Background: Most autoimmune diseases are more prevalent in women. Symptom severity, disease progression, response to therapy and overall survival differ between males and females with rheumatic diseases. Objectives: To identify the characteristics of autoimmune diseases presentation and treatment between male and female population using information from the Mexican Adverse Events Registry (BIOBADAMEX). Methods: BIOBADAMEX is a Mexican ongoing cohort that collects the information of patients using biologic and biosimilar drugs since 2016. For this study we included all patients enrolled in the registry and compared baseline clinical and disease characteristics, treatment and presence of adverse events between genders. We used logistic regression to analyze univariable associations. Results: A total of 655 participants were analysed, of which 82% were female (Table 1). We found women were older with a median of 53 years compared to 46 years in men (OR 1.02, CI 1.0-1.1). Smoking was higher in men (16%) compared to women (5%), (OR 0.3, CI 0.2-0.6). Women had longer disease duration, 9 years compared to 7 years in men (OR 1, CI 1.0-1.1). Rheumatoid arthritis (RA) was more prevalent in women (OR 2.7, CI 1-6.9), while ankylosing spondylitis (AS) and psoriatic arthritis (PsA) were more prevalent in men (OR 0.2, CI 0.1-0.4, and OR 0.3, CI 0.1-0.9 respectively). Women had more comorbidities than men (OR 1.8, CI 1.1-2.8) and used steroids more frequently (OR 1.7, CI 1.1-2.7). Differences in disease activity were not found, however we noticed high activity scores among participants. Table 1. Baseline characteristics in the cohort by sex Women n=532 (82% ) Men n=123 (18% ) Univariable a OR(95%CI ) Age, median (IQR) 53 (44-60) 47 (34-55) 1.02 (1.0-1.1)* Body Mass Index, median (IQR) 27 (23-31) 26 (23-30) 1.0 (0.9-1.1) Smoking, n(%) 28 (5) 18 (16) 0.3 (0.2- 0.6)* Disease duration, median (IQR) 9 (4-16) 7 (2-13) 1.0 (1.0-1.1)* Diagnosis, n(%): RA 414 (78) 37 (30) 2.4 (1.0-5.7)* AIJ 12 (2) 5 (4) 0.5 (0.1-1.9) AS 37 (7) 56 (46) 0.1 (0.1-0.4)* PsA 19 (4) 15 (12) 0.3 (0.1-0.8)* SLE 17 (3) 3 (2) 1.2 (0.3-5.2) Others 33 (6) 7 (6) 1 Disease Activity indexes, median (IQR) DAS28 a 4.9 (3.6-5.9) 4.9 (3.0-5.9) 1.1 (0.9-1.3) BASDAI b 4.8 (2.9-8) 5.3 (2.8-7.5) 0.9 (0.8- 1.1) ASDAS c 3.2 (1.9-4.5) 3.9 (2.5-4.7) 0.8 (0.6-1.2) SLEDAI d 14.5 (5.0-19.5) 25 (25.0-31.0) 0.6 (0.4-1.1) High blood pressure, n(%) 77 (15) 14 (12) 1.3 (0.7-2.4) Diabetes mellitus, n(%) 46 (9) 7 (6) 1.5 (0.7-3.5) High cholesterol, n(%) 41 (8) 8 (7) 1.2 (0.4-2.6) Other comorbidities, n(%): 173 (33) 26 (21) 1.8 (1.1 -2.8)* Use of previous biologic, n(%): 216 (40) 44 (36) 1.2 (0.8- 1.8) Use of