My deepest, most heartfelt, and sincere sympathy and condolences to the victims of this illness, their families, and friends. This is just horrendous and really must be stopped.
Shekelpal commented: "
...As to the experiment with the rat and the slime, I am not sure this would prove anything except that the rat may or may not get the illness from the slime. Also the rat is the natural host and the human is not so the nematode will behave differently and eventually dies in the human. The question they may have is the number of third stage nematodes that a human must ingest in order to contract the illness. I would think that something more similar to a human would have to be tested in order to get some idea because as the scientists pointed out they cannot do this experiment on humans."
Yes, rodents are probably more susceptible to infection by rat lungworm larvae than are humans, true enough; the point of such an experiment, though, is simply in establishing whether or not such rat lungworm larvae can be shed alive in slime and viably cause infection from slime trails (versus from being ingested sheltered within the body of slugs & snails, inside a living protective bunker, as it were). A positive result from such an experiment in lab rodents signals infectivity in general for slime, versus for the bodies
per se of invertebrates. We, of course, are hoping that the rodents would be negative for infection; if the more-susceptible rodents FAIL to develop rat lungworm infections from wet slime laden with rat lungworm larvae, then the odds of slime (wet or dry) being infective to humans would be essentially zero. This would be good news as it would sharpen our focus to the bodies of invertebrates, rather than their much more subtle trails.
If
positive in rodents, then slime trail infectivity to humans could reasonably be assumed to be dose related (even if the success of the rat lungworm larvae in humans is much lower than in rodents). The more consumed, the higher the risk.
The essential part about experiments (with due acknowledgment to Galileo Galilei for pointing this out and establishing the insight as a key tenet of science) is they assist to empirically reveal what is so regardless of theory -and so assist in casting light on the truth of matters, as by painting a more complete and accurate picture of what is going on. Progress in such matters tends to be frustratingly slow in part because tightly controlled experiments answer only one small question at a time and do not jump all the way to the final summary we all wish we had yesterday (if not sooner). Such limited experiments are still worth performing though, step by step, however slowly and methodically may be required, imho.
That said, two statements from the article which Damon kindly provided a link to [Kubota, 17JAN2009.
Disease is blamed on home-grown veggies. Honolulu Star Bulletin.
http://www.starbulletin.com/news/2009011...ggies.html] are confusing me. The article states "
...probably contracted the disease after eating vegetables containing larvae of a slug that carries the rat lungworm" and "
...warned that a species of slug on the Big Island has tiny larvae, about 1 to 2 millimeters long." This does not square with my understanding of either the rat lungworm lifecycle or slug & snail biology (and omits mentions of all the other potential intermediate hosts).
To dispense with the last point first, the CDC names invertebrates in general (including earthworms, freshwater prawns, slugs, and snails) as well as some vertebrates (frogs, but not fish) as potential intermediate hosts. Until proven otherwise, all invertebrates and amphibians (including coqui frogs) could be considered suspect as potential intermediate hosts if they have some contact with infective rodent feces &/or 1st or 2nd stage
A. cantonensis larvae.
My confusion stemming from the Star-Bulletin article relates to its use of the word "larvae" referring to the slugs, versus the nematodes. This is a significant difference.
My understanding is most if not all slugs and snails lay eggs which subsequently hatch out tiny little versions of the adults which produced them. Slugs & snails, unless I am mistaken, do not lay eggs which --like crustaceans-- hatch out into
larvae which then metamorphose through approximately 17 different stages (each of which looks totally different than the one before, is a different size, and eats something different) or --like insects-- metamorphoses through a number of different larval forms (such as a caterpillar, or a number of instars) on the way to becoming a pupae and then an adult (adults being capable of reproduction). Slugs and snails make eggs, the eggs hatch out little slugs & snails, and they grow larger as they munch their way from being immature juveniles into mature (reproductively enabled) adults, is my understanding. If someone knows differently then please do speak up, fer godssakes, and educate us all.
This article (Kubota, 17JAN2009) talks about the larvae of slugs carrying the rat lungworm disease. I think it may actually be juveniles instead of larvae (since larvae look different, eat different foods, live in different places, etc). Perhaps the word "larvae" is being used interchangeably with "juvenile" even though the larvae are of a nematode and INSIDE the juvenile slugs (and, perhaps, being shed in their slime trails, and in the bodies of other intermediate hosts as well). I further wonder how the heck a 1 to 2 mm slug is eating rat feces? Not whole and entire, that is for sure; maybe they could nibble at the edges of soft moist rat pellets.... It seems even more unlikely that
A. cantonensis larvae are being encapsulated and laid together inside the eggs of slugs, with slug embryos, by infected adult slugs. Yet the article asserts 1 to 2 mm slugs are infective for rat lungworm, and certainly --given the friends and neighbors who have been so seriously injured to date-- until we know otherwise we must take measures as if this rather remarkable assertion is God's own truth.
The reference in the article describing a small version of a Big Island slug is both bad news and good news. Bad news, because it is easy to not see a 1mm to 2mm slug hidden in leafy veggies. Good news, because a 1mm to 2mm slug is very vulnerable to attack if immersed in salt brine solution.
I have been assuming the rat lungworm larvae are being passed in larger slugs only (slugs big enough to have the mass and life experience to have encountered and successfully ingested rat feces with
A. cantonensis eggs in 'em) ...and the larger the slug the harder it falls. That is, a 1mm to 2mm sluglet will undergo lysis (burst apart cell by cell and be destroyed entire, like a starship exploding from one end to the other in a SciFi film) when immersed in a salt brine solution (and apparently, in distilled water). A big, fat, thick slug immersed in salt brine solution, by contrast, will writhe and begin to dissolve into greenish mucous from the outside ...but depending on how long it is exposed and how massive is the slug, even though the slug dies from having its surface layers dissolved the inner layers --untouched by the salt solution or distilled water-- may still be undisrupted. If the slug's inner tissues have not undergone lysis then they are protective bunkers for sheltering the rat lungworm larvae and so can still pass on infection.
