Posts filed under ‘Infecciones en transplantados’

Septic arthritis of a native knee joint due to Corynebacterium striatum.

J Clin Microbiol. 2014 May;52(5):1786-8.

Westblade LF1, Shams F, Duong S, Tariq O, Bulbin A, Klirsfeld D, Zhen W, Sakaria S, Ford BA, Burnham CA, Ginocchio CC.

Author information

1 Department of Pathology and Laboratory Medicine, Hofstra North Shore-LIJ School of Medicine, Hempstead, New York, USA.

Abstract

We report a case of septic arthritis of a native knee joint due to Corynebacterium striatum, a rare and unusual cause of septic arthritis of native joints. The isolate was identified by a combination of phenotypic, mass spectrometric, and nucleic acid-based assays and exhibited high-level resistance to most antimicrobials.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993712/pdf/zjm1786.pdf

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October 22, 2017 at 12:41 pm

A spontaneous joint infection with Corynebacterium striatum.

J Clin Microbiol. 2007 Feb;45(2):656-8.

Scholle D1.

Author information

1 Department of Medicine, Legacy Emanuel and Good Samaritan Hospitals, 1015 NW 22nd Ave., Portland, OR 97210, USA. dscholle@fastmail.fm

Abstract

Corynebacterium striatum is a ubiquitous saprophyte with the potential to cause bacteremia in immunocompromised patients. Until now, spontaneous infection of a natural joint has not been reported. When phenotyping failed, gene sequencing was used to identify the species. The isolate demonstrated high-level resistance to most antibiotics.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1829050/pdf/0827-06.pdf

 

October 22, 2017 at 12:39 pm

The Brief Case: Bacteremia Caused by Helicobacter cinaedi

Journal of Clinical Microbiology January 2017 V.55 N.1 P.5-9

Allen C. Bateman and Susan M. Butler-Wu* Department of Laboratory Medicine, University of Washington, Seattle, Washington, USA

Carey-Ann D. Burnham, Editor Washington University School of Medicine

CASE

A 61-year-old male with relapsed multiple myeloma presented to clinic with fatigue and chills.

The patient had undergone two rounds of autologous stem cell transplantation in 2012 and was undergoing chemotherapy with pomalidomide, cyclophosphamide, and dexamethasone.

He was admitted for neutropenic fever (absolute neutrophil count of 1.4 × 109/liter, temperature of 38.4°C). His physical exam was normal, and he denied any other symptoms.

Two sets of blood cultures were obtained (VersaTREK Redox; Trek Diagnostic Systems), and the patient was started on levofloxacin, vancomycin, and cefepime. His fever subsided after 24 h, and he was discharged home to complete a 30-day course of oral levofloxacin…

PDF

http://jcm.asm.org/content/55/1/5.full.pdf+html

October 19, 2017 at 3:04 pm

Moraxella osloensis, an emerging pathogen of endocarditis in immunocompromised patients?

Swiss Med Wkly. 2015 Sep 16;145:w14185.

Gagnard JC1, Hidri N2, Grillon A3, Jesel L4, Denes E5.

Author information

1 Infectious Diseases Department, Limoges Teaching Hospital, France.

2 Bacteriology Laboratory, Limoges Teaching Hospital, France.

3 Bacteriology Laboratory, Strasbourg Teaching Hospital, France.

4 Cardiology Department, Strasbourg Teaching Hospital, France.

5 CHU Dupuytren, 2 Ave Martin Luther King, LIMOGES, FRANCE.

Abstract

We report two cases of endocarditis due to Moraxella osloensis. Only one previous case of such infection has been described.

These infections occurred in immunocompromised patients (B-cell chronic lymphocytic leukaemia and kidney graft associated with Hodgkin’s disease) and both patients had a favourable outcome with a complete cure of their infectious endocarditis.

This bacterium could be an emerging pathogen revealed by MALDI-TOF. Indeed, its characterisation within the Moraxella group by use of biochemistry-based methods is difficult.

Moreover, this strain could be particularly involved in immunocompromised patients.

FULL TEXT

https://smw.ch/article/doi/smw.2015.14185

August 2, 2017 at 4:17 pm

Aspergilosis. Formas clínicas y tratamiento

Enf Infecciosas & Microbiologia Clínica Abril 2012 V.30 N.4

Jesús Fortún, Yolanda Meije, Gema Fresco, Santiago Moreno.

Servicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, Madrid, España

Resumen

La aspergilosis invasiva junto con la aspergilosis crónica pulmonar y la aspergilosis broncopulmonar alérgica, constituyen las formas clínicas de aspergilosis.

Aunque el número de especies de Aspergillus spp. es muy numeroso, Aspergillus fumigatus-complex es el agente etiológico más frecuente, independientemente de la forma clínica y la afección de base del paciente.

El incremento de los diferentes tratamientos inmunosupresores y el mayor uso de corticoides en pacientes con enfermedad obstructiva crónica han condicionado un mayor protagonismo de la aspergilosis en los últimos años.

El uso de galactomanano y las pruebas de imagen complementan las limitaciones microbiológicas en el diagnóstico de estos pacientes. Voriconazol y anfotericina liposomal constituyen la base del tratamiento en todas las formas de aspergilosis, y posaconazol, itraconazol, caspofungina y otras equinocandinas son alternativas eficaces.

