Diarrhoea up till now is still a major problem in Southeast Asia with high morbidity and mortality, particularly among children under 5 years of age, with the peak in children between 6 - 24 months. In Indonesia, in 1981, it was estimated that there are 60 million episodes with 300,000 - 500,000 deaths. In the Philippines, diarrhoea ranks as a second cause of morbidity (600 per 100,000 in 1974) and second cause of infant mortality (5 per 1,000 in 1974). In Thailand, in 1980, the morbidity rate was 524 per 100,000 and the mortality rate 14 per 100,000. In Malaysia, in 1976, diarrhoea was still ranking number 5 (3.1%) as a cause of total admission and number 9 (2.2%) as a cause of total deaths. In Singapore, diarrhoea still ranks number 3 as a cause of deaths (4% of total deaths). In Bangladesh, the overall attack rates imply a prevalence of 2.0% for the entire population, with the highest for under 5 groups i.e. 4.1%. The diarrhoea episode in rural population is 85.4%, 39% of them are children under 5. The most common enteropathogens found in all countries are rotavirus followed by Enterotoxigenic E. coli, Vibrio spp., Salmonella spp., Shigella spp. and Campylobacter. Malnutrition and decline of giving breast-feeding play an important role in causing high morbidity, besides socio-economic, socio-cultural and poor environmental sanitation.
Reassortant influenza A viruses bearing the H1 subtype of hemagglutinin (HA) and the N2 subtype of neuraminidase (NA) were isolated from humans in the United States, Canada, Singapore, Malaysia, India, Oman, Egypt, and several countries in Europe during the 2001-2002 influenza season. The HAs of these H1N2 viruses were similar to that of the A/New Caledonia/20/99(H1N1) vaccine strain both antigenically and genetically, and the NAs were antigenically and genetically related to those of recent human H3N2 reference strains, such as A/Moscow/10/99(H3N2). All 6 internal genes of the H1N2 reassortants examined originated from an H3N2 virus. This article documents the first widespread circulation of H1N2 reassortants on 4 continents. The current influenza vaccine is expected to provide good protection against H1N2 viruses, because it contains the A/New Caledonia/20/99(H1N1) and A/Moscow/10/99(H3N2)-like viruses, which have H1 and N2 antigens that are similar to those of recent H1N2 viruses.
Tropical Africa is not the only area where deadly viruses have recently emerged. In South-East Asia severe epidemics of dengue hemorrhagic fever started in 1954 and flu pandemics have originated from China such as the Asian flu (H2N2) in 1957, the Hong-Kong flu (H3N2) in 1968, and the Russian flu (H1N1) in 1977. However, it is especially during the last ten years that very dangerous viruses for mankind have repeatedly developed in Asia, with the occurrence of Alkhurma hemorrhagic fever in Saudi Arabia (1995), avian flu (H5N1) in Hong-Kong (1997), Nipah virus encephalitis in Malaysia (1998,) and, above all, the SARS pandemic fever from Southern China (2002). The evolution of these viral diseases was probably not directly affected by climate change. In fact, their emergential success may be better explained by the development of large industry poultry flocks increasing the risks of epizootics, dietary habits, economic and demographic constraints, and negligence in the surveillance and reporting of the first cases.
An influenza C virus was isolated from a Japanese traveler who had visited Malaysia in April 1999. Phylogenetic analysis indicated that the genome composition of this virus was distinct from that of any other strain isolated in Japan. The possibility that a genetically unique influenza C virus was introduced into Japan by a traveler is shown.
In the months of July and August 2003, an outbreak of acute respiratory illness caused by influenza A virus occurred among students in seven residential schools situated in the northern part (Perak) of Peninsular Malaysia. Out of 4989 students, aged 13 to 18 years (mean = 15.9), 1419 (28%) were effected by influenza-like illness. All patients were treated as outpatients except for 36 students who required admission for high fever, severe coughing and shortness of breath. Abnormal chest X-ray findings were noted for those that required inpatient management. Influenza A virus was isolated from 37 sputum specimens, 20 throat swabs and three nasal swab specimens from a total of 278 clinical samples obtained from 180 patients. Isolates from each of the outbreaks were sent to WHO Collaborating Centre for Reference and Research on Influenza, Melbourne, Australia for antigenic and genetic analysis. One school outbreak was due to influenza A (H1N1), A/New Caledonia/20/99-like virus while the other six school outbreaks were due to influenza A (H3N2) viruses which were A/Fujian/411/2002-like).
