Interim Recommendations for Clinical Use of Influenza Diagnostic Tests During the 2009-10 Influenza Season September 29, 2009, 6:00 PM ET
Objective To provide updated interim recommendations on influenza diagnostic testing for clinicians treating patients with suspected 2009 H1N1 influenza virus infection and to assist clinicians with testing decisions for the 2009-10 influenza season 1. These recommendations may be further revised as more information becomes available. These recommendations also can be adapted according to local epidemiologic and surveillance data and other state and local considerations. Clinical judgment is always an important part of testing and treatment decisions.
Summary Points Most patients with clinical illness consistent with uncomplicated influenza who reside in an area where influenza viruses are circulating do not require diagnostic influenza testing for clinical management. Patients who should be considered for influenza diagnostic testing include: Hospitalized patients with suspected influenza Patients for whom a diagnosis of influenza will inform decisions regarding clinical care, infection control, or management of close contacts. Patients who died of an acute illness in which influenza was suspected. When a decision is made to use antiviral treatment for influenza, treatment should be initiated as soon as possible without waiting for influenza test results. Antiviral treatment is most effective when administered as early as possible in the course of illness. (http://www.cdc.gov/h1n1flu/recommendations.htm) Clinicians should be aware that the sensitivities of rapid influenza diagnostic tests (RIDTs) and direct immunofluorescence assays (DFAs) are lower than real-time reverse transcriptase polymerase chain reaction (rRT-PCR) tests and viral culture. A negative RIDT or DFA result does not rule out influenza virus infection. (http://www.cdc.gov/h1n1flu/guidance/rapid_testing.htm). Further, these tests cannot distinguish between 2009 H1N1 and seasonal H1N1 or H3N2 influenza A viruses. If most circulating influenza viruses have similar antiviral susceptibilities (as is the case currently in the United States), information on the influenza A subtype may not be needed to inform clinical care. If identification of 2009 H1N1 influenza virus infection is required, testing with a rRT-PCR assay specific for 2009 H1N1 influenza or viral culture should be performed. Laboratory tests to diagnose 2009 H1N1 influenza, such as rRT-PCR, should be prioritized for hospitalized patients and immunocompromised persons with suspected influenza where RIDT or DFA testing is negative or to determine influenza A virus subtype in patients who have died from suspected or confirmed influenza A virus infection. Information on testing of pathology specimens for suspected 2009 H1N1 influenza virus infection can be found at (http://cdc.gov/h1n1flu/tissuesubmission.htm).
QUESTIONS & ANSWERS Influenza Diagnostic Testing During the 2009-2010 Flu Season September 29, 2009, 6:00 PM ET
For the Public How will I know if I have the flu this season? You may have the flu if you have one or more of these symptoms: fever, cough, sore throat, runny or stuffy nose, body aches, headache, chills, fatigue and sometimes, diarrhea and vomiting. Most people with 2009 H1N1 have had mild illness and have not needed medical care or antiviral drugs, and the same is true of seasonal flu. (More information is available on What To Do If You Get Sick this flu season.) Most people with flu symptoms do not need a test for 2009 H1N1 because the test results usually do not change how you are treated.
How can I know for certain if I have the flu this season? To know for certain, a test specific for flu would need to be performed. But most people with flu symptoms do not need a test for 2009 H1N1 flu because the test results usually does not change how you are treated.
What kinds of flu tests are there? A number of flu tests are available to detect influenza viruses. The most common are called “rapid influenza diagnostic tests” that can be used in outpatient settings. These tests can provide results in 30 minutes or less. Unfortunately, the ability of these tests to detect the flu can vary greatly. Therefore, you could still have the flu, even though your rapid test result is negative. In addition to rapid tests, there are several more accurate and sensitive flu tests available that must be performed in specialized laboratories, such as those found in hospitals or state public health laboratories. All of these tests are performed by a health care provider using a swab to swipe the inside of your nose or the back of your throat. These tests do not require a blood sample. For more information, see Seasonal Influenza Testing.
How well can these tests detect the flu? Rapid tests vary in their ability to detect flu viruses. Depending on the test used, their ability to detect 2009 H1N1 flu can range from 10% to 70%. This means that some people with a 2009 H1N1 flu infection have had a negative rapid test result. (This situation is called a false negative test result.) Rapid tests appear to be better at detecting flu in children than adults. None of the rapid tests currently approved by the Food and Drug Administration (FDA) are able to distinguish 2009 H1N1 flu from other flu viruses.
Bacterial Coinfections in Lung Tissue Specimens from Fatal Cases of 2009 Pandemic Influenza A (H1N1) --- United States, May--August 2009
In previous influenza pandemics, studies of autopsy specimens have shown that most deaths attributed to influenza A virus infection occurred concurrently with bacterial pneumonia (1), but such evidence has been lacking for 2009 pandemic influenza A (H1N1). To help determine the role of bacterial coinfection in the current influenza pandemic, CDC examined postmortem lung specimens from patients with fatal cases of 2009 pandemic influenza A (H1N1) for bacterial causes of pneumonia. During May 1--August 20, 2009, medical examiners and local and state health departments submitted specimens to CDC from 77 U.S. patients with fatal cases of confirmed 2009 pandemic influenza A (H1N1). This report summarizes the demographic and clinical findings from these cases and the laboratory evaluation of the specimens. Evidence of concurrent bacterial infection was found in specimens from 22 (29%) of the 77 patients, including 10 caused by Streptococcus pneumoniae (pneumococcus). Duration of illness was available for 17 of the 22 patients; median duration was 6 days (range: 1--25 days). Fourteen of 18 patients for whom information was available sought medical care while ill, and eight (44%) were hospitalized. These findings confirm that bacterial lung infections are occurring among patients with fatal cases of 2009 pandemic influenza A (H1N1) and underscore both the importance of pneumococcal vaccination for persons at increased risk for pneumococcal pneumonia and the need for early recognition of bacterial pneumonia in persons with influenza.
CDC receives tissue specimens routinely from patients with confirmed or suspected infectious diseases and provides histopathologic, immunohistochemical, and molecular evaluations. Early in the 2009 influenza A (H1N1) virus pandemic, CDC provided guidelines for submission of tissue specimens for evaluation of influenza virus infections.* Confirmed fatal cases of 2009 pandemic influenza A (H1N1) were defined as influenza-like illness or postmortem findings suggestive of viral pneumonia and laboratory-confirmed 2009 pandemic influenza A (H1N1) virus infection by real time reverse transcriptase--polymerase chain reaction (rRT-PCR). Respiratory specimens (i.e., lung, trachea, and large-airway specimens) collected at autopsy were submitted to CDC by medical examiners, hospitals, and local and state health departments for additional evaluation.
Specimens were received from 77 patients who had 2009 pandemic influenza A (H1N1) virus infection confirmed before death (N = 41) or after death (N = 36). Of the 77 cases evaluated, 56 (72%) had at least some clinical information available, and 35 (45%) had preliminary autopsy reports submitted with the tissue specimens. All specimens were examined using hematoxylin and eosin stain, Lillie-Twort tissue Gram stain, and Warthin-Starry silver stain (Figure). Tissue specimens also were evaluated by various immunohistochemical assays using antibodies that are specifically reactive with S. pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, or Haemophilus influenzae. All bacteria were evaluated by a broad-range PCR assay that targets a segment of the 16S ribosomal DNA gene in DNA extracted from formalin-fixed, paraffin-embedded tissue (2). PCR for lytA and spy genes and pneumococcal serotyping by multiplex PCR were conducted to further characterize streptococcal coinfections.†
Of the 77 confirmed cases evaluated, 22 had histopathologic, immnohistochemical, and molecular evidence of coinfection with an identified bacteria, including 10 cases with S. pneumoniae, six with S. pyogenes, seven with S. aureus, two with Streptococcus mitis, and one with H. influenzae; four cases involved multiple pathogens (Table). The median age of the 22 patients was 31 years (range: 2 months--56 years); 11 (50%) were male. The cases were reported from eight states: California, Hawaii, Illinois, New Jersey, New York, Texas, Utah, and Virginia.
