by seven SA tuf gene isolated from non-SLE individuals from different countries (downloaded from the GenBank database,https://www.ncbi.nlm.nih.gov/nucleotide/) and tuf gene SA collected from SLE patients enrolled in the present study.Results:We enrolled 118 patients (M/F 10/198; median age 45.5 years, IQR 13,2; median disease duration 120 months, IQR 144). Skin involvement is the most frequent disease manifestation (86 patients, 72.9%), followed by joint involvement (78 patients, 66.1%). Twenty-four patients (20.3%) were SA carriers (SA+), three of them resulted MRSA. SA+ patients showed a significantly higher prevalence of joint involvement (79.2%versus62.7%, P=0.01) and anti-dsDNA positivity (75.0%versus55.3%, P=0.004). Moreover, SA+ SLE showed a more active disease, in terms of SLEDAI-2k values [SA+: median 2 (IQR 3.75)versusSA-: median 0 (IQR 2), P=0.04). The phylogenetic analysis has been restricted on the 21 non-MRSA SA+ patients. The maximum likelihood phylogenetic tree of the first dataset revealed a statistically supported larger clade (A, N=17) and a smaller one (B, N=4; figure 1A). SLE patients located in the clade A showed a significantly higher prevalence of joint involvement (88.2%) in comparison with clade B (50.0%, PConclusion:The results of the present study confirmed the association between SA carriage status and disease activity, in terms of SLEDAI-2k values and anti-dsDNA positivity. The phylogenetic analysis ontufgene show a clustering ofSA+patients in two major clade (A and B). Interestingly thetufgenotype of clade A is significantly associated with a specific disease phenotype, characterized by joint involvement and positivity for anti-dsDNA. These findings support the hypothesis that bacterial genetic variants may be associated with specific disease features.References:[1]Rigante et al. Int J Mol Sci. 2015;[2]Wertheim et al Lancet Infect Dis. 2005;[3]Conti et al Arthritis Res Ther 2016;[4]Tong et al Clin Microbiol Rev. 2015;[5]Rhee et al Infect Control Hosp Epidemiol. 2015Disclosure of Interests:Giulio Olivieri: None declared, Fulvia Ceccarelli: None declared, Alessandra Lo Presti: None declared, silvia angeletti: None declared, Carlo Perricone: None declared, Giancarlo Iaiani: None declared, Lucia De Florio: None declared, francesca antonelli: None declared, Luigino Amori: None declared, Cristina Garufi: None declared, Francesca Romana Spinelli Grant/research support from: Pfizer, Speakers bureau: Lilly, BMS, Celgene, cristiano Alessandri: None declared, Guido Valesini: None declared, Massimo Cicozzi: None declared, Fabrizio Conti Speakers bureau: BMS, Lilly, Abbvie, Pfizer, Sanofi

Spinal infections are rare (their incidence is estimated in about the 5% of all osteomyelitis) and severe pathologies. They are usually identified with different names, as disk space infection, spondylodiscitis, and vertebral osteomyelitis. Spondylodiscitis is the most frequent among spinal infections. The etiology might be due to bacteria, fungi, and parasites and might affect many anatomical structures. The reported incidence is increased in the last years.[1,2] The disease can be classified according to the involved anatomical structure: Vertebral osteomyelitis Discitis and spondylodiscitis Spinal canal infections Adjacent soft tissue infections. In adult patients, the terms osteomyelitis and spondylodiscitis can be considered as more appropriate since an isolated discitis is rarely an isolated entity,[3] but in pediatric patients, it can be occasionally found.[4] The diagnosis might be challenging, often causing a delay in the identification of the pathology. On the basis of a clinical suspicion, the diagnosis can be formulated with a rational use of radiological, microbiological, and bioptic examinations.

