Ida Luzzi

Occurrence and resistance to antibiotics of Campylobacter jejuni and Campylobacter coli in animals and meat in northeastern Italy.

A study was carried out in northeastern Italy during 2000 and 2001 to investigate the occurrence of Campylobacter jejuni and Campylobacter coli in animals, cattle, pigs, and broilers, and raw meat, beef, pork, and chicken. Campylobacter spp. were detected in 53.9% of the cattle, 63.5% of the pigs, and 82.9% of the broilers examined. Chicken meat was frequently contaminated (81.3%), while lower rates were found in pork meat (10.3%) and beef (1.3%). The resistance to antibiotics of the strains was also investigated, and compared to that of human clinical isolates. C. coli was generally more resistant than C. jejuni. Resistance to quinolones was frequently observed in C. coli isolated in chicken meat (78.6%); slightly lower rates were found in C. jejuni isolated in broilers (42.2%), chicken meat (52.8%), and humans (38.2%). C. coli was also frequently resistant to tetracycline in all sources, while resistance to streptomycin was most frequently observed in pig isolates (89.4%).

Enteropathogens associated with childhood diarrhea in Italy

Background. Infectious diarrheal diseases remain an important cause of childhood morbidity in industrialized countries. The knowledge of the etiology and epidemiology of childhood diarrhea in a given area is needed to plan any measure designed to prevent or ameliorate diarrheal illness and to develop practice guidelines for the most appropriate stool examination procedures. Methods. We evaluated 618 children with diarrhea and 135 controls prospectively for viral, bacterial and parasitic enteric pathogens. Diarrheagenic Escherichia coli was identified by gene probes specific to different virulence factors. Stool filtrates were examined for the presence of free bacterial toxins by a cell culture cytotoxicity assay. Clinical and epidemiologic data were recorded and analyzed in relation to microbiologic findings. Results. Enteropathogens were identified in 59% of children with diarrhea and in 10.4% of asymptomatic controls. The agents mainly associated with disease were rotavirus (23.6%), Salmonella (19.2%) and Campylobacter (7.9%). Rotavirus was significantly more frequent among children observed as inpatients whereas Campylobacter was significantly more common in outpatients. Infections with diarrheagenic E. coli, Shigella flexneri, Yersinia enterocolitica, Crypto-sporidium and Giardia were observed in a limited number of patients. The clinical presentation of children was not sufficiently characteristic to permit presumptive diagnosis of a specific pathogen. Conversely the presence of blood and/or leukocytes in stools had a high positive predictive value for Salmonella or Campylobacter infection. Conclusion. The results of this study will be useful for planning strategies to prevent and control diarrheal diseases in our country.

Polymorphic DNA repair and metabolic genes: a multigenic study on gastric cancer

Risk factors for gastric cancer (GC) include inter-individual variability in the inflammatory response to Helicobacter pylori infection, in the ability of detoxifying DNA reactive species and repairing DNA damage generated by oxidative stress and dietary carcinogens. To evaluate the association between polymorphic DNA repair genes and GC risk, a case-control study including 314 histologically confirmed GC patients and 548 healthy controls was conducted in a GC high-risk area in Tuscany, Italy. Polymorphic variants of base excision repair (APE1-D148E, XRCC1-R194W, XRCC1-R399Q and OGG1-S326C), nucleotide excision repair (XPC-PAT, XPA-23G>A, ERCC1-19007T>C and XPD-L751Q), recombination (XRCC3-T241M) and alkylation damage reversal (MGMT-L84F) were tested for their potential role in the development of GC by using logistic regression models. The same population was also characterised for GSTT1 and GSTM1 variant alleles to search for possible functional interactions between metabolic and DNA repair genotypes by two-way interactions using multivariate logistic models. No significant association between any single DNA repair genotype and GC risk was detected with a borderline association with the XPC-PAT homozygous genotype [odds ratio (OR) =1.42; 95% confidence interval (CI) 0.94-2.17]. Gene-gene interaction analysis revealed combinations of unfavourable genotypes involving either multiple DNA repair polymorphisms or DNA repair and GST-specific genotypes. The combination of the XPC-PAT and the XPA variant alleles significantly increased GC risk (OR=2.15; 95% CI 1.17-3.93, P=0.0092). A significant interaction was also found between the APE1 wild-type genotype and either the single GSTT1 (OR=4.90; 95% CI 2.38-10.11, P=0.0079) or double GSTM1-GSTT1 null (OR=7.84; 95% CI 3.19-19.22, P=0.0169) genotypes or the XPA-mutant allele (OR=3.56; 95% CI 1.53-8.25, P=0.0012). These findings indicate that a complex interaction between host factors such as oxidative stress, antioxidant capacity and efficiency of multiple DNA repair pathways underlies the inter-individual variability in GC risk.