Duration of illness was available for 17 of the 22 patients; median duration was 6 days (range: 1--25 days). Fourteen of 18 patients with information available sought medical care while ill, and eight were hospitalized. Of the seven hospitalized patients with information available, all required mechanical ventilation. Seven of nine patients with information available on antimicrobial therapy were treated with antibiotics. Sixteen of the 21 patients for whom previous medical history was known had underlying medical conditions that were known to increase the risk for influenza-associated complications (16 patients) (3) or that were indications for vaccination with 23-valent pneumococcal polysaccharide vaccine (PPSV23) (15 patients).§
Reported by: J Louie, MD, C Jean, MPH, California Dept of Public Health. T-H Chen, MD, S Park, MD, R Ueki, Hawaii State Dept of Health. T Harper, MD, Stroger Hospital of Cook County; Chicago Dept of Public Health. E Chmara, MD, Northern Region Medical Examiner Office; New Jersey Dept of Health and Senior Svcs. J Myers, Erie County Medical Center; R Stoppacher, MD, Onondaga County Medical Examiner's Office; C Catanese, MD, Orange County Medical Examiner's Office; City of New York Office of the Chief Medical Examiner; New York City Dept of Health and Mental Hygiene; New York State Dept of Health. N Farley, MD, Valley Forensics, P.L.L.C.; Texas Dept of State Health Svcs. E Leis, MD, Utah Office of the Medical Examiner; Utah Dept of Public Health. C DiAngelo, MD, Northern District Office of the Chief Medical Examiner, Virginia; Virginia Dept of Health. AM Fry, MD, L Finelli, DrPH, Influenza Div, MG Carvalho, PhD, B Beall, PhD, M Moore, MD, C Whitney, MD, Div of Bacterial Diseases, National Center for Immunization and Respiratory Diseases; Infectious Diseases Pathology Br, National Center for Zoonotic, Vector-Borne, and Enteric Diseases; DM Blau, DVM, PhD, EIS Officer, CDC.
Editorial Note: During previous influenza pandemics, bacterial coinfections caused by S. pneumoniae, H. influenzae, S. aureus, and group A Streptococcus have been important contributors to morbidity and mortality (1,4). However, two early reviews of severe cases of 2009 pandemic influenza A (H1N1) showed no evidence of bacterial pneumonia among 30 hospitalized patients with laboratory-confirmed cases in California (5) and 10 intensive-care patients in Michigan (6). These reports might have led to a perception that bacterial coinfections are playing a limited role or no role in influenza deaths during the current pandemic. However, failure to document bacterial lung infections might reflect the difficulty of establishing specific bacterial diagnoses among persons with bacterial coinfections. Routine clinical tests used to identify bacterial infections among patients with pneumonia do not detect many of these infections. For example, <10% of patients who are hospitalized with clinically diagnosed pneumonia have blood cultures that are positive for bacterial infections (7). Histopathologic evaluation and testing of lung tissue, especially using PCR and immunochemistry methods, can detect many bacterial lung infections missed by standard clinical methods (2). The findings in this report indicate that, as during previous influenza pandemics, bacterial pneumonia is contributing to deaths associated with pandemic H1N1 and that histopathologic methods can be used to identify bacterial coinfections after death.
Although the findings in this report confirm the presence of bacterial lung coinfection, the results cannot be used to assess the prevalence of bacterial pneumonia among patients who have died from pandemic H1N1. The cases in this report do not come from a systematic sample and might not be representative of all pandemic H1N1 deaths or all pandemic H1N1 deaths associated with bacterial pneumonia. Systematic research is needed to determine the incidence and outcome of bacterial lung coinfections among patients with pandemic H1N1 virus infection and to quantify the role of these infections in fatal cases.
Medical examiners and coroners have an important role in the surveillance of deaths caused by the 2009 pandemic influenza A (H1N1) virus (8). Histopathologic techniques can assist with postmortem diagnosis of coinfections in patients in whom culture, antemortem or postmortem, does not detect bacteria. When autopsies are performed for patients with confirmed or suspected influenza who die after acute respiratory disease, a pathological evaluation of respiratory tissues should be conducted and should include testing for both viral and bacterial pathogens (8).
The findings in this report are subject to at least three limitations. First, not all potential bacterial pathogens (e.g., Legionella species) were evaluated. Second, the analysis of patient characteristics was based on limited patient information. Because medical records and death certificates generally were not available, no conclusion could be drawn about whether the cause of death was influenza, bacterial infection, or both. Third, because assessments of bacterial coinfections were conducted at autopsy, inadequate sampling, collection of specimens from unaffected portions of the lung, or prolonged illness and treatment before death might have prevented identification of bacteria.
The most common bacteria found in patients described in this report were S. pneumoniae. This infection was documented in 10 of the 22 patients. Although no data were available on the vaccination status of the 22 patients, one patient was aged <5 years and was therefore a candidate for pneumococcal conjugate vaccine, and 15 others had underlying medical conditions that were indications for PPSV23 vaccine (9,10). Persons at greatest risk for invasive pneumococcal disease include young children, older adults, and persons of any age with certain conditions, including chronic lung or cardiovascular disease and immunosuppressive conditions. All children aged <5 years should receive pneumococcal conjugate vaccine according to current Advisory Committee on Immunization Practices (ACIP) recommendations (9). In addition, PPSV23 is recommended for all persons aged 2--64 years with certain health conditions and all persons aged ≥65 years.¶ Available vaccination coverage data indicate that only a small proportion of persons aged 2--64 years in the United States who are recommended by ACIP to receive pneumococcal vaccine have received the vaccine. One study indicated that only 16% of persons aged 18--49 years with indications for PPSV23 vaccine had received the vaccine.** Because of the higher rates of 2009 pandemic H1N1 illness and death among persons aged 2--64 years, providers should target persons in this group who have existing ACIP indications for PPSV23 to receive the vaccine.
The findings in this report also underscore the importance of managing patients with influenza who also might have bacterial pneumonia with both empiric antibacterial therapy and antiviral medications.†† In addition, public health departments should encourage the use of pneumococcal vaccine, seasonal influenza vaccine, and, when the vaccine becomes available, pandemic influenza A (H1N1) 2009 monovalent vaccine.
References Morens DM, Taubenberger, Fauci AS. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness. J Infect Dis 2008;198:962--70. Guarner J, Packard MM, Nolte KB, et al. Usefulness of immunohistochemical diagnosis of Streptococcus pneumoniae in formalin-fixed, paraffin-embedded specimens compared with culture and gram stain techniques. Am J Clin Pathol 2007;127:612--8. CDC. Prevention and control of seasonal influenza with vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2009. MMWR 2009;58(No. RR-8). Brundage JF, Shanks GD. Deaths from bacterial pneumonia during the 1918--19 influenza pandemic. Emerg Infect Dis 2008;14:1193--9. CDC. Hospitalized patients with novel influenza A (H1N1) virus infection---California, April--May, 2009. MMWR 2009;58:536--41. CDC. Intensive-care patients with severe novel influenza A (H1N1) virus infection---Michigan, June 2009. MMWR 2009;58:749--52. Metersky ML, Ma A, Bratzler DW, Houck PM. Predicting bacteremia in patients with community-acquired pneumonia. Am J Respir Crit Care Med 2004;169:342--7. Nolte KB, Lathrop SL, Nashelsky MB, et al. "Med-X": a medical examiner surveillance model for bioterrorism and infectious disease mortality. Hum Pathol 2007;38:718--25. CDC. Preventing pneumococcal disease among infants and young children: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2000;49(No. RR-9). CDC. Prevention of pneumococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1997;46(No. RR-8). * Additional information available at http://www.cdc.gov/h1n1flu/tissuesubmission.htm.
† Additional information available at http://www.cdc.gov/ncidod/biotech/strep/protocols.htm.
§ Additional information available at http://www.cdc.gov/h1n1flu/guidance/ppsv_h1n1.htm.
¶ Additional information available at http://www.cdc.gov/h1n1flu/guidance/ppsv_h1n1.htm.
** Additional information available at http://www.cdc.gov/flu/professionals/vaccination/pdf/NHIS89_07ppvvaxtrendtab.pdf.
†† Additional information available at http://www.cdc.gov/h1n1flu/recommendations.htm.
Murió una nena de síndrome urémico hemolítico en Córdoba 13:17|Tenía casi tres años y otro chiquito, de uno, que concurría a la misma guardería está internado en grave estado con un cuadro similar. La enfermedad está relacionada con el consumo de carne en mal cocida.Una nena de casi tres años murió tras ser internada con un cuadro de síndrome urémico hemolítico (SUH) en Córdoba, mientras que un chiquito que asistía a la misma guardería que ella está internado con un cuadro similar.
La nena tenía dos años y medio y había ingresado el jueves pasado a la Clínica de la Concepción, de la capital provincial, con un cuadro de diarrea con sangre. Falleció al día siguiente, según confirmaron hoy autoridades médicas del centro asistencial al diario La Voz del Interior.
