COX-2-derived prostaglandins as mediators of the deleterious effects of nicotine in chronic kidney disease.

Tobacco smoking has been identified as a risk factor in the progression of chronic kidney disease (CKD). In previous studies, we showed that nicotine induces cyclooxygenase (COX)-2 expression in vivo and in vitro and that the administration of nicotine in vivo worsens the severity of renal injury in a model of subtotal renal ablation. In the present study, we tested the role of COX-2-derived prostaglandins on the deleterious effects of nicotine in CKD. Sham and 5/6 nephrectomy (5/6Nx) rats received tap water or nicotine (100 µg/mL) in the drinking water for 12 wk. Additional groups also systemically received the COX-2 inhibitor NS-398 (1.5 mg·kg-1·day-1 via osmotic minipump). The administration of nicotine worsened renal injury and proteinuria in 5/6Nx rats and increased proteinuria in sham rats. 5/6Nx rats had increased cortical production of the prostaglandins PGE2, PGI2, PGD2, and PGF2α and of thromboxane A2. In these rats, nicotine reduced the production of all prostaglandins examined except thromboxane A2. Treatment with the COX-2 inhibitor NS-398 resulted in complete inhibition of all prostaglandins studied and ameliorated renal injury and proteinuria in 5/6Nx rats on nicotine but not in 5/6 Nx rats on tap water. Nicotine also reduced the expression of megalin in all groups examined, and this was partially prevented by COX-2 inhibition. In the present study, we showed that in CKD, nicotine worsens renal injury at least in part by producing an imbalance in the production of prostaglandins. This imbalance in the production of prostaglandins likely plays a role in the deleterious effects of smoking on the progression of CKD.

Novel giardicidal compounds bearing proton pump inhibitor scaffold proceeding through triosephosphate isomerase inactivation.

Giardiasis is a worldwide parasitic disease that affects mainly children and immunosuppressed people. Side effects and the emergence of resistance over current used drugs make imperative looking for new antiparasitics through discovering of new biological targets and designing of novel drugs. Recently, it has determined that gastric proton-pump inhibitors (PPI) have anti-giardiasic activity. The glycolytic enzyme, triosephosphate isomerase (GlTIM), is one of its potential targets. Therefore, we employed the scaffold of PPI to design new compounds aimed to increase their antigiardial capacity by inactivating GlTIM. Here we demonstrated that two novel PPI-derivatives (BHO2 and BHO3), have better anti-giardiasic activity than omeprazole in concentrations around 120-130 µM, without cytotoxic effect on mammal cell cultures. The derivatives inactivated GlTIM through the chemical modification of Cys222 promoting local structural changes in the enzyme. Furthermore, derivatives forms adducts linked to Cys residues through a C-S bond. We demonstrated that PPI can be used as scaffolds to design better antiparasitic molecules; we also are proposing a molecular mechanism of reaction for these novel derivatives.

Long term renal survival in patients undergoing T-Cell depleted versus conventional hematopoietic stem cell transplants.

Calcineurin inhibitor (CNI)-sparing T-cell depleted (TCD) hematopoietic stem cell transplants (HSCTs) are presumed to be less nephrotoxic than conventional HSCTs. We evaluated incidence and risk factors for kidney failure and chronic kidney disease (CKD) in 231 TCD and 212 conventional HSCT recipients. Kidney failure required a median glomerular filtration rate (GFR) <60 ml/min/1.73 m2 for ⩾100 days anytime after 180-days post-HSCT. Two-year cumulative incidence (CI) of kidney failure was 42% in the conventional versus 31% in the TCD group (P=0.005). TCD, age, acute kidney injury and number of toxic CNI levels all impacted on kidney failure, which was associated with increased all-cause mortality (hazard ratio 2.86 (95% CI: 1.88-4.36), P<0.001). Renal recovery occurred in 28% of kidney failure patients whereas the remaining patients were defined to have CKD. In those with baseline GFR>60 ml/min/1.73 m2, only exposure to nephrotoxic medications was associated with CKD (P=0.033). In the myeloablative-conditioning subgroup only total body irradiation was associated with CKD (P=0.013). Of all patients, five (1.13%) required dialysis. These results confirm an impact of TCD on kidney failure but not CKD for which other risk factors such as radiation or nephrotoxic drug exposure may have a role.

