Posted on 06/24/2009 8:04:24 AM PDT by metmom
Within minutes, six-year-old Rubjit Thindal went from happily chatting in the back seat of the car to collapsing and dying in her father's arms.
"If we had known it was so serious, we would have called 911,'' Kuldip Thindal, Rubjit's distraught mother, said in Punjabi yesterday. "She just had a stomach ache -- she wasn't even crying.''
Rubjit was pronounced dead at hospital barely 24 hours after showing signs of a fever. Later, doctors told her parents she had the H1N1 influenza virus. She is believed to be the youngest person in Canada with the virus to have died.
(Excerpt) Read more at news.guelphmercury.com ...
Did you read post 300 yet ?
UK:
GP suffering from swine flu dies
Page last updated at 13:48 GMT, Monday, 13 July 2009 14:48 UK
http://news.bbc.co.uk/2/hi/uk_news/8148162.stm
A Bedfordshire GP who died had the swine flu virus, according to NHS East of England.
Dr Michael Day died on Saturday in the Luton and Dunstable Hospital, but the NHS said the exact cause of death in the case is still unknown.
A swab test taken from Dr Day at the hospital has been confirmed as being positive for the H1N1 swine flu virus.
A six-year-old girl, Chloe Buckley, from north west London died on Thursday after contracting swine flu.
New flu resembles feared 1918 virus, study finds
http://www.reuters.com/article/marketsNews/idUSN1316618720090713
Jul 13, 2009
By Maggie Fox
WASHINGTON, July 13 (Reuters) - The new H1N1 influenza virus bears a disturbing resemblance to the virus strain that caused the 1918 flu pandemic, with a greater ability to infect the lungs than common seasonal flu viruses, researchers reported on Monday.
Tests in several animals confirmed other studies that have shown the new swine flu strain can spread beyond the upper respiratory tract to go deep into the lungs — making it more likely to cause pneumonia, the international team said.
Some good informative sites On H1N1
Here is a site with an interesting interactive map with the latest h1n1 articles.
http://outbreaks.globalincidentmap.com/home.php
Attached Images outbreaks.jpg (63.9 KB, 42 views)
Great Site A+
Pandemic Alert
from you can find news reports , numbers , etc.. found here very intersting website .
Just click to get on the main forum
http://www.singtomeohmuse.com/viewtopic.php?t=3232&postdays=0&postorder=asc&start=705
Another Good Site
Link where article came from
Another Great Site Just Go the the last page of the thread
Here ia a link to another site with good info on the flu
Comprehensive Flu Thread, Latest reports, States, Countries, Closings.
http://www.timebomb2000.com/vb/showthread.php?t=330395&page=59
Yes.
I am no expert, neither do I play one on TV but from everything I have read about the 1918 influenza, and what is happening with H1N1, I suspected we were in for another 1918 like event. What you posted confirms my concerns, this is as I feared and VERY FRIGHTENING! Lord willing the powers that be will be able to come up with medicines and vacines in time to prevent another potential loss of 100 MILLION lives.
UW study of swine flu virus finds it more virulent than regular flu
By Mark Johnson of the Journal Sentinel
Posted: July 13, 2009
http://www.jsonline.com/features/health/50634332.html
An international team of scientists led by a University of Wisconsin-Madison virologist has produced a highly detailed portrait of the new swine flu virus that has killed 211 people in the U.S., suggesting it is more virulent than previously thought and contradicting assertions that the virus appears similar to seasonal flu.
What makes the new H1N1 virus different and more deadly than common seasonal influenza is its ability to infect cells deep in the lungs where it can cause scarring and pneumonia, according to a fast-tracked report Monday in the journal Nature.
The new study sends “a very clear message” that doctors and patients in the U.S. must adopt a new approach to influenza, said UW virologist Yoshihiro Kawaoka, who led the group of more than 50 scientists in Madison and Japan who are studying the H1N1 virus.
“Seeing physicians early and getting anti-viral drugs is not common practice,” Kawaoka said. “That has to be changed.”