Además, trascendió que personal de Epidemiología del Ministerio de Salud concurrió a la guardería a la que asistía la chiquita para evaluar la situación, dado que otro nene, de un año y 9 meses, está internado desde el lunes afectado también por el síndrome urémico hemolítico. La enfermedad suele estar relacionada con el consumo de carne mal cocida.
En tanto, una chiquita de un año de Capilla de los Remedios está internada desde el jueves a causa del síndrome en la terapia intensiva del Hospital de Niños. La jefa del servicio de Nefrología, Elida Inchaurregui informó que su estado es grave. En el Hospital de Río Cuarto otro chico está internado con SUH, pero se recupera favorablemente.
El SUH compromete el funcionamiento de los riñones, destruye los glóbulos rojos y puede provocar alteraciones neurológicas. En lo que va del año, en Córdoba se registraron 29 casos de la enfermedad, "menos de los que había el año pasado para la misma época", indicó la médica. En 2008, en la provincia hubo en total 59, cinco más que en 2007. Copyright 1996-2009 Clarín.com - All rights reserved file2799month502
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Ω DPT Website: Pharmacotherapy for Substance Use Dis... 2583. Ω Substance Abuse Treatment Advisory: OxyContin Pres... 2582. Ω Substance Abuse Treatment Advisory, Vol 5, Issue 2... 2581. Ω Substance Abuse in Brief Fact Sheet Pain Managemen... 2580. CDC 2009 H1N1 Flu | 2009 H1N1 Flu: International S... 2579. CDC H1N1 Flu | Updated Interim Recommendations for... 2578. WHO | Pandemic (H1N1) 2009 - update 66 2577. Educating the Public About Removal of Essential-Us... 2576. Investigadores de la Universidad de Granada descub... 2575. FDA Approves Donor Screening Test for Antibodies t... 2574. FDA Announces Second Annual Science Writers Sympos... 2573. - EPARs human use - Isentress//raltegravir 2572. - European Medicines Agency - Human Medicines - Orph... 2571. - European Medicines Agency - Human Medicines - Medi... 2570. - EPARs human use - Keppra//Levetiracetam 2569. - EPARs human use - Prezista//darunavir 2568. - EPARs human use - Luminity//Perflutren 2567. - EPARs human use - Jalra//vildagliptin 2566. - EPARs human use - Xiliarx//vildagliptin 2565. - EPARs human use - Galvus//vildagliptin 2564. - EPARs human use - ViraferonPeg//Peginterferon alfa... 2563. - EPARs human use - Avastin//Bevacizumab 2562. - EPARs human use - PegIntron//Peginterferon alfa-2b... 2561. Soluciones de acceso y fijación para una mejor vis... 2560. enfermedades genéticas: nuevo mecanismo 2559. Emerging Issues in the Use of Methadone 2558. Hiberix - Haemophilus b Conjugate Vaccine (Tetanus... 2557. Draft Guidance for Industry: Clinical Consideratio... 2556. QuickStats: Percentage of Adults Aged ≥18 Years Wh... 2555. Licensure of a Haemophilus influenzae Type b (Hib)... 2554. Updated Recommendations from the Advisory Committe... 2553. Update on Vaccine-Derived Polioviruses --- Worldwi... 2552. National, State, and Local Area Vaccination Covera... 2551. Nonfatal Scald-Related Burns Among Adults Aged ≥65... 2550. List of Determinations Including Written Request 2549. Medical, Statistical, and Clinical Pharmacology Re... 2548. Microbiological Data for Systemic Antibacterial Dr... 2547. Approved Drug Products with Therapeutic Equivalenc... 2546. en determinados escenarios clínicos, la detección ... 2545. la artrosis incrementa el número de células madre ... 2544. ∞ Guidance for Industry: Considerations for Allogene... 2543. MALARIA 2542. Aún los bajos niveles de plomo dañan el desarrollo... 2541. El análisis genético ayuda a detectar cada vez ant... 2540. * IntraMed - Artículos - Manejo de la epistaxis 2539. * IntraMed - Artículos - Epistaxis: ¿qué hacer? 2538. FDA Approves Vaccines for 2009 H1N1 Influenza Viru... 2537. CDC H1N1 Flu | Asthma Information for Patients and... 2536. Roflumilast mejora la función pulmonar y reduce la... 2535. Vaccines Approved for H1N1 Influenza Virus 2534. Generic Drug Roundup: September 2009 2533. papel clave de las monoamina oxidasas en la person... 2532. El osteocito regresa al estudio de la osteoporosis... 2531. El trastorno bipolar en niños suele ser tardío y e... 2530. El IPTi disminuye un 30% los episodios de malaria ... 2529. Nueva vía molecular para atacar el bacilo de Koch 2528. AHRQ Patient Safety Network 2527. European Medicines Agency - Human Medicines - Medi... 2526. Information on Natalizumab (marketed as Tysabri) 2525. AHRQ Effective Health Care Program - Research Revi... 2524. Information for Healthcare Professionals - Intrave... 2523. Muertes H1N1 muestran que es diferente a otras gri... 2522. H1N1 - gripe porcina - ISID / GLOBAL: estable 2521. micobacterias atípicas / ISID - U.S.A. 2520. Gripe A(H1N1) y cardiopatía, una mala combinación 2519. - EPARs human use - Oprymea//pramipexole 2518. tapentadol en Fase III 2517. nuevo antiviral: evita que el virus de la gripe mu... 2516. Neumococo: Promueven el uso de una vacuna 2515. Medications Effective in Reducing Risk of Breast C... 2514. Influenza A (H1N1) 2009 Monovalent Vaccine Safety ... 2513. Influenza A (H1N1) 2009 Monovalent Vaccines Compos... 2512. Influenza A (H1N1) 2009 Monovalent Vaccines Questi... 2511. Influenza A (H1N1) 2009 Monovalent 2510. FDA MedWatch August 2009 2509. ► The Pink Book: Epidemiology and Prevention of Vacc... 2508. - EPARs human use - Yentreve//duloxetine hydrochlori... 2507. Medication management guideline. 2506. Fall management guideline. 2505. Cardiovascular disease - primary prevention. 2504. Hypertension - detection, diagnosis and management... 2503. Febuxostat for the management of hyperuricaemia in... 2502. - EPARs human use - Aldara//Imiquimod 2501. H1N1 - gripe porcina - signos y síntomas 2500. Infliximab for acute exacerbations of ulcerative c... 2499. Content of a complete routine second trimester obs... 2498. Clinical practice guideline for the management of ... 2497. NGC - Compare - Comparison 2496. Progestogen-only pills. 2495. Progestogen-only injectable contraception. 2494. EFNS guidelines for the use of intravenous immunog... 2493. Particle Beam Radiation Therapy Promising but Unpr... 2492. bacterias resistentes 2491. H1N1 - gripe porcina - OMS / GLOBAL: 3205 muertes 2490. CDC H1N1 Flu | Questions and Answers Monitoring In... 2489. Denosumab, seguro y eficaz en el manejo de fractur... 2488. - EPARs human use - Lyrica//Pregabalin 2487. - EPARs human use - Apidra//Insulin glulisine 2486. TUBERCULOSIS resistente en Irán 2485. linfoma MALT 2484. doxorrubicina liposomal pegilada retrasa el tiempo... 2483. La QT metronómica es útil, pero aún se desconocen ... 2482. The effect of traumatic brain injury on the health... 2481. The effect of a quality improvement collaborative ... 2480. Patient activation and adherence to physical thera... 2479. Death or hospitalization of patients on chronic he... 2478. Overuse of tympanostomy tubes in New York metropol... 2477. H1N1 - gripe porcina - ARGENTINA: 514 decesos 2476. Mental Health Needs of Low-Income Children With Sp... 2475. H1N1 - gripe porcina - estrategia sanitaria global... 2474. Muchos medicamentos para la osteoporosis previenen... 2473. Task Force recomienda hacer estudios a los adolesc... 2472. El uso de fármacos antipsicóticos atípicos aumenta... 2471. Estudio financiado por AHRQ halla menor riesgo de ... 2470. Según un nuevo estudio de la AHRQ, no está comprob... 2469. Family History and Improving Health: Structured Ab... 2468. - EPARs human use - Enbrel//Etanercept 2467. - EPARs human use - Synagis//Palivizumab 2466. - EPARs human use - Privigen//human normal immunoglo... 2465. - EPARs human use - Cetrotide//Cetrorelix (as acetat... 