Swine flu worse in Mexico than US, but why?

[cartski]

Uhh, so the obvious question is what are the toilet facilities like in the mexican areas with high incidence? flush, outhouse, hole & pipe, "honey pot"....

And then are there reports of busted sewer pipes empyting out onto streets as was the case with the Amoy Gardens (?) and SARS?

And are there traps in the toilet pips in the apartments, the lack of which was also a factor creating negative pressure and bacteria in the Amoy Garden blocks.

It would be interesting to see a detailed geographic distribution of the cases in Mexico.

[Dutchy]

If I understand well the possible problems caused by a pandemic:

from an individual point of view the most important thing is: will I or my dear ones fall ill and die?

From a national or global view the thing is: will many people, mild or not mild, fall ill at the same time? If so, there will be problems with infrastructure, infrastructure of everything (shops, energy, healthcare, you name it).

"Infrastructure" can't work without people. So if you have a shortage of people running all kinds of infrastructure , shortage through illness, or absentism, society can have a hard time to function like it does every day.

So from a general point of view it seems the point is'nt: "is it mild" , or "why worse in Mexico", or "what is the cfr" , but "is it contagious and spreading fast, making many victims" .

Time will tell.

[vinny]

Swine Flu Probe Slowed by Backlog in Mexican Sample Testing

May 1 (Bloomberg) -- Swine flu samples caught in a laboratory backlog in Mexico are slowing the probe into the severity of the virus that’s sweeping across the world, experts including the World Health Organization’s Francesco Checchi say.

Mexico, the first country known to be hit by the new H1N1 flu strain that has reached 11 nations, has about 35,000 samples waiting to be analyzed, said Dick Thompson, a spokesman at the World Health Organization. Those samples, which experts say hold the key to understanding the virus, are held in a guarded laboratory surrounded by walls, gates and guards, that’s less than 4 miles from downtown Mexico City.

The WHO on April 29 called a flu pandemic “imminent,” and 13 people are confirmed to have died from H1N1 infection. Scientists say they need to how far the virus has spread in Mexico, where 12 of the deaths occurred, and how often it kills, to predict whether it will be as lethal as the so-called Spanish flu that killed about 50 million people in 1918.

“While we know of a given number of confirmed swine flu deaths, we do not know by any means the actual number of swine influenza cases that have occurred in Mexico,” Checchi, a WHO epidemiologist, said in an April 28 e-mail. “It is extremely difficult to assess just how lethal the virus is in Mexico.”

Much more on
http://www.bloomberg.com/apps/news?p...uDo&refer=home

[gsgs]

has it been mentioned ? :
Mexico is high above the sea-level, air is thinner

the other regions with outbreak are also high above sea-level ?


looking at niman's map ... all the Mexican outbreak regions seem to be high abov sea-level.
Can someone confirm ?


I speculate that the virus only transmits efficiently above sea-level and spreads
worse and is milder in other regions (in summer)


do we have a graphic program to superimpose niman's map with a sea-level-colored map ?

[AlaskaDenise]

Originally Posted by tropical

Until now, influenza in the terms of seasonal flu, and pandemic flu, was always be a respiratory disease.

The various gastro versions until now fallen into "virosis", or "paraflu" (flu simil like).

Saying that influenza was some times an non respiratory disease seems something new for me, or maybe from all these proliferated bugs even that is now changing, and we will (if survived) starts sheding flu viruses like ducks ...?

It depends on the predominant binding receptors. a2,3 tend to bind to the intestines and lower lungs, while a2,6 tends to bind to upper respiratory.

In http://www.ncbi.nlm.nih.gov/pubmed/16022777...

Influenza A H5N1 replication sites in humans.

Tissue tropism and pathogenesis of influenza A virus subtype H5N1 disease in humans is not well defined. In mammalian experimental models, H5N1 influenza is a disseminated disease. However, limited previous data from human autopsies have not shown evidence of virus dissemination beyond the lung. We investigated a patient with fatal H5N1 influenza. Viral RNA was detected by reverse transcription-polymerase chain reaction in lung, intestine, and spleen tissues, but positive-stranded viral RNA indicating virus replication was confined to the lung and intestine. Viral antigen was detected in pneumocytes by immunohistochemical tests. Tumor necrosis factor-? mRNA was seen in lung tissue. In contrast to disseminated infection documented in other mammals and birds, H5N1 viral replication in humans may be restricted to the lung and intestine, and the major site of H5N1 viral replication in the lung is the pneumocyte.

Perhaps, (in my non-expert opinion) it is because H5N1 is still more avian, which has more a2,3 receptors.

However, various influenzas can contain a fair number of a2,3 receptors which yield intestinal symptoms.

.

[tropical]

Thanks AD and hello,

I'm aware of the receptors throat/lung story about bird flu (learned at FT/...).
Also that the viruses could be find elsewhere in the body than in the lungs.

