Posts filed under ‘Metodos diagnosticos’

“Urinary Tract Infection”—Requiem for a Heavyweight

The Journal of the American Geriatrics Society  May 19, 2017

Thomas E. Finucane MD

Johns Hopkins Bayview Medical Center, Baltimore, Maryland

Abstract

“Urinary tract infection” (“UTI”) is an ambiguous, expansive, overused diagnosis that can lead to marked, harmful antibiotic overtreatment. “Significant bacteriuria,” central to most definitions of “UTI,” has little significance in identifying individuals who will benefit from treatment. “Urinary symptoms” are similarly uninformative. Neither criterion is well defined. Bacteriuria and symptoms remit and recur spontaneously. Treatment is standard for acute uncomplicated cystitis and common for asymptomatic bacteriuria, but definite benefits are few. Treatment for “UTI” in older adults with delirium and bacteriuria is widespread but no evidence supports the practice, and expert opinion opposes it.

Sensitive diagnostic tests now demonstrate that healthy urinary tracts host a ubiquitous, complex microbial community. Recognition of this microbiome, largely undetectable using standard agar-based cultures, offers a new perspective on “UTI.” Everyone is bacteriuric. From this perspective, most people who are treated for a “UTI” would probably be better off without treatment. Elderly adults, little studied in this regard, face particular risk. Invasive bacterial diseases such as pyelonephritis and bacteremic bacteriuria are also “UTIs.”

Mindful decisions about antibiotic use will require a far better understanding of how pathogenicity arises within microbial communities. It is likely that public education and meaningful informed-consent discussions about antibiotic treatment of bacteriuria, emphasizing potential harms and uncertain benefits, would reduce overtreatment. Emphasizing the microbiome’s significance and using the term “urinary tract dysbiosis” instead of “UTI” might also help and might encourage mindful study of the relationships among host, aging, microbiome, disease, and antibiotic treatment…..

FULL TEXT

http://onlinelibrary.wiley.com/doi/10.1111/jgs.14907/full

PDF

http://onlinelibrary.wiley.com/doi/10.1111/jgs.14907/epdf

July 20, 2017 at 8:24 am

The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

Front. Microbiol. 23 January 2017   

Cristian Dotto1, Andrea Lombarte Serrat1, Natalia Cattelan2, María S. Barbagelata1†, Osvaldo M. Yantorno2, Daniel O. Sordelli1, Monika Ehling-Schulz3, Tom Grunert3 and Fernanda R. Buzzola1*

1 Departamento de Microbiología, Parasitología e Inmunología, Facultad de Medicina, Instituto de Investigaciones en Microbiología y Parasitología Médica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad de Buenos Aires, Buenos Aires, Argentina

2 Facultad de Ciencias Exactas, Centro de Investigación y Desarrollo de Fermentaciones Industriales (CINDEFI), Centro Científico Technológico Consejo Nacional de Investigaciones Científicas y Tócnicas (CTT CONICET La Plata), Universidad Nacional de La Plata, La Plata, Argentina

3 Functional Microbiology, Institute for Microbiology, University of Veterinary Medicine, Vienna, Austria

Aspirin has provided clear benefits to human health. But salicylic acid (SAL) -the main aspirin biometabolite- exerts several effects on eukaryote and prokaryote cells. SAL can affect, for instance, the expression of Staphylococcus aureus virulence factors.

SAL can also form complexes with iron cations and it has been shown that different iron chelating molecules diminished the formation of S. aureus biofilm. The aim of this study was to elucidate whether the iron content limitation caused by SAL can modify the S. aureus metabolism and/or metabolic regulators thus changing the expression of the main polysaccharides involved in biofilm formation.

The exposure of biofilm to 2 mM SAL induced a 27% reduction in the intracellular free Fe2+ concentration compared with the controls. In addition, SAL depleted 23% of the available free Fe2+ cation in culture media. These moderate iron-limited conditions promoted …

FULL TEXT

https://doi.org/10.3389/fmicb.2017.00004

 

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July 19, 2017 at 6:53 pm

Increasing Macrolide and Fluoroquinolone Resistance in Mycoplasma genitalium.

Emerg Infect Dis. May, 2017 V.23 N.5 P.809-812.