2464. Portex Uncuffed Pediatric-Sized Tracheal Tubes (si... 2463. Science Report - Revista Digital de CEDEPAP TV / ... 2462. FDA Updates "Warning Letters" Web page 2461. FDA Clears a Test for Ovarian Cancer 2460. Release No. 0433.09 2459. WHO | Measures in school settings 2458. WHO | Pandemic (H1N1) 2009 - update 65 2457. Statement by Dr. Anthony Fauci, Director, National... 2456. Influenza (H1N1) 2009 Outbreak and School Closure,... 2455. → ArrayTrack™ Publications 2454. H1N1 - gripe porcina - USA: vacuna unidosis 2453. OSELTAMIVIR: resistencia - primer caso en USA 2452. H1N1 - gripe porcina - VENEZUELA: 55 decesos 2451. - European Medicines Agency - Human Medicines - Orph... 2450. H1N1 - gripe porcina - CHILE: actualización 2449. Vacunación contra el rotavirus e ingresos por gast... 2448. National Survey on Drug Use and Health: Results fr... 2447. NIAID Launches 2009 H1N1 Influenza Vaccine Trial i... 2446. - EPARs human use - Trevaclyn//nicotinic acid / lar... 2445. - EPARs human use - Tredaptive//nicotinic acid / lar... 2444. - EPARs human use - Sutent//SUNITINIB 2443. → ArrayTrack™ News 2442. Update: Influenza Activity --- United States, Apri... 2441. Notice to Readers: National Child Passenger Safety... 2440. ▲ National Laboratory Inventories for Wild Polioviru... 2439. ♠ Receipt of Influenza Vaccine During Pregnancy Amon... 2438. ♠ Oseltamivir-Resistant 2009 Pandemic Influenza A (H... 2437. DENGUE - QUINTANA ROO [México]: blindaje 2436. H1N1 - gripe porcina: MÉXICO - repunte de casos 2435. - European Medicines Agency - Withdrawals of Applica... 2434. - EPARs human use - Tasigna//nilotinib 2433, - EPARs human use - Revlimid//lenalidomide 2432. - EPARs human use - Cubicin//Daptomycin 2431. El virus de la gripe A(H1N1) llega al fondo de los... 2430. Penumbra Neuron 5F Select Catheter 2429. Questions and Answers about CDC’s Revised Recommen... 2428. Updated Interim Recommendations for the Use of Ant... 2427. CDC H1N1 Flu | Interim Guidance for State and Loca... 2426. SARM - ISID/USA 2425. ► Positron Emission Tomography for Nine Cancers (Bla... 2424. ► Potential Conflict of Interest in the Production o... 2423. ► Reviews of Selected Pharmacogenetic Tests for Non-... 2422. investigación del CIBER de Enfermedades Respirator... 2421. * IntraMed - Artículos - Tos: etiología poco frecuen... 2420. * IntraMed - Artículos - Síncope: nueva guía de la A... 2419. Hay que controlar el VPH en cérvix y ano de hombre... 2418. October 9, 2009: Cellular, Tissue and Gene Therapi... 2417. - EPARs human use - Kepivance//Palifermin 2416. - EPARs human use - Alimta//pemetrexed 2415. El primer ensayo de la vacuna contra la gripe A en... 2414. La UE aprueba el everolimus para el cáncer renal a... 2413. WHO | Pandemic (H1N1) 2009 - update 64 2412. Poor clinical sensitivity of rapid antigen test fo... 2411. A Model-based Assessment of Oseltamivir Prophylaxi... 2410. CDC 2009 H1N1 Flu | 2009 H1N1 U.S. Situation Updat... 2409. CDC 2009 H1N1 Flu | 2009 H1N1 Flu: International S... 2408. MedSun: Newsletter #40, September 2009 2407. H1N1 - gripe porcina - PERÚ: muertes 2406. * IntraMed - Artículos - Pancreatitis aguda isquémic... 2405. red internacional de teleictus 2404. - EPARs human use - Kogenatebayer//blood coagulation... 2403. - EPARs human use - Adenuric//febuxostat 2402. Negative Pressure Wound Therapy Devices [AHRQ] 2401. H1N1 - gripe porcina - ARGENTINA: 512 muertes 2400. Nuevo grupo de trabajo sobre enfermedades autoinmu... 2399. * IntraMed - Artículos - Tratamiento de la artrosis ... 2398. - EPARs human use - Axura//Memantine hydrochloride 2397. - EPARs human use - Ebixa//Memantine hydrochloride 2396. - EPARs human use - Myozyme//Alglucosidase alfa 2395. Viral infections. In: Guidelines for prevention an... 2394. Parasitic infections. In: Guidelines for preventio... 2393. Mycobacterial infections. In: Guidelines for preve... 2392. Fungal infections. In: Guidelines for prevention a... 2391. Bacterial infections. In: Guidelines for preventio... 2390. ACR Appropriateness Criteria® sudden onset of cold... 2389. ACR Appropriateness Criteria® multiple gestations.... 2388. ACR Appropriateness Criteria® endometrial cancer o... 2387. ACR Appropriateness Criteria® abnormal vaginal ble... 2386. Pemetrexed for the treatment of malignant pleural ... 2385. OSELTAMIVIR: resistencia estadísticamente previsib... 2384. * IntraMed - Artículos - Hiperfosfatemia e Insuficie... 2383. H1N1 - gripe porcina - BRASIL: 657 muertes 2382. - EPARs human use - Renagel//sevelamer 2381. H1N1 - gripe porcina - ISID / USA: brote 2380. H1N1 - gripe porcina - ISID / inmunización segura 2379. Medidas adecuadas permiten controlar eficazmente r... 2378. * IntraMed - Artículos - Diagnóstico de feocromocito... 2377. * IntraMed - Artículos - Comparación de la adrenalec... 2376. * IntraMed - Artículos - Asociación entre hiperplasi... 2375. * IntraMed - Artículos - Tumores suprarrenales descu... 2374. CANADA - Health Indicators 2009 2373. 10 Patient Safety Tips for Hospitals 2372. identificar y controlar la anemia en pacientes onc... 2371. FDA - Correction of Alert issued on 09/03/2009 2370. H1N1 - gripe porcina - ARGENTINA/OMS: contagio sos... 2369. The AHRQ Informed Consent and Authorization Toolki... 2368. - EPARs human use - Bondenza//Ibandronic acid 2367. - EPARs human use - Adrovance//Alendronate sodium tr... 2366. H1N1 - gripe porcina - ISID/USA: muertes 2365. CDC Guidance on Helping Child Care and Early Child... 2364. Technical Report for State and Local Public Health... 2363. Máscaras, clave en protección H1N1 trabajadores sa... 2362. H1N1 causa muerte de 2.837 personas 2361. HIV/SIDA - ISID 2360. ├ substancias letales - paco 2359. ◊ TRANSPLANTE de INTESTINO 2358. Integration of Mental Health/Substance Abuse and P... 2357. Myfortic (mycophenolic acid) 2356. H1N1 - gripe porcina - ISID / SALUD GLOBAL 2355. H1N1 - gripe porcina - ISID / GLOBAL 2354. * IntraMed - Artículos - Sindrome de hipereosinofili... 2353. - EPARs human use - NovoRapid//Insulin aspart 2352. - EPARs human use - Angiox//Bivalirudin 2351. - EPARs human use - Integrilin//Eptifibatide 2350. Influenza Virus Vaccine Actions 2349. Guidelines for the Prevention and Treatment of Opp... 2348. Erratum: Vol. 56, No. 53 2347. Notice to Readers: Sickle Cell Awareness Month -- ... 2346. QuickStats: Percentage of Adults Aged ≥18 Years Wh... 2345. Laboratory Surveillance for Wild and Vaccine-Deriv... 2344. Inadvertent Ingestion of Marijuana --- Los Angeles... 2343. Surveillance for Pediatric Deaths Associated with ... 2342. España: las Sociedades de Primaria valoran la situ... 2341. Crece la cifra de fallecidos por la gripe A(H1N1) ... 2340. AHRQ Patient Safety Network 2339. Research Activities, September 2009: Acute Care/Ho... 2338. Research Activities, September 2009: Mental Health... 2337. Blood Establishment Computer Software: Understandi... 2336. AHRQ Patient Safety Network: Indiana Medical Error... 2335. AHRQ Effective Health Care Program - Research Revi... 2334. Vaccines: Pubs/SurvManual/main page 2333. "U.S. Food & Drug Administration (FDA)" - New cla... 2332. - EPARs human use - Increlex//mecasermin 2331. - EPARs human use - NutropinAq//Somatropin, recombin... 2330. - EPARs human use - Zeffix//lamivudine 2329. CDC H1N1 Flu | 2009 H1N1 Influenza Vaccine and Pre... 2328. FDA - Guidance on Tacrolimus 2327. Public Health Emergency Preparedness: Planning for... 2326. Treatment for Overactive Bladder in Women: Structu... 2325. Prevention and Control of Seasonal Influenza with ... 2324. Use of Influenza A (H1N1) 2009 Monovalent Vaccine 2323. ACIP Provisional Recommendations for Measles-Mumps... 