Beverage purchases from stores in Mexico under the excise tax on sugar sweetened beverages: observational study
M Arantxa Colchero, Barry M Popkin, Juan A Rivera, Shu Wen Ng2

Statement from Agriculture Secretary Tom Vilsack: World Organization for Animal Health Recommends United States’ BSE Risk Status Be Upgraded

출처 : http://www.usda.gov/wps/portal/usda/usdamediafb?contentid=2013/02/0030.xml&printable=true&contentidonly=true

WASHINGTON, Feb. 20, 2013–Agriculture Secretary Tom Vilsack made the following statement about notification received today from the Scientific Commission for the World Organization for Animal Health (OIE) recommending that the United States’ risk classification for bovine spongiform encephalopathy (BSE) be upgraded to negligible risk:

“I am very pleased with this decision and recommendation by the OIE’s Scientific Commission. This is a significant achievement for the United States, American beef producers and businesses, and federal and state partners who work in coordination to maintain a system of three interlocking safeguards against BSE that protect our public and animal health. Being classified as negligible risk for BSE by the OIE will also greatly support our efforts to increase exports of U.S. beef and beef products. In recommending that the United States receive negligible risk classification, the Commission stated that the risk assessments submitted for their evaluation were robust and comprehensive, and that both our surveillance for, and safeguards against, BSE are strong. U.S. beef and beef products are of the highest quality, wholesome and produced to the highest safety standards in the world. The United States continues to press for normalization of beef trade with several nations in a manner that is based on science and consistent with international standards. U.S. food and agricultural exporters and consumers worldwide benefit when countries adopt international standards.”

BACKGROUND

Last year, the United States submitted an application and supporting information to the OIE’s Scientific Commission to upgrade the United States’ risk classification from controlled to negligible. The Commission, in turn, conducted a thorough review before recommending that the risk classification for the United States be upgraded to negligible. Before the OIE’s annual General Assembly meeting in Paris, France, in May 2013, delegate countries will have the opportunity to review the Commission’s recommendation. The United States expects that formal adoption of negligible risk status for the United States will occur at the General Assembly meeting in May, when it is considered.

The OIE determines a country’s risk status based on actions the country has taken to manage the risk of the disease. These actions include instituting a strong ruminant-to-ruminant feed ban, strictly controlling imports of animals and animal products from countries at risk for the disease, and conducting appropriate surveillance.

The OIE Code, which is based on the latest science and current knowledge concerning BSE, provides guidelines for the safe trade of animals and products based on the country’s risk status and the risk presented by the specific item being traded. Negligible risk is the lowest risk level under the OIE Code. Countries defined as negligible risk have conducted extensive surveillance and testing in domestic cattle to demonstrate a minimal risk for BSE.

The OIE administers and governs the foundational international standards on animal health as well as trade in livestock and animal products. With a total of 178 Member Countries, including the United States, the OIE is recognized as a reference organization by the World Trade Organization (WTO), the only global international organization dealing with the rules of trade between nations. The official recognition of disease status by OIE of Member Countries is of great significance for international trade and constitutes one of the most important links between the OIE and WTO.

The United States has a longstanding system of three interlocking safeguards against BSE that protects public and animal health in the United States, the most important of which is the removal of specified risk materials from all animals presented for slaughter. The second safeguard is a strong feed ban that protects cattle from the disease. The third safeguard is our ongoing BSE surveillance program that allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population.

일본, 대만 등 주변국의 미국산 쇠고기 수입 상황

1) 일본

* 20개월 미만 수입조건 유지

* 미국이 TPP 협상 개시조건으로 ‘쇠고기’ ‘자동차’ ‘우체국 보험’을 3대 선결조건으로 요구 중.

2) 대만

*2010.1.5 여야 합의로 식품법 11조 개정. 미국산 소 내장, 간 쇠고기(ground beef), 뇌, 척수, 눈, 머리뼈(頭骨) 등 6개 위험 부위 수입금지. (11조 “전염병 발생 지역이 아니더라도 최근 10년간 광우병 혹은 인간광우병이 발생한 적이 있는 국가와 지역의 소 머리뼈, 뇌, 눈, 척수, 분쇄육(간고기), 내장, 기타 부산물은 제1항의 인체건강 유해물질에 포함된다.”). 개정된 식품법은 대만과 미국 정부가 협상 끝에 2009년 10월 서명한 의정서에 위배되지만, 현재까지 WTO에 제소당하지도 않았음.

*2010.4.20 대만정부, 미국산 소의 혀(牛舌), 횡격막(橫隔膜), 고환(睾丸) 등 3개 부위 수입금지. 위생서 楊志良 서장은 “소혀는 내장기관으로 볼 수 없지만, 국민 여론을 반영하여 잠시 수입을 중단하기로 한다”고 강조함.

*2011.4.13 미국산 쇠고기 양지머리 3.6톤과 냉동 돼지고기 볼살 16톤에서 페일린(락토파민)이 또 검출되었으며, 올해 처음으로 캐나다산 냉동 돼지껍질 24.6톤에서도 페일린이 검출됨. 대만정부는 미국산 쇠고기를 수입한 해당 업체는 두 번째 적발된 것이며, 앞으로 100% 수입검역 실시 예정 발표. 페일린 잔류최대허용치(MRL) 설정 문제로 미국산 쇠고기 수입 중단됨.

3) 멕시코

멕시코의 미국산 쇠고기 수입조건

* 연령 : 30개월 이하(2008년 3월 미측 요구로 기존 24개월에서 30개월로 관련 규정을 개정함)

* 뼈 포함 쇠고기

* 간, 염통, 혀, 볼살 등 수입가능

* 수출증명(EV) 프로그램 의무

4) 호주

* 2010,4 미국-오스트레일리아 협상 결과. 오스트레일리아 측에서 수입전면금지 2년간 연장하기로 결정.

* 이후 WTO 제소 등의 후속조치 없었음

□ 뉴질랜드 현지작업장 점검 결과

1. 점검일시 : 2005.3.27∼4.10

2. 점검 작업장명 : 14개소

3. 점검내용

○ 뉴질랜드 육류 위생관리 정부조직 체계, 수출작업장 인증체계

○ 가축질병 발생현황

○ 미생물 잔류물질 관리체계

○ 작업장 시설기준, 위생관리기준, 작업장 HACCP 관리 등 점검

4. 점검결과

○ ME 86 작업장의 바닥 및 컨베이어벨트 비위생적 관리가 시정될 수 있도록 뉴질랜드 농림부의 감독강화 요청

※ 2010년 이전의 현지점검결과

□ 호주 현지작업장 점검 결과

1. 점검일시 : 2005.3.27∼4.10

2. 점검 작업장명 : 15개소

3. 주요 점검내용

○ 수출작업장 인증체계

○ 작업장 수의사 및 검사원 자격, 임무 및 교육

○ 검역검사청(AQIS) Meat Program

○ 가축질병 발생현황

○ 국가잔류물질 조사

○ 작업장 시설기준, 위생관리기준, 작업장 HACCP 관리 등 점검

4. 점검결과

○ 수출작업장 위생관리 감독 강화 요청

- 현지점검시 확인된 위생관리 지적사항(발골작업시 육류 및 Box 동시접촉, 열탕소독조 온도관리 등)이 수출작업시 재발되지 않도록 AQIS 감독 강화

○ 위생관리 권장 사항

- 금속성 이물질 검사, Box 포장실 위생관리, 일반세균 검사결과에 대한 개선조치 보완사항에 대하여는 식육의 오염을 방지할 수 있도록 조치

□ 멕시코 현지작업장 점검 결과

1. 점검일시 : 2009.11.22∼12.1

2. 점검 작업장명

3. 주요 점검내용

○ 수입위생조건 준수여부

○ 수출작업장 시설기준 점검

○ 위생관리기준(SSOP) 및 위생요소중점관리기준(HACCP)운용

○ 잔류물질 및 미생물관리 적정여부 등 점검

4. 점검결과

○ 작업장(Est. 451)은 작업장 시설 및 위생관리가 양호하나, 제품의 오염방지 및 위생관리 측면에서 일부 시설의 보완이 필요하여 개선조치 완료 후 승인이 가능함

< 보완 사항 >

① 포장실 : 가공장과 구획 ② 종업원 화장실 : 출입문 개선(자동문) ③ 급냉실 : 온도 조정(-35℃ 유지)

○ 2개의 작업장(Est. 142, 101)은 작업장 시설 및 HACCP 운용이 점검기준에 미달되어 승인이 어려움

- Est 142 : 수출 및 국내제품의 구분 적재가 불가, HACCP 운용 미비

- Est 101 : 도축장 출입구 위치 부적정, 내장처리실 비위생, 가공장내 포장실 미구획 등

□ 미국 현지작업장 점검 결과

1. 점검일시 : 2009.3.29∼4.13

2. 점검 작업장명 : 22개소

3. 주요 점검내용

○ 작업장의 SSOP(위생관리기준), HACCP(위해요소중점관리기준)

○ 도축우 생체검사, SRM(특정위험물질) 제거 관련 규정 준수 여부

○ 30개월령 이하 품질관리시스템 운용 및 수입위생조건 준수 현황

○ 969작업장의 변질 쇠고기 발생원인 및 FSIS(식품안전검사청) 조치사항 조사 등

4. 점검결과

□ 작업장의 위생관리(SSOP, HACCP) 상태는 양호하며 생체검사, 연령감별, SRM 제거 및 수출제품 QSA 운용이 수입위생조건에 부합됨

○ 도축소 연령감별 : 치아감별법을 사용하여 서류는 보조적 수단으로 활용

○ 도축소 원산지 확인

- 캐나다산 소 수입․사육․도축과정 서류는 9CFR 93.418 규정에 의해 잘 관리되고 있으며, 도축시 AMS(농업유통국)에 작업계획서 제출

○ SRM(두부, 편도, 척수, 척주, 회장원위부, 등배신경절) 제거

- 도구는 구분하여 사용(척수 제거 전용흡입기, 전용칼 등) 하며, 모든 SRM은 전용용기로 수송하여 폐기 처리

○ QSA 운용 현황

- 30개월 이상 제품 박스에 파란색 스티커 부착 또는 별도 코드번호 부여

- 수출인증(EV)프로그램에 의하여 캐나다산이 한국으로 수출되는 경우 캐나다에서 수입되어 100일 이상 사육되었다는 증명서 첨부

- AMS(농업유통국)에서 정기적으로 QSA 및 EV 프로그램에 대한 검증 실시

□ 현지점검 결과상 수출중단(미승인)조치 한 사례(일시, 도축장명 포함)

○ 점검일시 : 2009.11.22∼12.1

○ 멕시코 수출작업장 3개소 미승인

- TIF 451 (Alimentos San Mateo, S.A. de C.V)

- TIF 101 (Frigorifico de la Cuenca del Papaloapan, S.A. de C.V)

- TIF 142 (RYC Alimentos S.A. de C.V.)

□ 미국 도축장에 문제가 있을시 수출중지를 하기 위해 필요한 절차

○ 동일한 육류작업장에서 생산된 별개의 로트에서 최소 2회의 식품 안전위해가 발견된 경우, 해당 육류작업장은 개선조치가 취해질 때 까지 중단 조치할 수 있음(미국산 쇠고기 및 쇠고기 제품 수입위생조건 제24조)

□ 현행 “미국산 쇠고기 및 쇠고기 제품 수입위생조건”에는 한국정부가 한국으로 쇠고기 수출 자격이 있는 것으로 인정한 국가로부터 미국으로 합법적으로 수입된 소 또는 도축 전 최소한 100일 이상 미국 내에서 사육된 소에서 생산된 경우에 미국산 쇠고기로 인정하여 국내에 수출할 수 있도록 규정하고 있음

○ 캐나다산 생우가 수입된 후 즉시 도축되어 수출할 수 없음. 다만, 캐나다등 제3국산 송아지가 미국내에서 100일 이상 사육는 경우 수출할 수 있음. 이 경우 미측에 증명을 별도로 요구하지 않고 있어 파악 되지 않음.

韓, 올들어 美쇠고기 수입 日 제쳐
연합뉴스 | 입력 2010.05.27 12:02 |

USMEF “韓, 4월 수입은 세계 2위”

(서울=연합뉴스) 김병수 기자 = 올해 들어 한국의 미국산 쇠고기 수입이 크게 늘면서 한국의 수입량이 일본을 앞지른 것으로 나타났다고 미국 육류수출협회(USMEF)가 27일 밝혔다.

그동안 일본은 규모나 가격면에서 미국산 쇠고기의 3번째 큰 시장으로, 한국은 4대 시장으로 꼽혀왔다.

