Table of Contents:

Foreword

Introduction

I. Storm Gathering

1. 1918

2. Master of Metamorphosis

3. H5N1

4. Playing Chicken

5. Worse Than 1918?

6. When, Not If

II. When Animal Viruses Attack

1. The Third Age

2. Man Made

3. Livestock Revolution

4. Tracing the Flight Path

5. One Flu Over the Chickenís Nest

6. Coming Home to Roost

7. Guarding the Henhouse

III. Pandemic Preparedness

1. Cooping Up Bird Flu

2. Race Against Time

3. Tamiflu

IV. Surviving the Pandemic

1. Donít Wing It

2. Our Health in Our Hands

3. Be Prepared

V. Preventing Future Pandemics

1. Tinderbox

2. Reining in the Pale Horse

Topics

References 1-3,199

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What specifically about intensive production has the world’s leading public and animal health authorities up in arms? An industry trade journal listed some factors that make intensive poultry facilities such “ideal”1687 “breeding grounds for disease”1688 : “poor ventilation, high stocking density, poor litter conditions, poor hygiene, high ammonia level, concurrent diseases and secondary infections.”1689

The first ingredient in the recipe to potentially increase the virulence of bird flu is overcrowding. In modern broiler production, 20,000 to 30,000 day-old chicks are placed on the floor atop coarse wood shavings or other litter material in an otherwise barren shed.1690 As they grow bigger, rapidly reaching slaughter-weight, the crowding grows more and more intense. According to the standard reference manual for commercial chicken production, “Under standard commercial conditions chickens weighing 4.5 to 6 lbs have little more than a half a square foot of living space per bird in the last two weeks of their 42–47 days of life.”1691 As one researcher reported, “[I]t looks as though there is white carpet in the sheds—when the birds are fully grown you couldn’t put your hand between the birds, if a bird fell down it would be lucky to stand up again because of the crush of the others.”1692 “Obviously,” Louisiana State University veterinary scientists write, under these conditions, “the potential for a disastrous epidemic is very high.”1693

The majority of egg-laying hens in the world are confined in battery cages1695 —barren wire enclosures so small that each hen is allotted less space than a standard letter-sized piece of paper.1696 A hen needs 291 square inches of space to flap her wings, 197 square inches to turn around, and 72 square inches just to stand freely.1697 Currently, U.S. commercial battery facilities allow each bird an average of 64 square inches.1698 With up to ten birds per cage and thousands of cages stacked vertically in multiple tiers, layer warehouses can average more than 100,000 chickens per shed.1699

The Royal Geographical Society notes, “Massive demand for chicken has led to factory (battery) farming which provides ideal conditions for viruses to spread orally and via excreta which inevitably contaminates food in the cramped conditions that most birds are kept in.”1700

Europe is moving away from this level of intensification, for both egg-laying chickens and chickens raised for meat. In 2005, the European Commission proposed legislation to impose a maximum stocking density for broiler chickens throughout Europe.1701 In sharp contrast to the U.S. “standard commercial…half a square foot of living space per bird,” certain organic standards in Britain already require more than 150 square feet per bird.1702 For the health and welfare of egg-laying hens, the European Parliament voted to ban conventional battery-cage systems entirely by 2012.1703

In a joint consultation, the WHO, FAO, and OIE noted that the sheer number of intense contacts between birds with increasing flock density serves to spread and amplify disease agents like bird flu.1704 This is supported by research showing that, not surprisingly, increasing chicken stocking densities result in an increased burden of infectious disease agents.1705 In pigs, respiratory diseases1706 such as chronic pleuritis and pneumonia have been strongly correlated to increased crowding of pigs per pen1707 and per building,1708 corresponding to increased levels of bacteria cultured right out of the air.1709 In 1918, Army regiments whose barracks allowed only 45 square feet per soldier had a flu incidence up to ten times that of regiments afforded 78 square feet per man.1710

Not only does increased poultry density enable the enhanced spread of bird flu, but Webster’s group considers it a “big factor” in the rise of highly pathogenic viruses in the first place. The “more hosts in close confinements,” the more easily the virus can mutate into a form capable of infecting humans and eventually spreading throughout the human population.1711 The more animals there are to easily jump between, the more spins the virus may get at the roulette wheel gambling for the pandemic jackpot that may be hidden in the lining of the chickens’ lungs. Research on the evolution of antibiotic resistance, for example, has shown that “intensive production” can “vastly increase the occurrence of very rare genetic events.”1712 Influenza viruses don’t just need to proliferate; they need to evolve.