The study also found that people exposed to the deadly 1918 influenza appear to have antibodies that neutralize swine flu. This may explain why relatively few elderly people have died in the recent H1N1 outbreak. So far, the virus has killed four people in Wisconsin, including two children.
Kawaoka and his colleagues infected mice, ferrets, pigs and nonhuman primates with the H1N1 virus, using samples of the virus obtained from patients in California, Wisconsin, the Netherlands and Japan. They found that while seasonal flu usually infects only cells in the upper respiratory system - the nose, throat and larynx - swine flu was able to take root and grow in the lungs.
In mice with swine flu, the lungs essentially filled with fluid until they could not take in oxygen and the animals died. Other animals in the study did not die from the swine flu.
“There is a misunderstanding about this virus,” Kawaoka said. “People think this pathogen may be similar to seasonal influenza. This study shows that is not the case.”
“This swine influenza,” he added, “is more (virulent) than seasonal influenza. That is for sure.”
Some skepticism
However, some experts remain unconvinced that the H1N1 virus is substantially more deadly than seasonal flu.
Fall awaited
He said the number of new swine flu cases in Milwaukee has dropped off rapidly in recent weeks, but health officials are concerned about what will happen in the fall, when children return to school.
“It’s either going to start coming back two weeks into school or it won’t, and if it doesn’t, all bets are off,” he said.
Henrickson and others have been studying the flu outbreak in Milwaukee, where more cases have been reported than in many entire states. He said H1N1 is more concentrated than the seasonal influenza.
Many researchers are now studying the genetic evolution of the H1N1 strain. The hope is that learning how the virus evolves will help health care officials plan for it better and produce a more effective vaccine.
Scientists studying the virus in animals are likely to continue searching for specific markers of virulence.
“The 1918 virus had several virulence factors,” Siegel said, “including the ability to destroy the mitochondria of cells,” an ability that H1N1 has yet to demonstrate. The mitochondria generate energy for cells; when they’re destroyed, the cells die.
Thanks DvdMom.
More info with differing views ..
Swine flu’s edge: lesions in lungs
http://www.theage.com.au/world/swine-flus-edge-lesions-in-lungs-20090714-djfx.html
July 14, 2009 - 11:17AM
The way swine flu multiplies in the respiratory system is more severe than ordinary winter flu, a new study in animals finds.
Tests in monkeys, mice and ferrets show that swine flu thrives in greater numbers throughout the respiratory system, including the lungs, and causes lesions, instead of staying in the nose and throat as seasonal flu does.
In addition, blood tests show many people born before the 1918 flu pandemic seem to have immunity to swine flu but not to the seasonal flu that hits every year.
The research by a top University of Wisconsin flu researcher was released on Monday and will be published in the journal Nature.
“I’m very concerned because clearly the (swine flu) virus is different from seasonal influenza,” said study lead author Yoshishiro Kawaoka. “It’s a lot more severe.”
But it is still not as severe as the 1918 influenza, he said.
With only a few months since swine flu was identified, doctors are still trying to get a handle on this flu strain and how it differs from the yearly seasonal flu.
The latest study paints a more pessimistic picture of the flu’s strength and the vulnerability of the elderly than how federal US health officials have been portraying the situation.
Officials at the federal Centres for Disease Control and Prevention said on Monday that swine flu is behaving differently to seasonal flu and they are not comparing its virulence to the run-of-the-mill influenza, which kills about 36,000 Americans a year. The CDC had no immediate comment on the Nature study.
Unlike seasonal flu, the new swine flu is continuing into the northern summer, and has caused severe illness mostly in younger people instead of the elderly, the CDC said.
The CDC’s Dr. Anne Schuchat said late last month that people aged over 65, and maybe people over 50 “are less likely to get ill with this virus even when they’re in a family with somebody who has it.”
A CDC study in May also found that one-third of older people had some immunity to swine flu.
Kawaoka did not find that. He checked blood samples from a wide number of age groups. With two exceptions, he found only people who were born before the 1918 pandemic to have immunity.
W. Paul Glezen, a flu epidemiologist at the Baylor College of Medicine in Houston, Texas, who was not part of the study, said he would tend to agree with the earlier CDC study on immunity, especially since the latest figures show younger people became sicker.
