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INFLUENZA A (H1N1) - WORLDWIDE (81): EPIDEMIC ANALYSIS
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A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>
In this update:
[1] Epidemic pneumonia
[2] Origins
[3] CFR estimations
[4] Tamiflu resistance - Japan
******
[1] Epidemic pneumonia
Date: Tue 29 Jun 2009
Source: The New England Journal of Medicine [edited]
<http://content.nejm.org/cgi/content/full/NEJMoa0904023>
[The following paper appeared in the 29 June issue of the New England
Journal of Medicine. - Mod.CP]
G Chowell, SM Bertozzi, MA Colchero, H Lopez-Gatell, C Alpuche-Aranda, M
Hernandez, et al. Severe respiratory disease concurrent with the
circulation of H1N1 influenza. N Engl J Med 2009 (10.1056/NEJMoa0904023)
Abstract
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Background: In the spring of 2009, an outbreak of severe pneumonia was
reported in conjunction with the concurrent isolation of a novel
swine-origin influenza A (H1N1) virus (S-OIV), widely known as swine flu,
in Mexico. Influenza A (H1N1) subtype viruses have rarely predominated
since the 1957 pandemic. The analysis of epidemic pneumonia in the absence
of routine diagnostic tests can provide information about risk factors for
severe disease from this virus and prospects for its control.
Methods: From 24 Mar to 29 Apr 2009, a total of 2155 cases of severe
pneumonia, involving 821 hospitalizations and 100 deaths, were reported to
the Mexican Ministry of Health. During this period, of the 8817
nasopharyngeal specimens that were submitted to the National
Epidemiological Reference Laboratory, 2582 were positive for S-OIV. We
compared the age distribution of patients who were reported to have severe
pneumonia with that during recent influenza epidemics to document an age
shift in rates of death and illness.
Results: During the study period, 87 per cent of deaths and 71 per cent of
cases of severe pneumonia involved patients between the ages of 5 and 59
years, as compared with average rates of 17 per cent and 32 per cent,
respectively, in that age group during the referent periods. Features of
this epidemic were similar to those of past influenza pandemics in that
circulation of the new influenza virus was associated with an off-season
wave of disease affecting a younger population.
Conclusions: During the early phase of this influenza pandemic, there was a
sudden increase in the rate of severe pneumonia and a shift in the age
distribution of patients with such illness, which was reminiscent of past
pandemics and suggested relative protection for persons who were exposed to
H1N1 strains during childhood before the 1957 pandemic. If resources or
vaccine supplies are limited, these findings suggest a rationale for
focusing prevention efforts on younger populations.
--
communicated by:
ProMED-mail rapporteur Mary Marshall
[The authors add the following in their Discussion. "Of note, during the
study period, there was proportionately lower morbidity among persons who
were 60 years of age or older, the age group in which all persons were born
before the 1957 pandemic. With an annual influenza incidence of 15 to 20
per cent, most of these persons would have been 1st exposed to influenza A
(H1N1) strains, which disappeared from circulation after the 1957 A (H2N2)
influenza pandemic. Francis described the concept of "original antigenic
sin," in which the immune response is greatest to antigens to which 1st
exposure occurred in childhood. According to this concept, persons born
before 1957 who were exposed in childhood to influenza A (H1N1) viruses
might be better protected against this viral subtype than those who were
1st exposed to other influenza A subtypes, H2N2 and H3N2, at a later date.
Age shifts in mortality to younger populations during pandemics have been
described from the reemergence of a subtype. Although persons who were born
after 1977 may have been 1st exposed to an influenza A (H1N1) subtype
virus, such strains rarely predominate. In this data series, persons who
were 60 years of age or older were proportionately less likely to have
severe pneumonia, a consideration for future strategies for vaccine allocation.
