MGRS Monoclonal gammopathy of RENAL SIGNIFICANCE.
50% of Myeloma patients have renal disease. 10% on dialysis
19 April 2013
17 April 2013
ProMED: RICIN
RICIN - USA: (WASHINGTON, DC) LETTERS
******************************
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: Wed 17 Apr 2013
Source: Chicago Tribune, Reuters report [edited]
<http://www.chicagotribune.
A letter addressed to President Barack Obama contained a substance
that preliminarily tested positive for the deadly poison ricin,
authorities said on Wed 17 Apr 2013.
News that the letter to Obama was being investigated came as a flurry
of other reports of suspicious letters and a package caused the
evacuation of parts of 2 Senate buildings and set nerves in Washington
on edge.
The letter contained "a granular substance that preliminarily tested
positive for ricin," an FBI statement said. But the statement added:
"There is no indication of a connection to the attack in Boston,"
where 3 people were killed in bombings at the Boston Marathon on
Monday [15 Apr 2013].
The USA Secret Service said the letter to Obama was received at a mail
screening facility on Tue 16 Apr 2013. The mail facility that received
the letter was not located near the White House itself, Secret Service
spokesman Edwin Donovan said in a statement. "The Secret Service is
working closely with the US Capitol Police and the FBI in this
investigation," Donovan said.
Parts of the Russell and Hart Senate office buildings were cleared
while officials investigated suspicious letters and a package, a
Capitol Police spokesman said.
CNN read a statement from a spokesman to Senator Richard Shelby,
saying that Capitol Police were investigating a suspicious package
that had been delivered to their office.
Senator Carl Levin said one of his Michigan regional offices had
received a suspicious-looking letter, but it was not opened.
Authorities are investigating, Levin said in a statement.
On Tue 17 Apr 2013, USA authorities intercepted a letter sent to
Mississippi Senator Roger Wicker that preliminary tests showed
contained the deadly poison ricin.
[Byline: Susan Cornwell]
- --
Communicated by:
ProMED-mail
<promed@promedmail.org>
[ProMED-mail awaits more information regarding the presumed ricin.
The following is extracted (citations removed) from: Lutwick LI,
Gradon J, Zellen J: Category B Biotoxins. In Lutwick LI, Lutwick SM
(eds), Beyond Anthrax: Bioterror - The Weaponization of Infectious
Diseases. Springer-Humana, New York, 2009, New York, pp. 181-206:
"Ricin is found in castor beans from the plant _Ricinus communis_ and
is a residual product of the production of castor oil. The oil has
applications as a purgative, an engine lubricant, and as a component
of brake and hydraulic fluid. The industry is no longer active in the
United States but the oil is produced in large quantities in other
areas of the world. Importantly, the oil, if properly prepared, does
not contain the toxin.
"One million tons of castor beans are used each year for producing the
oil. The waste mash from the oil production process can have as much
as 5 percent ricin by weight and is easily and inexpensively isolated
via a simple process in a low technology setting using materials
easily obtainable. Ricin is easily prepared in liquid or crystalline
forms or as a readily aerosolized, lyophilized powder. The toxin is
stable and can be poisonous in its native form in the beans.
"Ricin is a 66 kD [kiloDalton] globular protein with a toxic mode of
action of inhibiting protein synthesis in eukaryotic cells. The
mechanism is due to the enzymatic removal of a single adenine residue
from (amino acid 4324) close to the 3-prime end of 28S ribosomal RNA.
The removal prevents elongation factor-2 from binding. Structurally it
is made up of 2 approximately equal molecular weight subunits, the A
and B chains, linked by a disulfide bond. The B chain facilitates
binding to cell surfaces and entry into the cell through binding to
terminal galactose moieties of cellular membrane glycolipids and
glycoproteins.
"The clinical presentation of ricin poisoning depends on whether the
exposure is parenteral, inhaled, or ingested. In mice, the dose found
to be lethal to 50 percent (LD50) of animals was found to be 3-5
microg/kg in inhalation or intravenous exposures and 20-25 microg/kg
in intraperitoneal, subcutaneous, or intragastric administration. The
time to death in the mice was 60 hours for inhalation, 90 hours for
intravenous, and 80-100 hours for the other exposures. It is important
to note that there is a variation of as much as 2 logarithms
[100-fold] in the microg/kg dose of ricin between animals, with the
horse seeming to be the most sensitive and the frog and chicken the
least.