Currently circulating influenza B viruses can be divided into two antigenically and genetically distinct lineages referred to by their respective prototype strains, B/Yamagata/16/88 and B/Victoria/2/87, based on amino acid differences in the hemagglutinin surface glycoprotein. During May and July 2005, clinical specimens from two early season influenza B outbreaks in Arizona and southeastern Nepal were subjected to antigenic (hemagglutinin inhibition) and nucleotide sequence analysis of hemagglutinin (HA1), neuraminidase (NA), and NB genes. All isolates exhibited little reactivity with the B/Shanghai/361/2002 (B/Yamagata-like) vaccine strain and significantly reduced reactivity with the previous 2003/04 B/Hong Kong/330/2001 (B/Victoria-like) vaccine strain. The majority of isolates were antigenically similar to B/Hawaii/33/2004, a B/Victoria-like reference strain. Sequence analysis indicated that 33 of 34 isolates contained B/Victoria-like HA and B/Yamagata-like NA and NB proteins. Thus, these outbreak isolates are both antigenically and genetically distinct from the current Northern Hemisphere vaccine virus strain as well as the previous 2003-04 B/Hong Kong/330/2001 (B/Victoria lineage) vaccine virus strain but are genetically similar to B/Malaysia/2506/2004, the vaccine strain proposed for the coming seasons in the Northern and Southern Hemispheres. Since these influenza B outbreaks occurred in two very distant geographical locations, these viruses may continue to circulate during the 2006 season, underscoring the importance of rapid molecular monitoring of HA, NA and NB for drift and reassortment.
The development of highly pathogenic avian H5N1 influenza viruses in poultry in Eurasia accompanied with the increase in human infection in 2006 suggests that the virus has not been effectively contained and that the pandemic threat persists. Updated virological and epidemiological findings from our market surveillance in southern China demonstrate that H5N1 influenza viruses continued to be panzootic in different types of poultry. Genetic and antigenic analyses revealed the emergence and predominance of a previously uncharacterized H5N1 virus sublineage (Fujian-like) in poultry since late 2005. Viruses from this sublineage gradually replaced those multiple regional distinct sublineages and caused recent human infection in China. These viruses have already transmitted to Hong Kong, Laos, Malaysia, and Thailand, resulting in a new transmission and outbreak wave in Southeast Asia. Serological studies suggest that H5N1 seroconversion in market poultry is low and that vaccination may have facilitated the selection of the Fujian-like sublineage. The predominance of this virus over a large geographical region within a short period directly challenges current disease control measures.
ESWI recommends that the 25 European Union nations strive to vaccinate one-third of their collective population every year by 2010. This translates into an annual vaccine usage of 150 million doses for a population of 455 million. However, the current vaccine usage in Europe is 79 million doses, meaning that only 40% of ESWI's recommended target population is being vaccinated in the EU-25. Indeed, the EU's current risk groups equal about 28% of its population, but it is estimated that less than 62% are being vaccinated with the current vaccine supply--the equivalent of 17% of the total population. Clearly, as ESWI noted in its concluding position paper at the Malta conference, "a large proportion of those traditionally assumed to be at most risk from influenza are not being vaccinated." How to change this and minimize the consequences of a pandemic? "It's very interesting how the arithmetic works, given the goal of immunizing 75 percent of Europe's high-risk group, " said Dr K.Nichol of the University of Minnesota Medical Center who chaired the session. "If you go from a trivalent vaccine to a monovalent one, then you triple the number of doses you can manufacture. Thus, you could produce enough doses for the entire population of the EU." However, there is no coordinated approach in Europe, meaning such an optimistic scenario is unlikely in the medium-term. For the time being, emphasis must be on raising public awareness and raising vaccination rates at the local level, starting with health care workers themselves. Here the role and attitude of health policy officials and--critically--health care workers are crucial. These front-line policy and healthcare professionals constitute both the problem and the solution to a more effective influenza vaccine effort in Europe: they know first-hand the institutional obstacles blocking progress--i.e., lack of resources, poorly focused public information campaigns, etc.--but their own work practices and attitudes can be misdirected, too. To identify the issues and help the participants produce a set of recommendations, ESWI brought in Penny Lawson from to facilitate Dr.K. Nichol to steer this session's workshop debate. The participants were a diverse group of 35 health care workers from Australia, Finland, France, Germany, Malaysia, Malta, Netherlands, Norway, Poland, Portugal, Spain, Sweden and the UK.