It will, of course, take some experiments to determine whether this idea will work, but I suggest the method for whatever it may be worth. I am in Alaska at the moment, will not be on the Big Island again until 07-14FEB, and do not yet have my own lab set up there or I would test it myself. Nonetheless, people are becoming grievously ill so untested as this suggestion is I make the it for whatever it may be worth (noting that avoiding leafy slug-exposed veggies altogether may be a better course for the time being, and using distilled water as recommended by the public health authorities on the basis of experimental results is of course the way to go if you can afford to do so, but I expect the single-application distilled water soak will become prohibitively expensive very quickly, especially for folks who grow in quantity). As a suggestion then, were it me, this is how I would recommend proceeding:
1) Dissolve as much salt in a 5 gallon bucket of water as will go into solution (heat the water to encourage better saturation). Label this bucket "A."
2) Prep a second 5 gallon bucket of clean (filtered or otherwise sanitized) fresh water. Label this bucket "B."
3) Wearing waterproof gloves inspect veggies for slugs & snails, remove and discard all visible slugs and snails, then immerse leafy veggies potentially exposed to slugs, snails, &/or other potential vectors of
A. cantonensis infection in bucket A, agitate the veggies (to insure the brine reaches all niches and crevices in the veggies), and soak for as long as you deem necessary to kill and lyse the largest slug you can envision escaping your detection inside the veggies. 1mm - 2mm slugs should curl and drop off the veggies the instant the brine hits them, with tissue lysis following swiftly. Larger slugs may be more resistant- you will need to test slugs of various sizes in small samples of the brine solution from your bucket A to see what happens and how long it takes to happen. Wear gloves. If your brine solution is inadequate in strength to knock out and dissolve the slugs, then I would discontinue the effort.
4) If the brine immersion, agitation, and soaking for
N minutes solidly appears to be 100% effective in detaching, killing, and dissolving slugs and other potential vectors, then immerse and agitate the brine-purged veggies in bucket B to remove the bulk of the salt solution and debris from the veggies.
5) In a sink, rinse the veggies thoroughly in clean single-use water to remove remaining traces of salt solution and debris.
6) Inspect carefully before deciding to consume.
This method, if effective, would have the advantage of being affordable and practical since the solutions in buckets A and B (particularly A) are reusable many times. Distilled water will cease to be effective as soon as salts dissolve into it.
Slug tissues are composed of cells with flexible membranes, like delicate balloons, and so are easily disrupted by salt solutions. Plant tissues are composed of cells with relatively tough and rigid walls (which is how trees manage to stay upright); the plant cells will resist lysis for far longer in strong salt solutions than will animal cells. In other words, slug tissues and the rat lungworm larval tissues they contain should have long since been ripped apart by the salt content differences before the veggies start breaking down.
A caveat to this suggestion: snails, as opposed to slugs, are armored in a shell which could afford protection from salt solution attack. If snails clamp down against the leaf surface so tightly as to exclude contact with salt solution (or distilled water, for that matter) then this strategy would be ineffective. Also, some species of snails have a shield (called an operculum) with which they can block the opening of their shell; that is, they can pull vulnerable soft tissues inside, seal off the opening, and wait out an assault. So, do not be fooled into thinking a snail is no longer infective for
A. cantonensis simply because it drops off of a veggie when hit with salt solution (or DW); particularly if equipped with an operculum its tissues may still be infective.
It is easy to think others are foolish to take any risk whatsoever, but try saying that when you have hungry kids to feed and scarce funds. The reality may be that some people need to use the produce from their gardens even if there is some risk involved. Given this reality, any reasonable steps and measures which can be taken to reduce the risks involved may be welcome. Toward this end the above is offered.
Some other suggestions I found interesting and informative may be perused at Cardiff University's website on slug control:
http://www.cf.ac.uk/biosi/staffinfo/wocs2.html
While there are distinct risks and potential problems in attempting to use one species to control another (as witness the mongoose in Hawaii vis a vis rats) and the importation of any live material into Hawaii is subject to prior approval, it is of note in the realm of biological warfare a nematode weapon has been used successfully on slugs:
http://www.nemasysinfo.com/slugs.shtml ...How ironic if one type of nematode, that in Nemasys, proves to be the nemesis of another type of nematode --
Angiostrongloides cantonensis-- by wiping the rat lungworm's slug host out of Puna's gardens. Silver bullets are few and far between, however, so an integrated approach working every possible angle for reducing and eliminating this monstrous malady is a more likely pathway to success.
This has been an awfully long post but then this is an awfully important topic. To add one last note on the comments and discussion, I hope folks do not embark on a jihad against planaria simply because they might carry
A. cantonensis larvae after ingesting slugs and snails. This, imho, would be counterproductive (as, btw, is killing spiders). Planaria and spiders are both natural predators on our common enemies, slugs and mosquitos. I do not know how many slugs and snails a planarian will eat in the course of its life, but the average spider eats around 2,000 (two thousand) insects. Yes, they look alien and can bite people, but every time I encounter a spider in my house I carry it outside and let it go; better one live spider than 2,000 live insects, I figure, especially if hundreds of those insects are mosquitoes carrying dengue fever and suchlike. Same deal with the planaria; they may look creepy to some folks but in the bigger scheme of things they kill disease-carrying & food-destroying slugs and snails and so are our friends. Let's treat them like friends, eh?
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