Summary:
Swine flu is the most recent pandemic scare. Specifically, this pandemic
is supposed to occur as a result of a mutation in the common H1N1 flu type. Since
H1N1 has predominated in the U.S. in the last two flu seasons, there will be deaths involved
with that type. Every year there are deaths due to influenza, predominantly in
the elderly and in very young children.
But the distinction necessary here is whether
the Mexican variation is spreading to the U.S.
and infecting healthy individuals with a potentially lethal strain? At this point,
because the CDC of Maine is announcing confirmed cases before genetic confirmation can be obtained, we must assume that somewhere
someone has jumped from scientific evidence to hysteria.
The purchase of millions of dollars worth of
Tamiflu (oseltamivir) is also somewhat suspicious as a protective tactic. Already
a large percentage of H1N1 cases are resistant to Tamiflu and we have no information on medline showing that Tamiflu is effective
against this outbreak. So we are purchasing a false insurance policy.
Given the current hysteria, we should all stockpile
our garlic and elderberry again. Both are as likely to be as effective as Tamiflu.
Elderberry has been specifically shown to be effective against the H1N1 strains. But
a far more effective route to prevention would be to follow the flu and cold prevention guidelines (found on the What Do I
Treat? Page).
I trust the
hysteria will pass, and we will know if this is indeed a threat. If you are overly concerned, please read about
the avian flu threat, which was more credible and did not result in a pandemic. The real problem here is how
often the CDC can cry wolf before we stop listening. Someone needs to stop shouting pandemic every time we have
a mutation, because they happen every year.
MMWR Morb Mortal Wkly Rep. 2009 Apr 24;58(15):400-2.
Links
Swine Influenza A (H1N1) infection in two children--Southern California, March-April 2009.Centers for Disease Control and Prevention (CDC).
On April 17, 2009, CDC determined that two
cases of febrile respiratory illness occurring in children who resided in adjacent counties in southern California were caused by infection with a swine influenza A (H1N1) virus. The viruses from
the two cases are closely related genetically, resistant to amantadine and rimantadine, and contain a unique combination of
gene segments that previously has not been reported among swine or human influenza viruses in the United States or elsewhere. Neither child had contact with pigs; the source of
the infection is unknown. Investigations to identify the source of infection and to determine whether additional persons have
been ill from infection with similar swine influenza viruses are ongoing. This report briefly describes the two cases and
the investigations currently under way. Although this is not a new subtype of influenza A in humans, concern exists that
this new strain of swine influenza A (H1N1) is substantially different from human influenza A (H1N1) viruses, that a large
proportion of the population might be susceptible to infection, and that the seasonal influenza vaccine H1N1 strain might
not provide protection. The lack of known exposure to pigs in the two cases increases the possibility that human-to-human
transmission of this new influenza virus has occurred. Clinicians should consider animal as well as seasonal influenza virus
infections in their differential diagnosis of patients who have febrile respiratory illness and who 1) live in San Diego and
Imperial counties or 2) traveled to these counties or were in contact with ill persons from these counties in the 7 days preceding
their illness onset, or 3) had recent exposure to pigs. Clinicians who suspect swine influenza virus infections in a patient
should obtain a respiratory specimen and contact their state or local health department to facilitate testing at a state public
health laboratory.
PMID: 19390508
JAMA. 2009 Mar 11;301(10):1034-41. Epub 2009
Mar 2. Links
Comment in:
JAMA. 2009 Mar 11;301(10):1066-9.
Infections with oseltamivir-resistant influenza
A(H1N1) virus in the United States.Dharan NJ, Gubareva LV, Meyer JJ, Okomo-Adhiambo M, McClinton RC, Marshall SA, St George
K, Epperson S, Brammer L, Klimov AI, Bresee JS, Fry AM; Oseltamivir-Resistance Working Group.
Collaborators (44)
Ahmed F, Nalluswami K, Bascom SD, Berisha V,
Boulton RB, Cohen J, Corkren E, Crockett M, Dao C, Deyde VM, Hall H, Patton M, Sheu TG, Wallis TR, Hales C, Sunenshine R,
Erhart LM, Komatsu K, Sunenshine R, Goodin K, Hanson M, Koepsell J, Rietberg K, Haupt T, Laplante JM, Mingle L, Linchangco
P, Louie J, Moore A, McHugh L, Moore Z, Najera R, Park S, Rajan R, Person CJ, Yousey-Hindes K, Powell RJ, Reisdorf E, Shult
PA, Van TT, Richards SM, Siston A, Stoute A, Van Houten C Jr.