steroids, n(%): 215 (42) 34 (29) 1.7 (1.1 -2.7)* Use of DMARD, n(%): 418 (79) 89 (72) 1.4 (0.9-2.2) Adverse events b , n(%): 69 (13) 14 (11) 1.2 (0.7-2.1) Severe b , n(%): 12 (17) 3 (21) 0.8 (0.2-3.1) Univariable logistic regression analysis. *p<0.05. a n=469, b n=99, c n=71, d n=19, Table 1. Analysis of association between change (Δ) in FMD and relevant parameters by univariate and multivariate linear regression analysis. Univariate Rho (p ) Multivariate Beta (p ) Δ FMD (%) (r 2 =0.30 ) Change ADMA (µmol/l) -0.63 (<0.001) -0.25 (0.01) MDA (nmol/ml) -0.58 (<0.001) -0.18 (0.02) SOD (U/ml) 0.48 (<0.001) NS GSH (U/ml) 0.02 (0.75) NS HOMA -0.21 (0.001) NS eGFR (ml/min/ 1.73 m 2 ) -0.03 (0.62) NS hsCRP (mg/l) -0.45 (<0.001) NS PTX3 (ng/ml) -0.49 (<0.001) -0.21 (0.01) SBP (mmHg) -0.26 (<0.001) NS DBP (mmHg) -0.11 (0.12) NS Hemoglobin (g/dl) 0.07 (0.32) NS Total Cholesterol (mg/dl) -0.05 (0.49) NS Triglyceride (mg/dl) -0.11 (0.12) NS LDL (mg/dl) -0.12 (0.07) NS HDL (mg/dl) 0.02 (0.82) NS HbA1c (%) -0.26 (<0.001) NS Figure 1. Scatter-plot graphs between FMD and ADMA, MDA, CuZn-SOD, PTX-3. Conclusion: In our study we found sex differences regarding age and disease duration, being higher in women. As expected, the prevalence of RA was higher in women and AS and PsA in men. Overall, women used more steroids than men. An interesting finding was that patients had high disease activity. Future longitudinal analyses will allow us to analyse sex differences in disease progression and treatment response. References: [1] Ortona E et al. Ann Ist Super Sanita 2016;52(2):205-12 [2] Ngo ST et al. Front Neuroendocrinol 2014;3(3):347-69 Disclosure of Interests: Vijaya Rivera Teran: None declared, Deshire Alpizar-Rodriguez: None declared, Sandra Sicsik: None declared, Fedra Irazoque-Palazuelos Consultant of: Bristol-Myers Squibb, Janssen, Pfizer Inc, Roche and UCB, Dafhne Miranda: None declared, David Vega-Morales: None declared, Julio Cesar Casasola: None declared, Sandra Carrilo: None declared, angel castillo: None declared, Sergio Duran Barragan: None declared, Omar Muñoz: None declared, Aleni Paz: None declared, Angélica Peña: None declared, Alfonso Torres: None declared, Daniel Xavier Xibille Friedmann Consultant of: Lilly, Abbvie, Speakers bureau: Lilly, Abbvie, Azucena Ramos: None declared, José Francisco Moctezuma: None declared, Francisco Aceves: None declared, Estefania Torres: None declared, Natalia Santana: None declared, Miguel Vazquez: None declared, Erick Zamora: None declared, Francisco Guerrero: None declared, Claudia Zepeda: None declared, Melanea Rivera: None declared, Kitzia Alvarado: None declared, Cesar Francisco Pacheco Tena: None declared

