Archive for June 29, 2012

Updated Recommendations for Use of Tetanus Toxoid, Reduced Diphtheria Toxoid, and Acellular Pertussis (Tdap) Vaccine in Adults Aged 65 Years and Older — Advisory Committee on Immunization Practices (ACIP), 2012

MMWR Weekly  June 29, 2012  V.61  N.25  P.468-470

Since 2005, the Advisory Committee on Immunization Practices (ACIP) has recommended a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine booster dose for all adolescents aged 11 through 18 years (preferred at 11 through 12 years) and for those adults aged 19 through 64 years who have not yet received a dose. In October 2010, despite the lack of an approved Tdap vaccine for adults aged 65 years and older, ACIP recommended that unvaccinated adults aged 65 years and older be vaccinated with Tdap if in close contact with an infant, and that other adults aged 65 years and older may receive Tdap. In July 2011, the Food and Drug Administration (FDA) approved expanding the age indication for Boostrix (Glaxo Smith Kline Biologicals, Rixensart, Belgium) to aged 65 years and older. In February 2012, ACIP recommended Tdap for all adults aged 65 years and older. This recommendation supersedes previous Tdap recommendations regarding adults aged 65 years and older…



June 29, 2012 at 3:19 pm

SHEA guideline for management of healthcare workers who are infected with hepatitis B virus, hepatitis C virus, and/or human immunodeficiency virus.

Infect Control Hosp Epidemiol. Mar 2010  V.31 N.3 P.203-32.

Henderson DK, Dembry L, Fishman NO, Grady C, Lundstrom T, Palmore TN, Sepkowitz KA, Weber DJ; Society for Healthcare Epidemiology of America.

National Institutes of Health Clinical Center, Bethesda, Maryland 20892-1504, USA.


June 29, 2012 at 1:50 pm

When to initiate combined antiretroviral therapy to reduce mortality and AIDS-defining illness in HIV-infected persons in developed countries: an observational study.

Ann Intern Med. Apr.19, 2011  V.154 N.8 P.509-15.

HIV-CAUSAL Collaboration, Cain LE, Logan R, Robins JM, Sterne JA, Sabin C, Bansi L, Justice A, Goulet J, van Sighem A, de Wolf F, Bucher HC, von Wyl V, Esteve A, Casabona J, del Amo J, Moreno S, Seng R, Meyer L, Perez-Hoyos S, Muga R, Lodi S, Lanoy E, Costagliola D, Hernan MA.

Collaborators (1153)

Harvard School of Public Health, Boston, MA, USA.



Most clinical guidelines recommend that AIDS-free, HIV-infected persons with CD4 cell counts below 0.350 × 10(9) cells/L initiate combined antiretroviral therapy (cART), but the optimal CD4 cell count at which cART should be initiated remains a matter of debate.


To identify the optimal CD4 cell count at which cART should be initiated.


Prospective observational data from the HIV-CAUSAL Collaboration and dynamic marginal structural models were used to compare cART initiation strategies for CD4 thresholds between 0.200 and 0.500 × 10(9) cells/L.


HIV clinics in Europe and the Veterans Health Administration system in theUnited States.


20, 971 HIV-infected, therapy-naive persons with baseline CD4 cell counts at or above 0.500 × 10(9) cells/L and no previous AIDS-defining illnesses, of whom 8392 had a CD4 cell count that decreased into the range of 0.200 to 0.499 × 10(9) cells/L and were included in the analysis.


Hazard ratios and survival proportions for all-cause mortality and a combined end point of AIDS-defining illness or death.


Compared with initiating cART at the CD4 cell count threshold of 0.500 × 10(9) cells/L, the mortality hazard ratio was 1.01 (95% CI, 0.84 to 1.22) for the 0.350 threshold and 1.20 (CI, 0.97 to 1.48) for the 0.200 threshold. The corresponding hazard ratios were 1.38 (CI, 1.23 to 1.56) and 1.90 (CI, 1.67 to 2.15), respectively, for the combined end point of AIDS-defining illness or death. Limitations: CD4 cell count at cART initiation was not randomized. Residual confounding may exist.


Initiation of cART at a threshold CD4 count of 0.500 × 10(9) cells/L increases AIDS-free survival. However, mortality did not vary substantially with the use of CD4 thresholds between 0.300 and 0.500 × 10(9) cells/L.


June 29, 2012 at 1:48 pm



Sergio Muryán, Diego Mc – Loughlin y Eduardo Malvino


June 29, 2012 at 1:46 pm

Ultrastructural examination of two cases of stromal microsporidial keratitis.

J Med Microbiol. 2004 Aug;  V.3  N.8  P.775-81.

Rauz S, Tuft S, Dart JK, Bonshek R, Luthert P, Curry A.

Corneal and External Diseases Service, Moorfields Eye Hospital NHS Trust, City Road, London EC1V 2PD, UK.


Two cases with chronic stromal keratitis are described in immunocompetent hosts where the diagnosis was originally thought to be herpetic or adenoviral disease. Light microscopy and ultrastructural examination of corneal tissue by electron microscopy were performed following penetrating keratoplasty (case 1) and corneal biopsy (case 2). Specimens from both cases were analysed for viral identification by PCR. Two different species of Microsporidia were identified. Case 1 represents the fourth reported case of corneal stromal Vittaforma corneae where the spores measured 3.3 x 1.4 microm, arranged in characteristic linear groups of about four to eight. Each spore contained a diplokaryotic nucleus and a single row of ten polar tube coils. By contrast, case 2 is the first reported case of stromal keratitis caused by Trachipleistophora hominis. In this case, spores measured 4 x 2.4 microm, located typically within packets. In this species, the polar tube was arranged as a single row of about 10-13 profiles. Viral DNA could not be amplified by PCR. In conclusion, microsporidial stromal keratitis should be considered in culture-negative cases refractory to medical therapy. As microbiological culture techniques are unsuccessful, diagnosis may only be established following histopathological and ultrastructural examination of corneal tissue.