Glezen also agreed with Kawaoka that the swine flu “appears to be more virulent than the seasonal” flu.
For his study, Kawaoka tested three monkeys with swine flu and three with seasonal flu. His data showed at least twice as much virus appeared in all parts of the lungs, the tonsils, windpipe and nose for the swine flu-infected monkey
Swine flu cases expected to spike when school starts
Posted On: Tuesday, Jul. 14 2009
By Rebecca LaFlure
Killeen Daily Herald
http://www.kdhnews.com/news/story.aspx?s=34532
A spike in swine flu cases is likely once school starts in August, local health officials say. Area hospitals have taken steps to contain the virus as they brace for a possible surge in patients.
“I expect that we’ll see a second wave if not in August, definitely in September,” said Shirley Hudley, an infection control prevention nurse at Metroplex Hospital in Killeen.
“I believe that once we hit the second wave, we will see a decline in numbers, but we’re going to see an increase before any of that happens.”
The H1N1 virus has steadily spread across Central Texas. As of last week, 172 confirmed cases have been reported in Bell County, with one resulting in death.
In June, the Killeen Independent School District announced its first confirmed swine flu case, which was at Rancier Middle School.
The possible resurgence of swine flu this fall would come during the start of the regular flu season. Health officials expect to see a combination of both the H1N1 virus and seasonal flu.
Currently, Metroplex Hospital is preparing for an increased demand, Hudley said. The biggest step is to make sure the hospital has the proper supplies to treat and prevent the spread of both swine and seasonal flu.
The symptoms of H1N1 flu are similar to the symptoms of regular seasonal influenza; they include fever, lethargy, lack of appetite and coughing. Some people also have reported a runny nose, sore throat, nausea, vomiting and diarrhea.
“We make sure we have enough supply of the (seasonal) flu vaccine for our employees to start out with, and enough masks and enough hand wash gel to prevent spread, even to our employees,” she said.
The federal government recently allotted $350 million to help the country prepare for the H1N1 flu virus and seasonal flu.
A swine flu vaccine could be available by October, but details are still up in the air.
Danielle Schmitz, executive director of the Central Texas Regional Advisory Council, said so far, swine flu has been about as dangerous as regular seasonal flu and not as severe as originally thought. Just how problematic it will be during the fall is undetermined.
For now, local health officials urge people to take steps to help stop the spread of the virus.
“The biggest part here is: Stay away from people who are sick,” Hudley said.
“People also need to remember to wash their hands frequently with soap and water, use alcohol-based hand sanitizers, and make sure to avoid touching eyes, nose and mouth. If they do, they should wash their hands immediately.”
Also, adopting other healthy habits can help build immunity to the virus. The Centers for Disease Control and Prevention advises people to get plenty of sleep, be physically active, manage stress, drink plenty of fluids and eat nutritious food.
For more information on the swine flu, go to www.bellcountyhealth.org, www.dshs.state.tx.us/swineflu or www.cdc.gov.
1918 Pandenic H1N1 Human/Swine Recombination
Recombinomics Commentary 14:41
July 14, 2009
It has become almost common wisdom that the virus that caused the 1918 flu pandemic was an avian strain introduced into the human population shortly before the pandemic erupted. But a new study disputes that hypothesis, arguing instead that genes of the 1918 virus had circulated in mammalian hosts, most likely pigs and humans, for several years before 1918.
The origins of the 1918 virus, which is estimated to have killed at least 20 million people, are still controversial. After painstakingly piecing together the genome of the extinct strain, a team led by virologist Jeffery Taubenberger, then at the Armed Forces Institute of Pathology in Washington, D.C., concluded in 2005 that the virus most closely resembled viruses of avian origin; the team suggested it had become transmissible between humans after a couple of key changes
The above comments on the recent PNAS paper as well as the Nature paper in 2005 provides some background on the data supporting a human / swine origin of 1918. The sequence of a 1917 avian isolate clearly demonstrated that avian sequences in 1917 were similar to current avian sequences and easily distinguished from mammalian sequences, such as pandemic 1918 H1N1, seasonal H1N1 and swine H1N1.
