Roland Posted October 23, 2006 Report Posted October 23, 2006 THATwould be gordon Chambers... in regards the German Test where pigeon have been give Avian flu that not only AFFECTS THE Brain by giving large doses he wrote firstly Briefly - a recently published study (July, 2006) from Germany showed that, yes, pigeons can be infected by the hot strain (Highly Pathogenic H5N1) of the virus killing chickens and some humans in SE Asia. Five of 14 experimental pigeons inoculated by nostril and eye died in a period of 5 to 19 days; the remaining nine birds lived and didn't have any sign of infection - but blood samples from these nine showed that they had significant levels of antibodies to this strain, indicating that they had been infected. The only tissue that appeared to be infected by this virus was the brain; furthermore none of these infected pigeons shed or transmitted the virus to healthy chickens housed with them. However the researchers are presently studying the subject of shedding in greater depth. It's a good news (no shedding)/bad news (yes, pigeons can be infected by this strain) story. I've just submitted an article based on this study to the RP Digest, CU yearbook/Tom Cosstick (health officer), Feather Fancier, BHW and several other international magazines, asking for some priority in publishing for the sake of providing up-to-date info for fanciers, if it's found to be an acceptable article. Gord. Then. This past week on two different nights, Global news showed state and federal officials in Alaska capturing wild ducks to test for H5N1 virus - I believe they said they were going to try to get 20,000 samples. I'm the same as Tom - so far I haven't seen reports of infections yet, but I'm sure they're coming. However my point in posting the update was to give fanciers info to show that this hot strain can infect pigeons but that experimental birds didn't shed virus - which is an important point to argue if pigeons are targeted as a cause of the spread of this agent. I wish that the people who did the work I reported on had done one more experiment - expose a group of normal healthy pigeons to infected chickens to see if the kind of exposure that pigeons could have in a natural outbreak would also infect them. Often in experiments, massive doses of virus are given to experimental birds - really unnnatural exposure, far more than they might encounter in a natural exposure. So I think this would be an important part of of this study, and I contacted please note...
Roland Posted October 23, 2006 Report Posted October 23, 2006 please note Gord Chalmers wrote: ...Often in experiments, massive doses of virus are given to experimental birds - really unnnatural exposure, far more than they might encounter in a natural exposure. So I think this would be an important part of of this study, and I contacted the author to ask if he might do that yet (since he is doing more work on the shedding angle). Gord. Then on the 25th September -------------------------------------------------------------------------------- This past week on two different nights, Global news showed state and federal officials in Alaska capturing wild ducks to test for H5N1 virus - I believe they said they were going to try to get 20,000 samples. I'm the same as Tom - so far I haven't seen reports of infections yet, but I'm sure they're coming. However my point in posting the update was to give fanciers info to show that this hot strain can infect pigeons but that experimental birds didn't shed virus - which is an important point to argue if pigeons are targeted as a cause of the spread of this agent. I wish that the people who did the work I reported on had done one more experiment - expose a group of normal healthy pigeons to infected chickens to see if the kind of exposure that pigeons could have in a natural outbreak would also infect them. Often in experiments, massive doses of virus are given to experimental birds - really unnnatural exposure, far more than they might encounter in a natural exposure. So I think this would be an important part of of this study, and I contacted the author to ask if he might do that yet (since he is doing more work on the shedding angle). Gord. Please note Gord Chalmers wrote: ...Often in experiments, massive doses of virus are given to experimental birds - really unnnatural exposure, far more than they might encounter in a natural exposure. So I think this would be an important part of of this study, and I contacted the author to ask if he might do that yet (since he is doing more work on the shedding angle). Gord.