Systemic rheumatic diseases have significant morbidity and mortality, due in large part to concurrent infections. The lung has been reported among the most frequent sites of infection in patients with rheumatic disease, who are susceptible to developing pneumonia sustained both by common pathogens and by opportunistic microorganisms. Patients with rheumatic disease show a peculiar vulnerability to infectious complications. This is due in part to intrinsic disease-related immune dysregulation and in part to the immunosuppressive treatments. Several therapeutic agents have been associated to a wide spectrum of infections, complicating the management of rheumatic diseases. This review discusses the most frequent pulmonary infections encountered in rheumatic diseases, focusing on opportunistic agents, consequent diagnostic challenges and appropriate therapeutic strategies.

The aim of the study was to evaluate the effect of risedronate on bone mineral density (BMD) and bone turnover markers in HIV-infected osteoporotic males, according to their gonadal status. HIV patients were followed up for 24 months and divided into two groups: patients with osteoporosis or osteopenia with fractures (group A, n = 20) and those without (group B, n = 21). Group A and B were further divided according to the presence of reduced androgenizations. Both groups were treated with cholecalciferol 800 I.U. and calcium (Ca) 1,000 mg orally every day for the first 12 months. Risedronate 75 mg for two consecutive days a month orally was then added in group A, for another 12 months. Group B continued treatment with Ca and vitamin D. Every 6 months each patient underwent biochemical evaluation, and BMD measurement. A significant increase in lumbar BMD was observed in HIV males with adequate androgenization after 12 months of risedronate treatment in group A together with a reduction of bone turnover markers. BMD remained stable with a concomitant significant slight reduction of bone turnover markers in group B. Risedronate increased BMD and reduced bone turnover markers to a greater extent in patients with adequate androgenization compared to osteoporotic HIV males with symptomatic hypoandrogenization.

Objective.The differential diagnosis between rheumatic diseases and infectious conditions is a great challenge in clinical practice. Adult-onset Still’s disease (AOSD) is a rare systemic inflammatory syndrome that shares several clinical and laboratory variables with sepsis. Interleukin (IL)-18 is overexpressed in AOSD, suggesting a possible role as a disease biomarker. The aim of our study was to detect IL-18 serum levels in a cohort of patients with AOSD and sepsis and to address its possible role as a biomarker for differential diagnosis.Methods.A group of unselected patients with AOSD diagnosed according to the Yamaguchi criteria and consecutive patients with sepsis diagnosed according to the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference criteria were enrolled. The clinical and laboratory data were collected. In the AOSD group, disease activity was assessed by Pouchot’s and Rau’s criteria. IL-18 serum levels were detected by ELISA.Results.Thirty-nine patients with AOSD and 18 patients with sepsis were enrolled. Two out of 18 patients with sepsis (11.1%) also fulfilled the Yamaguchi criteria. A significant difference was found in IL-18 serum levels between patients with active and inactive disease (p < 0.001), and it positively correlated with disease activity (p = 0.0003), ferritin serum level (p = 0.016), and erythrocyte sedimentation rate (p = 0.041). IL-18 was significantly increased in patients with AOSD when compared with sepsis (p = 0.014). For a cutoff of 148.9 pg/ml, this test had a specificity of 78.3% and a sensitivity of 88.6%.Conclusion.We have demonstrated that IL-18 can be a biomarker for differential diagnosis between AOSD and sepsis.