Murray GL, Bradshaw CS, Bissessor M, Danielewski J, Garland SM, Jensen JS, Fairley CK, Tabrizi SN.

Abstract

Escalating resistance to azithromycin and moxifloxacin is being reported for Mycoplasma genitalium in the Asia-Pacific region.

Analyzing 140 infections, we found pretreatment fluoroquinolone-resistance mutations in parC (13.6%) and gyrA (5%). ParC S83 changes were associated with moxifloxacin failure.

Combined macrolide/fluoroquinolone-resistance mutations were in 8.6% of specimens, for which recommended therapies would be ineffective.

PDF

https://wwwnc.cdc.gov/eid/article/23/5/pdfs/16-1745.pdf

July 19, 2017 at 3:56 pm

Pneumocystis jiroveci pneumonia: comparative study of cases in HIV-infected patients and immunocompromised non-HIV-infected patients.

Rev Chilena Infectol. August 2014 V.31 N.4 P.417-24.

[Article in Spanish]

Cerón I, Rabagliati R, Langhaus J, Silva F, Guzmán AM, Lagos M.

Abstract

BACKGROUND:

Although P. jiroveci pneumonia affects immunocompromised (IC) patients of any etiology, clinical features and prognostic outcomes are different depending if they are patients with HIV infection or other causes of IC.

OBJECTIVES:

To compare clinical and laboratory features as well as outcomes of P. jiroveci pneumonia in HIV versus non-HIV patients.

METHODS:

Retrospective review of clinical records of HIV and non-HIV patients with P. jiroveci pneumonia managed at the Hospital Clínico Universidad Católica in Santiago, Chile, between 2005 and 2007.

RESULTS:

We included 28 HIV and 45 non-HIV patients with confirmed P. jiroveci pneumonia. The non-HIV population was older (65 vs 36,2 years, p < 0,01), had shorter duration of symptoms (7 [1-21] vs 14 [2-45] days, p < 0,01), required more invasive techniques (60 vs 21%, p < 0,01) and RT-PCR to confirm the diagnosis (93 vs 68%, p < 0,01), were more frequently treated at intensive care units (58 vs. 25%, p < 0,01) requiring artificial ventilation (56 vs 11%, p < 0,01), and had a higher attributable mortality (33% vs 0%, p < 0,01).

CONCLUSIONS:

Our study confirmed that P. jiroveci pneumonia in non-HIV IC patients is more severe, more difficult to diagnose and has higher mortality that in HIV patients. Therefore, it is mandatory to optimize diagnostic and therapeutic strategies for this patients group

PDF

http://www.scielo.cl/pdf/rci/v31n4/art07.pdf

July 18, 2017 at 3:44 pm

Pneumocystis pneumonia in hospitalized patients: a detailed examination of symptoms, management, and outcomes in human immunodeficiency virus (HIV)-infected and HIV-uninfected persons.

Transpl Infect Dis. 2012 Oct;14(5):510-8.

McKinnell JA1, Cannella AP, Kunz DF, Hook EW 3rd, Moser SA, Miller LG, Baddley JW, Pappas PG.

Author information

1 Division of Infectious Diseases, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.

Abstract

BACKGROUND:

Pneumocystis jirovecii pneumonia (PCP) is a life-threatening infection for immunocompromised individuals. Robust data and clear guidelines are available for prophylaxis and treatment of human immunodeficiency virus (HIV)-related PCP (HIV-PCP), yet few data and no guidelines are available for non-HIV-related PCP (NH-PCP). We postulated that prevention and inpatient management of HIV-PCP differed from NH-PCP.

METHODS:

We performed a retrospective case review of all pathologically confirmed cases of PCP seen at the University of Alabama Medical Center from 1996 to 2008. Data on clinical presentation, hospital course, and outcome were collected using a standardized data collection instrument. Bivariate analysis compared prophylaxis, adjunctive corticosteroids, and clinical outcomes between patients with HIV-PCP and NH-PCP.

