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There is no resistance to Citrus Black Spot and once a tree has been infected there is no known cure causing tree removal to be the best option. Both Federal and State governments have recommended the following preventative measures.
To control "Guignardia citriparpa" fungicides like copper and/or strobilurins should be applied monthly from early May to the middle of September (in the northern hemisphere). Applications of the fungicides are recommended in early April (northern hemisphere) if that month has experienced more rainfall than usual resulting in the ideal conditions for citrus black spot to form.
Table 1. Recommended Chemical Controls for Citrus Black Spot
1)Lower rates can be used on smaller trees. Do not use less than minimum label rate.
2)Mode of action class for citrus pesticides from the Fungicide Resistance Action Committee (FRAC) 20111. Refer to ENY-624, "Pesticide Resistance and Resistance Management," in the 2012 Florida Citrus Pest Management Guide for more details.
3)Do not use more than 4 applications of strobilurin fungicides/season. Do not make more than 2 sequential applications of strobilurin fungicides.
Another method of control is to accelerate the leaf litter decomposition under the trees in citrus groves. Accelerating this decomposition reduces the chance for ascospore inoculation which generally takes place in the middle of March. There are three possible methods to hasten this decomposition. One method is the increase the mircrosprinkler irrigation in the grove to half an hour for at least five days of the week. This form of control should continue for about a month and a half. The second method is to apply urea or ammonium to the leaf litter. The last and final method to accelerate leaf decomposition is to apply lime or calcium carbonate to the litter. Urea, lime, and calcium carbonate reduce the number of fungal structures and spore production. Since the fungus requires wet conditions to thrive, air flow in the citrus grove should be maximized to reduce leaf wetness.
Along with these methods it is also important to get rid of debris such as fallen fruit or twigs in a manner that reduces the chances of infecting other plants. Citrus Black Spot can colonize and reproduce on dead twigs. To dispose of citrus debris it should either be heated to a minimum of 180℉ for two hours, incinerated, buried in a landfill, or fed to livestock. Plant trash should be moved with caution if at all to avoid spreading the infectious ascospores. Any trees that are infected with citrus black spot should be removed from the grove and disposed of. These trees must be removed because those that are declining and stressed will often have off season bloom. If there is more than one age of fruit present on the tree, it is possible for the asexual spores on the fruit to be transferred to new fruit, intensifying the disease. This off season blooming is often more problematic with Valencia oranges when old and new crops overlap.
"F. oxysporum" is a major wilt pathogen of many economically important crop plants. It is a soil-borne pathogen, which can live in the soil for long periods of time, so rotational cropping is not a useful control method. It can also spread through infected dead plant material, so cleaning up at the end of the season is important.
One control method is to improve soil conditions because "F. oxysporum" spreads faster through soils that have high moisture and bad drainage. Other control methods include planting resistant varieties, removing infected plant tissue to prevent overwintering of the disease, using soil and systemic fungicides to eradicate the disease from the soil, flood fallowing, and using clean seeds each year. Applying fungicides depends on the field environment. It is difficult to find a biological control method because research in a greenhouse can have different effects than testing in the field. The best control method found for "F. oxysporum" is planting resistant varieties, although not all have been bred for every forma specialis.
"F. oxysporum" f. sp. "batatas" can be controlled by using clean seed, cleaning up infected leaf and plant material and breeding for resistance. Fungicides can also be used, but are not as effective as the other two because of field conditions during application. Fungicides can be used effectively by dip treating propagation material.
Different races of "F. oxysporum" f. sp. "cubense", Panama disease on banana, can be susceptible, resistant and partially resistant. It can be controlled by breeding for resistance and through eradication and quarantine of the pathogen by improving soil conditions and using clean plant material. Biological control can work using antagonists. Systemic and soil fungicides can also be used.
The main control method for "F. oxysporum" f. sp. "lycopersici", vascular wilt on tomato, is resistance. Other effective control methods are fumigating the infected soil and raising the soil pH to 6.5-7.
The most effective way to control "F. oxysporum" f. sp. "melonis" is to graft a susceptible variety of melon to a resistant root-stock. Resistant cultivars, liming the soil to change soil pH to 6-7, and reducing soil nitrogen levels also help control "F. oxysporum" f. sp. "melonis".
The fungus "Trichoderma viride" is a proven biocontrol agent to control this disease in an environment friendly way.
Strawberry foliar nematodes are difficult to manage due to their robust life cycle. While dormant, they are quite difficult to kill, and they remain viable in dry debris for more than one year. Adult nematodes can survive desiccation and lie dormant for several years. Eggs can stay dormant until survival conditions are optimal for growth. Once eggs or nematodes are present in the soil, they are nearly impossible to eradicate because they can move laterally in the soil to escape non-optimal conditions. They are found in most foliar tissue, including the leaves, stems, buds, and crowns, making it difficult to control the disease on the plant itself once it has been infected
Many plant diseases are managed chemically, but due to a ban of nematicides there are currently no nematicides available for any type of foliar nematode. Some insecticides, pesticides, and plant product extracts from plants such as Ficus and Coffee (of which many pesticides and nematicides are neem-based ) can be used to reduce the numbers of strawberry foliar nematode (a reduction of 67-85%), but none of these chemicals can completely eradicate the nematodes once they are present in the soil. These chemicals affect all stages of the life cycle because they target the nervous system. One chemical, ZeroTol, a broad-spectrum fungicide and algaecide, was shown be to 100% potent against nematodes living in a water suspension, but the study does not show how nematodes are affected in soil or outside of a laboratory environment.
An alternative method of control is a hot water treatment, which affects all stages of the life cycle and can be used on whole plants. This treatment has been used for 60 years with some effect in greenhouse plants, but not on a widespread agricultural level. The difficulty in this treatment is that exposure times to hot water and the temperature of the water must be optimized so that the nematodes are killed, but the cultivar remains undamaged. One study, which researched five California strawberry cultivars including Chandler, Douglas, Fern, Pajaro, and Selva, demonstrated that the minimum-maximum exposure times and temperatures that killed the nematodes but did not harm the cultivars were: 20–30 minutes at 44.4⁰C, 10–15 minutes at 46.1⁰C, and 8–10 minutes at 47.7⁰. The study also found that fruit production was more sensitive to the treatment than mere survival of the plant, so the minimum exposure times are recommended when using plants for fruit production, and the maximum time is recommended when using plants for propagation.
One of the best and most practiced forms of management to reduce the local and geographical spread of the disease is sanitation. Removing the infected leaves of the plant can reduce spread in the individual plant, but because the nematode is found in most foliar tissue the nematodes may already be present in other tissues before the leaf symptoms appear. The nematodes can also move on the outside of the plant surface when water is present, so the nematodes can move around the outside surface of the plant and infect new tissues. Therefore, once plants show any signs of infection, they should be removed and destroyed. Reducing or eliminating overhead irrigation can prevent dispersal of the nematode through water splashing, and keeping the foliage dry prevents the nematodes from moving on the outside of the plant. Plants should be placed further apart to allow water to dry quickly after irrigation. In the greenhouse or nursery, soils, containers, and tools should be sterilized on a regular basis, and the floor and storage areas should be free from plant debris.
The most important form of management is prevention of introduction of the nematode to the environment. One should avoid planting infected plants, and it is recommended that new plants (especially in a personal lawn or greenhouse) be planted in an isolated area to monitor the plant for the development of symptoms before transplanting the plant near established plants. This will prevent the established plants from getting infected from a new, infected plant. All symptomatic plants should be destroyed immediately. Dead plant material should also be handled with caution. Vermiform nematodes can survive and reproduce in compost piles of dead plant material by feeding on fungi that are commonly found in compost. As a result, infected plants should be burned and sterilized to prevent the nematodes from infecting soil (which results directly from burying the material), or other plants (from allowing the plant to remain rooted in the soil near other plants as it dies).
The bacteria can survive in the rhizosphere of other crops such as tomato, carrots, sweet potato, radish, and squash as well as weed plants like lupin and pigweed, so it is very hard to get rid of it completely. When it is known that the bacterium is present in the soil, planting resistant varieties can be the best defense against the disease. Many available beet cultivars are resistant to "Pectobacterium carotovorum" subsp. "betavasculorum", and some examples are provided in the corresponding table. A comprehensive list is maintained by the USDA on the Germplasm Resources Information Network.
Even though some genes associated with root defense response have been identified, the specific mechanism of resistance is unknown, and it is currently being researched.
Fungicidal agents such as azadirachtin and phytoallexin have been used against some muscardine pathogens. Silkworm breeders dust their cages with slaked lime to discourage fungal growth. In India a dust of chaff soaked in formalin is applied to the larvae.
Some bacteriophages, viruses that infect bacteria, have been used as effective controls of bacterial diseases in laboratory experiments. This relatively new technology is a promising control method that is currently being researched. Bacteriophages are extremely host-specific, which makes them environmentally sound as they will not destroy other, beneficial soil microorganisms. Some bacteriophages identified as effective controls of "Pectobacterium carotovorum" subsp. "betavasculorum" are the strains ΦEcc2 ΦEcc3 ΦEcc9 ΦEcc14. When mixed with a fertilizer and applied to inoculated calla lily bulbs in a greenhouse, they reduced diseased tissue by 40 to 70%. ΦEcc3 appeared to be the most effective, reducing the percent of diseased plants from 30 to 5% in one trial, to 50 to 15% in a second trial. They have also been used successfully to reduce rotting in lettuce caused by "Pectobacterium carotovorum" subsp. "carotovorum", a different bacterial species closely related to the one that causes beet vascular necrosis.
While it is more difficult to apply bacteriophages in a field setting, it is not impossible, and laboratory and greenhouse trials are showing bacteriophages to potentially be a very effective control mechanism. However, there are a few obstacles to surmount before field trials can begin. A large problem is that they are damaged by UV light, so applying the phage mixture during the evening will help promote its viability. Also, providing the phages with susceptible non-pathogenic bacteria to replicate with can ensure there is adequate persistence until the bacteriophages can spread to the targeted bacteria. The bacteriophages are unable to kill all the bacteria, because they need a dense population of bacteria in order to effectively infect and spread, so while the phages were able to decrease the number of diseased plants by up to 35%, around 2,000 Colony Forming Units per milliliter (an estimate of living bacteria cells) were able to survive the treatment. Lastly, the use of these bacteriophages places strong selection on the host bacteria, which causes a high probability of developing resistance to the attacking bacteriophage. Thus it is recommended that multiple strains of the bacteriophage be used in each application so the bacteria do not have a chance to develop resistance to any one strain.
Sodium chloride is believed to mitigate the reproduction of Velvet, however this treatment is not itself sufficient for the complete eradication of an outbreak. Additional, common medications added directly to the fish's environment include copper sulfate, methylene blue, formalin, malachite green and acriflavin, all of which can be found in common fish medications designed specifically to combat this disease. Additionally, because Velvet parasites derive a portion of their energy from photosynthesis, leaving a tank in total darkness for seven days provides a helpful supplement to chemical curatives. Finally, some enthusiasts recommend raising the water temperature of an infected fish's environment, in order to quicken the life cycle (and subsequent death) of Velvet parasites; however this tactic is not practical for all fish, and may induce immunocompromising stress.
Leaf rust is a fungal disease of barley caused by "Puccinia hordei". It is also known as brown rust and it is the most important rust disease on barley.
Pustules of leaf rust are small and circular, producing a mass of orange-brown powdery spores. They appear on the leaf sheaths and predominantly on the upper leaf surfaces. Heavily infected leaves die prematurely.
Citrus Black Spot is a fungal disease caused by Guignardia citricarpa. This Ascomycete fungus affects citrus plants throughout subtropical climates, causing a reduction in both fruit quantity and quality. Symptoms include both fruit and leaf lesions, the latter being critical to inter-tree dispersal. Strict regulation and management is necessary to control this disease since there are currently no citrus varieties that are resistant.
Fusarium wilt is a common vascular wilt fungal disease, exhibiting symptoms similar to Verticillium wilt. The pathogen that causes Fusarium wilt is "Fusarium oxysporum" ("F. oxysporum"). The species is further divided into forma specialis based on host plant.
Strawberry foliar nematode is a disease common in strawberries and ornamental plants that can greatly affect plant yield and appearance, resulting in a loss of millions of dollars of revenue. Symptoms used to diagnose the disease are angular, water soaked lesions and necrotic blotches. "Aphelenchoides fragariae" is the nematode pathogen that causes the disease. Its biological cycle includes four life stages, three of which are juvenile. The nematode can undergo multiple life cycles in one growing season when favorable conditions are present. They can infect the crowns, runners, foliage, and new buds of the plant via stylet penetration or through the stomata. The best management practices for this disease are sanitation, prevention of induction of the pathogen to the environment, and planting clean seed or starter plants.
Wheat yellow rust ("Puccinia striiformis" f.sp. "tritici"), also known as stripe rust, is one of the three wheat rust diseases principally found in wheat grown in cooler environments. Such locations are generally associated with northern latitudes or cooler seasons.
As R.P. Singh, J. Huerta-Espino, and A.P. Roelfs say in their (undated) comprehensive review of literature on the wheat rusts for UN FAO:
"Although Gadd first described stripe rust of wheat in 1777, it was not until 1896 that Eriksson and Henning (1896) showed that stripe rust resulted from a separate pathogen, which they named P. glumarum. In 1953, Hylander et al. (1953) revived the name P. striiformis."
Yellow red muscardine is caused by "Paecilomyces fumosoroseus". It can produce reddish patches on the external body and powdery masses of spores internally.
White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.
Initially, infected fish are known to "flash", or sporadically dart from one end of an aquarium to another, scratching against objects in order to relieve their discomfort. They will also "clamp" their fins very close to their body, and exhibit lethargy. If untreated, a 'dusting' of particles (which are in fact the parasites) will be seen all over the infected fish, ranging in color from brown to gold to green. In the most advanced stages, fish will have difficulty respiring, will often refuse food, and will eventually die of hypoxia due to necrosis of their gill tissue.
White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.
There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.
There is no cure for Schamberg's disease; however, the itching can be controlled by a cortisone cream, and Colchicine treatment has been successfully used to prevent recurrence of the symptoms. This condition is not life-threatening or a major health concern. The only problem that patients will encounter is the itching and discoloration of the skin. It is recommended that patients take a vitamin C supplement to promote collagen production, which will help make the skin look and feel healthier. To prevent further irritation of the lesions, patients should avoid food with artificial colors and preservatives. Some people can be allergic to preservatives, which can cause the body to initiate an allergic reaction by further irritating those lesions. Several research studies have indicated that Schamberg's disease can be controlled and the number of lesions can be reduced with use a drug called aminaphtone. This drug helps improve capillary fragility and it prevents and controls the purpuric lesions.
A patient with Schamberg's disease can live a normal and healthy life. Since there is no proven cure for this condition, the patient will have to endure the lesions on his or her skin. With appropriate treatments, the condition may get better. Although the skin lesions are not life-threatening, it may cause a cosmetic concern for some individuals. Skin lesions may cause psychological discomfort, where patients may require reassurance to help with stress and anxiety. There are a few rare cases of T-cell lymphoma that has developed from Schamberg's disease.This is not a cause for concern, since the risk factors associated with Schamberg's disease are relatively low.
Different therapeutic modalities have been attempted to repigment the lesions of nevus depigmentosus such as PUVA, excimer laser, and different grafting techniques. PUVA therapy has not been shown to be beneficial. Successful repigmentation was reported in a single case with 14 sessions of excimer laser treatment. Though the repigmentation of nevus depigmentosus is possible by grafting techniques, the results are inconsistent and recurrence is possible. In consideration of the experience of other authors and us, the quality and retention of pigment are unpredictable. These factors need to be considered while consulting and offering any treatment to the patient of nevus depigmentosus.
"Narrowband UVB therapy as an effective treatment for Schamberg's disease."
This research article proposed that narrowband UVB therapy can be considered as a treatment for pigmented purpura. A study was done on a 33 year old man who had a 3 month history of widespread pigmented purpura. Oral prescription of prednisolone and topical ointment helped controlled the purpuric eruptions, but when the medication was stopped, the rash recurred. Researchers placed the patient on a UV therapy for 5 months. The patient showed signs of improvement, where new purpuric eruptions stopped and some of the pigmented purpura disappeared. However, when the dose of the UV therapy was decreased, the patient showed signs of recurrence. Researchers want to monitor the patient for two years to see if the purpuric eruptions will stop and they believe that this patient will have promising results.
"Successful treatment of generalized childhood Schamberg's disease with narrowband ultraviolet B therapy."
This research article demonstrated two cases where two children had purpuric rashes. The children were placed on UVB therapy and were monitored weekly for purpuric eruptions. One of the child received 10 treatments of UVB therapy, while the other child received 20 treatments. The child that received the 20 treatments did not show signs of purpuric eruptions and the skin lesions disappeared. However, the child that received the 10 treatments, showed signs of recurrence. Most of the rash disappeared, but some of it reappeared on the body. Researchers believe that the narrowband UVB therapy used on children has proven to remove and control the skin lesions.
White plague is a suite of coral diseases of which three types have been identified, initially in the Florida Keys. They are infectious diseases but it has proved difficult to identify the pathogens involved. White plague type II may be caused by the gram negative bacterium "Aurantimonas coralicida" in the order Rhizobiales but other bacteria have also been associated with diseased corals and viruses may also be implicated.
In 1977, a disease of scleractinian corals appeared on reefs off the Florida Keys in the United States and was termed white plague. It caused white lesions and was shown to be an infectious disease, being particularly prevalent in "Mycetophyllia ferox". This disease caused little mortality and occurred sporadically, but was still present in the area in 1984. It is now known as white plague type 1.
In 1995, a new coral disease was described as an epizootic disease in the same reefs in the Florida Keys. Many species of coral found in the area were affected and the mortality rate of these was up to 38%. The pathogen involved was found to be a previously unknown species of bacterium in the order Rhizobiales, which was placed in the newly created genus "Aurantimonas" and given the name "Aurantimonas coralicida", and the disease was described as white plague type 2. The pathogen was isolated from a diseased colony of "Dichocoenia stokesi" and cultured in the laboratory, subsequently being used to inoculate two healthy colonies which then developed the disease. In the next few months, it had spread over of reef and was killing seventeen species of coral. Over the next four years, it spread further, but interestingly, was most severe in different regions each year.
However, white plague is an enigmatic disease. Further research cast into doubt the role of "A. coralicida" as a causative agent by finding that bacterium on healthy parts of colonies of "Orbicella annularis" affected by white plague disease but absent from diseased parts. In these diseased colonies, an α-proteobacterium similar to one which causes a disease in juvenile oysters has been implicated, being found on the diseased parts of the coral but not on the sound tissues. These anomalous findings may be caused by the fact that there are two or more diseases with similar symptoms, both known as white plague.
In 1999, a third and still more virulent variant appeared in the northern Florida Keys. White plague type III mostly affected "Colpophyllia natans" and "Orbicella annularis".
A white-plague like disease reported from the Red Sea in 2005 has been shown to be caused by a different bacterial pathogen, "Thalassomonas loyana". Further research has shown that viruses may be involved in white plague infections, the coral small circular ssDNA viruses (SCSDVs) being present in association with diseased tissue. This group of viruses is known to cause disease in plants and animals.
A related condition, bisphosphonate-associated osteonecrosis of the jaw (BON), has been described as a side-effect of amino-bisphosphonates, a class of phosphorus-based drugs that inhibit bone resorption and are used widely for treating osteoporosis, bone disease in cancer and some other conditions.
BON, sometimes called "bis-phossy jaw",
is primarily associated with the use of intravenous bisphosphonates in the treatment of cancer. The percentage incidence of BON from this use is approximately 1000 times higher than the incidence of BON caused by the use of oral bisphosphonates.
Leukoedema is a harmless condition, and no treatment is indicated. People may be alarmed by the appearance and benefit from reassurance.