USMEF에 따르면 올해 1분기 한국의 미국산 쇠고기 수입량은 1만8천763t으로, 1만8천487t을 수출한 일본보다 약간 많았다. 가격면에서는 한국의 수입 규모가 7천820만달러로 일본(9천530만달러)보다 적었다.

이는 일본의 경우 도축 당시 20개월 미만의 미국산 쇠고기만을 수입하는 반면, 한국은 30개월령 미만의 쇠고기를 수입한 데 따른 것으로 분석된다.

USMEF는 “작년에 한국의 미국산 쇠고기 수입은 양적으로 11%, 가격면에선 24% 인상적인 증가를 보였다”면서 “최근 한국의 수입관련 자료를 보면 훨씬 더 긍정적”이라고 밝혔다.

USMEF는 한국의 올해 1분기 미국산 쇠고기 수입은 작년 같은 기간에 비해 66% 늘어난 것으로, 한국의 전체 쇠고기 수입량 중 미국산이 차지하는 비중이 30%를 넘었다고 말했다.

또 USMEF는 구체적인 수치는 제시하지 않은 채 자료에 따르면 4월 들어 한국의 미국산 쇠고기 수입은 80%나 증가했다며 한국이 멕시코에 이어 두번째 미국산 쇠고기 수입국으로 올라선 것으로 보인다고 덧붙였다.

bingsoo@yna.co.kr

(끝)

doi:10.1016/S0140-6736(09)61638-XCite or Link Using DOI
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)61638-X/fulltext

Infection and death from influenza A H1N1 virus in Mexico: a retrospective analysis

Santiago Echevarría-Zuno MD a, Juan Manuel Mejía-Aranguré PhD b, Alvaro J Mar-Obeso MD b, Concepción Grajales-Muñiz MD b, Eduardo Robles-Pérez MSc b, Margot González-León MD b, Manuel Carlos Ortega-Alvarez MSc b, Cesar Gonzalez-Bonilla PhD b, Ramón Alberto Rascón-Pacheco MSc b, Dr Víctor Hugo Borja-Aburto PhD b

Summary

Background

In April, 2009, the first cases of influenza A H1N1 were registered in Mexico and associated with an unexpected number of deaths. We report the timing and spread of H1N1 in cases, and explore protective and risk factors for infection, severe disease, and death.

Methods

We analysed information gathered by the influenza surveillance system from April 28 to July 31, 2009, for patients with influenza-like illness who attended clinics that were part of the Mexican Institute for Social Security network. We calculated odds ratios (ORs) to compare risks of testing positive for H1N1 in those with influenza-like illness at clinic visits, the risk of admission for laboratory-confirmed cases of H1N1, and of death for inpatients according to demographic characteristics, clinical symptoms, seasonal influenza vaccine status, and elapsed time from symptom onset to admission.

Findings

By July 31, 63 479 cases of influenza-like illness were reported; 6945 (11%) cases of H1N1 were confirmed, 6407 (92%) were outpatients, 475 (7%) were admitted and survived, and 63 (<1%) died. Those aged 10—39 years were most affected (3922 [56%]). Mortality rates showed a J-shaped curve, with greatest risk in those aged 70 years and older (10·3%). Risk of infection was lowered in those who had been vaccinated for seasonal influenza (OR 0·65 [95% CI 0·55—0·77]). Delayed admission (1·19 [1·11—1·28] per day) and presence of chronic diseases (6·1 [2·37—15·99]) were associated with increased risk of dying.

Interpretation

Risk communication and hospital preparedness are key factors to reduce mortality from H1N1 infection. Protective effects of seasonal influenza vaccination for the virus need to be investigated.

Funding

None.

======================

Older People at Greater Risk of Swine Flu Death

출처 : HealthDay Wed Nov 11, 11:48 pm ET

WEDNESDAY, Nov. 11 (HealthDay News) — A study of H1N1 swine flu in Mexico finds that while babies and people under the age of 40 are most likely to get sick, elderly people have the highest death rates.

The research, published online Nov. 11 in The Lancet, analyzed medical records of patients at clinics in the Mexican Institute for Social Security network, who became sick with flu-like illnesses between April 28 and July 31, 2009.

The researchers found 63,479 cases of flu-like illness. Of the 6,945 confirmed cases of H1N1 swine flu, about 1 percent (63 patients) died. Seven percent (475 patients) were admitted to the hospital and lived.

Of those aged 70 and older who got sick, 10.3 percent died. By contrast, 0.9 percent of those aged 20 to 29 died, the study authors noted.

The researchers found that the risk of infection fell by 35 percent in those who received vaccinations for seasonal flu. Chronic disease boosted the risk of death by six times.

Those who didn’t go to the hospital within four days after developing symptoms boosted their risk of death by 20 percent for each extra day they delayed a hospital visit.

Pregnant women made up 6 percent of the deaths in Mexico. That rate is a bit lower than in the United States (8 percent) over the same time period.

“In Mexico, all pregnant workers were sent home during the peak of the pandemic, which probably accounts for this difference,” Dr. Victor Borja-Aburto of the Mexican Institute for Social Security in Mexico City, and colleagues wrote.

Guillermo Domínguez-Cherit, MD; Stephen E. Lapinsky, MB, BCh, MSc; Alejandro E. Macias, MD; Ruxandra Pinto, PhD(Stat); Lourdes Espinosa-Perez, MD; Alethse de la Torre, MD; Manuel Poblano-Morales, MD; Jose A. Baltazar-Torres, MD; Edgar Bautista, MD; Abril Martinez, MD; Marco A. Martinez, MD; Eduardo Rivero, MD; Rafael Valdez, MD; Guillermo Ruiz-Palacios, MD; Martín Hernández, MD; Thomas E. Stewart, MD; Robert A. Fowler, MD, MS(Epi)

JAMA. 2009;302(17):(doi:10.1001/jama.2009.1536).

Objective  To describe baseline characteristics, treatment, and outcomes of consecutive critically ill patients in Mexico hospitals that treated the majority of such patients with confirmed, probable, or suspected 2009 influenza A(H1N1).

Design, Setting, and Patients  Observational study of 58 critically ill patients with 2009 influenza A(H1N1) at 6 hospitals between March 24 and June 1, 2009. Demographic data, symptoms, comorbid conditions, illness progression, treatments, and clinical outcomes were collected using a piloted case report form.

Main Outcome Measures  The primary outcome measure was mortality. Secondary outcomes included rate of 2009 influenza (A)H1N1–related critical illness and mechanical ventilation as well as intensive care unit (ICU) and hospital length of stay.

Results  Critical illness occurred in 58 of 899 patients (6.5%) admitted to the hospital with confirmed, probable, or suspected 2009 influenza (A)H1N1. Patients were young (median, 44.0 [range, 10-83] years); all presented with fever and all but 1 with respiratory symptoms. Few patients had comorbid respiratory disorders, but 21 (36%) were obese. Time from hospital to ICU admission was short (median, 1 day [interquartile range {IQR}, 0-3 days]), and all patients but 2 received mechanical ventilation for severe acute respiratory distress syndrome and refractory hypoxemia (median day 1 ratio of PaO₂ to fraction of inspired oxygen, 83 [IQR, 59-145] mm Hg). By 60 days, 24 patients had died (41.4%; 95% confidence interval, 28.9%-55.0%). Patients who died had greater initial severity of illness, worse hypoxemia, higher creatine kinase levels, higher creatinine levels, and ongoing organ dysfunction. After adjusting for a reduced opportunity of patients dying early to receive neuraminidase inhibitors, neuraminidase inhibitor treatment (vs no treatment) was associated with improved survival (odds ratio, 7.4; 95% confidence interval, 1.8-31.0).

Conclusion  Critical illness from 2009 influenza A(H1N1) in Mexico occurred in young individuals, was associated with severe acute respiratory distress syndrome and shock, and had a high case-fatality rate.

INTRODUCTION

On April 21, 2009, the Centers for Disease Control and Prevention reported the detection of 2 cases of human infection with 2009 influenza A(H1N1) in California.¹ The greatest initial burden of critical illness and death occurred in Mexico² between March 18, 2009, and June 1, 2009, with 5029 cases and 97 documented deaths.^2-6 By August 30, 2009, there were more than 116 046 cases with 2234 deaths in the Americas and 277 607 documented cases and at least 3205 deaths worldwide.^{2, 7}

We report on 58 patients in Mexico who developed critical illness from confirmed, probable, or suspected 2009 influenza A(H1N1). This early information may be of considerable value for (1) the early identification of individuals at risk of becoming critically ill and who may benefit from targeted interventions including vaccination and antiviral therapy; (2) pandemic health care resource planning; and (3) providing baseline 2009 influenza A(H1N1)–associated morbidity and mortality data, comparing experiences in different jurisdictions, and identifying changes in disease virulence over time.

METHODS

Study Design

We retrospectively studied all critically ill patients with confirmed, probable, or suspected 2009 influenza A(H1N1) in Mexico admitted between March 24, 2009, and June 1, 2009, to 6 hospitals that were reference centers for the care of patients with influenza (Figure 1). Identification of all such patients was achieved by examining admission logs for all patient care areas, in collaboration with critical care and infectious diseases physicians in each participating hospital and with regional health authorities in Mexico.

We classified patients according to case definitions (confirmed, probable, or suspected) developed by the World Health Organization, Centers for Disease Control and Prevention, and the National Microbiology Laboratory (see eAppendix).^8-10 We defined critically ill patients as those admitted to an adult or pediatric intensive care unit (ICU); requiring mechanical ventilation; having a fraction of inspired oxygen (FIO₂) greater than or equal to 60%; or receiving intravenous infusion of inotropic or vasopressor medication during the hospitalization.

To evaluate the proportion of patients who became critically ill, we compared our study population with the total number of inpatients diagnosed with confirmed, probable, or suspected 2009 influenza A(H1N1) and treated at any of the participating hospitals by June 1, 2009. All patients admitted to these 6 hospitals with respiratory symptoms or fever were routinely screened for 2009 influenza A(H1N1) during the outbreak period.

Case Report Generation, Dissemination, and Ethics Approval

Investigators in Canada collaborated with colleagues in Mexico and developed a data collection form with input from critical care personnel, infectious diseases clinicians, and clinical researchers, including the Canadian Critical Care Trials Group.¹¹ Research ethics board review and approval was granted by Sunnybrook Health Sciences Centre on April 30, 2009, and subsequently by the ethics boards of participating jurisdictions in Mexico. The data collection form was posted on academic institutional and critical care society Web sites on or after May 3, 2009.^12-14 Data collection in Mexico commenced on May 1, 2009, was entered by study site personnel, transmitted to the coordinating center in Toronto, then checked for errors through manual and electronic inspection using prespecified range limits.

Data Collection

Data collection included 2009 influenza A(H1N1) and critical illness eligibility criteria, demographic data, and details of influenza contact, symptoms, comorbid conditions, clinical characteristics, time course of the acute illness, microbiology samples, and treatments (eAppendix). Severity of illness was assessed using the Acute Physiology and Chronic Health Evaluation II (APACHE II) score for adults or Pediatric Risk of Mortality III score for children.^15-16 Reporting of ventilatory parameters, arterial blood gas values, and chest radiograph findings, as well as Sequential Organ Failure Assessment (SOFA) scores, was performed on days 1, 3, 7, 14, and 28, using the values closest to 8:00 AM where appropriate.¹⁷ Outcome variables included duration of mechanical ventilation, ICU and hospital length of stay, and ICU and hospital mortality at 14, 28, and 60 days from onset of critical illness.

From the largest referral centers, we were able to collect more detailed information on the total number of patients presenting to the emergency department with influenzalike illness as well as those admitted to the hospital and to the ICU, and to calculate the proportion of patients critically ill with influenza-related pneumonia as a function of total number of ICU beds. In the largest centers, we also collected detailed information on health care worker exposure and illness to assess risk posed to health care professionals through care of patients with 2009 influenza A(H1N1).

Analysis

Descriptive data are presented as frequencies (percentages) for discrete variables and as means (SDs) or medians (interquartile ranges [IQRs]) for continuous variables. Because few patients remained alive and in the ICU at 28 days, nonoutcome variables are presented on days 1, 3, 7, and 14 but not day 28. To determine if there were differences in baseline characteristics between patients who survived vs those who died, we used a 2-sample t test or the Wilcoxon rank sum test for continuous variables and a ² test or Fisher exact test for the discrete variables. Analyses to detect differences in treatment variables between survivors and nonsurvivors are at risk of confounding due to immortal time bias—ie, patients who die quickly have less “opportunity” to be exposed to certain therapies. Therefore, we restricted comparisons of neuraminidase use to patients who did not die within the first 3 days after admission to the hospital and adjusted for differences in severity of illness using the APACHE II score in a multiple logistic regression model.