Effects of the reactive oxygen species hydrogen peroxide and hypochlorite on endothelial nitric oxide production.

Reactive oxygen species (ROS) hydrogen peroxide (H(2)O(2)) and hypochlorite (HOCl) participate in the pathogenesis of ischemia/reperfusion injury, inflammation, and atherosclerosis. Both NO and ROS are important modulators of vascular tone and architecture and of adhesive interactions between leukocytes, platelets, and vascular endothelium. We studied the effect of H(2)O(2) and HOCl on receptor-dependent (bradykinin [10(-6) mol/L] and ADP [10(-4) mol/L]) and receptor-independent mechanisms (calcium ionophore A23187 [10(-6) mol/L]) of NO production by porcine aortic endothelial cells (ECs). Changes in the level of EC cGMP (the second messenger of NO) were used as a surrogate of NO production. EC cGMP increased 300% in response to bradykinin and A23187 and 200% in response to ADP. Exposure of ECs to H(2)O(2) (50 micromol/L) for 30 minutes significantly impaired cGMP levels in response to ADP, bradykinin, and the receptor-independent NO agonist A23187. In contrast, preincubation with HOCl (50 micromol/L) impaired cGMP production only in response to ADP and bradykinin but not A23187. These concentrations of H(2)O(2) and HOCl did not result in increased EC lethality as assessed by lactate dehydrogenase release. Neither H(2)O(2) nor HOCl affected EC cGMP production in response to NO donor sodium nitroprusside, which suggests that guanylate cyclase is resistant to these oxidants. We also demonstrated that neither H(2)O(2) nor HOCl affects endothelial NO synthase (eNOS) catalytic activity as measured by conversion of L-arginine to L-citrulline in EC homogenates supplemented with eNOS cofactors. The present studies show that H(2)O(2) impairs NO production in response to both receptor-dependent and receptor-independent agonists and that these effects are due, at least in part, to inactivation of eNOS cofactors, whereas HOCl inhibits NO production by interfering with receptor-operated mechanisms at the level of the cell membrane. Concentrations of H(2)O(2) and HOCl used in the present studies have been shown to be generated in vivo during inflammation and ischemia/reperfusion. Therefore, we infer that these effects of H(2)O(2) and HOCl on EC NO production may contribute to disregulated vascular tone and altered leukocyte-EC interactions that occur in vascular injury as a result of those causes in which ROS generation is involved.

Cigarette smoke-induced endothelium dysfunction: role of superoxide anion.

OBJECTIVES: Cigarette smoking is strongly associated with coronary artery disease and atherosclerosis. While smoking has been shown to impair endothelium-dependent vasorelaxation, the mechanisms involved are not completely understood. We investigated the role of superoxide anion and vasoconstricting prostanoids in cigarette smoke induced endothelial dysfunction. METHODS: Endothelial function was assessed in rat aortic rings exposed to cigarette smoke-treated Krebs buffer, by measuring agonist stimulated endothelium-dependent vasorelaxation. Treatment with superoxide dismutase (SOD) as well as ifetroban, thromboxane A2/prostaglandin endoperoxide H2 (TxA2/PGH2) receptor blocker and indomethacin (cyclooxygenase inhibitor) was used to investigate the role of superoxide anion and vasoconstricting eicosanoids on cigarette smoke-induced endothelial dysfunction. The effect of cigarette smoke on endothelial nitric oxide synthase (eNOS) catalytic activity was measured by conversion of L-arginine to L-citrulline in rat aortas and rat endothelial cell homogenates supplemented with eNOS cofactors. RESULTS: Relaxations to receptor-dependent agonists, acetylcholine and adenosine diphosphate (ADP), as well as to a receptor-independent agonist, A23187 (Ca2+ ionophore) were significantly impaired by cigarette smoke. Cigarette smoke did not impair relaxations to sodium nitroprusside, indicating preserved guanylate cyclase activity. Further, cigarette smoke did not affect eNOS catalytic activity in homogenates from either endothelial cells or aortas previously exposed to cigarette-smoketreated Krebs buffer. Treatment with SOD or ifetroban and in a lesser degree by indomethacin prevented cigarette-smoke-induced endothelial dysfunction. CONCLUSIONS: Taken together, our results suggest that cigarette smoking causes an increase in vascular superoxide production which results in decreased nitric oxide (NO) bioactivity and concomitantly increases production of cyclooxygenase dependent and independent vasoconstricting eicosanoids.

