The Topic of This Month Vol. 31, No. 9 (No. 367)

2009/10 influenza season, Japan
(IASR 31: 248-250, September 2010)

The 2009/10 season, from week 36 of 2009 (September) to week 34 of 2010 (August), experienced an epidemic whose pattern was entirely different from the average year on account of the pandemic (H1N1) 2009 caused by influenza A(H1N1)pdm (abbreviated as AH1pdm below) virus which was first isolated in May 2009 in Japan (see p. 250 of this issue).

Incidence of Influenza: Under the National Epidemiological Surveillance of Infectious Diseases (NESID), 5,000 influenza sentinels (3,000 pediatric and 2,000 internal medicine clinics) weekly report clinically diagnosed influenza cases.  Weekly cases per sentinel on the nationwide level reached over 1.0, an indicator of the start of the influenza epidemic, in week 33 of 2009, and the epidemic lasted as long as for 29 weeks till week 8 of 2010.  The epidemic peak was in week 48 of 2009 (39.7 cases/sentinel), which was 2-3 months earlier than the average year; the familiar epidemic peak in January-February was absent in 2010 (Fig. 1, upper panel and

The peak incidence of this season was the second highest in the past 10 seasons following the 2004/05 season.  However, as the epidemic lasted long, the cumulative number of cases per sentinel (411.66) of this season (from week 36 of 2009 to week 34 of 2010) far exceeded that of the 2004/05 season (320.38), and was the highest since the influenza patient survey started in 1987/88.  The estimated total number of patients who visited medical facilities in Japan including non-sentinel facilities from week 28 of 2009 to week 10 of 2010 was 20,660,000 (95% confidence interval: 20,460,000-20,860,000) (provisional value). 

The epidemic starting from Okinawa in week 31 spread to Tokyo in week 38 and then to Hokkaido, Fukuoka and Aichi in week 40 each attaining the number of patients per sentinel point higher than 10.0.  The epidemic spread to all over Japan from week 41 on (

Influenza encephalopathy is categorized as “acute encephalitis”, a category V infectious disease that requires report of all the cases.  The number of influenza encephalopathy reported from week 28 of 2009 to week 3 of 2010 was total 285 (AH1pdm, 240 cases; type A, subtype unknown, 38 cases; type B, 1 case; type unknown, 6 cases)  (as of January 27, 2010). 

Isolation/detection of influenza virus: Total 12,295 influenza viruses were isolated by the prefectural and municipal public health institutes in 2009/10 season (as of August 24, 2010, Table 1).  In addition, there were 9,894 cases that were detected by PCR alone.  Among the total 22,189 isolated/PCR-detected viruses, 12,435 were derived from influenza sentinels and 9,754 from elsewhere (Table 2).

Ninety-eight percent of influenza virus detected in 2009/10 season was AH1pdm.  The seasonal AH1 that prevailed till 2008/09 season was not detected at all after week 36 of 2009, and AH3 and type B influenza viruses very rarely (Fig. 2).  From people who came back from abroad, detected were AH1pdm (38 cases), AH3 (11 cases), and type B (1 case) (In 2008/09 season, reported were 770 AH1pdm, 40 AH1, 177 AH3 and 3 type B cases, Table 2).  Among AH1pdm strains analyzed in 2009/10, 1.0% had oseltamivir resistance associated with H275Y mutation (see p. 253 of this issue and

AH1pdm first isolated in week 19 of 2009 was continuously reported at a rate exceeding 500 cases/week from week 28 of 2009 and the reporting started to decline in week 4 of 2010 (Fig. 1).  Isolation/detection of AH1pdm from the influenza sentinel clinics started to increase from week 32, attained its peak in week 44 and then gradually declined (Fig. 1, upper panel).  AH3 was reported every week till week 41 of 2009, but then disappeared for 16 weeks until week 8 of 2010 when it started to be reported in small numbers.  The report of type B was almost absent after week 29 of 2009, but, from week 2 of 2010, its Victoria lineage started to reappear (Fig. 3).  Outbreaks of AH1pdm, B and AH3 occurred in May to August of 2010, when number of patients declined (IASR 31: 172-173 and 235-236, 2010 and p. 264 of this issue).

AH1pdm was most frequently isolated from 15-19 year olds in 2008/09 season and from 5-9 year olds in 2009/10 season (Fig. 4 & Fig. 5).  Populations most infected by AH3 and type B were 0-4 olds and 5-9 olds, respectively.

Antigenic characteristics of 2009/10 isolates: AH1pdm isolates were all similar to A/California/7/2009pdm (2009/10 vaccine strain) in their antigenicity (see p. 253 of this issue).  Most AH3 isolates resembled A/Perth/16/2009, which was antigenically different from the 2008/09-2009/10 vaccine strain A/Uruguay/716/2007.  The main type B isolates were of Victoria-lineage and resembled B/Brisbane/60/2008 (2009/10 vaccine strain).  Isolates of B/Yamagata-lineage were resembled B/Bangladesh/3333/2007 which was a B/Florida/4/2006 (2008/09 vaccine strain)-like strain and belonged to a different HA group.

Immunological status of Japanese population against AH1pdm: According to the data of National Epidemiological Surveillance of Vaccine-Preventable Diseases that was obtained with serum samples collected from July to September in 2009, frequency of anti-A/California/7/2009pdm HI antibody positives (titer higher than 1:40) was highest among population older than 85 years (40%); probably, this group had antibody already before the pandemic (H1N1) 2009.  Among the population below the age of 84, the antibody-positive population was highest in age group 15-19, which was most affected in the early stage of the epidemic (21% in contrast to 1-3% among those under 14 years of age). The population having HI antibody titer higher than 1:40 (i.e., infected population) among the population under 30 years of age was estimated to be about 3,000,000, which largely exceeded the estimated number of patients that visited clinics (about 1,800,000) during weeks 28-40 (see p. 260 of this issue).

Vaccination in 2009/10 season: The quantity of seasonal vaccine produced in 2009/10 season was for 23,130,000 persons (2 doses/person), and the quantity of vaccine used was for 20,390,000 persons.  The vaccination coverage of the elderly (older than 65 years) in compliance with the Preventive Vaccination Law was 50% (56% in 2008/09 season).  The pandemic vaccine was estimatedly administered until June 2010 to 18,000,000 persons focusing on immunization-privileged groups.

Vaccine strains selected for 2010/11 season: Vaccine strains selected for AH1, AH3 and B were, respectively, A/California/7/2009pdm derived from AH1pdm (replacing seasonal AH1), A/Victoria/210/2009, and B/Brisbane/60/2008 belonging to the Victoria lineage (same as for 2009/10) (see p. 262 of this issue).  For 2010/11 season, the above three strains are used to produce a trivalent vaccine replacing the trivalent seasonal vaccine and the monovalent AH1pdm vaccine produced separately in 2009/10 season.  Immunization of the 2010/11 season will start in October 2010.

Conclusion: The incident of the pandemic (H1N1) 2009 in 2009/10 reminded us again the importance of patient and pathogen surveillances in grasping epidemic profiles (see p. 251 of this issue).  For both seasonal and pandemic influenza, it is important to follow the occurrence of influenza patients through sentinel surveillance, outbreak surveillance and severe-case surveillance.  Virus isolation should be conducted throughout the year for monitoring of possible antigenic, genomic and drug-sensitivity changes and for collection of appropriate vaccine candidate strains.

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