RESULTS:

Our analysis of the cohort included 97 cases of PCP; 65 HIV and 32 non-HIV cases. Non-HIV cases rarely received primary prophylaxis (4% vs. 38%, P = 0.01) and received appropriate antibiotics later in the course of hospitalization (5.2 days vs. 1.1 days, P < 0.005). Among transplant patients, NH-PCP was diagnosed a mean of 1066 days after transplantation and most patients were on low-dose corticosteroids (87%) at the time of disease onset. No significant differences in adjunctive corticosteroid use (69% vs. 77%, P = 0.39) and 90-day mortality (41% vs. 28%, P = 0.20) were detected.

CONCLUSIONS:

Patients who have undergone organ or stem cell transplant remain at risk for PCP for many years after transplantation. In our cohort, patients who developed NH-PCP were rarely given prophylaxis, and initiation of appropriate antibiotics was significantly delayed compared to cases of HIV-PCP. Medical providers should be aware of the ongoing risk for NH-PCP, even late after transplantation, and consider more aggressive approaches to both prophylaxis and earlier empirical therapy for PCP.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3889465/pdf/nihms-536426.pdf

July 18, 2017 at 3:43 pm

LEPTOSPIROSIS – GUIA para el Equipo de Salud. Ministerio de Salud de la Nación Argentina – ABRIL 2014

INDICE

Pág 3. Información para el equipo de salud:

  1. Introducción
  2. Manifestaciones clínicas
  3. ¿Cuándo sospechar leptospirosis?
  4. ¿Cómo confirmar leptospirosis?
  5. ¿Cómo notificar el caso de leptospirosis?
  6. ¿Cómo se trata el paciente con leptospirosis?
  7. Flujograma de manejo de casos sospechosos de leptospirosis
  8. Diagnóstico diferencial
  9. ¿Qué hacer si se confirma?
  10. ¿Cómo se tratan los casos caninos de leptospirosis?
  11. Prevención de la leptospirosis en la familia y la comunidad

Pág 25. Recomendaciones para la organización de las actividades en el Equipo de Salud

  1. ¿Qué pueden Ud y su equipo de salud hacer para contribuir al control de la leptospirosis en su área?

Pág 29. Información para la población

  1. ¿Qué es la leptospirosis?
  2. ¿Cómo se transmite la leptospirosis?
  3. ¿Cómo ingresa la bacteria?
  4. ¿Cuáles son los síntomas de la leptospirosis?
  5. ¿Qué hacer en caso de padecer de algunos de los síntomas mencionados antes?
  6. ¿Cuál es el tratamiento?

7 ¿Cómo afecta la enfermedad a los animales domésticos?

  1. ¿Qué podemos hacer para prevenir la leptospirosis?

Pág 35. Anexos

  1. Muestras clínicas para examen
  2. Notificación a través del Módulo SIVILA del SNVS
  3. Bioseguridad
  4. Laboratorios de la Red de leptospirosis
  5. Algoritmo de diagnóstico y notificación por laboratorio
  6. Ficha de notificación de casos de síndrome febril
  7. Ficha de notificación de caso leptospirosis canina

PDF

http://www.msal.gob.ar/images/stories/bes/graficos/0000000489cnt-guia-medica-leptospirosis.pdf

July 17, 2017 at 8:32 am

Leptospirosis. Puesta al día

Rev. Chil. infectol. Junio 2007 V.24 N.3 P.220-226

Enna Zunino M. y Rolando Pizarro P.

Hospital Dr. Lucio Córdova Santiago, Chile

Resumen

Se revisan los aspectos clínicos, diagnóstico de laboratorio y alternativas terapéuticas para la leptospirosis.

Destaca en la epidemiología el riesgo ocupacional y laboral y la falta de datos, por no haber constituido en Chile tema de vigilancia epidemiológica hasta el año 2000.

Los datos clínicos evidencian una notable heterogeneidad de manifestaciones, muchas veces inespecíficas. La complejidad del diagnóstico diferencial que plantea hace necesario incluirlo en el análisis causal de múltiples situaciones clínicas.

El diagnóstico de laboratorio es aún complejo y poco accesible. Aunque es todavía controvertido, el análisis de la literatura apoya el beneficio del tratamiento antimicrobiano con varias alternativas de elección.

PDF

http://www.scielo.cl/pdf/rci/v24n3/art08.pdf

July 17, 2017 at 8:30 am

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