"The 1st symptoms of toxicity generally occur 6-12 hours after
exposure but can occur as early as 3 hours. This is longer than many
of the chemical agents affecting the lung and more rapid than
infectious agents. In humans, as seemed to have occurred in the Georgi
Markov assassination, multiorgan failure occurred with a prominently
elevated white blood cell count. [Markov was a Bulgarian communist
defector who was killed in London in 2003 by a ricin pellet injected
into his leg from a modified umbrella point -- see
<http://edition.cnn.com/2003/
"As a weapon of bioterrorism, ricin would most likely be dispersed as
an aerosol although contamination of food and water supplies is also
feasible. Although easily obtained, massive quantities of toxin are
necessary to create a large scale effect. Because signs and symptoms
are non-specific, detection of an attack would require a high index of
suspicion based on clinical and epidemiologic factors. The finding of
a geographic cluster of patients with acute lung injury should arouse
suspicion of an attack via an aerosolized agent, although the list of
potential culprits is extensive and includes chemical as well as
biologic agents. Ricin cases do not exhibit mediastinitis, as with
anthrax, and they do not demonstrate any response to antibiotic
therapy as would be expected with an infectious etiology. Pulmonary
edema may develop one to 3 days after ricin exposure, in contrast to
staphylococcal enterotoxin B or phosgene where time to development of
pulmonary edema is 12 and 6 hours respectively.
"There are limited data describing the outcome from an inhalation
exposure. In the 1940s, sublethal and accidental exposures were said
to have occurred and were manifest 4-8 hours after exposure with
fever, cough, shortness of breath, and nausea. Studies in rodents
suggest an inhaled ricin aerosol could lead to necrosis of the upper
and lower airway, respiratory distress syndrome and respiratory
failure. Chest x-ray would be expected to show bilateral infiltrates.
In animal studies death occurred in 36 to 72 hours and was dose
dependent. In primates, symptoms and time to death were also dose
related and associated with alveolar flooding, fibropurulent
pneumonia, and necrotizing tracheitis. Death occurred 36 to 48 hours
after challenge following a 8-24 hour preclinical period." - Mod.LL
BMJ: PSA @ 40, 50,& 60 clinically indicated.
- Andrew J Vickers, attending1,
- David Ulmert, research fellow23,
- Daniel D Sjoberg, research biostatistician1,
- Caroline J Bennette, PhD student4,
- Thomas Björk, associate professor3,
- Axel Gerdtsson, resident3,
- Jonas Manjer, associate professor5,
- Peter M Nilsson, professor6,
- Anders Dahlin, data manager7,
- Anders Bjartell, professor3,
- Peter T Scardino, chair2,
- Hans Lilja, attending clinical chemist, professor2891011
- Correspondence to: H Lilja, Memorial Sloan-Kettering Cancer Center, 1275 York Ave (Box 213), New York, NY 10065, USA liljah@mskcc.org
- Accepted 13 March 2013
Abstract
Objective
To determine the association between concentration of prostate specific
antigen (PSA) at age 40-55 and subsequent risk of prostate cancer
metastasis and mortality in an unscreened population to evaluate when to
start screening for prostate cancer and whether rescreening could be
risk stratified.
Design Case-control study with 1:3 matching nested within a highly representative population based cohort study.
Setting Malmö Preventive Project, Sweden.
Participants
21 277 Swedish men aged 27-52 (74% of the eligible population) who
provided blood at baseline in 1974-84, and 4922 men invited to provide a
second sample six years later. Rates of PSA testing remained extremely
low during median follow-up of 27 years.
Main outcome measures Metastasis or death from prostate cancer ascertained by review of case notes.
Results
Risk of death from prostate cancer was associated with baseline PSA:
44% (95% confidence interval 34% to 53%) of deaths occurred in men with a
PSA concentration in the highest 10th of the distribution of
concentrations at age 45-49 (≥1.6 µg/L), with a similar proportion for
the highest 10th at age 51-55 (≥2.4 µg/L: 44%, 32% to 56%). Although a
25-30 year risk of prostate cancer metastasis could not be ruled out by
concentrations below the median at age 45-49 (0.68 µg/L) or 51-55 (0.85
µg/L), the 15 year risk remained low at 0.09% (0.03% to 0.23%) at age
45-49 and 0.28% (0.11% to 0.66%) at age 51-55, suggesting that longer
intervals between screening would be appropriate in this group.