Guest Posted October 27, 2006 Report Posted October 27, 2006 i heard that a vet in canada did some tests and 80% of pigeon breeds dont get it,only the fancy inbred breeds, ben There's a lot of confusion around. There's experiments, experimental infection in labs (using massive doses of one particular strain of H5 or H7 types of highly pathogenic avian influenza virus). Then there's the natural world outside laboratories, a few wild pigeons found dead from different strains of H5 type of highly pathogenic avian influenza virus. Then there's racing pigeons. They have few if any opportunities of coming into contact with highly pathogenic avian influenza in the natural world, and there's no recorded case of one catching it, carrying it, dying of it, or spreading it. Pigeons are also immune to Low Pathogenic Avian influenza, so it cannot convert to the highly pathogenic type in the pigeon's body. A chicken for example catching Low Pathogenic Avian influenza will be turned into a highly pathogenic avian influenza virus factory ... and infect everything round about it.
bill_bennie Posted October 31, 2006 Report Posted October 31, 2006 Here we go again....."NEW & STRONGER", coming out of Asia. http://news.yahoo.com/s/hsn/20061030/hl_hsn/vaccineresistantbirdfluspreadinginasia
Guest Posted October 31, 2006 Report Posted October 31, 2006 There's an interesting report on the WHO website on the human infections in Turkey Dec 2005/Jan 2006. http://www.who.int/wer/2006/wer8143.pdf Page 6 - Family B kept 25 chickens and 2 pet pigeons; 3yo child played with the pigeons, hospitalised and survived. Page 6 - Family C kept 4 ducks and 4 pet pigeons, 5yo child child played with the pigeons, hospitalised and survived. Other family members involved in slaughtering the AI-infected chickens and ducks, unfortunately not so lucky. Page 7 - Discussion - bit on pigeons very interesting. Another case of 'people in charge' not obtaining enough information on the virus and another chance to find out what happens to pigeons in an AI-infected environment was missed. Thats two chances gone this year (that we know of).
Guest Posted November 9, 2006 Report Posted November 9, 2006 Current Wild Bird Surveillance results posted by DEFRA make interesting reading. Discovery of different strains of avian influenza in wild birds in all three categories [caught live, shot for sampling, found dead ]. All are in SE England, including 1 x H5 [doesn't give the N or number]. http://www.defra.gov.uk/animalh/diseases/notifiable/disease/ai/wildbirds/survey-results.htm
Guest Posted December 8, 2006 Report Posted December 8, 2006 This is a translation from German of that part of the scientific paper which describes the experiment which was used to support Dr Kaleta's theory that racing pigeons could act as mechanical carriers of avian flu during long distance races. I do not expect the Table to upload properly, it appears just before 'Discussion' in the paper. I have added it at the end 'as a pic'. ON THE ABILITY TO SURVIVE AND DISINFECTION OF AVIAN INFLUENZA A-VIRUSES Dr. Ayhan Yilmaz and Professor Erhard F. Kaleta (Giessen) Introduction Conventional bird flu and Newcastle disease (atypical bird flu) are epidemics in domestic poultry of paramount significance. Both lead to considerable losses and to lasting impacts on international commerce. There have therefore been significant efforts worldwide to eliminate or contain their spread. Combating conventional bird flu has overwhelmingly involved the culling of affected stocks. On the other hand, Newcastle disease has been combated in most countries through immunisation by means of both live and inactivated vaccines. Conventional bird flu has been denoted in relation to the virus as highly pathogenic influenza A (HPAI) of the haemoglutin-subtype H5 and H7 and the atypical bird flu has been denoted as Newcastle disease. A diagnostic differentiation on the basis of clinical manifestations is not possible due to the extensive similarities. The cause of conventional bird flu is the highly pathogenic viruses of the H5 and H7 subtypes of the orthomyxoviridae family, while the atypical bird flu is caused by the paramyxoviruses of serogroup 1. The orthomyxoviridae virions are enveloped pleomorphic, mostly spherical and carry single-strand RNA as base material (Van Regenmortel et all, 2000). The spreading or transmission of the virus occurs horizontally only through infected animals and their excretions, as well as untreated animal products, including inanimate vectors (Werner and Kaleta, 2004). The pressing reasons which have given rise to the renewed work on the ability to survive and the possibilities of chemical disinfection have been the numerous outbreaks of conventional bird flu over the last year (Alexander, 2003) – in Italy through the highly pathogenic AIV –subtype H7N1 and other subtypes (Capua and Minelli, 2001: Capua et al, 2003), in Texas, USA, through the subtype H5N2, in Canada through the subtype H7N3 and through the subtype H5N1 in various south Asian countries and most recently in August 2004 through the subtype H5N2 in a province of South Africa. This report is concerned with the