Cytotoxin-Associated Gene-A–Positive Helicobacter pylori Strains Are Associated With Atherosclerotic Stroke

Background—It is uncertain whether Helicobacter pylori is associated with ischemic syndromes and whether this association is mediated by the induction of atherosclerosis. In this study, we tested the hypothesis that atherosclerotic stroke shows a selective association with virulent H pylori strains. Methods and Results—The seroprevalence of infection by H pylori and by strains bearing the cytotoxin-associated gene-A (CagA), a strong virulence factor, was assessed by ELISA in 138 patients with large-vessel stroke (group A), in 61 patients with cardioembolic stroke (group B), and in 151 healthy control subjects. The 3 groups had a similar socioeconomic status. Serum levels of C-reactive protein were also measured by ELISA. The prevalence of infection was 71% in group A, 63.9% in group B, and 70.2% in the control group (P =NS), whereas the prevalence of CagA-positive strains was higher in group A than in group B (42.8% versus 19.7%, respectively; odds ratio 3.04, 95% CI 1.43 to 6.49;P <0.001) and higher in group A than in the control group (42.8% versus 17.9%, respectively; odds ratio 4.3, 95% CI 2.12 to 8.64;P <0.001), after adjusting for main cardiovascular risk factors and social class. A trend toward a difference in C-reactive protein was observed between CagA-positive (2.00±3.43 [mean±SD] mg/dL) and CagA-negative (1.31±1.72 [mean±SD] mg/dL) patients (P =0.072, Mann-Whitney U test). Conclusions—The association between H pylori and acute cerebrovascular disease seems to be due to a higher prevalence of more virulent H pylori strains in patients with atherosclerotic stroke.

Tetracycline and Streptomycin Resistance Genes, Transposons, and Plasmids in Salmonella enterica Isolates from Animals in Italy

ABSTRACT Fifty-eight multidrug-resistant Salmonella enterica strains of 20 serotypes, isolated from animal sources in Italy, were analyzed for tet(A) and strA-strB, conferring tetracycline and streptomycin resistance, respectively. The strA and strB genes were highly prevalent in Salmonella strains of our collection, being detected in 84% of the streptomycin-resistant strains. In many strains, the strA and strB genes were linked to a particular Tn5393-derivative transposon characterized by the presence of the insertion sequence IS1133, previously identified only in the plant pathogen Erwinia amylovora. Sixty-eight percent of the tetracycline-resistant strains were tet(A) positive, indicating that this gene is widely diffused in Salmonella strains circulating in animals in Italy. Most of the tet(A) genes were localized within a deleted Tn1721 transposon variant. Two prevalent repN and repI1 resistance plasmids were identified in Salmonella isolates of our collection.

Occurrence of Vibrio and other pathogenic bacteria in Mytilus galloprovincialis (mussels) harvested from Adriatic Sea, Italy

Sixty-two samples of Mytilus galloprovincialis (mussels) harvested from approved shellfish waters in the Adriatic Sea were examined for the presence of Vibrio, Salmonella, Campylobacter, and verocytotoxin producing Escherichia coli. Vibrio spp. were isolated from 48.4% of samples; the species most frequently found were V. alginolyticus (32.2%) and V. vulnificus (17.7%), followed by V. cincinnatiensis (3.2%), V. parahaemolyticus (1.6%), V. fluvialis (1.6%) and V. cholerae non-O1 (1.6%). V. parahaemolyticus resulted negative to Kanagawa-phenomenon and to PCR amplification of tdh gene. V. cholerae resulted negative to PCR amplification of sto gene. No Salmonella, Campylobacter, or E. coli verocytotoxin-producing strains were isolated. The results of this study suggest the potential risk of ingesting raw or undercooked mussels due to the frequent presence of potentially pathogenic Vibrio species.

Antibiotic Resistance Genes and Salmonella Genomic Island 1 in Salmonella enterica Serovar Typhimurium Isolated in Italy

ABSTRACT Fifty-four epidemiologically unrelated multidrug-resistant Salmonella enterica serovar Typhimurium isolates, collected between 1992 and 2000 in Italy, were analyzed for the presence of integrons. Strains were also tested for Salmonella genomic island 1 (SGI1), carrying antibiotic resistance genes in DT104 strains. A complete SGI1 was found in the majority of the DT104 strains. Two DT104 strains, showing resistance to streptomycin-spectinomycin and sulfonamides, carried a partially deleted SGI1 lacking the flost, tetR, and tetA genes, conferring chloramphenicol-florfenicol and tetracycline resistance, and the integron harboring the pse-1 gene cassette, conferring ampicillin resistance. The presence of SGI1 was also observed in serovar Typhimurium strains belonging to other phage types, suggesting either the potential mobility of this genomic island or changes in the phage-related phenotype of DT104 strains.