The Kaplan-Meier method was used to determine the probability of survival over the duration of follow-up and to generate survival curves, censoring at 60 days all individuals discharged from the hospital alive. We compared the discriminative ability of the day-1 SOFA and APACHE II scores on mortality by testing the difference in C statistics (area under the receiver operating characteristic curve).

All statistical tests were 2-tailed, and factors were considered statistically significant at  < .05. SAS version 9.2 (SAS Institute Inc, Cary, North Carolina) was used for all analyses.

RESULTS

Characteristics of Study Patients and Hospitals

During the study period 899 patients with confirmed, probable, or suspected 2009 influenza A(H1N1) were assessed and admitted to study hospitals having a mean of 289 (SD, 167) beds and 16 (SD, 8) critical care beds. Critical illness occurred in 58 patients (6.5%) admitted to the hospital (29 confirmed, 14 probable, 15 suspected). There were no significant differences in demographics, severity of illness, comorbid conditions, or mortality among those with confirmed, probable, or suspected 2009 influenza A(H1N1), and they are described as a single group.

As a result of increased patient volumes, many experienced delay in admission to the ICU, and 4 remained in the emergency department until death. During the period of data collection, there were 5029 cases of 2009 influenza A(H1N1) and 97 deaths in all of Mexico.¹⁸ This cohort from 6 hospitals represents approximately one-quarter of all deaths in Mexico during the study period. We have described the temporal burden of influenza and H1N1 on the largest study center, outlining the number of cases of influenzalike illness presenting to the emergency department and admitted to the hospital and cases of influenza-related illness admitted to the ICU (Figure 1). The usual capacity to care for critically ill patients was exceeded, necessitating care in other patient care areas and the addition of ICU beds and ventilators on 2 occasions.

Study patients were a median age of 44 (range, 10-83) years (Figure 2), 53% were female, and 2 were health care workers (Table 1). Only 2 children (10 and 14 years) were admitted to study centers with critical illness and had mean admission Pediatric Risk of Mortality III scores of 6.5 (SD, 2.1). Among all patients, symptoms included fever in 58 (100%); respiratory complaints (cough, dyspnea, or wheeze) in 57 (98%); generalized weakness in 41 (71%); myalgias in 35 (60%); headache in 33 (57%); and gastrointestinal symptoms of nausea, vomiting, or diarrhea in 18 (30%).

The median number of comorbid conditions was 2 (IQR, 1-4) (Table 1). Only 2 patients had a history of chronic obstructive pulmonary disease. Obesity was the most common comorbid condition (mean body mass index [BMI], 32 [SD, 12], calculated as weight in kilograms divided by height in meters squared). Twenty-one patients (36%) had a BMI greater than 30; 8 (14%) were morbidly obese (BMI >40).

Course of Illness and Treatments Received

Medical Therapies. Patients developed first symptoms a median of 6 (IQR, 4-8) days prior to hospitalization. Time from hospitalization to ICU admission was 1 (IQR, 0-3) day. Among 55 patients confirmed to have received medical therapies (unknown for 3), 52 (95%) were treated with antibiotics, while 45 (78%) received neuraminidase inhibitors (oseltamivir [44], zanamivir [6]), 8 received amantidine (14%), 1 rimantidine (2%), and 40 (69%) corticosteroids. Two patients received recombinant activated protein C. Two had received an influenza vaccination in 2008 or 2009.

Ventilation Support. Fifty-four patients, including 1 of 2 children, required mechanical ventilation (48 invasive, 22 noninvasive, 16 both) during the course of hospitalization (Table 2 and eTable).¹⁹ On the first day of critical illness, the mean FIO₂ was 72% (SD, 26%), set positive end-expiratory pressure (PEEP) was 13 (SD, 5) cm H₂O, and plateau pressure was 27 (SD, 7) cm H₂O. Median ratio of PaO₂ to FIO₂ was 83 (IQR, 59-145) mm Hg, with oxygen saturation of 88% (SD, 13%). Four patients received prone ventilation on their first day in the ICU, owing to severe hypoxia. Tidal volume per ideal body weight was 8.3 (SD, 3) mL/kg. Day 1 chest radiographs demonstrated bilateral disease in 95.6% of patients. Barotrauma occurred in 6 patients (10.3%) over the study. Patients received high FIO₂, high PEEP, and were commonly ventilated in the prone position. Only 1 patient received high-frequency oscillatory ventilation, and none was known to receive nitric oxide or extracorporeal membrane oxygenation.

Nonrespiratory Organ Dysfunction. A large number of patients (34 [58.6%]) initially required inotropic or vasoactive medications at day 1 (Table 2). Creatine kinase level was elevated (285 [IQR, 136-1159] IU/L). Initial other organ dysfunction was mild. Over the course of follow-up, hypotension requiring vasoactive medication support remained common at days 3, 7, and 14. Staphylococcus aureus was the most commonly identified cause of secondary bacterial pneumonia (4 patients).

Outcomes. After 60 days from the onset of critical illness, 24 of 58 patients (41.4%; 95% confidence interval [CI], 28.9%-55.0%) had died (Table 3, Figure 3). In Mexico, most (19) patients died within the first 2 weeks after becoming critically ill. An additional 4 patients died by day 28, with only 1 additional death occurring within 60 days.

Four patients died in the emergency department, 3 within 8 hours and 1 within 24 hours of arrival. All deaths within 28 days were primarily related to respiratory failure, with only 1 late death primarily related to multisystem organ dysfunction. The 2 included children both survived and were discharged from the hospital. Intensive care unit length of stay among survivors was 13.5 (IQR, 6-24) days, while nonsurvivors died 7.0 (IQR, 2-13) days after ICU admission (Table 3). Duration of mechanical ventilation among survivors was 15 (IQR, 8-26) days and among nonsurvivors was 7.5 (IQR, 3-13.5) days. Many patients received ventilation outside of the ICU.

Comparison of Survivors and Nonsurvivors. Patients who died were more likely to have a higher APACHE II and SOFA score, lower mean arterial pressure at admission, evidence of renal and hepatic organ injury, lower ratio of PaO₂ to FIO₂, and higher set PEEP at admission to the ICU (Table 4). There were no significant differences in tidal volume or ventilation strategies between survivors and nonsurvivors. Patients with higher creatine kinase levels had a greater likelihood of dying at 28 days. Both APACHE II and day-1 SOFA score were significantly associated with 28-day mortality (P < .001 for both), and there was no difference in predictive value (C = 0.83 and C = 0.87, respectively; P = .52). After excluding patients dying early (within 72 hours of illness onset), who may have had less opportunity to be exposed to neuraminidase inhibitors, survivors were more likely to have received treatment with neuraminidase inhibitors (odds ratio, 7.4; 95% CI, 1.8-31.0; P = .006).

Risk to Health Care Workers. Among the 3 largest centers caring for 65.6% of the patients in this series, 40 of 6755 health care workers (0.6%) developed 2009 influenza A(H1N1), including 10 of 2421 workers (0.5%) from clinical areas. Only 1 health care worker became critically ill, and this patient was believed to have acquired H1N1 outside of the workplace.

COMMENT

Our analysis of critically ill patients with 2009 influenza A(H1N1) reveals that this disease affected a young patient group. Fever and respiratory symptoms were harbingers of disease in almost all cases. There was a relatively long period of illness prior to presentation to the hospital, followed by a short period of acute and severe respiratory deterioration. These patients had severe hypoxia and acute respiratory distress syndrome and required high FIO₂, PEEP, and ventilatory pressures. Within 60 days, 41% of critically ill patients had died.

The mortality rate of 41% for 2009 influenza A(H1N1)–associated critical illness is not dissimilar to that for acute respiratory distress syndrome resulting from other influenza but is higher than that for severe acute respiratory syndrome (SARS), and deaths in Mexico appear to have been more directly related to respiratory rather than multiorgan failure.^20-22 The low median age and relatively good prior health of this critically ill group are different from those for seasonal influenza and SARS,²² in which older patients appear more susceptible to severe disease.

Although serologic studies suggest that 2009 influenza A(H1N1) is a novel influenza strain with little protection afforded by seasonal influenza vaccination, adults older than 60 years appear to have some preexisting immunity to this novel virus.²³ While a degree of cross-immunity might be afforded through a long history of annual vaccination, the specific effect of uncommon prior seasonal influenza vaccination, if any, is unclear. The age distribution of the general population in Mexico differs from that in many developed nations, with a much larger proportion of the population in lower age categories, and therefore it may not be surprising that young individuals comprise a greater proportion of those infected.²⁴

Approximately 18% of critically ill patients with SARS were health care workers.²² With SARS, viral shedding appeared to peak at about 7 days, coinciding with the time of ICU admission for many patients. Viral shedding in seasonal influenza is maximal near onset of the disease, then decreases rapidly.²⁵ These patients presented to the hospital and were admitted to the ICU a median of 6 days after disease onset, which may in part explain the apparent lack of nosocomial transmission among critically ill patients. Avian influenza A(H5N1) outbreaks would appear to have a significantly higher mortality than 2009 influenza A(H1N1) in patients requiring advanced organ support (approximately 90%, with median time from hospital admission to death of 6 days).^26-28 These baseline data will allow evaluation of whether the morbidity and mortality of this infection are worsening over time, which has been the case in many other pandemics.²⁹

We found that certain baseline characteristics of critically ill patients with 2009 influenza A(H1N1) may be associated with increased mortality, including cardiovascular, respiratory, and renal organ dysfunction. Novel findings include possible worse outcomes among patients presenting with an elevated creatine kinase level. Elevated creatine kinase levels and rhabdomyolysis have been previously reported to complicate seasonal influenza, although more commonly in children.^30-31 Obesity was the most common comorbid condition in these patients and was more prevalent (36%) in this series than the general population prevalence (30%) in Mexico.³² However, mortality was not significantly higher among obese patients compared with nonobese patients. Among other patient cohorts with undifferentiated acute respiratory distress syndrome, increased BMI has not emerged as a predictor of mortality.³³

A better understanding of these factors, which were common, or those that suggest a higher mortality may provide health care professionals an earlier opportunity to identify and treat high-risk groups. Importantly, we found in this cohort that either SOFA or APACHE II scores may help to identify patients at high risk of death. Some authors have previously suggested the use of SOFA scores for triage during pandemic periods, owing to their relative ease of calculation.³⁴

The strengths of this study include a large and detailed description of patients critically ill as a result of 2009 influenza A(H1N1). We have highlighted what appear to be differences in severity of illness, associations, and outcomes from other recent infectious respiratory outbreaks. The methods of rapid case report modification, research ethics approval, international dissemination, and analysis provide a potential example for future outbreak characterization¹¹ and potential for international comparisons among countries with different health care systems and capacity for care.

This study has several potential limitations. First, it represents a relatively early examination of the epidemiology of a severe infectious disease. Early reports risk overestimating the case-fatality rate through selective recognition and screening of the most severely ill patients. This may partially explain a high mortality in Mexico early in the outbreak; however, our cohort included all patients hospitalized with critical illness, not only those selected for admission to an ICU, thus minimizing the effect of selective triaging of critically ill patients (by age, comorbidity, etc) and minimizing the potential for overrepresentation of patients with certain characteristics or severity of illness. Also, the 6 hospitals participating in this cohort study had specific criteria for 2009 influenza A(H1N1) screening among all hospitalized patients, minimizing the risk of exposure ascertainment bias through overestimation of disease among only the sickest patients. For this early report, we deliberately included suspected, in addition to confirmed and probable, cases of 2009 influenza A(H1N1) because in the earliest stages of the outbreak, confirmatory testing was sometimes unavailable for patients who died rapidly and in settings with resources that did not initially permit testing. We performed all analyses in duplicate and found no significant differences in outcomes when including only confirmed and probable cases.