stability of the infectiousness of avian influenza a-virus (AIV) on feathers of various bird species and with the potential for chemical disinfection of AIV of the subtypes H5 and H7. On The Ability Of Avian Influenza A-Viruses To Survive By the term ‘tenacity’, we mean the retention of the ability of a sickness causing agent to infect and reproduce outside of an animal under natural conditions. This characteristic can also be denoted as the agent's ability to resist in the face of external influences. AIV is produced in great quantities in infected birds and shed in droppings as well as secretions from the eye conjunctiva, nose and throat. If this newly formed virus reaches a receptive animal within a short period, and under favourable conditions, an infection will follow via the upper respiratory tract and the digestive tract, followed by illness. If no receptive animal is reachable, the virus will perish within a certain period i.e. it loses its ability to infect and reproduce. Illness cannot be caused by an inactivated virus. Knowledge of the speed of inactivation and the conditions under which such an inactivation occurs is of high significance for the spread of the agent and for diagnostic investigation. (Boehm, 2002). It is known from many studies that the destruction of the infectiousness of every influenza A-virus is dependent on several factors. At the same time, these studies show that infectiousness abates in a logarithmic manner. Experience shows that temperature, humidity, pH value and structure as well as the chemical composition of the surrounding environment are of particular importance in the abatement of the infectiousness. The higher the temperature, the quicker the destruction of the infectiousness will occur. In recognition of this fact, the treatment of infected material with heat is established practice, whereby heat can be produced through pasteurisation (King, 1991), boiling, burning or in the laboratory through autoclaving. Under more natural conditions, heat can also be produced through composting and this is also regarded as effective practice. (Anonymous, 1997, Bergdorf, 1989; Beher and Gerdes, 2003). According to announcements by The World Organisation for Animal Health (OIE), Paris, AIV will be completely inactivated through exposure to 56oC for three hours or 60 oC for 30 minutes (OIE Disease Card, 2004). On the other hand, when freezing AIV, it will retain its infectiousness, to a degree in direct relation to the temperature of freezing, for very long periods (months to years). The humidity in the area surrounding the virus is likewise of high importance for the ability of AIV to survive. All influenza A-viruses are initially in a watery phase after being shed by infected animals. In water (pools, drinks, liquid manure) AIV survives for long periods of time. On the other hand, AIV is particularly susceptible to drying out. Loss of water occurs through drying out of the virus on its surfaces or through heating. In sugary and salt water but also in animal tissue, including muscles (Swayne and Suarez 2000), the infectiousness remains intact for weeks to months. The PH value of the humidity surrounding the virus has a direct influence on the ability of the AIV to survive. An acidic environment destroys the infectiousness, while a neutral or weak alkaline environment stabilises the reproductive ability of the AIV. The natural maturation of the flesh which accompanies the reducing PH value, is not enough in relation to the flesh of birds, to destroy the infectiousness of the AIV within a commensurate period of time. The structure and composition of the environment in which the AIV is situated, likewise has an effect on its stability. Proteins have a stabilising effect. On the other hand, oxygen and UV rays destroy the infectiousness. (Steet-Mund and Mahnel, 1980). Emulsification in fat or fat-protein mixtures retain the infectiousness. From these remarks, the following fundamental conclusions can be drawn: 1 The inactivation of the AIV outside of a susceptible animal results from a complex process, in which, under practical conditions, only factors which are difficult to control take part, such as temperature, humidity, pH-value, UV rays and oxygen environment. 2 The abatement of the infectiousness occurs logarithmically. It is therefore clear that the complete elimination of infectious AIV, at least theoretically, cannot be achieved. 