June 29, 2012 at 1:44 pm

Microsporidia: emerging ocular pathogens.

Indian J Med Microbiol. 2005 Apr V.23 N.2  P.80-91.

Joseph J, Vemuganti GK, Sharma S.

Jhaveri Microbiology Center, Hyderabad Eye Research Foundation, LV Prasad Eye Institute, LV Prasad Marg, Banjara Hills, Hyderabad, India.


Microsporidia are eukaryotic, spore forming obligate intracellular parasites, first recognized over 100 years ago. Microsporidia are becoming increasingly recognized as infectious pathogens causing intestinal, ocular, sinus, pulmonary, muscular and renal diseases, in both immunocompetent and immunosuppressed patients. Ocular microsporidiosis, though uncommon, could be isolated or part of systemic infections. It occurs mainly in two forms: keratoconjunctivitis form, mostly seen in immunocompromised individuals; stromal keratitis form seen in immunocompetent individuals. Recent reports indicate increasing number of cases of ocular microsporidiosis in immunocompetent individuals. The ocular cases present as superficial keratitis in AIDS patients, and these differ in presentation and clinical course from the cases seen in immunocompetent individuals which mainly appear to be as deep stromal keratitis. For most patients with infectious diseases, microbiological isolation and identification techniques offer the most rapid and specific determination of the etiologic agent, however this does not hold true for microsporidia, which are obligate intracellular parasites requiring cell culture systems for growth. Therefore, the diagnosis of microsporidiosis currently depends on morphological demonstration of the organisms themselves, either in scrapings or tissues. Although the diagnosis of microsporidiosis and identification of microsporidia by light microscopy have greatly improved during the last few years, species differentiation by these techniques is usually impossible and electron microscopy may be necessary. Immuno fluorescent-staining techniques have been developed for species differentiation of microsporidia, but the antibodies used in these procedures are available only at research laboratories at present. During the last 10 years, molecular techniques have been developed for the detection and species differentiation of microsporidia.

FULL TEXT;year=2005;volume=23;issue=2;spage=80;epage=91;aulast=Joseph

June 29, 2012 at 1:42 pm

Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America.

MMWR Recomm Rep. 2009 Apr 10 V.58  RR-4  P.1-207

Kaplan JE, Benson C, Holmes KH, Brooks JT, Pau A, Masur H; Centers for Disease Control and Prevention (CDC); National Institutes of Health; HIV Medicine Association of the Infectious Diseases Society of America.

CDC, Atlanta, Georgia, USA.


This report updates and combines earlier versions of guidelines for the prevention and treatment of opportunistic infections (OIs) in HIV-infected adults (i.e., persons aged >/=18 years) and adolescents (i.e., persons aged 13–17 years), last published in 2002 and 2004, respectively. It has been prepared by the Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH), and the HIV Medicine Association (HIVMA) of the Infectious Diseases Society of America (IDSA). The guidelines are intended for use by clinicians and other health-care providers, HIV-infected patients, and policy makers in theUnited States. These guidelines address several OIs that occur in theUnited Statesand five OIs that might be acquired during international travel. Topic areas covered for each OI include epidemiology, clinical manifestations, diagnosis, prevention of exposure; prevention of disease by chemoprophylaxis and vaccination; discontinuation of primary prophylaxis after immune reconstitution; treatment of disease; monitoring for adverse effects during treatment; management of treatment failure; prevention of disease recurrence; discontinuation of secondary prophylaxis after immune reconstitution; and special considerations during pregnancy. These guidelines were developed by a panel of specialists from theUnited Statesgovernment and academic institutions. For each OI, a small group of specialists with content-matter expertise reviewed the literature for new information since the guidelines were last published; they then proposed revised recommendations at a meeting held at NIH in June 2007. After these presentations and discussion, the revised guidelines were further reviewed by the co-editors; by the Office of AIDS Research, NIH; by specialists at CDC; and by HIVMA of IDSA before final approval and publication. The recommendations are rated by a letter that indicates the strength of the recommendation and a Roman numeral that indicates the quality of evidence supporting the recommendation, so that readers can ascertain how best to apply the recommendations in their practice environments. Major changes in the guidelines include 1) greater emphasis on the importance of antiretroviral therapy for the prevention and treatment of OIs, especially those OIs for which no specific therapy exists; 2) information regarding the diagnosis and management of immune reconstitution inflammatory syndromes; 3) information regarding the use of interferon-gamma release assays for the diagnosis of latent Mycobacterium tuberculosis (TB) infection; 4) updated information concerning drug interactions that affect the use of rifamycin drugs for prevention and treatment of TB; 5) the addition of a section on hepatitis B virus infection; and 6) the addition of malaria to the list of OIs that might be acquired during international travel. This report includes eleven tables pertinent to the prevention and treatment of OIs, a figure that pertains to the diagnois of tuberculosis, a figure that describes immunization recommendations, and an appendix that summarizes recommendations for prevention of exposure to opportunistic pathogens.


June 29, 2012 at 1:39 pm

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