Children are undoubtedly among the most vulnerable individuals to contract amebiasis and suffer amebic disease in communities where amebiasis is endemic, children are affected to a similar or greater degree than the adult population. The frequency of amebic infection and disease in the infantile population of a given community can be estimated from the number of recorded cases of intestinal and hepatic amebic disease, from seroepidemiologic studies, from institutional autopsies and from carrier analysis in the open population. Invasive intestinal amebiasis is more frequent in children than in adults. The classical amebic dysentery with frequent, blood-stained, mucus-containing stools with scarce fecal material, accompanied by abdominal cramps and tenesmus, is less frequent in children than in adults. A presumptive diagnosis of amebic abscess of the liver can be established in children by careful integration of the clinical syndrome. In endemic areas, fever and painful hepatomegaly should immediately suggest the possibility of amebic abscess of the liver.

BACKGROUND:Helicobacter pylori infection occurs mostly during childhood, but few studies on this age group have addressed the innate immune and the proliferative response to this infection. Mexico has a high H. pylori prevalence in children, but a low risk of gastric cancer. The aim of this work was to study the cellular responses of the gastric mucosa to this infection in Mexican children.METHODS:Antral and corpus gastric biopsies were obtained from 44 H. pylori-infected children (mean age 12 +/- 3.2 years) and 44 uninfected children (mean age 10 +/- 3 years). Mucosal cellular responses were studied by immunohistochemistry, using anti-Ki67 antibodies for proliferation studies, antihuman tryptase for mast cells, and antihuman CD68 for macrophages. T and B lymphocytes were stained with a commercial integrated system. The intensity of cellular responses was estimated histologically using the software KS300.RESULTS:Epithelium proliferation and infiltration of macrophages and T and B lymphocytes were significantly higher in H. pylori-infected than in uninfected children. A balanced increase of CD4, CD8, and CD20 lymphocytes was observed in infected children. However, activated mast cells were decreased, and infiltration of neutrophil and mononuclear cells was low. Epithelial proliferation was associated with polymorphonuclear infiltration but not with infiltration of macrophages or lymphocytes. Inflammation and proliferation was higher in CagA (+)-infected children.CONCLUSIONS:Mexican children respond to H. pylori infection with a low inflammatory response, a balanced increase of T and B lymphocytes, and a high regenerative activity.

Infection by Helicobacter pylori affects about 50% of the human population. Of those infected, 10% to 15% will develop peptic ulcer and up to 3% will present with gastric cancer. These estimates suggest that around 7% of the world's population will eventually develop H. pylori –associated

Background: Social and economic development together with demographic changes and health interventions have resulted in an increase in life expectancy and a rapidly ageing population in Mexico. Whether people will live longer active and independent lives is still, however, unknown. We will address this question, providing the first estimates of active life expectancy by age, sex and local regional area in Mexico.Methods: Active life expectancy was calculated using the Sullivan method with abridged life tables. Information on the older Mexican population covered by the Mexican Institute of Social Security (IMSS) and the number of deaths for the same group in the year 2000 was obtained from the Office for Health Statistics and Information at IMSS in Mexico. Information on ability to perform basic activities of daily living was obtained from the National Survey on Ageing carried out in IMSS during 1998 - 99.Results: For males and females combined, active life expectancy decreased from 26.9 years at 60 years to 5.7 years at 85 years. Women's life expectancy exceeded that of men but women lived more years dependent. Similarly, older people in geographical areas with longer life expectancy spent a lower proportion of remaining life active.Conclusion: The success in increasing life expectancy above average in some groups of older people covered by IMSS has been accompanied by increments in the proportion of remaining years dependent upon others for help in basic self-care activities.

Background:The cagA gene is a marker for the presence of the cag pathogenicity island, and the presence of cagA positive strains ofHelicobacter pylorican identify individuals with a higher risk of developing gastrointestinal diseases.Aims:To study the interaction betweenH pyloricagA(+) and cagA(−) strains and the gastric mucosa.Methods:Patients withH pyloriassociated gastritis and peptic ulcers were studied. Biopsies were obtained from the antrum, corpus, fundus, and incisura forH pyloriculture, and for in situ hybridisation studies. From each biopsy, multiple singleH pyloricolonies were isolated and propagated for DNA isolation, and cagA was detected by the polymerase chain reaction (PCR). For in situ detection ofH pylorian oligonucleotide specific for anH pyloricommon antigen and an oligonucleotide specific for cagA were used as probes. Biotinylated probes were incubated with biopsy sections, developed with streptavidin–horseradish peroxidase, and amplified with the tyramide system.Results:PCR results for cagA in isolated colonies confirmed the in situ hydridisation studies. In situ hybridisation identified cagA(+) bacteria in patients with cagA(+) isolates; cagA(−) bacteria in patients with cagA(−) isolates, and cagA(+) and cagA (−) bacteria in patients with both cagA(+) and cagA(−) isolates. CagA(−) bacteria usually colonised the mucous gel or the apical epithelial surface, whereas cagA(+) bacteria colonised the immediate vicinity of epithelial cells or the intercellular spaces.Conclusions:These results document a different in vivo interaction betweenH pyloricagA(+) orcagA(−) strains and the gastric mucosa.