[Antimicrobial resistance characteristics of clinical isolates of Streptococcus pyogenes]. / Características de la resistencia antimicrobiana de una colección clínica de Streptococcus pyogenes.

OBJECTIVE: To determine the antibiotic susceptibility of recent isolates of Streptococcus pyogenes and to evaluate the prevalence of macrolide-resistant phenotypes. MATERIAL AND METHODS: In 1999, we conducted a cross-sectional study at Mexico Children's Hospital "Federico Gomez", to analyze one hundred strains of S. pyogenes isolated from 1992 to 1998, in children with uncomplicated pharyngotonsillitis. Strains were frozen at the bacteriology lab until they were analyzed. Strains were tested for susceptibility against some beta-lactams, macrolides and clindamycin. Double-disk testing was carried out to evaluate erythromycin-resistant phenotypes. Data are presented using central tendency measures. RESULTS: All tested strains were not resistant to beta-lactams and clindamycin; 16% of the strains were resistant to macrolides and all of them belonged to phenotype M. CONCLUSIONS: Susceptibility testing is recommended to identify possible changes in antibiotic resistance to streptococci.

Clinical outcome of invasive infections in children caused by highly penicillin-resistant Streptococcus pneumoniae compared with infections caused by penicillin-susceptible strains.

BACKGROUND: In this report based on data from the Institutional Surveillance System during 1994-1998, we document the continuing emergence of drug-resistant Streptococcus pneumoniae strains at the Hospital Infantil de Mexico Federico Gómez in Mexico City. METHODS: We evaluate the clinical course of 49 invasive pneumococcal infection outside the central nervous system (CNS) by a number of factors including the site, severity, and place where the infection was acquired, the underlying health of the patient, and the adequacy of antimicrobial therapy. RESULTS: An underlying illness was present in 21 of 49 (43%) patients, 37 (75%) patients had taken previous antimicrobial therapy, and 25% of the infections were nosocomially acquired. Overall, 25 of 49 (51%) of the pneumococcal strains tested were pencillin-resistant; strains with the highest resistance to penicillin were also resistant to cephalosporins. Twenty-two percent of all strains were considered to be multidrug-resistant. Eleven of 25 penicillin-resistant strains were identified as multidrug-resistant, i.e., to erythromycin, TMP/SMX, and chloramphenicol. Ten serotypes accounted for 88% of the isolates, the most frequent serotypes being 23F, 14, 19V, 6A, and 6B. The overall case-fatality rate was 37% (18 of 49), with most deaths occurring within 3-5 days after antibiotic therapy was initiated. There was no difference in the case fatality rate between children with penicillin-nonsusceptible and penicillin-susceptible pneumococcal infections; instead; case-fatality rate correlated with severity of illness on admission and presence of underlying disease. CONCLUSIONS: Characterizing groups at risk for invasive pneumococcal disease could aid in the development of preventive programs and increase the benefits from wide use of future conjugated vaccines.

