Flu update

Hong Kong is preparing for the worst.
Remember the Hong Kong flu?
They don't take these things lightly.

The authority which manages all of Hong Kong's public hospitals fears an explosion of bird flu cases in the city early next year, a Chinese-language daily reported on Saturday, quoting a source at the authority.

"Spring is the peak season for human influenza. Once the human influenza virus mixes with bird flu, it will pose a big threat," Wen Wei Po said in a front-page story, quoting an unidentified source at the Hong Kong Hospital Authority.

"If bird flu explodes in the community, the first wave will be very severe. It will pose the biggest threat to young people," the pro-Beijing daily said.

Experts fear that the H5N1 bird flu virus could mutate and become easily transmissible between people, setting off a pandemic in which millions might die. The virus in its current form has killed around half of the people it has infected.

A study, published in the online medical journal Respiratory Research, suggested that if H5N1 did cause a pandemic, it could disproportionately affect the young and healthy as compared to seasonal flu, which kills many elderly but few young adults. In Hong Kong, the seasonal peak for human influenza is between January and March.

This link comes from H5N1 Blog.

Those interested in science might be interested in this.

The more you understand of this report from Respiratory Research, the less you'll like it: Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells.
[...]
If I understand what they're saying, H5N1 has a talent for provoking the immune system into inflaming and destroying the lung tissue where the virus is thriving. The abstract goes on to say that recent virus strains from Vietnam are even better at inducing "chemokines" than the original 1997 strain of H5N1.

Or this via another bird flu blog.

Bird flu might cause such severe disease and kill so many people because it makes the immune system 'overreact', say researchers.

They say that suppressing the immune response could be a way to treat infection by the H5N1 virus, which has killed 64 people in Asia — about half of all confirmed cases.

In a study published online today (11 November) by Respiratory Research, the researchers showed that lung cells infected with the virus produce considerably more 'messenger' chemicals than cells infected with a normal human flu virus.

These chemical messengers alert the immune system to send white blood cells to attack the source of infection.

The production of so many messenger molecules could explain why H5N1-infected people's lungs are "full" of a kind of white blood cell called macrophages, says lead researcher Malik Peiris of the University of Hong Kong.

(More)

New virus "very unstable", more changes seen -- expert

Via H5N1 blog, this from Reuters.

By Tan Ee Lyn

HONG KONG, May 12 (Reuters) - A leading virologist has described the new H1N1 influenza virus as "very unstable", meaning it could mix and swap genetic material when exposed to other viruses.

The new virus, which has infected 5,251 people in 30 countries and killed 61, has displayed great efficiency in spreading among people, said Guan Yi, a microbiologist with the University of Hong Kong.

"This virus has been around only a few months, it is very unstable ... and we know that its presence is dramatically increasing in human population, so the chance of it meeting with H5N1 is actually increased," Guan said in an interview on Tuesday.

"Both H1N1 and H5N1 are unstable so the chances of them exchanging genetic material are higher, whereas a stable (seasonal flu) virus is less likely to take on genetic material."

While H1N1 appears to be mild so far with many infected people recovering even without treatment, the H5N1 has a mortality rate of between 60 to 70 percent.

Experts are fearful about the emergence of a hybrid which combines the killing power of the H5N1 with the efficient transmissibility of H1N1. H5N1 is believed to be endemic in countries like China, Indonesia, Vietnam and Egypt.

Guan, an expert on both the H5N1 and SARS, has analysed the genetic sequences of the new virus, which is a triple reassortant containing genetic material from swine, human and bird.

He said there was a huge information gap due to a lack of regular surveillance on animal disease.

Each one of the eight gene segments in the new virus has been seen in pigs in the past 10 years, but experts have no clue when this new H1N1 virus strain first appeared and in which animal species it had been incubating, Guan said.

"We know when each gene segment appeared, but we don't know when this strain first appeared, there is an information gap of about five to 10 years, from 1999 to 2009. If there was regular surveillance, we would know when this virus came about," he said.

"We don't know if this reassortment happened in pigs or human ... It's likely to have come from pigs because all the segments have been found in pigs, but we can't be 100 percent sure."

Guan backed stringent moves taken by some governments to keep the virus at bay, such as quarantining.

"They are useful because we are now fighting for time to develop vaccines and antivirals, which will then minimise its impact on people (over the longer term)," he said.

"Already it appears to more virulent than seasonal flu because it is killing younger people and it appears to have higher mortality than seasonal flu, so it doesn't make sense to treat this like seasonal flu."

Seasonal flu kills about 250,000 to 500,000 people annually with a fatality rate of less than 0.1 percent.

A study published in Science on Monday estimated that the new H1N1 flu virus has a case fatality ratio of 0.4 percent based on confirmed and suspected deaths. (Editing by Jeremy Laurence)

Another cautionary note via John Robb's blog:

WHO The new H1N1 flu virus could still mutate into a more virulent form..

The 1918 influenza pandemic -- which killed tens of millions of people -- began mild and returned within six months in a much more lethal form, it said. The 1968 pandemic began relatively mild, with sporadic cases prior to the first wave, and remained mild in its second wave in most, but not all countries, it said.

Seasonal flu has a so-called "secondary attack rate" -- the percentage of contacts who catch it from an infected person -- of between 5 and 15 percent, according to the WHO. Current estimates of the secondary attack rate of H1N1 range from 22 to 33 percent.


The overall severity of a pandemic is further influenced by the tendency of pandemics to encircle the globe in at least two, sometimes three, waves.. [likely more given interconnection]

"It is in the realm of reasonable probability that H5N1 will reach the United States this summer or early autumn."

H5N1 Blog is one of the sites I look at almost daily. The snips are from all over the place, but this caught my eye this morning and I thought it should be posted. It should be noted that when mention is made of bird flu is is about instances of the virus that occur in the animal population, typically wild birds but also domestic poultry which contracts the disease from migratory birds.

This recent interview with Laurie Garrett is very informative. For example...

We now know that the H5N1 virus is particularly robust, and can survive suspended in fecal material for more than a month, making it possible that a flock of dead chickens spotted today may actually have become infected as a result of pecking its way through feces deposited weeks ago by a passing goose.
[...]
By June or July, if the biological imperatives continue to follow their course, H5N1 should turn up in eastern Siberia, and then Alaska, via the East Asia flyway. It might also at that time jump from Iceland, via Greenland, to northern Canada. Once in the Arctic zones of the Americas, H5N1 will be able to follow any, or all, of the four primary north/south flyways that span the Americas, from the Arctic to Tierra del Fuego. It is in the realm of reasonable probability that H5N1 will reach the United States this summer or early autumn.
Instead of simply sitting back and watching nature take its course, the global community should be proactive. Being ahead of the virus is akin to being ahead of the migrating birds. Instead of waiting for dead birds, and even dying people, to turn up in new areas, political leaders should heed the warnings from science and act accordingly - as, apparently, Sweden and the Netherlands are doing. The Swedes and Dutch looked at their maps, plotted the movements of infected birds, and last week ordered farmers to bring their flocks indoors, out of harm's way. In poorer regions of the world, where indoor facilities for animals may be unaffordable, simple nets and fences can radically decrease contact between wild and domestic birds, and mass public education campaigns warning people to avoid contact with sick birds or carcasses may decrease the likelihood of avian-to-human transmission of H5N1.

Of course in order to plan and execute constrtuctive global plans to prepare for what is as plainly in our future as a hurricane forcast those inleadership positions have to stop political carping and gamesmanship long enough to do a little bridge building.