Conclusion
Measurement of PSA concentration in early midlife can identify a small
group of men at increased risk of prostate cancer metastasis several
decades later. Careful surveillance is warranted in these men. Given
existing data on the risk of death by PSA concentration at age 60, these
results suggest that three lifetime PSA tests (mid to late 40s, early
50s, and 60) are probably sufficient for at least half of men.
Introduction
Screening
for prostate cancer with the prostate specific antigen (PSA) test
became widespread long before the availability of randomised evidence as
to its value. There is now evidence that PSA screening is associated
with reduced mortality from prostate cancer in men who would not
otherwise be screened,1 2
although this comes at considerable harms in terms of the number of men
who need to be screened, undergo biopsy, and be treated to prevent one
man experiencing prostate cancer metastasis or dying.
That
said, PSA screening is not a single intervention and men can be
screened in different ways. There is surprisingly little evidence to
support many aspects of contemporary screening guidelines. In
particular, the age at which screening starts and the frequency of PSA
testing is rarely justified in terms of empirical data. Recent evidence
has suggested that a single PSA measurement can predict the long term
risk of clinically relevant prostate cancer.3 4 5 6
This suggests that a baseline concentration could be used to determine
whether a man might benefit from subsequent PSA tests and, if so, when
these should be administered.
We used data from the
Malmö Preventive Project cohort to develop an evidence based schema for
prostate cancer testing. We retrospectively analysed PSA in previously
unthawed, archived, anticoagulated blood plasma obtained at baseline
from a large highly representative population based cohort of men who
had not been screened for PSA and had been followed for 25-30 years. As
such, the cohort provides a “natural experiment” for investigating the
association between PSA and long term prostate cancer outcomes.
Using
this cohort, we previously showed that PSA concentration at age 60 can
predict the risk of death from prostate cancer by age 85 (AUC of 0.90).
In particular, the 25 year risk of death from prostate cancer in men
with PSA below the median (≤1 µg/L) is low (0.2%) and suggests that half
of the men at age 60 could be exempt from further screening.7
We determined the risk of metastasis or death from prostate cancer
within 25-30 years based on PSA measured close to the time when
screening is normally recommended to begin. As there was little
screening for prostate cancer in our cohort, these results can be used
to determine which men are most likely to benefit from screening.
15 April 2013
USA: LEGAL RISK of GUIDELINES
From AMERICAN MEDICAL NEWS
Doctors win first safe harbor against ACA use in liability suits
■ States and Congress are urged to pass legislation based on an AMA model bill to prevent health reform criteria from exposing doctors to medical liability.
By
Alicia Gallegos
amednews staff
— Posted April 15, 2013
- WITH THIS STORY:
- » 5 ACA standards that could give plaintiffs an advantage in court
- » Related content
Physician leaders hope a first-of-its-kind bill
approved in Georgia protecting doctors from civil liability for
breaching federal health system reform requirements will be replicated
in other states.
Medical associations long have been
concerned that federal quality-of-care and payment reform measures,
such as those authorized by the Affordable Care Act, could be used to
fuel negligence accusations against individual physicians. The Georgia
law, drafted from American Medical Association model legislation,
prevents such health reform metrics from being used as evidence in
liability cases. Georgia's law states that payer guidelines and quality
criteria under federal law shall not establish a legal basis for
negligence or a standard of care for the purposes of determining medical
liability.
“We're saying if it's a breach in those
federal guidelines based on administrative behavior, let's make sure
that evidence is not admissible in court, and more than anything, let's
make sure that evidence is not being used as a determinant in the
standard of care,” said Marcus Downs, director of government relations
for the Medical Assn. of Georgia, which advocated for the enactment of
the shield law. “There could be some [administrative] wrongdoing, but it
is definitely not malpractice. It's definitely not negligence.”
The
passage of the Georgia bill, which at this article's deadline was
expected to be signed by Gov. Nathan Deal by the end of April, came as a
federal version of the legislation was being reintroduced in Congress.
The Standard of Care Protection Act would prohibit health system reform
provisions from being construed to establish a standard or duty of care
owed by a health professional to a patient in any liability case. A
similar version of the bill died in committee at the end of the last
Congress.
