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).

Leaf rust of barley is considered a relatively minor disease in the United States. However, sporadic outbreaks have occurred in the southeastern and Midwestern regions of the country.

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.

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.

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."

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.

Beet vascular necrosis and rot is a soft rot disease caused by the bacterium Pectobacterium carotovorum" subsp. "betavasculorum, which has also been known as "Pectobacterium betavasculorum" and "Erwinia carotovora" subsp. "betavasculorum". It was classified in the genus "Erwinia" until genetic evidence suggested that it belongs to its own group; however, the name Erwinia is still in use. As such, the disease is sometimes called Erwinia rot today. It is a very destructive disease that has been reported across the United States as well as in Egypt. Symptoms include wilting and black streaks on the leaves and petioles. It is usually not fatal to the plant, but in severe cases the beets will become hollowed and unmarketable. The bacteria is a generalist species which rots beets and other plants by secreting digestive enzymes that break down the cell wall and parenchyma tissues. The bacteria thrive in warm and wet conditions, but cannot survive long in fallow soil. However, it is able to persist for long periods of time in the rhizosphere of weeds and non-host crops. While it is difficult to eradicate, there are cultural practices that can be used to control the spread of the disease, such as avoiding injury to the plants and reducing or eliminating application of nitrogen fertilizer.

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.

Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.

While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.

There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.

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.

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 single-celled parasite's life cycle can be divided into three major phases. First, as a tomont, the parasite rests at the water's floor and divides into as many as 256 tomites. Second, these juvenile, motile tomites swim about in search of a fish host, meanwhile using photosynthesis to grow, and to fuel their search. Finally, the adolescent tomite finds and enters the slime coat of a host fish, dissolving and consuming the host's cells, and needing only three days to reach full maturity before detaching to become a tomont once more.

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 doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function. Improvements have also been reported from treating malnutrition associated with zinc deficiency and other minerals. Intracellular (red blood cell) assays are more sensitive than tests for plasma levels.

Schamberg's disease can only be properly diagnosed by a healthcare provider. While reviewing medical history is important to diagnose this condition, it is essential that the purpuric lesions are physically examined. A skin biopsy will be taken to determine capillaritis of dermal vessels. Capillaritis or pigmented purpura is skin condition that has brown-reddish patches on the skin, which is caused by leaky capillaries. The skin biopsy is sent to a laboratory for a pathological examination, where the biopsy is observed under a microscope. In addition to the skin biopsy, dermatologists will perform a dermatoscopy. With the results from the biopsy and from the dermatoscopy, a doctor will be able to identify that the skin lesions are in fact due Schamberg's disease. To ensure that the skin lesions are not caused by other skin conditions or infections, doctors will order a complete blood count (CBC) and other blood tests. Blood tests are usually normal and they are only performed to rule out other bleeding disorders that cause purpura. Since Schamberg's disease is usually asymptomatic, there is not a lot of other tests that can be performed. This condition is easy to diagnose because the appearance of skin lesions on the skin is the first indicator that the lesions are due to Schamberg's disease.

Schamberg's disease is caused by leaky blood vessels near the surface of the skin, capillaries, which allow red blood cells to slip through into the skin. The red blood cells in the skin then fall apart and release their iron, which is released from hemoglobin. The iron causes a rust color and this accounts for the orange tint of the rash that can be seen on the skin. The underlying cause of the leaky blood vessels is not known, but researchers are suggesting that there could be some potential triggers. Some possible triggers include viral infection, a hypersensitivity to some agent, and interaction of some medications, such as thiamine and aspirin. Even though there is no correlation with genetics, there have been a few cases where few people in a family had this condition.

Although the cause of capillary inflammation is unknown, certain preventive measures can be taken. Doctors may prescribe medications that enhance the circulation of blood, which can keep blood vessels strong and healthy. Daily intake of vitamin C has proven to be a natural home remedy that can prevent the onsite of any disease or infection. Doctors always recommend that their patients monitor what they eat because their diet could be a possible factor that contributes to this condition. A healthy body that receives nutritious meals is more likely to have a healthy life that does not revolve around a lot of health problems.

Feather duster budgerigars ("Melopsittacus undulatus"), sometimes called budgerigar mops, are budgerigars that have a condition characterised by overly long feathers that do not stop growing at usual periods, giving the bird the appearance of a feather duster. This condition is sometimes known as chrysanthemum feathering. The contour, tail and flight feathers do not stop growing, and they do not have the necessary barbs and barbules for the feather's structure to interlock. The shaft (calamus) is also curved, and so the feathers appear deformed and fluffed out. Individuals with this condition often appear less alert than nest mates. In addition, they are small and some have other defects such as microphthalmia. They lack vigour, often cannot fly and die within a year of hatching. There is no treatment for the condition; birds are often euthanized in the nest.

The condition may be a genetic disorder, caused by a herpesvirus, or perhaps caused by both.

Mees' lines or Aldrich–Mees' lines, also called leukonychia striata, are white lines of discoloration across the nails of the fingers and toes (leukonychia).