"Our outline of the age-stratification profile of risk provides a possible
foundation for control strategies on the basis of the biologic plausibility
of partial protection from earlier exposure. Further studies are under way
in Mexico to elucidate other potential risk factors for severity of S-OIV
infection to guide targeted control efforts." - Mod.CP]
******
[2] Origins
Date: Mon 29 Jun 2009
Source: ScienceDaily, News [edited]
<http://www.sciencedaily.com/releases/2009/06/090629200641.htm>
The current H1N1 swine flu strain has genetic roots in an illness that
sickened pigs at the 1918 Cedar Rapids Swine Show in Iowa, report
infectious disease experts at the University of Pittsburgh Graduate School
of Public Health in the New England Journal of Medicine. Their paper,
published online 29 Jun 2009 and slated for the 16 Jul 2009 print issue,
describes H1N1's nearly century-long and often convoluted journey, which
may include the accidental resurrection of an extinct strain.
"At the same time the 1918 flu pandemic was rapidly spreading among humans,
pigs were hit with a respiratory illness that closely resembled symptoms
seen in people," said senior author Donald S Burke, MD, dean, University of
Pittsburgh Graduate School of Public Health. "Early experiments confirmed
that this 1918 swine virus and a human strain emerged about the same time.
Since then, this ancestor virus has re-assorted genetically with other
influenza strains at least 4 times, leading to the emergence of the new
2009 strain, which has retained some similarities to the original virus."
In the paper, Dr Burke and lead author Shanta M Zimmer, MD, assistant
professor, University of Pittsburgh School of Medicine, describe the
temporary "extinction" of the H1N1 virus from humans in 1957 and its
subsequent re-emergence 20 years later. They note a small 230 person
outbreak of H1N1 in 1976 among soldiers in Fort Dix, New Jersey that did
not extend outside the military base. Then, H1N1 influenza re-emerged in
1977 among people in the former Soviet Union, Hong Kong and north eastern
China. Careful study of the genetic origin of the 1977 strain showed that
it was not the Fort Dix strain, but, surprisingly, was related closely to a
1950 human strain. Given the genetic similarity of these strains,
re-emergence was likely due to an accidental release during laboratory
studies of the 1950 strain that had been preserved as a "freezer" virus,
they said.
The authors hypothesize that concerns about the Fort Dix outbreak
stimulated a flurry of research on H1N1 viruses in 1976, which led to an
accidental release and re-emergence of the previously extinct virus a year
later. The re-emerged 1977 H1N1 strain has continued to circulate among
humans as seasonal flu for the past 32 years.
Although originally traced to Mexico, the exact physical origins of the
2009 H1N1 pandemic virus are unknown. Because the current strain shares
common ancestry with older flu strains, it is possible that portions of the
population may have partial immunity to the new pandemic virus.
The authors also go on to explain that the danger posed by a virus isn't
based solely on its lethality but also on its transmissibility, which is
the ability to jump from animals to humans and to survive by mutating to
adapt to its new human host. H1N1 influenza viruses have demonstrated this
ability throughout their history.
"Studying the history of emergence and evolution of flu viruses doesn't
provide us with a blueprint for the future, but it does reveal general
patterns, and this kind of information is critical if we are to be as
prepared as possible," said Dr Burke.
--
communicated by:
ProMED-mail rapporteur Susan Baekeland
*****
[3] CFR estimations
Date: Thu 2 Jul 2009
Source: Eurosurveillance, Volume 14, Issue 26, 2009 [edited]
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19255>
The emerging influenza pandemic: estimating the case fatality ratio
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By: N Wilson, M G Baker (Department of Public Health, University of Otago,
Wellington, New Zealand)
To determine appropriate influenza pandemic containment and mitigation
measures, health authorities need to know the approximate case fatality
ratio (CFR) for this new infection. We present 4 different methods for very
provisionally estimating the plausible range of the CFR for symptomatic
infection by this pandemic strain in developed countries. All of the
methods produce substantially lower values (range 0.06 percent to 0.0004
percent) than a previously published estimate for Mexico (0.4 percent). As
these results have many limitations, improved surveillance and serological
surveys are needed in both developed and developing countries to produce
more accurate estimates.
