Effect of dietary excess of branched-chain amino acids on performance and serum concentrations of amino acids in growing pigs.

Depressed performance and availability of some amino acids (AA) in pigs fed excess Leu diets appear to be related to lower feed intake. Surplus Ile and Val may help to overcome this effect. An experiment was conducted with 24 pigs (31.8 ± 1.2 kg initial BW) to evaluate the effect of dietary excess of either Leu alone or with surplus Ile and Val on performance and serum concentration (SC) of essential AA. Treatments were as follows: T1, basal diet; T2, basal plus 0.43% L-Leu (excess Leu); T3, basal added with 0.43% L-Leu, plus 0.20% L-Ile and 0.25% L-Val (excess LIV). The basal diet was formulated to contain 0.90% standardized ileal digestible Lys and added with crystalline L-Lys, L-Thr, DL-Met, L-Trp, L-Leu, L-Ile, L-His and L-Val to create essential AA:Lys ratios close to an ideal protein for growing pigs. All pigs were fed the same amount of feed twice a day (average, 3.42× the requirement of NEm). Blood samples were collected at 2.5 (absorptive) and 11.0 h (post-absorptive) post-prandial to analyse SC of AA. Excess of either Leu or LIV did not affect growth rate nor feed conversion. Excess Leu increased Leu SC and decreased Ile and Val SC (p < 0.05) at both absorptive and post-absorptive phases, but excess LIV restored the SC of Ile and Val. The SC of other essential AA was not affected by excess of either Leu or LIV. The SC of all AA during absorptive, on average, was about two times higher than that of post-absorptive phase. These results suggest that the reduced availability (SC) of Ile and Val in pigs consuming excess Leu diets is attributed to a reduced absorption and increased cellular degradation rates of them.

Expression of genes coding for selected amino acid transporters in small intestine, liver, and skeletal muscle of pigs fed excess branched-chain amino acids.

Excess Leu reduces the availability of Ile and Val in pigs likely by reducing absorption of the latter amino acids (AA). Twenty-four crossbred pigs were used to evaluate the effect of excess Leu alone or with surplus Ile and Val on the expression of cationic (b(0),(+)AT and CAT1) and neutral (B(0)AT1) AA transporters in the small intestine, liver, and skeletal muscle. Dietary treatments included: 1) basal diet; 2) basal plus 0.43% L-Leu (excess Leu); 3) basal plus 0.43% Leu, 0.20% L-Ile, and 0.25% L-Val (excess Leu, Ile, and Val). The basal diet contained 0.90% standardized ileal digestible Lys, as well as crystalline L-Lys, L-Thr, DL-Met, L-Trp, L-Leu, L-Ile, L-His, and L-Val. Diets 2 and 3 contained 52% more Leu and diet 3 contained 42% more Ile and Val compared with the basal diet. Excess Leu or excess Leu, Ile, and Val reduced b(0),(+)AT expression in the jejunum (P < 0.05) but had no effect in the ileum and liver. Excess Leu increased CAT1 expression in the ileum but reduced expression in the liver (P < 0.05). Excess Leu, Ile, and Val increased (P < 0.05) B(0)AT1 expression in the jejunum and tended to increase (P = 0.10) expression in the ileum. In general, b(0),(+)AT expression was higher but CAT1 expression was lower in the jejunum than in the ileum; B0AT1 was similarly expressed in the jejunum and ileum. Excess Leu or any branched-chain AA affects AA transporter expression, which may affect the absorption and availability of AA for animal growth.

Effect of L-lysine on expression of selected genes, serum concentration of amino acids, muscle growth and performance of growing pigs.

Lysine (Lys) is the first limiting amino acid (AA) in most feed formulations for pigs and most abundant, along with leucine, in muscle proteins. An experiment was conducted with 17 pigs (17.7 ± 0.05 kg initial BW) to identify a role of dietary Lys in the control of protein synthesis in pigs. Fourteen pigs were randomly assigned to one of the two wheat-based dietary treatments: Lys-deficient, 3.0 g/kg (DEF) and Lys-adequate, 10.8 g/kg (ADE). Samples from jejunum mucosa, liver, Longissumus and Semitendinosus muscles, and blood were collected. The other three pigs were sacrificed at the beginning of the trial to measure basal carcass composition. Weight gain, gain:feed ratio, Lys intake and loin eye area were greater in ADE than in DEF pigs (p < 0.01). Muscle-related carcass characteristics were better, and myosin heavy chain IIb expression (MyHC IIb) in Semitendinosus was higher in ADE than in DEF pigs. Expression of AA transporters CAT-1 was lower (p < 0.05), serum Lys was higher and serum Val was lower in pigs fed the ADE diet. The higher muscularity, MyHC IIb expression in Semitendinosus muscle and Lys serum of pigs fed the ADE diet suggest that Lys increases growth rate not only by functioning as protein construction unit but also as potential control of the protein synthesis process.