In land-based birds, it is advantageous for influenza viruses to switch from residing peacefully in the intestine to invading the respiratory tract, from being spread only through the water to also being spread through the air. To adapt, the virus must first survive by overwhelming host defenses. As shown in earlier examples, when animals are spread apart, the virus is presumably constrained by needing to keep the host healthy enough, long enough, to spread to another. Under extreme crowding conditions, though, natural biological checks and balances on virulence may no longer apply. Anthropologist and author Wendy Orent explained this in the Los Angeles Times:
H5N1 has evolved great virulence among chickens only because of the conditions under which the animals are kept—crammed together in cages, packed into giant warehouses. H5N1 was originally a mild virus found in migrating ducks; if it killed its host immediately, it too would die. But when its next host’s beak is just an inch away, the virus can evolve to kill quickly and still survive.1713
With tens if not hundreds of thousands of susceptible hosts crammed beak-to-beak, the virus can rapidly cycle from one bird to the next, accumulating adaptive mutations. With so many teachers, the virus may learn at an accelerated rate. French scientist C.J. Davaine was one of the first to demonstrate the concept of “serial passage.” How much anthrax-infected blood, he wondered, would it take to kill a rabbit?

Davaine showed that it took ten drops of blood swarming with anthrax to infect and kill a rabbit. Fewer than ten drops and the rabbit survived. But, when he took blood from the first rabbit and infected another, the second required a smaller infectious dose. The anthrax germ was learning. Passing from rabbit to rabbit, the anthrax adapted to its new host to become more and more deadly. By the fifth rabbit, instead of requiring ten drops to kill the rabbit, it only took 1/100th of one drop to kill. By the 15th passage the pathogen became so well adapted that it only took 1/40,000th of a single drop. After passing through 25 rabbits, just one-millionth of a drop could be fatal.

When a pathogen passes into a new environment, species, or even host, it may start out with low pathogenicity. But, when it passes from animal to animal, it can learn to become a more proficient killer.1714 Forget 25 hosts: broiler chicken sheds offer an average of 25,000 captive hosts, and some egg-laying hen sheds 250,000.1715

Once the virus burns through a chicken shed, its survival is again jeopardized—unless it can find new victims. Depending on the ambient conditions, influenza virus can only endure in wet manure for weeks at most.1716 The virus no longer has the luxury of being sheltered for months, lurking in the depths of some Canadian lake. It has very little time to find its way into another flock, so the virus hitches a ride on whatever it can find: footwear, clothing, tires, trucks, cages, crates, insects, rodents, or even the wind, blown out into the countryside by the colossal fans that ventilate the sheds. Mink fur farms are crowded enough to suffer influenza outbreaks, but unless there are multiple farms to which the virus can travel, the virus seems to inevitably fizzle out.1717

When spatial analyses were carried out of the spread of H5N1 in Asia, outbreaks corresponded to areas with the greatest numbers of chickens per square mile. When researchers overlaid a poultry density map of a country on a map of outbreaks, the maps lined up with statistical significance.1718 So, within a shed, on a farm, or even across an entire region, as the WHO’s Asian director put it, “outbreaks of avian influenza correspond to where [poultry] population density is very high.”1719

Large, crowded populations may be the only way a short-lived virus like influenza has been able to exist for millions of years. Viruses tend to have one of two “viral life strategies.”1720 There are persistent viruses like herpes, which have survived through the ages because they can hide within the body, only peeking out for a transient blistering rash in order to spread before going back underground to hide from the body’s defenses. Then there are the acute viruses like influenza, which have no place to hide. They only have a matter of days to spread before they kill the host or, more likely, the host kills them. Therefore, without a vast, dense population of susceptible hosts, the virus would quickly disappear.

Even in wild waterfowl, influenza is transient. There is no evidence that ducks carry the virus for more than a few weeks at a time, so the virus seems to rely on the fact that for 100 million years, aquatic birds like ducks and geese have gathered in mass congregations. Combined with efficient waterborne transmission, this rather unique circumstance of a densely crowded yet mobile population makes waterfowl essentially the only host in the animal kingdom thought able to continuously support such a short-lived infection.1721

In 1989, a bird flu virus jumped straight into horses in China, killed 20% of a herd, and then quickly disappeared.1722 Such epidemics seem necessarily self-limited since the population is restricted in size and not rapidly replenished with new hosts.1723 Unless we start circulating tens of thousands of horses through crowded megabarns, horse flu has little chance of taking root and, presumably, even less chance of posing a human threat. Only, perhaps, when the poultry population and density reached a critical mass—and one that was continuously repopulated—could chickens act as harbingers of viruses like H5N1.1724

Similar studies on influenza in commercial pig operations have come to the same conclusion. An increased density of pigs per pen, pigs per operation, and pigs per municipality all have been shown to be associated with increased risk of swine flu infection.1725 Whether talking about pigs in a shed or sniffly kids in a preschool, the greater the number of contacts, the greater the risk of spread. Pig farm researchers blame the increased risk in part on diminished air volume per animal, increasing the concentration of infectious particles and thereby facilitating aerosol spread.1726 It’s like a pig sneezing in one really big crowded elevator. A professor of Medical Microbiology at the University of Edinburgh concluded that “overcrowded farms are a hotbed of genetic mixing for flu viruses.”1727