[Clinico-microbiological characteristics of meningitis caused by penicillin-resistant Streptococcus pneumoniae]]. / Características clínico-microbiológicas de la meningitis por Streptococcus pneumoniae resistente a la penicilina.

OBJECTIVE: To evaluate the susceptibility to antibiotics of Streptococcus pneumoniae isolated from cerebrospinal fluid of children with meningitis. To describe and compare the clinical and microbiological characteristics, treatment and outcome among children infected with strains either susceptible or resistant to penicillin and cephalosporin. MATERIAL AND METHODS: A total of 38 children with pneumococcal meningitis were prospectively enrolled in the Institutional Surveillance Program for Pneumococcal Infections during 1994-1998. Clinical and laboratory data were collected by chart review. RESULTS: Of the 38 children, 24 (63%) were less than 2 years of age, 11 (28.9%) had drug-resistant S. pneumoniae, 18.4% had intermediate resistance, 10.5% high level resistance and 2.6% also showed high level resistance to cefotaxime. The only associated factors (by Fisher's exact test) associated to resistance were: previous use of antibiotics (p = 0.2), underlying disease (p < 0.001). Course of illness and clinical course were similar for children infected with penicillin or cefotaxime susceptible, vs. non-susceptible strains. CONCLUSIONS: Current levels of S. pneumoniae resistance to penicillin and cephalosporin are not associated to an increase in mortality in children with meningitis.

Angiotensin II induces superoxide anion production by mesangial cells.

BACKGROUND: The recognized role of angiotensin II (Ang II) in the pathogenesis of the progression of renal disease cannot be solely attributed to Ang II's hemodynamic effects. Indeed, growth stimulating signals driven by Ang II promote mesangial cell (MC) hypertrophy and extracellular matrix production, prominent features of progressive glomerular injury. Superoxide anion (O2-) avidly interacts with nitric oxide, an endogenous vasodilator that inhibits growth factor stimulated MC growth and matrix production. In addition, O2- acting as an intracellular signal is linked to growth related responses such as activation of mitogen activated protein (MAP) kinases. The studies reported herein were designed to investigate: (a) whether Ang II induces MC O2-production and (b) if increased O2- production elicits growth responses in MC. METHODS: MC were exposed to Ang II for 24 or 48 hours. In some experiments, in addition to Ang II, MC were exposed to: diphenylenieodonium (DPI), an inhibitor of the flavin containing NADH/NADPH oxidase; losartan (LOS), an Ang II type 1 (AT1) receptor blocker; PD 98059, a MAP kinases inhibitor; the protein kinase C inhibitors Calphostin C or H-7; and the tyrosine kinase inhibitors, herbymycin A or genistein. RESULTS: Ang II (10(-5) M to 10(-8) M) dose dependently increased MC O2- production up to 125% above control (ED 50 5 x 10(-7) M). LOS as well as DPI, and the PKC inhibitors blocked Ang II stimulated MC O2- production. Ang II dose dependently increased MC 3H-leucine incorporation, and MC protein content, two markers of MC hypertrophy, as well as 3H-thymidine incorporation, a marker of MC hyperplasia. PD98059, a specific inhibitor of MAP kinases prevented Ang II induced MC hypertrophy. Moreover, LOS, DPI, and the PKC inhibitors each independently inhibited MC 3H-leucine incorporation, thereby establishing the specificity of Ang II induced O2- in driving MC hypertrophy. CONCLUSIONS: The current studies demonstrate a previously unrecognized link between Ang II and MC O2- production that may participate in the pathophysiology of progressive renal disease by concomitantly affecting the hemodynamics of the glomerular microcirculation as well as growth related responses of MC to injury.

Nitric oxide production during Vibrio cholerae infection.