The Standard of Care Protection Act would
ensure that federal laws do not change the way health care professionals
practice medicine or treat patients through the threat of liability,
said Rep. Phil Gingrey, MD (R, Ga.), the bill's chief sponsor.
“This
legislation provides that lawsuits cannot be brought against health
care providers based simply on whether [they] followed national
guidelines created by the health care law,” Dr. Gingrey stated in an
email. “This bill reinforces my belief that medical decisions must be
made between patients and their doctors. The practice of medicine is not
one-size-fits-all. It must be protected from policies or rules that may
threaten a physician's ability to treat patients according to their
specific needs.”
The AMA supports the federal
legislation and also advocated for the Georgia law. In a statement, AMA
Board of Trustees member Patrice A. Harris, MD, praised Georgia's shield
law, saying federal reform statutes and regulations are intended to
enhance access to high-quality and efficient health care, not to justify
windfalls through lawsuits against physicians.
“Georgia
is the first state to take decisive action to prevent federal health
care reform laws and regulations from fueling the unrestricted excesses
of the state's broken medical liability system,” she said. “To hold the
line against tort abuse, Georgia relied on AMA model legislation to make
it clear that federal health care standards or guidelines cannot be
skewed to invent new legal actions against physicians.”
The
Georgia Trial Lawyers Assn. also worked with MAG on the state
legislation and was pleased with how the final bill turned out, said
Bill Clark, GTLA's director of political affairs. The association
successfully pushed for including a “goose-gander” provision in the bill
that also protects plaintiffs in medical liability suits from having
defendants introduce reform standard compliance as evidence.
“The
only way we were willing to allow the bill to go forward was to have it
go both ways,” Clark said. “If a physician can't be held accountable
for malpractice for failing to adhere to a payment guideline, then they
also shouldn't be able to use their compliance with a standard as
evidence that they complied with the standard of care. If it can't be
used against you as a sword, you also can't use it for a shield.”
The
director of policy for the American Assn. for Justice, Susan Steinman,
declined to comment on the Georgia law. The national association
represents trial attorneys.
Potential risks from reform
Without explicit legal protections, observers
said doctors who are sued for medical liability face various legal risks
from the ACA or other health system reform statutes.
To
find negligence, a plaintiff generally has to show — usually through
expert testimony — that his or her treatment did not meet the standard
of care observed by a reasonable physician, said Hal Dasinger, vice
president for government relations for The Doctors Company, a national
physician medical liability insurer. The Doctors Company supported the
Georgia law and is involved with promoting the federal legislation.
“Our
concern has been that plaintiff's counsel might attempt to use federal
guidelines developed, for example, to cost-effectively manage chronic
patients as evidence of negligence, by claiming that any treatment that
differed from the federal guidelines is beneath the standard of care,
rather than the result of an individual physician deciding what is in
the best interest of the patient,” Dasinger stated in an email.
Another
potential legal risk could come from the ACA's hospital value-based
purchasing program. Those provisions authorize payment adjustments for
certain hospitals based on designated health care performance criteria.
Whether a hospital-based physician met such criteria easily could be
raised in a medical negligence lawsuit to challenge the doctor's
credibility, Downs said.
Physicians' adherence to
hospital readmissions limits and prohibitions on payment for treating
hospital “never events” also are quality measures that could come up in
court. Plaintiffs could attempt to sway juries using such data, said Dan
Huff, a medical liability defense attorney based in Georgia.
Plaintiffs
alleging an undesired patient outcome could use the information to
argue that doctors “have no right to defend themselves or their actions,
because statutes and regulations have said these things should never
happen, and we're not going to pay them when they happen,” Huff said.
“If we have a gallbladder case we're defending about whether the
physician has met the standard of care, the plaintiff should not be
allowed to introduce evidence about the physician's readmissions rate,
complication rate or other issues that deal primarily with reimbursement
and payment.”
Federal shield bill redesigned
Despite their failed attempt to enact the
federal shield law in 2012, supporters are hopeful a newly redesigned
version of the measure will have a different outcome. The new bill has
been broadened beyond the provisions of the ACA and also would encompass
sections under the Social Security Act that deal with Medicare
payments.
Dr. Gingrey said the liability loopholes
created by the ACA should be addressed at the federal level. “The bill
makes clear that the care standards and guidelines detailed in federal
health care laws cannot be used to create new causes of legal action
against physicians, nor do they supersede state liability laws,” he
said.