Epidemic Intelligence Service, Office of Workforce
and Career Development Assigned to Influenza Division, Centers for Disease Control and Prevention, 1600 Clifton Rd, MS A-32,
Atlanta, GA 30333, USA. nfd6@cdc.gov
CONTEXT: During the 2007-2008 influenza season,
oseltamivir resistance among influenza A(H1N1) viruses increased significantly for the first time worldwide. Early surveillance
data suggest that the prevalence of oseltamivir resistance among A(H1N1) viruses will most likely be higher during the 2008-2009
season. OBJECTIVES: To describe patients infected with oseltamivir-resistant influenza A(H1N1) virus and to determine whether
there were any differences between these patients and patients infected with oseltamivir-susceptible A(H1N1) virus in demographic
or epidemiological characteristics, clinical symptoms, severity of illness, or clinical outcomes. DESIGN, SETTING, AND PATIENTS:
Influenza A(H1N1) viruses that were identified and submitted to the Centers for Disease Control and Prevention by US public
health laboratories between September 30, 2007, and May 17, 2008, and between September 28, 2008, and February 19, 2009, were
tested as part of ongoing surveillance. Oseltamivir resistance was determined by neuraminidase inhibition assay and pyrosequencing
analysis. Information was collected using a standardized case form from patients with oseltamivir-resistant A(H1N1) infections
and a comparison group of patients with oseltamivir-susceptible A(H1N1) infections during 2007-2008. MAIN OUTCOME MEASURES:
Demographic and epidemiological information as well as clinical information, including symptoms, severity of illness, and
clinical outcomes. RESULTS: During the 2007-2008 season, influenza A(H1N1) accounted for an estimated 19% of circulating
influenza viruses in the United States.
Among 1155 influenza A(H1N1) viruses tested from 45 states, 142 (12.3%) from 24 states were resistant to oseltamivir.
Data were available for 99 oseltamivir-resistant cases and 182 oseltamivir-susceptible cases from this period. Among resistant
cases, median age was 19 years (range, 1 month to 62 years), 5 patients (5%) were hospitalized, and 4 patients (4%) died.
None reported oseltamivir exposure before influenza diagnostic sample collection. No significant differences were found between
cases of oseltamivir-resistant and oseltamivir-susceptible influenza in demographic characteristics, underlying medical illness,
or clinical symptoms. Preliminary data from the 2008-2009 influenza season identified resistance to oseltamivir among 264
of 268 influenza A(H1N1) viruses (98.5%) tested. CONCLUSIONS: Oseltamivir-resistant A(H1N1) viruses circulated widely in the
United States during the 2007-2008 influenza
season, appeared to be unrelated to oseltamivir use, and appeared to cause illness similar to oseltamivir-susceptible A(H1N1)
viruses. Circulation of oseltamivir-resistant A(H1N1) viruses will continue, with a higher prevalence of resistance, during
the 2008-2009 season.
PMID: 19255110
MMWR Morb Mortal Wkly Rep. 2009 Apr 17;58(14):369-74.
Links
Update: influenza activity--United States, September 28, 2008-April 4, 2009, and composition
of the 2009-10 influenza vaccine.Centers for Disease Control and Prevention (CDC).
This report summarizes U.S. influenza activity from September 28, 2008, the start
of the 2008-09 influenza season, through April 4, 2009, and reports on the 2009-10 influenza vaccine strain selection. Low
levels of influenza activity were reported from October through early January. Activity increased from mid-January and peaked
in mid-February. Influenza A (H1N1) viruses have predominated overall this season, but influenza B viruses have been
isolated more frequently than influenza A viruses since mid-March. Widespread oseltamivir resistance was detected among
circulating influenza A (H1N1) viruses and a high level of adamantane resistance was identified among influenza A (H3N2)
viruses.
PMID: 19373198
MMWR Morb Mortal Wkly Rep. 2008 Jun 27;57(25):692-7.
Links
Influenza activity--United States and worldwide, 2007-08 season.Centers for Disease Control and Prevention
(CDC).
During the 2007-08 influenza season, influenza
activity peaked in mid-February in the United States
and was associated with greater mortality and higher rates of hospitalization of children aged 0-4 years, compared with each
of the previous three seasons. In the United States,
influenza A (H1N1) was the predominant strain early in the season; influenza A (H3N2) viruses increased in circulation
in January and predominated overall. While influenza A (H1N1), A (H3N2), and B viruses cocirculated worldwide, influenza A
(H1N1) viruses were most commonly reported in Canada, Europe, and Africa, and influenza B viruses were predominant in most
Asian countries. This report summarizes influenza activity in the United
States and worldwide during the 2007-08 influenza season (September 30, 2007-May 17, 2008).
PMID: 18583957
Emerg Infect Dis. 2009 Apr;15(4):552-60. Links
Oseltamivir-resistant influenza virus A (H1N1),
Europe, 2007-08 Season.Meijer A, Lackenby A, Hungnes O, Lina B, van-der-Werf S, Schweiger B, Opp M, Paget J, van-de-Kassteele
J, Hay A, Zambon M; European Influenza Surveillance Scheme.
Collaborators (117)
Lachner P, Popow-Kraupp T, Strauss R, Brochier
B, Sabbe M, Thomas I, Casteren V, Yane F, Georgieva T, Kojouharova M, Kotseva R, Kurchatova A, Aleraj B, Drazenovic V, Bagatzouni-Pieridou
D, Elia A, Havlickova M, Kyncl J, Glismann S, Mazick A, Nielsen L, Fleming DM, Lackenby A, Watson J, Zambon M, Sadikova O,
Sarv I, Ziegler T, Cohen JM, Enouf V, Lina B, Mosnier A, Valette M, van der Werf S, Buchholz U, Haas W, Schweiger B, Kossivakis
AG, Kyriazopoulou-Dalaina V, Mentis A, Spala G, Berencsi G, Csohán A, Jankovics I, Coughlan S, Domegan L, Duffy M, Joyce M,
O'Donnell J, O'Flanagan D, Ansaldi F, Crovari P, Donatelli I, Pregliasco F, Nikiforova R, Van Velicko I, Zamjatina N, Griskevicius
A, Kupreviciene N, Rimseliene G, Mossong J, Opp M, Barbara C, Melillo T, Arkema A, Meerhoff T, Paget WJ, van der Velden K,
Dijkstra F, Donker G, de Jong JC, Meijer A, Rimmelzwaan G, van der Sande M, Wilbrink B, Coyle P, Kennedy H, O'Neill H, Hungnes
O, Iversen B, Brydak L, Romanowska M, Falcăo IM, Falcăo JM, Rebelo de Andrade H, Alexandrescu V, Lupulescu E, Carman W, Gunson
R, Kean J, McMenamin J, Milic N, Nedeljkovic J, Blaskovicova H, Kristufkova Z, Sláciková M, Prosenc K, Socan M, Casas I, Larrrauri
A, de Mateo S, Ortiz de Lejarazu R, Pérez-Breńa P, Pumarola Suńé T, Vega Alonso T, Brytting M, Linde A, Penttinen P, Rubinova
S, Thomas Y, Witschi M, Yilmaz N, Aranova M, Mironenko A, Hay A, Jones R, Thomas D.
Netherlands Institute for Health Services Research,
Utrecht, the Netherlands.
In Europe,
the 2007-08 winter season was dominated by influenza virus A (H1N1) circulation through week 7, followed by influenza B virus
from week 8 onward. Oseltamivir-resistant influenza viruses A (H1N1) (ORVs) with H275Y mutation in the neuraminidase emerged
independently of drug use. By country, the proportion of ORVs ranged from 0% to 68%, with the highest proportion in Norway.
The average weighted prevalence of ORVs across Europe increased gradually over time, from
near 0 in week 40 of 2007 to 56% in week 19 of 2008 (mean 20%). Neuraminidase genes of ORVs possessing the H275Y substitution
formed a homogeneous subgroup closely related to, but distinguishable from, those of oseltamivir-sensitive influenza viruses
A (H1N1). Minor variants of ORVs emerged independently, indicating multiclonal ORVs. Overall, the clinical effect of ORVs
in Europe, measured by influenza-like illness or acute respiratory infection, was unremarkable
and consistent with normal seasonal activity.
PMID: 19331731
Clin Infect Dis. 2009 May 1;48(9):1254-6. Links
Influenza virus resistance to antiviral agents:
a plea for rational use.Poland GA, Jacobson RM, Ovsyannikova IG.
Mayo Vaccine Research Group, Department of
Internal Medicine, Mayo Clinic, Rochester, Minnesota,
USA.
Although influenza vaccine can prevent influenza
virus infection, the only therapeutic options to treat influenza virus infection are antiviral agents. At the current time,
nearly all influenza A/H3N2 viruses and a percentage of influenza A/H1N1 viruses are adamantane resistant, which leaves only
neuraminidase inhibitors available for treatment of infection with these viruses. In December 2008, the Centers for Disease
Control and Prevention released new data demonstrating that a high percentage of circulating influenza A/H1N1 viruses are
now resistant to oseltamivir. In addition, oseltamivir-resistant influenza B and A/H5N1 viruses have been identified. Thus,
use of monotherapy for influenza virus infection is irrational and may contribute to mutational pressure for further selection
of antiviral-resistant strains. History has demonstrated that monotherapy for influenza virus infection leads to resistance,
resulting in the use of a new monotherapy agent followed by resistance to that new agent and thus resulting in a background
of viruses resistant to both drugs. We argue that combination antiviral therapy, new guidelines for indications for treatment,
point-of-care diagnostic testing, and a universal influenza vaccination recommendation are critical to protecting the population
against influenza virus and to preserving the benefits of antiviral agents.
PMID: 19323631