It is possible that the 2009 influenza A(H1N1) experience described here is somewhat unique to Mexico and may be related to a variety of factors, including climate, air quality, and altitude (2240 m above sea level) in Mexico City; or, noting the long duration between illness onset and presentation to the hospital with severe disease, potential differences in the timing of access or presentation of the population to acute care compared with other settings. These critically ill patients presented to the hospital already very ill. Four patients died before admission to the ICU, 3 of these within 8 hours of presentation to the hospital. Despite these potential differences with other recently characterized outbreaks, the experience in Mexico may well represent a global “median” of illness presentation and outcome for 2009 influenza A(H1N1) more appropriate than reports only from the most well-resourced health care settings.²²

As of August 30, 2009, the World Health Organization reported 254 206 cases of 2009 influenza A(H1N1) and 2837 deaths, for a case-fatality rate of approximately 1%—yet this may well be an overestimate, because testing is no longer being reported in many jurisdictions.² The case-fatality rate in previous influenza pandemics has varied widely, and all such reports may be inaccurate owing to difficulty in assessing the denominator (ie, the total number of cases).³⁵ The Spanish flu of 1918 is reported as causing 50 million deaths in 500 million individuals infected (10% case-fatality rate), while the Hong Kong flu of 1968-1969 caused 33 000 deaths among 50 million infected (<0.1% case-fatality rate).³⁶ The case-fatality rate of avian influenza A(H5N1) was initially reported to be as high as 60% but is more likely in the range of 14% to 33%.²⁸

From the Mexico experience, it is clear that in certain environments, critical illness from 2009 influenza A(H1N1) may be associated with severe acute lung injury, refractory hypoxia, and a high mortality rate in young individuals. Influenza pandemics of the past century have been associated with a remarkably consistent epidemiologic curve, with peaks in the spring, fall, and later winter.⁷ Early recognition of disease by the consistent symptoms of fever and a respiratory illness during times of outbreak, with prompt medical attention including neuraminidase inhibitors and aggressive support of oxygenation failure and subsequent organ dysfunction, may provide opportunities to mitigate the progression of illness and mortality observed in Mexico.

AUTHOR INFORMATION

Corresponding Author: Robert Fowler, MD, MS(Epi), Sunnybrook Health Sciences Center, 2075 Bayview Ave D478, Toronto, ON M5N 3M5, Canada (rob.fowler@sunnybrook.ca ).

Published Online: October 12, 2009 (doi:10.1001/jama.2009.1536).

Author Contributions: Drs Dominguez-Cherit and Fowler had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Domínguez-Cherit, Lapinsky, Stewart, Fowler.

Acquisition of data: Domínguez-Cherit, Macias, Espinosa-Perez, de la Torre, Poblano-Morales, Baltazar-Torres, Bautista, A. Martinez, M. Martinez, Rivero, Valdez, Ruiz-Palacios, Hernández, Fowler.

Analysis and interpretation of data: Domínguez-Cherit, Lapinsky, Espinosa-Perez, Pinto, Stewart, Fowler.

Drafting of the manuscript: Domínguez-Cherit, Lapinsky, Macias, Pinto, Espinosa-Perez, de la Torre, Poblano-Morales, Baltazar-Torres, Bautista, A. Martinez, M. Martinez, Rivero, Valdez, Ruiz-Palacios, Hernández, Stewart, Fowler.

Critical revision of the manuscript for important intellectual content: Domínguez-Cherit, Macias, Espinosa-Perez, de la Torre, Ruiz-Palacios, Stewart, Fowler.

Statistical analysis: Pinto, Fowler.

Administrative, technical, or material support: Domínguez-Cherit, Lapinsky, Espinosa-Perez, Baltazar-Torres, Stewart, Fowler.

Study supervision: Domínguez-Cherit, Stewart, Fowler.

Financial Disclosures: None reported.

Participating Centers: Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán,” México City, México; Hospital General “Dr. Manuel Gea Gonzalez,” México City; School of Medicine Instituto Tecnologico de Monterrey, Monterrey City, México; Hospital Juarez de Mexico, México City; Hospital San Jose-Tec de Monterrey, Monterrey City, México; Instituto Nacional de Enfermedades Respiratorias, México City; Instituto Nacional de Diagnóstico y Referencia Epidemiológicos, México City.

Previous Presentations: Presented in part at the International Conference of the American Thoracic Society; May 20, 2009; San Diego, California.

Additional Contributions: We thank the following persons for providing input on the study design and conduct: Mexico: Instituto Nacional de Ciencias Medicas y Nutrición “Salvador Zubiran”: Delia Borunda-Nava, MD, Carlos Rodriguez-Osorio, MD, Silvio Antonio Ñamendys, MD, MSc, Antonio Fonseca, MD, Guadalupe Morales, RN, Martha Huertas, RN; Patricia Leal, MD, Arturo Galindo Fraga, MD, Rafael Franco, MD, Sarbelio Moreno-Espinosa, MD, MSc; Hospital General “Dr Manuel Gea Gonzalez” Influenza Committee: Simon Kawa Karasik, MD, Araceli Contreras Molina, RN, Rafael Figueroa Moreno, MD, Jose Jesús Acevedo Mariles, MD, Carlos Alberto San Juan Martínez, MD, Guillermo Bierzwinsky Sneider, MD, Laura Ramírez Preciado, MD, Alejandro Avalos Bracho, MD, Lucina Gutierrez Sánchez, RN, Antonio Martínez Conde, MD, Antonio Lavalle Villalobos, MD, Lorena Hernández Delgado, MD, Gerardo Lara Figueroa, MD, Hector Prado Calleros, MD, Jeremy Farrar, MD, Alejandro Flores (emergency room technician); Hospital de Especialidades CMN la Raza IMSS: Alejandro Sanchez Hurtado, MD, Claudia Lopez Nava, MD; Hospital Juarez de México: Jose M. Conde-Mercado, MD, Monica Cureño-Diaz, MD, Ariel Estrada-Aguilera, MD, Claudia Vazquez-Zamora, MD, Mayte Martinez-Velazquez, MD, David Hernandez-Lopez, MD; Hospital San Jose Tec de Monterrey: Javier Valero Gomez, MD, Carlos Diaz Olachea, MD, Estrella Gonzalez, MD; School of Medicine Tecnologico de Monterrey: Rocio Cabrera (bioengineer); and all the Intensive Care Unit and Medical Intensive Care Unit nurse staff for all the effort and devotion of their work at the Inistituto Nacional de Enferemedades Respiratorias. Canada and United States: John Marshall, MD, Arthur Slutsky, MD, Phil Hebert, MD, PhD, Blair Henry, MSc, Francois Lamontagne, MD, Gordon Rubenfeld, MD, MSc, Andy Simor, MD, Muhammad Mamdani, PharmD, MA, MPH, Judith Hall, MSc, Bryan Boodhoo, and the Li Ka Shing Knowledge Institute of St. Michael’s Hospital; Neill Adhikari, MDCM, MSc, Damon Scales, MD, PhD, Richard Mraz, PEng, Barry McLellan, MD, Karen Choong, MD, Kusem Menon, MD, MSc, Dominique Piquette, MD, MSc, Michael Christian, MD, Jeff Singh, MD, MSc, Orla Smith, MSc, Ellen McDonald, RN, Claudio Martin, MD, MSc, Francois Lellouche, MD, Nicole Zytaruk, RN, Lauralyn McIntyre, MD, MSc, Tom Stelfox, MD, PHD, John Granton, MD, Anand Kumar, MD, Ryan Zarychanski, MD, MSc, David Wensley, MD, Dermot Doherty, MD, Sandra Dial, MD, Sean Keenan, MD, MSc, Sheldon Magder, MD, David Hornstein, MD, David Leasa, MD, Rick Hall, MD, Mark Crowther, MD, MSc, Donald Griesdale, MD, Jamie Hutchison, MD, Jan Friedrich, MD, DPhil, Nial Ferguson, MD, MSc, Jacques Lacroix, MD, Peter Dodek, MD, MHSc, Philippe Jouvet, MD, PhD, Steve Webb, MD, Simon Finfer, MD, Jamie Cooper, MD, Allison McGeer, MD, Tex Kissoon, MD, Brian Cuthbertson, MB, ChB, Cathy Tansey, PhD, Ari Joffe, MD, Craig Coopersmith, MD, the American Thoracic Society, the Society of Critical Care Medicine, the University of Toronto Interdepartmental Division of Critical Care Medicine, and the Canadian Critical Care Trials Group.

Author Affiliations: Division of Pulmonary and Critical Care (Dr Domínguez-Cherit), Hospital Epidemiology Department (Drs de la Torre and Macias), Infectious Disease Department (Dr Ruiz-Palacios), and Department of Critical Care Medicine (Dr Rivero), Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán,” México City, México; Interdepartmental Division of Critical Care Medicine and Department of Medicine, University of Toronto and Mount Sinai Hospital, Toronto, Ontario, Canada (Dr Lapinsky); School of Medicine, Instituto Tecnologico de Estudios Superiores de Monterrey, Monterrey, México (Dr Espinosa-Perez); Interdepartmental Division of Critical Care Medicine and Department of Medicine, University of Toronto and Sunnybrook Health Sciences Centre, Toronto (Dr Pinto); Hospital Juarez de México, México City (Dr Poblano-Morales); Hospital de Especialidades Centro Medico La Raza, IMSS, México City (Dr Baltazar-Torres); Instituto Nacional de Enfermedades Respiratorias, México City (Dr Bautista); Department of Internal Medicine (Drs A. Martinez and M. A. Martinez) and Infectious Disease Hospital (Dr Valdez), Hospital General “Dr. Manuel Gea Gonzalez,” México City; Hospital San Jose-Tec de Monterrey, Monterrey City (Dr Hernández); Interdepartmental Division of Critical Care Medicine and Department of Medicine and Anaesthesia, University of Toronto, Mount Sinai Hospital, University Health Network, Toronto (Dr Stewart); and Interdepartmental Division of Critical Care Medicine and Department of Medicine, University of Toronto and Sunnybrook Health Sciences Centre, Toronto (Dr Fowler).

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JAMA-EXPRESS
Critically Ill Patients With 2009 Influenza A(H1N1) Infection in Canada

Anand Kumar, MD; Ryan Zarychanski, MD; Ruxandra Pinto, PhD; Deborah J. Cook, MD, MSc; John Marshall, MD; Jacques Lacroix, MD; Tom Stelfox, MD, PhD; Sean Bagshaw, MD, MSc; Karen Choong, MD; Francois Lamontagne, MD; Alexis F. Turgeon, MD, MSc; Stephen Lapinsky, MD; Stéphane P. Ahern, MD; Orla Smith, MSc; Faisal Siddiqui, MD; Philippe Jouvet, MD, PhD; Kosar Khwaja, MD; Lauralyn McIntyre, MD, MSc; Kusum Menon, MD, MSc; Jamie Hutchison, MD; David Hornstein, MD; Ari Joffe, MD; Francois Lauzier, MD; Jeffrey Singh, MD, MSc; Tim Karachi, MD; Kim Wiebe, MD; Kendiss Olafson, MD; Clare Ramsey, MD; Satendra Sharma, MD; Peter Dodek, MD, MHSc; Maureen Meade, MD, MSc; Richard Hall, MD; Robert Fowler, MD, MSc; for the Canadian Critical Care Trials Group H1N1 Collaborative

출처 : JAMA. 2009;302(17):(doi:10.1001/jama.2009.1496).
http://jama.ama-assn.org/cgi/content/full/2009.1496

Context  Between March and July 2009, the largest number of confirmed cases of 2009 influenza A(H1N1) infection occurred in North America.

Objective  To describe characteristics, treatment, and outcomes of critically ill patients in Canada with 2009 influenza A(H1N1) infection.

Design, Setting, and Patients  A prospective observational study of 168 critically ill patients with 2009 influenza A(H1N1) infection in 38 adult and pediatric intensive care units (ICUs) in Canada between April 16 and August 12, 2009.

Main Outcome Measures  The primary outcome measures were 28-day and 90-day mortality. Secondary outcomes included frequency and duration of mechanical ventilation and duration of ICU stay.

Results  Critical illness occurred in 215 patients with confirmed (n = 162), probable (n = 6), or suspected (n = 47) community-acquired 2009 influenza A(H1N1) infection. Among the 168 patients with confirmed or probable 2009 influenza A(H1N1), the mean (SD) age was 32.3 (21.4) years; 113 were female (67.3%) and 50 were children (29.8%). Overall mortality among critically ill patients at 28 days was 14.3% (95% confidence interval, 9.5%-20.7%). There were 43 patients who were aboriginal Canadians (25.6%). The median time from symptom onset to hospital admission was 4 days (interquartile range [IQR], 2-7 days) and from hospitalization to ICU admission was 1 day (IQR, 0-2 days). Shock and nonpulmonary acute organ dysfunction was common (Sequential Organ Failure Assessment mean [SD] score of 6.8 [3.6] on day 1). Neuraminidase inhibitors were administered to 152 patients (90.5%). All patients were severely hypoxemic (mean [SD] ratio of PaO₂ to fraction of inspired oxygen [FIO₂] of 147 [128] mm Hg) at ICU admission. Mechanical ventilation was received by 136 patients (81.0%). The median duration of ventilation was 12 days (IQR, 6-20 days) and ICU stay was 12 days (IQR, 5-20 days). Lung rescue therapies included neuromuscular blockade (28% of patients), inhaled nitric oxide (13.7%), high-frequency oscillatory ventilation (11.9%), extracorporeal membrane oxygenation (4.2%), and prone positioning ventilation (3.0%). Overall mortality among critically ill patients at 90 days was 17.3% (95% confidence interval, 12.0%-24.0%; n = 29).

Conclusion  Critical illness due to 2009 influenza A(H1N1) in Canada occurred rapidly after hospital admission, often in young adults, and was associated with severe hypoxemia, multisystem organ failure, a requirement for prolonged mechanical ventilation, and the frequent use of rescue therapies.

INTRODUCTION

The reemergence of pandemic influenza has been anticipated since the Hong Kong (H3N2) influenza pandemic of 1968. In recent years, there has been substantial concern that a pandemic would involve the novel H5N1 avian flu variant, which has demonstrated an ability to cause severe disease when transmitted to humans.^1-2 However, this spring the US Centers for Disease Control and Prevention reported the occurrence of a 2009 influenza A(H1N1) in 2 children in southern California.³ Subsequently, infection with this virus has been reported in virtually every country.^4-7 The World Health Organization declared the first phase 6 global influenza pandemic of the century on June 11, 2009.⁸

The largest numbers of confirmed cases have been documented in the United States, Mexico, Canada, Chile, and Australia.⁹ Mexico and Canada have both experienced large localized outbreaks of infection with severe illness requiring intensive care unit (ICU) admission and ventilator support. This report describes the epidemiological characteristics, clinical features, treatments, and outcomes of a multicenter cohort of critically ill adult and pediatric Canadian patients.

METHODS

Study Design

In response to an outbreak of 2009 influenza A(H1N1) in Mexico, members of the Canadian Critical Care Trials Group (CCCTG) designed a multicenter observational study of critically ill patients infected with 2009 influenza A(H1N1) (eAppendix). After several cycles of feedback and pilot testing, forms were widely disseminated to ICU physicians, and uploaded to the CCCTG and other critical care society Web sites on May 3, 2009.¹⁰ Data were collected retrospectively or prospectively on all patients with 2009 influenza A(H1N1)–related critical illness admitted to the ICU between April 16 and August 12, 2009. Research ethics board approval was granted by Sunnybrook Health Sciences Centre as the central coordinating center on April 30, 2009, and by each participating local research ethics board. The need for a priori informed consent was waived because of the noninterventional study design.

Data Collection

Eligible patients included all adult and pediatric critically ill individuals admitted to participating hospitals in Canada with confirmed, probable, or suspected 2009 influenza A(H1N1) infection, according to case definitions developed by the World Health Organization and the Canadian National Microbiology Laboratory.^10-11 Critically ill patients were defined as (1) those admitted to a pediatric or adult ICU or those requiring mechanical ventilation (invasive or noninvasive), (2) those with a fraction of inspired oxygen (FIO₂) concentration greater than or equal to 60%, or (3) those with the need for intravenous infusion of inotropic or vasopressor medication. Suspected cases of 2009 influenza A(H1N1) in the presence of a strong epidemiologic link were initially included because confirmatory testing was unavailable in some hospitals when diagnostic laboratories were overwhelmed with testing requests once the pandemic was under way.

Eligibility criteria were confirmed and data were recorded by research coordinators or site investigators at each center (eAppendix). Severity of illness was assessed in adults and children using the Acute Physiology and Chronic Health Evaluation (APACHE) II and Pediatric Risk of Mortality (PRISM) III scores.^12-13 Comorbidities, including major comorbidities defined a priori, were recorded as the presence of 1 or more of the following chronic medical conditions: congestive heart failure; cerebrovascular, neoplastic, chronic liver or renal diseases; and use of immunosuppressant medications.¹⁴

The primary outcome measure was mortality at 28 days after the onset of critical illness as defined by the eligibility criteria. Secondary outcomes included frequency and duration of mechanical ventilation and duration of ICU and hospital stay. Data were submitted to the coordinating center and checked for errors by manual inspection and electronic range limits.

Analysis

Descriptive statistics included frequency analysis (percentages) for categorical variables and means and standard deviations or medians and interquartile ranges (IQRs) for continuous variables. To test for differences in baseline characteristics between those with confirmed or probable and those with suspected disease, and those who survived vs those who died, a 2-sample t test or the Wilcoxon rank sum test was used for continuous variables as appropriate and the ² test or Fisher exact test was used for discrete variables. Daily variables are presented at days 1, 3, 7, and 14.

The Kaplan-Meier method in which patients discharged from the ICU alive were censored at 28 days was used to depict the probability of survival over the duration of follow-up and to generate survival curves. The discriminative ability of the day 1 APACHE II and SOFA scores on mortality were compared by testing the difference in C statistics (area under the receiver operating curve). The 95% confidence intervals (CIs) and P values were reported to reflect a 2-tailed level of .05. The statistical analyses were conducted using SAS version 9.1 (SAS Institute Inc, Cary, North Carolina).

RESULTS

Characteristics of Study Patients and Hospitals

Between April 16 and July 13, 2009, 215 critically ill patients were admitted to 38 study ICUs (median of 16 ICU beds^15-34; median hospital size, 463 beds [IQR, 238-524 beds]) with confirmed (n = 162), probable (n = 6), or suspected (n = 47) 2009 influenza A(H1N1) infection. Patients having confirmed or probable 2009 influenza A(H1N1) infection were significantly younger, had a longer duration of mechanical ventilation and ICU stay, and higher mortality than those with suspected disease. Therefore, all analyses were restricted to the 168 patients with confirmed or probable 2009 influenza A(H1N1) infection (Table 1). The mean (SD) age was 32.3 (21.4) years; 113 patients were female (67.3%), 50 were children (29.8%), and there were 43 aboriginal Canadians (25.6%). There were 52 critically ill patients from the greater Winnipeg region, in the province of Manitoba, and 116 patients were from other provinces (Figure 1). Sixteen cases originated from nosocomial transmission; none of these were health care workers.

Among adults, the mean (SD) APACHE II score was 19.7 (8.7); and among pediatric patients, the mean (SD) PRISM III score was 9.1 (9.8). At presentation, comorbidities were present in 165 patients (98.2%) (Table 2). However, major comorbidities were present in only 51 patients (30.4%). The most common individual comorbidities were chronic lung disease (41.1%), obesity (33.3%), hypertension (24.4%), and ever smoking (22.6%). The mean (SD) body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) was 34.6 (11.0) and 28 patients (23.7%) were morbidly obese (BMI >40). The most common presenting symptoms were fever (90.5%), respiratory symptoms (94.6%), weakness (55.9%), and myalgias (40.1%). Concomitant presenting conditions included possible bacterial pneumonia (54 cases; 32.1%), hypotension requiring vasopressors (23 cases; 13.7%), asthma or chronic obstructive pulmonary disease exacerbation (23 cases; 13.7%), altered level of consciousness (17 cases; 10.1%), acute kidney injury (12 cases; 7.1%), and ischemic chest pain (5 cases; 3.0%).

Course of Illness and Treatments Received

The median time from symptom onset to hospital admission was 4 days (IQR, 2-7 days)^2-7 and from hospitalization to ICU admission was 1 day (IQR, 0-2 days) after presentation to the hospital. Only 10 patients (6%) had received a seasonal influenza vaccination in either of the past 2 years. Most patients (70.8%) had bilateral chest radiograph infiltrates (41.1% with 4-quadrant involvement) and 72.6% had acute lung injury at the onset of critical illness.

Of all patients, 136 (81.0%) were mechanically ventilated on the first day of ICU admission; 128 (76.2%) invasively and 55 (32.7%) noninvasively. Forty-seven patients (85.4%) who received noninvasive ventilation ultimately required invasive ventilation. The mean (SD) day 1 ratio of PaO₂ to FIO₂ was 147 (128) mm Hg (Table 3); the mean (SD) day 1 FIO₂ value was 74% (26%) and the mean (SD) day 1 positive end-expiratory pressure (PEEP) was 9.8 (4.0) cm H₂O (eTable).

The mean daily PEEP was greater than 10 cm H₂O for the first 2 weeks of mechanical ventilation. Over the first 2 weeks of critical illness, tidal volumes ranged from 8 to 9.1 mL/kg of ideal body weight; and carbon dioxide elimination was not substantially impaired. Barotrauma occurred in 14 patients (8.3%). Therapies for oxygenation failure included neuromuscular blockade (47 patients; 28.0%), inhaled nitric oxide (23 patients; 13.7%), high-frequency oscillatory ventilation (20 patients; 11.9%), extracorporeal membrane oxygenation (7 patients; 4.2%), and prone positioning ventilation (5 patients; 3.0%) (eTable).

Inotropes or vasopressors were used in 55 patients (32.7%) on day 1 after the onset of critical illness (Table 3), often with high levels of sedatives to facilitate patient-ventilator synchrony. Drug treatments included neuraminidase inhibitors (152 patients [90.5%] for a median of 5 days^4-8), antibiotics (166 patients; 98.8%), and corticosteroids (85 patients; 50.6%).

Creatine kinase was moderately elevated over the first week of critical illness (median level, 580 U/L [IQR, 203-1728 U/L] by day 3; to convert creatine kinase to µkat/L, multiply by 0.0167) (Table 3). The mean leukocyte count was normal at admission and remained in the normal range for the first week. Clinical evidence of secondary bacterial pneumonia following ICU admission was found in 41 cases (24.4% of all patients) including 18 cases caused by Staphylococcus aureus and 5 cases caused by Streptococcus pneumoniae.

Outcomes

Among 168 critically ill patients with 2009 influenza A(H1N1) infection, 29 died (17.3%; 95% CI, 12.0%-24.0%). Eighteen patients died (10.7%; 95% CI, 6.6%-16.6%) within the first 14 days and 24 died (14.3%; 95% CI, 9.5%-20.7%) within 28 days from the onset of critical illness (Table 4 and Figure 2). Twenty-one of those who died were female (72.4%) and 8 were male (27.6%). Of 50 children, only 4 died (8.0%). Of 9 health care workers, 5 required mechanical ventilation and none died. The median length of ICU stay was 12 days (IQR, 5-20 days)^5-20; 12 days for survivors^5-22 and 10 days for nonsurvivors.^4-19 The median duration of ventilation was 12 days (IQR, 6-20 days) for both survivors^6-20 and nonsurvivors.^4-20 One patient died on a medical ward, while all others died in the ICU.

The primary reported causes of death included severe acute respiratory distress syndrome and hypoxemia, or complications thereof⁵; secondary infection and sepsis⁶; multiorgan dysfunction syndrome,² malignancy,² chronic obstructive pulmonary disease,¹ primary cardiac arrest¹; tension pneumothorax,¹ cerebral edema¹; and undetermined etiologies. Pulmonary embolism was believed to be contributory but not causal in 1 death.

Comparison of Survivors With Nonsurvivors

Patients who died were more likely to have higher severity of illness at presentation and greater organ dysfunction (Table 5). Although this overall population was young, older patients were more likely to die. There were no statistically significant differences in female sex distribution or aboriginal vs nonaboriginal status. The APACHE II and day 1 SOFA scores were significantly associated with overall mortality (P<.001 and P = .002, respectively) and there was no difference between the predictive value of these 2 scores (C statistics: 0.757 and 0.688, respectively; P = .13). Because nearly all patients received early treatment with neuraminidase inhibitors, we were unable to investigate differences in outcome due to treatment or timing of these agents (Figure 3).

Comparison of All Patients

As of August 22, 2009, in the general Canadian population, among 7107 reported cases, 1441 required hospitalization (20.3%), 278 were admitted to the ICU (3.9%) (the 215 admitted by July 13, 2009, are reported in this series).¹⁵ In comparing characteristics of all patients infected with 2009 influenza A(H1N1) infection, patients hospitalized, those admitted to the ICU, and those who died, the median age of patients was progressively greater along this continuum and there was a progressively greater proportion of patients with at least 1 underlying medical condition. The proportion of females was greater among those admitted to the ICU and among those who died compared with those infected and those admitted to hospital. There were a greater proportion of pregnant women requiring admission to the hospital and who died compared with the proportion among all of those infected.¹⁵

COMMENT

The spring outbreak of 2009 influenza A(H1N1) infection in Canada affected primarily young, female, and aboriginal patients without major comorbidities, and conferred a 28-day mortality of 14.3% among critically ill patients. A history of lung disease or smoking, obesity, hypertension, and diabetes were the most common comorbidities. Critical illness occurred rapidly after hospital admission and was associated with severe oxygenation failure, a requirement for prolonged mechanical ventilation, and the frequent use of rescue therapies.

We identified unusual features of severe disease in the current pandemic compared with most previous well-characterized pandemics, including the (probable) H2N2 1890 Russian influenza pandemic, the H2N2 1957 Asian influenza pandemic, and the H3N2 1968 Hong Kong pandemic.^16-18 In these previous influenza pandemics, an increased predilection for infection among children and young adults has been documented,^{9, 19} although mortality curves were U shaped with increased deaths in the very young and the aged.

Our data suggest that severe disease and mortality in the current outbreak is concentrated in relatively healthy adolescents and adults between the ages of 10 and 60 years, a pattern reminiscent of the W-shaped curve previously seen only during the 1918 H1N1 Spanish pandemic.^20-22 Few patients older than 60 years in this study were admitted to the ICU (Figure 1). A potential biological basis for this observation is that patients in this age group have a cross-reactive antibody to 2009 influenza A(H1N1) at much higher rates than younger patients.²³

The increased fraction of the aboriginal community presenting with severe 2009 influenza A(H1N1) infection is notable but not unique. This finding is reflected in the history of the 1918 H1N1 Spanish influenza pandemic during which mortality in aboriginal communities in North America (3%-9%) was many times higher than nonaboriginal communities (generally <0.75%).^24-29 In 1918, mortality within Alaskan and Labrador Inuit populations was 30% to 90%.^{24, 28-29} Although mortality was not substantially greater among aboriginal Canadians in this report, the number of patients with severe disease and knowledge of prior illness patterns in this community is cause for concern.

The tendency of females to develop severe 2009 influenza A(H1N1) infection in this series is striking. A general female susceptibility has not been observed in other influenza case series of variable severity including the initial reports of 2009 influenza A(H1N1) infections.^30-31 In most infectious diseases and related conditions such as sepsis and septic shock, males represent a larger proportion of cases and have a higher mortality.^32-33 The explanation for increased risk of severe disease and death among females in this report is unclear but the role of pregnancy as a risk factor has been noted in previous influenza pandemics.^34-35

The most common comorbidities among critically ill patients in our study were lung disease, obesity, hypertension, and a history of smoking or diabetes, each occurring in 30% to 40% of patients. All these conditions are known to be increased in frequency in the aboriginal population that comprises a substantial portion of cases within this cohort.³⁶ The extent to which these comorbidities contribute to severity of disease is unclear because a large portion of the aboriginal population (which may be a risk factor itself on the basis of genetic susceptibility) often have such comorbidities.

Among critically ill patients, obesity has been shown to be a risk factor for increased morbidity, but not consistently with mortality.^37-38 The association of obesity with severe 2009 influenza A(H1N1) infection has been reported by others³⁹ and may be a novel finding of this pandemic; however, even though obesity was more common in our series than in the general Canadian population (33% vs approximately 24%), we did not find a significant difference in BMI between survivors and nonsurvivors.⁴⁰

Critically ill patients with diabetes and hyperglycemia also are known to be at increased risk of complications and death; similarly, alcohol abuse, which is known to be a risk factor for acute respiratory distress syndrome, may have been a risk factor some patients in our series.⁴¹ These relationships also have been reported with seasonal influenza.⁴² The relative absence of serious comorbidities emphasizes that young, relatively healthy adults were the primary population affected by severe 2009 influenza A(H1N1) infection during this outbreak.

Patients with 2009 influenza A(H1N1) infection–related critical illness experienced symptoms for an average of 4 days prior to hospital presentation, but rapidly worsened and required care in the ICU within 1 to 2 days. Apart from the usual symptoms seen in seasonal influenza, these cases stand out for the presence of gastrointestinal tract symptoms, dyspnea, purulent sputum production, and occasional frothy lung fluid on cough or endotracheal aspiration. Chest radiographs demonstrating bilateral mixed interstitial or alveolar infiltrates were found in three-quarters of the patients.

Approximately one-third of patients required vasopressor support on day 1 following ICU admission; however, in many cases this appeared temporally associated with the need for substantial sedation to optimize ventilation. Broad-spectrum antibacterial agents were initiated in almost all patients because of the initial suspicion of community-acquired bacterial pneumonia. However, actual bacterial lung infection was typically documented later in the course of critical illness.

In addition, approximately one-third of patients in our cohort required advanced ventilatory support and rescue therapies for profound hypoxemic respiratory failure, including high levels of inspired oxygen and PEEP, pressure control, and airway pressure release ventilation, high-frequency oscillatory ventilation, prone positioning ventilation, neuromuscular blockade, inhaled nitric oxide, and extracorporeal membrane oxygenation. The fact that severe illness arises in a young, previously healthy population with a high probability of survival given the availability of appropriate resources has important societal implications.

In Winnipeg, Manitoba, Canada, site of the largest pandemic cohort of patients, the capacity for the care of critically ill patients was seriously challenged at the outbreak peak in June (Figure 1) with full occupancy of all regional ICU beds, similar to the 2002 Toronto, Ontario, Canada, experience with severe acute respiratory syndrome.⁴³ If, as expected, the prevalence of 2009 influenza A(H1N1) infection increases with the upcoming flu season, there will be an acutely increased demand for ICU care, including the need for rescue therapies that are not currently widely available.^44-46 Clinicians and policy makers will need to examine feasible methods to optimally expand and deploy ICU resources to meet this need.

This study has a number of strengths. It represents the largest series of patients with severe 2009 influenza A(H1N1) infection yet described, and includes both adults and children from geographically and racially diverse settings across Canada, which improves the generalizability of our results to other regions. These observations of the epidemiological risk factors, typical clinical features, response to therapy, and prognosis should aid in the recognition, diagnosis, and clinical management of such infections. Our finding that patients can often be supported through 2009 influenza A(H1N1) infection–related critical illness with prolonged, aggressive life support, and the expectation that the number of cases will likely increase substantially over the next 6 months, highlight important potential limitations in critical care capacity.

This study also has limitations. Our focus on severe disease requiring ICU admission may not reflect important presenting features in less severe cases. The ongoing deaths throughout the course of the study period suggest the possibility of late deaths after the observation period. This may result in a final hospital mortality rate that exceeds the mortality rate we are reporting. Although we describe cases in most regions of Canada, many were from an outbreak in a single province (Manitoba) and involved an aboriginal Canadian population near Winnipeg, which is Manitoba’s largest city. This may lead to overrepresentation or underrepresentation of certain comorbidities and clinical features.

In conclusion, we have demonstrated that 2009 influenza A(H1N1) infection–related critical illness predominantly affects young patients with few major comorbidities and is associated with severe hypoxemic respiratory failure, often requiring prolonged mechanical ventilation and rescue therapies. With such therapy, we found that most patients can be supported through their critical illness.

AUTHOR INFORMATION

Corresponding Author: Anand Kumar, MD, Section of Critical Care Medicine, Health Sciences Centre, JJ 399, 700 William Ave, Winnipeg, MB R3E-0Z3 Canada (akumar61@yahoo.com ).

Published Online: October 12, 2009 (doi:10.1001/jama.2009.1496).

Author Contributions: Drs Kumar and Fowler had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Kumar, Zarychanski, Cook, Marshall, Stelfox, Lamontagne, Lapinsky, Ahern, Hutchison, Joffe, Dodek, Hall, Fowler.

Acquisition of data: Kumar, Zarychanski, Cook, Marshall, Stelfox, Bagshaw, Choong, Lamontagne, Turgeon, Lapinsky, Ahern, Smith, Siddiqui, Khwaja, McIntyre, Menon, Hutchison, Hornstein, Joffe, Lauzier, Singh, Karachi, Ramsey, Sharma, Meade, Hall, Fowler.

Analysis and interpretation of data: Kumar, Zarychanski, Pinto, Cook, Lacroix, Stelfox, Ahern, Jouvet, Menon, Wiebe, Olafson, Ramsey, Sharma, Fowler.

Drafting of the manuscript: Kumar, Zarychanski, Pinto, Cook, Ahern, Hall, Fowler.

Critical revision of the manuscript for important intellectual content: Kumar, Zarychanski, Pinto, Cook, Marshall, Lacroix, Stelfox, Bagshaw, Choong, Lamontagne, Turgeon, Lapinsky, Smith, Siddiqui, Jouvet, Khwaja, McIntyre, Menon, Hutchison, Hornstein, Joffe, Lauzier, Singh, Karachi, Wiebe, Olafson, Ramsey, Sharma, Dodek, Meade, Fowler.

Statistical analysis: Kumar, Pinto, Fowler.

Obtained funding: Kumar, Ahern, Fowler.

Administrative, technical or material support: Cook, Marshall, Lacroix, Bagshaw, Lamontagne, Turgeon, Ahern, Smith, Siddiqui, Hutchison, Joffe, Lauzier, Sharma, Meade, Fowler.

Study supervision: Kumar, Cook, Lacroix, Siddiqui, Khwaja, Menon, Fowler.

Financial Disclosures: None reported.

Funding/Support: The Public Health Agency of Canada, the Ontario Ministry of Health and Long-term Care, the Heart and Stroke Foundation Canada, and the Canadian Institutes of Health Research provided support for this article.

Role of the Sponsor: The Public Health Agency of Canada, the Ontario Ministry of Health and Long-term Care, the Heart and Stroke Foundation Canada, and the Canadian Institutes of Health Research had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.

Canadian Critical Care Trials Group H1N1 Collaborative Writing Committee: Anand Kumar, Ryan Zarychanski, Ruxandra Pinto, Philippe Jouvet, Jacques Lacroix, John Marshall, Deborah J. Cook, Rob Fowler. Canadian Critical Care Trials Group H1N1 Collaborative Clinicians: Nova Scotia: Halifax: Richard Hall, Rob Green, Dietrich Heinzler, Lisa Julien, Debra Wright (Queen Elizabeth II Health Sciences Centre). Québec: Québec City: François Lauzier, Alexis Turgeon, Caroline Roy (CHA-Hôpital de l’Enfant-Jésus); François Lellouche, Marie-Claude Ferland (Institut Universitaire de Cardiologie et de Pneumologie de Québec). Longueuil: Germain Poirier (Hôpital Charles-LeMoyne). Sherbrooke: François Lamontagne (Centre Hospitalier Universitaire de Sherbrooke). Montreal: Phillippe Jouvet, Jacques Lacroix (CHU Sainte-Justine); Denny Laporta, David Hornstein (SMBD-Jewish General Hospital); Kosar Khwaja, Laura Banici (McGill University Health Centre); Stéphane P. Ahern, Yoanna Skrobic, Johanne Harvey (Hôpital Maisonneuve Rosemont); Martin Albert, Isabelle Arsenault (Hôpital du Sacré-Coeur de Montréal). Ontario: Ottawa: Lauralyn McIntyre, Claude Gaudet, Ray Saginur, Joe Pagliarello, Irene Watpool, Tracy Mcardle (Ottawa Hospital); Kusum Menon, Dermot Doherty, Sonny Dhanani, Roxanne Ward (Children’s Hospital of Eastern Ontario). Kingston: John Muscedere, Nicole Godfrey, Susan Fleury (Kingston General Hospital). Toronto: Robert Fowler, Ruxandra Pinto, Neill Adhikari (Sunnybrook Hospital); Stephen Lapinsky, Cheryl Ethier, Tom Stewart (Mount Sinai Hospital); Orla Smith, John Marshall, Jan Friedrich, Karen Burns (St Michael’s Hospital); Jeffrey M. Singh, John Granton, Nancy Brockest, Niall Ferguson, Andrea Matte (University Health Network); Jamie Hutchison (Hospital for Sick Children); Rob Cirone (St Joseph’s Health Centre). Hamilton: Deborah Cook, Ellen MacDonald, Kelly Wilton, Andrea Tkaczyk (St Joseph’s Healthcare); Karen Choong, Mark Duffett (McMaster University Children’s Hospital); Maureen Meade (Hamilton Health Sciences Center, general site); Andy Freitag (Hamilton Health Sciences Center, McMaster site); Tim Karachi (Hamilton Health Sciences Center, Henderson site). Guelph: Gerry Hollinger (Guelph General Hospital). London: Claudio Martin (London Health Sciences Centre). Windsor: Eli Malus, Maureen Hrytsyk (Hotel Dieu Grace Hospital). Thunder Bay: Ravi Agarwala (Thunderbay Regional Health Sciences Centre). Manitoba: Winnipeg: Anand Kumar, Ryan Zarychanski, Faisal Siddiqui, Duane Funk, Allan Garland, Wendy Janz, Nicole Marten, Kim Wiebe, Mandy Siddiqui, Clare Ramsey, Satendra Sharma, Kendiss Olafson, Stasa Veroukis, Murray Kesselman (Health Sciences Centre/St Boniface Hospital/Grace Hospital/Victoria Hospital/Concordia Hospital/Seven Oaks Hospital). Brandon: Charles Penner (Brandon Regional Health Authority). Alberta: Calgary: Tom Stelfox (Foothills Medical Centre). Edmonton: Sean M. Bagshaw (University of Alberta Hospital); Mark Heule (Misericordia Hospital); Curtis Johnston (Royal Alexandria Hospital); Marcia Johnson (Public Health Division, Alberta Health Services); Sean Norris (Sturgeon Hospital); Ari Joffe (Stollery Children’s Hospital). British Columbia: Vancouver: Peter Dodek (St Paul’s Hospital); Peter Skippen (BC Children’s Hospital); Donald E. G. Griesdale, Denise Foster (Vancouver General Hospital). New Westminster: Sean Keenan, Steven Reynolds (Royal Columbian Hospital).