The Doctor's Company was not aware of
legislation similar to Georgia's that is pending in other state
legislatures. However, Dasinger said it is only a matter of time before
other states follow the lead.
“With the victory in Georgia, it seems likely that other states will try to enact their own versions,” he said.
State
Rep. Edward Lindsey, a Republican who co-sponsored the Georgia law,
agreed. “I think it is good, pragmatic legislation, and I certainly
would think a lot of other states would look at it, just as we look at
other states when they pass pragmatic legislation.”
ADDITIONAL INFORMATION
Copyright © 2013 American Medical Association. All rights reserved.
14 April 2013
New York Paediatrician Henry KOPLIK born HENRI KOPLICK (1858-1927)
KOPLIK SPOTS
2. Koplik H. The diagnosis of the invasion of measles from a study of the exanthema as it appears on the buccal mucous membrane. Arch Pediatr1896;13:918-22. [PubMed]
2. Koplik H. The diagnosis of the invasion of measles from a study of the exanthema as it appears on the buccal mucous membrane. Arch Pediatr1896;13:918-22. [PubMed]
01 April 2013
NIH "MGUS" = MYELOMA
C. Ola Landgren, M.D., Ph.D.
Medical Oncology Branch and Affiliates
Head, Multiple Myeloma Section
Senior Investigator
National Cancer Institute
9000 Rockville Pike
Building 10, Room 13N240
Bethesda, MD 20892
Phone: 301-496-0670
Fax: 301-402-0172
landgreo@mail.nih.gov
Dr. Landgren received his M.D. in 1995 from the Karolinska Institute in Stockholm, Sweden. Following clinical training as a hematology/internal medicine specialist physician, he earned a Ph.D. with a focus on diagnostics and prognostics in Hodgkin lymphoma in 2002 at Karolinska Institute. He then served as an attending physician at Karolinska and conducted clinical research on lymphoproliferative malignancies and related precursors. He came to the National Cancer Institute’s (NCI) Division of Cancer Epidemiology and Genetics (DCEG) in 2004, where he served as an Investigator before he joined the Medical Oncology Branch.
Dr. Landgren's major research interests are in the treatment, causation, diagnostics and prognostics, and natural history of multiple myeloma and its precursor condition, monoclonal gammopathy of undetermined significance (MGUS). He also studies related hematologic malignancies and their precursor states, including chronic lymphocytic leukemia and monoclonal B-cell lymphocytosis (MBL); Waldenstrom’s macroglobulinemia, and IgM MGUS, as well as myeloproliferative neoplasms. His research focuses on treatment-, host-, disease-, and immune-related factors in the pathway from precursor to full-blown malignancy and their relation to outcome.
Dr. Landgren's Clinical Trial(s):
NCI’s Center for Cancer Research (CCR) is currently conducting the following trial(s) for patients with MGUS, smoldering myeloma, and multiple myeloma. Click on the trial(s) below for additional details, including a summary of key eligibility criteria, study outline, and information on how to contact the study team directly.
Head, Multiple Myeloma Section
Senior Investigator
National Cancer Institute
9000 Rockville Pike
Building 10, Room 13N240
Bethesda, MD 20892
Phone: 301-496-0670
Fax: 301-402-0172
landgreo@mail.nih.gov
Dr. Landgren received his M.D. in 1995 from the Karolinska Institute in Stockholm, Sweden. Following clinical training as a hematology/internal medicine specialist physician, he earned a Ph.D. with a focus on diagnostics and prognostics in Hodgkin lymphoma in 2002 at Karolinska Institute. He then served as an attending physician at Karolinska and conducted clinical research on lymphoproliferative malignancies and related precursors. He came to the National Cancer Institute’s (NCI) Division of Cancer Epidemiology and Genetics (DCEG) in 2004, where he served as an Investigator before he joined the Medical Oncology Branch.
Dr. Landgren's major research interests are in the treatment, causation, diagnostics and prognostics, and natural history of multiple myeloma and its precursor condition, monoclonal gammopathy of undetermined significance (MGUS). He also studies related hematologic malignancies and their precursor states, including chronic lymphocytic leukemia and monoclonal B-cell lymphocytosis (MBL); Waldenstrom’s macroglobulinemia, and IgM MGUS, as well as myeloproliferative neoplasms. His research focuses on treatment-, host-, disease-, and immune-related factors in the pathway from precursor to full-blown malignancy and their relation to outcome.