BACKGROUND Spontaneous spinal infections (SSIs) represent a rare and serious pathological entity. We tried to study a correlation between type of treatment, timing of treatment and clinical outcome through a multivariate analysis of an observational cohort study with the aim to define what is the optimal clinico-therapeutic management. METHODS We performed a retrospective observational cohort study on all consecutive patients observed in our Institute in a period of 13 years; from 2001 to 2014 we enrolled 50 consecutive patients with symptomatic spontaneous spinal infections (no previous surgery or recent infection in other site), confirmed with diagnostic imaging. The inclusion parameters were: diagnostic imaging, signs and symptoms positive for SSI, no history of recent infection or surgery. Of each parameter analyzed, we calculated mean and standard deviation and when necessary correlation (ρ), covariance (σ) and relation coefficient between type of treatment, timing of treatment and clinical outcome. RESULTS Our results suggest that an increase of one day from the onset of symptoms and the start of therapy leads to an increase in the Oswestry Disability Index Scale both at 6 months than at 1 year, with a statistical relevance, so our experience shows a statistically significant correlation and a positive co-variance between timing and outcome at 6 months and 1 year. CONCLUSIONS SSI are rare, very difficult to diagnose and represent a significant clinical problem. If not properly managed, they may lead to significant impact in the quality of life. The most relevant problem is not the treatment, conservative or surgical, but early diagnosis, so a careful physical, laboratory and imaging examination is fundamental, with an important help provided by isolation of the pathogen and histology. In our experience early diagnosis has a fundamental role. In the light of this, current treatment protocols may require a prompt and multidisciplinary management including infectivologists, neuroradiologists and spine surgeons.

Background Staphylococcus aureus (SA) is a commensal bacterium representing one of the most important components of the skin microbiome, mostly isolated in the anterior nares. A higher rate of SA nasal colonization in patients affected by Wegener’s granulomatosis and rheumatoid arthritis compared with healthy subjects (HS) has been described. No studies focusing on systemic lupus erythematosus (SLE) are available. We aimed at analyzing the prevalence of SA nasal carriers in an SLE cohort and evaluating correlation between nasal colonization and clinical, laboratory and therapeutic features. Methods We enrolled 84 patients with SLE (number of male/female patients 6/78; mean age 41.3 ± 12.2 years, mean disease duration 142.1 ± 103.8 months) and 154 HS blood donors. Patients with SLE underwent a physical examination and the clinical/laboratory data were collected. All the patients with SLE and the HS received a nasal swab for SA isolation and identification. Results SA nasal colonization prevalence was 21.4 % in patients with SLE and 28.6 % in HS (P not significant). We analyzed patients with SLE according to the presence (n = 18, SA-positive SLE) or the absence (n = 66, SA-negative SLE) of nasal colonization. Renal involvement was significantly more frequent in SA-positive SLE (11.6 % vs 3.0 %; P = 0.0009). Moreover, the presence of anti-dsDNA, anti-Sm, anti-SSA, anti-SSB, anti-RNP antibodies was significantly higher in SA-positive SLE (P

Background Recent clinical studies have shown that the presence of CC genotype in the rs12979860 region of IL28B gene is associated with an increase in the probability of spontaneous clearance of hepatitis C virus (HCV). Moreover, IL28B polymorphism seems to influence the probability of developing liver steatosis in chronic HCV patients. Aims The aims of our clinical study were 1) to verify the distribution of IL28B genotypes (CC, CT or TT) among subjects with spontaneous clearance of HCV infection and 2) to examine the correlation between IL28B polymorphism and hepatic steatosis among these subjects. Methods and patients We enrolled 41 subjects with spontaneous resolution of HCV infection (detectable serum anti-HCV but undetectable HCV-RNA) and 134 healthy controls from the same geographical area. The IL28B single-nucleotide polymorphism (SNP) rs12979860 was genotyped by using a Pyrosequencing™ technique. The presence of steatosis was assessed by liver biopsy or ultrasound examination in the 41 study subjects. Results CC, CT and TT-genotypes of the SNP rs1979860 were found in 66%, 24% and 10% of the subjects who spontaneously cleared HCV and in 31%, 54% and 15% of controls, respectively (p = 0.0003). Among the study subjects, females with CC-genotype were significantly more represented (p = 0.02). Hepatic steatosis did not correlate with IL28B genotype (p = 0,14) but only with a high body mass index (BMI) value (p = 0.03). Conclusions Female subjects carrying IL28B CC-genotype are significantly more represented among Italian patients who spontaneously cleared HCV infection. In addition, among these subjects, the presence of liver steatosis does not correlate with IL28B genotype but is solely related to the occurrence of high BMI. Thus, the association between IL28B polymorphism and steatosis in chronic HCV patients requires the presence of active HCV replication to occur, while in subjects who have cleared the infection, the mechanism(s) inducing liver steatosis are independent from IL28B profile.