Introduction
------------
The 1st published estimate of the case fatality ratio (CFR) for those
infected by the influenza A(H1N1)v pandemic strain was based on data from
Mexico [1]. This work estimated the CFR to be 0.4 per cent (range 0.3 per
cent to 1.5 per cent) based on confirmed and suspected influenza
A(H1N1)v-related deaths reported up to late April 2009. Since that date,
the new pandemic strain has spread globally, and new impact data are
available, but we were unable to identify new estimates of the CFR in the
literature. Yet this figure is critical if health authorities are to
produce reasonable estimates of the likely impact of the pandemic in their
particular countries. The estimated mortality burden is particularly useful
for calibrating appropriate containment and mitigation measures that
balance the likely health gains from interventions against their social and
economic costs.
Methods
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We considered 4 different ways to provide provisional estimates for
plausible ranges of CFRs in developed countries for this pandemic.
1. Multiplier method: This method used confirmed deaths and cases reported
to the World Health Organization (WHO), but with a range of multipliers for
the latter to adjust for under-ascertainment. These multipliers were based
on expert judgment that most symptomatic cases of the new pandemic involve
relatively mild symptoms and that the great majority of cases were not
being identified and reported. For example, spokespeople from the United
States (US) Centers for Disease Control and Prevention (CDC) have announced
"hundreds of thousands of cases that have occurred in the US" in late May
and mid-June 2009 [2,3]. Similarly, one estimate for the United Kingdom was
30 000 cases in the community in May 2009 [4]. Regarding the choice of a
multiplier to adjust data on laboratory-confirmed cases of pandemic
influenza, we considered the above assessments, which are specific to the
current pandemic, to be more informative than past experience with seasonal
influenza, which only provides very broad estimates of a potential
multiplier. For example, it has been estimated for seasonal influenza in
the US that there are 2.3 influenza cases in the community for every
outpatient consultation, and 84.1 for every case that is hospitalised
(derived from Molinari et al. [5]). But during a pandemic, patients are
encouraged to remain at home unless they have "severe illness" or are "at
high risk for influenza complications." In addition, laboratory testing
capacity can be quickly saturated in a pandemic, and priority is given to
those who require hospitalisation or are at high risk for severe disease
[6]. These processes will tend to push the ratio of community cases to
laboratory-confirmed cases upwards to the multiplier in the range of 10-30
that we judged reasonable for this analysis.
In the calculations, we used WHO data for cumulative cases and deaths as of
26 Jun 2009 [7] for all member countries of the Organisation for Economic
Cooperation and Development (OECD), but excluding data from Mexico. The
reason for this exclusion was that the epidemic appeared to have started in
Mexico, and we were concerned about the quality and sensitivity of
numerator data in the early stages of the epidemic there -- that is, when
it was not recognised that the new pandemic strain was spreading.
2. Community survey method: This method used an estimate for community
cases from a telephone survey done by the New York City Department of
Health [8]. It reported that 6.9 per cent of New Yorkers had symptoms of
influenza-like illness (ILI) between 1 and 20 May 2009. The report on this
survey did not publish confidence intervals, so we calculated these to be
5.6 per cent to 8.5 per cent (for the survey of 1005 households).
Furthermore, at the time of this survey, only 90 per cent of the influenza
samples tested in the city were of the current pandemic strain [9], and so
we adjusted the CFR estimate accordingly by this proportion. We
conservatively used the cumulative death toll for New York City at 3 weeks
after the time period used in this survey (when it was n=12) to allow for a
lag in illness progression and then in reporting fatalities to health
authorities [10]. We identified that there were no pandemic influenza
deaths prior to May 2009 [11], and the New York City population of 8 274
500 used in our calculations was that for 2007 [12].
3. Method extrapolating from seasonal influenza mortality: This method was
based on evidence that the elderly population appear to have a relatively
low mortality rate compared to other age groups in this pandemic. Data from
Canada on hospitalisations and deaths [13] and US data indicate a median
age of hospitalisation at 19 years and of death at 37 years [14]. Hence, we
assumed that a CFR for seasonal influenza in the age group of under 65
years could provide a crude approximation for the CFR of the new pandemic
strain. To obtain this value, we used the full range estimates that could
be derived from a detailed US study [15] that used 7 models for determining
excess mortality attributable to influenza. [These data are presented as a
table in the original text].
