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GIVEN the alarming spread of the highly pathogenic avian influenza (HPAI) or `bird flu', caused by the virus H5N1, across the globe and the increasing evidence of the role of migratory birds in its transmission, the outbreak of the disease in India was only a matter of time. On February 18, the Department of Animal Husbandry in the Ministry of Agriculture confirmed the country's first outbreak of bird flu. Molecular diagnostic tests at the High Security Animal Diseases Laboratory (HSADL) in Bhopal had established conclusively that it was H5N1 infection that was the cause of the death of thousands of chickens in the farms of Navapur in Nandurbar district of Maharashtra for over three weeks.
Preliminary investigations at the Regional Disease Diagnostic Laboratory (RDDL), Pune, had indicated the possibility of the outbreak of Newcastle or Ranikhet disease and some crucial time may have been lost in this wrong diagnosis. According to the report presented to the World Health Organisation (WHO) and the World Organisation of Animal Health (OIE), the outbreak is estimated to have begun on January 27.
Even as the locus of the disease appeared to be shifting away from the South-East Asian region, which has witnessed several outbreaks since it first emerged in Hong Kong in 1997, to Europe, Africa and West Asia, the Indian subcontinent, though surrounded by the affected regions, had curiously escaped infection until recently. Last year, a highly pathogenic form of H5N1 affected migratory waterfowl - primarily the bar-headed geese, but gulls and ducks as well - in the Qinghai lake in China. The outbreak occurred in April and by June more than 6,000 birds belonging to various species had died. In 2004, research showed that H5N1 had become progressively more lethal among mammals and could kill wild waterfowl, long considered disease-free. The bar-headed geese and ducks now appear less susceptible to the lethal infection and their migratory route is suspected to be the cause of the spread of H5N1 to newer destinations.
Between July and August 2005, avian influenza outbreaks were reported from Mongolia, Siberia and Kazakhstan. By the end of the year it had reached Turkey, Croatia, Romania, Greece and Ukraine. In January, the infection moved to northern Iraq and in early February Nigeria became the first African nation to witness the outbreak in a large commercial farm. In February alone 13 countries, including India, reported their first cases of H5N1 infection in birds to international agencies.
The migration route of wild waterfowl from Central Asia in the East-Asian-Australasian flight pathway overlaps the areas that have witnessed H5N1 outbreaks. The Central Asian-Indian flight pathway is the one along which bird species from the Qinghai lake migrate southwards to the subcontinent and could well have been the source of the infection detected in India. Scientific studies comparing viruses from different outbreaks in birds have found that viruses from the recently affected countries, all of which lie along bird migratory pathways, are almost identical to viruses detected in dead birds in the Qinghai lake.
According to a research work published in the latest issue of the Proceedings of the National Academy of Sciences (PNAS), United States, the H5N1 virus has been circulating continuously in the poultry of south-eastern China for a decade and has been repeatedly introduced into neighbouring regions such as Vietnam and distant regions such as Indonesia through the establishment of colonies of the N5N1 virus by the movement of both poultry and migratory birds. The Qinghai lake outbreak has been linked to previous outbreaks in Jianxi province, 1,700 km away. The conclusions are based on a detailed genetic analysis of samples from 13,000 migratory birds and 50,000 market poultry in China. Now we also know that the H5N1 strain that has travelled as far as Turkey and Nigeria in January is the same as that found in infected geese in the Qinghai lake.
"The occurrence of the disease in India," said a WHO release after the outbreak, "is part of a recent pattern of rapid geographical spread of the virus in wild and domestic birds." The genetic sequencing of the virus isolates from India will throw light on the role of migratory birds in the Indian outbreak. While it is true that the period is well past the migratory season, migratory birds still seem to be the most plausible cause of the spread, says S.K. Bandopadhyay, Commissioner, Animal Husbandry.
Although the virus has been isolated from the poultry tissue samples and the sequencing has been completed, identification of the genotype and the strain of H5N1 involves application of `gene blasting' techniques against all sequences of known H5N1 strains in a database. The genotype associated with the current rapid spread as well as the earlier spread across South-East Asia is the Z genotype as against the one that affected Japan and Korea and the one that affected Indonesia. A task force set up under the chairmanship of N.K. Ganguly, Director-General of the Indian Council of Medical Research, will conduct investigation into the source of infection.
