The first approach, which is the best approach at an effective management practice would be to eradicate or severely damage the Mountain and Cherry Leafhopper population because the leafhoppers are the number one vectors for this pathogen. To do this, pesticides (i.e. acephate, bifenthrin, cyfluthrin) could be applied or biological control (predators of the leafhopper) could be used. There should be a pre-season application of control measures as well as a post-season application. This is to maximize the effort at controlling both types of leafhoppers (Cherry and Mountain), thus cutting down the starting inoculum at both stages in the life cycle.

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

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.

Treatment is symptomatic.

Treatment does not require a doctor's attention unless the case is severe, with most affected using a topical anti-itch cream (diphenhydramine) and a cortisone solution (hydrocortisone). Do not scratch the area, and avoid any clothing that may irritate the affected area; scratching will result in localized swelling and intense itching.

Upon exiting the water, prompt removal of swim clothing (while it is still wet) followed by a warm sea-water shower largely negates the risk of Seabather's eruption even in endemic areas. A hot freshwater shower with soap (paying particular attention to the hair and areas covered by the suit) is a somewhat less-effective alternative if uncontaminated seawater is unavailable. The contaminated swimsuit should be machine washed with laundry soap and dried in warm air.

Animals can be affected as well, and a cortisone solution for humans can be used on dogs.

Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .

Coral diseases, comprising the diseases that affect corals, injure the living tissues and often result in the death of part or the whole of the colony. These diseases have been occurring more frequently in the twenty-first century as conditions become more stressful for many shallow-water corals. The pathogens causing the diseases include bacteria, fungi and protozoa, but it is not always possible to identify the pathogen involved.

The following treatments, while once recommended, are considered of no use or harmful, including tourniquets, incisions, suction, application of cold, and application of electricity. Cases in which these treatments appear to work may be the result of dry bites.

- Application of a tourniquet to the bitten limb is generally not recommended. There is no convincing evidence that it is an effective first-aid tool as ordinarily applied. Tourniquets have been found to be completely ineffective in the treatment of "Crotalus durissus" bites, but some positive results have been seen with properly applied tourniquets for cobra venom in the Philippines. Uninformed tourniquet use is dangerous, since reducing or cutting off circulation can lead to gangrene, which can be fatal. The use of a compression bandage is generally as effective, and much safer.

- Cutting open the bitten area, an action often taken prior to suction, is not recommended since it causes further damage and increases the risk of infection; the subsequent cauterization of the area with fire or silver nitrate (also known as "infernal stone") is also potentially threatening.

- Sucking out venom, either by mouth or with a pump, does not work and may harm the affected area directly. Suction started after three minutes removes a clinically insignificant quantity—less than one-thousandth of the venom injected—as shown in a human study. In a study with pigs, suction not only caused no improvement but led to necrosis in the suctioned area. Suctioning by mouth presents a risk of further poisoning through the mouth's mucous tissues. The well-meaning family member or friend may also release bacteria into the person's wound, leading to infection.

- Immersion in warm water or sour milk, followed by the application of snake-stones (also known as "la Pierre Noire"), which are believed to draw off the poison in much the way a sponge soaks up water.

- Application of a one-percent solution of potassium permanganate or chromic acid to the cut, exposed area. The latter substance is notably toxic and carcinogenic.

- Drinking abundant quantities of alcohol following the cauterization or disinfection of the wound area.

- Use of electroshock therapy in animal tests has shown this treatment to be useless and potentially dangerous.

In extreme cases, in remote areas, all of these misguided attempts at treatment have resulted in injuries far worse than an otherwise mild to moderate snakebite. In worst-case scenarios, thoroughly constricting tourniquets have been applied to bitten limbs, completely shutting off blood flow to the area. By the time the person finally reached appropriate medical facilities their limbs had to be amputated.

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.

Until the advent of antivenom, bites from some species of snake were almost universally fatal. Despite huge advances in emergency therapy, antivenom is often still the only effective treatment for envenomation. The first antivenom was developed in 1895 by French physician Albert Calmette for the treatment of Indian cobra bites. Antivenom is made by injecting a small amount of venom into an animal (usually a horse or sheep) to initiate an immune system response. The resulting antibodies are then harvested from the animal's blood.

