Posts filed under ‘Infecciones del SNC’

ESCMID guideline: diagnosis and treatment of acute bacterial meningitis.

Clin Microbiol Infect. 2016 May;22 Suppl 3:S37-62.

van de Beek D1, Cabellos C2, Dzupova O3, Esposito S4, Klein M5, Kloek AT1, Leib SL6, Mourvillier B7, Ostergaard C8, Pagliano P9, Pfister HW5, Read RC10, Sipahi OR11, Brouwer MC12; ESCMID Study Group for Infections of the Brain (ESGIB).

Author information

1 Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands.

2 Department of Infectious Diseases, Hospital Universitari de Bellvitge, Barcelona, Spain.

3 Department of Infectious Diseases, Charles University, Third Faculty of Medicine, Prague, Czech Republic.

4 Pediatric Highly Intensive Care Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy.

5 Department of Neurology, Klinikum Großhadern, Munich, Germany.

6 Institute for Infectious Diseases, University of Bern, Bern, Switzerland.

7 Department of Intensive Care Medicine, Groupe Hospitalier Bichat-Claude Bernard, Paris, France.

8 Department of Clinical Microbiology, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark.

9 Department of Infectious Diseases, “D. Cotugno” Hospital, Naples, Italy.

10 Department of Infectious Diseases, Southampton General Hospital, Southampton, United Kingdom.

11 Department of Infectious Diseases and Clinical Microbiology, Ege University, Izmir, Turkey.

12 Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands. Electronic address: m.c.brouwer@amc.uva.nl

FULL TEXT

http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(16)00020-3/fulltext

PDF

http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(16)00020-3/pdf

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November 22, 2017 at 11:58 am

Follow-up brain imaging of 37 children with congenital Zika syndrome: Case series study

BMJ 2017 Oct 13; 359:j4188

Calheiros de Lima Petribu N et al.

Abstract

Objective

To compare initial brain computed tomography (CT) scans with follow-up CT scans at one year in children with congenital Zika syndrome, focusing on cerebral calcifications.

Design

Case series study.

Setting

Barão de Lucena Hospital, Pernambuco state, Brazil.

Participants

37 children with probable or confirmed congenital Zika syndrome during the microcephaly outbreak in 2015 who underwent brain CT shortly after birth and at one year follow-up.

Main outcome measure

Differences in cerebral calcification patterns between initial and follow-up scans.

Results

37 children were evaluated. All presented cerebral calcifications on the initial scan, predominantly at cortical-white matter junction. At follow-up the calcifications had diminished in number, size, or density, or a combination in 34 of the children (92%, 95% confidence interval 79% to 97%), were no longer visible in one child, and remained unchanged in two children. No child showed an increase in calcifications. The calcifications at the cortical-white matter junction which were no longer visible at follow-up occurred predominately in the parietal and occipital lobes. These imaging changes were not associated with any clear clinical improvements.

Conclusion

The detection of cerebral calcifications should not be considered a major criterion for late diagnosis of congenital Zika syndrome, nor should the absence of calcifications be used to exclude the diagnosis.

FULL TEXT

http://www.bmj.com/content/359/bmj.j4188

PDF

http://www.bmj.com/content/bmj/359/bmj.j4188.full.pdf

 

November 16, 2017 at 8:12 am

Specific Biomarkers Associated With Neurological Complications and Congenital Central Nervous System Abnormalities From Zika Virus–Infected Patients in Brazil

Journal of Infectious Diseases July 15, 2017 V.216 N.2 P.172–181

Yiu-Wing Kam; Juliana Almeida Leite; Fok-Moon Lum; Jeslin J L Tan; Bernett Lee …

Background

Zika virus (ZIKV) infections have been linked to different levels of clinical outcomes, ranging from mild rash and fever to severe neurological complications and congenital malformations.

Methods

We investigated the clinical and immunological response, focusing on the immune mediators profile in 95 acute ZIKV-infected adult patients from Campinas, Brazil. These patients included 6 pregnant women who later delivered during the course of this study. Clinical observations were recorded during hospitalization. Levels of 45 immune mediators were quantified using multiplex microbead-based immunoassays.