Effect of L-valine supplementation to a wheat-based diet with leucine excess on performance, gene expression, and serum concentration of amino acids.

Excess Leu in the diet reduces the expression of the cationic AA transporter b(0,+), absorption of Lys and Arg, feed intake, and ADG of pigs. Because Val competes with Leu for absorption, surplus Val may correct some of these effects. An experiment was conducted to analyze the effect of surplus Val in a basal wheat (Triticum aestivum) diet fortified with free Lys, Thr, and Met and containing excess Leu and Ile on performance, expression of genes encoding b(0,+), and serum concentrations of AA. Sixteen pigs (30.3 ± 2.1 kg BW) were used. Treatments were wheat based with excess Leu and Ile (T1) and T1 plus 0.44% L-Val (T2). At the end of the 21-d study, 12 pigs were euthanized; jugular blood was collected to analyze serum AA and jejunal mucosa to measure expression of b(0,+). Surplus Val increased (P < 0.05) ADG and G:F and serum Val, Lys, and Arg but did not affect (P > 0.10) b(0,+) expression. Although analyzed Val content in the basal diet was lower than calculated, the increased serum Lys and improved pig performance may suggest that excess Leu limits Val availability and that surplus Val could correct some of the negative effects of excess Leu.

Motor vehicle crash fatalities by race/ethnicity in Arizona, 1990-96.

OBJECTIVE: To compare rates of motor vehicle crash (MVC) fatalities among different race/ethnic groups in urban and rural Arizona. METHOD: Using the Fatality Analysis Reporting System and the National Center for Health Statistics Multiple Cause of Death file, MVC fatalities in Arizona from 1990-96 inclusive were classified by gender, race/ethnicity, and urban or rural residence. Age adjusted rates of total, occupant, pedestrian, and alcohol related fatalities were calculated. The total MVC fatality rate for each race/ethnic group was then adjusted for proportion of rural residence. RESULTS: Compared with non-Hispanic whites (NHWs), American Indians had raised relative risks for MVC fatality in all gender and residence subgroups. Hispanic females and rural Hispanic males had lower relative risks, as did rural African-American men. Raised relative risks for American Indian men and women included all subgroups: total, occupant, pedestrian, and alcohol related. Hispanic and African-American men both had raised relative risks of pedestrian related fatalities, and Hispanic men had a slightly higher relative risk while Hispanic women had a lower relative risks, for alcohol related fatality. Hispanic men and women and African-American men had lower occupant fatality rates. Close to half (45%) of the excess MVC fatality among American Indians can be attributed to residence in rural areas, where MVC fatality rates are higher. There were 1.85 occupants in crashes involving NHW deaths compared with 2.51 for Hispanics and 2.71 for American Indians (p<0.001). The proportion of occupants not using a seatbelt was higher in Hispanics and American Indians in both urban and rural areas. CONCLUSION: The major disparity in MVC fatality in Arizona is among American Indians. The higher MVC fatality rates among American Indians occur in all age groups, in both urban and rural areas, and among occupants and pedestrians. Rural residence, lower rates of seatbelt use, higher rates of alcohol related crashes, a greater number of occupants, and higher rates of pedestrian deaths all contribute to the American Indian MVC fatality disparity. High rates of pedestrian fatality occur in men in all three race/ethnic minorities in Arizona and among American Indian women. In contrast to other studies, African-Americans and Hispanics did not have raised total MVC fatality rates and compared to NHWs actually had lower rates in the rural areas of the state.

Tumor necrosis factor-alpha drives HIV-1 replication in U937 cell clones and upregulates CXCR4.

U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-alpha and viral replication was inhibited by neutralization of endogenous TNF-alpha. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-alpha, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-alpha as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-alpha may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.