Additional Contributions: We thank our patients and the health care professionals who have delivered exemplary care to these patients in the face of uncertain risks. We also thank the following research assistants, who have worked tirelessly in the last several months: Davie Wong, Joel Braun, Aaron Guinn, Allison Stasiuk, Joan Tien, Raji Kaler, Alyson Mahar, Phil Hebert, MD, Blair Henry, MSc, Richard Mraz, PEng, Barry McLellan, MD, Michael Christian, MD, Steve Webb, MD, Simon Finfer, MD, Jamie Cooper, MD, Allison McGeer, MD, Tex Kissoon, MD, Brian Cuthbertson, MD, Mark Crowther, MD, MSc, Cathy Tansey, PhD, Craig Coopersmith, MD, and Arthur Slutsky, MD; Muhammad Mamdani, PharmD, Judith Hall, MSc, Magda Melo, MSc, Bryan Boodhoo, MSc (University of Toronto Interdepartmental Division of Critical Care Medicine); and Rachel Rodin, MD (Applied Health Research Centre, Li Ka Shing Knowledge Institute of St Michael’s Hospital); and the National Microbiology Laboratory of Canada, Winnipeg, the American Thoracic Society, and the Society of Critical Care Medicine. The persons listed in this section were not financially compensated for their work.

Author Affiliations: Section of Critical Care Medicine, Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada (Drs Kumar, Siddiqui, Wiebe, Olafson, Ramsey, and Sharma); Department of Medical Oncology and Hematology, Cancercare Manitoba, Winnipeg (Dr Zarychanski); Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada (Drs Pinto and Fowler); Departments of Clinical Epidemiology and Biostatistics (Drs Cook and Meade) and Medicine (Dr Karachi), McMaster Children’s Hospital (Dr Choong), McMaster University, Hamilton, Ontario, Canada; Department of Critical Care Medicine, St Michael’s Hospital, Toronto, Ontario, Canada (Dr Marshall and Ms Smith); Department of Pediatrics, CHU Sainte-Justine, Université de Montréal, Montréal, Quebec, Canada (Drs Lacroix and Jouvet); Departments of Critical Care Medicine and Community Health Sciences, University of Calgary, Calgary, Alberta, Canada (Dr Stelfox); Division of Critical Care Medicine, University of Alberta, Edmonton (Drs Bagshaw and Joffe); Department of Medicine, Centre Hospitalier, Université de Sherbrooke, Sherbrooke, Quebec, Canada (Dr Lamontagne); Centre de Recherche du CHA, Hôpital de l’Enfant-Jésus, Université Laval, Quebec City, Quebec, Canada (Drs Turgeon and Lauzier); Intensive Care Unit, Mount Sinai Hospital (Dr Lapinsky) and University Health Network (Dr Singh), University of Toronto, Toronto, Ontario, Canada; Department of Medicine, Hôpital Maisonneuve-Rosemont, University of Montréal, Montréal, Quebec, Canada (Dr Ahern); Trauma Services, McGill University Health Centre, Montréal, Quebec, Canada (Dr Khwaja); Clinical Epidemiology Unit, Ottawa Health Research Institute, Ottawa, Ontario, Canada (Dr McIntyre); Clinical Research Unit, Children’s Hospital of Eastern Ontario, Ottawa (Dr Menon); Department of Critical Care Medicine, Hospital for Sick Children, Toronto, Ontario, Canada (Dr Hutchison); SMBD-Jewish General Hospital, Montréal, Québec, Canada (Dr Hornstein); University of British Columbia, Vancouver (Dr Dodek); and Department of Anesthesia, Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada (Dr Hall).

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Caring for the Critically Ill Patient Section Editor: Derek C. Angus, MD, MPH, Contributing Editor, JAMA (angusdc@upmc.edu ).

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Swine flu risk to youths, healthy adults: studies

출처 : AFP Mon Oct 12, 9:43 pm ET

신종 인플루엔자 유행이 잦아드는 듯하더니 다시 감염 발생 소식이 들리고 있다. 지난 4월말부터 멕시코를 중심으로 발생한 ‘돼지 독감’으로 불린 이 질병은 전 세계로 확산됐고 지금도 감염인을 낳고 있다. 세계보건기구(WHO)가 집계한 바에 따르면 지난 5월17일까지 39개국에서 8480명의 감염인이 발생했다. 한국에도 지금까지 3명의 감염인이 발생한 것으로 확인됐다. 감염인 발생이 한풀 꺾이고 있지만 세계 보건당국은 여전히 긴장의 끈을 늦추지 않고 있다.

‘신종’ 바이러스의 유행

이번 신종 인플루엔자 바이러스는 돼지 독감, 조류 독감, 인간 독감 바이러스 유전자가 혼합된 ‘신종’ 바이러스인 것으로 알려지고 있다. 보통 독감 바이러스는 해당 종을 넘어 전염되지 않는다. 그런데 간혹 유전자 변형이 일어나 조류나 돼지 독감 바이러스가 사람에게 감염되기도 한다. 더 나아가 사람에게 감염된 동물 독감 바이러스가 인간 사이에 감염되면 사건이 커지게 된다. 이렇게 될 경우 감염이 급속도로 확산되고 감염의 결과도 치명적일 수 있기 때문이다.

현재까지 상황을 종합하면, 이번 바이러스의 감염력과 치사율은 그리 높지 않은 것으로 평가되고 있다. 그러나 전 세계 보건 당국은 긴장의 끈을 늦추지 않고 있다. 적절한 대응이 이루어지지 않을 경우 예기치 못한 사태가 발생할 가능성을 완전히 배제할 수 없기 때문이다.

2000년대 들어 조류 독감의 유행이 확인되면서, ‘신종’ 바이러스에 대한 대중의 관심이 높아졌다. 초창기에는 아시아 몇몇 나라의 문제로 치부되었으나 대륙 간 전염의 가능성에 대한 언급이 늘어나면서 이제는 전 세계적인 문제로 여겨지고 있다. 이러한 인식 변화에 중요한 역할을 한 것은 세계보건기구이다. 세계보건기구는 2005년부터 조류 독감 등 동물 기원 독감 바이러스의 위험성을 강조하기 시작했다. 세계보건기구는 이러한 독감 바이러스가 빈부격차, 남반구와 북반구, 남녀노소를 가릴 것 없이 모든 이들에게 위험할 수 있다고 경고했다. 특히 몇몇 전문가들은 1918년 독감 유행보다 더욱 위험한, 전세계적으로 유래 없는 재앙이 올 가능성이 있다고 주장했다.

바이러스 확산과 국가 안보 이데올로기 유포

이러한 주장에 정면으로 반대하는 이들도 있다. 이들은 “바이러스에 대한 과다하고 조작된 공포는 거대 국제 기구, 초국적 제약회사, 정부 등이 예산을 마련하고 국민을 관리하기 위해 개발해낸 과다광고에 불과하다”고 주장한다. 소위 ‘음모론’이다. 이러한 주장은 과학기술, 국제기구, 제약회사 등에 대한 불신이 강한 제3세계 국민 및 생태주의자들에게 설득력 있게 받아들여지고 있다. 이러한 음모론은 과학적 설득력이 약하지만 그러한 음모론이 나온 배경에 관심을 기울일 필요가 있다. 모든 종류의 음모론은 주류 집단이 이야기하는 것 이면에 숨은 진실의 한 조각을 보여주기 때문이다. 동물 기원 독감 바이러스 문제도 마찬가지다.

국제기구 및 미국 등 선진국 정부에 대한 불신이 이러한 음모론이 번성하는 데 일조하고 있다. 이 바이러스에 대한 위험은 국제기구와 선진국 정부가 앞장서 유포하고 있는데, 이는 꿍꿍이가 있는 것 아니냐는 것이다. 특히 미국 정부는 이러한 바이러스 감염에 대한 대응을 ‘국가 안보’ 차원에서 접근하는 경향이 있어 인권 운동 그룹의 신경을 건드린다. 미국 정부는 이러한 바이러스의 유행이 국가 안전에 크나큰 위협이 될 수 있고, 생물학적 테러의 도구가 될 수도 있으므로, 유사시에는 엄격한 이주 제한, 이동과 여행의 제한, 국경지대 방어, 강력한 감시 시스템이 필요하다는 입장을 가지고 있다. 그런데 이러한 위험에 대한 강조 및 공포 조장 전략은 국가 안보라는 허구의 가치를 위해 개인의 권리를 제한하는 정책을 정당화하는 것이라는 의심을 살 만하다. 특히 미국 정부는 ‘국가 안보’라는 이데올로기를 위해 ‘테러의 위험’을 과장되게 강조하는 경향이 있어, 이것도 그러한 정책의 일환이라는 의심을 사는 것이다.

감염인이 아닌 제약회사를 위한 치료제

다른 한편으로는, 감염이 발생할 때 선진국 정부가 대개 교역이나 이동을 제한하기 때문에 제3세계 국가 경제에 치명적 타격을 가할 수 있어 불만이 생긴다. 이러한 바이러스 유행은 일반적으로 제3세계에서 시작되는 경우가 많은데, 바이러스 유행과 함께 ‘봉쇄’가 시작되면, 해당 국가 경제는 치명적 타격을 받을 수 있다. 이럴 경우 제3세계 국민들은 별로 심각하지도 않은 문제를 가지고 선진국이 오버하고 있다는 인상을 받게 된다. 선진국 정부가 말로는 ‘전 세계의 위험’이므로 공동 대처가 필요하다고 하지만, 실질적으로는 자국의 이익만을 생각하고 행동하는 이중적 태도를 보이기 때문이다.

바이러스에 대한 대응책의 일환으로 백신 및 치료제 확보가 강조됨에 따라 불만과 의심은 더욱 커진다. 세계보건기구는 각국에 충분한 양의 치료제를 확보하라고 권고하지만 정작 제3세계 국가는 비싼 약가 때문에 그렇게 하지 못하는 경우가 허다하다. 정말 그렇게 ‘전 세계 인류를 위협하는 문제’라면 유행하고 있는 지역에 무상으로 혹은 싼 값으로 약을 공급해 더 이상 유행이 퍼지지 않도록 하는 것이 합리적이고 윤리적이다. 그러나 제약회사도 국제기구도 그러한 정책은 펴지 않는다. 이 역시 말과 행동이 다른 이중적 행태다. 게다가 바이러스 유행이 생길 때마다 해당 제약기업은 약품 판매와 주가 상승으로 엄청난 부를 챙기는 현실이다.

음모론이 나름의 의미가 있는 것과 별개로 독감 바이러스의 위험은 실존한다. 문제의 ‘크기와 심각성’에 대해서는 논의가 필요하지만 문제의 ‘존재’ 자체는 사실이다. 그러나 문제에 대한 진단과 해법이 현재와 같은 구도에서 이루어진다면 그 문제를 올바로 해결하기 힘들다. 오히려 음모론만 키울 수도 있다. 현재의 방식은 문제의 근본적 원인을 진단하지 못하고 있고, 그에 따라 해법도 근본적이지 못하기 때문이다.