"'Review of Aerosol Transmission of Influenza A Virus"

For some reason CDC linked this piece, then it became unavailable.
I found it in a Google cache, so I figure it is okay to capture it here for future reference. There is a lot of valuable information here, and the number of references makes me think there are any number of litigious reasons its publication might be delayed or prevented altogether.

I haven't taken time to remove the footnote citations for easy reading, but I have a saved copy if anyone is interested.

Abstract

In theory, influenza viruses can be transmitted through aerosols, large droplets, or direct contact with secretions (or fomites). These 3 modes are not mutually exclusive. Published findings that support the occurrence of aerosol transmission were reviewed to assess the importance of this mode of transmission. Compelling evidence in the literature indicates that aerosol transmission of influenza is an important mode of transmission, which has obvious implications for pandemic influenza planning, and in particular for recommendations about the use of N95 respirators as part of personal protective equipment.

Concerns about the likely occurrence of an influenza pandemic in the near future are increasing. The highly pathogenic strains of influenza A (H5N1) virus circulating in Asia, Europe, and Africa have become the most feared candidates for giving rise to a pandemic strain.

Several authors have stated that large-droplet transmission is the predominant mode by which influenza virus infection is acquired (1–3). As a consequence of this opinion, protection against infectious aerosols is often ignored for influenza, including in the context of influenza pandemic preparedness. For example, the Canadian Pandemic Influenza Plan and the US Department of Health and Human Services Pandemic Influenza Plan (4,5) recommend surgical masks, not N95 respirators, as part of personal protective equipment (PPE) for routine patient care. This position contradicts the knowledge on influenza virus transmission accumulated in the past several decades. Indeed, the relevant chapters of many reference books, written by recognized authorities, refer to aerosols as an important mode of transmission for influenza (6–9).

In preparation for a possible pandemic caused by a highly lethal virus such as influenza A (H5N1), making the assumption that the role of aerosols in transmission of this virus will be similar to their role in the transmission of known human influenza viruses would seem rational. Because infection with influenza A (H5N1) virus is associated with high death rates and because healthcare workers cannot as yet be protected by vaccination, recommending an enhanced level of protection, including the use of N95 respirators as part of PPE, is important. Following are a brief review of the relevant published findings that support the importance of aerosol transmission of influenza and a brief discussion on the implications of these findings on pandemic preparedness.

Influenza Virus Aerosols

By definition, aerosols are suspensions in air (or in a gas) of solid or liquid particles, small enough that they remain airborne for prolonged periods because of their low settling velocity. For spherical particles of unit density, settling times (for a 3-m fall) for specific diameters are 10 s for 100 μm, 4 min for 20 μm, 17 min for 10 μm, and 62 min for 5 μm; particles with a diameter <3>10,11).
The median diameters at which particles exhibit aerosol behavior also correspond to the sizes at which they are efficiently deposited in the lower respiratory tract when inhaled. Particles of >6-μm diameter are trapped increasingly in the upper respiratory tract (12); no substantial deposition in the lower respiratory tract occurs at >20 μm (11,12). Many authors adopt a size cutoff of <5>10–20 μm will settle rapidly, will not be deposited in the lower respiratory tract, and are referred to as large droplets (10–12).

Coughing or sneezing generates a substantial quantity of particles, a large number of which are <5–10>10)]. In addition, particles expelled by coughing or sneezing rapidly shrink in size by evaporation, thereby increasing the number of particles that behave as aerosols. Particles shrunken by evaporation are referred to as droplet nuclei (10–12). This phenomenon affects particles with a diameter at emission of <20>10). Droplet nuclei are hygroscopic. When exposed to humid air (as in the lungs), they will swell back. One would expect that inhaled hygroscopic particles would be retained in the lower respiratory tract with greater efficiency, and this hypothesis has been confirmed experimentally (11,12). Aerosols, though heavily diluted, remain airborne and thus can be carried over large distances, which may create a potential for long-range infections. The occurrence of long-range infections is affected by several other factors. These include the infectious dose, the amount of infectious particles produced, the duration of shedding of the infectious agent, and the persistence of the agent in the environment (11). Inferring an absence of aerosols because long-range infections are not frequently observed is incorrect.

Humans acutely infected with influenza A virus have a high virus titer in their respiratory secretions, which makes generation of virus aerosols possible. The viral titer measured in nasopharyngeal washes culminates on approximately day 2 or 3 after infection and can reach up to 107 50% tissue culture infective dose (TCID50)/mL (13,14). The persistence of the infectivity of influenza virus in aerosols has been studied in the laboratory. In experiments that used homogeneous aerosolized influenza virus suspensions (mean diameter 6 μm), virus infectivity (assessed by in vitro culture) at a fixed relative humidity undergoes an exponential decay; this decay is characterized by very low death rate constants, provided that the relative humidity was in the low range of 15%–40% (15,16). These results are consistent with those of an older study (admittedly performed in a more rudimentary manner) in which infectious influenza viruses in an aerosol could be demonstrated for up to 24 h by using infection in mice as a detection method, provided that the relative humidity was 17%-24% (17). In all these studies, the decay of virus infectivity increased rapidly at relative humidity >40%. The increased survival of influenza virus in aerosols at low relative humidity has been suggested as a factor that accounts for the seasonality of influenza (15,16). The sharply increased decay of infectivity at high humidity has also been observed for other enveloped viruses (e.g., measles virus); in contrast, exactly the opposite relationship has been shown for some nonenveloped viruses (e.g., poliovirus) (11,15,16).

Experimental Influenza Infection

Experimental infection studies permit the clear separation of the aerosol route of transmission from transmission by large droplets. Laboratory preparation of homogeneous small particle aerosols free of large droplets is readily achieved (13,18). Conversely, transmission by large droplets without accompanying aerosols can be achieved by intranasal drop inoculation (13).
Influenza infection has been documented by aerosol exposure in the mouse model, the squirrel monkey model, and human volunteers (12,13,17–19). Observations made during experimental infections with human volunteers are particularly interesting and relevant. In studies conducted by Alford and colleagues (18), volunteers were exposed to carefully titrated aerosolized influenza virus suspensions by inhaling 10 L of aerosol through a face mask. The diameter of the aerosol particles was 1 μm–3 μm. Demonstration of infection in participants in the study experiment was achieved by recovery of infectious viruses from throat swabs, taken daily, or by seroconversion, i.e., development of neutralizing antibodies. The use of carefully titrated viral stocks enabled the determination of the minimal infectious dose by aerosol inoculation. For volunteers who lacked detectable neutralizing antibodies at the onset, the 50% human infectious dose (HID50) was 0.6–3.0 TCID50, if one assumes a retention of 60% of the inhaled particles (18). In contrast, the HID50 measured when inoculation was performed by intranasal drops was 127–320 TCID50 (13). Additional data from experiments conducted with aerosolized influenza virus (average diameter 1.5 μm) showed that when a dose of 3 TCID50 was inhaled, ≈1 TCID50 only was deposited in the nose (12). Since the dose deposited in the nose is largely below the minimal dose required by intranasal inoculation, this would indicate that the preferred site of infection initiation during aerosol inoculation is the lower respiratory tract. Another relevant observation is that whereas the clinical symptoms initiated by aerosol inoculation covered the spectrum of symptoms seen in natural infections, the disease observed in study participants infected experimentally by intranasal drops was milder, with a longer incubation time and usually no involvement of the lower respiratory tract (13,20). For safety reasons, this finding led to the adoption of intranasal drop inoculation as the standard procedure in human experimental infections with influenza virus (13).

