Archive for February, 2012
Recurrent Guillain-Barré Syndrome Following Vaccination
Clin Infect Dis March 2012 V.54 N.6 P.800-804
Roger Baxter1, Ned Lewis1, Nandini Bakshi2, Claudia Vellozzi3, Nicola P. Klein1, and the CISA Network
1Kaiser Permanente Vaccine Study Center
2The Permanente Medical Group, Oakland, California
3Immunization Safety Office, Centers for Disease Control and Prevention, Atlanta, Georgia
Background.
Guillain-Barré syndrome (GBS) is an acute polyradiculopathy, thought to be autoimmune, which has been reported following vaccinations. The Advisory Committee on Immunization Practices recommends not administering influenza vaccine to individuals who have had a history of GBS within 6 weeks of a prior influenza vaccination if they are not at high risk of severe complications from influenza illness.
Methods.
We identified GBS cases from the Kaiser Permanente Northern California databases from 1995 into 2006 using hospital discharge codes; each medical record was neurologist-reviewed and only GBS-confirmed cases were included for follow-up. We followed confirmed cases through 2008 for vaccinations and recurrent GBS.
Results.
We identified 550 cases of GBS over 33 million person-years. Following their GBS diagnoses, 989 vaccines were given to 279 of these individuals, including 405 trivalent inactivated influenza vaccines (TIV) administered to 107 individuals with a prior diagnosis of GBS. Among the 550 total cases of GBS, 18 initially had onset within 6 weeks of TIV; of these, 2 were revaccinated with TIV without a recurrence of GBS. Only 6 individuals of 550 (1.1%) had a second (recurrent) diagnosis of GBS. Among these 6 individuals, none had any vaccine exposure at all in the 2 months prior to the second onset of GBS.
Conclusions.
In our population of over 3 million members, during an 11-year period, risk of GBS recurrence was low. There were no cases of recurrent GBS after influenza vaccination and none within 6 weeks after any vaccine.
http://cid.oxfordjournals.org/content/54/6/800.full.pdf+html
Systemic Antibiotic Therapy for Chronic Osteomyelitis in Adults
Clin Infect Dis Feb 2012 V.54 N.3 P.393-407
Ellie J. C. Goldstein, Section Editor
Brad Spellberg1,2 and Benjamin A. Lipsky3,4
1Division of General Internal Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance
2David Geffen School of Medicine at UCLA, Los Angeles, California
3VA Puget Sound Health Care System
4University of Washington, Seattle
Abstract
The standard recommendation for treating chronic osteomyelitis is 6 weeks of parenteral antibiotic therapy. However, oral antibiotics are available that achieve adequate levels in bone, and there are now more published studies of oral than parenteral antibiotic therapy for patients with chronic osteomyelitis. Oral and parenteral therapies achieve similar cure rates; however, oral therapy avoids risks associated with intravenous catheters and is generally less expensive, making it a reasonable choice for osteomyelitis caused by susceptible organisms. Addition of adjunctive rifampin to other antibiotics may improve cure rates. The optimal duration of therapy for chronic osteomyelitis remains uncertain. There is no evidence that antibiotic therapy for >4–6 weeks improves outcomes compared with shorter regimens. In view of concerns about encouraging antibiotic resistance to unnecessarily prolonged treatment, defining the optimal route and duration of antibiotic therapy and the role of surgical debridement in treating chronic osteomyelitis are important, unmet needs.
http://cid.oxfordjournals.org/content/54/3/393.full.pdf+html
Hospital-acquired infections due to gram-negative bacteria.
N Engl J Med. 2010 May 13 V.362 N.19 P.1804-13.
Peleg AY, Hooper DC.
Source
Division of Infectious Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. apeleg@bidmc.harvard.edu
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3107499/pdf/nihms296483.pdf
Comment in
N Engl J Med. 2010 Oct 7;363(15):1482; author reply 1483-4.
http://www.nejm.org/doi/pdf/10.1056/NEJMc1006641
Burkholderia cepacia complex: beyond pseudomonas and acinetobacter.
Indian J Med Microbiol. 2011 Jan-Mar V.29 N.1 P.4-12.
Gautam V, Singhal L, Ray P.
Source
Department of Medical Microbiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. r_vg@yahoo.co.uk
Abstract
Burkholderia cepacia complex (BCC) is an important nosocomial pathogen in hospitalised patients, particularly those with prior broad-spectrum antibacterial therapy. BCC causes infections that include bacteraemia, urinary tract infection, septic arthritis, peritonitis and respiratory tract infection. Due to high intrinsic resistance and being one of the most antimicrobial-resistant organisms encountered in the clinical laboratory, these infections can prove very difficult to treat and, in some cases, result in death. Patients with cystic fibrosis (CF) and those with chronic granulomatous disease are predisposed to infection by BCC bacteria. BCC survives and multiplies in aqueous hospital environments, including disinfectant agents and intravenous fluids, where it may persist for long periods. Outbreaks and pseudo-outbreaks of BCC septicaemia have been documented in intensive care units, oncology units and renal failure patients. BCC is phenotypically unremarkable, and the complex exhibits an extensive diversity of genotypes. BCC is of increasing importance for agriculture and bioremediation because of their antinematodal and antifungal properties as well as their capability to degrade a wide range of toxic compounds. It has always been a tedious task for a routine microbiological laboratory to identify the nonfermenting gram-negative bacilli, and poor laboratory proficiency in identification of this nonfermenter worldwide still prevails. In India, there are no precise reports of the prevalence of BCC infection, and in most cases, these bacteria have been ambiguously reported as nonfermenting gram-negative bacilli or simply Pseudomonas spp. The International Burkholderia cepacia Working Group is open to clinicians and scientists interested in advancing knowledge of BCC infection/colonisation in persons with CF through the collegial exchange of information and promotion of coordinated approaches to research.
FULL TEXT
Isolation of Staphylococcus aureus from the urinary tract: association of isolation with symptomatic urinary tract infection and subsequent staphylococcal bacteremia.
Clin Infect Dis. 2006 Jan 1 V.42 N.1 P.46-50.
Muder RR, Brennen C, Rihs JD, Wagener MM, Obman A, Stout JE, Yu VL.
Source
Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, USA.Robert.Muder@med.va.gov
Abstract
BACKGROUND:
Staphylococcus aureus is frequently isolated from urine samples obtained from long-term care patients. The significance of staphylococcal bacteriuria is uncertain. We hypothesized that S. aureus is a urinary pathogen and that colonized urine could be a source of future staphylococcal infection.
METHODS:
We performed a cohort study of 102 patients at a long-term care Veterans Affairs facility for whom S. aureus had been isolated from clinical urine culture. Patients were observed via urine and nasal cultures that were performed every 2 months. We determined the occurrence of (1) symptomatic urinary tract infection concurrent with isolation of S. aureus (by predetermined criteria), (2) staphylococcal bacteremia concomitant with isolation of S. aureus from urine, and (3) subsequent episodes of staphylococcal infection.
RESULTS:
Of 102 patients, 82% had undergone recent urinary catheterization. Thirty-three percent of patients had symptomatic urinary tract infection at the time of initial isolation of S. aureus, and 13% were bacteremic. Eight-six percent of the initial urine isolates were methicillin-resistant S. aureus. Seventy-one patients had follow-up culture data; 58% of cultures were positive for S. aureus at > or =2 months (median duration of staphylococcal bacteriuria, 4.3 months). Sixteen patients had subsequent staphylococcal infections, occurring up to 12 months after initial isolation of S. aureus; 8 late-onset infections were bacteremic. In 5 of 8 patients, the late blood isolate was found to have matched the initial urine isolate by pulsed-field gel electrophoresis typing.