Antivenom is injected into the person intravenously, and works by binding to and neutralizing venom enzymes. It cannot undo damage already caused by venom, so antivenom treatment should be sought as soon as possible. Modern antivenoms are usually polyvalent, making them effective against the venom of numerous snake species. Pharmaceutical companies which produce antivenom target their products against the species native to a particular area. Although some people may develop serious adverse reactions to antivenom, such as anaphylaxis, in emergency situations this is usually treatable and hence the benefit outweighs the potential consequences of not using antivenom. Giving adrenaline (epinephrine) to prevent adverse effect to antivenom before they occur might be reasonable where they occur commonly. Antihistamines do not appear to provide any benefit in preventing adverse reactions.

There is no effective treatment or antidote for ciguatera poisoning. The mainstay of treatment is supportive care. There is some evidence that calcium channel blockers like nifedipine and verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hot and cold. Some medications such as amitriptyline may reduce some symptoms, such as fatigue and paresthesia, although benefit does not occur in every case.

Mannitol was once used for poisoning after one study reported symptom reversal. Follow-up studies in animals and case reports in humans also found benefit from mannitol. However, a randomized, double-blind clinical trial found no difference between mannitol and normal saline, and based on this result, mannitol is no longer recommended.

Long term management of chronic Ciguatera includes avoiding trigger food and environmental triggers, and managing symptoms with medications and or lifestyle.

Caution may be needed with anesthesia and should be discussed with your healthcare providers.

Yellow-band disease has severely affected reef building corals in the Caribbean. This disease have been associated with lower coral fecundity, altered tissue composition and a lower activites of antixenobiotic and antioxidant enzymes. Compared to the late 1990s, current data suggests that the disease remains a severe epidemic. In one study, 10 meter belt transects were taken at various depths, sampling coral colonies in the Lesser Antilles. At a depth of 5 m, yellow band rings and lesions were found on 79% of the colonies per transect, and only 21% of the colonies in this depth range appeared healthy.

Recent research indicates that yellow-band disease continues to be in an infectious phases in the Caribbean. It has been

found to cause infection in Pacific coral as well.

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

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.

Black band disease is a coral disease in which corals develop a black band. It is characterized by complete tissue degradation due to a pathogenic microbial consortium. The mat is present between apparently healthy coral tissue and freshly exposed coral skeleton.

Black band disease was first observed on reefs in Belize in 1973 by A. Antonius, who described the pathogen he found infecting corals as "Oscillatoria membranacea", one of the cyanobacteria. The band color may be blackish brown to red depending on the vertical position of a cyanobacterial population associated with the band. The vertical position is based on a light intensity-dependent photic response of the cyanobacterial filaments, and the color (due to the cyanobacterial pigment phycoerythrin) is dependent on the thickness of the band. The band is approximately thick and ranges in width from to White specks may be present on surface, at times forming dense white patches. The pathogenic microbial mat moves across coral colonies at rates from to a day. Tissue death is caused by exposure to an hypoxic, sulfide-rich microenvironment associated with the base of the band.

Initial treatments for minor erythrasma can begin with keeping the area clean and dry and with antibacterial soaps. The next level would be treated with topical fusidic acid, miconazole cream, and antibacterial solution such as clindamycin HCL to eradicate the bacteria. For aggressive types of Erythrasma, oral antibiotics like macrolides(erythromycin or azithromycin)can be prescribed. Below is a figure showing the different types and subtypes of therapies.

There is no current agreement on the most optimal treatment for this disease. There are plenty of limitations on these treatments such as more irritation, possible allergic reactions, and ulcerations. These treatments are suitable for most ages, but for young children it should be monitored very closely. Erythrasma if treated and found early on, is not fatal and the patient will live a full life. In more severe cases, it can be an indicator for another disease such as diabetes.

Various Caribbean folk and ritualistic treatments originated in Cuba and nearby islands. The most common old-time remedy involves bed rest subsequent to a guanabana juice enema. Other folk treatments range from directly porting and bleeding the gastrointestinal tract to "cleansing" the diseased with a dove during a Santería ritual. In Puerto Rico, natives drink a tea made from mangrove buttons, purportedly high in B vitamins, to flush the toxic symptoms from the system. There has never been a funded study of these treatments.