ABSTRACT The prevalence and type diversity of human astroviruses (HAstV) in children with symptomatic and asymptomatic infections were determined in five localities of Mexico. HAstV were detected in 4.6 (24 of 522) and 2.6% (11 of 428) of children with and without diarrhea, respectively. Genotyping of the detected strains showed that at least seven (types 1 to 4 and 6 to 8) of the eight known HAstV types circulated in Mexico between October 1994 and March 1995. HAstV types 1 and 3 were the most prevalent in children with diarrhea, although they were not found in all localities studied. HAstV type 8 was found in Mexico City, Monterrey, and Mérida; in the last it was as prevalent (40%) as type 1 viruses, indicating that this astrovirus type is more common than previously recognized. A correlation between the HAstV infecting type and the presence or absence of diarrheic symptoms was not observed. Enteric adenoviruses were also studied, and they were found to be present in 2.3 (12 of 522) and 1.4% (6 of 428) of symptomatic and asymptomatic children, respectively.

Background. Experimental evidences have suggested that a Th1 response is unable to eliminate H. pylori colonization; whereas a Th2 response, like the one induced by vaccination, reduces H. pylori infection in animal models. Some parasitic infections induce a polarized Th2 response, which theoretically would favor a reduced H. pylori prevalence. The aim of this work was to study the possible association between parasitic infections and H. pylori prevalence.Materials and Methods. The study population included 120 children and 188 adults from a low socioeconomic level village. H. pylori prevalence was determined in serum by ELISA; parasitic infections were identified in feces by microscopic examination; and total serum IgE levels, as an indirect indicator of some parasitic infections, were determined by ELISA.Results. In children, H. pylori prevalence was no different between those with and without intestinal parasitic infection. By contrast, adults with intestinal parasitic infection had a significantly lower H. pylori prevalence than adults without parasites (62.6% compared with 80.4%; p=0.006, OR 2.45). Also in adults, but not in children, total IgE levels were significantly higher in those without H. pylori infection than in those with H. pylori infection (P<0.001).Conclusions. Intestinal parasitic infections and serum IgE levels showed an age-dependent association with H. pylori prevalence. In adults, but not in children, intestinal parasitic infections and increased IgE levels where associated with a reduced H. pylori prevalence.

ABSTRACT This report is of a community-based case control study to assess whether the severity of acute diarrhea by rotavirus (RV) in young children is associated with a particular VP7 (G) or VP4 (P) RV serotype. Five hundred twenty children younger than 2 years of age with diarrhea lasting less than 3 days were age and gender matched with 520 children with no diarrhea. The G and P serotypes were determined with specific monoclonal antibodies, and the VP4 serotype specificity in a subgroup was confirmed by genotyping. Infection with a G3 serotype led to a higher risk of diarrhea than infection with a G1 serotype. Infection with a G3-nontypeable-P serotype was associated with more severe gastroenteritis than infection with a G3 (or G1) P1A[8] serotype. A child with diarrhea-associated dehydration was almost five times more likely to be infected with a G3-nontypeable-P serotype than a child without dehydration (P < 0.001). Moreover, the two predominant monotypes within serotype P1A[8] had significantly different clinical manifestations. In this study, the severity of RV-associated diarrhea was related to different P serotypes rather than to G serotypes. The relationship between serotype and clinical outcomes seems to be complex and to vary among different geographic areas.