2322. ACIP Provisional Recommendations for the Use of Co... 2321. DENGUE - ISID - GLOBAL 2320. ► Studies in Animals Suggest 2009 H1N1 Virus May Hav... 2319. - EPARs human use - Avandamet//Rosiglitazone maleate... 2318. - EPARs human use - Avandia//rosiglitazone 2317. -● European Medicines Agency - EMEA monthly medicines... 2316. HIV - New guidelines 2009 2315. ACR Appropriateness Criteria® acute pyelonephritis... 2314. ACR Appropriateness Criteria® recurrent lower urin... 2313. ACR Appropriateness Criteria® recurrent symptoms f... 2312. ACR Appropriateness Criteria® renal failure. 2311. ACR Appropriateness Criteria® staging of bronchoge... 2310. Clinical practice guideline for the evaluation of ... 2309. The management of encephalitis: clinical practice ... 2308. Prevention and management of obesity (mature adole... 2307. Osteoarthritis. The care and management of osteoar... 2306. Post myocardial infarction: secondary prevention i... 2305. Eating disorders during pregnancy and postpartum. 2304. El ESC de Barcelona presenta 15 grandes ensayos mu... 2303. NCCN Trends August 2009 2302. Tumor Necrosis Factor (TNF) Blockers (marketed as ... 2301. WHO | Pandemic (H1N1) 2009 - update 63 2300. ├ Tokyo-172 BCG Vaccination Complications, Taiwan | ... 2299. ► Susceptibilities of Nonhuman Primates to CWD | CDC... 2998. ◊ Reemergence of Strongyloidiasis, Northern Italy | ... 2297. ◊ Human Plasmodium knowlesi Infection | CDC EID 2296. ◊ Program to Eradicate Malaria in Sardinia | CDC EID... 2295. ◊ Infectious Disease Modeling and Military Readiness... 2294. → Merkel Cell Polyomavirus | CDC EID 2293. → Avian and Human Isolates of C. dubliniensis | CDC ... 2292. → Zygomycosis, France | CDC EID 2291. → Gordonia sputi Bacteremia | CDC EID 2290. → Relapsing Fever Spirochete in Seabird Tick, Japan ... 2289. → Chlamydia trachomatis Infections | CDC EID 2288. WHO | Preparing for the second wave: lessons from ... ARCHIVO DEL BLOG AGOSTO • ▼ 2009 (2297) o ▼ agosto (472) 2287. Biologics PREA Labeling Changes 2286. Guidance for Industry - Recommendations for Manage...
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Independent Lineage of Lymphocytic Choriomeningitis Virus in Wood Mice (Apodemus sylvaticus), Spain Juan Ledesma, Cesare Giovanni Fedele, Francisco Carro, Lourdes Lledó, María Paz Sánchez-Seco, Antonio Tenorio, Ramón Casimiro Soriguer, José Vicente Saz, Gerardo Domínguez, María Flora Rosas, Jesús Félix Barandika, and María Isabel Gegúndez Author affiliations: Universidad de Alcalá, Madrid, Spain (J. Ledesma, L. Lledό, J.V. Saz, M.I. Gegúndez); Instituto de Salud Carlos III, Madrid (C.G. Fedele, M.P. Sánchez-Seco, A. Tenorio); Consejo Superior de Investigaciones Científicas, Seville, Spain (F. Carro, R.C. Soriguer); Consejería de Sanidad y Bienestar Social de la Junta de Castilla y León, Burgos, Spain (G. Domínguez); Centro de Biologia Molecular Severo Ochoa, Madrid (M.F. Rosas); and NEIKER-Instituto Vasco de Investigación y Desarrollo Agrario, Vizcaya, Spain (J.F. Barandika)
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Abstract To clarify the presence of lymphocytic choriomeningitis virus (LCMV) in Spain, we examined blood and tissue specimens from 866 small mammals. LCMV RNA was detected in 3 of 694 wood mice (Apodemus sylvaticus). Phylogenetic analyses suggest that the strains constitute a new evolutionary lineage. LCMV antibodies were detected in 4 of 10 rodent species tested.
Lymphocytic choriomeningitis virus (LCMV) is a ubiquitous rodent-borne virus belonging to the family Arenaviridae, whose genome consists of 2 single strands of RNA, named small (S) and large (L), respectively. The S segment encodes the nucleocapsid protein (NP) and the glycoprotein precursor (GPC). The L segment encodes a viral RNA-dependent RNA polymerase and a zinc-binding protein. The common house mouse (Mus musculus) is the principal reservoir for LCMV. Infected mice can shed the virus in large quantities throughout their lives. Some epidemiologic studies show that ≈9% of wild mice are infected with LCMV (1,2), and other species of rodents have been reported to be possible reservoirs of LCMV (2–4).
Humans become infected with LCMV by inhaling contaminated feces or urine, through bite wounds, by vertical route, or after organ transplants (5). LCMV is responsible for aseptic meningitis and encephalitis (6) and may cause congenital malformations or abortion (7). In Spain, 1 case of encephalitis caused by LCMV has been reported (8), and recently, LCMV infection has been detected in 4 patients with aseptic meningitis (9). LCMV infection in rodents and the general population has also been demonstrated by serologic tests (2). The aim of this study was to improve our knowledge of LCMV in rodents in Spain.
The Study A total of 866 small mammals were trapped from July 2003 through June 2006 in 19 Spanish provinces. Of those captured, 833 were rodents from 10 species: 694 wood mice (Apodemus sylvaticus), 17 yellow-necked mice (A. flavicollis), 27 house mice (M. musculus), 6 Algerian mice (M. spretus), 21 Norway rate (Rattus norvegicus), 50 bank voles (Myodes [Clethrionomys] glareolus), 9 snow voles (Chionomys [Microtus] nivalis), 3 Orkney voles (Microtus arvalis), 3 Mediterranean pine voles (Microtus [Pitymys] duodecimcostatus), and 3 garden dormice (Eliomys quercinus). Thirty-three were insectivores (18 shrews [Sorex spp.] and 15 white-toothed shrews [Crocidura russula]). Tissue samples (lungs, kidneys, spleens) were obtained in all cases and stored at –20°C in RNAlater solution (Ambion Inc., Austin, TX, USA) to preserve the RNA and inactivate the virus. Serum samples were only available from 665 specimens.
Serum samples were assayed against LCMV, diluted 1:16 as previously described (9), but using immunoglobulins against mice or rats as secondary antibodies. Western blot assays confirmed 25 of the 35 positive serum specimens detected by the immunofluorescence antibody (IFA) assay. The overall prevalence of antibodies against LCMV was 3.76%. Antibodies were detected in 4 species: A. sylvaticus (21/536, 3.92%), M. musculus (2/24, 8.33%), M. spretus (1/6, 16.67%), and R. norvegicus (1/21, 4.76%). Titers ranged from 16 to 2,048 by IFA assay.
LCMV-related genome was detected in 3 of 866 specimens corresponding to A. sylvaticus mice trapped in Sierra Nevada (SN05), Cabra (CABN), and Grazalema (GR01), 3 well-preserved natural areas in the southern Spain. Only serum specimens from 2 of these rodents were available, and LCMV antibodies were detected in only 1 sample.
Briefly, pools were prepared by mixing 3- to 4-mm pieces of lung, kidney, and spleen from each trapped animal; the mixture was homogenized and their nucleic acid extracted by using RNeasy Mini Kit (QIAGEN, Hilden, Germany) in accordance with the manufacturer's instructions. The extracted RNA was analyzed by reverse transcription and nested PCR. The first round was performed with primers AREN1+ (5´-2367CWATRTANGGCCAICCITCICC2388-3´) and AREN1– (5´-2789TNRWYAAYCARTTYGGIWCIRTKCC2813-3´) and primers AREN2+ (5´-2396CANANYTTRTANARNAIRTTYTCRTAIGG2424-3´) and AREN2– (5´-2567AGYYTNKNNGCNGCIGTIAARGC2589-3´) for nested PCR. The symbols + and – correspond to sense and antisense sequences, respectively. Indicated positions correspond to those of LCMV-Armstrong 53b (GenBank accession no. M20869). Primers were designed on conserved motifs of the NP gene and were able to detect arenaviruses from the Old World and from the New World. Amplification products of the expected size (194 bp) were purified and sequenced. Positive results were also obtained when each tissue from these 3 animals was analyzed separately. Viral isolation was not attempted because samples were inactivated with RNA later.
The complete S segment sequence of every detected virus was obtained from lung lysates by using primers designed based on LCMV conserved sequences of the S segments available in GenBank that enable amplification of overlapping complementary DNAs (sequences of the primers are available upon request). The lengths of the S-segments were 3,357, 3,364, and 3,366 nt for samples GR01, SN05, and CABN, respectively (GenBank accession nos. FJ895882–FJ895884, respectively). As expected for LCMV, the sequences defined 2 nonoverlapping genes (genes GPC and NP, with 498 and 558 aa, respectively) arranged in ambisense direction, separated by an intergenic noncoding region, and flanked by 5´ and 3´ ends. Sequence comparison with the complete S segment from other LCMV strains showed deletions and insertions of nucleotides in the noncoding regions (information available on request).
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Surveillance System for Infectious Diseases of Pets, Santiago, Chile Javier López, Katia Abarca, Jaime Cerda, Berta Valenzuela, Lilia Lorca, Andrea Olea, and Ximena Aguilera Author affiliations: Chilean Society of Veterinary Infectious Diseases, Santiago, Chile (J. López, B. Valenzuela, L. Lorca); Pontificia Universidad Católica de Chile, Santiago (K. Abarca, J. Cerda); and Ministry of Health, Santiago (A. Olea, X. Aguilera)
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Abstract Pet diseases may pose risks to human health but are rarely included in surveillance systems. A pilot surveillance system of pet infectious diseases in Santiago, Chile, found that 4 canine and 3 feline diseases accounted for 90.1% and 98.4% of notifications, respectively. Data also suggested association between poverty and pet diseases.
Communicable diseases challenge health systems and require coordinated efforts for their control. Surveillance systems for human communicable diseases have been implemented since the 19th century. Surveillance of animal infections started later and focused on livestock production. More recently, in response to emerging zoonoses such as avian influenza and West Nile virus infection, novel surveillance systems for wild animals have been implemented (1). Although pet-borne infections have become increasingly relevant to human health, systematic notification of these infections is not currently conducted, except for rabies.
Pets (domesticated dogs and cats that live in close proximity to humans) may pose several risks to their owners' health and create occupational hazards for professionals such as veterinarians. They can also serve as sentinels for several diseases by alerting persons to the presence of infectious agents in a community (2). These features emphasize the need for surveillance systems of pet infectious diseases, especially those that can be transmitted to humans (3).
In Chile, as in other countries, pet infectious diseases, except for rabies, have not been included in any surveillance system; for this reason, information about their epidemiology is scarce. Thus, a pilot surveillance system for infectious disease of pet dogs and cats was implemented for a 2-year period in Santiago, Chile.
The Study During October 2004–September 2006, the sentinel surveillance system was implemented in 61 veterinary clinics (30 during the first year and another 31 during the second year) located in 34 districts of Santiago (population 5.4 million). Pet population estimates (1,117,192 dogs; 518,613 cats) were derived from a study conducted previously in Santiago (4) and corresponded to a rate of ≈1 sentinel centers per 27,000 pets. Sentinel centers were asked to participate on a voluntary basis and were grouped similarly to the human health services, following geographic criteria.
Of the 12 notifiable infectious diseases in the surveillance system, 5 were nonzoonotic (distemper, canine infectious tracheobronchitis, feline respiratory complex disease, feline leukemia, and hemorrhagic gastroenteritis), and 7 were zoonotic (giardiasis, brucellosis, leptospirosis, rabies, ehrlichiosis, scabies, and tinea infection). Definitions were established for suspected and confirmed cases of each disease. Laboratory confirmation was required for diagnosis of giardiasis, brucellosis, leptospirosis, and rabies. Personnel from each sentinel center recorded their data on a website. They were trained in operative definitions and procedures, which included submitting a weekly report of the total number of cases seen. Participation in the study was voluntary; no funding or incentives were offered.
During the 2-year period, 8,167 cases were reported: 6,974 (85.4%) in dogs and 1,193 (14.6%) in cats. Of these dogs and cats, 4,415 (63.3%) and 730 (61.2%), respectively, were males. Also, 4,524 (64.9%) dogs and 503 (42.2%) cats were <1 year of age. Data submitted during the first year of surveillance accounted for 67.5% of canine and 66.7% of feline diseases notifications.
A negative correlation was found between the average number of notifications per sentinel center (ANC) and time (8 trimesters) for dogs (ρ –0.95, p<0.01) and cats (ρ –0.93, p<0.01). A positive correlation, although not statistically significant, was found between the average poverty rate of the districts located in each health service (5) and the ANC for dogs (ρ +0.77, p = 0.07) and cats (ρ +0.43, p = 0.40) (Table 1).
During the 2-year surveillance period, 4 canine diseases (hemorrhagic gastroenteritis, distemper, scabies, and infectious tracheobronchitis) accounted for 90.1% of notifications, and 3 feline diseases (respiratory disease complex, feline leukemia, and tinea) accounted for 98.4% of notifications (Table 2). For each disease, ANC during the first year of surveillance was calculated for centers located in South–East Health Service (SEHS), which had the highest poverty rate of its districts, and East Health Service (EHS), which had the lowest. For canine diseases, the ratios of ANC for SEHS/ANC for EHS were 3.5 (scabies), 2.5 (distemper), 2.2 (hemorrhagic gastroenteritis), and 1.8 (infectious tracheobronchitis); for feline diseases, these ratios were 1.2 (respiratory disease complex), 1.1 (feline leukemia), and 0.7 (tinea).
For each of the 7 diseases, we calculated the following ratio: total no. notifications for the whole surveillance period for all sentinel centers for pets <1 year of age/total no. notifications for the whole surveillance period for all sentinel centers for pets >1 year of age. Diseases most commonly occurring in pets <1 year of age were hemorrhagic gastroenteritis (10.9) and distemper (3.1); on the contrary, diseases whose ratio favors pets >1 year of age were feline leukemia (0.17) and infectious tracheobronchitis (0.43). Scabies in dogs, feline respiratory disease complex, and tinea in cats had ratios of ≈1.00 (1.07, 0.96, and 0.92, respectively).
Conclusions This pilot surveillance system indicated that overall notifications predominated for pets with 3 characteristics: canine, male, and age <1 year. These characteristics partially reflect the species and sex distribution of pets in the city, as shown by a household survey of 2,100 homes in 7 districts of Santiago during 2001, which showed that 55.7% of household pets were dogs (62.3% males, 16.0% <1 year of age), and 23.5% were cats (57.9% males, 15.0% <1 year of age) (M.A. Daza, 2002, unpub. data). However, according to our data, the predominance of notifications for animals <1 year of age seems to represent a higher risk associated with being <1 year of age.
The finding that 4 canine and 3 feline diseases were most frequently reported may be useful in many settings, such as disease control prioritization and identification of topics of interest for investigation. From a human health perspective, 1 canine disease (scabies) was zoonotic and 2 others (hemorrhagic gastroenteritis and infectious tracheobronchitis) included zoonotic agents in their list of possible etiologies; thus, the information provided by the surveillance system is useful for human physicians and policy makers. This finding is especially relevant because certain pet diseases may occur on a socioeconomic gradient, affecting a greater proportion of persons in the lowest socioeconomic districts. This socioeconomic gradient could have been underestimated in our study because pet owners in Chile must pay for the healthcare of their pets, and the likelihood of diagnostic tests being performed for diseases requiring laboratory confirmation is low, especially in the poorest areas of the city. We also did not account for the overall number of veterinary clinics that exist in each district, making estimation of disease notification rates among districts or health services, impossible. The finding that the most prevalent diseases were preventable by vaccination (e.g., distemper) raises questions about the coverage and quality of vaccinations among pets in Santiago.
The validity of this pilot surveillance system is limited because the overall ANC showed a declining trend during the 2 years of surveillance. This trend probably does not represent reduced incidence of infectious diseases among pets in Santiago; on the contrary, it may illustrate the difficulty of maintaining a private surveillance system based on professional motivation, a key element for ensuring the sustainability of such a system over time.
This pilot surveillance system may motivate other investigations regarding zoonotic infections of pets in Chile. The resulting information would provide the data needed to calculate disease incidence rates and establish unbiased comparisons, which can be used to further the goal of improved pet and human health.
Dr López is a clinical veterinarian and member of the Chilean Society of Veterinary Infectious Diseases. His research interests include canine and feline arthropod-transmitted diseases such as anaplasmosis, ehrlichiosis, and rickettsiosis and other parasitic infections of pets.