Vibrio cholerae induces massive intestinal fluid secretion that continues for the life of the stimulated epithelial cells. Enhanced regional blood flow and peristalsis are required to adapt to this obligatory intestinal secretory challenge. Nitric oxide (NO) is a multifunctional molecule that modulates blood flow and peristalsis and possesses both cytotoxic and antibacterial activity. We demonstrate that, compared with those in asymptomatic control subjects, levels of stable NO metabolites (NO2-/NO3-) are significantly increased in sera from acutely ill Peruvian patients with natural cholera infection as well as from symptomatic volunteers from the United States infected experimentally with V. cholerae. In a rabbit ileal loop model in vivo, cholera toxin (CT) elicited fluid secretion and dose-dependent increases in levels of NO2-/NO3- in the fluid (P < 0.01). In contrast, lipopolysaccharide (LPS) elicited no such effects when applied to the intact mucosa. NO synthase (NOS) catalytic activity also increased in toxin-exposed tissues (P < 0.05), predominantly in epithelial cells. The CT-induced NOS activity was Ca2+ dependent and was not suppressed by dexamethasone. In conclusion, symptomatic V. cholerae infection induces NO production in humans. In the related animal model, CT, but not LPS, stimulated significant production of NO in association with increases in local Ca(2+)-dependent NOS activity in the tissues.

Glomerular and vascular tissues do not down-regulate nitric oxide synthesis during protracted endotoxemia.

Down-regulation of cytokines is implicated as an important component of the phenomenon of tolerance to bacterial products in humans and animals. Since many effects of endotoxin and cytokines are mediated by nitric oxide, this study was designed to evaluate in vivo the L-arginine:NO pathway in endotoxin tolerance. Sublethal injections of E. coli lipopolysaccharide (LPS, 1 mg/kg body wt, i.p.) were given to rats daily for five days. Blood levels of NO2-/NO3-, stable metabolites of nitric oxide (NO), significantly increased on day 1 (baseline, 89.64 +/- 40, day 1, 260.32 +/- 36 nmol/ml; P < 0.05) but returned to baseline levels on day 5 (77.60 +/- 5 nmol/ml). However, urinary NO2-/NO3- remained significantly elevated several-fold throughout the study period (baseline, 121.25 +/- 11.4, day 1, 899.35 +/- 15.8, day 5, 250.23 +/- 21.4 nmol/hr/100 g body wt). Glomeruli and aortae obtained from these rats showed increased NO production that was maintained at similar levels even at day 5 (glomeruli: control, 0.01 +/- 0.0, day 1, 22.4 +/- 0.3, and day 5, 22.0 +/- 2.5, P < 0.05 vs. control; aortae; control, 0.01 +/- 0.0, day 1, 4.3 +/- 2.2, and day 5, 5.4 +/- 1.0 nmol/hr/mg protein, P < 0.05 vs. control, respectively); this further increased significantly in response to in vitro LPS challenge. However, peritoneal macrophages, liver and spleen showed an initial increase in NO production that decreased significantly by the fifth day of LPS and could not be further stimulated by in vitro LPS challenge. Thus, in vivo NO synthesis is down-regulated during protracted LPS. Our results show that the process is relatively specific to the liver, spleen and macrophages, and is qualitatively and quantitatively different in vascular tissues such as aortae and glomeruli.

Hydrogen peroxide downregulates IL-1-driven mesangial iNOS activity: implications for glomerulonephritis.

In glomerulonephritides, autacoids such as nitric oxide (NO), reactive oxygen species, and prostanoids are produced in increased amounts in response to cytokines such as interleukin-1 (IL-1). These autacoids influence the expression of glomerular injury by their direct as well as interactive actions. We studied the effect of hydrogen peroxide (H2O2) on NO production in rat mesangial cells. We demonstrate that transient exposure of mesangial cells to H2O2 prior to sustained exposure to IL-1 decreased extracellular accumulation of NO2/NO3 and cellular guanosine 3,'5'-cyclic monophosphate (cGMP) content. H2O2 markedly impaired inducible nitric oxide synthase (iNOS) activity induced by IL-1 directly measured by the conversion of L-[14C]arginine to L-[14C]citrulline. Such impairment in iNOS activity was accompanied by a parallel reduction in iNOS protein abundance but not by a reduced expression of iNOS mRNA. The inhibitory effect of H2O2 on NOS activity was further supported by peroxide-induced impairment in IL-1-driven, NO-dependent synthesis of prostaglandin E2. Our studies thus provide the first direct evidence of a posttranscriptional inhibitory effect of H2O2 on iNOS activity. Additionally, our studies uncover the existence of a previously unrecognized effect of H2O2 on the production of NO that may exert influence on the severity of glomerular injury during glomerular inflammation.