Results

Whereas 11.6% of patients had neurological complications, 88.4% displayed mild disease of rash and fever. Several immune mediators were specifically higher in ZIKV-infected patients, and levels of interleukin 10, interferon gamma-induced protein 10 (IP-10), and hepatocyte growth factor differentiated between patients with or without neurological complications. Interestingly, higher levels of interleukin 22, monocyte chemoattractant protein 1, TNF-α, and IP-10 were observed in ZIKV-infected pregnant women carrying fetuses with fetal growth–associated malformations. Notably, infants with congenital central nervous system deformities had significantly higher levels of interleukin 18 and IP-10 but lower levels of hepatocyte growth factor than those without such abnormalities born to ZIKV-infected mothers.

Conclusions

This study identified several key markers for the control of ZIKV pathogenesis. This will allow a better understanding of the molecular mechanisms of ZIKV infection in patients.

PDF

https://watermark.silverchair.com/api/watermark?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAdgwggHUBgkqhkiG9w0BBwagggHFMIIBwQIBADCCAboGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMuj_a-VAMddE_zlaHAgEQgIIBi63-XH3OORdTvNkyg01iIpJuW3POLRfocSGreL0dwgD_6lfvv3yIkhP83MPEjgbyM9hazTt8DxQ_2IqEP6eND0h1g-VCwKcveB1byxBTEz8KSJ33u-ZLO-0iet2RmKK6HMazACV8sW8KfaiLYfdKTUnyv4RSn2jfuq4U0F2hnTo_1WGmLFnsCrbfRbbQHnrudA9e_MPedHJfZAnRm53kkbzUtza0KfnfJx80cCVKJu2wGYXY5INohc43UMAEgsI2wAbXr7Xwd2RE8CXHlNPJnhI8YYhhjz_Yj4dnOfsSbzwL0inCX7tnqdFt5GsWbaM7Oa3zpl391yhxwE1HYUvCOZnyEAQpu2XTB_4h6ko7T1WDr_Jd-4H9W1HtVK1_ILzddKywF3yVCYmk35oC1RXv9gPslai0Hkjlpnb46k9VPEeQOOhXMzRYU7koX2RpuWfXAah7nfzaS0evT50mVl2GoS7mcMwtfDNFOCP_5mujf0ZaGhrTLgav_RbLq-dKMQA7DP0LVlBEsjtL61zI

September 27, 2017 at 8:50 am

Successful CAZ-avibactam treatment of MDR-KPC-positive Kleb pneumoniae infection in a patient with traumatic brain injury.

MEDICINE August 2017 V.96 N.31 P e7664

Rationale

Carbapenem-resistant Enterobacteriaceae infections are a serious health care problem, because of the high mortality. Carbapenem resistance is mainly caused by carbapenemases production, including Klebsiella pneumoniae carbapenemase (KPC).

Ceftazidime-avibactam is a new cephalosporin/β-lactamase inhibitor combination for the treatment of complicated urinary, intra-abdominal infections, and nosocomial pneumonia caused by gram negative, or other serious gram-negative infections.

Patient concerns

We showed the case of a 27-year-old patient, hospitalized for traumatic brain injury and chest trauma, with KPC-producing Klebsiella pneumoniae infection.

Diagnoses

Blood and bronchial aspirate culture analysis detected an infection caused by MDR Klebsiella pneumoniae, resistant to meropenem, ertapenem, piperacillin/tazobactam, amoxicillin/clavulanic acid, aztreonam, ceftazidime, cefotaxime, cefepime, amikacin, ciprofloxacin, trimethoprim/sulfamethoxazole, colistin while it showed an intermediate sensitivity to gentamicin and was sensitive to ceftazidime-avibactam. Molecular analyses revealed that the isolate belonged to the epidemic clone sequence type 258 (ST258) carrying blaKPC-3, blaTEM-1, and blaSHV-11genes.