Additional support for the view that the lower respiratory tract (which is most efficiently reached by the aerosol route) is the preferred site of infection is provided by studies on the use of zanamivir for prophylaxis. In experimental settings, intranasal zanamivir was protective against experimental inoculation with influenza virus in intranasal drops (21). However, in studies on prophylaxis of natural infection, intranasally applied zanamivir was not protective (22), but inhaled zanamivir was significantly protective (22,23). These experiments and observations strongly support the view that many, possibly most, natural influenza infections occur by the aerosol route and that the lower respiratory tract may be the preferred site of initiation of the infection.

Epidemiologic Observations

In natural infections, the postulated modes of transmission have included aerosols, large droplets, and direct contact with secretions or fomites because the virus can remain infectious on nonporous dry surfaces for <48>24). Because in practice completely ruling out contributions of a given mode of transmission is often difficult, the relative contribution of each mode is usually difficult to establish by epidemiologic studies alone. However, a certain number of observations are consistent with and strongly suggestive of an important role for aerosol transmission in natural infections, for example the "explosive nature and simultaneous onset [of disease] in many persons" (9), including in nosocomial outbreaks (25). The often-cited outbreak described by Moser et al. on an airplane with a defective ventilation system is best accounted for by aerosol transmission (26). Even more compelling were the observations made at the Livermore Veterans Administration Hospital during the 1957–58 pandemic. The study group consisted of 209 tuberculous patients confined during their hospitalization to a building with ceiling-mounted UV lights; 396 tuberculous patients hospitalized in other buildings that lacked these lights constituted the control group. Although the study group participants remained confined to the building, they were attended to by the same personnel as the control group, and there were no restrictions on visits from the community. Thus, it was unavoidable at some point that attending personnel and visitors would introduce influenza virus in both groups. During the second wave of the pandemic, the control group and the personnel sustained a robust outbreak of respiratory illness, shown retrospectively by serology to be due to the pandemic strain influenza A (H2N2), whereas the group in the irradiated building remained symptom free. The seroconversion rate to influenza A (H2N2) was 19% in the control group, 18% in personnel, but only 2% in the study group (27,28).

Whereas UV irradiation is highly effective in inactivating viruses in small-particle aerosols, it is ineffective for surface decontamination because of poor surface penetrations. It is also ineffective for large droplets because the germicidal activity sharply decreases as the relative humidity increases (28). Furthermore, because the installation of UV lights was set up in such a way as to decontaminate the upper air of rooms only, large droplets would not have been exposed to UV, whereas aerosols, carried by thermal air mixing, would have been exposed (27,28). So in effect in this study only the aerosol route of infection was blocked, and this step alone achieved near complete protection.

The converse occurrence, blocking only the large droplet and fomites routes in natural infections, can be inferred from the studies on the use of zanamivir for prophylaxis described previously. In experimental settings, intranasally applied zanamivir was protective against an experimental challenge with influenza by intranasal drops (21). However, in studies on prophylaxis of natural disease, intranasal zanamivir was not protective (22), which leads to the conclusion that natural infection can occur efficiently by a route other than large droplets or fomites. As noted above, inhaled zanamivir was significantly protective (22,23).

Discussion and Implications for Infection Control during Influenza A (H5) Pandemic
In principle, influenza viruses can be transmitted by 3 routes: aerosols, large droplets, and direct contact with secretions (or with fomites). These 3 routes are not mutually exclusive and, as noted above, may be difficult to disentangle in natural infections.

For the purpose of deciding on the use of N95 respirators in a pandemic, showing that aerosol transmission occurs at appreciable rates is sufficient. Evidence supporting aerosol transmission, reviewed above, appears compelling. Despite the evidence cited in support of aerosol transmission, many guidelines or review articles nevertheless routinely state that "large droplets transmission is thought to be the main mode of influenza transmission" (or similar statements) without providing supporting evidence from either previously published studies or empirical findings. Despite extensive searches, I have not found a study that proves the notion that large-droplets transmission is predominant and that aerosol transmission is negligible (or nonexistent). Reports on many outbreaks suggest that influenza aerosols are rapidly diluted because long-range infections occur most spectacularly in situations of crowding and poor ventilation (25,26). However, even if long-range infections do not readily occur when sufficient ventilation exists, this does not rule out the presence at closer range of infectious particles in the micron or submicron range, against which surgical masks would offer little protection (29,30). Many infection control practitioners have argued that the introduction of large-droplets precautions in institutions has proven sufficient to interrupt influenza outbreaks and therefore that aerosol transmission appears negligible. This evidence is, unfortunately, inconclusive because of several confounding or mitigating factors. First, unless precise laboratory diagnosis is obtained, respiratory syncytial virus outbreaks can be mistaken for influenza outbreaks (9), which would artificially increase the perceived "effectiveness" of large-droplets precautions against influenza. Second, serologic studies are often not conducted, and therefore asymptomatic infections are not documented (among healthcare workers a large fraction of influenza infections are asymptomatic or mistaken for another disease [31]). Third, since we are in an interpandemic period and the viruses currently circulating have been drifting from related strains for decades, we all have partial immunity against these viruses, immunity that is further boosted in vaccinated healthcare workers. It has even been argued that after several decades of circulation the current human influenza viruses are undergoing gradual attenuation (32). Finally, surgical masks (used in large-droplets precautions) do not offer reliable protection against aerosols, but they nevertheless have a partially protective effect, which further confuses the issue (29,30).
In contrast, the situation with a pandemic strain of influenza A (H5) would become only too clear because no one would have any degree of immunity against such a virus, vaccines would not be available for months, and these viruses would likely be highly virulent. Even though efficient human-to-human transmission of the A (H5N1) virus has not yet been observed (by any mode), transmission of influenza A (H5N1) from geese to quails has been demonstrated in the laboratory (33). Thus, even in the current incarnation of A (H5N1), infection by the virus can generate aerosols that are infectious for highly susceptible hosts. As far as we know, 1 of the main blocks to efficient human-to-human transmission of influenza A (H5N1) is the virus's current preference for specific sialic acid receptors. The current strains still prefer α-2,3–linked sialic acids, which is typical of avian influenza viruses, whereas human influenza viruses bind preferentially to α-2,6–linked sialic acids (34–36). In all likelihood, 1 of the mutations required for influenza A (H5N1) to give rise to a pandemic strain would be to change its receptor affinity to favor the α-2,6–linked sialic acids. For the influenza A (H1N1) pandemic strain of 1918, this change required only 1 or 2 amino acid substitutions (36). Once a highly transmissible strain of influenza A (H5) has arisen, it will likely spread in part by aerosols, like other human influenza viruses.

Recent studies have shown that whereas epithelial cells in the human respiratory tract express predominantly the α-2,6 sialic acid receptor, cells expressing the α-2,3 receptor were detected only occasionally in the upper respiratory tract; however, measurable expression of α-2,3–linked sialic acid receptors was found in some cells in the alveolar epithelium and at the junction of alveolus and terminal bronchiole (35). Binding of influenza A (H5N1) virus can be demonstrated in human tissue sections from the respiratory tract in a distribution corresponding to that of the α-2,3 receptors in the respiratory tract (34,35). This pattern of virus binding correlates well with autopsy findings, which show extensive alveolar damage (34,37), and also correlates well with the observation that recovery of the A (H5N1) virus is much more difficult from nasal swabs than from throat swabs (37). Thus, in the respiratory system the current strains of A (H5N1) appear to infect mostly (perhaps exclusively) the lower respiratory tract. If that is indeed the case, it in turn suggests that human cases of avian influenza were acquired by exposure to an aerosol, since large droplets would not have delivered the virus to the lower respiratory tract. (Another hypothesis might be gastrointestinal infection, followed by viremia and dissemination, but not all patients have gastrointestinal symptoms [37]). Given the strong evidence for aerosol transmission of influenza viruses in general, and the high lethality of the current strains of avian influenza A (H5N1) (37), recommending the use of N95 respirators, not surgical masks, as part of the protective equipment seems rational.
Several infection control guidelines for influenza have recently been published, some specifically aimed at the current strains of A (H5N1), others as part of more comprehensive pandemic plans that address the emergence not only of a pandemic form of A (H5) but also of other types of pandemic influenza viruses. Even though to date human-to-human transmission of A (H5N1) remains very inefficient, the high lethality of the infection and potential for mutations call for prudence. The use of N95 respirators is included in the 2004 recommendations of the Centers for Disease Control and Prevention for healthcare workers who treat patients with known or suspected avian influenza (38). The World Health Organization's current (April 2006) guidelines for avian influenza recommend the use of airborne precautions when possible, including the use of N95 respirators when entering patients' rooms (39).