4. Method extrapolating from a more "mature" epidemic: This method was
restricted to data from Canada and assumed that the epidemic there was
relatively advanced in that the trend data for cases and hospitalisations
were suggestive of a peak in early June 2009 with a subsequent waning of
the epidemic in the following 3 weeks [17]. To calculate the CFR, we
assumed that the epidemic in Canada was half complete in terms of
cumulative deaths (with n=21 deaths confirmed as of 26 Jun 2009 [17]),
which is possibly a conservative assumption given the low level of new
hospitalisations in late June 2009. We also assumed that the cumulative
total of symptomatic cases would ultimately reach between 5 per cent of the
total population (which is within the range of seasonal influenza) and
around 30 per cent (which is about the value predicted by modelling for a
pandemic with an R0 value of 1.5 [18] as estimated for the current pandemic
using the Mexican data [1]).
Results
-------
The 4 different methods produced a wide range of estimates for the CFR in
developed countries, from 0.0004 per cent to 0.06 per cent, a range of
150-fold (table 2). The ranges for each model overlapped with at least one
other model. When these CFR estimates were applied to a country with a
population of 10 million that ultimately experienced a cumulative incidence
of symptomatic infection with the pandemic strain of 30 per cent, the total
number of deaths would range from 12 to 1800.
Table: Case fatality ratio for symptomatic infection with influenza
A(H1N1)v pandemic strain in developed countries, estimated by 4 different
methods [abbreviated]:
Method / Range of CFR (per cent) / Projected number of deaths in developed
country of 10 million inhabitants
1 / 0.004 - 0.06 / 120 - 1800
2 / 0.01 - 0.03 / 300 - 900
3 / 0.002 - 0.003 / 60 - 90
4 / 0.0004 - 0.003 / 12 - 90
Discussion
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All these estimated CFRs are substantially lower than the previously
published estimate (0.4 per cent for Mexico). They also differ markedly
from the simplistic estimate that would be derived from using surveillance
data available only for confirmed cases reported to WHO (that is, CFR =
0.29 per cent, based on 110 deaths in 38 409 cases for the 29 OECD
countries used in this analysis [7]). A low CFR would be consistent with
the mild 1st wave seen in previous pandemics which caused widespread
infection but low mortality [19]. It could also be related to the
relatively young age of the majority of cases and the use of highly
effective modern treatment for those who are seriously ill.
Although based on the most current data possible, all the methods used
still have substantial limitations. The multiplier method merely relied on
the judgment (from other experts as well as ours) of widespread and
relatively mild disease that is not being reported. Nevertheless, the
suggestion of widespread community spread in the US is broadly consistent
with the community survey in New York City and another community survey in
the US with around 6 per cent cumulative incidence of ILI [14].
The New York City survey was limited by asking only about ILI that occurred
during a 20 day period in May 2009 and by ignoring illness in April 2009
even though there were hospitalisations in New York City in that month.
Therefore, the method using this survey could have overestimated the CFR,
although the opposite could have occurred if some of the reported ILI
symptoms were due to other respiratory infections and allergic conditions
such as hay fever.
The method that extrapolated from seasonal influenza mortality data in
people under 65 years of age was limited in that it effectively considered
no aspects of the epidemiology of the new pandemic influenza virus other
than the age distribution -- that is, that it seems to affect younger age
groups more than older age groups. Yet there is little information
comparing the current pandemic strain with seasonal influenza strains in
terms of mortality risk in this younger age group. Furthermore, the data
from which the estimated range was derived may be outdated in that modern
medical care has progressed since the early part of the period used in the
particular US study [15] that the estimates were based on.
Although the Canadian epidemic appears to be waning, the method using the
crude extrapolation of the course of this epidemic was very simplistic.
Indeed, rather than being half complete, this epidemic wave could continue
throughout the northern hemisphere summer and beyond.
