Submitted to: International Symposium on Avian Influenza
Publication Type: Abstract Only
Publication Acceptance Date: February 10, 2009
Publication Date: April 5, 2009
Citation: Swayne, D.E. 2009. Mechanisms of transmission and spread of H5N1 high pathogenicity avian influenza virus in birds and mammals [abstract]. Abstracts of the 7th International Symposium on Avian Influenza, April 5-8, 2009, Athens, Georgia. p. 50-51. Technical Abstract: The Eurasian-African H5N1 high pathogenicity avian influenza (HPAI) virus has crossed multiple species barriers to infect poultry, captive and wild birds, carnivorous mammals and humans. The specific transmission mechanisms are unclear in most cases, but experimental studies and field data suggest multiple mechanisms. Poultry transmission has occurred bird-to-birds on the same premise as well as spread of the virus between premises. Experimental studies have demonstrated the ease of infecting poultry through respiratory route (intranasal exposure) to the virus; i.e. doses as low as 2log10 EID50 causing 50% mortality in chickens. However, the ability to transmit was related to the virus strain and dose of challenge virus suggesting adaptation of individual virus strains to different bird species. HPAI viruses have been easily transmitted between chickens in separate cages when housed in the same room or chickens in direct contact. Exposure of caged chickens to a infected chickens undergoing simulated live poultry market slaughter resulted in transmission of the virus with illness and death. The virus was recovered from the room air suggesting transmission via inhalation. The virus has also been transmitted through feeding of infected meat to gulls, chickens and domestic ducks, but such transmission required 3-4log10 more virus than intranasal (IN) exposure. Similarly, the viruses have been transmitted through intragastric inoculation of virus in water or in infected meat, or by consumption of contaminated water. Human infections have been associated with direct or indirect contact with live or dead poultry while in carnivores, consumption of infected birds or their products have been associated with infections. Experimental studies in ferrets with H5N1 HPAI virus have shown efficient transmission by IN inoculation, but inefficient transmission by respiratory droplets or direct contact. Exposure of ferrets to the same air space as infected chickens in a simulated live poultry market resulted in aerogenous transmission. Experimental studies in ferrets and pigs have demonstrated transmission of H5N1 HPAI virus by oral or direct digestive tract exposure which closely mimicked human and other mammal infections and disease, but required a much higher dose of virus than exposure via IN inoculation. Oral consumption of infected meat initiated infection via the tonsil followed by nasal cavity infection, but with one strain of virus, A/Vietnam/1203/04 (H5N1) strain, ferrets were simultaneous infection via the upper digestive tract with spread to liver and pancreas, and via the respiratory tract. Five H5N1 and one H7N3 HPAI viruses in orally consumed infected meat caused infection in ferrets, but production of such infections was dependent on virus strain and the amount of virus in the meat. Cooking or pasteurization was effective at killing the virus. These results suggest consumption of infected raw poultry products could produce human infections based on the ferret model, but the rarity of human avian influenza (AI) cases associated with eating raw infected products and the ease with killing avian influenza viruses (AIV) by cooking, AI has not become a food safety issue. Human infections have mainly resulted from exposure to live infected poultry or poultry during processing. Consumption of raw infected poultry or their products can explain transmission in various carnivores. Some H7 viruses have been transmitted via conjunctival exposure.