Objective.To assess the performance of serial QuantiFeron-TB Gold In-Tube (QFT-GIT) tests in patients with rheumatic diseases during longterm systemic treatment with biologic therapy, evaluating conversions and reversions in relation to the clinical outcome.Methods.We conducted a prospective study on patients awaiting biologic agents. At baseline, they had chest radiographs, QFT-GIT tests, and tuberculin skin tests (TST); QFT-GIT was repeated at 3, 6, 12, and 18 months after onset of biologic therapy. In patients with no evidence of latent tuberculosis infection (LTBI) at baseline, TST was repeated at 12 months of biologic treatment.Results.Among patients (n = 102; women 65.7%; median age 47 yrs, range 20–82), 14 (13.7%) were considered as having LTBI because of a minimum of 1 abnormal screening test. The agreement between QFT-GIT and TST was 88% (κ = 0.14). During biologic treatment, both patients with (n = 14) and those without (n = 88) evidence of LTBI at baseline showed conversions and reversions in QFT-GIT results at different timepoints. These fluctuations were not paralleled by significant clinical changes. The TST repeated at 12 months in patients with no evidence of LTBI at baseline continued to be negative. The median baseline interferon-γ (IFN-γ) concentration was not significantly different from that observed at each subsequent timepoint.Conclusion.Dynamic changes occur with serial IFN-γ release assay testing in patients treated with biologic therapy that do not correlate with clinical outcome. A careful and integrated evaluation of the patient, including clinical information, should guide the treatment decision. This study was underpowered for definite conclusions and further studies are needed to determine the significance of these findings.

Objective Osteoporosis and hypogonadism are common in men with HIV infection. Ageing Male Symptoms (AMS) scale measures symptoms related to hypogonadism. FRAX provides 10-year probability of major fractures. We investigated the role of AMS scale combined with FRAX without bone mineral density (BMD), in identifying HIV men with bone fragility. Design Cross-sectional observational study. Methods Fifty HIV-positive men treated with highly active antiretroviral therapy and 27 controls underwent hormonal evaluation, BMD scan and spine X-ray. The AMS questionnaire was administered. Results Osteoporosis was found in 24·0% of HIV patients and in 3·7% of controls (P = 0·05). In HIV patients, 9 radiological vertebral fractures were found (none in controls, P = 0·04). Calculated free testosterone suggested hypogonadism in 26% of HIV patients vs 4% of controls (P = 0·04); an abnormal AMS score (≥27) was found in 62% HIV patients compared with 41% controls (P = 0·04). ROC curves showed that FRAX for major fracture had a 23% sensitivity and a 100% specificity in identifying HIV patients with bone fragility (P = 0·002, with the threshold of 7% at which bisphosphonate therapy is cost-effective). Considering a value of AMS ≥27, we obtained an 82·6% sensitivity and a 42·9% specificity (P = 0·04). The combination of AMS and FRAX score achieved a 77·3% sensitivity and a 69% specificity (P = 0·02, cut-off 34). Conclusion Combination of FRAX (without BMD) and AMS improved sensitivity of FRAX alone in identifying HIV patients at fracture risk, at the expense of reduced specificity.

Screening for latent tuberculosis infection (LTBI) prior to the prescribing of anti-TNF agents and monitoring for infection during treatment are recommended. The feasibility of novel screening tools, including QuantiFERON-TB Gold In-Tube (QFT-GIT), remains unclear in the setting of immunosuppression. The aim of this study was to evaluate the usefulness of serial QFT-GIT during biologic therapy to assess whether dynamic changes in IFN-γ levels may be helpful in identifying reactivation of LTBI or newly acquired TB. We conducted a prospective study on patient candidates to TNF inhibitors. QFT-GIT was performed at baseline and after 3 and 6 months since biologic onset. A further follow-up period of 6 months was observed. Among patients enrolled (n = 119; F = 69 %; median age = 47 years, range 18–80), 24 had at least 1 risk factor for LTBI. Ninety-six were taking immunosuppressants at the time of TB testing. At baseline, 5 patients displayed positive, 93 negative, and 21 indeterminate QFT-GIT results. We observed QFT-GIT conversions and reversions in 12 patients with LTBI and in 73 without LTBI. QFT-GIT results changed of 28 % at month 3 and of 21 % at month 6; the greatest change was observed in patients with indeterminate results that became negative (15 %; p

Objective: To evaluate whether an inter-individual variability in the activity of thymidine kinase (TK) and deoxycytidine kinase (dCK), which are involved in the first step of phosphorylation of some nucleoside analogues, exists in antiretroviral-naive, HIV-seropositive patients. Design: Forty-five randomly selected antiretroviral-naive HIV-infected patients were recruited, together with 26 healthy volunteers with no concurrent infection and under no pharmacological treatment. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from venous blood and their TK and dCK activities evaluated. CD4 T cells and HIV-RNA were measured in HIV-infected patients, too. Results: There was a broad range of variability in TK activity in HIV-infected individuals. Furthermore, the activity in PBMC was significantly higher in HIV-infected individuals than in healthy volunteers. dCK activity in seropositive patients was significantly lower than in healthy volunteers. A marked inter-individual variability in dCK levels was observed in the HIV-infected group. No correlations were found between TK or dCK activities and plasma viral load, CD4 cell count, sex or age of patients. Conclusions: A marked range of inter-individual variability of TK and dCK activities in PBMC exists in HIV-infected individuals but not in healthy volunteers, indicating that the activity of enzymes with key roles in drug activation could vary greatly from one patient to another. Furthermore, TK expression is greater in HIV-infected individuals than in healthy volunteers. Better understanding of the viral or cellular factors that contribute to this variability, as well as their effect on responses to antiretroviral treatment, may aid optimization of the management of HIV-infected patients.

Background Staphylococcus aureus (SA) is a commensal bacterium which can be isolated mostly in the anterior nares. In immunosuppressive patients, SA could cause various infections, ranging from minor skin infections to severe pneumonia. Data from literature reported a prevalence of SA nasal carriage of about 25% in healthy subjects (HS). Patients affected by Wegener9s granulomatosis and Rheumatoid Arthritis showed significantly higher rates of SA nasal colonisation compared with HS. In contrast, there are no studies concerning the patients with Lupus Erythematosus Systemic (SLE). Objectives We aimed to analyse the prevalence of SA nasal carriers in a cohort of SLE patients. Secondly, we evaluated the correlations between the presence of nasal colonization and clinical, laboratory and therapeutical features. Methods We enrolled 84 SLE patients (ACR criteria 1997, M/F 6/78; mean age 41.3±12.2 years, mean disease duration 141.5±102.6 months) and 154 HS blood donors, enrolled as control group. At each visit, SLE patients underwent a complete physical examination and the clinical/laboratory data were collected in a standardized, computerized, and electronically-filled form. The evaluation of serum complement C3 and C4 levels and determination of autoantibodies was obtained. Disease activity was assessed with the SLEDAI-2K. All the SLE patients and HS received a nasal swab in both anterior nares; the swabs were sent to microbiological laboratory for isolation and identification of SA. Results SA nasal colonization prevalence was 23.8% in SLE patients and 28.6% in HS (P=NS). None of the detected SA were Methicillin-resistant. We analysed SLE patients according with the presence (N=20, group 1) or the absence (N=64, group 2) of the nasal colonization. Group 1 patients showed a significant higher frequency of renal involvement compared with group 2 (15.0% vs 3.1%; P=0.0009). Moreover, the presence of anti-dsDNA, RNP, SSA and SSB antibodies was significantly higher in group 1 (P Conclusions In the present study we analysed the prevalence of SA nasal colonization in SLE patients, showing similar results in SLE patients and HS control group. Interestingly, in SLE patients the nasal colonization was associated with a more active disease, as demonstrated by higher values of disease activity indices, most frequent renal involvement and positivity for several autoantibodies. This association could be explained by two different hypothesis: first, the presence of SA nasal colonization could act as trigger for autoimmune process, perpetuating inflammatory condition. The second hypothesis suggests that the more active disease, requiring more aggressive immunosuppressant treatment, could facilitate the development of the nasal colonization. Further studies are needed to better clarify the relationship between SLE and SA. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4226