Selective inhibition of HIV replication in primary macrophages but not T lymphocytes by macrophage-derived chemokine.

Macrophage-derived chemokine (MDC) has been reported to inhibit different HIV-1 strains in activated peripheral blood mononuclear cells (T cell blasts), although other investigators have not confirmed these findings. Here we demonstrate that MDC inhibits the replication of CCR5-dependent (R5) HIV-1(BaL) in monocyte-derived macrophages (MDM), but not in T cell blasts, although with variable potency depending on donor variability. Analysis of HIV-1(BaL) proviral DNA synthesis in MDM indicated that the suppressive effect of MDC did not involve inhibition of early events such as entry or reverse transcription. Finally, an inverse correlation was observed between the levels of endogenous MDC secreted by uninfected MDM of different donors and the efficiency of different HIV strains, including two primary isolates with different coreceptor usage, to replicate in these cells. Thus, MDC represents an example of a chemokine inhibiting HIV replication in macrophages acting at one or more postentry levels in the virus life cycle.

Upregulated expression of interleukin-8, RANTES and chemokine receptors in human astrocytic cells infected with HIV-1.

Human immunodeficiency virus (HIV) infection of the central nervous system (CNS) affects primarily microglial cells and astrocytes. Infection of these latter cells occurs independently of CD4 and is characterised by preferential accumulation of 2 Kb mRNA, encoding mostly Nef, and by low levels of 4.5 and 9 Kb RNAs. We have investigated the potential role of chronic HIV infection of human astrocytic cells on the expression of pro-inflammatory cytokines, chemokines and their receptors by comparing the infected TH4-7-5 with its parental uninfected 85HG66 cell lines. Upregulated levels of tumour necrosis factor-alpha (TNF-alpha) and of certain chemokines, namely interleukin-8 (IL-8) and regulated upon activation normal T cell expressed and secreted (RANTES), were observed in the infected versus uninfected cells, whereas monocyte chemotactic protein-1 (MCP-1) was comparably expressed in both cell lines. This pattern of expression was confirmed in primary foetal astrocytes transiently transfected with HIV. In addition, CXCR1, CXCR2 and CCR2b, receptors for IL-8 and MCP-1, respectively, were also found to be upregulated in TH4-7-5 versus 85HG66. CXCR4, the receptor of stromal cell derived factor-1 (SDF-1) and co-receptor for syncytium inducing HIVs, was comparably expressed in infected and uninfected astrocytic cells, whereas CCR5 was not detected in either cell line. Furthermore, treatment of TH4-7-5 cells with TNF-alpha or IL-1beta stimulated RNA and protein secretion of IL-8, MCP-1, and RANTES as well as HIV expression. Thus, our findings suggest that HIV infection of astrocytic cells can contribute to the establishment of a chronic inflammatory state in the CNS, eventually resulting in HIV encephalitis, by increasing the secretion of pro-inflammatory cytokines, such as TNF-alpha and several chemokines. Overexpression of chemokine receptors including CCR2b, CXCR1 and CXCR2 in infected astrocytic cells may contribute to HIV-induced damage of the CNS via autocrine/paracrine activation of astrocytes.

Inhibition of CXCR4-dependent HIV-1 infection by extracellular HIV-1 Tat.

Certain chemokines inhibit HIV replication through binding to cell surface receptors which also act as viral coreceptors. Based on our previous observations that HIV-1 Tat can interact with alpha- and beta-chemokine receptors, we investigated the potential effect of extracellular Tat (ecTat) on infection and replication of CCR5-dependent (R5) and CXCR4-using (X4) HIV-1 strains in primary activated peripheral blood mononuclear cells (PBMC) of uninfected donors. Receptor desensitization and binding competition studies were used to determine chemokine receptor binding by ecTat. Standard HIV replication assays based on reverse transcriptase (RT) activity determination in culture supernatants of PBMC and real time PCR for HIV-1 gag DNA were used to determine potential effects on early (entry or RT) steps of infection. ecTat bound to CXCR4 expressing monocytes and mitogen-activated PBMC, and competed with the natural ligand of CXCR4, SDF-1alpha (stromal cell-derived factor-1alpha) in calcium mobilization assays. EcTat inhibited replication of the X4 HIV-1 (LAI/IIIB strain) in activated PBMC at concentrations close to those of SDF-1alpha, whereas it only modestly interfered with R5 HIV-1 (BaL) replication in PBMC. Both SDF-1alpha and ecTat inhibited accumulation of X4 HIV-1 gag DNA, indicating interference with viral entry and/or RT. Our data show the surprising and counter-intuitive observation that ecTat selectively represses X4 HIV replication. This could favour spreading of R5 viruses, a condition observed in vivo immediately after transmission and in the early asymptomatic phase of infection.

