Some herbaceous hosts naturally have the Cherry X Disease. Once the spreads to the cherry hosts, with the help of the mountain leafhoppers, the cherry leafhoppers can spread the disease around to other woody hosts. Here are some approaches at management with each host type:

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.

"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.

Currently, fungicides and other chemical and biological control agents have proven fairly unsuccessful, or only successful in vitro or in greenhouses, in the face of Panama disease of bananas. The most commonly used practices include mostly sanitation and quarantine practices to prevent the spread of Panama disease out of infected fields. However, the most effective tool against Panama disease is the development of banana trees resistant to "Fusarium oxysporum f. sp. Cubense". Unfortunately, the clonal reproduction of banana has led to a consequential lack of other varieties. Efforts are being made to produce resistant varieties, but with bananas being triploids which do not produce seeds, this is not an easy task. Creating clones from tissue cultures, rather than suckers, has proven somewhat successful in breeding resistant varieties, however these tend to have decreased success in stress-tolerance, yield, or other beneficial traits necessary for commercial varieties. Nevertheless, these efforts are leading to the best control measure for Panama disease of banana.

Recently, an R gene (RGA2) was transformed into Cavendish bananas which confers disease resistance to Fusarium wilt tropical race 4. This is the first case of successful resistance in the field and is a promising step towards preventing the loss of the Cavendish cultivars that are a huge portion of banana export production and subsistence of many communities.

In Queensland, a farm in Tully, 1500 km north of Brisbane, was quarantined and some plants were destroyed after TR4 was detected on March 3, 2015. After an initial shutdown of the infected farm, truckloads of fruit left in April with harvesting allowed to resume under strict biosecurity arrangements. The government says it is not feasible to eradicate the fungus. Researchers like Wageningen’s Kema say the disease will continue to spread, despite efforts to contain it, as long as susceptible varieties are being grown. The disease was again detected in Tully in July 2017, prompting Biosecurity Queensland to impose quarantine conditions.

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.

Lethal yellowing (LY) is a phytoplasma disease that attacks many species of palms, including some commercially important species such as the coconut and date palm. In the Caribbean it is spread by the planthopper "Haplaxius crudus" (former name "Myndus crudus") which is native to Florida, parts of the Caribbean and Central America. The only effective cure is prevention, i.e. planting resistant varieties of coconut palm and preventing a park or 'golf course like' environments which attracts the planthopper. Some cultivars, such as the Jamaica Tall coconut cultivar, nearly died out by lethal yellowing. Heavy turf grasses and similar green ground cover will attract the planthopper to lay its eggs and the nymphs develop at the roots of these grasses. The planthoppers' eggs and nymphs may pose a great threat to coconut growing countries' economies, into which grass seeds for golf courses and lawns are imported from the Americas.

It is not clearly understood how the disease was spread to East Africa as the planthopper "Haplaxius crudus" is not native in East Africa.

The only explanation is that it was imported with grass seed from Florida that was used to create golf courses and lawns in beach resorts. There is a direct connection between green lawns and the spread of lethal yellowing in Florida. Even so-called 'resistant cultivars' such as the Malayan Dwarf or the Maypan hybrid between that dwarf and the Panama Tall were never claimed to have a 100% immunity. The nymphs of the planthoppers develop on roots of grasses, hence the areas of grass in the vicinity of palm trees is connected with the spread of this phytoplasma disease. The problem arose as a direct result of using coconut and date palms for ornamental and landscaping purposes in lawns, golf courses and gardens together with these grasses. When these two important food palms were grown in traditional ways (without grasses) in plantations and along the shores, the palm groves were not noticeably affected by lethal yellowing. There is no evidence that disease can be spread when instruments used to cut an infected palm are then used to cut or trim a healthy one. Seed transmission has never been demonstrated, although the phytoplasma can be found in coconut seednuts, but phytosanitary quarantine procedures that prevent movement of coconut seed, seedlings and mature palms out of an LY epidemic area should be applied to grasses and other plants that may be carrying infected vectors.

Beside coconut palm ("Cocus nucifera"), more than 30 palm species have also been reported as susceptible to lethal phytoplasmas around the globe.

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.

Anti-venoms are commercially prepared antibodies to toxins in animal bites. They are specific for each bite. There are several anti-venoms commercially available in Brazil, which have been shown to be effective in controlling the spread of necrosis in rabbits. When administered immediately, they can almost entirely neutralize any ill effects. If too much time is allowed to pass, the treatment becomes ineffective. Most victims do not seek medical attention within the first twelve hours of being bitten, and these anti-venoms are largely ineffective after this point. Because of this, anti-venoms are not being developed more widely. They have, however, been proven to be very effective if administered in a timely manner and could be utilized in Brazil as a legitimate technique.