CONCLUSIONS:
S. aureus is a cause of urinary tract infection among patients with urinary tract catheterization. The majority of isolates are methicillin-resistant S. aureus. S. aureus bacteriuria can lead to subsequent invasive infection. The efficacy of antistaphylococcal therapy in preventing late-onset staphylococcal infection in patients with persistent staphylococcal bacteriuria should be tested in controlled trials.
Application of TaqMan low-density arrays for simultaneous detection of multiple respiratory pathogens.
J Clin Microbiol. 2011 Jun V.49 N.6 P.2175-82.
Kodani M, Yang G, Conklin LM, Travis TC, Whitney CG, Anderson LJ, Schrag SJ, Taylor TH Jr, Beall BW, Breiman RF, Feikin DR, Njenga MK, Mayer LW, Oberste MS, Tondella ML, Winchell JM, Lindstrom SL, Erdman DD, Fields BS.
Source
Division of Bacterial Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. MKodani@cdc.gov
Abstract
The large and growing number of viral and bacterial pathogens responsible for respiratory infections poses a challenge for laboratories seeking to provide rapid and comprehensive pathogen identification. We evaluated a novel application of the TaqMan low-density array (TLDA) cards for real-time PCR detection of 21 respiratory-pathogen targets. The performance of the TLDA was compared to that of individual real-time PCR (IRTP) assays with the same primers and probes using (i) nucleic acids extracted from the 21 pathogen strains and 66 closely related viruses and bacteria and (ii) 292 clinical respiratory specimens. With spiked samples, TLDA cards were about 10-fold less sensitive than IRTP assays. By using 292 clinical specimens to generate 2,238 paired individual assays, the TLDA card exhibited 89% sensitivity (95% confidence interval [CI], 86 to 92%; range per target, 47 to 100%) and 98% specificity (95% CI, 97 to 99%; range per target, 85 to 100%) overall compared to IRTP assays as the gold standard with a threshold cycle (C(T)) cutoff of 43. The TLDA card approach offers promise for rapid and simultaneous identification of multiple respiratory pathogens for outbreak investigations and disease surveillance.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3122721/pdf/zjm2175.pdf
Role of Chlamydia pneumoniae in atherosclerosis.
Clin Sci (Lond). 2008 Apr V.114 N.8 P.509-31.
Watson C, Alp NJ.
Source
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Abstract
Cardiovascular disease, resulting from atherosclerosis, is a leading cause of global morbidity and mortality. Genetic predisposition and classical environmental risk factors explain much of the attributable risk for cardiovascular events in populations, but other risk factors for the development and progression of atherosclerosis, which can be identified and modified, may be important therapeutic targets. Infectious agents, such as Chlamydia pneumoniae, have been proposed as contributory factors in the pathogenesis of atherosclerosis. In the present review, we consider the experimental evidence that has accumulated over the last 20 years evaluating the role of C. pneumoniae in atherosclerosis and suggest areas for future research in this field.
Antimicrobial Drug Resistance in Peru
Emerging Infectious Diseases March 2012 V.18 N.3
To the Editor: In Latin American countries, rates of antimicrobial drug resistance among bacterial pathogens are high. Data on these rates inPeruare incomplete (1), and no institution inPeruhas participated in multinational surveillance studies (2–4). To document the antimicrobial drug resistance profile of key pathogens, we organized a surveillance network of clinical laboratories from 9 hospitals (public, general, tertiary care, and quaternary care) inLima, the capital ofPeru. Over a 12-month period (April 2008–March 2009), we consecutively collected positive bacterial blood culture isolates (other than coagulase-negative staphylococci) from each of the 9 hospitals. Only the first isolate per patient was included. Patients’ age and hospital ward were recorded. Identification and susceptibility testing were performed at the Institute of Tropical Medicine Alexander von Humboldt (Lima,Peru).