End-stage renal disease: why aren't improvements in hypertension treatment reducing the risk?

Although we have seen a decreased incidence of some of the complications of hypertension, such as myocardial infarction and stroke, the same cannot be said for end-stage renal disease (ESRD). The disparity brings up the question of why improvements in hypertension control apparently do not bring improvement in the incidence of ESRD. Some of the factors likely at play include variation in the mechanisms at work in hypertensive patients of different races and variation in the degree to which antihypertensive agents affect systemic blood pressure and glomerular capillary pressure. These and other factors relating to hypertension and ESRD are the focus of this review.

Prevalence, incidence, and determinants of syphilis in female commercial sex workers in Mexico City.

GOAL: To determine the prevalence and the incidence of serologic markers for syphilis, and the characteristics associated with the risk of infection in female commercial sex workers in Mexico City. To identify female commercial sex workers at greater risk of infection with syphilis. STUDY DESIGN: The authors performed a cross-sectional study of 3,100 female commercial sex workers who sought human immunodeficiency virus testing at a National Council on AIDS clinic between January 1992 and April 1993. The authors collected information about socioeconomic and demographic characteristics, history of sexually transmitted diseases, sexual practices, and preventive measures against such diseases. All of the women provided a blood sample for identification of infection markers and in a subgroup of 1,802 women, repeat samples were obtained to estimate the rate of seroconversion to syphilis. RESULTS: Prevalence of syphilis was 8.2%, with an incidence of 2.4 per 100 person years. A positive linear relation between age and time working in commercial sex and prevalence of infection markers was observed. Women with less education, born in states other than Mexico City, and who worked on the street had significantly greater risks of infection with syphilis. CONCLUSIONS: Frequency of infection by both estimators is relatively low in the women studied. Characteristics related with periods of exposure such as age and time working in commercial sex, as well as socioeconomic and demographic characteristics, such as place of birth, education, and type of work site, were significantly related to the frequency of infection.

PIP: The goal of this study was to determine the prevalence and the incidence of serologic markers for syphilis and the characteristics associated with the risk of infection in female commercial sex workers (CSWs) in Mexico City. It also sought to identify female CSWs at greater risk of infection with syphilis. The authors performed a cross-sectional study of 3100 female CSWs who sought human immunodeficiency virus testing at a National Council on AIDS clinic between January 1992 and April 1993. The authors collected information about socioeconomic and demographic characteristics, history of sexually transmitted diseases, sexual practices, and preventive measures against such diseases. All of the women provided a blood sample for identification of infection markers, and in a subgroup of 1802 women repeat samples were obtained to estimate the rate of seroconversion to syphilis. Prevalence of syphilis was 8.2%, with an incidence of 2.4/100 person-years. A positive linear relation between age and time working in commercial sex and prevalence of infection markers was observed. Women with less education, born in states other than Mexico City, and who worked on the street had significantly greater risks of infection with syphilis. Frequency of infection by both estimators is relatively low in the women studied. Characteristics related to periods of exposure such as age and time working in commercial sex, as well as socioeconomic and demographic characteristics, such as place of birth, education, and type of work site, were significantly related to the frequency of infection.

Pathophysiology of the vascular wall: the role of nitric oxide in renal disease.