The Nature paper of 2005 identified 10 polymorphisms which were said to be pandemic -specific because they were in the 1918 pandemic sequence but not avian sequences. However, these markers were simply mammalian markers and were not only in the H1N1 1918 pandemic sequence but also in seasonal H1N1 and swine H1N1. Thus, the markers did not identify changes that created a pandemic strain, but instead provided additional data supporting a human / swine origin of 1918, as had been seen from phylogenetic analysis.
The swine origin is also supported by the recent Nature paper showing that sera from patients alive in 1918 had antibodies that not only saw the 1918 pandemic H1N1 strain, but also the current 2009 pandemic strain which is a swine H1N1. Thus, both the antibody data as well as phylogenetic analysis support a mammalian (human and swine) origin of 1918.
However, detailed analysis of the 8 gene segments of the 1918 virus show that it is a recombinant with alternating blocks of swine and human polymorphisms. In fact approximately 90% of the polymorphisms in each of the eight gene segments can be found in two parental sequences, WSN/33 representing human H1N1 and swine/Iowa/15/1931 representing swine H1N1. Although there are some avian polymorphisms, the vast majority of polymorphisms is mammalian and can in fact be found in two isolates from the early 1930’s.
These data have important implications for the current pandemic strain, because it is a swine H1N1 which can efficiently transmit in humans. It has spread throughout the human population worldwide, and now is in position for further adaptation to human host via recombination with seasonal H1N1, which is well adapted to humans.
There are several obvious candidates in seasonal H1N1 which could significantly impact swine H1N1. One of the 10 markers identified in the 2005 Nature paper was PB2 E627K. This polymorphism is in virtually all influenza A seasonal flu isolates. It allows for most efficient replication at 33 C, which leads to upper respiratory infections and a preference for seasonal spread, when cold temperatures keep the human nose close to the optimal temperature for E627K. In contrast, the avian version, E627, allows for most efficient replication at 41 C, the body temperature of birds. Since the swine H1N PB2 is avian, it has E627, which may lead to less efficient transmission in the winter, but higher transmission in the summer, and associated replication the lower respiratory tract. E627K was reported in one isolate in Shanghai but was only found in the sequences from the original sample as well as the first clone. The second clone had reverted back to E627.
Another potential acquisition from seasonal H1N1 is H274Y. Although this isn’t a mammalian specific polymorphisms, it is present on almost 100% of seasonal H1N1 and has a history of jumping from one genetic background to another. It has been reported in three pandemic swine isolates, including a patient traveling from San Francisco to Hong Kong who had not received oseltamivir, raising concerns of a fit pandemic H1N1 with H274Y. Moreover, this isolate and other related isolates without H274Y also have a receptor binding domain change D225E, which may be important in establishing dominance via genetic hitching. A change at the same position, D225N, was associated with the establishment of H3N2 seasonal flu with adamantane resistance, S31N.
Thus, the movement of swine H1N1 into the human population creates the environment for rapid adaptation to human hosts and the acquisition of key polymorphisms from seasonal H1N1, which could cause significant problems in the upcoming months.
http://www.recombinomics.com/News/07140901/H1N1_1918_Human_Swine.html
1918 Pandenic H1N1 Human/Swine Recombination
Recombinomics Commentary 14:41
July 14, 2009
It has become almost common wisdom that the virus that caused the 1918 flu pandemic was an avian strain introduced into the human population shortly before the pandemic erupted. But a new study disputes that hypothesis, arguing instead that genes of the 1918 virus had circulated in mammalian hosts, most likely pigs and humans, for several years before 1918.
The origins of the 1918 virus, which is estimated to have killed at least 20 million people, are still controversial. After painstakingly piecing together the genome of the extinct strain, a team led by virologist Jeffery Taubenberger, then at the Armed Forces Institute of Pathology in Washington, D.C., concluded in 2005 that the virus most closely resembled viruses of avian origin; the team suggested it had become transmissible between humans after a couple of key changes
The above comments on the recent PNAS paper as well as the Nature paper in 2005 provides some background on the data supporting a human / swine origin of 1918. The sequence of a 1917 avian isolate clearly demonstrated that avian sequences in 1917 were similar to current avian sequences and easily distinguished from mammalian sequences, such as pandemic 1918 H1N1, seasonal H1N1 and swine H1N1.