The aims of the study were to determine the attack rate of influenza-like illness among inhabitants of five old folk homes nationwide using influenza vaccine as a probe and the effectiveness of influenza vaccination in prevention of influenza-like illness. We conducted a nonrandomized, single-blind placebo control study from June 2003 to February 2004. VAXIGRIP(R) 2003 Southern hemisphere formulation was used. Among 527 subjects, the attack rates of influenza-like illness in the influenza vaccine group were 6.4, 4.6 and 2.4% during the first, second and third 2-month periods, respectively. The attack rates of influenza-like illness in the placebo group were 17.7, 13.8 and 10.1%. Influenza vaccination reduced the risk of contracting influenza-like illness by between 14, and 45%. The vaccine effectiveness in reducing the occurrence of influenza-like illness ranged from 55 to 76%, during the 6-month study followup. The presence of cerebrovascular diseases significantly increased the risk of influenza-like illness (p < 0.005). Vaccine recipients had fewer episodes of fever, cough, muscle aches, runny nose (p < 0.001) and experience fewer sick days due to respiratory illness. Subjects who received influenza vaccination had clinically and statistically significant reductions in the attack rate of influenza-like illness. Our data support influenza vaccination of persons with chronic diseases and >50 year olds living in institutions.
The influenza epidemic of 2006/'07 began late in the season, like the two previous influenza epidemics. In week 8 a peak of modest height was reached. As usual, the causal strains were mainly A/H3N2 viruses and to a lesser extent A/H1N1 and B viruses. A new A/H1N1 virus variant has emerged, an event that on average takes place only every 10 years. However, almost all A/H1N1 virus isolates belonged to the old variant and were similar to the vaccine virus. The A/H3N2 virus isolates appeared to deviate from the vaccine strain, but after antigenic cartographic analysis and correction for low avidity they proved also closely related to the vaccine strain. The few type B virus isolates belonged to the B/Yamagata/16/88 lineage, whereas the used B vaccine virus had been chosen from the B/Victoria/2/87 lineage. The vaccine therefore will have provided almost optimal protection against the circulating influenza A/H1N1 and A/H3N2 viruses but not against the influenza B viruses. For the 2007/'08 influenza season the World Health Organization has recommended the following vaccine composition: A/Solomon Islands/3/06 (H1N1) (new), A/Wisconsin/67/05 (H3N2), and B/Malaysia/2506/04.
Determining the local circulating strain of influenza is essential to prevent and control epidemics. In the years 2004 and 2005, the National Influenza Center of Thailand received 3,854 and 3,834 specimens, respectively, from patients throughout the country, including submissions from 4 established influenza surveillance sentinel sites. In 2004, of 539 influenza-positive specimens, 461 were positive for influenza A and 78 were positive for influenza B by isolation. Influenza A subtyping revealed that 249, 197, and 15 isolates were H1N1, H3N2, and H5N1, respectively. In 2005, of 748 influenza-positive specimens, 492 were influenza A and the remaining 256 were influenza B. The results of influenza A subtyping indicated that 55, 437, and 5 isolates were H1N1, H3N2, and H5N1. All isolated strains of subtype H1N1 were A/New Caledonia/20/99-like. The isolated strains of H3N2 were A/Fujian/411/2002-like in the first half of the year 2004, while those in the latter half of 2004 gradually drifted to a mixture of A/Wellington/1/2004-like, A/California/7/2004-like, and A/Wisconsin/67/2005-like, and this mixture continued through the end of 2005. The influenza B strains were B/Sichuan/379/99-like, B/Hong Kong/330/2001-like, B/Shanghai/361/2002-like and B/Malaysia/2506/2004-like. The strains circulating in the years 2004 and 2005 were antigenically similar to the vaccine formulas recommended in the same period by WHO. Our results underscore that local influenza surveillance plays an important role in responding to epidemics and potential pandemics.