Nitric oxide (NO) is formed in the endothelium by the constitutive enzyme NO synthase from the substrate amino acid L-arginine. As an endogenous vasodilator it contributes to renal arteriolar tone and modulates relaxation of the mesangium, thus contributing to regulation of glomerular microcirculation. NO also plays a role in regulating renal sodium excretion and renin release. It has antiplatelet and antithrombogenic effects and thus helps prevent thrombosis within the glomerular capillaries. In sepsis and sepsis-related syndromes, NO has a renoprotective role in that it aids in maintaining renal vasodilation and inhibiting platelet adhesion and aggregation. More knowledge of these effects may lead to the design of therapeutic interventions for preventing glomerular injury.

[Prevalence of antitreponemal antibodies in 3,098 female prostitutes in Mexico City]. / Prevalencia de anticuerpos antitreponémicos en 3098 mujeres dedicadas a la prostitución en la ciudad de México.

This paper describes a serological survey applied to 3098 female commercial sex workers, in order to determine the prevalence of syphilis. The women attend regularly an AIDS orientation center sponsored by CONASIDA in Mexico City. The laboratory tests included the rapid plasma reagin assay (presumptive analysis) and the fluorescent treponemal antibody-absorption technique (confirmatory test). No primary syphilis cases were detected and the prevalence of latent asymptomatic syphilis was 8.2% (255/3098). The sensitivity and specificity of the presumptive test compared to the confirmatory test were 74% and 98% respectively, and the positive predictive value was 77% and the negative predictive value 98%. All seropositive women received the standard penicillin treatment for syphilis. Considerations of importance are offered regarding interpretation and usefulness of this kind of research.

[The resistance and serotyping of 83 strains of Streptococcus pneumoniae isolated from asymptomatic carriers and ill children]. / Resistencia y serotipificación de 83 cepas de Streptococcus pneumoniae aisladas de niños portadores asintomáticos y enfermos.

Eight-three isolates of Streptococcus pneumoniae obtained from children hospitalized with several infections in Mexico City and Cuernavaca, and from healthy children attending a day-care center in Cuernavaca, from January to September 1992, were screened for antimicrobial resistance patterns by in vitro susceptibility testing against antimicrobial agents of potential use in the treatment of diseases caused by S. pneumoniae (39 infected patients and 44 from healthy children). 21.6% of strains were resistant to penicillin, 52% of the strains were multiresistant without a commun pattern. Children attending a day-care center had a higher rate of S. pneumoniae strains resistant to one or more antimicrobial than hospitalized children. Serotypes or serogroups 6, 23F, 14 and 19 were most prevalent. There are evidence that strain 23F has an intercontinental link, this strain is associated with disseminated diseases and multiresistance to antimicrobials. The results indicate that changes can occur in the susceptibility of S. pneumoniae and that selective susceptibility testing and epidemiologic studies in hospitalized patients and children in day-care centers are necessary.

[Human papillomavirus infection in women with and without abnormal cervical cytology]. / Infección por el virus del papiloma humano en mujeres con y sin citología cervical anormal.

This study sought to define the prevalence rates of human papillomavirus (HPV) infection and cytologic abnormalities in 3,257 sexually active females 13 to 45 years of age, undergoing routine cervical cytologic screening in the outpatient clinic of an urban hospital. One hundred and fifty patients (4.6%) showed cytologic evidence of cervical human papillomavirus infection (abnormal Pap). We selected a control group (n = 150) with negative cervical cytologic smears. Cells collected were analysed for HPV-DNA by PCR amplification method with probes for HPV types 6.11, 16.18 and 33. The HPV-DNA was detected in 21/300 (7.0%). The prevalence of cervical HPV-DNA types among women with negative cytology was 5.3% (8/150) and 8.6% (13/150) among women with abnormal Pap. The risk of HPV infection seems to be related with age at first intercourse, younger age and number of sexual partners. We did not find relation with the use of oral contraceptives smoking and history of prior sexually transmitted disease.