One of the unanswered questions about the transmission of influenza H5N1 is the mode. We presume, probably correctly, that person to person spread is the main mode, mediated by coughing, breathing, sneezing. Whether the infective material is small enough to remain suspended in the air for long periods or whether it is primarily in large droplets that settle out quickly is a matter of importance still under debate but both possibilities pertain to person to person spread via the respiratory tract. Then there is the question of the role of inanimate objects, like door knobs, arm rests or personal physical contact, like shaking hands. There is evidence that the virus remains replicable in the environment for extended periods, although its replicable lifetime on hands may be much shorter, on the order of minutes. There is also the lingering suspicion that there may be other live reservoirs of the virus besides birds in nature we are not aware of. Even with poultry, a recognized reservoir. how the virus gets from birds to humans is a matter of debate. Is it through the bird respiratory tract or intestinal tract or feces laden dust? Finally, can a human contract H5N1 infection from water or food contaminated with the virus? If food is properly cooked it will kill the virus, although undercooked or raw food or its handling during preparation can still presumably infect someone (how, isn't quite clear). What about water?
The issues are not just drinking water but also recreational water (lakes, streams, oceans) that might be contaminated by infected wild aquatic birds or wastewater discharges. Swimming exposes the conjunctiva of the eye (the thin tissue covering the front of the eyeball which has receptors for influenza virus), not to mention the nose and throat, both suspected sites of viral entry. Drinking water is also a concern. So it is important to have studies that try to nail down some of the unknowns.
A report out of Cornell University says neither drinking water nor wastewater containing viral discharges is likely to be a problem (the paper is published in Environmental Engineering Science and can be downloaded in .pdf format here). The Cornell researchers used the H5N2 subtype of influenza A (low pathogenic for birds and not known to be pathogenic for humans) as a surrogate for H5N1. They showed that the usual water and wastewater treatment modalities of chlorine and UV light were effective in inactivating the virus. Virus was placed into at two temperatures into water and small scale bacterial digesters (the method used in wastewater treatment plants). Each was treated with chlorine (the most common disinfectant in use in water and waste water treatment) and UV light (used primarily in wastewater treatment but also in some drinking water systems). Bacteria and viruses differ greatly in their sensitivity to treatment and no virus is thought to be indicative of the sensitivity of most other viruses. Thus the use of a relatively close avian influenza virus (H5N2) to test the sensitivity of H5N1 to treatment is a reasonable step.
We'll skip a detailed description of the experimental protocol (you can find them in the paper and they are worth reading just to see how difficult some of these seemingly straightforward questions can be to answer). The persistence of the virus as a replicating entity in water at 4 degrees C. (about 40 degrees F.) is better and longer than at 37 degrees C. (body temperature), but in buffered water was consistently and constantly present for more than 50 hours. At 4 degrees C. in buffered water it was still there after two weeks. Thus the stuff doesn't just disappear in the environment. It can be around for days or weeks after being deposited. In anaerobic digesters the virus was undetectable at 72 hours. The virus seemed quite sensitive to UV irradiation, although this method is used in only a small percentage of drinking water systems. We have previously discussed the use of UV lights in health care facilities as a possible prophylactic measure and these data seem to support the idea in a different context.
The data on chlorine disinfection is somewhat harder to interpret. Viruses vary widely in their sensitivity to chlorine, so it isn't a given that chlorine disinfection will inactivate H5N1. The paper gives a Ct (contact time) value of 8 mg.min/L for the virus. Ct is the product of free available chlorine and the time it is in contact with the virus. The average free available chlorine in US drinking water systems is about 1 mg/L (1 ppm) and the paper cites average and median contact times of 237 minutes and 60 minutes, respectively, based on a literature review. This would give average and median Ct's of 237 and 60 mg.min/L, far in excess of the inactivating levels found in this paper.
The apparent large Ct safety margin is reassuring, although these are average and median Ct's. A median contact time of 60 minutes means half the systems had contact times less than 60, so half the systems had Cts with a safety margin less than ten fold, not quite so reassuring. Much depends on the distribution in the lower tail and the upper tail of the Ct inactivation estimate. And of course all of this only holds good for conditions similar to the bench experiments of this paper. The results do not tell us with certainty what would happen in a more natural and usual water and waste water environment. What happens when the virus is inside clumps of feces, for example, or in water of different pH or salt make-up?
There are also a number of treatment methods not tested here, among them ozone (now being used increasingly because of the resistance of parasite cysts to chlorine), chlorine dioxide, chloramines and some others. Many small water supplies (almost always groundwater sources), have no treatment at all, so none of this would apply in those cases.
This paper appears to be well done and provides good information. We need more work like it, although unfortunately this kind of work is not the road to academic stardom. It may not be elegant, but it is very, very useful.
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This is good news. The UV component will obviously be more important in winter for stagnant and non-treated water. I'm getting increasingly optimistic that the risk of a H5N1 pandemic will diminish this year to practically zero, though I know we're not out of the woods yet. Hopefully, the lessons that have been learned will be absorbed for future outbreaks of other influenza strains, and other zoonotic diseases.
Certainly still puts a dent in swimming at the local hole. Especially those New Year's Polar Bear dips.
Marissa: You're "increasingly optimistic that the risk of a H5N1 pandemic will diminish this year to practically zero, though [you] know we're not out of the woods yet." Why, pray tell?
Have I missed something incredibly obvious? Or extremely subtle?
Despite what appears to be a seasonal lull in reported cases, it seems to me that the data from many fronts are increasingly disturbing!
With respect, it seems to me that the only reason you might say the above is that you're drinking the koolaid...