An account of ciguatera poisoning from a linguistics researcher living on Malakula island, Vanuatu, indicates the local treatment: "We had to go with what local people told us: avoid salt and any seafood. Eat sugary foods. And they gave us a tea made from the roots of ferns growing on tree trunks. I don't know if any of that helped, but after a few weeks, the symptoms faded away."

Senescent leaves of "Heliotropium foertherianum" (Boraginaceae), also known as octopus bush, a plant used in many Pacific islands as a traditional medicine to treat ciguatera fish poisoning, contain rosmarinic acid and derivatives, which are known for their antiviral, antibacterial, antioxidant and anti-inflammatory properties. Rosmarinic acid may remove the ciguatoxins from their sites of action, as well as being an anti-inflammatory.

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.

Skeletal eroding band (SEB) is a disease of corals that appears as a black or dark gray band that slowly advances over corals, leaving a spotted region of dead coral in its wake. It is the most common disease of corals in the Indian and Pacific Oceans, and is also found in the Red Sea.

So far one agent has been clearly identified, the ciliate "Halofolliculina corallasia". This makes SEB the first coral disease known to be caused by a protozoan. When "H. corallasia" divides, the daughter cells move to the leading edge of the dark band and produce a protective shell called a lorica. To do this, they drill into the coral's limestone skeleton, killing coral polyps in the process.

A disease with very similar symptoms has been found in the Caribbean Sea, but has been given a different name as it is caused by a different species in the genus "Halofolliculina" and occurs in a different type of environment.

Stony corals and soft corals are subject to disease in the same way as other organisms. This may not have been obvious in the past but is becoming increasingly apparent in the twenty-first century. The ill health is the result of the corals being subjected to increasing amounts of stress as the physical environment in which they live becomes less suited to their needs.

Corals live within a precise range of environmental conditions including water temperature, salinity and water quality. Variations outside the normal range of these parameters may make the corals less able to grow and reproduce successfully. Of themselves these variations may be insufficient to kill the corals, but they make them more susceptible to disease organisms. The main factor that causes stress to the corals is climate change, with an increase in sea temperatures, particularly affecting shallow-water corals in the tropics. One of the consequences of heat stress is that the coral expels its zooxanthellae and becomes bleached. The rise in sea temperature is also expected to increase the frequency and severity of tropical storms; these adversely affect corals through mechanical damage to reefs, through increased wave action, and through the stirring up and re-deposition of sediment. Other stress factors include increased pollution, increased ultraviolet radiation, and a reduction in the aragonite saturation of surface seawater that is connected with ocean acidification. Although stressed corals are more susceptible to coral diseases, it is infectious organisms that actually cause these diseases. Pathogens so far identified include bacteria, fungi and protozoans.

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.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

"Verticillium" wilt begins as a mild, local infection, which over a few years will grow in strength as more virile strains of the fungus develop. If left unchecked the disease will become so widespread that the crop will need to be replaced with resistant varieties, or a new crop will need to be planted altogether.

Control of "Verticilium" can be achieved by planting disease free plants in uncontaminated soil, planting resistant varieties, and refraining from planting susceptible crops in areas that have been used repeatedly for solanaceous crops. Soil fumigation can also be used, but is generally too expensive over large areas.

In tomato plants, the presence of ethylene during the initial stages of infection inhibits disease development, while in later stages of disease development the same hormone will cause greater wilt. Tomato plants are available that have been engineered with resistant genes that will tolerate the fungus while showing significantly lower signs of wilting.

"Verticillium albo-altrum", "Verticilium dahliae" and "V. longisporum" can overwinter as melanized mycelium or microsclerotia within live vegetation or plant debris. As a result, it can be important to clear plant debris to lower the spread of disease. "Verticilium dahliae" and "V. longisporum" are able to survive as microsclerotia in soil for up to 15 years.

Susceptible tomato seedlings inoculated with arbuscular mycorrhizal fungi and "Trichoderma Harzianum" show increased resistance towards "Verticillium" wilt.