But speaking of human seasonal flu's and the few pandemic at least after the 1918, all the times they must have included the respiratory component, so it must be respiratory(?)

To a human flu virus to not be respiratory, it must be changed in a way that it could not transmit itself by respiratory ways (?).

So, maybe here is only an read/write glitch,
actualy your text want's to point to the fact that this novel virus have upgraded into itself both the ways of transmission because of the receptors: respiratory and not respiratory, so both primary human (droplets/respiratory) and primary avian (shedding intestinal viruses) in one?

Originally Posted by AlaskaDenise

It depends on the predominant binding receptors. a2,3 tend to bind to the intestines and lower lungs, while a2,6 tends to bind to upper respiratory.

In http://www.ncbi.nlm.nih.gov/pubmed/16022777...

Influenza A H5N1 replication sites in humans.



Perhaps, (in my non-expert opinion) it is because H5N1 is still more avian, which has more a2,3 receptors.

However, various influenzas can contain a fair number of a2,3 receptors which yield intestinal symptoms.

.

[Forelle]

The first 7 cases are from Tlalpan and Magdalena Contreras, as far as I know.

Tlalpan is here:

and Magdalena Contreras is here:

They are next to one another.

Here is some more information on Wikipedia:
Tlalpan
Magdalena Contreras

Por la delegación corre el último rio vivo del Distrito Federal, el Río Magdalena, que sufre un grave problema de contaminación.

I don't know where the other (so far) 9 cases are from.

[Forelle]

Actually, there are 19 death cases so far. Here is a table with the locations:
http://www.prevencioninfluenza.gob.mx/
Unfortunately, it just mentions Mexico City (= Distrito Federal) and not its delegaciones.

[Forelle]

I think the question is rather answered, as this article (and others plus the Mexican conference with the Health Minister) show:
http://www.king5.com/topstories/stor...S.db58678.html

"This unfortunate death is consistent with the two other confirmed H1N1 deaths in Texas, where both suffered underlying health issues," said Dr. Goldbaum in a press release. "This death reminds us that influenza can be a very serious illness, especially if a person has underlying health problems."

Whenever more information on the confirmed deaths in Mexico was released, it was said that those people suffered underlying health issues, too (I already mentioned a few here in this forum).

[HenryN]

INFLUENZA A (H1N1) - WORLDWIDE (17)
***********************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

Date: Fri 8 May 2009
From: Marcel Jonges
<Marcel.Jonges@RIVM.NL>


Travel-associated influenza A (H1N1) with a virus containing a mutation in PB2
------------------------------------------------------------------------------
In the Netherlands, the 2nd laboratory confirmed human case of
influenza A (H1N1) virus infection was reported on 7 May 2009. A
53-year-old woman returned on the 30 Apr 2009 from Cancun, Mexico.
During the flight she developed an unproductive cough. Then, 2 days
later on 2 May 2009, she had a temperature of 38.6C and a sore throat
and consulted a general practitioner. Samples were submitted for
diagnostic evaluation and both the patient and her husband were
treated with oseltamivir. The patient recovered completely and
uneventfully, and samples collected 4 days later tested negative. The
virus was analyzed for presence of antiviral resistance markers in
the neuraminidase and for human adaptation markers in the PB2 protein
by direct sequencing.

The sequence data suggested that the virus was susceptible to both
oseltamivir and zanamivir. The amino acid 627 in PB2 (glutamicacid)
was not human-host-adapted, similar to recent swine influenza A
(H1N1) viruses. However, a glutamic acid to glycine amino acid
substitution was detected at position 677 in PB2. This mutation was
not observed in any of the A (H1N1) sequences submitted since 27 Apr
2009. Lam et al. (2008) postulated that this substitution could
reflect adaptation to mammalian hosts of highly pathogenic avian
influenza A (H5N1) viruses (1), as it was found to be under positive
selection based on phylogenetics of Indonesian viruses. Based on the
position of the mutation it might contribute to more efficient
human-to-human transmission by enhanced replicative efficiency of the
polymerase of the influenza A (H1N1) virus in humans [PB2 is a
polymerase component. - Mod.CP]. Experiments are underway to test the
relevance of this finding.

Reference:
----------
(1) Lam TT, Hon CC, Pybus OG, Kosakovsky Pond SL, Wong RT, Yip CW,
Zeng F, Leung FC, Evolutionary and transmission dynamics of
reassortant H5N1 influenza virus in Indonesia, PLoS Pathog. 2008 Aug
22;4(8):e1000130.