These methods tended to focus on correcting for under-ascertainment of the
denominator, yet there is also a potential bias from underascertainment of
the numerator of the CFR. Particularly in the early stages of an epidemic,
there will be a lag in reported deaths and other severe outcomes.
Sophisticated statistical methods have been proposed for obtaining adjusted
CFR estimates using data from the early phase of an epidemic [20], and
these result in adjustment for various time lags and an upward shift of the
CFR. However, such adjustments would probably have little effect on the
estimates presented in this article which are based on data from country
epidemics which have progressed well beyond their early stages (for
example, the Canadian data). There is also the potential for
under-recognition of deaths attributable to influenza in those with serious
co-morbidities, but this can only be addressed by careful research studies
and post-epidemic modelling to determine total excess deaths. Nevertheless,
this bias might be relatively smaller in this pandemic where more deaths
involve young people. Also, once the new influenza A(H1N1)v strain was
recognised, there is likely to have been increased sensitivity for
diagnosing influenza-related deaths (at least in developed countries where
hospitalisation is likely to precede influenza-related death).
All of the presented methods have limitations and could be refined using
additional data to provide more robust estimates. Ultimately, such
estimates require enhanced surveillance, outbreak investigations in a range
of settings, and carefully designed population studies, ideally with
serological testing [21]. Additionally, the ranges of CFRs for
disadvantaged populations in developed countries and for most of the
population in developing countries are likely to be much higher than those
estimated here, given likely differences in disease transmission,
co-morbidity, access to antivirals and standards of medical care.
Conclusion
----------
We present several methods for provisionally estimating the plausible range
for the CFR of the emerging influenza pandemic in developed countries. All
methods used have significant limitations, but they collectively suggest
that infection with this particular pandemic strain is likely to cause
illness with a relatively low CFR compared to an earlier estimate and also
to historical standards. A further reason for presenting this range of
methods is to encourage data collection that can start to reduce the
uncertainty around this important pandemic parameter.
References
----------
1. Fraser C, Donnelly CA, Cauchemez S, Hanage WP, Van Kerkhove MD,
Hollingsworth TD, et al. Pandemic potential of a strain of influenza A
(H1N1): early findings. Science 2009; 324(5934): 1557-61.
2. CDC. CDC telebriefing on investigation of human cases of novel influenza
A (H1N1). 18 June 2009. Atlanta: CDC; 2009. Available from:
<http://www.cdc.gov/media/transcripts/2009/t090618.htm>.
3. CDC. Update on the novel influenza A H1N1 virus and new findings
published today. 22 May 2009. Atlanta: CDC; 2009. Available from:
<http://www.cdc.gov/media/transcripts/2009/t090522.htm>.
4. Lean G. UK swine flu toll is really 30 000, says leading scientist.
London: The Independent; 24 May 2009. Available from:
<http://www.independent.co.uk/life-style/health-and-families/health-news/uk-swine-flu-toll-is-really-30000-says-leading-scientist-1690130.html>.
5. Molinari NA, Ortega-Sanchez IR, Messonnier ML, Thompson WW, Wortley PM,
Weintraub E, et al. The annual impact of seasonal influenza in the US:
measuring disease burden and costs. Vaccine 2007; 25(27): 5086-96.
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patients with swine-origin influenza A (H1N1) virus infection (4 May).
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7 WHO. Influenza A(H1N1) - update 54. 26 June 2009. Geneva: WHO; 2009.
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8. New York City Department of Health and Mental Hygiene (NYCDHMH).
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<http://www.nyc.gov/html/doh/downloads/pdf/cd/h1n1_citywide_survey.pdf>.
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10. NYCDHMH. Health Department survey suggests that 7 per cent of New
Yorkers had flu-like illness in May (press release 10 June 2009). New York:
NYCDHMH; 2009. Available from:
<http://www.nyc.gov/html/doh/html/pr2009/pr041-09.shtml>.