3 The time factor is of utmost importance in relation to all measures to eliminate AIV in contaminated materials. It is down to the wisdom, expertise and experience of those people who are concerned with the elimination of highly pathogenic AIV (and NDV) to make the correct considerations and to come to quick, professional, sound decisions in specific occurrences of a pandemic. Trialling The Means Of Disinfection For AIV According To German Veterinary Association (DVG) Guidelines, Comite Europeen De Normalisation (CEN) Guidelines And Guidelines Of The German Federal Office For Health It can be derived from the knowledge of the loss of AIV infectiousness outside the susceptible animal, that there is a need for a controlled and accelerated inactivation of the AIV. This can be achieved through focussed disinfection. According to the recommendations of the OIE, the following means of disinfection come into consideration: oxidising agents, lipid dilution/lotion agents, formalin or commercial preparations/compounds. The guidelines of the German Federal Ministry for Nutrition, Agriculture and Forestry on the means and processes for carrying out the disinfection of notifiable animal pandemics (Stand 1997) designates the following as effective against enveloped viruses (column 7a: limited virucide) in the disinfection of the virus of conventional bird flu (avian flu): the surface disinfecting agent formalin (2% - for 2 hours), peracetic acid (1% for 1 hour) and commercial disinfecting agents which have been tested according to DVG guidelines. They have an inactivating effect within 2 hours at most and have been recorded in the latest 12th DVG list (anonymous, 2003a) as effective in twice the concentration of the recommended concentration (anonymous, 1997). The examination of the effectiveness of chemical disinfection agents under laboratory conditions in the area of animal husbandry currently takes place according to guidelines of the German Veterinary Medicine Society in Giessen (anonymous, 2000) and within the European Union, according to the development and testing guidelines of the CEN (anonymous, 2003b). Materials and Methods Due to its easy handling and fruitful virus reproduction, the subtype H7N1 (Influenza A/Carduelis/Germany/72) is used in all test procedures. In an experiment to explain the question of “The ability of Influenza A-Virus to survive on Feathers”, moulted feathers (back, stomach, wing and tail) were coated with 0.1 ml of AIV (diluted in a phosphate retaining common salt solution, PBS) died and preserved at room temperature. At various times, the remaining virus was placed quantitatively in HEF cultures through titration. To determine the resistance of the AIV in relation to disinfecting agents, 5 differing commercial preparations were subjected to testing. At the moment, there are no single European virucide testing rules in relation to chemical disinfection agents in the area of animal husbandry. Therefore, the following were tested according to: DVG guidelines (anonymous, 2000a): the barn disinfecting agent Venno FF Super (20% glutadehyde, 12% oligomer, pentaerithritose condensate) and Venno Vet 1 super (55% formic acid, 7% glyoxal acid; Guidelines of the German Federal Office for Health (anonymous, 1982, 1983): the hand disinfecting agent Manorapid Synergy 63 (14% propane 2, 0.115% 1, 3 dibutanol) and poly-alcohol hand anti-septic; CEN Guidelines (anonymous 2003b): the compound Halamid (1000% natrium –p – toluolsulfonchloromide) During this process several parameters were taken into account such as time, concentration, organic load, surface composition, surrounding temperature as well as water hardness. On the clarification of the question as to whether a difference in resistance exists between the H7 and H5 subtypes, additional comparative disinfection tests were carried out with subtypes H7N1 (A/Carduelis/Germany/72), H5N2 (A/chicken/Pennsylvania/1370/83) and H5N9 (A/turkey/Ontario/7732/66). Formic acid served as a reference disinfection agent. One ml of virus-containing allantois fluid was mixed with 1ml of formic acid in double the concentration of the desired end concentration. Negative controls were treated with PBS. After a reaction time of 15 minutes at a temperature of 20 oC, 0.1ml samples were analysed on the remaining virus. Primary chicken embryo(fibrolasten) HEF cultures were used as a verification system. The details of the virus verification are subject to DVG guidelines (anonymous, 2000) The disinfection agent experiments carried out according to DVG guidelines used suspension and germ carrying tests, those carried out according to guidelines of the German Federal Office For Health and the CEN used only suspension tests. While the suspension tests ascertained the inactivation kinetics in the liquid phase, in germ carrying tests carried out according to DVG guidelines, 0.1ml of virus suspension was dried on wood and lint germ carriers with 40% serum additive and then treated with 4ml of the disinfection agent dilutions. As a result of the protective function of the proteins and the porosity of the germ carrying surface, the virions are especially hard to inactivate on wood germ carriers. Lint germ carriers on the other hand, are relatively easy to disinfect. Therefore tests with lint germ carriers were ruled out during our research. Results Longevity of AIV on Feathers AIV can occur in the excretions of infected poultry, in the body of the animal itself and in the plumage of the poultry. During elimination campaigns and the safe disposal of the carcass, there is a regular unintentional scattering of the feathers in the immediate vicinity. Therefore it is crucial to establish how long AIV is able to survive on feathers. In experiments to resolve this question, moulted feathers were coated with 0.1ml virus suspension. The virus contaminated feathers were stored at room temperature and at various times, the remaining infectious virus measured. The titrations produced the following findings: 1 Between 0 and 1 hours, a reduction in the virus titer occurred through the drying out of the AIV on the feathers. 2 Infectious virus is detectable on the feathers of all bird species up to 24 hours after application. 3 Infectious AIV is detectable the longest on the Peking duck. The mechanism of the longer retention period of the AIV on the feathers of this species is still unknown. 4 Infectious virus remains on the feathers of chickens up to 48 hours after application. 5 No significant differences exist between the feathers of the chicken, pigeon and common buzzard in relation to the residual virus level. These results show that, under the conditions used here, the virus level on the contaminated feathers decreases as the period of storage increases. However, infectious AIV remains detectable for at least 2 days. Discussion Although influenza A-viruses, with regard to their lower ability to survive in nature and resilience compared to chemical-physical noxa, are among the unstable viruses (Hausmann and Graffe, 1956, 1957; Albrecht, 1957; Albrecht et al. 1957-58;Henneberg und Hoeppner, 1960; Sprossig and Muecke, 1968; King, 1991; Davison et al., 1999; Lu et al., 2003), particular factors can favour their survival outside the host organism or in animal products. In this regard, lower environmental temperatures or the protective functions of organic substances are particularly effective. Under such circumstances the virus particles in products or in animal waste can remain infectious for weeks. (Alexander, 2000; Swayne and Suarez, 2000). Haas and colleagues (1995) established that influenza A-viruses in liquid dung perish within an hour at 55 oC but are inactivated at 20 oC after two weeks and at 5 oC after 9 weeks. Our research to determine the ability to survive on feathers shows that AIV was no longer detectable on the feathers of chickens, pigeons and common buzzards after 72 hours, while it remained infectious on duck feathers at up to 96 hours. The minimum infectious dose of AIV for chicken embryos stands at 1 to 10 augmentable virus particles (Lu et al., 2003). Where even a very low amount of infectious AIV remains on feathers which have been unintentionally scattered during the disposal of animal carcasses, avoiding the scattering of feathers contaminated in cases of a pandemic attracts a substantial practical and epidemiological significance. Unlike non-enveloped viruses, viruses which are enveloped are relatively easy to disinfect. The enveloped viruses of the orthomyxoviridae family are no exception to this rule. Our research also confirms that the disinfection of AIV in its fluid phase doesn’t present fundamental problems. The tested alcohol-based hand disinfection agent inactivated the virus within a few seconds. The disinfection of AIV on porous, absorbent surfaces was however particularly difficult. After every increase of the degree of protein load and through temperature reduction, a reduction of the effectiveness was observed. In spite of these extremely aggravated conditions, the tested hand disinfection agent could achieve disinfection within relatively short residence times and acceptable concentrations. The disinfection of enveloped viruses depends on the physical and chemical denaturation of the virus envelope. The construction principle of the envelope is, apart from the surface proteins haemoglutin and neuraminidase, almost identical with all AIV subtypes. Consequently, there may not be any noteworthy differences in the resistance between the AIV subtypes with regard to the means of chemical disinfection. Our research confirms this assertion. Hardly any differences could be established between the subtypes H7N1, H5N2 and H5N9 with regard to resilience against formic acid. Summary On feathers which are experimentally contaminated with AIV and stored at room temperature, a slow decrease in the concentration of the infectious virus will occur spontaneously. Infectious virus can however be detected for more than two days on the AIV coated feathers. Infectious virus was detectable on the feathers of chickens and pigeons up to two days after the application of the AIV. On duck feathers, low amounts of virus were present even up to four days. All tested chemical disinfection agents (commercial names: Venno FF Super, Venno Vet 1 Super, Poly-alcohol hand anti-septic, Manorapid Synergy and Halamid), which were tested as commercial preparations for their effectiveness, led to complete disinfection within a short period in suspension and germ carrying experiments. The required residence times and concentrations of disinfection agent are almost identical for the tested AIV of subtype H7N1 and are not substantially different from the values which are entered for the disinfection of the cytopathogenic virus Newcastle disease in the 12th list of the DVG tested and listed chemical disinfection agents. Formic acid disinfected AIV subtypes H5 and H7 in low concentration. Consequently, formic acid is suitable as a reference disinfection agent in terms of the CEN guidelines.
