Giovanna Barbuti

Objective: We previously identified, using a synthetic peptide, namely peptide 4.33 (p4.33), a subgroup of anti‐CENP‐A antibodies (Abs) recognizing an epitope shared between the CENP‐A region spanning amino acids 1‐17 (Ap1‐17) and the E2 component of the mitochondrial pyruvate dehydrogenase complex (PDC‐E2), the major mitochondrial target autoantigen in primary biliary cholangitis (PBC). Here, we evaluated whether anti‐p4.33 Ab positivity may be associates with a higher prevalence of antimitochondrial Ab (AMA) in systemic sclerosis (SSc) patients. Methods: Serum samples from 145 anti‐CENP ^pos SSc patients were tested for anti‐CENP‐A, ‐Ap1‐17, and ‐p4.33 Abs by ELISA. Subsequently, 32 anti‐Ap1‐17 ^pos /p4.33 ^pos and 32 anti‐Ap1‐17 ^pos /p4.33 ^neg were randomly selected and tested for AMA by immunoblotting. Results: Of 145 anti‐CENP ^pos patients, 128 (88.2%) were anti‐CENP‐A ^pos patients, of which 103 (80.5%) were positive for anti‐Ap1‐17 Abs and 66 (51.6%) were positive for anti‐p4.33 Abs. Of 32 selected anti‐Ap1‐17 ^pos /p4.33 ^pos patients, 15 (46.9%) were also positive for AMA targeting PDC‐E2 and/or the branched chain 2‐oxo acid dehydrogenase complex (BCOADC‐E2). In the Ap1‐17 ^pos /p4.33 ^neg group, AMA were detected in only two patients (6.25%). AMA positivity was statistically different between groups. Anti‐p4.33 Ab levels were directly associated more than anti‐Ap1‐17 Ab levels with AMA levels. Sequence homology analyses demonstrated that anti‐p4.33 Abs recognize an epitope (kPsaP) strongly overlapping with those of Ap1‐17, PDC‐E2, and BCOADC‐E2, also expressed by viral and bacterial proteins. Conclusions: Anti‐p4.33 Abs may be a useful biomarker to define a subset of SSc patients with a higher prevalence of AMA. Our findings also support the hypothesis that pathogens can trigger autoimmunity.

The safety of groundwater resources is a serious issue, particularly when these resources are the main source of water for drinking, irrigation and industrial use in coastal areas. In Italy, 85% of the water used by the public is of underground origin. The aim of this report is to analyze the main factors that make groundwater vulnerable. Soil characteristics and filtration capacity can promote or hinder the diffusion of environmental contaminants. Global climate change influences the prevalence and degree of groundwater contamination. Anthropic pressure causes considerable exploitation of water resources, leading to reduced water availability and the progressive deterioration of water quality. Management of water quality will require a multidisciplinary, dynamic and practical approach focused on identifying the measures necessary to reduce contamination and mitigate the risks associated with the use of contaminated water resources.

Nosocomial environmental contamination plays an important role in the transmission of several health care-associated pathogens. Control of surfaces contamination can reduce the risk of cross-infection in hospitals. The aim of our study is to evaluate the disinfectant effectiveness of hydrogen peroxide and silver ions, against nosocomial multidrug-resistant strains, when it's used directly on surfaces. Staphylococcus aureus ATCC 6538, Pseudomonas aeruginosa ATCC 15442 and the same multidrug-resistant clinical isolates were selected to study the effectiveness of the disinfectant used in suspension or on the clean and dirty surface. Regarding the suspension activity test, the hydrogen peroxide and silver ions resulted effective after 5 min for ATCC strains and after 10 min for multidrug-resistant isolates; about the surface activity test, its action resulted after 10 min for ATCC strains and after 15 min for multidrug-resistant isolates. Moreover, it was more effective when used in the absence or in presence of a low concentration of biological materials. In a complex environment such as hospital wards, to have a disinfectant notoriously effective but more easy and quick to use would be an useful solution to treat small surfaces occasionally contaminated by biological materials.

Candidemia is a major infectious complication in neonatal patients. The isolation of yeasts from blood is still the “gold standard” for its diagnosis, but other laboratory markers (i.e., circulating antigens) have been studied with varying specificities and sensitivities. The aim of this study was to evaluate the role of procalcitonin for the diagnosis of candidemia in neonatal patients at high risk. To verify if the use of different commercial methods can highlight dissimilar results of sensitivity and/or specificity, the determination of procalcitonin serum levels was estimated by two systems. Overall, 90 patients from a Neonatal Intensive Care Units were enrolled, of whom six developed Candida bloodstream infection. Four of six infants with candidemia had slight increase of procalcitonin values (0.5–1 ng/mL). Only one baby showed very high levels but he had fungal and bacterial sepsis at the same time, while no elevation was observed in the sixth patient. No statistically significant difference was observed between two different methods at the time of monitoring (p > 0.643). Both methods showed a sensitivity of 83.3 % at diagnosis, while the specificity was 73.8 and 63.1 % by methods A and B, respectively. In the light of the low sensibility and specificity of this assay, we can assume that the determination of procalcitonin would not seem to play a significant role in the diagnosis of fungal infection in neonatal patients.

This study aim was to determine the prevalence of microorganisms in the respiratory tract of patients with cystic fibrosis (CF) admitted to the CF Reference Centre in Southern Italy between 2002-2010. Microbiology assessment of samples (sputum and tracheal aspirates) collected from patients with pulmonary exacerbation admitted to hospital was carried out. All patients were registered in a database and clinical and microbiological data were retrospectively analysed. Overall, 188 patients were included and a total of 1217 samples were analysed. The most common microorganisms were Staphylococcus aureus (78.7% of the patients) and Pseudomonas aeruginosa (58%), followed by Candida albicans (19.1%), Haemophilus influenzae (13.3%) and Aspergillus fumigatus (9.6%). Compared to similar studies performed in other European countries, our microbiological data, especially the low occurrence of filamentous fungi, suggest a specific local epidemiology, probably related to some uncommon CFTR mutations, which are specific to Southern Italy.

Following the publication of the Italian Guidelines for the control and prevention of legionellosis an environmental and clinical surveillance has been carried out in Southeastern Italy. The aim of the study is to identify the risk factors for the disease, so allowing better programming of the necessary prevention measures.

The gram-positive pathogen Streptococcus pneumoniae is the most common cause of community-acquired pneumonia and is responsible for high morbidity and mortality worldwide. A major feature of pneumococcal pneumonia is an abundant neutrophil infiltration. In this work we observed that the R6 nonencapsulated S. pneumoniae strain induced a higher oxidative burst in neutrophils compared with its capsulated progenitor D39, by triggering neutrophil NADPH oxidase to produce more reactive oxygen intermediates (ROI) and by interfering with the neutrophil kinase signalling pathway. In addition, we evaluated the possibility that the capsule, lacking in R6 but present in D39, could modulate the S. pneumoniae-induced neutrophil respiratory burst. In this respect, three knock-out isogenic mutants (D39ΔCPS2E, D39ΔCPS-R6 and R6ΔCPS-R6) that were unable to synthesize the capsule, were tested for their capability of inducing the release of neutrophil-ROIs. The results indicate that the mutants behaved similarly to their wild-type parental strains in enhancing respiratory burst activity, suggesting that the capsule itself is not directly involved in modulating the neutrophil oxidative burst induced by S. pneumoniae, but that other genetic differences between D39 and R6 present elsewhere in the genome could be responsible for these mechanisms.