Antimicrobial Drug Resistance in Human Nontyphoidal Salmonella Isolates in Europe 2000–2004: A Report from the Enter-net International Surveillance Network

A 5-year survey, from 2000 to 2004, of results of antimicrobial susceptibility testing for 11 antimicrobials for 134,310 isolates of nontyphoidal salmonellas from cases of human infection in 10 European countries has demonstrated an overall increase in the occurrence of resistance, from 57% to 66% over the period of study. In contrast, multiple resistance (to four or more antimicrobial drugs) has declined from 18% to 15%. The most significant increase in resistance has been to nalidixic acid (14% to 20%), particularly in Salmonella enterica serovar Enteritidis (10% to 26%), the most common serovar. For England and Wales this increase has for the most part been attributed to infections linked to contaminated eggs originating outside the United Kingdom. For Salmonella Typhimurium, the second most prevalent serovar, there has been an overall decline in the occurrence of resistance to ampicillin, chloramphenicol, and tetracyclines, attributed to a decline in the occurrence of multiresistant Salmonella Typhimurium DT 104. For Salmonella Virchow, a serotype with a predilection for invasive disease, there has been a substantive increase in resistance to most antimicrobials, attributed to the spread of drug-resistant strains associated with poultry. Because of the widespread importation of foods, it is important that controls to reduce the emergence and spread of drug-resistant strains of Salmonella are internationally implemented.

Interleukin-1 gene polymorphisms and gastric cancer risk in a high-risk Italian population

OBJECTIVES:Host genetic factors, including the IL1 gene cluster, play a key role in determining the long-term outcome of Helicobacter pylori infection. The aim of the study was to investigate the relationship between selected IL1 loci polymorphisms and gastric cancer risk in an Italian population.METHODS:In a case-control study we compared the IL1B−31 and IL1B+3954 biallelic and IL1RN pentaallelic variable number of tandem repeats (VNTR) polymorphisms in 185 gastric cancer patients and 546 controls randomly sampled from the general population of an area at high gastric cancer risk (Tuscany, Central Italy).RESULTS:Genotype frequencies of the IL1B−31 T/C, IL1B+3954 C/T, and IL1RN polymorphisms among our population controls were in Hardy-Weinberg equilibrium. In multivariate analyses, no increase in gastric cancer risk was observed for the IL1B−31*C− and IL1B+3954*T− carriers; a significant 50% increase emerged for IL1RN*2 allele carriers (OR = 1.49; 95% CI: 1.01–2.21).Analyses based on combined genotypes showed also that the association with IL1RN*2 allele was limited to two-variant allele carriers who were also homozygous for the IL1B−31*T allele (OR = 2.23; 95% CI: 1.18–4.23) with a statistically significant interaction between these two genotypes (p= 0.043). Haplotype analysis showed an increased risk for the haplotype IL1RN*2/IL1B−31*T.CONCLUSIONS:Our results suggest that host genetic factors (such as the IL1RN and the IL1B−31 polymorphisms) interact in the complex process of gastric carcinogenesis in this high-risk Italian population. Overall, this effect appears more modest than previously reported in other populations, supporting the hypothesis that other still-to-be-defined factors are important in gastric carcinogenesis. These findings might be due to a haplotype effect.

GSTT1 and GSTM1 gene polymorphisms and gastric cancer in a high-risk italian population

Glutathione S‐Transferases (GSTs) are a family of phase II enzymes involved in the detoxification of potential carcinogens and provided of a strong antioxidant function by neutralizing electrophiles and free radicals. The GSTM1 and GSTT1 isoenzymes exhibit deletion polymorphisms, resulting in a lack of activity, and the null genotypes have been associated with increased cancer risk at several sites, including the stomach, although with contrasting results. We carried out a case‐control study to evaluate whether these polymorphisms modulate the risk of developing gastric cancer (GC). Genotypes for GSTM1 and GSTT1 were obtained from a series of 175 histologically confirmed GC patients and a large series of 546 healthy controls randomly sampled from the general population of Tuscany, an area at high GC risk. No difference in the frequency of GSTM1 null genotype was observed between cases and controls, whereas the GSTT1 null genotype was more frequent among cases (p = 0.04). Multivariate single‐gene analyses adjusted for possible confounders showed that the GSTT1 null genotype, but not the GSTM1 null genotype, was associated with an increased GC risk. Combined‐genotype analyses showed a significantly increased GC risk only for the double null (GSTM1‐GSTT1) genotype (OR = 2.27; 95% CI: 1.14–4.53). A statistically significant positive interaction between the 2 null genotypes was observed (p = 0.02). Our findings suggest that only subjects lacking both GSTM1 and GSTT1 activity are at increased GC risk. This study provides further support to the hypothesis that the risk of developing GC is influenced by inter‐individual variation in both carcinogen detoxification and antioxidant capacity.