bill_bennie Posted December 11, 2006 Report Posted December 11, 2006 The latest form this side of the pond. http://news.yahoo.com/s/ap/20061210/ap_on_he_me/bird_flu_1
Guest Posted December 12, 2006 Report Posted December 12, 2006 In case you felt that nothing was going on during November because there were few posts here, there was a lot going on off-screen, on the mechanical carriers question. The following email was sent to Peter Bryant on 4th December, and in his reply to me he says it may be brought up with DEFRA at the planned 14th December meeting. Mr Bryant, Dr Kaleta feathers experiment - the pigeon as AI mechanical carriers question. Sorry I have not been back in touch sooner. I have had the relevant parts of the paper translated from German into English. Further and follow-up enquiries have taken longer than I expected. The paper is very informative and gives good lay-person information on the virus and most importantly, what kills it. You will see that the feathers experiment was based on moulted feathers, and conducted in a laboratory environment. The purpose of the experiment was to make the clean-up operations after an AI cull safer by establishing if the feathers which litter the area after such a cull could be contaminated with AI and become a means of spreading the infection. Because the virus survived for two days on a pigeon feather Dr Kaleta extrapolated this to hypothesise that a racing pigeon competing in a long distance race could carry live virus home with it. He did not take into account any of the factors he outlined in his paper which could kill the virus during such a flight, for example air movement over the bird drying out the virus, or UV sunlight on the feathers. I am in email correspondance with Dr Kaleta. He plans to continue with feather experiments and I hope to convince him to re-do the original experiment. The main add-ons would be 'in a wind tunnel', UV light present, and with the racing pigeon feathers coated in secretions from the pigeon's tear, salivary and preen glands, respectively. These secretions are basically extensions of the pigeon's immune system. Dr Kaleta is keen to establish if the immune substance IgA is present in pigeon's tear duct or salivary gland secretions, as IgA is known by him to kill AI virus. I have discovered a paper which shows that IgA is present in pigeon milk, so there is every likelihood it exists elsewhere in the pigeon's body too, as part of its immune system. I have attached the paper which gives the IgA pigeon milk reference, and the feathers experiment paper. I will forward seperately my last email from Dr Kaleta in which he confirms he has no knowledge of pigeons that have actually been mechanical carriers, his reference to IgA killing AI and his thoughts on future experiments to discover whether IgA [immunoglobulin] exists in pigeons.
Guest Posted December 12, 2006 Report Posted December 12, 2006 Hi my wife is manager of a medical practice and I don't want to dampen the optimism for the coming channel season, but she is having regular mailfrom the dept of health NOW on avaian flu, she tells me the indications are that they are still very concerned. Lets hope this is beaurocrats being cautious
Guest Posted December 12, 2006 Report Posted December 12, 2006 This is the email from Dr Kaleta referred to in the previous post: Sir, thank you for your messages of Nov. 20 and Nov. 23 2006! Currently, I have no definite prove that racing pigeons were indeed carriers of infectious influenza A viruses from one place to an other. Nobody is willing to infect or contaminate racing pigeons and let them participate in racing. Therefore, direct studies with such pigeons are impossible. In an attempt to simulate such role, we contaminated feathers of various avian species including pigeons with AI virus and found that this virus does survive on feathers for times that are long anough for long distance transport. We did not yet evaluate all likely factors that may influence the rates of survival of AI virus. Further experimentation is necessary to illucidate these factors. Among thinkable factors are - as you also mentioned - temperature, humidity, pH value and structure of the feathers. It is my intention to continue with feather - AIV experiments. Current plans are to investigate - the age of feathers from pigeons and ducks - e.g. newly developed and moulted old feathers - modes of removal of bacterial and fungal contamination of feathers - we washed feathers in a washing machine that we use normally for glass laboratory equipment. The water contains a detergent (producer Merck, Darmstadt) that consists of non-ionic tensides, phosphates, sodium hydroxide and alcali salts, pH 12.2. The washing removed all bacteria and fungy that might be present on feathers as natural contaminants. Alternatively