The Nature paper of 2005 identified 10 polymorphisms which were said to be pandemic -specific because they were in the 1918 pandemic sequence but not avian sequences. However, these markers were simply mammalian markers and were not only in the H1N1 1918 pandemic sequence but also in seasonal H1N1 and swine H1N1. Thus, the markers did not identify changes that created a pandemic strain, but instead provided additional data supporting a human / swine origin of 1918, as had been seen from phylogenetic analysis.
The swine origin is also supported by the recent Nature paper showing that sera from patients alive in 1918 had antibodies that not only saw the 1918 pandemic H1N1 strain, but also the current 2009 pandemic strain which is a swine H1N1. Thus, both the antibody data as well as phylogenetic analysis support a mammalian (human and swine) origin of 1918.
However, detailed analysis of the 8 gene segments of the 1918 virus show that it is a recombinant with alternating blocks of swine and human polymorphisms. In fact approximately 90% of the polymorphisms in each of the eight gene segments can be found in two parental sequences, WSN/33 representing human H1N1 and swine/Iowa/15/1931 representing swine H1N1. Although there are some avian polymorphisms, the vast majority of polymorphisms is mammalian and can in fact be found in two isolates from the early 1930’s.
These data have important implications for the current pandemic strain, because it is a swine H1N1 which can efficiently transmit in humans. It has spread throughout the human population worldwide, and now is in position for further adaptation to human host via recombination with seasonal H1N1, which is well adapted to humans.
There are several obvious candidates in seasonal H1N1 which could significantly impact swine H1N1. One of the 10 markers identified in the 2005 Nature paper was PB2 E627K. This polymorphism is in virtually all influenza A seasonal flu isolates. It allows for most efficient replication at 33 C, which leads to upper respiratory infections and a preference for seasonal spread, when cold temperatures keep the human nose close to the optimal temperature for E627K. In contrast, the avian version, E627, allows for most efficient replication at 41 C, the body temperature of birds. Since the swine H1N PB2 is avian, it has E627, which may lead to less efficient transmission in the winter, but higher transmission in the summer, and associated replication the lower respiratory tract. E627K was reported in one isolate in Shanghai but was only found in the sequences from the original sample as well as the first clone. The second clone had reverted back to E627.
Another potential acquisition from seasonal H1N1 is H274Y. Although this isn’t a mammalian specific polymorphisms, it is present on almost 100% of seasonal H1N1 and has a history of jumping from one genetic background to another. It has been reported in three pandemic swine isolates, including a patient traveling from San Francisco to Hong Kong who had not received oseltamivir, raising concerns of a fit pandemic H1N1 with H274Y. Moreover, this isolate and other related isolates without H274Y also have a receptor binding domain change D225E, which may be important in establishing dominance via genetic hitching. A change at the same position, D225N, was associated with the establishment of H3N2 seasonal flu with adamantane resistance, S31N.
Thus, the movement of swine H1N1 into the human population creates the environment for rapid adaptation to human hosts and the acquisition of key polymorphisms from seasonal H1N1, which could cause significant problems in the upcoming months.
http://www.recombinomics.com/News/07140901/H1N1_1918_Human_Swine.html
Anyone known what kind of flu the Hong Kong flu was?
I wonder if that might not be because older people have generally been urged to get flu shots and many have for years. Could it be that there might be some residual immunity from all those shots, and that those shots may have contained enough similar sections of the virus to impart partial immunity?
Hong Kong flu: A pandemic of influenza A (H3N2) in 1968-69. This virus was first detected in Hong Kong in early 1968 and spread to the United States later that year. where it caused about 34,000 deaths, making it the mildest pandemic in the 20th century. Also known as Hong Kong influenza.