Interventions

After various combined antibiotic therapies without improvements, he was treated with ceftazidime-avibactam, on a compassionate-use basis.

Outcomes

With ceftazidime-avibactam monotherapy clinical and microbiological clearance was obtained. A week after the end of the therapy microbiological analysis was repeated and a positive rectal swab for KPC-Klebsiella pneumoniae was found, becoming negative after 1 month. Moreover, the patient did not show any relapses for up to 18 weeks.

Lessons

This case indicates that ceftazidime-avibactam monotherapy could be efficacious against KPC positive Klebsiella pneumoniae infections.

FULL TEXT

http://journals.lww.com/md-journal/Fulltext/2017/08040/Successful_ceftazidime_avibactam_treatment_of.24.aspx

August 5, 2017 at 9:21 am

A case report of intraventricular tigecycline therapy for intracranial infection with extremely drug resistant A baumannii.

MEDICINE August 2017 V.96 N.31

Fang, Yu-Qing MDa; Zhan, Ru-Cai MDb; Jia, Wei MDc; Zhang, Bao-Qing MMd; Wang, Jian-Jun MDb,*

Section Editor(s): Rosca., Elena Cecilia

Rationale

Intracranial infection with Acinetobacter baumannii is a tough problem due to the presence of multiresistance and drugs poor penetration through the blood brain barrier (BBB). Tigecycline is effective to cure A baumannii, but it can only be used intravenously which is also difficult to pass BBB. So, it will be a breakthrough if intraventricular (IVT) tigecycline is used in the clinical therapy. However, this treatment has been reported quite rarely until now.

Patient concerns

We described a case of a 50-year-old male worker whose clinical futures were high fever and cerebral rigidity after neurosurgery.

Diagnoses

Intracranial infection with extensive drug resistant (XDR) A baumannii.

Interventions

The patient was treated with IVT tigecycline.

Outcomes

The symptoms of intracranial infection disappeared. The temperature of this patient decreased to normal and cerebral rigidity disappeared. The cerebrospinal fluid culture became negative, with normal levels of white blood cell, glucose and chlorine.

Lessons

IVT tigecycline therapy maybe effective to intracranial infection with XDR A baumannii. However, more studies will further demonstrate the therapeutic values of IVT tigecycline to intracranial infection, and not only restricted to A baumannii infections.

FULL TEXT

http://journals.lww.com/md-journal/Fulltext/2017/08040/A_case_report_of_intraventricular_tigecycline.41.aspx

August 5, 2017 at 9:15 am

Vancomycin-resistant enterococcal infections: epidemiology, clinical manifestations, and optimal management.

Infect Drug Resist. 2015 Jul 24;8:217-30.

O’Driscoll T1, Crank CW2.

Author information

1 Department of Pharmacy Practice, Chicago College of Pharmacy, Downers Grove, IL, USA.

2 Pharmacy Services, Rush-Copley Medical Center, Aurora, IL, USA.

Abstract

Since its discovery in England and France in 1986, vancomycin-resistant Enterococcus has increasingly become a major nosocomial pathogen worldwide.

Enterococci are prolific colonizers, with tremendous genome plasticity and a propensity for persistence in hospital environments, allowing for increased transmission and the dissemination of resistance elements.

Infections typically present in immunosuppressed patients who have received multiple courses of antibiotics in the past.

Virulence is variable, and typical clinical manifestations include bacteremia, endocarditis, intra-abdominal and pelvic infections, urinary tract infections, skin and skin structure infections, and, rarely, central nervous system infections.

As enterococci are common colonizers, careful consideration is needed before initiating targeted therapy, and source control is first priority.

Current treatment options including linezolid, daptomycin, quinupristin/dalfopristin, and tigecycline have shown favorable activity against various vancomycin-resistant Enterococcus infections, but there is a lack of randomized controlled trials assessing their efficacy.

Clearer distinctions in preferred therapies can be made based on adverse effects, drug interactions, and pharmacokinetic profiles.