11. NYCDHMH. Health Department updates flu status (press release, 2 May
2009). New York: NYCDHMH; 2009. Available
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Census Bureau; 2009. Available from:
<http://factfinder.census.gov/servlet/SAFFPopulation?_submenuId=population_0&_sse=on>.
13. Public Health Agency of Canada. FluWatch: June 14, 2009 to June 20,
2009 (Week 24). Public Health Agency of Canada. Ottawa; 2009. Available
from: <http://www.phac-aspc.gc.ca/fluwatch/08-09/w24_09/index-eng.php>.
14. CDC. CDC telebriefing on investigation of human cases of novel
influenza A (H1N1). 26 June 2009. Atlanta: CDC; 2009. Available from:
<http://www.cdc.gov/media/transcripts/2009/t090626.htm>.
15. Thompson WW, Weintraub E, Dhankhar P, Cheng PY, Brammer L, Meltzer MI,
et al. Estimates of US influenza-associated deaths made using four
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16. United States Census Bureau. Quick table (QT-P1A): age and sex for the
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from:
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18. Milne GJ, Kelso JK, Kelly HA, Huband ST, McVernon J. A small community
model for the transmission of infectious diseases: comparison of school
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pandemic. PLoS One 2008; 3(12): e4005.
19. Miller MA, Viboud C, Balinska M, Simonsen L. The signature features of
influenza pandemics--implications for policy. N Engl J Med 2009; 360(25):
2595-8.
20. Ghani AC, Donnelly CA, Cox DR, Griffin JT, Fraser C, Lam TH, et al.
Methods for estimating the case fatality ratio for a novel, emerging
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reducing uncertainty in an emerging influenza pandemic. N Engl J Med 28 May
2009; [E-pub ahead of print].
--
communicated by:
ProMED-mail <promed@promedmail.org>
[The authors have indicated that their methods tended to focus on
correcting for underascertainment of the denominator. All methods used have
significant limitations, but they collectively suggest that infection with
this particular pandemic strain is likely to cause illness with a
relatively low CFR compared with an earlier estimate and also to historical
standards. - Mod.CP]
******
[4] Tamiflu resistance - Japan
Date: Thu 2 Jul 2009
Source: Reuters News [edited]
<http://www.reuters.com/article/internal_ReutersNewsRoom_ExclusivesAndWins_MOLT/idUSTRE5614TW20090702>
Japan has confirmed its 1st case of a genetic mutation of the new H1N1
influenza that shows resistance to Tamiflu [oseltamivir], the main
antiviral flu drug, a health ministry official said on Thursday [2 Jul 2009].
The World Health Organization has declared a global pandemic is under way
from the virus, known as swine flu, which has so far been treatable with
Tamiflu, made by Switzerland's Roche. Takeshi Enami, an official at Japan's
health ministry, said that the patient's sensitivity to Tamiflu had yet to
be tested.
The patient, who was confirmed in May 2009 with the H1N1 strain of the flu
in the Osaka prefecture of western Japan, has since recovered, and no other
cases of the new flu have been confirmed around the patient, Enami said. He
could not confirm the age or the sex of the patient.
The 1st case of H1N1 that did not respond to Tamiflu was a patient in Denmark.
Earlier this week, WHO said that the case, revealed by Roche and Danish
officials on Monday [29 Jun 2009], was an isolated one and did not amplify
the severity of the virus. Resistance to Tamiflu has been previously
documented in the deadly bird flu virus H5N1 and seasonal H1N1 flu.
--
communicated by:
ProMED-mail <promed@promedmail.org>
[Dr Irene Lai of SOS International has provided the following information
with regard to the 1st occurrence of Tamiflu-resistance (in Denmark).