Up-regulation of CCR2 chemokine receptor expression and increased susceptibility to the multitropic HIV strain 89.6 in monocytes exposed to glucocorticoid hormones.

Glucocorticoid hormones (GC) are potent antiinflammatory agents widely used in the treatment of diverse human diseases. The present study was aimed at assessing the effect of GC on chemokine receptor expression in human monocytes. Dexamethasone (Dex) up-regulated mRNA expression of the monocyte chemotactic protein (MCP-1, CCL2) chemokine receptor CCR2. The effect was selective in that other chemokine receptors were not substantially affected. Stimulation by Dex was observed after 4 h of exposure at concentrations of 10(-7) to 10(-5) M. Steroids devoid of GC activity were inactive, and the GC receptor antagonist, RU486, inhibited stimulation. Dex did not affect the rate of nuclear transcription, but augmented the CCR2 mRNA half-life. Augmentation of CCR2 expression by Dex was associated with increased chemotaxis. Finally, Dex treatment induced productive replication of the HIV strain 89.6, which utilizes CCR2 as entry coreceptor, in freshly isolated monocytes. Together with previous findings, these results indicate that at least certain pro- and antiinflammatory molecules have reciprocal and divergent effects on expression of a major monocyte chemoattractant, MCP-1, and of its receptor (CCR2). Augmentation of monocyte CCR2 expression may underlie unexplained in vivo effects of GC as well as some of their actions on HIV infection.

Envelope-dependent restriction of human immunodeficiency virus type 1 spreading in CD4(+) T lymphocytes: R5 but not X4 viruses replicate in the absence of T-cell receptor restimulation.

The human immunodeficiency virus (HIV) replicates in activated CD4(+) T lymphocytes. However, only CD4(+) Th2 and Th0, but not Th1, CD4(+) T-cell clones have been reported to efficiently support HIV-1 replication. This dichotomous pattern was further investigated in the present study in Th1, Th2, or Th0 cell lines derived from umbilical human cord blood and in T-cell clones obtained from the peripheral blood mononuclear cells (PBMC) of healthy adults. Both primary and laboratory-adapted HIV-1 strains with CCR5 as the exclusive entry coreceptor (R5 viruses) efficiently replicated in Th1, Th2, and Th0 cells. In sharp contrast, CXCR4-dependent (X4) viruses poorly replicated in both polarized and unpolarized CD4(+) T cells, including adults' PBMC infected several days after mitogenic stimulation. Unlike the X4 HIV-1(NL4-3), a chimera in which the env gene had been replaced with that of the R5 HIV-1(NL(AD8)), efficiently replicated in both Th1 and Th2 cells. This X4-dependent restriction of HIV replication was not explained by either the absence of functional CXCR4 on the cell surface or by the inefficient viral entry and reverse transcription. T-cell receptor stimulation by anti-CD3 monoclonal antibodies fully rescued X4 HIV-1 replication in both Th1 and Th2 cells, whereas it did not alter the extent and kinetics of R5 HIV-1 spreading. Thus, R5 HIVs show a replicative advantage in comparison to X4 viruses in their ability to efficiently propagate among suboptimally activated T lymphocytes, regardless of their polarized or unpolarized functional profiles. This observation may help to explain the absolute predominance of R5 HIVs over X4 viruses observed after viral transmission and during early-stage disease.

Human CD34(+) cells express CXCR4 and its ligand stromal cell-derived factor-1. Implications for infection by T-cell tropic human immunodeficiency virus.