also UV radiation (common UV lamp) was used. Do you have any possible alternatives? - coating of sterilized washed or UV treated feathers with single or several fatty acids - as you proposed. If you have access to these chemically pure fatty acids I would be delighted to test these! Although fatty acids (and other compounds) are derived from the uropygeal gland, it is not clear which if any additional compounds are involved. I am thinking on secretions of the salivary glands and also of the lacrimal glands. The beak - oral cavity - is used to spread the uropygeal "oil" on feathers by birds. I am not aware of a reference on the chemical composition of the secretions of salivary glands and their possible effect on survival / inactivation of virus. However, the lacrimal fluid may contain IgA that can neutralize AIV infectivity. I am a member of the advisory board of the German pigeon federation. The next "Deutsche Brieftaubenausstellung" will be held in the city of Dortmund on Jan. 12-14 2007. I will attend this meeting. In case that you will also come we will likely find some time to discuss in more detail our common interests including additional future research activities. Sincerely yours Prof. Dr. Erhard F. Kaleta
Guest Posted December 13, 2006 Report Posted December 13, 2006 Hi my wife is manager of a medical practice and I don't want to dampen the optimism for the coming channel season, but she is having regular mailfrom the dept of health NOW on avaian flu, she tells me the indications are that they are still very concerned. Lets hope this is beaurocrats being cautious I think we have to remain very cautious, we are after all in the high risk winter period where both human and avian flu virus are 'doing the rounds'. I think it is very important to continue to distance racing pigeons from avian flu in the public mind. I think that is best done by establishing through scientific studies that nature has equipped the pigeon with an immune system which can kill or neutralise highly pathogenic avian flu virus. Such an immune system is absent in the chicken and the duck. The pigeon is usually only overcome in a laboratory experiment and then only after the bird has been given enough virus to kill an elephant, viral loads that the bird is unlikely to encounter in the natural world. Should the chicken or duck encounter even a tiny viral load in the wild, they will become infected and infectious, become turned into AI production factories and spread virus thro whole flocks of poultry ... and wild waterfowl .... and humans in close contact with them. And remember too that heat and UV light kill AI virus. Our racing takes place during the warmest and therefore 'safest' parts of the year when temperatures are at their highest and UV light is at its strongest.
Guest Posted December 24, 2006 Report Posted December 24, 2006 Not good news http://news.bbc.co.uk/1/hi/world/middle_east/6207797.stm
Pompey Mick Posted January 4, 2007 Report Posted January 4, 2007 HERE ARE A COUPLE OF EXTRACTS FROM A RECENT REPORT ON THE DURABILITY OF AVIAN FLU, THE SECOND ONE IS INTERESTING IN RELATION TO DEFRA'S STANCE ON 'MECHANICAL TRANSFER' ‘Jan. 3 (Bloomberg) -- Bird flu viruses are unlikely to survive sewerage and drinking water treatment systems, making it doubtful contaminated faeces could infect plant workers and spread through tap water, scientists at Cornell University said..’ ‘Avian flu viruses don't survive well outside of a host, the Cornell researchers said.’
Guest Posted January 8, 2007 Report Posted January 8, 2007 New World Health Organisation's boss' view last week http://news.bbc.co.uk/1/hi/world/asia-pacific/6232849.stm
Guest bristolkev Posted January 8, 2007 Report Posted January 8, 2007 report today http://www.24dash.com/health/15048.htm
Guest Posted January 9, 2007 Report Posted January 9, 2007 report today http://www.24dash.com/health/15048.htm With respect, I feel this report is something to fill a news gap ... ´no news´ because there is no new news on AI. The ´if a cold snap develops´ is of course very relevant, but comparing this winter with last, it appears remote. Spain is around 13C average just now. Poland which saw temperatures of -20C to -30C last winter (leading to the pigeon show hall roof collapse) is around 10C just now. So the severe cold throughout Europe last winter isn´t happening this year. We´ll suffer in other ways of course, flies and other vermin eggs will also survive in greater numbers. AI loves cold temps, but cannot survive as well in hot. So, to me, for now, looking quite promising that there won´t be the same AI outbreaks in Europe that we had during and following last winters severe winter weather.
Guest bristolkev Posted January 9, 2007 Report Posted January 9, 2007 thanks bruno,thats good news...fingers crossed.