Currently, several pandemic plans differ considerably in their recommendations for infection control precautions and PPE. The current version of the Canadian pandemic plan recommends surgical masks only, disregarding data that support the aerosol transmission of influenza (4). The US pandemic plan (5), as well as the British plans from both the National Health Service acknowledges the contribution of aerosols in influenza but curiously recommends surgical masks for routine care; the use of N95 respirators is reserved for protection during "aerosolizing procedures" (5,40). These recommendations fail to recognize that infectious aerosols will also be generated by coughing and sneezing. The Australian Management Plan for Pandemic Influenza (June 2005) recommends N95 respirators for healthcare workers recommends FFP2 respirators (equivalent to N95 respirators) Given the scientific evidence that supports the occurrence of aerosol transmission of influenza, carefully reexamining current recommendations for PPE equipment would appear necessary.

Bird Flu Update

CFR has a summary of what is curently known (and unknown) about H5N1, including an ABC News report that is cautiously reassuring.

With regard to raising this flag, Hinrichs says that for a bird influenza virus to reach the level of a pandemic and become dangerous to humans, three things must occur. First, the bird virus must be virulent or capable of causing disease. Second, it must be a new virus that can avoid our existing immune system. And third, the virus must be able to spread from human to human.

"At the present time, the current H5N1 virus has only the first two characteristics," he says. "Dr. Kawaoka's research findings add to our ability to detect the basic element of the third characteristic, the ability to pass infection from human to human.
***
"By analogy, the current H5N1 virus is like an enemy that possesses a nuclear device, has the intention of using the nuclear device, but does not have a delivery missile," Hinrichs says. "When all three are present, the enemy becomes fully capable, and we must increase our readiness to respond."

So far, not a single case of human-to-human transmission of H5N1 has been recorded. Also, the United States remains apparently untouched by H5N1, as no human or bird cases have yet been reported in the country.

"The generals may propose, but H5N1 will dispose."

Crawford Kilian at H5N1...

Pakistan is now just the eastern edge of a disaster extending west to Jordan and Syria. Every country from India to the Mediterranean and the Black Sea is either at war, facing impending war, or struggling to cope with the consequences of its neighbours' wartime difficulties. Three of those countries have nuclear weapons. At least six have experienced outbreaks of H5N1.

When the Germans were planning their big offensive for the spring of 1918, they do not seem to have paid much attention to the influenza that was already weakening their divisions. But by the time they launched their assault on the western front, H1N1 had already defeated them.

Whatever happens in Pakistan, Afghanistan, and Iraq in the coming weeks, avian flu will follow its own course. The generals may propose, but H5N1 will dispose.
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From Wikipedia, Spanish Flu...

The 1918 flu pandemic, commonly referred to as the Spanish flu, was a category 5 influenza pandemic caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1.
[...]
While in most places less than one-third of the population was infected, only a small percentage of whom died, in a number of towns in several countries entire populations were wiped out.

Even in areas where mortality was low, those incapacitated by the illness were often so numerous as to bring much of everyday life to a stop. Some communities closed all stores or required customers not to enter the store but place their orders outside the store for filling. There were many reports of places with no health care workers to tend the sick because of their own ill health and no able-bodied grave diggers to bury the dead. Mass graves were dug by steam shovel and bodies buried without coffins in many places.

Just saying...

H5N1 Watch -- Experts Are On the Job

This summary from the NY Times is not easy reading for laymen. Too many references to the particulars of biochemistry and such. But I find scanning it to be reassuring. Despite the hype smart people all over the world are keeping watch on the spread of this deadly virus, waiting to react swiftly when a mutation occurs jumping the species barrier to humans, triggering a human-to-human strain. When that happens, the much talked about pandemic will be underway.
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...even though the human death toll from H5N1 is still below 200, scientists around the world are racing to study the ways in which it might mutate to spread easily among humans.

The 1918 Spanish flu, they argue, was not even noticed until it had killed thousands. It might have been gathering virulence for years, hidden in the background of seasonal flu deaths.

Today’s H5N1 flu is probably changing more slowly, because health officials have been vigilant about attacking clusters of cases, which presumably wipes out the most dangerous strains. Whenever several human cases appear, even in remote villages in Indonesia or Egypt, local officials and World Health Organization teams move in to kill all the local poultry and dose all the humans with antiviral drugs — the so-called Tamiflu blanket strategy.
[...]
...flus mutate incessantly wherever they move, and in viral samples from Asia, the Middle East and Africa, many individual changes that look potentially dangerous have been spotted.

In May 2005, for example, the virus in China escaped in migratory birds going north and traveled across Russia, Europe and Africa. It became known as the Qinghai strain after the lake in Northern China where thousands of ducks and geese were found dead. (The older strain in Southern China and Southeast Asia is sometimes called the Fujian strain.)

The Qinghai strain has a mutation known as PB2 E627K. (The abbreviation can be read this way: at position No. 627 on polymerase basic protein 2, the amino acid called glutamic acid, abbreviated by scientists as E, has been replaced by lysine, known as K.)

The change helps the virus grow at the temperatures found in human noses, which are cooler than the insides of birds’ intestines.

It is “characteristic of a gene that’s been in mammals,” said Dr. Robert G. Webster, a virologist at St. Jude Children’s Research Hospital in Memphis. “It says to me that it was in a mammalian species in China, and got back into ducks. But what species? We don’t know.”

The Qinghai strain has now reached about 50 countries.

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Thanks H5N1 Blog for the link.

H5N1 Report -- Two Points

News of the bird flu virus is "in a trough," according to this dedicated blogmaster.

Many of us, I suspect, follow H5N1 because it's provided a good, suspenseful narrative. The cases have been few, so we can often learn the names and backgrounds of the victims. The virus has moved rapidly and surprisingly, leaping from Egypt to Nigeria. Even its pauses have surprised: Who would have thought H5N1 would kill two people in northern Iraq (and maybe a third in the middle of the country), and then drop out of sight?

The humans involved have contributed to the narrative: the hapless Indonesians, the methodical Vietnamese, the sometimes-mysterious Chinese, the stoic French. Politicians everywhere have memorized their key line: "No need to panic. Please pass the chicken."
But narrative demands ever-increasing anxiety, news of fresh disasters that heighten suspense before the inevitable announcement (whether from Jakarta or Mumbai or Los Angeles) that a cluster of cases are inarguably human-to-human.

That climactic point, by the rules of narrative, provides a natural conclusion to Volume I. Volume II then follows the pandemic itself, perhaps rounding out the trilogy with a volume on the post-pandemic world.