Background A great challenge in clinical practice is the differential diagnosis between rheumatic inflammatory diseases, such as Adult Onset Still’s disease (AOSD), and sepsis. Indeed, these conditions share several clinical and laboratory findings. Recent studies have investigated the cytokine profile in patients with AOSD and sepsis detecting elevated serum levels of different cytokines, including interleukin (IL)-18. This cytokine plays a pivotal role in AOSD, by driving the inflammatory process. Objectives To investigate IL-18 serum levels in AOSD and to assess whether IL-18 could be used as a biomarker to discriminate between patients with AOSD and sepsis. Methods We measured IL-18 serum levels by a commercial ELISA kit (Immuno Pharmacology Research, Italy), in a cohort of patients with AOSD (diagnosed according to Yamaguchy criteria) and in patients sepsis (diagnosed according to American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference). In AOSD, disease activity was evaluated with Rau’s criteria, and patients were defined “active” if they scored ≥4. Area under the receiver operating characteristic curve (ROC-AUC) analysis was used to evaluate the diagnostic utility of the IL-18. Results Thirty patients with AOSD (F 18, M 12, mean age 39.6 years, range 18-69) and 7 patients with sepsis (F 4 M 3, mean age 35.1 years, range 30-55) were enrolled. Mean IL-18 serum level in AOSD patients [1298.7 pg/ml (range 0–6015)] was significantly higher from mean IL-18 serum level in sepsis [113.5 pg/ml (range 52–328), P=0.008]. ROC-AUC analysis of the serum concentration of IL-18 indicated that it was significantly diagnostic of AOSD, especially when active. The ROC-AUC analysis for the serum level of the IL-18 between patients with AOSD and sepsis was 0.712. At a cutoff point of 179 pg/ml, corresponding to the greatest sum of specificity and sensitivity, the specificity was 69.7% and the sensitivity was 87.5% for detection of AOSD (likelihood 2.89). When disease activity was scored according to Rau’s criteria, 21/30 (70%) patients were identified as active. These patients showed mean IL-18 serum levels (1793 pg/ml, range 0-6015) significantly higher than patient with “non active” disease (145.5 pg/ml, range 0-685, P=0.0039), as well as higher than sepsis (P=0.007). The ROC-AUC analysis for the serum level of the IL-18 between active patients with AOSD and sepsis was 0.845. At a cutoff point of 223 pg/ml, the specificity was 87.5% and the sensitivity was 80.9% for detection of AOSD (likelihood 6.48). Conclusions A significant difference in IL-18 serum levels between patients with AOSD and sepsis was found, especially in those patients with active disease. This evidence may confirm the potential utility of IL-18 in the differential diagnosis between AOSD and sepsis. Disclosure of Interest None Declared

Although the association between inflammatory bowel disease and gastrointestinal infections has been suggested, the mechanisms involved in the pathogenesis of Crohn's disease (CD) are still undetermined. We report the case of a man, who presented with mesenteric adenitis initially due to a Yersinia pseudotubercolosis infection, who was later diagnosed with Crohn's disease. This case is in keeping with recent evidence in the literature which suggests that CD is a disease linked to abnormal immune responses to enteric bacteria in genetically susceptible individuals.