References Kahn LH. Confronting zoonosis, linking human and veterinary medicine. Emerg Infect Dis. 2006;12:556–61. Paddock CD, Brenner O, Vaid C, Boyd DB, Berg JM, Joseph RJ, et al. Short report: concurrent Rocky Mountain spotted fever in a dog and its owner. Am J Trop Med Hyg. 2002;66:197–9. Mauer WA, Kaneene JB. Integrated human–animal disease surveillance. Emerg Infect Dis. 2005;11:1490–1. Ibarra L, Morales MA, Acuña P. Demographic aspects of dog and cat populations in Santiago City, Chile [in Spanish]. Avances en Ciencias Veterinarias. 2003;18:13–20. Ministry of Central Planning. National Socioeconomic Characterization Survey. 2006 [cited 2008 Nov 10]. Available from: http://www.mideplan.cl/casen Tables Table 1. Average number of notifications per sentinel center, according to health service, Santiago, Chile, October 2004–September 2005 Table 2. Diseases reported for dogs and cats, Santiago, Chile, October 2004-September 2006
Suggested Citation for this Article López J, Abarca K, Cerda J, Valenzuela B, Lorca L, Olea A, et al. Surveillance system for infectious diseases of pets, Santiago, Chile. Emerg Infect Dis [serial on the Internet]. 2009 Oct [date cited]. Available from http://www.cdc.gov/EID/content/15/10/1674.htm
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Tick-borne Encephalitis from Eating Goat Cheese in a Mountain Region of Austria Heidemarie Holzmann, Stephan W. Aberle, Karin Stiasny, Philipp Werner, Andreas Mischak, Bernhard Zainer, Markus Netzer, Stefan Koppi, Elmar Bechter, and Franz X. Heinz Author affiliations: Medical University of Vienna, Vienna, Austria (H. Holzmann, S.W. Aberle, K. Stiasny, F.X. Heinz); Regional Hospital, Rankweil, Austria (P. Werner, S. Koppi); and Austrian Public Health Authorities, Vorarlberg, Austria (A. Mischak, B. Zainer, M. Netzer, E. Bechter)
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Abstract We report transmission of tick-borne encephalitis virus (TBEV) in July 2008 through nonpasteurized goat milk to 6 humans and 4 domestic pigs in an alpine pasture 1,500 m above sea level. This outbreak indicates the emergence of ticks and TBEV at increasing altitudes in central Europe and the efficiency of oral transmission of TBEV.
Tick-borne encephalitis virus (TBEV) is a human pathogenic flavivirus that is endemic to many European countries and to parts of central and eastern Asia (1). Even though vaccination can effectively prevent TBE (2), >10,000 cases are reported annually for hospitalized persons in areas of Europe and Asia to which TBE is endemic. TBEV occurs in natural foci characterized by ecologic habitats favorable for ticks, especially in wooded areas within the 7°C isotherm (3). The major route of virus transmission is tick bites, but TBEV also can be transmitted during consumption of nonpasteurized milk and milk products from infected animals, primarily goats (3). Outbreaks resulting from oral virus transmission are rare in central Europe but more common in eastern Europe and the Baltic states (3). Our investigation of TBEV transmitted by milk from a goat in an alpine pasture in a mountainous region provides evidence for a changing TBEV epidemiology in central Europe and the expansion of ticks and TBEV to higher regions.
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch West Nile Virus Infection in Plasma of Blood and Plasma Donors, United States Christina B. Planitzer, Jens Modrof, Mei-ying W. Yu, and Thomas R. Kreil Author affiliations: Baxter Bioscience, Vienna, Austria (C.B. Planitzer, J. Modrof, T.R. Kreil); and US Food and Drug Administration, Bethesda, Maryland, USA (M.-y.W. Yu)
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Abstract This study investigated the association of ongoing West Nile virus (WNV) infections with neutralizing antibody titers in US plasma-derived intravenous immune globulin released during 2003–2008. Titers correlated closely with the prevalence of past WNV infection in blood donors, with 2008 lots indicating a prevalence of 1%.
West Nile virus (WNV) is a flavivirus endemic to the United States; typically, hundreds of clinical cases of infection occur each year. The observed number of clinical WNV infections as collated by ArboNET (www.cdc.gov) and the incidence of asymptomatic WNV infections as shown by nucleic acid testing (NAT) of the US blood supply (1) indicate that ≈3 million WNV infections occurred in humans during 1999– 2008.
Because the immune system elicits WNV neutralizing antibodies in response to WNV infection, detectable levels of WNV neutralizing antibodies in the blood of persons with previous WNV infection is expected. Consequently, lots of immune globulin-intravenous (human) (IGIV) manufactured from plasma collected in the United States contain WNV neutralizing antibodies (2). Those IGIV lots, each prepared from several thousand plasma donations to ensure a broad spectrum of antibodies, can be used as an epidemiologic tool that enables the surveillance of thousands of persons in a community through analysis of comparatively few samples. In this study, we demonstrated the increasing trend of WNV-neutralizing antibody titers in lots of IGIV.
Comparing these titers with those of persons with confirmed past WNV infection provides an independent measure of the percentage of the US population previously infected with WNV. Several WNV vaccine trials are ongoing or imminent, so information about the prevalence of past WNV infection in the United States is valuable for planning the demonstration of vaccine efficacy. Low incidence and lack of highly WNV-endemic areas in the United States preclude classic vaccine field trials because of study size requirements and cost-logistics difficulties.
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Human Rickettsialpox, Southeastern Mexico Jorge E. Zavala-Castro, Jorge E. Zavala-Velázquez, Gaspar F. Peniche-Lara, and Justo E. Sulú Uicab Author affiliation: Universidad Autónoma de Yucatán, Mérida, Mexico
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Abstract The detection of Rickettsia akari in 2 human patients increased the diversity of rickettsioses affecting the public health in the southeast of Mexico. Rickettsialpox should be considered in the differential diagnosis with other febrile illnesses for the correct diagnosis and accurate treatment of this potential threat to human health.
Rickettsialpox is an illness characterized by fever, headache, papulovesicular rash over the trunk and extremities, and, in 80% of cases, appearance of an eschar. Rickettsia akari, the etiologic agent of rickettsialpox, is commonly transmitted by the bite of the house-mouse mite, Liponyssoides sanguineus. Human cases of rickettsialpox, as well as infected mites and potential reservoirs of R. akari, have been found in several countries, including the United States, Turkey, Croatia, and Ukraine (1–5). Despite the presence of the house mouse (Mus musculus) around the world, in Latin America human cases caused by R. akari have not been reported, and rickettsial diseases caused by antigenically related rickettsiae have been confined to R. rickettsii, R. felis, R. prowasekii, R. typhi, and R. parkeri (6–11). We report 2 human cases of R. akari infection in the Yucatan Peninsula of Mexico.
The Study Patient 1 was a 9-year-old girl who came to the public hospital in Merida, Yucatan, in May 2008. Her illness had started abruptly with high fever and headache, then evolved over a 12-day period to include nausea, vomiting, hemorrhagic conjunctivitis, excessive lacrimation, and epistaxis. She was treated empirically with antipyretic drugs and had a slight improvement; 3 days after beginning treatment, fever and epistaxis returned with myalgia; irritability; papulovesicular rash involving the extremities, thorax, and oral mucosa; vaginal and gingival bleeding; and disseminated ecchymoses. Clinical laboratory studies showed hemoglobin 9.9 g/dL and hematocrit 29.0% (reference ranges 12–18 g/dL and 31%–51%, respectively), thrombocytopenia (45 × 103 platelets/mL [reference range 140–440 × 103 platelets/mL]), prolonged prothrombin and thromboplastine times (20 s and 64 s [reference range 10–15 s and 25–35 s, respectively]), neutrophilia, and elevated transaminase (aspartate transaminase 100 mU/mL [reference range 14–36 mU/mL], alanine transaminase 148 mU/mL [reference range 9–52 mU/mL]). The girl was hospitalized in the intensive care unit with a preliminary diagnosis of shock from dengue hemorrhagic fever.
Patient 2 was a 32-year-old woman in whom rickettsialpox was diagnosed in July 2008. She reported visiting a suburban area and being bitten by an unidentified arthropod. Her illness started abruptly with fever, headache, myalgia, and arthralgia in her extremities. The patient showed signs of dengue fever and was treated symptomatically. Three days after the first symptoms, a papulovesicular rash appeared on her extremities and thorax. Clinical laboratory results showed thrombocytopenia (100 × 103 platelets/mL [reference range 140–440 × 103 platelets/mL]) with slightly prolonged clotting times of thrombin and prothrombin, and neutrophilia.