Hepatitis E Virus Infection in HIV-infected Persons
Emerging Infectious Diseases March 2012 V.18 N.3
Nancy F. Crum-Cianflone , Jennifer Curry, Jan Drobeniuc, Amy Weintrob, Michael Landrum, Anuradha Ganesan, William Bradley, Brian K. Agan, Saleem Kamili, and The Infectious Disease Clinical Research Program HIV Working Group
Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA (N.F. Crum-Cianflone, J. Curry, A. Weintrob, M. Landrum, A. Ganesan, W. Bradley, B.K. Agan); Naval Medical Center San Diego, San Diego, California, USA (N.F. Crum-Cianflone); Naval Medical Center Portsmouth, Portsmouth, Virginia, USA (J. Curry); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (J. Drobeniuc S. Kamili); Walter Reed Army Medical Center, Washington DC, USA (A. Weintrob); San Antonio Military Medical Center, San Antonio, Texas, USA (M. Landrum); National Naval Medical Center, Bethesda (A. Ganesan)
To determine whether hepatitis E virus (HEV) is a cause of hepatitis among HIV-infected persons, we evaluated 1985–2009 data for US military beneficiaries. Evidence of acute or prior HEV infection was detected for 7 (4%) and 5 (3%) of 194 HIV-infected persons, respectively. HEV might be a cause of acute hepatitis among HIV-infected persons.
http://wwwnc.cdc.gov/eid/article/18/3/pdfs/11-1278.pdf
Influence of empiric therapy with a beta-lactam alone or combined with an aminoglycoside on prognosis of bacteremia due to gram-negative microorganisms.
Antimicrob Agents Chemother. 2010 Sep V.54 N.9 P.3590-6.
Martínez JA, Cobos-Trigueros N, Soriano A, Almela M, Ortega M, Marco F, Pitart C, Sterzik H, Lopez J, Mensa J.
Source
Department of Infectious Diseases, Hospital Clinic-IDIBAPS, Villarroel 170, 08036 Barcelona, Spain. jamarti@clinic.ub.es
Abstract
Evidence supporting the combination of aminoglycosides with beta-lactams for gram-negative bacteremia is inconclusive. We have explored the influence on survival of empirical therapy with a beta-lactam alone versus that with a beta-lactam-aminoglycoside combination by retrospectively analyzing a series of bacteremic episodes due to aerobic or facultative gram-negative microorganisms treated with single or combination therapy. The outcome variable was a 30-day mortality. Prognostic factors were selected by regression logistic analysis. A total of 4,863 episodes were assessed, of which 678 (14%) received combination therapy and 467 (10%) were fatal. Factors independently associated with mortality included age greater than 65 (odds ratio [OR], 2; 95% confidence interval [CI], 1.6 to 2.6), hospital acquisition (OR, 1.5; 95% CI, 1.2 to 1.9), a rapidly or ultimately fatal underlying disease (OR, 2.5; 95% CI, 2 to 3.2), cirrhosis (OR, 1.9; 95% CI, 1.4 to 2.6), prior corticosteroids (OR, 1.5; 95% CI, 1.1 to 2), shock on presentation (OR, 8.8; 95% CI, 7 to 11), pneumonia (OR, 2.8; 95% CI, 1.9 to 4), and inappropriate empirical therapy (OR, 1.8; 95% CI, 1.3 to 2.5). Subgroup analysis revealed that combination therapy was an independent protective factor in episodes presenting shock (OR, 0.6; 95% CI, 0.4 to 0.9) or neutropenia (OR, 0.5; 95% CI, 0.3 to 0.9). Combination therapy improved the appropriateness of empirical therapy in episodes due to extended-spectrum beta-lactamase (ESBL)- or AmpC-producing Enterobacteriaceae and Pseudomonas aeruginosa. In patients with gram-negative bacteremia, we could not find an overall association between empirical beta-lactam-aminoglycoside combination therapy and prognosis. However, a survival advantage cannot be discarded for episodes presenting shock or neutropenia, hence in these situations the use of combination therapy may still be justified. Combination therapy also should be considered for patients at risk of being infected with resistant organisms, if only to increase the appropriateness of empirical therapy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2934963/pdf/0115-10.pdf