El pronóstico depende de la forma clínica y las características del huésped, pero es sombrío fundamentalmente en las formas invasivas diseminadas.

abstract

http://www.elsevier.es/es-revista-enfermedades-infecciosas-microbiologia-clinica-28-articulo-aspergilosis-formas-clinicas-tratamiento-S0213005X12000316

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July 17, 2017 at 8:11 am

Cytomegalovirus (CMV) DNA Quantitation in Bronchoalveolar Lavage Fluid From Hematopoietic Stem Cell Transplant Recipients With CMV Pneumonia

Journal of Infectious Diseases May 15, 2017 V.215 N.10 P.1514-1522

EDITOR’S CHOICE

Michael Boeckh  Terry Stevens-Ayers  Giovanna Travi  Meei-Li Huang  Guang-Shing Cheng Hu Xie  Wendy Leisenring  Veronique Erard  Sachiko Seo  Louise Kimball  …

Background.

Quantitative cytomegalovirus (CMV) DNA–specific polymerase chain reaction (PCR) analysis is widely used as a surveillance method for hematopoietic stem cell transplant (HCT) recipients. However, no CMV DNA threshold exists in bronchoalveolar lavage (BAL) to differentiate pneumonia from pulmonary shedding.

Methods.

We tested archived BAL fluid samples from 132 HCT recipients with CMV pneumonia and 139 controls (100 patients with non-CMV pneumonia, 18 with idiopathic pneumonia syndrome [IPS], and 21 who were asymptomatic) by quantitative CMV and β-globin DNA–specific PCR.

Results.

Patients with CMV pneumonia had higher median viral loads (3.9 log10 IU/mL; interquartile range [IQR], 2.6–6.0 log10 IU/mL) than controls (0 log10 IU/mL [IQR, 0–1.6 log10 IU/mL] for patients with non-CMV pneumonia, 0 log10 IU/mL [IQR, 0–1.6 log10 IU/mL] for patients with IPS, and 1.63 log10 IU/mL [IQR, 0–2.5 log10 IU/mL] for patients who were asymptomatic; P < .001 for all comparisons to patients with CMV pneumonia). Receiver operating characteristic curve analyses and predictive models identified a cutoff CMV DNA level of 500 IU/mL to differentiate between CMV pneumonia and pulmonary shedding, using current CMV pneumonia prevalence figures. However, different levels may be appropriate in settings of very high or low CMV pneumonia prevalence. The presence of pulmonary copathogens, radiographic presentation, or pulmonary hemorrhage did not alter predictive values.

Conclusion.

CMV DNA load in BAL can be used to differentiate CMV pneumonia from pulmonary shedding.

PDF

https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jid/215/10/10.1093_infdis_jix048/3/jix048.pdf?Expires=1499397143&Signature=ZGqgqbQ9a2uE12bomeqsVGChCW1Y3N54DapASFYI-SwrBn~eaUCXlNiXdKohVR-mw9Lx4NsjrxxqpIuvbiiGy8rpCb0sOLHdUlt8eA-mB7oZe249GgBvS8Oz9pXG-D7qBtEJ3jMI235GXMaYneGNv50wGHU6Nu3jzmffhXrz9GqjXrO5u80MlMtQDeB3DtOQVMl5vF4~dLL4o~OSWN4hI6gwqaR998s1l5iSspqNsU4suq4TmFlwcNLrmBpSA8z8XRVsKsS~7RrBDsGENU5SDxXp1AZmY50mHB3fvKjpnLXPdvQdedi3wHLfereEU5i7PaZ3MBlPz-RvtbGiMXjMUA__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q

July 5, 2017 at 10:24 pm

Estimating the burden of invasive and serious fungal disease in the United Kingdom

Journal of Infection January 2017 V.74 N.1

Matthew Pegorie a, David W. Denning b,c,d, *, William Welfare a,d

a Public Health England North West Health Protection Team (Greater Manchester), UK

bNational Aspergillosis Centre, University Hospital of South Manchester, Manchester, UK

c The University of Manchester, Manchester, UK

d Manchester Academic Health Sciences Centre, University of Manchester, UK

Background: The burden of fungal disease in the UK is unknown. Only limited data are systematically collected. We have estimated the annual burden of invasive and serious fungal disease.

Methods: We used several estimation approaches. We searched and assessed published estimates of incidence, prevalence or burden of specific conditions in various high risk groups. Studies with adequate internal and external validity allowed extrapolation to estimate current UK burden. For conditions without adequate published estimates, we sought expert advice.

Results: The UK population in 2011 was 63,182,000 with 18% aged under 15 and 16% over 65. The following annual burden estimates were calculated: invasive candidiasis 5142; Candida peritonitis complicating chronic ambulatory peritoneal dialysis 88; Pneumocystis pneumonia 207e587 cases, invasive aspergillosis (IA), excluding critical care patients 2901e2912, and IA in critical care patients 387e1345 patients, <100 cryptococcal meningitis cases. We estimated 178,000 (50,000e250,000) allergic bronchopulmonary aspergillosis cases in people with asthma, and 873 adults and 278 children with cystic fibrosis. Chronic pulmonary aspergillosis is estimated to affect 3600 patients, based on burden estimates post tuberculosis and in sarcoidosis.

Conclusions: Uncertainty is intrinsic to most burden estimates due to diagnostic limitations, lack of national surveillance systems, few published studies and methodological limitations. The largest uncertainty surrounds IA in critical care patients. Further research is needed to produce a more robust estimate of total burden

PDF

http://www.journalofinfection.com/article/S0163-4453(16)30273-0/pdf

March 25, 2017 at 5:40 pm

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