Rickettsiosis was diagnosed on the basis of PCR amplification and sequencing of bacterial genes; immunofluorescent assay (IFA) and restriction fragment length polymorphism (RFLP) analyses confirmed the diagnosis and identified the Rickettsia species. Blood was collected in 3.8% sodium citrate as anticoagulant, and DNA was extracted immediately by QIAamp DNA kit (QIAGEN, Valencia, CA, USA) following the manufacturer's instructions. PCR amplification was performed by using genus-specific primers for the rickettsial 17-kDa protein gene (5´-GCTCTTGCAACTTCTATGTT-3´ and 5´-CATTGTTCGTCAGGTTGGCG-3´) (434-bp PCR fragment) and the outer membrane protein B (ompB) primers (5´-ATGGCTCAAAAACCAAATTTTCTAA-3´ and 5´-GCTCTACCTGCTCCATTATCTGTACC-3´) (996-bp PCR fragment). The positive controls used were DNA of R. felis, R. rickettsii, R. akari, R. typhi, R. conorii, and R. honei, provided by the Rickettsial and Ehrlichial Diseases Research Laboratory (University of Texas Medical Branch, Galveston, TX, USA); 1 reaction without DNA was used as a negative control. To avoid contamination, DNA of the positive controls and the patients was handled separately.
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Poor Clinical Sensitivity of Rapid Antigen Test for Influenza A Pandemic (H1N1) 2009 Virus Jan Felix Drexler, Angelika Helmer, Heike Kirberg, Ulrike Reber, Marcus Panning, Marcel Müller, Katja Höfling, Bertfried Matz, Christian Drosten, and Anna Maria Eis-Hübinger Author affiliation: Institute of Virology, Bonn, Germany
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Abstract Influenza A pandemic (H1N1) 2009 virus RNA was detected by reverse transcription–PCR in 144 clinical samples from Bonn, Germany. A common rapid antigen–based test detected the virus in only 11.1% of these samples. The paramount feature of rapid test–positive samples was high virus concentration. Antigen-based rapid tests appear unsuitable for virologic diagnostics in the current pandemic.
In April 2009, a novel human influenza virus A (H1N1) variant, influenza A pandemic (H1N1) 2009 virus, was identified in Mexico and the United States (1). Efficient human-to-human transmission facilitated global spread of this virus. On June 11, 2009, the World Health Organization (WHO) raised its pandemic alert level to Phase 6, indicating ongoing pandemic transmission. By July 27, WHO had registered 134,503 laboratory-confirmed cases and 816 confirmed deaths caused by pandemic (H1N1) 2009 virus infection worldwide (2).
In Germany, 5,324 cases were confirmed by July 30 (3). Almost 50% (n = 2,184) of these cases occurred in the federal state of North Rhine-Westphalia in western Germany, where our institution is located. As of July 30, we had tested 1,838 suspected cases and confirmed 221. All testing was based on real-time reverse transcription–PCR (RT-PCR) specific for the hemagglutinin (HA) gene of pandemic (H1N1) 2009 virus in clinical specimens. Although the real-time RT-PCR format provides considerably decreased turnaround times in molecular diagnostics, delays associated with shipping of samples and laboratory-based testing are a concern when many patients have to be seen in short time. Antigen-based rapid assays can be used as bedside tests and have been successfully applied in studies of influenza caused by the seasonal strains A (H1N1) and A (H3N2) (4).
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Acute Q Fever and Scrub Typhus, Southern Taiwan Chung-Hsu Lai, Yen-Hsu Chen, Jiun-Nong Lin, Lin-Li Chang, Wei-Fang Chen, and Hsi-Hsun Lin Author affiliations: E-Da Hospital and I-Shou University, Kaoh siung City, Taiwan (C.-H. Lai, J-.N. Lin, W.-F. Chen, H.-H. Lin); Kaohsiung Medical University, Kaohsiung City (C.-H. Lai, Y-H. Chen, J.-N. Lin, L.-L. Chang); and National Yang-Ming University, Taipei, Taiwan (H.-H. Lin)
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Abstract Acute Q fever and scrub typhus are zoonoses endemic to southern Taiwan. Among the 137 patients with acute Q fever (89, 65.0%) or scrub typhus (43, 31.4%), we identified 5 patients (3.6%) who were co-infected with Coxiella burnetii and Orientia tsutsugamushi.
Q fever is a worldwide zoonosis in humans caused by Coxiella burnetii infection. Ticks are the main arthropod vectors of C. burnetii; the major animal reservoirs include goats, sheep, cattle, and domestic cats. Humans are infected mainly by inhaling organism-contaminated aerosols (1). Scrub typhus, caused by Orientia tsutsugamushi infection, is endemic to eastern Asia and the western Pacific region. O. tsutsugamushi is transmitted vertically in mites (particularly Leptotrombidium species) by the transovarial route, and horizontally in rodents through trombiculid larval (chigger) bites. Humans contract scrub typhus by being bitten by chiggers infected with O. tsutsugamushi; such bites occur accidentally during agriculture or field recreational activities (2).
Although the major arthropod vectors, animal reservoirs, and routes of transmission to humans are different for C. burnetii and O. tsutsugamushi, co-infection may occur when humans have been exposed to an environment where arthropod vectors and animal reservoirs are prevalent. In southern Taiwan, acute Q fever and scrub typhus are endemic zoonoses (3–5), and co-infection with the 2 pathogens may occur. We report 5 cases of co-infection with the agents of acute Q fever and scrub typhus.
EID Journal Home > Volume 15, Number 10–October 2009
Volume 15, Number 10–October 2009 Dispatch Orangutans Not Infected with Plasmodium vivax or P. cynomolgi, Indonesia Balbir Singh and Paul Cliff Simon Divis Author affiliation: Universiti Malaysia Sarawak, Kuching, Sarawak, Malaysia
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Abstract After orangutans in Indonesia were reported as infected with Plasmodium cynomolgi and P. vivax, we conducted phylogenetic analyses of small subunit ribosomal RNA gene sequences of Plasmodium spp. We found that these orangutans are not hosts of P. cynomolgi and P. vivax. Analysis of >1 genes is needed to identify Plasmodium spp. infecting orangutans.
Parasites belonging to the genus Plasmodium cause malaria and are usually host specific. For example, humans are natural hosts for P. falciparum, P. vivax, P. malaria, and P. ovale, and orangutans are naturally infected with P. pitheci and P. silvaticum (1,2). However, simian malaria parasites can infect humans (1); for example, P. knowlesi, normally associated with infections in long-tailed and pig-tailed macaques, has recently been found to have caused malaria in humans in several countries in Southeast Asia (3–8). This finding raises the possibility that other zoonotic malaria parasites may emerge in humans.
Malaria parasites have distinct small subunit ribosomal RNA (SSU rRNA) genes that are developmentally regulated (9). Each Plasmodium species has at least 2 types of SSU rRNA genes, and the stage-specific expression of these genes varies among species. In general, the A-type genes are transcribed or expressed mainly during the asexual stages, and the S-type genes are transcribed mainly during the sporozoite stage. P. vivax also has O-type genes, which are expressed during ookinete and oocyst development. Phylogenetic analysis of the P. vivax and P. cynomolgi SSU rRNA genes has indicated that the genes appear to have evolved as a result of 2 gene duplication events (10). A more recent study, involving SSU rRNA sequence data from a much larger number of Plasmodium spp., demonstrated that gene duplication events giving rise to the A-type and S-type sequences took place independently at least 3 times during the evolution of Plasmodium spp. (11).
Reid et al. (12) analyzed the DNA sequences of SSU rRNA genes of Plasmodium spp. from blood of orangutans in Kalimantan, Indonesia. Using phylogenetic analysis, they concluded that, in addition to P. pitheci and P. silvaticum, the orangutans were infected with the human malaria parasite P. vivax and the macaque malaria parasite P. cynomolgi. Their report implies that human and macaque malaria parasites could be transmitted to orangutans and that orangutans could act as reservoir hosts for at least 1 of the human malaria parasites.
When taxonomic inferences of species within a genus are made from phylogenetic trees, trees must be reconstructed by using orthologous genes and must include as many species sequences as possible. However, Reid et al. used sequence data of only the S-type SSU rRNA genes for P. vivax, P. cynomolgi, and P. knowlesi and data of only the A-type genes for P. inui and P. fragile. Furthermore, they analyzed sequence data from only 4 simian malaria parasites. Nishimoto et al. recently included data from 10 simian malaria parasites (11). We therefore reanalyzed the SSU rRNA sequence data of malaria parasites of orangutans together with the A-type, S-type, and O-type SSUrRNA gene sequence data for various Plasmodium spp.
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