Human CD34(+) hematopoietic progenitor cells obtained from bone marrow (BM), umbilical cord blood (UCB), and mobilized peripheral blood (MPB) were purified and investigated for the expression of the chemokine receptor CXCR4 and its ligand, stromal cell-derived factor-1 (SDF-1). CXCR4 was found present on the cell surface of all CD34(+) cells, although it was expressed at lower density on MPB with respect to BM CD34(+) cells. Freshly isolated and in vitro-cultured CD34(+) cells also coexpressed SDF-1 mRNA, as determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Of interest, CD34(+)/CD38(+) committed progenitor cells, unlike primitive CD34(+)/CD38(-) cells, expressed SDF-1 mRNA. Supernatants from in vitro-cultured CD34(+) cells contained substantial (3 to 8 ng/mL) amounts of SDF-1 by enzyme-linked immunosorbent assay and induced migration of CD34(+) cells. Because CD34(+) cells express low levels of CD4, the primary receptor of the human immunodeficiency virus (HIV), and CXCR4 is a coreceptor for T-cell tropic (X4) HIV strains, we investigated the susceptibility of CD34(+) cells to infection by this subset of viruses. Lack of productive infection was almost invariably observed as determined by a conventional RT activity in culture supernatants and by real-time PCR for HIV DNA in CD34(+) cells exposed to both laboratory adapted (LAI) and primary (BON) X4 T-cell tropic HIV-1 strain. Soluble gp120 Env (sgp120) from X4 HIV-1 efficiently blocked binding of the anti-CD4 Leu3a monoclonal antibody (MoAb) to either human CD4(+) T cells or CD34(+) cells. In contrast, sgp120 interfered with an anti-CXCR4 MoAb binding to human T lymphocytes, but not to CD34(+) cells. However, CXCR4 on CD34(+) cells was downregulated by SDF-1. These results suggest that CXCR4 and its ligand SDF-1 expressed in CD34(+) progenitors may play an important role in regulating the local and systemic trafficking of these cells. Moreover, these findings suggest multiple and potentially synergistic mechanisms at the basis of the resistance of CD34(+) cells to X4 HIV infection, including their ability to produce SDF-1, and the lack of CXCR4 internalization following gp120 binding to CD4.

Human immunodeficiency virus replication induces monocyte chemotactic protein-1 in human macrophages and U937 promonocytic cells.

We have recently described a significant correlation between human immunodeficiency virus-1 (HIV-1) RNA replication and monocyte chemotactic protein-1 (MCP-1) levels in the cerebrospinal fluid (CSF) of individuals with the acquired immunodeficiency syndrome (AIDS) with HIV encephalitis (E). Because local macrophages (microglia) are the cells predominantly infected in the brain, we investigated whether in vitro HIV infection affects MCP-1 production in mononuclear phagocytes (MP). MCP-1 secretion and expression were consinstently upregulated over constitutive levels in human monocyte-derived macrophages (MDM) infected with the M-tropic R5 BaL strain of HIV-1. HIV replication was required for this effect, as demonstrated by the absence of chemokine upregulation after infection in the presence of 3'-azido-3'-deoxythimidine (AZT) or cell-exposure to heat-inactivated (triangle up degrees ) virus. MCP-1 induction was not restricted to HIV-1 BaL, but was also observed during productive infection of MDM with two primary isolates differing for entry coreceptor usage and of U937 cells with the X4 HIV-1 MN strain. Based on the observation that exogenous HIV-1 Tat induced MCP-1 expression in astrocytes, we also investigated its role in MDM and U937 cells. Exogenous Tat induced MCP-1 production from MDM in a concentration-dependent manner, however, it was not effective on uninfected U937 cells or on the chronically infected U937-derived cell line U1. Transfection of Tat-expressing plasmids moderately activated HIV expression in U1 cells, but failed to induce MCP-1 expression in this cell line or in uninfected U937 cells. HIV replication-dependent expression of MCP-1 in MP may be of particular relevance for the pathogenesis of HIV infection in nonlymphoid organs such as the brain.

[Wilson's disease ("hepatic form") in a region endemic for schistosomiasis mansoni: clinical presentation of 25 patients]. / Doença de Wilson ("forma hepática") em região endêmica para esquistossomose mansoni: apresentação clínica de 25 pacientes.