There could be several reasons why fewer people in the US died due to this virus. First, the Hong Kong flu virus was similar in some ways to the Asian flu virus that circulated between 1957 and 1968. Earlier infections by the Asian flu virus might have provided some immunity against the Hong Kong flu virus that may have helped to reduce the severity of illness during the Hong Kong pandemic.
Second, instead of peaking in September or October, like pandemic influenza had in the previous two pandemics, this pandemic did not gain momentum until near the school holidays in December. Since children were at home and did not infect one another at school, the rate of influenza illness among schoolchildren and their families declined.
Third, improved medical care and antibiotics that are more effective for secondary bacterial infections were available for those who became ill.
BUMP!
This article touches on the 1918 immunity
More evidence that the new H1N1 virus is more dangerous than seasonal flu: The new Kawaoka paper
A paper has just come out from Dr. Yoshihiro Kawaoka’s group describing their findings regarding the respective dangers of the new, pandemic H1N1 and seasonal flu (see reference below). Although this work supports two recent studies with ferrets suggesting that the new H1N1 causes more illness than seasonal flu, the new study provides additional insights into the pathology caused by H1N1.
Mice, ferrets, monkeys and pigs were given either the new H1N1 or a seasonal H1N1 intranasally. The following new H1N1 strains were used:
* A/California/04/09
* A/Wisconsin/WSLH049/09
* A/Wisconsin/WSLH34939/09
* A/Netherlands/603/09
* A/Osaka/164/09
These strains were all isolated from individuals with mild disease except A/Wisconsin/WSLH34939/09 which came from a person who had been hospitalised.
In mice, ferrets and monkeys the new H1N1 strains caused more severe disease than the seasonal H1N1 strain. However, in pigs, few clinical signs were observed with the new H1N1 suggesting that the virus may be spread asymptomatically in this species.
The amount of virus necessary to kill 50% of the mice was examined with the different strains. Less virus was required to kill mice with most of the new H1N1 strains than with the seasonal H1N1 . A/Wisconsin/WSLH049/09 was equally lethal to the mice as seasonal H1N1. Of the new H1N1 strains, A/Wisconsin/WSLH34939/09 was the most lethal. This is the strain isolated from an individual that had been hospitalised.
Striking differences in lung pathology in mice, monkeys and ferrets were observed between animals that received the new H1N1 virus as compared to animals that received seasonal H1N1. In particular, the lungs of monkeys that received the new H1N1 exhibited similar pathological changes to those seen in animals exposed to H5N1.
Transmission between ferrets by aerosol droplets was similar in animals infected with seasonal or pandemic H1N1.
One notable, and surprising, finding of this study was that neutralising activity was found in sera collected from the residents of nursing home that were born before 1920, but none in those born after. Thus, only those exposed to the 1918 virus are likely to have antibodies that recognise the new H1N1. Therefore, the relative paucity of deaths among people in the 60 to 89 age range cannot be explained by exposure to a virus that conferred cross-protection to the new H1N1.
In comparing this study with the two previous studies using ferrets, I am again struck by the parallels between the severity of disease observed in its human host and the ability of particular isolates to cause disease in animals. A/Wisconsin/WSLH34939/09, which was the only strain isolated from an individual who had been hospitalised, was the most lethal in mice. This adds further support for my hypothesis that the new H1N1 is unstable and causing variable disease due to variations in the virus itself.
Future studies explicitly comparing pathology in animals caused by virus isolated from patients with different clinical outcomes may be informative. If this association holds up, sequence analysis may provide clues into which variants of the virus are most likely to cause severe disease.
Reference:
Itoh, et al. (2009) In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses. Nature, doi:10.1038/nature08260
swine flu
Karaoka and his team looked at nursing home residents and workers from 1999 and from workers and patients in a hospital from this year (2009). Almost all the sera with neutralizing antibodies came from people born before 1920, a fact they interpreted as meaning that the current swine flu is related to the original 1918 virus before it diverged
The Associated Press
Posted: 07/14/2009 10:56:23 AM PDT
VALLEJO, Calif.—Nurses at a northern California hospital say inadequate masks and air-filters have resulted in medical staffers becoming ill while caring for three swine flu patients. ...
http://www.mercurynews.com/breakingnews/ci_12834125
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.