Although combination therapies and newer agents such as tedizolid, telavancin, dalbavancin, and oritavancin hold promise for the future treatment of vancomycin-resistant Enterococcus infections, further studies are needed to assess their possible clinical impact, especially in the treatment of serious infections.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521680/pdf/idr-8-217.pdf

August 1, 2017 at 9:06 pm

Telavancin: a novel semisynthetic lipoglycopeptide agent to counter the challenge of resistant Gram-positive pathogens.

Ther Adv Infect Dis. March 2017 V.4 N.2 P.49-73.    

Das B1, Sarkar C2, Das D3, Gupta A4, Kalra A1, Sahni S1.

Author information

1 Department of Pharmacology, All India Institute of Medical Sciences (AIIMS) Rishikesh, Rishikesh, India.

2 Department of Pharmacology & Clinical Pharmacology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) Shillong, Shillong, India.

3 Department of Computer Science & Engineering, Faculty of Engineering, Manipal University Jaipur, Dehmi Kalan, Jaipur Ajmer Expressway, Rajasthan, India.

4 Department of Surgery, All India Institute of Medical Sciences (AIIMS) Rishikesh, Rishikesh, India.

Abstract

Telavancin (TD-6424), a semisynthetic lipoglycopeptide vancomycin-derivative, is a novel antimicrobial agent developed by Theravance for overcoming resistant Gram-positive bacterial infections, specifically methicillin-resistant Staphylococcus aureus (MRSA).

The US Food and Drug Administration (USFDA) had approved telavancin in 2009 for the treatment of complicated skin and skin structure infections (cSSSIs) caused by Gram-positive bacteria, including MRSA (S. aureus, Streptococcus agalactiae, Streptococcus pyogenes, Streptococcus anginosus group, or Enterococcus faecalis).

Telavancin has two proposed mechanisms of action. In vitro, telavancin has a rapid, concentration-dependent bactericidal effect, due to disruption of cell membrane integrity. Telavancin has demonstrable in vitro activity against aerobic and anaerobic Gram-positive bacteria. Telavancin and vancomycin have similar spectra of activity. Gram-negative bacteria are usually non-susceptible to telavancin.

Telavancin has been successfully tested in various animal models of bacteremia, endocarditis, meningitis, and pneumonia. Phase II Telavancin versus Standard Therapy for Treatment of Complicated Skin and Soft-Tissue Infections due to Gram-Positive Bacteria (FAST 1 and FAST 2) and phase III [Assessment of Telavancin in Complicated Skin and Skin Structure Infections 1 (ATLAS 1 and ATLAS 2)] clinical trials have been conducted for evaluating telavancin’s efficacy and safety in cSSSIs.

Phase III clinical trials have been carried out for evaluating telavancin’s safety and efficacy in nosocomial pneumonia [Assessment of Telavancin for Treatment of Hospital acquired Pneumonia 1 and 2 (ATTAIN 1 and ATTAIN 2)].

A phase II randomized, double-blind, clinical trial has been carried out for evaluating telavancin’s safety and efficacy in uncomplicated S. aureus bacteremia [Telavancin for Treatment of Uncomplicated S. aureus Bacteremia (ASSURE)]. Pacemaker lead-related infective endocarditis due to a vancomycin intermediate S. aureus (VISA) strain (non-daptomycin susceptible) was successfully treated with parenteral telavancin for 8 weeks.

Telavancin extensively binds to serum albumin (~93%) and has a relatively small volume of distribution. Telavancin is not biotransformed by any cytochrome P450 microsomal enzymes and excreted mainly in the urine. Though well-tolerated, worrisome adverse effects, including renal dysfunction and QTc prolongation are of potential concern.

Given its extensive binding to plasma proteins, long half-life, and a long post-antibiotic effect, it represents a promising addition to the therapeutic armamentarium in combating infections caused by resistant Gram-positive pathogens, namely, MRSA.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5467880/pdf/10.1177_2049936117690501.pdf

July 11, 2017 at 4:04 pm

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