BACKGROUND:Few reports exist on inflammation and interleukin (IL)-8 response in H. pylori-infected children. The aim of this study was to determine the intensity of inflammation, density of colonization and magnitude of IL-8 response in children with and without H. pylori infection.MATERIALS AND METHODS:We studied 45 children with dyspeptic symptoms, 21 infected with H. pylori and 24 without infection. Antrum and corpus gastric biopsies were obtained and studied for H. pylori infection with an immunofluorescence technique and for IL-8 with an immunohistochemical assay. Biopsy specimens were stained with hematoxilin and eosin and gastritis was graded according to the Sydney system. The magnitudes of the IL-8 response and H. pylori colonization were estimated microscopically with image analyzer software.RESULTS:In H. pylori-infected children, mild mono-nuclear cell infiltration was found in 50%, and no neutrophils in 40% of cases. In the antrum but not in the corpus, the intensity of colonization correlated with neutrophil and mononuclear cell infiltration. The IL-8 response was significantly higher in the antrum (p <.05) and corpus (p <.02) of infected children, and was localized mainly in the surface and crypts of the epithelium. No correlation was found between the magnitude of the IL-8 response and the infiltration of either neutrophil or mononuclear cells.CONCLUSIONS:In H. pylori-infected children, poor mononuclear and neutrophil infiltration was observed. Infection was associated with a higher IL-8 response by gastric epithelial cells. The density of colonization but not the IL-8 response correlated with neutrophil cell infiltration.

OBJECTIVES: Little is known concerning the magnitude of reinfection versus recrudescence of Helicobacter pylori (H. pylori) infection after eradication treatment. The aims of this study were to determine the magnitude of H. pylori reinfection versus recrudescence, and to identify possible risk factors for reinfection.METHODS: Children and adults with upper GI symptoms treated at the Centro Medico Nacional Siglo XXI (Instituto Mexicano del Seguro Social, in Mexico City, Mexico) were studied. H. pylori infection was diagnosed with urea breath test (UBT), histology, and culture. Infected patients received triple therapy, and those who became UBT negative 4 - 6 wk after treatment were considered as eradicated and were included in the study. A cohort of 141 patients in whom the disease was eradicated was monitored for recurrence with UBT at 3, 6, 9, 12, 18, and 24 months. H. pylori was isolated from gastric biopsy samples before treatment and at recurrence and isolates compared by genotyping.RESULTS: During this period, 32 (22.7%) cases of recurrence were documented the majority occurring during yr 1. In nine of the 32 (28.1%) cases, recurrence was eradicated spontaneously, suggesting these were transient reinfections. Recurrence rates were significantly higher in the subjects 41-60 yr of age than in younger or older subjects. H. pylori isolates from 12 recurrence cases were genotyped; nine (75%) were classified as true reinfection and three as recrudescence.CONCLUSIONS: In our population, recurrence rate is high in adults and transient reinfection is common. In several cases, reinfection occurred by multiple strains, which suggests that soon after eradication, patients are exposed to multiple sources of reinfection. (C) 2003 by Am. Coll. of Gastroenterology.

Few studies have analyzed the immune response to Helicobacter pylori CagA and urease antigens across age groups in the same population. The aim of this study was to analyze the serologic immunoglobulin G (IgG) response to CagA and urease proteins in children and adults with gastrointestinal symptoms and belonging to the same population and similar socioeconomic levels. The serologic response was studied in 352 children and 293 adults with gastrointestinal symptoms. IgG antibodies against CagA and urease were tested by enzymelinked immunosorbent assay methods using highly purified recombinant antigens. H. pylori infection was defined as a positive result in a serologic assay using whole-cell H. pylori extracts as the antigen. We found, in H. pylori-positive children, a seroprevalence of 46.9% to CagA and 16.2% to urease, whereas in H. pylori-positive adults, a seroprevalence of 78.9% to CagA and 59% to urease was found. In children, the magnitude of the response to CagA was significantly higher and the response to urease was significantly lower than those in adults. The kinetics of serologic response to CagA and to urease across age groups was contrastably different. Whereas CagA is a strong immunogen, urease is a poor immunogen during natural infection. These differences in the humoral response may be important for the short-term or long-term outcome of the infection. These results add to our knowledge of the epidemiology of H. pylori infection.

