Panama disease is a plant disease of the roots of banana plants. It is a type of Fusarium wilt, caused by the fungal pathogen "Fusarium oxysporum f. sp. cubense" (Foc). The pathogen is resistant to fungicide and cannot be controlled chemically.

During the 1950s, Panama disease wiped out most commercial Gros Michel banana production. The Gros Michel banana was the dominant cultivar of bananas, and the blight inflicted enormous costs and forced producers to switch to other, disease-resistant cultivars. New strains of Panama disease currently threaten the production of today's most popular cultivar, Cavendish.

Cherry X disease also known as Cherry Buckskin disease is caused by a plant pathogenic phytoplasma. Phytoplasma's are obligate parasites of plants and insects. They are specialized bacteria, characterized by their lack of a cell wall, often transmitted through insects, and are responsible for large losses in crops, fruit trees, and ornamentals. The phytoplasma causing Cherry X disease has a fairly limited host range mostly of stone fruit trees. Hosts of the pathogen include sweet/sour cherries, choke cherry, peaches, nectarines, almonds, clover, and dandelion. Most commonly the pathogen is introduced into economical fruit orchards from wild choke cherry and herbaceous weed hosts. The pathogen is vectored by mountain and cherry leafhoppers. The mountain leafhopper vectors the pathogen from wild hosts to cherry orchards but does not feed on the other hosts. The cherry leafhopper which feeds on the infected cherry trees then becomes the next vector that transmits from cherry orchards to peach, nectarine, and other economic crops. Control of Cherry X disease is limited to controlling the spread, vectors, and weed hosts of the pathogen. Once the pathogen has infected a tree it is fatal and removal is necessary to stop it from becoming a reservoir for vectors.

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.

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:

Two external symptoms help characterize Panama disease of banana:

- Yellow leaf syndrome, the yellowing of the border of the leaves which eventually leads to bending of the petiole.

- Green leaf syndrome, which occurs in certain cultivars, marked by the persistence of the green color of the leaves followed by the bending of the petiole as in yellow leaf syndrome. Internally, the disease is characterized by vascular discoloration. This begins in the roots and rhizomes with a yellowing that proceeds to a red or brown color in the pseudostem.

These symptoms often get confused with the symptoms of bacterial wilt of banana, but there are ways to differentiate between the two diseases:

- Fusarium wilt proceeds from older to younger leaves, but bacterial wilt is the opposite.

- Fusarium wilt has no symptoms on the growing buds or suckers, no exudates visible within the plant, and no symptoms in the fruit. Bacterial wilt can be characterized by distorted or necrotic buds, bacterial ooze within the plant, and fruit rot and necrosis.

Once a banana plant is infected, it will continue to grow and any new leaves will be pale in color. Recovery is rare, but if it does occur any new emerging suckers will already be infected and can propagate disease if planted.

"Fusarium oxysporum f. sp. cubense" (Foc) is most prominent in banana and plantain, but some other similar relatives are also susceptible to infection. Different races of the disease are used to classify different major hosts affected by Foc. Race 1 was the initial outbreak which destroyed much of the world's Gros Michel bananas. Cavendish bananas are resistant to race 1, but tropical race 4 (or subtropical race 4) is the classification for Foc which affects Cavendish. Race 2 affects a cooking and dessert banana, Bluggoe.

"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.

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.

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.

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.

Loxoscelism () is a condition occasionally produced by the bite of the recluse spiders (genus "Loxosceles"). The area becomes dusky and a deep open sore forms as the skin around the bite dies (necrosis). It is the only proven type of necrotic arachnidism in humans. While there is no known therapy effective for loxoscelism, there has been research on antibiotics, surgical timing, hyperbaric oxygen, potential antivenoms and vaccines. Because of the number of diseases that may mimic loxoscelism, it is frequently misdiagnosed by physicians.

Loxoscelism was first described in the United States in 1879 in Tennessee. Although there are up to 13 different "Loxosceles" species in North America (11 native and two nonnative), "Loxosceles reclusa" is the species most often involved in serious envenomation. "Loxosceles reclusa" has a limited habitat that includes the Southeast United States. In South America, "L. laeta", "L. intermedia" (found in Brazil and Argentina), and "L. gaucho" (Brazil) are the three species most often reported to cause necrotic bites.

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.

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.

Although Tyzzer’s disease is commonly found in laboratory animals worldwide, infected wild animal populations have been identified in North America and Australia. Specific locations where the disease has been reported in the United States include Connecticut, Idaho, Iowa, Maryland, Michigan, Montana, Ohio, Wisconsin, and Wyoming. In Canada, it has been reported in British Columbia, Manitoba, Ontario, and Saskatchewan. Outbreaks in these locations are primarily attributed to muskrat populations; however infected cottontail rabbits have been discovered in Maryland.

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.

The amphibian chytrid fungus appears to grow best between 17 and 25 °C, and exposure of infected frogs to high temperatures can cure the frogs. In nature, the more time individual frogs were found at temperatures above 25 °C, the less likely they were to be infected by the amphibian chytrid. This may explain why chytridiomycosis-induced amphibian declines have occurred primarily at higher elevations and during cooler months. Naturally produced cutaneous peptides can inhibit the growth of "B. dendrobatidis" when the infected amphibians are around temperatures near 10 °C (50 °F), allowing species like the northern leopard frog ("Rana pipiens") to clear the infection in about 15% of cases.

Although many declines have been credited to the fungus "B. dendrobatidis", some species resist the infection and some populations can survive with a low level of persistence of the disease. In addition, some species that seem to resist the infection may actually harbor a nonpathogenic form of "B. dendrobatidis".

Some researchers contend the focus on chytridiomycosis has made amphibian conservation efforts dangerously myopic. A review of the data in the IUCN Red List found the threat of the disease was assumed in most cases, but no evidence shows, in fact, it is a threat. Conservation efforts in New Zealand continue to be focused on curing the critically endangered native Archey's frog, "Leiopelma archeyi", of chytridiomycosis, though research has shown clearly that they are immune from infection by "B. dendrobatidis" and are dying in the wild of other still-to-be identified diseases. In Guatemala, several thousand tadpoles perished from an unidentified pathogen distinct from "B. dendrobatidis".

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 .

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.

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.

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.

Surra (from the Marathi "sūra", meaning the sound of heavy breathing through nostrils, of imitative origin) is a disease of vertebrate animals. The disease is caused by protozoan trypanosomes, specifically "Trypanosoma evansi", of several species which infect the blood of the vertebrate host, causing fever, weakness, and lethargy which lead to weight loss and anemia. In some animals the disease is fatal unless treated.

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.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

The cause of Grover's disease is unknown. Suspected triggers of disease activity include heat and sweating, sunlight, and adverse reaction to medications as well as ionizing radiation, end-stage renal disease/hemodialysis, and mechanical irritation or prolonged bed rest.

Some cases of Grover's disease have been associated with medications such as sulfadoxine-pyrimethamine, ribavirin, cetuximab, and interleukin-4 [1,8-15]. One series of 300 patients with Grover's disease reported an association with other coexisting dermatoses including atopic dermatitis, contact dermatitis, and xerosis cutis. Finally, smaller series have detailed an association with pyoderma gangrenosum, bacterial and viral infections, and occasionally, malignancies.

No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease.