The recommended organic spray for late blight is copper. The prices for copper are astronomical on account of copper just costs a lot right now. Last year as usual I grew my tomatoes from seeds. Hearing about late blight, I tried an experiment with straw mulch for my big tomatoes, which is one recommended response. I had my cherries in pots. My neighbor bought his tomato plants. When the blight hit, his plants all dropped dead in a period of two days. My straw-mulched plants didn't do too well, since I was not used to using a straw mulch and didn't notice they needed water as often as I would have otherwise. They did get blight eventually, but it didn't matter much, since the lack of water seriously cut into their production. The plants in pots did okay. Eventually, they did get blight, no doubt from my neighbor's plants. The one that lived longest was Matt's Wild Cherry. I decided that this year I would not grow any tomatoes, that I would buy them from areas of the country that aren't getting late blight, because I just had a feeling that the late blight would be back. Sure enough, it is in PA (I'm 15 mi from PA in NY, so it's just a matter of time). A friend of mine who grows a lot of his own food is growing Matt's Wild Cherry for tomatoes this year and foregoing the copper. Good soil? My plants had very good soil. But it's soil, not a force field. When there is that much disease around, it doesn't matter how good the soil is.

Here is an article about RRD/RRV from the Ohio State University BYGLers (Buckeye Yard and Garden onLine) discussed the relatively recent appearance of rose rosette disease (RDD) on Knock Out roses. Roses in this group have been heavily used in landscapes because of their relative adaptability to a wider range of landscape conditions compared to their hybrid-tea cousins. However, in recent years, RDD has become a serious issue in Ohio landscapes, particularly in mass plantings. RDD was first reported in 1941 on multiflora rose Manitoba, Canada, Wyoming, northeastern California, and Nebraska; however, it took many years for scientific sleuthing to reveal the exact cause of the disease and the mechanism for disease transmission. Indeed, until very recently, the pathogen was thought to be a phytoplasma; these are prokaryotic (no nucleus) cells that lack crosswalls. However, phytoplasmas did not "fit" with the discovery that RDD is transmitted by an eriophyid mite, specifically the ROSE LEAF CURL MITE (Phyllocoptes fructiplilus) that inhabits the shoot tips and leaf petal bases of roses. Phytoplasmas inhabit plant phloem and eriophyid mites do not have the phloem-piercing mouthparts of leafhoppers or psyllids; two common vectors of phytoplasma diseases. Research published in 2011 by scientists from the University of Arkansas and Oregon State University showed the true causal agent for RDD to be a new negative-strand RNA virus that has been tagged, ROSE ROSETTE VIRUS (RRV). Readers may recognize the name because "RRV" was used before on the road to discovering the true culprit when it was believed a virus was involved prior to the phytoplasma side-trip. A virus once again "fits" because virus particles are not limited to phloem and may be readily available within a range of plant tissue to hitch-hike on eriophyid mites. Currently, the disease is diagnosed based on observed symptoms since there is no laboratory method to detect the virus; however now that the virus has been identified, diagnostic tests may be developed. The mite alone causes little damage; however, the virus produces a range of symptoms that first become evident in the spring and intensify as the season progresses. Infected plants produce succulent bright red shoots covered in stunted, twisted stems, and leaves. The leaves may also appear red, chlorotic, or a combination of both symptoms and the shoots may be covered by an abnormally high number of thorns. The twisted growth may be mistaken for damage caused by a plant growth-regulator herbicide such as 2, 4-D. The disease is lethal to multiflora rose and it was originally thought that the pathogen was specific to this non-native noxious weed. However, it has become clear in the intervening years that RDD also infects virtually all cultivated roses. Once plants become infected, all parts of the plants are infectious. Pruners used on infected plants can spread the pathogen to non-infected plants. There are no pesticides available that will control the disease, so management focuses on removing the pathogen by removing infected plants. Entire plants, including the roots, should be removed and destroyed; while the pathogen does not survive in the soil, it will survive in roots. If possible, rose growers should focus their attention on eliminating nearby multiflora rose plants since the plants can serve as reservoirs for this disease. Here is a link that might be useful: OSU article about RRD

Some comments about the UFL sites. First, I would agree the information is presented well in a clean-looking, easy-to-read format and I find the illustrations of the trees helpful. The problems that I've had with it though is they would appear to have more than one publication for the same species posted in different locations on the web that often contain contradictory information. Their labeling of invasive potential is another area that I have a problem with. Almost every noxious weed they have a fact sheet for, they say has "little, if any" potential. Furthermore, I have long wondered why and or how they are able to compile this information when a great deal of the species they've written about won't even grow in Florida. Never the less, they will describe availability of certain trees or cultivars but it's unclear as to who that is relevant to. There are some discrepancies that I often find with size, growth rates, shapes and fruiting but do enjoy reading that site just for entertainment value and because the illustrations of a "middle aged __________ " can't be beat.

To all who have wished me a speedy recovery: Thank You! I am feeling steadily better (1 month out), and expect to be back to full strength shortly. @Alisande, If you think you may have babeseosis at the moment, then insist on being tested. Same with anaplasmosis, both are less-difficult than Lyme to diagnose from blood smears, I believe. (The issue with the blood supply, aside from the traditional head-in-the-sand attitude of the blood industry, and of course the cost, is that there is no rapid-enough test for babeseosis -or possibly the other tick-borne diseases -to work with the need for fresh blood.) But as I mentioned, anaplasmosis has distinct, characteristic, changes in routine blood work that are almost diagnostic. I can check next time I am in the medical library if there are specific changes in the case of babeseosis. I may have that info for erlichiosis, if you'd like to know it. Anaplasmosis has distinctive mullberry shaped artifacts (morullae) in the disease-specific blood smears (as does erlichiosis, I believe). Babeseosis is different but unless you, like I, have had malaria it's pretty distinctive in the blood test for it. The tests aren't inexpensive (the unadjusted street price for them is $500-$1,000 -each- but my insurance company whacked both of them down considerably. Since you're on Medicare, you'd only pay a percentage of the CMS-negotiated cost which is likely to be as aggressively moderated as that of my own insurance company's contractual rate. Since all three are bacterial, not spirochete, -caused it doesn't require the complex analysis of PCR bands that Lyme does. But frankly if I was on my second continuous month of Lyme I would have pretty awful constitutional symptoms from that lengthy treatment alone. I can barely make it out the 30 days of a single course before I have disturbed sleep, night sweats, muscle aches and pains, etc. Part of my fierceness about discovering ticks early is to avoid the need for the lengthy course of anti-Lyme doxy. Since doxy won't really do anything for babeseosis - and other drugs will - why keep taking what may be the wrong cure? I don't think you would experience symptoms from babeseosis or anaplasmosis (or even Lyme) infection before locating the tick. The incubation time needed to get sick from a still-attached tick would have resulted in a deer tick as big as a green pea, a nasty pearly-grey tight blob. It's hard to imagine you wouldn't have noticed it well before getting sick if it was still attached. Don't you itch like mad when you have a tick attached for more than a few hours, not to mention days? I'd be wild! BTW, the tick-hours-of-bite measurement has a built in problem: the aging relies on analysis of stomach digestive contents. But that assumes, and it is not always true, that the bite the tick was discovered making is the only bite, not a second one. Also you mentioned you squashed the critter in removing it. You might want to consider beginning more intensive searches for ticks on your body twice a day in order to not miss one. I have hair so long I can sit on it so I do realize it can be hard to check your scalp and hair. I have also found attached ticks under my breasts, in my belly button, on various unmentionable parts of my bottom, and even larval ones between my toes and fingers. I usually keep my long hair tied up in pigtail outdoors. I tuck the pigtail down the back of my shirt to minimize the likelihood of ticks getting caught in my hair. Of course I always have a hat on outside for sun protection, so my head and scalp are less-common tick areas. I do tick-checks at least twice every day of the year, unless I am away from home overnight in the city. It's just like brushing your teeth. I'm not convinced that Lyme "lurks in your body" but given that it is caused by spirochete I suppose it's possible. (Another spirochete-caused illness, syphillis, has a proven habit of lingering on and re-occurring, often despite treatment.) I know, for certain, that I have had Lyme (from clearly positive blood tests), been treated successfuly and subsequently had lengthy periods of profound physiological, and mental stress, without Lyme popping back up and adding to the problems. And I still have one band for Lyme on the latest PCR, which indicates an old, resolved infection, so there's no question it's still visible in my blood, but not thankfully making a pest of itself. I also still have serological evidence of malaria in my blood and I haven't had any illness from it in more than fifty years! But the bacterial diseases (anaplasmosis, babeseosis and erlichiosis) seem extremely unlikely lurkers and later-pouncers, especially if treated. What I definitely think they can do, however, is damage other organs and systems resulting in consequential, long-term problems (like the poor fellow described above who lost his spleen as a result of a babeseosis infection.) Your description of high fevers, muscle aches and pains, etc., sound much more like anaplasmosis than Lyme. Did you have any "regular" blood tests done at the time? The average time from bite to onset of symptoms with anaplasmosis is 8 days. I could look that time up for erlichiosis and babseosis, if needed. I don't know enough about Fibro, but aren't night sweats and aches and pains part of that, too? You may not need to go to any doctor more specialized than your primary care doc to check for the bacterial tick-borne illnesses. And then you'll be able to know, and treat, any that are there. I didn't get any hint that the tests for them lead to confusing, or contradictory results, as I know the Lyme test can, because it is a different, and more complicated test.. If you test negative for them, including having normal routine blood results, you can cross them off your list of worries and look elsewhere. (And get off the wretched doxy!) HTH, L.