According to the press release from Denmark's State Serum Institute
(<http://www.ssi.dk/sw174.asp?PAGE=3D1&ArtNo=3D3651423>), the strain
isolated from the Danish patient remains sensitive to the alternate
neuraminidase inhibitor, zanamivir. In that case, the resistance arose in a
person who was on post-exposure prophylaxis with Tamiflu [oseltamivir]. -
Mod.CP]
[see also:
Influenza A (H1N1) - worldwide (80): Argentina, human to pig 20090701.2376
Influenza A (H1N1) - worldwide (79): case count 20090701.2372
Influenza A (H1N1) - worldwide (78): Tamiflu resistance, DK 20090630.2359
Influenza A (H1N1) - worldwide (77): case count 20090627.2338
Influenza A (H1N1) - worldwide (76): comments on 1918 virus (03) 20090625.2309
Influenza A (H1N1) - worldwide (74): susp. origin 20090624.2303
Influenza A (H1N1) - worldwide (73): case count, epidemiology 20090622.2288
Influenza A (H1N1) - worldwide (72): case count, epidemiology 20090619.2261
Influenza A (H1N1) - worldwide (70): risk factors 20090619.2260
Influenza A (H1N1) - worldwide (69): other viral infections 20090618.2254
Influenza A (H1N1) - worldwide (68): southern hemisphere 20090618.2253
Influenza A (H1N1) - worldwide (65): antivirals in pregnancy 20090616.2224
Influenza A (H1N1) - worldwide (64): case count, pandemic 20090616.2221
Influenza A (H1N1) - worldwide (62): Egypt, Lebanon 20090611.2150
Influenza A (H1N1) - worldwide (62): Egypt, Lebanon 20090611.2150
Influenza A (H1N1) - worldwide (60): Egypt (Cairo) 20090608.2117
Influenza A (H1N1) - worldwide (59): Worldwide 20060608.2117
Influenza A (H1N1) - worldwide (58): USA, Africa 20090607.2109
Influenza A (H1N1) - worldwide (57): Brazil, USA 20090605.2090
Influenza A (H1N1) - worldwide (55) 20090603.2056
Influenza A (H1N1) - worldwide (47): China, epidemiology 20090526.1962
Influenza A (H1N1) - worldwide (45) 20090525.1951
Influenza A (H1N1) - worldwide (42) 20090523.1929
Influenza A (H1N1) - worldwide (39) 20090521.1903
Influenza A (H1N1) - worldwide (37) 20090520.1893
Influenza A (H1N1) - worldwide (34) 20090518.1863
Influenza A (H1N1) - worldwide (31) 20090516.1835
Influenza A (H1N1) - worldwide (29) 20090515.1824
Influenza A (H1N1) - worldwide (26) 20090514.1798
Influenza A (H1N1) - worldwide (23) 20090511.1764
Influenza A (H1N1) - worldwide (21) 20090510.1749
Influenza A (H1N1) - worldwide (19) 20090509.1733
Influenza A (H1N1) - worldwide (17) 20090508.1722
Influenza (H1N1) - worldwide (15) 20090507.1709
Influenza A (H1N1) - worldwide (13) 20090506.1695
Influenza A (H1N1) - worldwide (11): coincident H3N2 variation 20090505.1679
Influenza A (H1N1) - worldwide (09) 20090504.1673
Influenza A (H1N1) - worldwide (07) 20090503.1658
Influenza A (H1N1) - worldwide (05) 20090503.1657
Influenza A (H1N1) - worldwide (03) 20090501.1646
Influenza A (H1N1) - worldwide (02): case counts 20090430.1638
Influenza A (H1N1) - worldwide 20090430.1636
Influenza A (H1N1) "swine flu": worldwide (07), update, pandemic 5
20090429.1622
Influenza A (H1N1) "swine flu": Worldwide 20090427.1583
Influenza A (H1N1) virus, human: worldwide 20090426.1577
Influenza A (H1N1) virus, human - New Zealand, susp 20090426.1574
Influenza A (H1N1) virus, human - N America (04) 20090426.1569
Influenza A (H1N1) virus, human - N America 20090425.1552
Acute respiratory disease - Mexico, swine virus susp 20090424.1546
Influenza A (H1N1) virus, swine, human - USA (02): (CA, TX) 20090424.1541
Influenza A (H1N1) virus, swine, human - USA: (CA) 20090422.1516
Influenza A (H1N1) virus, swine, human - Spain 20090220.0715]
.....................cp/mpp/msp/sh
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