This is a time of watchful waiting. In a later post he notes that the current outbreak of mumps can be seen as a dress rehersal of what could be a more virulent threat in the event of a flu outbreak.

He mentioned in the first post something that I find both interesting and important: pigeons apparently will not be vectors for the virus. For some reason they are not prone to catch or carry the disease.

From the London Daily Mail:

Researcher David Swayne said: "Pigeons are not uniformly susceptible like chickens or ducks."

Infected pigeons carried the virus for about 10 days. But they were infectious for only two days and then at levels below what it would normally take to infect a chicken.

From WISTV, Columbia, S.C.:

Wildlife disease specialists have been conducting tests on the city pests, and found the birds just aren't susceptible to the virus. They're not totally immune, but research shows pigeons catch the H5N1 virus only when exposed to very high doses and even then carry the disease very briefly. Pigeons didn't even get infected after high levels of virus were squirted directly into their mouths. "So that's good news," according to one researcher.

Instead, US government scientists looking for the first signs of the deadly strain are focusing on wild migratory birds, not birds like pigeons, starlings and sparrows that stay close to home.

It makes me wonder what causes variable rates of infection from one bird species to another. How are migratory birds different from populations that stay put year-round? I'm not an expert, but respiratory endurance over miles of flying immediately comes to mind, which leads me to speculate that the immune systemns of non-migrating birds must be better. Ventilating the lungs reduces the incidence of pneumonia in humans (which is why binding the chest for rib fractures was abandoned years ago). Relatively shallow breathing, then, should correlate with a strong immune system.

So why would chickens be vulnerable? Could it be that generations of inbreeding aimed at getting faster growth, combined with the widespread use of agricultural pharmaceutical additives may have significantly compromised the immune systems of commercially raised poultry?

Ducks? I dunno. They are more than just "swimming chickens." Aren't they migratory? Miles of flying and all that.

In any case, I am reassured that the ubiquitous pigeons are apparently not at risk. (Yet. There is no way to know what direction new mutations might take.)

H5N1 -- Drawing a line between concern and panic

It's nice to finally write a post about H5N1 that doesn't have to start with an explanation, thanks to recent publicity about avian flu. Unfortunately that same publicity has given rise to the usual spate of inappropriate responses, illustrating the old adage about "a little knowledge is a dangerous thing."

H5N1 Blog points to a short piece from Canada that focuses the picture in a short summary worth repeating. I don't think anyone will mind my reproducing it here.

Dizzying explosion of 'bird flu' events, coverage create confusion

Helen Branswell, Canadian Press, October 20, 2005

TORONTO (CP) - To many people trying to make sense of their newspapers or newscasts these days, it must seem like actresses Tippi Hedren (The Birds) and Sandra Bullock (Speed) conspired to write a script for a really bad horror movie.

Lethal bird viruses lurking to infiltrate the lungs of innocent people, threatening to turn a seasonal respiratory ailment into a mutant killer flu. Migratory birds winging the virus from Asia to Russia towards the heart of Europe. Ashen-faced public health authorities warning of potential fatalities ranging from the merely awful to the barely conceivable.

Pandemic influenza has a steep learning curve, ladies and gentlemen. It's time to strap on the crampons.

Setting the record straight

Experts are worried we may be watching a pandemic unfold, but there's no evidence yet that one has started. The noise and fury is about what's thought to be a serious looming threat, not an actuality.

"I think there are some people in the public who think probably with the attention that pandemic human influenza is actually here. And it isn't," notes Dr. Ross Findlater, Saskatchewan's chief medical officer of public health.

Since late 2003, a very deadly strain of avian influenza called H5N1 has been infecting and killing domestic poultry, some wild birds, zoo tigers and on rare occasions people in Southeast Asia. But it isn't spreading in a sustained fashion among people.

If it mutates to be able to do that, it would trigger a pandemic, a wave of illness that would sweep around the globe. There's no way of knowing if it ever will do that or how soon it will if it does.

About that flu shot

It seems a few people around the country are presenting themselves at flu shot clinics thinking they can get a shot to protect against "bird flu." That is not the case.

The shots offered at the clinics protect against the three main strains of human flu experts believe will circulate this winter. They won't offer any protection against a pandemic strain when it emerges.

Flu, bird flu and pandemic influenza

At the heart of the confusion is, well, more confusion. Most people aren't entirely sure what flu is for starters. Unless you've had a bad case of the flu, you won't necessarily know if the bug you have is influenza or one of the myriad pathogens that provoke respiratory hell every winter.
Human influenza causes severe cold-like illness, with fatigue, muscle aches and the potential to progress to pneumonia caused by a secondary bacterial infection.

Bird flu - more accurately called avian influenza - is a term that actually describes a large range of viruses that live in the guts of some species of wild water birds. Occasionally domestic poultry become infected with one of those viruses, which can trigger an outbreak of avian influenza among flocks.

Very occasionally a novel strain of avian flu will cross the species barrier and start transmitting easily among people. Or a bird flu virus will swap genetic material with a human or a pig flu virus, giving it the ability to transmit easily among humans. That's the start of a flu pandemic.

The death and taxes thing

Politicians occasionally talk about flu pandemics with the modifier "if" attached. That's wishful thinking.

"The first big issue is 'if', because a lot of people are still talking 'if' - and that's a fundamental misperception," says Dr. Allison McGeer, one of Canada's leading infectious disease experts.
They can't tell you when or how often, but the experts are united - flu pandemics will continue to occur.

The myth of quarantine

George W. Bush recently talked about using the National Guard to cordon off affected parts of the U.S. when a pandemic strikes. Nice notion, but it can't work.

Flu is too infectious a disease to be contained through quarantine. And people can pass on the virus before they know they're sick, so how would you know who to quarantine if you tried?

"Quarantine will not work. Closing the borders will not work. Closing schools will not work. Nothing will stop the transmission of the pandemic," says McGeer, head of infection control at Toronto's Mount Sinai Hospital.

Lowering expectations

People may be tempted to think modern medicine can curb pandemic influenza. Heck, it stopped SARS.

In actuality, experts say medicine still doesn't have much to offer when an individual goes into acute respiratory distress syndrome - which can be triggered by pandemic influenza. When hundreds or thousands in a community need medical care, the sheer volume of illness will swamp medical systems, planners believe.

Infectious disease expert Dr. William Schaffner says there has to be some realism attached to discussions about how much any government can do to prepare for pandemic flu. Schaffner, from Vanderbilt University School of Medicine in Nashville, likens it to preparing for a hurricane.
"We can't prevent the hurricane. But what we're trying to do is gear ourselves up so that our response to the hurricane is as good as we can reasonably hope it can be," he says. "There is out there an expectation of perfection on the part of some people in the government and many citizens. They expect us to be 'completely prepared.' That's not a relevant concept when you're dealing with hurricanes. It's not a relevant concept when it comes to potential pandemic influenza."

Back to that vaccine

Canada and some other countries have plans in place to make pandemic vaccine. But because we don't know in advance what strain of flu will cause the next pandemic, it can't be prepared in advance.

Making vaccine isn't a quick process.

"If you could get full production of a licensed vaccine up within six months of the start of a pandemic, we'll be doing very, very, very, very well," says Dr. Perry Kendall, chief medical officer of health for British Columbia.

"So if we're talking about a pandemic that comes in a number of waves, each of which lasts about 15 or 16 weeks, separated by some months, then we won't have vaccine for the first wave.

"But we might be able to get vaccine ready for the second wave and give it to the most vulnerable people - health care workers, essential service workers, police, firemen, etc. ... before then giving it to the broader population."

Avian Flu update

Lots of stuff coming in...

The Next Pandemic?
A special section in the July/August 2005 issue of Foreign Affairs.
Editor's Note
As a call to action, the July/August issue of Foreign Affairs includes a special set of articles...[more]

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AN OUTBREAK of avian flu among wild and domestic birds in Russia is spreading west and starting to approach Europe, public health officials said yesterday.
The first cases of bird flu have been reported in the Chelyabinsk region of Siberia, close to the Ural mountains that separate Europe from Asia, though scientists are not yet certain that the virus found there is the deadly H5N1 strain.
Roads were cordoned off and hundreds of chickens were slaughtered in Chelyabinsk yesterday to contain the apparent advance of avian flu, first reported in Siberia in July and being spread westward by migrating birds. [More from the Times of London]

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The CDC predicts that a "medium-level epidemic" could kill up to 207,000 Americans, hospitalize 734,000, and sicken about a third of the U.S. population. Direct medical costs would top $166 billion, not including the costs of vaccination. An H5N1 avian influenza that is transmittable from human to human could be even more devastating: assuming a mortality rate of 20 percent and 80 million illnesses, the United States could be looking at 16 million deaths and unimaginable economic costs. This extreme outcome is a worst-case scenario; it assumes failure to produce an effective vaccine rapidly enough to make a difference and a virus that remains impervious to some antiflu drugs. But the 207,000 reckoning is clearly a conservative guess. [Laurie Garrett, Senior Fellow for Global Health at the Council on Foreign Relations and author of The Coming Plague and Betrayal of Trust writing in Foreign Affairs. Very long. See addendum below.]

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Thanks Hugh Hewett and Stones Cry Out

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A blog was started at the end of March, Avian Flu - What we need to know, for the purpose of keeping up with Avian Flu. There have been posts almost daily. Good one to bookmark or add to the aggregator.

Addendum...
It's two days later and I have read through that Laurie Garrett paper cited above. It prints out to ten pages if you stretch the margins and use two column format. Pretty long.

There are a lot of if's, buts, mays and possiblies in the thing which makes it clear that there is no way to know with any kind of assurance what may happen. It's like predicting the big one in California, or speculating about the odds of an asteroid hitting earth. The difference is that big ones and asteroids don't seem to occur with the frequency of pandemics, so I would be careful not to dismiss the threat lightly.

If the president is reading about the great flu outbreak of 1918 I would guess he is weighing the political aspects of what could happen if there is a global disaster and he did too little, against another Y2K puff that triggered what turned out to be an unfounded exercise in overkill. Shades of duck and cover! The article suggest that any catastrophe that manifests could happen this next season or... and this strikes me as more likely...it could continue to loom for several years to come. The longer the delay, the less likely will be a political will that might cause anything constructive to be pushed through, either by Congress or by some future administration.

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Snips that struck me as interesting...

...as of May 1, about 109 people were known to have contracted it, and it killed 54 percent (although this statistic does not include any milder cases that may have gone unreported). Since it first appeared in southern China in 1997, the virus has mutated, becoming heartier and deadlier and killing a wider range of species.

... in a normal flu season about 200,000 Americans are hospitalized, 38,000 of whom die from the disease, with an overall mortality rate of .008 percent for those infected.
[In the event of a global disaster] the international community would look to the United States, Canada, Japan, and Europe for answers, vaccines, cures, cash, and hope. How these wealthy governments responded, and how radically the death rates differed along worldwide fault lines of poverty, would resonate for years thereafter.

Nearly half of all deaths in the United States in 1918 were flu related. Some 675,000 Americans -- about 0.6 percent of the population of 105 million and the equivalent of 2 million American deaths today -- perished from the Spanish flu. [Statistics are incomplete. Many people perished in what we now refer to as the Third World.]... many historians and biologists believe that nearly a third of all humans suffered from influenza in 1918-19 -- and that of these, 100 million died.

Most strains of the flu do not kill people directly; rather, death is caused by bacteria, which surge into the embattled lungs of the victim. But the Spanish flu that circulated in 1918-19 was a direct killer. Victims suffered from acute cyanosis, a blue discoloration of the skin and mucous membranes. They vomited and coughed up blood, which also poured uncontrollably from their noses and, in the case of women, from their genitals. The highest death toll occurred among pregnant women: as many as 71 percent of those infected died. If the woman survived, the fetus invariably did not. Many young people suffered from encephalitis, as the virus chewed away at their brains and spinal cords. And millions experienced acute respiratory distress syndrome, an immunological condition in which disease-fighting cells so overwhelm the lungs in their battle against the invaders that the lung cells themselves become collateral damage, and the victims suffocate. Had antibiotics existed, they may not have been much help.

Influenza viruses contain eight genes, composed of RNA and packaged loosely in protective proteins. Like most RNA viruses, influenza reproduces sloppily: its genes readily fall apart, and it can absorb different genetic material and get mixed up in a process called reassortment. When influenza successfully infects a new species -- say, pigs -- it can reassort, and may switch from being an avian virus to a mammalian one. When that occurs, a human epidemic can result.

From 1998 to 2001 the virus went through multiple reassortments and moved back to domestic birds, spreading almost unnoticed in Chinese chicken flocks. It continued to evolve at high speed: 17 more reassortments occurred, and in January 2003 the "Z" virus emerged, a mutant powerhouse that had become tougher, capable of withstanding a wider range of environmental challenges. The Z virus spread to Vietnam and Thailand, where it evolved further, becoming resistant to one of the two classes of antiflu drugs, known as amantadines, or M2-inhibitors.

Over the course of this brief but rapid evolution, the H5N1 virus developed in ways unprecedented in influenza research. It is not only incredibly deadly but also incredibly difficult to contain. The virus apparently now has the ability to survive in chicken feces and the meat of dead animals, despite the lack of blood flow and living cells; raw chicken meat fed to tigers in Thailand zoos resulted in the deaths of 147 out of a total of 418. The virus has also found ways to vastly increase the range of species it can infect and kill. Most strains of influenza are not lethal in lab mice, but Z+ is lethal in 100 percent of them. It even kills the very types of wild migratory birds that normally host influenza strains harmlessly. Yet domestic ducks, for unknown reasons, carry the virus without a problem, which may explain where Z+ hides between outbreaks among chickens.

The medical histories of those who have died from H5N1 influenza are disturbingly similar to accounts of sufferers of the Spanish flu in 1918-19. Otherwise healthy people are completely overcome by the virus, developing all of the classic flu symptoms: coughing, headache, muscle pain, nausea, dizziness, diarrhea, high fever, depression, and loss of appetite. But these are just some of the effects. Victims also suffer from pneumonia, encephalitis, meningitis, acute respiratory distress, and internal bleeding and hemorrhaging. An autopsy of a child who died of the disease in Thailand last year revealed that the youth's lungs had been torn apart in the all-out war between disease-fighting cells and the virus.

The scarcity of flu vaccine, although a serious problem, is actually of little relevance to most of the world. Even if pharmaceutical companies managed to produce enough effective vaccine in time to save some privileged lives in Europe, North America, Japan, and a few other wealthy nations, more than six billion people in developing countries would go unvaccinated. Stockpiles of Tamiflu and other anti-influenza drugs would also do nothing for those six billion, at least 30 percent of whom -- and possibly half -- would likely get infected in such a pandemic.

In the summer of 1918, influenza killed far more soldiers than did bombs, bullets, or mustard gas. By October, some 46 percent of the French army was off the field of battle -- ailing, dying, or caring for flu victims. ...In the event of a modern pandemic, the U.S. Department of Defense, with the lessons of World War I in mind, would undoubtedly insist that U.S. troops in Iraq and Afghanistan be given top access to vaccines and antiflu drugs. About 170,000 U.S. forces are currently stationed in Iraq and Afghanistan, while 200,000 more are permanently based elsewhere overseas. All of them would potentially be in danger: in late March, for example, North Korea conceded it was suffering a large-scale H7N1 outbreak -- taking place within miles of some 41,000 U.S. military forces. It is impossible to predict how such a pandemic influenza would affect U.S. operations in Iraq, Afghanistan, Colombia, or any other place.

Although there is little evidence that isolation measures have ever slowed the spread of influenza -- it is just too contagious -- most governments would likely resort to quarantines in a pandemic crisis.

In 1971, the great American public health leader Alexander Langmuir likened flu forecasting to trying to predict the weather, arguing that "as with hurricanes, pandemics can be identified and their probable course projected so that warnings can be issued. Epidemics, however, are more variable [than hurricanes], and the best that can be done is to estimate probabilities."

H5N1 (Birtd Flu or Avian Flu) Update

The worldwide spread of the H5N1 virus continues but the mortality numbers, although still shocking, are trending downward. I have not read any opinions why this is happening, but my guess would be that a growing awareness of the dangers and nature of the disease may be more widespread as officials in affected areas increase their scrutiny. Occasional reports of officieal mass destruction of poultry flocks (chickens, ducks, geese) are certain to draw attention. Also, China and other countries have poultry vaccination policies in place.

(Most Americans are unaware, but our own poultry supply is routinely vaccinated against one or two common diseases among chickens.)

Official data from WHO list only laboratory confirmed cases, so their official numbers are low. Many more cases never get recorded because the most severe outbreaks are in what we carelessly call Third World countries.

Official record-keeping starting in 2003 reports 413 confirmed cases, of which 256 (nearly 62 percent) died.

Hat tip to Crawford Kilian for his excellent, tireless efforts at H5N1 blog.

Bird Flu watch -- best advice at this moment

I'm stealing half a post here:

It's been confirmed in north Germany today (and let me remind you, the suspected human H5N1 case was the cook on a ship which had last docked in Germany), Iran and Austria. Nor is it "expanding" into new territory. It's been there. There were reports of relatively large die-offs in northern Iran since last fall. There were incidents in Germany.

This is not the spring migration, which is still to come - this is 'fessing up after increased monitoring. You won't find what you won't seek. Since any country that found H5N1 was going to get quarantined, every country had a very good reason not to seek. The whole thing has been purely political. There was no way to stop an infection spread by migrating birds, so there was no reason at all to step forward and invite economic distress before it was unavoidable.

And don't think that if these birds made it to Europe in the fall that they didn't make the much shorter hop to NA. The Qinghai strain was far closer to Alaska in the fall than to the Baltic. The US poultry industry quietly instituted an H5N1 sampling program for poultry sent to market in January. Ask yourselves why. I watch the hawks disappear around here and I know what I think. I don't think the Qinghai strain made it to south GA last fall, but I think a milder strain did. I think the Qinghai strain made it into NA last fall, and will spread this year as the weather warms. We're going to find out in a few months if I'm right.

If you eat eggs, hardboil them. Ten minutes boiling. Don't fry them. They might not get hot enough during frying to kill the virus. Don't prepare chicken for cooking without gloves and wash your hands after you have touched eggs. Bleach is by far your best friend. Stock up and use it. Get used to not touching your face unless you have just washed your hands. Get used to taking off your shoes at the door when you come home. Wash the doorknobs and taps at home down once a day with bleach.

You can be (and testing demonstrates that people have been) exposed to even the most virulent strain of flu without getting sick. A high initial dose of the virus gives it the jump on your body's immune system. A low dose will be overcome by your natural defenses. When you have never been exposed to a particular flu virus before, your body is slower to gear up to fight it. Don't be afraid of exposure - just make sure that you avoid a high exposure.

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(The other half of the same post addresses antisemitism, which together with bird flu is the other of twin political plagues in our time. I have no quibble about the main point but I do not agree with some of the writer's conclusions.

(This is delicate ground on which we tread. Any discussion of Jews and Israel is by definition a string of hot-button topics: religion, politics, bigotry, race, culture and history. Any of these frames of reference with regard to Israel or Jews is subject to inflammatory ideas, but taken together, tumbling one after another, can quickly paint a Jackson Pollock-looking picture.

(A question is raised {What is the reason for all of this "nuance"? } regarding what I would rather call discernment, a careful handling of ideas that calls for as much delicacy as the movement of a scalpel in the hand of a surgeon. My point is quickly illustrated in the next few lnes which conclude that anyone advocating nuance -- like me -- is either a hysteric or a coward.

(There follows a couple of bracing references to bears and facism, not intended to be open to debate, so I dare not open any. So go learn something from Maxed Out Mama whose attention to everything she writes about is as intense as a laser, even if I don't always care to be standing in the beam.)

Flu awareness: more people are catching on

At last. Those of us who have been paying attention to H5N1 are moving from the lunatic fringe to the mainstream. When I see signs urging people to get vaccinated I know that there is still a lot of ignorance (there is no vaccine for the bad strain being monitored) but at least an awareness is growing. Public discussions will inevitably lead to talk of panic, but with enough discussion and education I think that scenario can be better controlled. The more people read, learn and ask questions, the less likely a panic will ensue.

This is a good sign.

The page views since I set up H5N1 last March total 72,150, so 20% of all page views have been just since last Tuesday. Before the ABC News "Primetime" item on avian flu, I'd been getting perhaps 500 page views per day. That night and the following day, the number spiked to just over 6,000 in 24 hours, and it's been interesting to see that it settled down to four times the previous average.
[...]
While many other sites link to H5N1, they don't seem to bring many visitors here. But I hope that if you're here, you'll follow the links to the other flu blogs and news sources. No one site can give a real overview of the situation, but a few minutes' surfing can keep you remarkably up to date.

Nothing dramatic to report.
Yet.
If and when the virus mutates into a human-to-human strain, that is when the the alarm bells will start ringing. To date there has been species jumping, but human cases have been associated with contaminated animals (chicken, swine), not other humans.

Stay tuned and keep reading.

H5N1 up to the minute

World Health Organization FAQ is a comprehensive resource. Thanks H5N1 blog. Come to think of it, that blog is also a wellspring of timely reporting.

The most comprehensive treatment of the subject I have read is the Laurie Garrett article in Foreign Affairs, July-August, 2005. It prints out to about ten pages or so, and makes for interesting reading. Among other things she offers this historical caveat:

In January 1976, 18-year-old Private David Lewis staggered his way through a forced march during basic training in a brutal New Jersey winter. By the time his unit returned to base at Fort Dix, Lewis was dying. He collapsed and did not respond to his sergeant's attempts at mouth-to-mouth resuscitation.

In subsequent weeks, U.S. Army and CDC scientists discovered that the virus that had killed Lewis was swine flu. Although no other soldiers at Fort Dix died, health officials panicked. F. David Matthews, then secretary of health, education, and welfare, promptly declared, "There is evidence there will be a major flu epidemic this coming fall. The indication is that we will see a return of the 1918 flu virus that is the most virulent form of flu. In 1918, a half million people died [in the United States]. The projections are that this virus will kill one million Americans in 1976."

At the time, it was widely believed that influenza appeared in cycles, with especially lethal forms surfacing at relatively predictable intervals. Since 1918-19, the United States had suffered through influenza pandemics in 1957-58 and 1968-69; the first caused 70,000 deaths and the second 34,000. In 1976, scientists believed the world was overdue for a more lethal cycle, and the apparent emergence of swine flu at Fort Dix seemed to signal that another wave had come. The leaders of the CDC and the Department of Health, Education, and Welfare (HEW) warned the White House that there was a reasonably high probability that a catastrophic flu pandemic was about to hit. But opinion was hardly unanimous, and many European and Australian health authorities scoffed at the Americans' concern. Unsure of how to gauge the threat, President Gerald Ford summoned the polio-fighting heroes Jonas Salk and Albert Sabin to Washington and found the long-time adversaries in remarkable accord: a flu pandemic might truly be on the way.

On March 24, 1976, Ford went on national television. "I have just concluded a meeting on a subject of vast importance to all Americans," he announced. "I have been advised that there is a very real possibility that unless we take effective counteractions, there could be an epidemic of this dangerous disease next fall and winter here in the United States. ... I am asking Congress to appropriate $135 million, prior to the April recess, for the production of sufficient vaccine to inoculate every man, woman, and child in the United States."

Vaccine producers immediately complained that they could not manufacture sufficient doses of vaccine in such haste without special liability protection. Congress responded, passing a law in April that made the government responsible for the companies' liability. When the campaign to vaccinate the U.S. population started four months later, there were almost immediate claims of side effects, including the neurologically debilitating Guillain Barré Syndrome. Most of the lawsuits -- with claims totaling $3.2 billion -- were settled or dismissed, but the U.S. government still ended up paying claimants around $90 million.

Swine flu, however, never appeared. The head of the CDC was asked to resign, and Congress never again considered assuming the liability of pharmaceutical companies during a potential epidemic. The experience weakened U.S. credibility in public health and helped undermine the stature of President Ford. Subsequently, an official assessment of what went wrong was performed for HEW by Dr. Harvey Fineberg, a Harvard professor who is currently president of the Institute of Medicine.

Fineberg concluded:"In this case the consequences of being wrong about an epidemic were so devastating in people's minds that it wasn't possible to focus properly on the issue of likelihood. Nobody could really estimate likelihood then, or now. The challenge in such circumstances is to be able to distinguish things so you can rationally talk about it. In 1976, some policymakers were simply overwhelmed by the consequences of being wrong. And at a higher level [in the White House] the two -- likelihood and consequence -- got meshed."

Fineberg's warnings are well worth remembering today, as scientists nervously consider H5N1 avian influenza in Asia. The consequences of a form of this virus that is transmittable from human to human, particularly if it retains its unprecedented virulence, would be disastrous. But what is the likelihood that such a virus will appear?

Faith Communities Can Prepare for Bird Flu

[Reposted from April 26 with additional links. I was impressed with the idea so I emailed this post to anyone able to spread the word.]

It's not my habit to dispatch mass emails, but in this case it is an idea that deserves spreading.

I have been following Crawford Killian's H5N1 Blog for the last few years. News cycles have stopped headlining the threat of a bird flu pandemic but the threat remains real. Because human to human transmission of the disease remains rare, fatalities from the H5N1 strain are still statistically small, but the virus is slowly making its way through animal populations around the world.

All that stands between the disease among birds (mainly chickens) and among humans is a mutant strain that can be passed from one human to another. A human to human (H2H) mutation of this flu could be a ticking pandemic bomb depending on how severe symptoms might appear in its victims. As of this writing the WHO has validated 381 cases worldwide which have resulted in 240 fatalities.

Concerned readers can do their own homework, but the purpose of this email is to propogate an idea that has widespread implications, not only for a possible disease pandemic but any number of widespread catastrophies. Food shortages (now in the news), natural disasters, troubles of human origin either deliberate or accidental, and regional/local events calling for a rapic outside response come to mind.

This story is from Calgary. It's about bird flu, but the implications are much bigger. The moment I saw it I envisioned a trans-denominational network of task-oriented people of faith, crossing doctrinal boundaries to close ranks in the face of possible threats. We hear a lot about "faith initiatives." and this is an excellent example.

Marg Pollon knows her particular spiritual calling can be a lonely road.

Pollon has been urging faith communities in Calgary to make plans to play important, supportive roles in battling any major global pandemic.

But when talk of bird flu or a similar medical threat disappears from the daily headlines for long stretches, such a potential disaster goes out-of-sight, out-of-mind.

"I do feel like Noah sometimes," Pollon says with a smile.

"When I talk about pandemic preparedness, peoples' eyes can glaze over."

But Pollon soldiers on, convinced that Christian churches and their congregations can carry out vital work side-by-side with medical authorities should such a modern plague land on our collective doorsteps.

"It would be a living demonstration that the Christian message is authentic," says Pollon, who runs the Bridges of Love ministry. "My goal has always been to get churches out of their buildings and into their communities."

Pollon is the key organizer of a two-day conference of pandemic preparedness, set for May 14 to 15 at Rocky Mountain College, 4039 Brentwood Rd. N.W.

She's hoping representatives of many city churches will attend to see where their congregation might fit into a master pandemic plan.

"Churches can do a lot more than offer pastoral care and host funerals," Pollon reasons. "If large numbers of people fall ill, who is going to give medications to seniors, deliver food to shut-ins and offer child care when parents are sick?

"Churches already have the internal networks and grassroots connections to their neighbourhoods. Some are set up to host people by being involved in Inn from the Cold. Others have great kitchen systems to prepare food. It's about finding your best niche."

Pollon says a key issue is getting area churches talking to each other to make sure service duplication is limited. And while a pandemic's probability remains low, its impact could be devastating.

"And if it never comes, we will have still built these networks and connections between churches and their communities," says Pollon.

"We've been lucky in Calgary in that we haven't had a lot of emergencies or disasters in recent years. But that doesn't mean it can't happen here."

More information and registration is available online at www.bridges oflove.net or by calling Pollon directly at 263-5683.

A related website is Bridges of Love.

Predictions of the impact that an influenza Pandemic would cause range from two million to over one billion deaths worldwide, over the course of several months. The associated social and economic impact would reach even further. The timing of such an upheaval cannot be predicted but from all predictions it is considered to be very likely in the next five years. This will not be something happening ‘over there’ or ‘to them’. Our families, our churches, our organizations will all be affected, in whatever country or city we live. Governments are taking action and the business sector is also taking this threat very seriously.

How could the local church assist the health authorities and government agencies? Could the church stand in the ‘gap’ and be the shining light in the community? How will the church prepare? How will Christians individually as well as the church body respond?

H5N1 again:

This from The Salt Lake Tribune describes how the Mormon network in that state is prepared to help locally in the event of any widespread need.

Assuming there is enough vaccine to go around, Garrison said there aren't enough clinics or nurses to inject it.

Instead, Garrison's plan calls for training thousands of volunteers to give their neighbors and friends shots at their local churches. The county's 300,000 residents could be vaccinated in one day and expect waits of 10 minutes, said Garrison, who was recently named a Utah Public Health Hero by the Utah Public Health Association.

"We don't want to repeat what happened in New Orleans with Katrina. Everyone learned a great deal about what can happen if you're not prepared," said Garrison, who is on the Davis County Board of Health and lives in Kaysville.

The plan, which can be implemented for other outbreaks and is being copied by other counties, would set up vaccination clinics at local churches. People who don't want to go to a church would go to county facilities.

The county's 64 emergency vaccination centers would each have 188 volunteers with 36 people giving shots at one time. Once the county got word that it was getting the vaccine, the call would go out for volunteers, who would then be trained by the Davis Applied Technology Center, Garrison said.

He has no doubt that enough volunteers will step up.

"We're very well known for volunteerism and wanting to help our neighbors with no regard to their religious affiliation," he said.