Brazil has a young population and areas of endemic mansoni schistosomiasis where Wilson's disease might be easily misdiagnosed in patients erroneously classified as having either the hepatosplenic or the hepatointestinal form of the helminthiasis. Twenty five patients with the "hepatic form" of Wilson's disease (14 males and 11 females) were investigated in Belo Horizonte, MG; the mean age was 13.7 years (3 to 22). Nineteen had hepatomegaly (76%) and nine splenomegaly (36%). Twenty two (88%) had cirrhosis. The Kaiser-Fleisher ring was detected in fifteen (60%). Four (16%) had clear neurological abnormalities. Eleven (44%) had ascitis and/or jaundice. Ninety one point three per cent and 92% had low ceruloplasmin and copper serum levels respectively. Eighty four point two per cent showed an increased 24 hours urinary copper excretion; seven patients in whom hepatic copper was determined had increased values. Six out of nine had at least a ten fold increase in 24 hours urinary copper excretion following penicillamine use ("penicillamine test"). Three out of 19 patients (15.8%) had mansoni schistosoma ova in stools examination, a common prevalence in our population. Their biopsies showed inactive cirrhosis without schistosomiasis-associated alterations. At least fourteen patients (56%) could be misdiagnosed as having hepatointestinal or hepatosplenic schistosomisis when in fact they suffered from Wilson's disease with or without asymptomatic intestinal schistosomiasis, losing the chance of an early treatment. The follow-up time of 22 patients was 52 months (1 to 96); eight (36.3%) died, four from bleeding esphageal varices, three from terminal hepatic failure and one from fulminant liver failure. The majority of the patients, including those who died, had abandomned the use of penicillamine or had taken it irregularly, due mainly to its highly expensive cost. A 17 year old patient underwent a successful liver transplant in 1989.

Interleukin-6 induces monocyte chemotactic protein-1 in peripheral blood mononuclear cells and in the U937 cell line.

Induction of chemokine gene expression from peripheral blood mononuclear cells (PBMCs) stimulated by proinflammatory cytokines plays an important role in both wound repair and response to infectious agents. In the present study, we show that the proinflammatory cytokine interleukin-6 (IL-6) potently induced mRNA expression and secretion of the CC chemokine monocyte chemotactic protein 1 (MCP-1) in PBMCs. In addition, because human immunodeficiency virus (HIV) infection in vivo and in vitro has been shown to dysregulate the production of and/or the response to cytokines, PBMCs from both healthy uninfected and HIV-infected individuals were studied for their constitutive and IL-6-induced expression of MCP-1. No substantial differences were observed between the two groups of individuals. In addition, IL-6 upregulated MCP-1 expression in the promonocytic cell line U937 and in its chronically HIV-infected counterpart, U1. In these cell lines, IL-6 selectively induced MCP-1 and not other chemokines, including regulated upon activation normal T cells expressed and secreted (RANTES), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and IL-8. IL-6 induction of MCP-1 was partially inhibited by hydrocortisone in U1 cells. Thus, IL-6 activates PBMCs to secrete MCP-1, a CC chemokine pivotal for monocyte recruitment in tissue and organs in which important inflammatory events occur.

Prevalencia del estreptococo beta hemolitico del grupo A en 1,574 preescolares de jardines de ninos. / Prevalence of beta hemolytic Streptococcus of A group in 1,574 preschool child

Se estudiaron los cultivos faringeos de 1,352 preescolares y se concluyo que la prevalencia de estreptococos beta hemolitico fue de 7.6%. No hubo cardiopatias. De todos modos un numero que no se puede precisar, de estos pacientes son, ademas de portadores, potencialmente susceptibles de enfermar del corazon. Se hace enfasis en la conveniencia de llevar a cabo este plan de encuesta y profilaxis primaria en Mexico, en forma mas amplia

[Primary prevention of rheumatic fever. Occurrence of beta hemolytic Streptococcus of the A group in 11,314 students in Magdalena Contreras]. / Estudios sobre la prevención primaria de fiebre reumática. I. Prevalencia de estreptococo beta hemolítico del grupo A, en 11,314 escolares de la Magdalena Contreras

A study was made in 11,314 school-age children to determine the prevalence of streptococcus pyogenes group A. The children studied belonged to a low socioeconomic group of one of the political boroughs of the Federal District. The prevalence found was 6.86%. There were no differences in the percentage of carriage according to the school surveyed or the school grade studied. However, marked differences were found when the presence of arthralgias was related to the carriage of streptococcus. Children complaining of artharlgias showed twice as much streptococcus in their pharynx than the ones not carrying it.