In cases where a large dermonecrotic lesion has developed, sometimes surgery is attempted to remove the dead tissue. This is not ideal, since it will usually leave a large open sore behind, but in certain cases, still occurs. Skin graft to cover the ulcer are rarely needed but may help with appearance.

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.

The hypothesis that pesticide use has contributed to declining amphibian populations has been suggested several times in the literature. Interactions between pesticides and chytridiomycosis were examined in 2007, and sublethal exposure to the pesticide carbaryl (a cholinesterase inhibitor) was shown to increase susceptibility of foothill yellow-legged frogs ("Rana boylii") to chytridiomycosis. In particular, the skin peptide defenses were significantly reduced after exposure to carbaryl, suggesting pesticides may inhibit this innate immune defence, and increase susceptibility to disease.

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.

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.

The use of antifungals and heat-induced therapy has been suggested as a treatment of "B. dendrobatidis." " "However, some of these antifungals may cause adverse skin effects on certain species of frogs. And although we do use them to treat species that are infected by chytridiomycosis, the infection never fully eradicates. A study done by Rollins-Smith and colleagues suggests that itraconazole is the antifungal of choice when it comes to treatment of "Bd." This is favored in comparison to amphotericin B and chloramphenicol because of their toxicity, specifically chloramphenicol as it is correlated with leukemia in toads. This becomes a difficult situation because without treatment, frogs will suffer from limb deformities and even death, but may also suffer skin abnormalities with treatment. Treatment of chytridiomycosis isn’t always successful, and some frogs are not able to handle the treatment process. It is important to consult with a veterinarian before treating frogs that suffer from chytridiomycosis"."

Individuals infected with "B. dendrobatidis" are bathed in intraconazole solutions, and within a few weeks, previously infected individuals test negative for "B. dendrobatidis" using PCR assays. Heat therapy is also used to neutralize "B. dendrobatidis" in infected individuals. Temperature-controlled laboratory experiments are used to increase the temperature of an individual past the optimal temperature range of "B. dendrobatidis". Experiments, where the temperature is increased beyond the upper bound of the "B. dendrobatidis" optimal range of 25 to 30 °C, show its presence will dissipate within a few weeks and individuals infected return to normal. Formalin/malachite green has also been used to successfully treat individuals infected with chytridiomycosis. An Archey's frog was successfully cured of chytridiomycosis by applying chloramphenicol topically. However, the potential risks of using antifungal drugs on individuals are high.

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 .

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

The reservoirs of the disease are carrier chickens which could be health but harboring the disease or chronically sick chickens. The disease affects all ages of chickens. The disease can persist in the flock for 2-3 weeks and signs of the disease are seen between 1–3 days post infection. Transmission of the disease is through direct interaction, airborne droplets and drinking contaminated water. Chicken having infection and those carriers contribute highly to the disease transmission

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

The main methods of controlling surra has been chemotherapy, and chemoprophylaxis in animals.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Pacheco's disease is an eponymously named disease; it is named after the Brazilian veterinarian, Genesio Pacheco, who first came across the disease in 1929, in an outbreak affecting the turquoise-fronted amazon parrot, "Amazona aestiva". Initially, Pacheco's disease was thought to be a manifestation of avian psittacosis. The causative agent of the disease, a herpesvirus, was not identified until 1975.

An acute form of the disease, which is generally fatal unless treated, occurs in horses, donkeys, mules, cattle, buffalo, deer, camels, llamas, dogs, and cats. This form is caused by "Trypanosoma evansi" (Steel 1885) (Balbiani 1888), and is transmitted by horse-flies, and also by the vampire bat, "Desmodus rotundus", in South-America. This form occurs in South America, Northern Africa, and the Middle East. This was the first form of pathogenic trypanosome discovered and was first described by Griffith Evans in 1880 while he was working in India.

A chronic form of the disease, which is milder but persistent, occurs in pigs, sheep, and goats. This form is caused by "Trypanosoma suis" and is transmitted by tsetse. This form occurs in Africa.

Surra is also known from other countries; an unspecified form is locally common in Mindanao, in the Philippines.

Sweating causes lesions to form, but lesions aggravated by sweat usually return to "normal" fairly quicklyavoiding sweat is not a reason to avoid exercise. Minor outbreaks can be controlled with prescription strength topical cortisone creams. More severe eruptions usually clear up after treatment for one to three months with Accutane or tetracycline. If these fail or the outbreak is severe, PUVA phototherapy treatments, antifungal pills and cortisone injections are alternatives.

Some research has suggested a correlation of Grover's disease with mercury toxicity in which case Dimercaptosuccinic acid might help.

Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs.