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THE AVIAN FLU IS COMING!

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Summary: Avian flu has been here, is here, and will continue to be here. It has been transmissible, is transmissible, and will continue to be transmissible. The chances of a global pandemic are always present, but the numbers of deaths and disease are greatly inflated by expanding a tiny infected pool onto the entire population. We are far more likely to die of cancer, heart disease, and car accidents than the Avian flu, even if it hits Augusta. If you are worried, black elderberry makes a reasonably good pancake topping.
The Avian Flu is coming! The Avian Flu is coming!



By Christopher Maloney, N.D.



Actually, it has been here for 100 years. It was first recognized in Italy, has undergone multiple mutations, and will be with us for the rest of our lives.


Bird flu is endemic (always there) in wild bird populations. Unless we kill all wild fowl, the Avian flu will be there for us to worry about.


What will happen when it reaches the U.S.? Well, it has already been to America. (Emerg Infect Dis. 2004 Dec;10(12):2196) It struck in British Columbia, where two chicken farmers came down with (gasp!) "confirmed avian influenza infection. Symptoms included conjunctivitis and mild influenzalike illness." No one died.


The projections on death rates for the U.S. are absolutely staggering, because they are based on confirmed reports of influenza and confirmed deaths. Keep in mind that confirmed deaths are solid, but confirmed reports of the virus are likely to be highly underreported. Become a chicken farmer for a moment. You have the choice of getting yourself checked every time you get a sniffle, and if you are positive you get to slaughter your entire livelihood and live in quarantine. So naturally, the death to survival rate is highly skewed and we are all shaking our hands in dismay about the coming pandemic. Confirmed deaths for SARS were 800 for 8000 confirmed cases (10%). The projections based on a maximum of 23 deaths from Avian flu put the death rate at almost 50%. That is because the confirmed cases are only about double the death rate.


Ah, but the death rate will be much higher because the avian flu will make the deadly switch to human-to-human transmission! Actually, it already has. (N Engl J Med. 2005 Jan 27;352(4):333) Analysis of the Thai outbreak concluded: "disease in the mother and aunt probably resulted from person-to-person transmission of this lethal avian influenza virus." If the virus was transmitting from person-to-person, why was the Thai death rate only 32, with confirmed cases at only 44? They weren't slaughtering the people, just the chickens. That should have been the beginning of the pandemic, right there.


Conveniently, a designer drug has hit the market to specifically counteract the coming pandemic. Tamiflu is here to save us, which is good because its competitor caused serious neurological problems in 25% of those taking it (Tamiflu only affected 5%). (Infect Control Hosp Epidemiol. 2004 Nov;25(11):955-61) We should note that Tamiflu is only effective on the specific flu strains, that it was introduced in 2003 and already 18% of children present with resistant strains, and unless it gets purchased in mass quantities for the coming pandemic, its "shelf life will expire."


So what are we to do? Well, black elderberry is effective against: "human influenza viruses type A/Shangdong 9/93 (H3N2), A/Beijing 32/92 (H3N2), A/Texas 36/91 (H1N1), A/Singapore 6/86 (H1N1), type B/Panama 45/90, B/Yamagata 16/88, B/Ann Arbor 1/86, and of animal strains from Northern European swine and turkeys, A/Sw/Ger 2/81, A/Tur/Ger 3/91, and A/Sw/Ger 8533/91" (J Altern Complement Med. 1995 Winter;1(4):361-9) It works: "A complete cure was achieved within 2 to 3 days in nearly 90% of the SAM-treated group and within at least 6 days in the placebo group" and it doesn't depend on a specific gene for treatment, unlike the Tamiflu.


But don't believe me, read all the studies for yourself. Everything I just quoted is below, all taken directly from medline.


In the articles, oseltamivir is Tamiflu. My apologies for the medicalese. The shorthand is that it says exactly what I said above, because I did not have a preconceived notion about the Avian flu, I just want to help people cope with it.


Infect Control Hosp Epidemiol. 2004 Nov;25(11):955-61. Related Articles, Links

Adverse effects of amantadine and oseltamivir used during respiratory outbreaks in a center for developmentally disabled adults.

McGeer AJ, Lee W, Loeb M, Simor AE, McArthur M, Green K, Benjamin JH, Gardner C.

Department of Microbiology, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.

BACKGROUND AND OBJECTIVES: Antiviral prophylaxis is recommended for the control of institutional influenza A outbreaks. In long-term-care institutions other than nursing homes, neither the seriousness of influenza nor the risks and benefits of antiviral prophylaxis is clearly understood. We studied the severity of illness due to influenza among adults residing in a center for the developmentally disabled and assessed adverse reactions to amantadine and oseltamivir prophylaxis. METHODS: Data were collected from the charts of consenting residents. Complications of upper respiratory tract illness were recorded. Potential adverse events were documented during amantadine and oseltamivir therapy, and during a baseline period with neither medication. RESULTS: The median age of the 287 participants was 46.4 years. Only 15 (5%) were older than 65 years, and 69 (24%) had chronic underlying medical illness placing them at high risk for influenza. Of the 122 residents with an upper respiratory tract infection, 16 (13%) developed pneumonia, 12 (9.8%) were hospitalized, and 5 (4%) died. Twenty-eight (25%) of 112 residents had an adverse neurologic event while receiving amantadine prophylaxis, compared with 3 (2.7%) receiving no antiviral medication and 5 (4.5%) receiving oseltamivir (P < .001). Sixteen percent of the residents discontinued amantadine due to adverse events; in contrast, adverse events were identified in 2.9% of the residents prescribed oseltamivir, and none discontinued therapy. CONCLUSIONS: Viral respiratory tract infections are associated with a high risk of complications in this population. The rate of adverse neurologic events associated with amantadine was significantly higher than that associated with oseltamivir.

PMID: 15566030 [PubMed - indexed for MEDLINE]

Antivir Chem Chemother. 2004 Sep;15(5):261-8.

Treatment of mannan-enhanced influenza B virus infections in mice with oseltamivir, ribavirin and viramidine.

Smee DF, Wandersee MK, Wong MH, Bailey KW, Sidwell RW.

Institute for Antiviral Research, Department of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA. dsmee@cc.usu.edu

Mannan, a polysaccharide preparation from Saccharomyces cerevisiae, has previously been shown to enhance influenza virus replication in mice by inhibiting host defense collectins. The use of mannan in infections may serve to broaden the types of influenza viruses that can be studied in rodent infection models. When mannan was co-administered with influenza B/Sichuan/379/99 virus to mice, the animals died from the infection, whereas mice infected with only virus survived. Three types of influenza A (H1N1) and another influenza B (Hong Kong/330/01) virus infection were also enhanced by mannan, but not four types of influenza A (H3N2) viruses. Mannan was used at 0.16 or 0.5 mg/mouse for optimal disease-enhancing activity using influenza B/Sichuan/379/99 virus. Using this model, influenza B/Sichuan/379/99 infections were treated with oseltamivir, ribavirin or viramidine (the carboxamidine derivative of ribavirin). When oral gavage treatments started 4 h before virus and mannan challenge, oseltamivir was effective at 2.5, 5 and 10 mg/kg/day. Ribavirin was active at 20, 40 and 80 mg/kg/day. Viramidine was effective at 80 and 160 mg/kg/day but not at 40 mg/kg/day. Active drug doses improved lung consolidation scores and lung weights, with decreases in lung virus titres also noted. Arterial oxygen saturation values in treated groups were significantly better than those of the placebo group on days 7-11 of the infection. Oseltamivir (5 mg/kg/day) and ribavirin (40 mg/kg/day) were used alone and in combination to determine how late after infection they could be beneficially administered. Ribavirin alone was very effective (90-100% survival of mice) when treatments started as late as 3 days after infection. Forty percent survival was evident even when treatments started 4 days post-infection. Oseltamivir was active starting treatments 1 day after virus exposure, but lost considerable efficacy when treatments began after that time. The combination of ribavirin and oseltamivir appeared to be no better than ribavirin alone, due to the stronger beneficial effect of ribavirin in this model. The overall results demonstrate that mannan can be used to enhance certain non-lethal influenza virus infections sufficiently to allow antiviral studies.

PMID: 15535048 [PubMed - indexed for MEDLINE]

Commun Dis Intell. 2003;27(4):542-7.

Surveillance for neuraminidase inhibitor resistance in human influenza viruses from Australia.

Hurt AC, Barr IG, Durrant CJ, Shaw RP, Sjogren HM, Hampson AW.

WHO Collaborating Centre for Reference and Research on Influenza, Melbourne, Australia. Aeron_Hurt@csl.com.au

Two hundred and forty-five human influenza A and B viruses isolated in Australia between 1996 and 2003 were tested for their sensitivity to the NA inhibitor drugs, zanamivir and oseltamivir using a fluorescence-based neuraminidase inhibition assay. Based on mean IC50 values, influenza A viruses (with neuraminidase subtypes N1 and N2) were more sensitive to both the NA inhibitors than were influenza B strains. Influenza A viruses with a N1 subtype and influenza B strains both demonstrated a greater sensitivity to zanamivir than to oseltamivir carboxylate, whereas influenza A strains with a N2 subtype were more susceptible to oseltamivir carboxylate. A comparison of IC50 values for viruses isolated before and after the release of the NA inhibitors in Australia, found there was no significant difference in the sensitivity of strains to either neuraminidase inhibitor and none of the isolates tested showed clinically significant resistance.

PMID: 15508516 [PubMed - indexed for MEDLINE]

Expert Rev Anti Infect Ther. 2003 Aug;1(2):337-42. Related Articles, Links

A designer drug against influenza: the NA inhibitor oseltamivir (Tamiflu).

Oxford JS, Mann A, Lambkin R.

Retroscreen Virology Ltd, Bart's and The London, Queen Mary's School of Medicine and Dentistry, 327 Mile End Road, London E1 4NS, UK.

The description of the first two designer antiviral drugs to fight influenza was a ground breaking advance. Targeted against the influenza neuraminidase enzyme these inhibitors have been shown to reduce both the severity and duration of influenza illness. Importantly, it is expected that these neuraminidase inhibitors would be effective against influenza pandemic strain and could therefore be vital at reducing the potentially devastating consequences of such an outbreak. Despite the demonstrated efficacy of these drugs, they are not commonly used, particularly in the UK, and there is substantial concern that in the event of a pandemic or even a severe epidemic there could be substantial morbidity and mortality. SARS has shown that the public and media response to a serious epidemic is not always rational and this could easily become panic if it became apparent that treatment was possible, but not available.

Publication Types:

* Review

* Review, Multicase

PMID: 15482128 [PubMed - indexed for MEDLINE]

J Infect Dis. 2004 Nov 1;190(9):1627-30. Epub 2004 Sep 28. Related Articles, Links

Influenza viruses resistant to the antiviral drug oseltamivir: transmission studies in ferrets.

Herlocher ML, Truscon R, Elias S, Yen HL, Roberts NA, Ohmit SE, Monto AS.

Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, Michigan 48109, USA.

Three type A influenza viruses, each of which has a distinct neuraminidase-gene mutation and is resistant to the neuraminidase inhibitor oseltamivir, have been isolated. Previously, in the ferret model, an R292K mutant of a type A (H3N2) virus was not transmitted under conditions in which the wild-type virus was transmitted. This model was used to investigate whether the E119V mutant of a type A (H3N2) virus and the H274Y mutant of a type A (H1N1) virus would be transmitted under similar circumstances. Both mutant viruses were transmitted, although the H274Y mutant required a 100-fold-higher dose for infection of donor ferrets and was transmitted more slowly than was the wild type. Both the mutant and the wild-type viruses retained their genotypic characteristics.

PMID: 15478068 [PubMed - indexed for MEDLINE]

Clin Infect Dis. 2004 Aug 15;39(4):459-64. Epub 2004 Aug 2.
Comment in:

* Clin Infect Dis. 2004 Aug 15;39(4):465-7.

* Clin Infect Dis. 2005 Feb 1;40(3):492-3.

Detection and control of influenza outbreaks in well-vaccinated nursing home populations.


Monto AS, Rotthoff J, Teich E, Herlocher ML, Truscon R, Yen HL, Elias S, Ohmit SE.

Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI 48109-2029, USA. asmonto@umich.edu

BACKGROUND: Influenza outbreaks continue to occur in nursing homes despite high vaccination coverage among residents. Recommendations for outbreak control in institutions such as nursing homes advises use of antiviral drugs to reduce influenza transmission. METHODS: Influenza surveillance was performed among elderly residents of nursing homes in Michigan during 2 influenza seasons. The antiviral drug oseltamivir was used for outbreak control at the discretion of nursing home staff once influenza transmission was confirmed by virus isolation or rapid antigen detection. RESULTS: During 2000-2001, influenza was not confirmed in any of the 28 participating homes, despite transmission of types A (H1N1) and B in the community. During 2001-2002, influenza type A (H3N2) transmission was confirmed in 8 (26%) of 31 participating homes; influenza vaccine coverage among residents was 57%- 98% in outbreak-associated homes. Oseltamivir was used in all homes with influenza transmission; outbreak control varied according to the rapidity of outbreak recognition and the extent of antiviral use. Reported adverse events were primarily gastrointestinal reactions and rashes. Analysis of the usefulness of rapid antigen detection tests for outbreak recognition indicated a sensitivity of only 77% (specificity, 92%). CONCLUSIONS: Oseltamivir was reasonably well tolerated, and its use, along with continued promotion of vaccination coverage among nursing home residents and staff, should be a valuable addition to institutional outbreak-control strategies.

PMID: 15356805 [PubMed - indexed for MEDLINE]

Lancet. 2004 Aug 28-Sep 3;364(9436):759-65. Related Articles, Links

Comment in:

* Lancet. 2004 Aug 28-Sep 3;364(9436):733-4.

Resistant influenza A viruses in children treated with oseltamivir: descriptive study.

Kiso M, Mitamura K, Sakai-Tagawa Y, Shiraishi K, Kawakami C, Kimura K, Hayden FG, Sugaya N, Kawaoka Y.

Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.

BACKGROUND: Oseltamivir is an effective inhibitor of influenza virus neuraminidase. Although viruses resistant to oseltamivir emerge less frequently than those resistant to amantadine or rimantadine, information on oseltamivir-resistant viruses arising during clinical use of the drug in children is limited. Our aim was to investigate oseltamivir resistance in a group of children treated for influenza. METHODS: We analysed influenza A viruses (H3N2) collected from 50 children before and during treatment with oseltamivir. We sequenced the genes for neuraminidase and haemagglutinin and studied the mutant neuraminidases for their sensitivity to oseltamivir carboxylate. FINDINGS: We found neuraminidase mutations in viruses from nine patients (18%), six of whom had mutations at position 292 (Arg292Lys) and two at position 119 (Glu119Val), which are known to confer resistance to neuraminidase inhibitors. We also identified another mutation (Asn294Ser) in one patient. Sensitivity testing to oseltamivir carboxylate revealed that the neuraminidases of viruses that have an Arg292Lys, Glu119Val, or Asn294Ser mutation were about 10(4)-10(5)-fold, 500-fold, or 300-fold more resistant than their pretreatment neuraminidases, respectively. Oseltamivir-resistant viruses were first detected at day 4 of treatment and on each successive day of the study. More than 10(3) infectious units per mL of virus were detected in some of the patients who did not shed drug-resistant viruses, even after 5 days of treatment. INTERPRETATION: Oseltamivir-resistant mutants in children being treated for influenza with oseltamivir arise more frequently than previously reported. Furthermore, children can be a source of viral transmission, even after 5 days of treatment with oseltamivir.

PMID: 15337401 [PubMed - indexed for MEDLINE]

J Int Med Res. 2004 Mar-Apr;32(2):132-40.

Randomized study of the efficacy and safety of oral elderberry extract in the treatment of influenza A and B virus infections.

Zakay-Rones Z, Thom E, Wollan T, Wadstein J.

Department of Virology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Elderberry has been used in folk medicine for centuries to treat influenza, colds and sinusitis, and has been reported to have antiviral activity against influenza and herpes simplex. We investigated the efficacy and safety of oral elderberry syrup for treating influenza A and B infections. Sixty patients (aged 18-54 years) suffering from influenza-like symptoms for 48 h or less were enrolled in this randomized, double-blind, placebo-controlled study during the influenza season of 1999-2000 in Norway. Patients received 15 ml of elderberry or placebo syrup four times a day for 5 days, and recorded their symptoms using a visual analogue scale. Symptoms were relieved on average 4 days earlier and use of rescue medication was significantly less in those receiving elderberry extract compared with placebo. Elderberry extract seems to offer an efficient, safe and cost-effective treatment for influenza. These findings need to be confirmed in a larger study.

Publication Types:

* Clinical Trial

* Multicenter Study

* Randomized Controlled Trial

PMID: 15080016 [PubMed - indexed for MEDLINE]

Posit Health News. 1998 Fall;(No 17):12-4. Related Articles, Links

A new triple combination therapy.

Konlee M.

AIDS: Elderberry, chondroitin, and glucosamine sulfate have been found to block HIV replication at three distinct points in the replication cycle. For quadruple therapy, a reverse transcriptase inhibitor such as olive leaf extract or Epivir (3TC) could be added. In one case, a female, taking no HIV drugs, used an elderberry extract, called Sambucol, with olive leaf extract and experienced a viral load drop from 17,000 to 4,000. Instructions are given for making both alcohol-free and alcohol-based elderberry extracts. In 1993, researchers at Jerusalem?s Hebrew University Medical School found in a placebo-controlled double-blind study that Sambucol led to a rapid recovery from influenza and inhibited replication of nine other strains of the flu virus. A theory is that elderberry renders viruses nonfunctional by staining and coating them. Another promising treatment is soil based organisms, which improved Natural Killer cell function in a person with CFIDS.
>
Publication Types:

* Newspaper Article

PMID: 11366542 [PubMed - indexed for MEDLINE]

J Altern Complement Med. 1995 Winter;1(4):361-9. Related Articles, Links

Inhibition of several strains of influenza virus in vitro and reduction of symptoms by an elderberry extract (Sambucus nigra L.) during an outbreak of influenza B Panama.

Zakay-Rones Z, Varsano N, Zlotnik M, Manor O, Regev L, Schlesinger M, Mumcuoglu M.

Department of Virology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

A standardized elderberry extract, Sambucol (SAM), reduced hemagglutination and inhibited replication of human influenza viruses type A/Shangdong 9/93 (H3N2), A/Beijing 32/92 (H3N2), A/Texas 36/91 (H1N1), A/Singapore 6/86 (H1N1), type B/Panama 45/90, B/Yamagata 16/88, B/Ann Arbor 1/86, and of animal strains from Northern European swine and turkeys, A/Sw/Ger 2/81, A/Tur/Ger 3/91, and A/Sw/Ger 8533/91 in Madin-Darby canine kidney cells. A placebo-controlled, double blind study was carried out on a group of individuals living in an agricultural community (kibbutz) during an outbreak of influenza B/Panama in 1993. Fever, feeling of improvement, and complete cure were recorded during 6 days. Sera obtained in the acute and convalescent phases were tested for the presence of antibodies to influenza A, B, respiratory syncytial, and adenoviruses. Convalescent phase serologies showed higher mean and mean geometric hemagglutination inhibition (HI) titers to influenza B in the group treated with SAM than in the control group. A significant improvement of the symptoms, including fever, was seen in 93.3% of the cases in the SAM-treated group within 2 days, whereas in the control group 91.7% of the patients showed an improvement within 6 days (p < 0.001). A complete cure was achieved within 2 to 3 days in nearly 90% of the SAM-treated group and within at least 6 days in the placebo group (p < 0.001). No satisfactory medication to cure influenza type A and B is available. Considering the efficacy of the extract in vitro on all strains of influenza virus tested, the clinical results, its low cost, and absence of side-effects, this preparation could offer a possibility for safe treatment for influenza A and B.

Publication Types:

* Clinical Trial

* Randomized Controlled Trial

PMID: 9395631 [PubMed - indexed for MEDLINE]

Pediatr Ann. 2005 Jan;34(1):42-52. Related Articles, Links

When animal viruses attack: SARS and avian influenza.

Lee PJ, Krilov LR.

Division of Pediatric Infectious Diseases, Winthrop University Hospital, Mineola, NY, USA.

SARS and avian influenza have many common features. They both arose in Asia and originated from animal viruses. They both have the potential to become pandemics because human beings lack antibodies to the animal-derived antigens present on the viral surface and rapid dissemination can occur from the relative ease and availability of high speed and far-reaching transportation methods. Pediatricians, in particular, should remain alert about the possibility of pandemic illnesses in their patients. Annual rates of influenza in children may be 1.5 to 3 times those in the adult population, and infection rates during a community epidemic may exceed 40% in preschool-aged children and 30% in school-aged children. Infected children also play a central role in disseminating influenza, as they are the major point of entry for the virus into the household, from which adults spread disease into the community. Of course, children younger than 24 months also are at high risk for complications from influenza. A 1999 Centers for Disease Control and Prevention projection of an influenza pandemic in the US paints a grim picture: 89,000 to 207,000 deaths, 314,000 to 734,000 hospitalizations, 18 million to 42 million outpatient visits, and 20 million to 47 million additional illnesses, at a cost to society of at least dollars 71.3 billion to dollars 166.5 billion. High-risk patients (15% of the population) would account for approximately 84% of all deaths. Although SARS has been kind to the pediatric population so far, there are no guarantees that future outbreaks would be as sparing. To aid readers in remaining up-to-date with SARS and avian influenza, some useful websites are listed in the Sidebar. Two masters of suspense, Alfred Hitchcock and Stephen King, may have been closer to the truth than they ever would have believed. Both birds and a super flu could bring about the end of civilization as we know it. But all is not lost--to paraphrase Thomas Jefferson, the price of health is eternal vigilance. Although we may not be able to prevent future pandemics, mankind has the ability to recognize new diseases and outbreaks as they occur, to study these infections and find ways to contain and treat them, and to implement the necessary measures to defeat them.

Publication Types:

* Review
* Review, Tutorial

PMID: 15693215 [PubMed - indexed for MEDLINE]

Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9654-8.
Avian-to-human transmission of H9N2 subtype influenza A viruses: relationship between H9N2 and H5N1 human isolates.

Lin YP, Shaw M, Gregory V, Cameron K, Lim W, Klimov A, Subbarao K, Guan Y, Krauss S, Shortridge K, Webster R, Cox N, Hay A.

Division of Virology, National Institute for Medical Research, Mill Hill, London, United Kingdom. Dise. lyipu@nimr.mrc.ac.uk

In 1997, 18 cases of influenza in Hong Kong (bird flu) caused by a novel H5N1 (chicken) virus resulted in the deaths of six individuals and once again raised the specter of a potentially devastating influenza pandemic. Slaughter of the poultry in the live bird markets removed the source of infection and no further human cases of H5N1 infection have occurred. In March 1999, however, a new pandemic threat appeared when influenza A H9N2 viruses infected two children in Hong Kong. These two virus isolates are similar to an H9N2 virus isolated from a quail in Hong Kong in late 1997. Although differing in their surface hemagglutinin and neuraminidase components, a notable feature of these H9N2 viruses is that the six genes encoding the internal components of the virus are similar to those of the 1997 H5N1 human and avian isolates. This common feature emphasizes the apparent propensity of avian viruses with this genetic complement to infect humans and highlights the potential for the emergence of a novel human pathogen.

PMID: 10920197 [PubMed - indexed for MEDLINE]

Dtsch Med Wochenschr. 2005 Apr 15;130(15):946-8.

[Is avian influenza a risk for humans?]

[Article in German]

Allwinn R, Doerr HW.

Institut fur Medizinische Virologie und Reisemedizinische Impfambulanz, Frankfurt/Main. allwinn@em.uni-frankfurt.de

Avian influenza is an infectious disease of birds, caused by type A strains of the influenza virus. The disease, which was first identified in Italy more than 100 years ago, occurs worldwide. Avian influenza viruses are mainly distributed by migratory birds. Different mammals like swine, horse and finally humans are susceptible for avian influenza viruses. The high possibility of genomic changes like gene shift and drift is caused by the segmented RNA genome. During the avian flu outbreak in East Asia at the end of 2003 the virus also killed several humans in Vietnam and Thailand. That avian influenza could also infect humans has been known since 1997. The H5N1 flu outbreak seemed successfully controlled, but currently new cases in poultry and humans in Vietnam, Thailand, China and Indonesia are recognized. Also another avian influenza A strain type H9N2 was prevalent in chickens of local markets in Hong Kong. Because of the natural virus reservoir like wild and/ or domesticated ducks and others, actually there is little chance of eradicating avian influenza. Furthermore the virus could mutate and jump to humans with the threat of a global influenza pandemic.

PMID: 15812719 [PubMed - indexed for MEDLINE]

MMWR Morb Mortal Wkly Rep. 2004 Feb 13;53(5):97-100. Related Articles, Links

Comment in:

* Ann Emerg Med. 2005 Jan;45(1):88-92.


Outbreaks of avian influenza A (H5N1) in Asia and interim recommendations for evaluation and reporting of suspected cases--United States, 2004.

Centers for Disease Control and Prevention (CDC).

During December 2003-February 2004, outbreaks of highly pathogenic avian influenza A (H5N1) among poultry were reported in Cambodia, China, Indonesia, Japan, Laos, South Korea, Thailand, and Vietnam. As of February 9, 2004, a total of 23 cases of laboratory-confirmed influenza A (H5N1) virus infections in humans, resulting in 18 deaths, had been reported in Thailand and Vietnam. In addition, approximately 100 suspected cases in humans are under investigation by national health authorities in Thailand and Vietnam. CDC, the World Health Organization (WHO), and national health authorities in Asian countries are working to assess and monitor the situation, provide epidemiologic and laboratory support, and assist with control efforts. This report summarizes information about the human infections and avian outbreaks in Asia and provides recommendations to guide influenza A (H5N1) surveillance, diagnosis, and testing in the United States.

PMID: 14961001 [PubMed - indexed for MEDLINE]

Uirusu. 2004 Jun;54(1):93-6. Related Articles, Links

[Avian influenza virus]

[Article in Japanese]
Kida H.
Department of Disease Control Hokkaido University Graduate School of Veterinary Medicine, Kita18, Nishi 9, Kita-ku, Sapporo 060-0818. kida@vetmed.hokudai.ac.jp
Recent outbreaks of highly pathogenic avian influenza in chickens and ducks that occurred in 9 Asian countries including Japan alarmed to realize that there is no border for infections and gave a rise to great concern for human health as well as for agriculture. This H5N1 virus jumped the species barrier and caused severe disease with high mortality in humans in Viet Nam and Thailand; 15 deaths of 22 cases and 8 of 12, respectively. A second concern was the possibility that the situation could give rise to another influenza pandemic in humans since genetic reassortment may occur between avian and human influenza viruses when a person is concurrently infected with viruses from both species. This process of gene swapping inside the human body can give rise to a new subtype of the influenza virus to which humans would not have immunity. The outbreaks also emphasized the need to continue active surveillance on avian influenza throughout the year to undertake aggressive emergency control measures as soon as an infection is detected.
Publication Types:
* Review
* Review, Multicase
* Review, Tutorial
PMID: 15449909 [PubMed - indexed for MEDLINE]

Emerg Infect Dis. 2004 Dec;10(12):2196-9.
Human illness from avian influenza H7N3, British Columbia.

Tweed SA, Skowronski DM, David ST, Larder A, Petric M, Lees W, Li Y, Katz J, Krajden M, Tellier R, Halpert C, Hirst M, Astell C, Lawrence D, Mak A.
British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada. aleina.tweed@bccdc.c
Avian influenza that infects poultry in close proximity to humans is a concern because of its pandemic potential. In 2004, an outbreak of highly pathogenic avian influenza H7N3 occurred in poultry in British Columbia, Canada. Surveillance identified two persons with confirmed avian influenza infection. Symptoms included conjunctivitis and mild influenzalike illness.
PMID: 15663860 [PubMed - indexed for MEDLINE]

Tijdschr Diergeneeskd. 2004 Dec 1;129(23):782-96.
[Avian influenza: eradication from commercial poultry is still not in sight]
[Article in Dutch]
Landman WJ, Schrier CC.
Gezondheidsdienst voor Dieren, Arnsbergstraat 7, 7418 EZ Deventer.
Avian influenza viruses are highly infectious micro-organisms that primarily affect birds. Nevertheless, they have also been isolated from a number of mammals, including humans. Avian influenza virus can cause large economic losses to the poultry industry because of its high mortality. Although there are pathogenic variants with a low virulence and which generally cause only mild, if any, clinical symptoms, the subtypes H5 and H7 can mutate from a low to a highly virulent (pathogenic) virus and should be taken into consideration in eradication strategies. The primary source of infection for commercial poultry is direct and indirect contact with wild birds, with waterfowl forming a natural reservoir of the virus. Live-poultry markets, exotic birds, and ostriches also play a significant role in the epidemiology of avian influenza. The secondary transmission (i.e., between poultry farms) of avian influenza virus is attributed primarily to fomites and people. Airborne transmission is also important, and the virus can be spread by aerosol in humans. Diagnostic tests detect viral proteins and genes. Virus-specific antibodies can be traced by serological tests, with virus isolation and identification being complementary procedures. The number of outbreaks of avian influenza seems to be increasing - over the last 5 years outbreaks have been reported in Italy, Hong Kong, Chile, the Netherlands, South Korea, Vietnam, Japan, Thailand, Cambodia, Indonesia, Laos, China, Pakistan, United States of America, Canada, South Africa, and Malaysia. Moreover, a growing number of human cases of avian influenza, in some cases fatal, have paralleled the outbreaks in commercial poultry. There is great concern about the possibility that a new virus subtype with pandemic potential could emerge from these outbreaks. From the perspective of human health, it is essential to eradicate the virus from poultry; however, the large number of small-holdings with poultry, the lack of control experience and resources, and the international scale of transmission and infection make rapid control and long-term prevention of recurrence extremely difficult. In the Western world, the renewed interest in free-range housing carries a threat for future outbreaks. The growing ethical objections to the largescale culling of birds require a different approach to the eradication of avian influenza.
Publication Types:
* Review
* Review, Tutorial
PMID: 15624878 [PubMed - indexed for MEDLINE]

N Engl J Med. 2005 Jan 27;352(4):333-40. Epub 2005 Jan 24.
Comment in:
* N Engl J Med. 2005 Jan 27;352(4):323
* N Engl J Med. 2005 Jan 27;352(4):405-7.
Probable person-to-person transmission of avian influenza A (H5N1).

Ungchusak K, Auewarakul P, Dowell SF, Kitphati R, Auwanit W, Puthavathana P, Uiprasertkul M, Boonnak K, Pittayawonganon C, Cox NJ, Zaki SR, Thawatsupha P, Chittaganpitch M, Khontong R, Simmerman JM, Chunsutthiwat S.
Bureau of Epidemiology, Department of Disease Control, Thai Ministry of Public Health, Nonthaburi, Thailand. kum@health.moph.go.th

BACKGROUND: During 2004, a highly pathogenic avian influenza A (H5N1) virus caused poultry disease in eight Asian countries and infected at least 44 persons, killing 32; most of these persons had had close contact with poultry. No evidence of efficient person-to-person transmission has yet been reported. We investigated possible person-to-person transmission in a family cluster of the disease in Thailand. METHODS: For each of the three involved patients, we reviewed the circumstances and timing of exposures to poultry and to other ill persons. Field teams isolated and treated the surviving patient, instituted active surveillance for disease and prophylaxis among exposed contacts, and culled the remaining poultry surrounding the affected village. Specimens from family members were tested by viral culture, microneutralization serologic analysis, immunohistochemical assay, reverse-transcriptase-polymerase-chain-reaction (RT-PCR) analysis, and genetic sequencing. RESULTS: The index patient became ill three to four days after her last exposure to dying household chickens. Her mother came from a distant city to care for her in the hospital, had no recognized exposure to poultry, and died from pneumonia after providing 16 to 18 hours of unprotected nursing care. The aunt also provided unprotected nursing care; she had fever five days after the mother first had fever, followed by pneumonia seven days later. Autopsy tissue from the mother and nasopharyngeal and throat swabs from the aunt were positive for influenza A (H5N1) by RT-PCR. No additional chains of transmission were identified, and sequencing of the viral genes identified no change in the receptor-binding site of hemagglutinin or other key features of the virus. The sequences of all eight viral gene segments clustered closely with other H5N1 sequences from recent avian isolates in Thailand. CONCLUSIONS: Disease in the mother and aunt probably resulted from person-to-person transmission of this lethal avian influenzavirus during unprotected exposure to the critically ill index patient. Copyright 2005 Massachusetts Medical Society.
Publication Types:
* Case Reports
PMID: 15668219 [PubMed - indexed for MEDLINE]

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