Roland Posted January 30, 2007 Report Posted January 30, 2007 -------------------------------------------------------------------------------- http://news.yahoo.com/s/afp/20070129/wl_asia_afp/healthflutaiwan_070129184741 Taiwan eyes mass production of bird flu vaccines in 2008 Mon Jan 29, 3:40 PM ET TAIPEI (AFP) - A Taiwanese research team said it had produced a bird flu vaccine that had passed initial animal tests. "The vaccine against the H5N1 strain has passed tests on mice," said Pele Chuang, the head of a 25-member team at the National Health Research Institute. The H5N1 bird flu strain is potentially deadly to humans. The vaccine, using cell culture technology, needs validation by the health ministry before human tests are undertaken. They are due to be completed before the end of June next year. If all goes to plan, mass production of the vaccines -- running up to a million doses a year -- would begin late 2008, Chuang said. "This is a milestone considering when we started last year, we started from scratch, and now we have developed the capability to produce vaccines," he said. The research project has cost the government some 40 million Taiwan dollars (1.22 million US). Institute officials said the ability to produce indigenous vaccines could be crucial in the event of an outbreak. Bird flu has killed more than 160 people worldwide since late 2003 and there are fears it could mutate and trigger a deadly human flu pandemic. A less virulent H7N3 strain was twice detected in samples of bird droppings in Taiwan in 2005 and again in January 2006. In 2003, Taiwan slaughtered 467,000 birds, mostly chickens, after the H5N2 strain was discovered on chicken farms on the offshore island of Kinmen.
Pompey Mick Posted January 30, 2007 Report Posted January 30, 2007 Hopefully news like this will reduce the FEAR of Avian Flu by the Public ,and likewise the Authorities and help allay the general panic that is associated with this virus.
Guest Posted January 30, 2007 Report Posted January 30, 2007 Taken from the OIE Website Updated : 30-Jan-2007 H5N1 strain in Hungary is 99.4 percent same as last year The H5N1 avian influenza strain isolated from the outbreak notified by Hungary is 99.4 percent similar to the strain that infected some countries of Europe last year, the OIE's Reference Laboratory for avian influenza in Weybridge (UK) confirmed yesterday. “This information tells us that the genetic characterisation of the virus isolated in Hungary has still not mutated significantly ” Dr Bernard Vallat, OIE Director General, explained. Avian and human influenza viruses are known to be able to mutate or exchange genetic material to form new strains. In certain conditions, these can be more deadly to both animals and humans. Since the start of the H5N1 crisis in late 2003, the OIE calls for increased global monitoring and control measures of the virus at animal source. Transparent sharing and sequencing of virus samples is also key to tracking the least genetic evolution of the virus and trigger appropriate global rapid response mechanisms. January 2007 Still no information on how the geese on this farm became infected tho.
Bilco Posted January 31, 2007 Report Posted January 31, 2007 It is now generally accepted and acknowledged, that Bird ‘Flu (H5N1) is NOT primarily spread by migrating birds. A very few cases were linked to this source of distribution, and both the Poultry Industry and National Tourism, the major sufferers in any ensuing panic, were quick to pounce on migratory birds as the danger. It wasn’t. The danger came from the Poultry Industry’s own distribution network of chicks, carcases, the spread of manure on fields, sale of contaminated faeces to animal feed manufacturers, etc. Wild birds themselves were the victims of biosecurity lapses within the Industry’s many outlets, and fearful of the backlash from the consumer public if the truth were known, the blame was cast on them rather than let the truth be known. Migratory birds do not migrate east to west, but the trading route that follows the old “Silk Road” from China to the west, took the infection to Thailand, Indonesia, Korea, Laos, Japan, Turkey, India, Egypt, Nigeria, and Hungary, etc, to a tiny degree. Right along the commercial poultry sales routes. The backyard poultry production sources were less risky in terms of infection than the closed “biosecure” commercial poultry farms who all had contact with each other. The “isolated” outbreaks associated with wild bird passage proved to be carried by aircraft instead, in the boxes, wrappings, hands and feet of handlers, and in the chicks and poultry themselves. DEFRA now knows this, so we should look to see the draconian restrictions of 2006 lifted, or at least very much eased in the immediate future. Cheers,
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