[Byline: Marcel Jonges, Adam Meijer, Pieter Overduin, Titia Kortbeek,
Rob van Kessel, Paul Bijkerk, Martin Schutten, Theo Bestebroer,
Charles Boucher, Guus Rimmelzwaan, Ron Fouchier, Ab Osterhaus, and
Marion Koopmans
At the National Institute for Public Health and the Environment,
Bilthoven, the Netherlands, and the Erasmus Medical Center,
Rotterdam, the Netherlands]

--
Marcel.Jonges
National Institute for Public Health and the Environment
Centre for Infectious Disease Control
P.O. Box 1
3720 BA, Bilthoven
The Netherlands
<Marcel.Jonges@RIVM.NL>

[The identification of a single mutation in the PB2 gene (encoding
the major component of the viral polymerase) of this Netherlands
isolate of the novel 2009 strain of influenza A (H1N1) virus is an
interesting finding only previously reported in the case of avian
influenza A (H5N1) virus. It is conceivable that such a mutation
might influence the transmissibility and the host range of the virus.
However, it would be premature to draw such a conclusion since there
appears to have been no onward transmission of the virus to any other
person. Nonetheless this is clearly a site which should be kept under
surveillance in future studies. - Mod.CP]

[The Netherlands can be located on the HealthMap/ProMED-mail
interactive map at:
<http://healthmap.org/r/00by>
-CopyEd.EJP]

[see also:
Influenza A (H1N1) - worldwide (16): case counts 20090507.1715
Influenza A (H1N1) - worldwide (15) 20090507.1709
Influenza A (H1N1) - worldwide (14): case counts 20090507.1702
Influenza A (H1N1) - worldwide (13) 20090506.1695
Influenza A (H1N1) - worldwide (12): case counts 20090505.1681
Influenza A (H1N1) - worldwide (11): coincident H3N2 variation 20090505.1679
Influenza A (H1N1) - worldwide (10): case counts 20090504.1675
Influenza A (H1N1) - worldwide (09) 20090504.1673
Influenza A (H1N1) - worldwide (08): case counts 20090503.1660
Influenza A (H1N1) - worldwide (07) 20090503.1658
Influenza A (H1N1) - worldwide (06): case counts 20090502.1654
Influenza A (H1N1) - worldwide (05) 20090503.1657
Influenza A (H1N1) - worldwide (04): case counts 20090501.1648
Influenza A (H1N1) - worldwide (03) 20090501.1646
Influenza A (H1N1) - worldwide (02): case counts 20090430.1638
Influenza A (H1N1) - worldwide 20090430.1636]
....................cp/ejp/dk

[HenryN]

Originally Posted by niman

INFLUENZA A (H1N1) - WORLDWIDE (17)
***********************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

Date: Fri 8 May 2009
From: Marcel Jonges
<Marcel.Jonges@RIVM.NL>


Travel-associated influenza A (H1N1) with a virus containing a mutation in PB2

"Travel-associated influenza A (H1N1)" is pure propaganda (in HEADLINE). Promed continues to embarass scientific community with nonsense posts.

[Siegfried X]

This is from CIDRAP, May 8:

WHO experts held a conference call yesterday with Mexican officials to discuss clinical findings in the patients who died from severe swine flu infections, Sylvie Briand, acting director of the WHO's Global Influenza Program, said today at a media briefing. Mexican health officials have identified two high-risk groups: previously healthy young people who deteriorated rapidly with acute pneumonia and people with chronic health conditions such as cardiovascular disease or tuberculosis. Briand said viral pneumonia has played a role in the deaths, but bacterial pneumonia has been less of a factor, unlike in other pandemics. Authorities have found that causes of death are typically respiratory failure or organ failure.

[AlexanderSJones]

One of the Mexican isolates had two SNPs in PB2 , not seen in any other isolates...



There is evidence that the Mexican swine flu strain is NOT the same as the North American strain -- contrary to the pronouncement of Dr. Frank Plummer at the Canadian National Laboratory of Microbiology -- who held a press conference yesterday...


Regarding the genetic analysis of Mexican Swine Flu vs. Canadian Swine Flu -- There are SNPs on PA and PB2 , which are ONLY present in the Mexican strain -- a sequence released by Dr. Plummer's own laboratory! The fact that this difference was in his own data should bring into question the credibility of government health labs' ability and will to protect the public interest..


Suppose we use New York / Canada as the consensus strain. There are two unique polymorphisms found ONLY in Mexico (so far, anyway):



L275I on PA
N82S on PB2

[nomadic wench]

One of the Mexican isolates had two SNPs in PB2 , not seen in any other isolates...

That's interesting. In plain English does that mean just one patient?

Were other Mexican isolates the same as the N.American ones?

[AlexanderSJones]

Yes, at least one isolate (patient) had this -- A/Mexico/InDRE4487/2009(H1N1). But curiously, this particular published sequence had no information on the patient, age, location, etc. The two SNPs on this strain are different from all other sequences around the world, and occur on the PA gene and the PB2 gene.

[English Teacher]

This is really interesting, but what does it MEAN, Alexander?

[gsgs]

the mutations are not in another published Mexican virus
nor in a close Arizona virus.
So it's presumably just a variation which didn't spread