Helicobacter pylori genome contains a gene (HP1338) that encodes a nickel-dependent regulator homologous to the Escherichia coli nickelresponsive regulator NikR. Due to limited identity with E. coli NikR, H. pylori nikR was only able to partially complement a nikR deficient E. coli strain, and displayed a pleiotropic metal-dependent regulatory function. A non-polar isogenic mutant deleted for the nikR gene was constructed, and native and maltose binding protein-fused recombinant NikR proteins were purified. The NikR protein was shown to be essential for H. pylori resistance to high nickel (>300 μM) and cobalt (>2μM) ion concentrations in vitro, but was not essential for the colonization of mouse gastric mucosa. Using a differential gene expression analysis, we screened a DNA macroarray for genes that were differentially expressed in parental and nikR deficient H. pylori strains grown under either normal or nickel overload (250 μM) conditions. We showed that H. pylori NikR can mediate directly or indirectly the regulation of a series of nickel-activated or –repressed genes. The transcriptome data were further confirmed for 10 of these genes in slot blot DNA/RNA hybridization experiments from RNA prepared from three independent bacterial cultures. Based on gel shift and ß-galactosidase assays with the intergenic region between nikR and the exbB/exbD divergent operon, we provide evidence that NikR is an autoregulator which binds to the intergenic region, and we suggest that it might also control the exbB/exbD/tonB operon that provides energy for ferric iron uptake systems. Thus, as previously suggested for Fur in H. pylori, NikR appears to act as a global regulator for the metabolism of the divalent cations within a highly complex regulated network.

The response to 2 consecutive protease inhibitor (PI) combination regimens was evaluated in a cohort of HIV-1-infected children. Twelve children, most of whom had been heavily treated, received a 3-drug treatment: saquinavir in hard gelatin capsules (SQVhgc) + zidovudine (ZDV) + didanosine. When this treatment failed it was replaced by a 4-drug regimen: ritonavir + SQVhgc + ZDV + lamivudine. A mild and temporary decrease in viral load (VL) was observed with the initial regimen (p=0.22). Therapy failure occurred in 7 patients (58%) within 9 months and in another 3 (25%) within 9-18 months. The 7 children who failed within 9 months received the subsequent boosted regimen, leading to a significant and lasting reduction in VL ( p = 0.001). None of the patients failed on the boosted regimen: 5/7 achieved a VL of < 400 copies/ml and 3/7 achieved a VL of < 50 copies/ml. Our results suggest that a 4-drug regimen including 2 PIs produces a better and more sustained response than a 3-drug regimen including only 1 PI, and that a good, sustained response is possible with subsequent boosted regimens even in heavily treated children.

The protozoan parasite Entamoeba histolytica is the etiological agent of human amebiasis. The pathology of the disease starts with the cytolysis of the host target cells by amoebae. It is initiated by the adhesion of trophozoites to the host cells, through surface lectin via specific receptors. These adherence lectins have been demonstrated to be highly conserved, and can be recognised by serum antibodies from patients with invasive amebiasis. Some of these molecules have been used as antigens in serologic studies, which has been very helpful in the diagnosis of invasive intestinal amebiasis. However, false-positive serologic reactivity can occur using E. histolytica extracts and purified antigens. Additional problems are because the extracts display a great enzymatic activity. Several diagnostic methods, using different molecules and techniques, have been described. However, the problem still remains since these tests are not capable of differentiating between amoebic liver abscess (ALA) and intestinal amebiasis.Here, the research has been addressed to the 66-kDa antigen, which is a part of the outer membrane proteins from the E. histolytica strain HM1-IMSS trophozoites. First of all, we characterized the 66-kDa antigen in order to prove the relevance. We found that the 66-kDa antigen is a part of the plasma membranes and is distributed rather homogeneously on the cell surface of trophozoites. Apparently, the 66-kDa antigen is a glycoprotein. Using a monoclonal antibody (MAb), we found 25% of inhibition in the erythrophagocytosis by the trophozoites. Starting form one monoclonal antibody, we prepared an anti-idiotype (anti-Id) antibody reagent, with the purpose of searching for the different expressions of the idiotype between the sera from ALA and the intestinal amebiasis patients. Moreover, we produced the antibody Ab3 that is capable of recognising the 66-kDa antigen; it means that the Ab2 displays the internal image of the antigen. We found that 91.6% of the serum from ALA patients displayed the expression of the Id. In contrast, 15.7% of the E. histolytica asymtomatic cyst carriers displayed the Id expression, 6.6% of the patients with another parasite infection, and 11% of the negative controls (serum from umbilical cords of newborn babies). Our results showed that the expression of the Id could be differentiated among the AHA patients from the other groups with a 91.6% sensibility and 88.3% specificity.

