WHO slow to respond, says top Mexican medic

MEXICO’S chief epidemiologist accused the World Health Organisation of being slow to respond to the country’s warning about a health crisis that turned into a global swine flu scare and called for an investigation.

WHO slow to respond, says top Mexican medic

Dr Miguel Angel Lezana said his centre alerted the Pan American Health Organisation on April 16 about alarming occurrences of flu and atypical pneumonia in Mexico. But no action was taken until eight days later when the WHO said it was “very, very concerned” the outbreak could grow into a pandemic.

“It seems it should have been more immediate,” said Dr Lezana, director of the National Epidemiology Centre.

WHO officials said yesterday the health body had been informed on about April 9 of unusual cases of “suspicious influenza” from Mexico that had begun in late March, but that US and Canadian laboratories identified the virus on April 24, when the organisation responded rapidly.

In Mexico, new cases and the death rate were levelling off, the country’s top medical officer said.

Health authorities said they have confirmed 300 swine flu cases and 12 deaths due to the virus.

“The fact that we have a stabilisation in the daily numbers, even a drop, makes us optimistic,” Mexican health secretary Jose Angel Cordova said. “Because what we’d expect is geometric or exponential growth. And that hasn’t been the situation.”

But as Mexico shut down non-essential government and private business yesterday to begin a five-day break aimed at further slowing the spread of the virus, the country’s epidemiology chief faulted WHO and its regional branch, PAHO, for not stepping in earlier.

Dr Lezana said that after a rash of flu and pneumonia cases emerged in Mexico in April, his department was so alarmed that it notified by email the local office of PAHO, as called for by international protocols.

“The procedure is very clearly established,” Dr Lezana said. “You have to notify the local office, then it sends the notification to the regional office. They analyse the data and decide whether to send it to the WHO in Geneva.”

But four days later, PAHO still had not responded, so the National Epidemiology Centre again contacted the local PAHO office and asked for an explanation and whether more information was needed, Dr Lezana said.

PAHO responded that the alert was being handled, he said. But Dr Lezana said that as far as he knew, the PAHO regional office in Washington and WHO took no action until April 24, when WHO announced an epidemic was under way.

Dr Lezana had learned just the day before, from a testing of a sample that Mexico sent to a lab in Canada, that people were coming down with a new, mutated and lethal swine flu virus. By then, more than 1,000 people had been sickened in Mexico.

PAHO spokesman Daniel Epstein confirmed to The Washington Post that the agency got a message from Mexican authorities on April 16 about an unusual disease outbreak.

Mr Epstein told the newspaper that it was impossible for authorities in Geneva not to have learned of the unusual outbreak at the same time, describing a system that sends messages through to WHO headquarters automatically.

WHO officials in Geneva confirmed the organisation had received reports from Mexico of cases of suspicious influenza and that the organisation reacted quickly when the new flu virus was identified on April 24.

“Once we knew that this illness was caused by a new influenza virus ... we moved into operation within a matter of hours,” WHO spokesman Thomas Abraham told reporters. HERE are some questions and answers about the science of swine flu, the H1N1 virus that’s sweeping the world:

What exactly is a virus?

It’s a tiny packet of only eight genes wrapped in a cloak of proteins, much smaller than a bacterium. Unlike bacteria, a virus is only half alive. It can’t eat or reproduce on its own, but must take over the genetic machinery of a living cell. Most viruses are harmless; some are useful, but others, such as the flu virus, can be deadly.

What makes this swine flu virus special?

It’s a novel combination of bird, pig and human viral genes which has not been found before, so people have no immunity to it. It’s a descendant of the H1N1 virus that killed tens of millions of people worldwide in 1918-1919, mixed in with recent strains of swine and bird flu viruses. The 1918 virus originated in birds and then jumped to humans. The new virus apparently jumped from a pig to a five-year-old boy in Mexico, who passed it to other humans.

What does H1N1 stand for?

It’s the initials of two sugar proteins (their scientific names are hemagglutinin and neuramidinase) that sit on the surface of the virus and do its dirty work. There are 16 types of the H protein, numbered H1 through H16, and 9 types of the N protein, numbered N1 through N9. That makes 144 possible combinations of the virus, a constantly changing challenge for prevention or treatment. A new combination, H2N2, caused a brief swine flu epidemic in 1957. An H3N2 strain was the source of another epidemic in 1968. The bird flu virus that started spreading from south-east Asia a decade ago is an H5N1 combination.

How does the H protein work?

The H protein looks like a little spike that fits into a notch, called a receptor, on the outside of an animal or human cell and lets the virus enter. Once inside, the virus hijacks the DNA in the cell’s nucleus and uses it to make copies of itself.

What does the N protein do?

After infection, it opens a passage in the cell wall and releases the new baby viruses, which can now invade other cells. Without the N protein, infection would be limited to the first cell, rarely enough to cause disease.

How do medicines such as Tamiflu and Relenza work?

They block the action of the N protein so the virus can’t spread. They’re not vaccines to prevent an infection, but drugs to limit its impact. They should be taken as soon as possible since the virus reproduces most rapidly between 24 and 72 hours after illness begins.

How does a new virus develop?

When the genes that govern the H and N proteins reproduce, random changes – mutations – can occur in their DNA. The changes gradually accumulate, ultimately producing a virus that may be more lethal or may penetrate a target cell more easily. Another possibility is gene-swapping. This can happen when a cell is infected by viruses from different creatures, say a chicken and a pig. The cell becomes a “mixing bowl”, whipping up a new virus. In the new strain of H1N1, pieces of human, bird and pig genes are all scrambled up.

How does this H1N1 virus differ from the H1N1 that caused the Spanish flu pandemic in 1918-1919?

That virus developed various changes over the years. So far, H1N1 is not as virulent as the previous strain, but that could change. The earlier pandemic began mildly in 1918, but returned in a devastating wave six months later. Experts fear that could happen again. Hence they are rushing to develop a vaccine by the autumn.

How does one person catch H1N1 from others?

The virus can be transmitted through the air – by a cough or a sneeze – or by a handshake or by touching an infected surface, such as a doorknob.

Why does this disease seem to be more deadly in Mexico than in the US or other countries?

That may be an illusion. The first US death has now occurred in Texas and more fatalities are expected.

Why does H1N1 seem to attack healthy young adults more than sick and elderly people?

Young adults have a healthy immune system that launches a massive counterattack of antibodies against the flu virus. Unfortunately, the counterattack can cause an overwhelming inflammation that damages other organs, such as the lungs. Elderly people with weaker immune systems are less likely to suffer from such harmful inflammation.

Compiled by Robert S Boyd

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