바이러스를 유행시키는 사회경제적 요인을 봐야

독감 바이러스는 늘 인류와 더불어 존재해 왔다. 그리고 독감 바이러스는 늘 신종 바이러스를 만든다. 그러므로 신종 바이러스의 발생 자체를 억제할 수는 없다. 하지만 최근 문제되고 있는 독감 바이러스는 종간(種間) 감염을 일으키는 신종 바이러스라는 데 문제가 있다. 동물 독감 바이러스와 인간 독감 바이러스가 복잡하게 혼합되면서 그 위험성이 더 커지고 있다. 이런 점에서 최근의 독감 바이러스 위험의 원인을 기업화된 축산업에서 찾는 이들이 많다. 기업화된 축산업은 좁은 공간에 많은 동물을 키워 감염의 위험성을 높이고, 배설물을 사료로 쓰는 등 질병 발생에 취약한 조건을 제공한다. 그러므로 기업화된 축산업에 대한 규제를 강화하지 않는 한, 유행을 예방할 수 없다는 주장이 제기된다. 이번에 유행하고 있는 신종 인플루엔자도 미국의 대표적 축산기업인 ‘스미스필드’사의 돼지 사육장에서 유래한 것이라는 주장이 제기되고 있다. 그 주장을 과학적으로 확인하기는 쉽지 않지만, 최근 축산기업의 행태가 신종 바이러스의 출현과 유행에 영향을 끼치고 있는 것만은 부인할 수 없다.

늘 존재하는 바이러스의 위험을 더욱 크게 만드는 요인 중 사회경제적 요인도 빼놓을 수 없다. 대부분의 독감은 발생하더라도 조기에 발견해서 적절히 대처하면 대규모 확산을 예방할 수 있다. 그런데 사회경제적 취약지역에서 독감이 발생하면, 발견도 대처도 제대로 못하게 되어 문제가 커지게 된다. 의료 시스템이 불완전한 나라에서 환자를 조기 발견하기란 힘든 일이고, 환자를 확인하더라도 비싼 약을 사지 못해 제 때에 투여하지 못한다면 제대로 치료되지 못해 바이러스가 확산되기 때문이다. 이번 신종 인플루엔자가 멕시코에서 대유행한 이유는 나프타(NAFTA) 이후 붕괴된 멕시코의 의료 시스템 때문이라는 주장이 제기되고 있는 것도 이 때문이다. 이러한 주장을 하는 이들은 그래서 이번 인플루엔자를 ‘나프타 독감’이라고 불러야 한다고 말한다.

하지만 문제 인식과 해결 노력에 있어 과학에 대한 맹신은 경계해야 할 요소이다. 신종 인플루엔자의 확산 자체가 과학의 불확실성을 웅변하는 것이다. 우리는 우리가 무엇을 모르고 있는지조차 모른다. 우리는 신종 인플루엔자 확산을 통해 과학의 불확실성에 대해 깨달아야 하고, 우리가 안전 대책을 충분히 세우고 있는 것처럼 과장해서는 안 된다. 신종 인플루엔자로 인한 위험이 얼마나 커질 것인지, 향후 또다시 이보다 더 큰 위험이 도래할 것인지 등에 대해 ‘확실히’ 예측할 수 있는 이들은 아무도 없다. 위험을 과소평가하고 과학기술에 의한 안전을 맹신할 때 자연은 인간의 예측을 넘는다. 우리가 막아야 할 것은 자연 자체가 아니라 인간으로 인한 문제들이다.

이윤추구보다는 근본적 해결이 필요

신종 인플루엔자 문제는 단순히 생물학적 바이러스의 위험에 국한된 것이 아니다. 바이러스의 위험을 더욱 극단적으로 만드는 것은 축산기업, 제약기업, 그리고 그러한 기업에 친화적인 선진국 정부와 국제기구 등의 권력 관계이다. 그러므로 이 문제의 해결 방식이 오히려 문제의 원인을 제공한 거대 축산기업이나 제약기업에 게 도움이 되는 방식이어서는 곤란하다.

그런 측면에서 백신과 약품에 의존하는 방식보다는 적절한 감시 체계, 신속한 대응 체계 등 하부 구조를 마련하는데 우선순위를 두어야 한다. 그리고 백신과 약품은 강제실시나 복제품 생산 등을 통해 저렴하게 공급되어야 하고, 이를 국가가 관할하여 이윤이 발생하지 않도록 해야 한다. 또한 위험에 대한 과다한 공포로 그 효과조차 입증되지 않은 예방 및 관리 대책을 마련하면서 개인의 권리를 제약하거나 침해하지 않도록 주의하여야 한다. 문제의 근본적 해결을 위해서는 자본의 탐욕에 족쇄를 채우고 국제사회 및 일국적 차원에서 불균등하게 분포되어 있는 권력 관계를 바꾸어야 함은 물론이다.

이상윤(건강과대안 상임연구원) / 5월20일자 인권오름 및 5월21일자 프레시안

모든 역병에 대해 그렇듯이 이번 신종 인플루엔자에 대해서도 음모론이 떠돈다. 그중 한가지는 인도네시아 보건장관의 음모론이다. 수파리 보건장관은 “이번 인플루엔자 바이러스가 선진국에서 인위적으로 만들어졌을 수 있다”고 말했다고 한다. 이 보건장관은 조류독감이 문제가 되었을 때도 “선진국들이 제약회사의 이익을 위해 바이러스를 만들어 퍼뜨렸을 가능성이 있다”고 주장한 바 있다. 인도네시아는 “선진국이 빈국으로부터 바이러스 균주를 받아 백신을 개발하고 이를 비싸게 되파는 것은 공정하지 않다”며 2006년부터 조류독감 균주를 세계보건기구에 제공하는 것을 거부하기도 했다.

인도네시아 보건장관의 음모론을 지지하려는 것은 아니다. 그러나 사스부터 조류독감, 이번의 북미독감 또는 신종 A형 인플루엔자(이하 IA)까지 계속 신종 바이러스 질환이 문제가 되고 있지만 세계보건기구가 권고하는 대비책은 전혀 효과적이지 못하다. 백신을 준비하고 항바이러스치료제를 구입하라고 하지만 대다수의 나라들은 그럴 기술도 돈도 없다. 정작 필요한 지역보건의료체계는 가난한 나라에서는 붕괴돼 있다. 그리고 그 치료제와 백신은 대기업들이 특허를 가지고 있어 엄청난 이익을 올린다.

이번의 IA 사태에서도 가장 이익을 보고 있는 것은 타미플루와 리렌자의 독점판매회사들인 로슈와 글라소스미스클라인(GSK)이다. 이들은 조류독감 등으로 이미 천문학적인 이익을 올렸다. 타미플루를 좀더 자세히 살펴보면 타미플루의 특허는 길리어드가 가지고 있고 로슈가 가진 것은 그 판매권이다. 2005년부터 3년 동안 로슈가 길리어드에 지불한 로열티만 11조 원이 넘는다. 그런데 길리어드의 전임 대표이사는 바로 미 국방부장관을 지낸 럼스펠드다. 그는 국방부장관 재임 때도 길리어드의 지분을 포기하지 않았으며 바로 그가 전 세계 미군에게 타미플루를 일괄지급하라고 명령한 장본인이었다. 여기에 조류독감 유행과 타미플루 사재기가 어느 정도 끝나서 로슈와 길리어드의 이익이 2008년에 절반 정도로 줄어들자 때마침 IA가 나타나서 또다시 길리어드와 로슈의 주가가 하늘 높은 줄 모르고 치솟는다? 정말로 ‘제약회사 음모론’을 믿고 싶을 정도다.

지금 전 세계는 또다시 타미플루 확보를 위한 ‘전쟁’에 돌입했다. 타미플루의 약값은 천정부지다. 멕시코에서 타미플루 10알에 최근 1백 달러가 넘는다고 한다. 한국 정부도 이번에 8백33억 원의 추경예산으로 타미플루 보유량을 2백50만 명 분 늘리겠다고 발표했다. 그래봤자 최소한 인구의 20퍼센트까지 항바이러스제를 확보하라는 전 세계적 전문가들과 세계보건기구가 권고한 양의 절반밖에 안되고 지금은 살 수도 없다.

로슈ㆍ길리어드ㆍ럼스펠드

그런데 이상한 일이 있다. 똑같은 성분이지만 인도의 시플라라는 제약회사가 생산한 안티플루라는 약은 타미플루보다 훨씬 싸서 지금도 5분의 1 가격이다. WTO 지적재산권협정의 예외로 돼있는 인도에서는 로슈의 특허권이 없기 때문이다. 이 인도제약회사의 약을 사면 되지 않을까? 다른 방법도 있다. 2005년 조류독감 유행 시기에 한국 정부는 이미 국내제약회사들에게 생산능력이 있는지를 물어봤다. 이때 16개 제약회사가 생산능력이 있다고 답했으며 그중 한 회사는 시제품까지 정부에 제출했다. 특허를 하늘처럼 받드는 WTO에서도 인정하고 있는 특허에 대한 정부사용(정부에 의한 강제실시) 제도는 공익적이거나 비상업적 목적인 경우에는 정부가 특허를 일단 사용하고 나중에 로슈나 길리어드에게 일정량(대략 3~4퍼센트)의 로열티만 지불하면 되는 제도다. 정부가 의지만 있으면 당장 한국의 제약회사에 타미플루 복제약 생산을 허가하거나 이게 시간이 걸린다면 인도약을 수입하면 된다.

그러나 한국은 정부에 의한 특허권 강제실시를 특허법 106조에 “전쟁이나 이에 준하는 상황”에만 가능하다고 규정해서 이를 스스로 제한하고 있다. 특허법이 가장 강력하다는 미국에서조차 이렇게 규정하고 있지는 않다. 법은 당장 한국 정부가 뜯어고치면 된다. 이미 중국이 타미플루의 강제실시에 들어갔고 대만도 2005년에 그렇게 했으며 멕시코, 뉴질랜드, 이스라엘이 인도의 복제약 수입을 타진하고 있다는 보도다. 그러나 한국 정부는 그럴 의향이 없다고 한다.

대기업과 선진국 정부들 간의 특허권에 대한 동맹은 타미플루에서만이 아니라 인플루엔자 백신의 특허에도 동일하다. 인플루엔자만이 아니다. 치료약이 있음에도 매년 3백만 명의 에이즈 환자가 죽어야만 하고 결핵과 말라리아로 매년 3백만 명이 죽는다. 에이즈 치료제의 특허를 가진 기업이 바로 로슈와 GSK가 포함된 거대 다국적 제약사들임은 두말할 필요도 없다.

IA의 진정한 원인에 대해서는 이미 여러 논자들이 지적하고 있다. 거대 다국적 식품기업들의 공장식 가축사육방식으로 인한 변종 인플루엔자의 창궐 가능성과 이에 대한 기업과 정부의 무대책이 신종 인플루엔자가 계속해서 발생하는 진정한 원인이다.

여기에 덧붙여야 할 것은 멕시코의 의료제도 붕괴다. 멕시코에서 사망자가 많이 나온 원인은 바로 멕시코의 의료민영화 때문이다. 멕시코 국민 중 우리 나라와 같은 건강보험에 가입돼 있는 사람들은 46퍼센트에 불과하다. 이마저도 본인부담금이 너무 높다. 나머지 50퍼센트는 시설도 약도 제대로 갖추지 못한 보건소만 이용할 수 있다. 오직 4퍼센트에 해당하는 특권층만이 메트라이프나 ING 등의 다국적 민영보험사가 운영하는 의료보험에 가입해 미국이나 멕시코 대기업들이 운영하는 사립병원의 의료혜택을 누린다. 신종 인플루엔자를 북미자유무역협정 즉 나프타(NAFTA) 독감이라고 부르는 것은 멕시코 의료제도가 나프타로 더 악화했다는 의미에서도 올바른 명칭이다.

사람들의 건강과 생명이 거대기업들의 이윤보다 우선시돼야 한다는 것이 촛불의 요구였다. 그러나 오늘날 IA 사태에서 볼 수 있는 것은 지금의 신자유주의적 자본주의 체제는 촛불의 요구와는 거리가 멀다는 것이다. 촛불 1주년인 지금 이명박 정부는 한미, 한EU FTA를 통해 특허를 더욱 강화시키고 또 의료민영화 정책을 계속 추진하겠다고 한다. 진정 무서운 것은 신종 인플루엔자가 아니라 인간의 생명보다 기업의 이윤을 우선시하는 지금의 자본주의 체제이고 이명박 정부다. 따라서 박멸해야 할 것도 신종 인플루엔자만이 아니다.

우석균 (보건의료단체연합 정책실장, 연구공동체 ‘건강과 대안’ 부대표) / 레프트21 5월9일자 기고