There are no reports, to our knowledge, on the expression of Lewis (Le) antigens in Helicobacter pylori isolates from children. The aim of this study was to compare the expression of Le antigens by H. pylori isolates from children and from adults. Totals of 278 clones from 22 children with recurrent abdominal pain and 293 clones from 22 adults with (n=10) or without (n=12) duodenal ulcer were studied. Expression of Le(x) and Le(y) antigens was determined by ELISA, using monoclonal anti-Le antibodies. The Le phenotype of the patients was determined in gastric juice with a hemagglutination assay. Clones expressing Le(x) were more common in children than in adults (55.4% vs. 33.4%, respectively; P<.001), and Le(y) was more common in adults than in children (81.6% vs. 66%, respectively; P<.01). A trend analysis showed a significant decline in frequency of clones expressing Le(x) with age (P=.021). In this community, expression of Le antigens differs in H. pylori isolates obtained from children versus adults.

BACKGROUND:Enterococcus spp. is an important nosocomial and community-acquired pathogen. Recent studies have documented the increasing importance of this pathogen in children, particularly in the hospital setting. Our objective in this study was to report the frequency of antimicrobial resistance in enterococci and to determine the characteristics of high-level gentamicin resistance (HLGR) plasmids in Enterococcus faecalis clinical isolates. METHODS:Two hundred eighty-nine enterococcal isolates were collected during an 18-month period from a tertiary-care pediatric hospital in Mexico City. Isolates were screened for antibiotic resistance, including HLGR. High-level, gentamicin-resistant E. faecalis strains were selected for pulsed-field electrophoresis (PFGE) typing and plasmid analysis. Transferability of resistance markers was carried out using filter matings. RESULTS:Seventy-six percent of isolates were E. faecalis, 10% were E. avium, 5.2% E. faecium, 5.2% E. raffinossus, 1.38% E. malodoratus, 0.6% E. hirae, and 0.6% E. casseliflavus. Antimicrobial resistance was ampicillin and penicillin 29%, imipenem 17%, and vancomycin 3%, HLGR 5%. The following 15 high-level, gentamicin-resistant isolates were identified: six E. faecalis; four E. avium; three E. faecium, and two E. casseliflavus. Five of the six E. faecalis isolates were different by PFGE and transferred gentamicin and streptomycin resistance on filter membranes. Transfer frequencies ranged from 8.2 x 10(-4) to 6.92 x 10(-5) transconjugants/recipient cell. The plasmid content of donors and transconjugants were homogeneous (one plasmid of 47 kb). CONCLUSIONS:In this pediatric hospital, antimicrobial resistance in Enterococcus spp. is common. Frequency of high-level, gentamicin-resistant strains is low. Mechanism of HLGR appears to be due to a single plasmid dissemination.

ABSTRACT The susceptibilities to three antimicrobials of 195 Helicobacter pylori strains isolated from Mexican patients is reported; 80% of the strains were resistant to metronidazole, 24% were resistant to clarithromycin, and 18% presented a transient resistance to amoxicillin. Resistance to two or more antimicrobials increased significantly from 1995 to 1997.