I'd like to discuss this aspect:
"The persistence of the virus as a replicating entity in water at 4 degrees C. (about 40 degrees F.) is better and longer than at 37 degrees C. (body temperature), but in buffered water was consistently and constantly present for more than 50 hours. At 4 degrees C. in buffered water it was still there after two weeks. Thus the stuff doesn't just disappear in the environment. It can be around for days or weeks after being deposited."
in relation to the fact that over the next couple of weeks somewhere between 50 and 70 million people in India will indulge in a series of mass bathing ceremonies at the conflux of three rivers (Ganges and I forget the other two) which are - per bird migratory maps - right on one of the main migration routes from China.
Marissa...take heed. We are definitely not out of the woods yet, and not likely to be for some time if people continue to ignore the dangers.
MiH: You have a point (or rather a speculation), but remember that the Ganges is not a buffered flask. There are a lot of other organisms there and they may or may not affect the persistence of H5N1 in that water. Consider that the virus persists for considerable periods on hard, inanimate surfaces but maybe ten minutes or less on hands. The reason may be that the hands are a biological organ and has ingredients less hospitable to viral persistence (e.g., RNAase). So don't leap to far to your conclusions.
Speaking of water---there may be a severe problem if everyone starts taking lots of Tamiflu.
Tamiflu persists unchanged in water after it is eliminated---and wild birds drinking that water may encourage Tamiflu resistance developing in the influenza viruses present in their bodies.
Here is the study:
http://www.watertechonline.com/news.asp?mode=4&N_ID=65566
Link is wrong above.
Here is the correct link---sorry:
http://www.infectioncontroltoday.com/hotnews/71h46463763090.html
Earl: Thanks for reminding us. We posted on it at length in October here.
Tejas, Mary: I didn't say we're out of the woods yet. Despite recent outbreaks, things are looking up. If ther aren't large numbers of birds infected, or human cases, opportunities for the virus to recombine or mutate diminish. It's a case of probabilities.
Marissa. As always, I am very interested in your opinions...but I will respectfully disagree with you on this one.
As a farm animal veterinarian, I have observed the ebb and flow of emerging and re-emerging diseases with inter-emergence periods as long as fifty-years.
Everything I have learned tells me that the important stuff going on with H5N1, is occurring behind the scenes and beyond our senses.
The reason we are not seeing more positive tests, in my opinion, is because the virus has mutated away from survelliance tests that weren't very accurate in the first place.
Also, the more we learn about what we don't know, the more it becomes apparent that pathogen evolution parallels that of higher life forms; leaps rather than small steps.
I believe that H5N1 is on a well worn pathway...and the best evidence for its imminent emergence as a pandemic potential virus is in the history of H1N1.
A sleeping dragon may be sleeping but is still a dragon.
Didn't more people die of H5N1 in 2006 than the previous three years combined?
And, it is in mammal species, not just birds, (and it doesn't always kill some species of birds) I suppose on at least a few continents, now. Not much surveillance going on in Africa I'd guess...
Things are not looking up; our "modern" systems are barely squeaking by now; they cannot take any sort of illness/fatality surge nor JIT chain disruption!
Months (over a year's worth) have been wasted that could have been educating the public and building more resiliant communities; getting our priorities in order...
Also, next time we're with other people;
see how many times they touch their eyes, nose or mouth
in the "but maybe ten minutes or less on hands"
window of opportunity (never mind the coughers and sneezers).
And back to the subject of bird flu in water...
I noticed today a couple of articles in the Vietnam newspaper that might raise more speculation (at least in my over-speculative mind). There is a massive die off of catfish in the mekong delta (being blamed on pollution) in the same area where there is widespread avian flu among the water bird population. Now, just how coincidental is that?
We already have proof that bird feces can be loaded with the virus, and bird feces drops to the bottom of still waters. Where do catfish feed? On the bottom. So as they are gobbling up those little crustaceans, insect larvae and such in the muck, they are also ingesting large quantities of potentially virus laden poo. Another thought: what about the bottom dwelling invertebrates they eat? These are living in virus laden poo...might some of them not become reservoirs for it? Just speculation... But I wonder if anyone has checked the catfish for H5N1?
MIH brings up some really good damned points.... The Mekong is a warm river for the better part. No snow or ice fed streams to cool it off. So the gig was last summer that this stuff would survive like 5 days in doo-doo and dirt at 98 degrees, then 30+ days at about 39 degrees. So a river wouldnt be a breeding ground, but a holding ground. I have films that my brother took when he returned to Vietnam four years ago and the place is lousy with waterfowl and side of the river types of birds. They also like the shallows where the river catfish and other fish hide in the weeds and reeds for feeding. So suppose it stayed alive and all it did was constanty recirculate by eating a contaminated fish, that in turn makes them sick and they drop contaminated doo into the river which is eaten by the bottom feeders and then up the river food chain it goes again. If you could prove that connection, its Nobel time again. Testing the fish wouldnt work though alone. You would have to conclusively prove first that it stayed alive in water (now that would be something for a big yay), that it was transmissible in fish, then fish to birds. Now I can tell you for a fact that people eat loads of fish out of the Mekong so someone had better prove at least that it doesnt for a start. Else mankind will be on the endangered species list.
Dear All,
I have previously posted questions about pond farming and implications for spread of bird flu to fish. I am glad to see new information on this.
We used to enjoy pond farm catfish but have stopped buying it or ordering it at restaurants. The thought of chicken farm waste fed to pond catfish just is not appetizing. I have been researching the kosher proscriptions for fish and they seem sound to us: no bottom feeding fish including catfish, shrimp, shellfish, etc.
We, in this part of the country, have not been able to safely consume catfish from the Ohio River for decades.
Love,
Library Lady