Outbreaks of HPAI in poultry were considered rare. Only 24 outbreaks of HPAI, barring the current ones, have been recorded worldwide since 1959. Of these 14 occurred in the past decade. The majority, according to WHO, had limited geographical spread, a few remained confined to a single farm or flock, and only one spread internationally. Research done in July 2004 had concluded that H5N1 had found a new ecological niche in poultry but had not yet fully adapted to that host.
Influenza viruses belong to the family of viruses known as Orthomyxoviridae and are classified into three types: A, B and C. Type A is the most common and usually causes the most serious epidemics. Type B outbreaks can also cause epidemics but the infection is milder. Type C has never been implicated in a large epidemic. Type A viruses can infect several animal species, including birds, pigs, horses, seals and whales. Birds are a particularly important species because all known subtypes of type A viruses circulate among wild birds.
According to Robert G. Webster of St. Jude Children's Hospital, Tennessee, U.S., and co-workers, in the natural host, the 16 subtypes of influenza A viruses "coexist in perfect harmony with their hosts". In these natural hosts, the researchers point out, the viruses remain in "evolutionary stasis, showing minimum evolution at the amino acid level over extended periods". However, after transfer to a new type of host, either avian or mammalian, the viruses seem to evolve rapidly. Evidence had suggested that wild waterfowl introduced avian influenza viruses in their low pathogenic forms to poultry but did not carry or directly spread the highly pathogenic form. The current wave of bird flu may indeed be this evolutionary phase where the benign equilibrium between the influenza A viruses and their natural hosts may have changed.
These changes have affected the patterns of virus transmission, the extent of its geographic spread and the effect on poultry. However, since 1997, when the first human infection was documented, they do not seem to have had any discernible impact on the disease in humans as yet.
Till date, while over 150 million domesticated birds have been killed by the virus or culled to stem its spread, the total number of human infections worldwide has been only 170. But the growing number suggests an increased propensity of the virus to infect humans.
Also, given the present mortality rate of 50 per cent among humans (92/170), the pathogenicity appears to be high. If the apparent mortality rate of 15 per cent among poultry is correct, then the H5N1 in the present infection may be a low pathogenic avian influenza (LPAI) virus, Bandopadhyay feels. As the number of reported poultry deaths may not be accurate, a more definitive statement on the pathogenicity of the strain can be made only after an Intravenous Pathogenicity Index Test (IVPI) - in-vivo trials on four-to-eight-week-old chickens - is completed, which would take about three to four weeks, he said.
As regards the pathogenicity of the virus, there is no `rule of thumb' as there is no correlation between a particular genotype and virulence. It depends on the presence of three basic amino acids at the cleavage site of the HA protein. To be able to bind to a host cell, the HA glycoprotein of the virus breaks into two sub-units, HA1 and HA2, in the presence of a certain enzyme. Now for an LPAI virus, HA should have only one amino acid at the cleavage site, which enables binding with cells of only tissues of respiratory and intestinal tracts. If there are more amino acids at the cleavage site, the virulence of the virus is high as it can cause multi-organ damage.
As regards human infection, tests have been carried out on samples from 95 quarantined persons, both at the National Institute of Virology (NIV) and at the National Institute for Communicable Diseases (NICD), Delhi. Of these 12 are reported to have upper respiratory tract infection (URTI). The others have been handling diseased chickens in various farms.
One of the samples has shown equivocal evidence of the presence of the virus when tested at the NICD with the highly sensitive Real-Time Reverse Transcriptase Polymerase Chain Reaction (RT-PCR). The same is yet to be tested at the NIV before a conclusive statement can be made. With no human deaths reported, the virus strain is certainly lowly pathogenic in humans.
There is, however, globally no evidence of human-to-human transmission of the disease yet. But as the virus evolves and there is mixing of human and virus genes, the probability of a mutation causing person-to-person transmission increases.
A highly pathogenic mutant with transmission among humans will have a global pandemic potential. While migratory birds may be implicated for the geographic spread of H5N1, only eradication and biosecurity measures can prevent the inevitable. Early detection and aggressive control measures allowed Japan, South Korea and Malaysia to eradicate the virus soon after its introduction into those countries' poultry.
In other countries of Asia, however, delayed detection and response has resulted in the entrenchment of the virus. Indian authorities may have responded well but there may have been a crucial delay in detection.
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