Dr. Landgren's Clinical Trial(s):
NCI’s Center for Cancer Research (CCR) is currently conducting the following trial(s) for patients with MGUS, smoldering myeloma, and multiple myeloma. Click on the trial(s) below for additional details, including a summary of key eligibility criteria, study outline, and information on how to contact the study team directly.
Videocast/Podcast Details:The quality of these videocasts is dependent on the speed of your Internet connection. Many videocasts are streamed directly to your computer by software on the NIH VideoCasting Web site. Others require that you have a standalone player installed on your computer to handle the streaming. If you do not have a standalone player installed or if you are having problems viewing the videocast, please visit http://videocast.nih.gov/faq/.
| CC Grand Rounds: (1) Therapeutic Gene Delivery: Using
Hematopoietic Stem Cells in Sickle Cell Disease (2) Multiple Myeloma and
Its Precurser (MGUS): Looking into the Future Speaker(s): John F. Tisdale, M.D., Senior Investigator, Molecular and Clinical Hematology Branch, NHLBI Ola Landgren, M.D., Ph.D., Investigator, Medical Oncology Branch, Center for Cancer Research, NCI April 16, 2010 60 minutes http://videocast.nih.gov/launch.asp?15720 |
| Eradicating Multiple Myeloma Speaker(s): C. Ola Landgren, M.D., Ph.D., Head, Multiple Myeloma Section, Medical Oncology Branch and Affiliates, NCI September 15, 2010 3 minutes, 32 seconds http://bethesdatrials.cancer.gov/rss/videocastdetail.aspx?webcastid=9 |
| NIH Director's Seminar Series: Multiple Myeloma and its Precursor Disease: the Future is Already Here Speaker(s): C. Ola Landgren, M.D., Ph.D. Head, Multiple Myeloma Section, Medical Oncology Branch and Affiliates, NCI April 20, 2012 50 minutes http://videocast.nih.gov/Summary.asp?File=17227 |
29 March 2013
NEW CORONA VIRUS
New virus is MORE deadly than Sars, warn scientists after second Briton dies taking death toll to 11
- New research shows coronavirus affects many organs and kills quickly
- 'It could be more virulent than Sars' says microbiologist
- Announced this week that second British man has died from virus
|
A new virus which has claimed the life of a second Briton is potentially more deadly than Sars, scientists have warned. The mysterious coronavirus, which has emerged in the Middle East, attacks the respiratory system and was only identified six months ago.
So far there have been 11 deaths - with the World Health Organisation this week saying a second British man has died.
Killer: A new virus which has claimed the life
of a second Briton is potentially more deadly than Sars, scientists have
warned. This image shows a microscope image of coronavirus
Speaking to the South China Morning Post, microbiologist Yuen Kwok-yung, said if the virus mutated further it could cause a deadly pandemic.
'It could be more virulent [than Sars]', he said. 'The Sars coronavirus infects very few human cell lines. But this new virus can infect many types of human cell lines, and kill cells rapidly.'
Seventeen cases have been announced since the WHO issued an alert in September last year, most of them with links to the Middle East.
This week it was announced that a 73-year-old man from the United Arab Emirates had also died from the virus.
He was flown to hospital in Munich last week and died on Tuesday, the World Health Organisation said.
Source: Experts believe the coronavirus originated in bats
The source of coronavirus is not known, but experts believe it originated in bats.
Animals which could host the virus include monkeys, pigs and even rabbits
Scientists say the new virus is from the same viral family that causes the common cold and also triggered the outbreak of Sars which swept the world from Asia in late 2003, leaving 775 dead.
Symptoms of coronavirus - which doctors say spreads rapidly around the body within 48 hours of infection - include severe breathing difficulties, fever, coughing and pneumonia.
It can also attack the kidneys, according to health experts.
In a statement issued late on Tuesday, the WHO said it was encouraging governments to watch for all severe respiratory infections and especially for any unusual patterns they might take.
For the moment, the U.N. agency said, it was not advising countries to set up any special screening for the virus at entry points and was not recommending any of the travel or trade restrictions introduced during the SARS epidemic.
The first reported case of infection by the previously little-known virus was a Qatari man who had also traveled to Saudi Arabia. Earlier in 2012, a 60-year-old Saudi national was believed to have died from it.
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