Long-distance spread of the disease occurs through the planting of infected trees, as well as budding and grafting of infected tissue. To prevent the establishment of the disease, guidelines typically call for testing of rootstocks and budwood before planting, removal of all trees known and suspected to be infected and eradication of ornamental and wild cherry trees from the surrounding area.

Short-distance spread of the disease occurs through transmission of the viruses by insect vectors. Little cherry virus-2 is spread by scale insects of the family Pseudococcidae, primarily the apple mealybug ("Phenacoccus aceris"). In areas where the apple mealybug is commonplace, application of insecticides prior to cutting infected trees are routinely used to stop the spread of little cherry disease within orchards. Little cherry virus-1 is spread by an unknown vector.

Little cherry disease likely originated in Japan and spread with ornamental cherry trees world-wide; many of the top cherry producing nations in the world have reported infections, including USA, Italy and Spain.

There is no known cure for little cherry disease and tolerance breeding programs have not yielded any cultivars able to withstand the effects of the disease for more than a few seasons. Thus, prevention of spread has been the focal point in combating the disease.

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.

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:

Shot hole disease (also called Coryneum blight) is a serious fungal disease that creates BB-sized holes in leaves, rough areas on fruit, and concentric lesions on branches. The pathogen that causes shot hole disease is "Wilsonomyces carpophilus".

Control of Leucostoma Canker is possible through a combination of pest and crop management techniques following life cycles of the trees. The strategy is implemented following techniques aimed at reducing number of pathogenic inoculum, minimizing dead or injured tissues to prevent infection, and improving tree health to improve rapid wound healing. Chemical controls have not been very effective at controlling this disease with no fungicides registered specifically for control of "Leucostoma" spp., and demethylation-inhibiting (DMI) fungicides having almost no effect on "L. persoonii".

Dead arm, sometimes grape canker, is a disease of grapes caused by a deep-seated wood rot of the arms or trunk of the grapevine. As the disease progresses over several years, one or more arms may die, hence the name "dead arm". Eventually the whole vine will die. In the 1970s, dead-arm was identified as really being two diseases, caused by two different fungi, "Eutypa lata" and "Phomopsis viticola" (syn. "Cryptosporella viticola").

Dead arm is a disease that causes symptoms in the common grapevine species, "vitis vinifera", in many regions of the world. This disease is mainly caused by the fungal pathogen, "Phomopsis viticola", and is known to affect many cultivars of table grapes, such as Thompson Seedless, Red Globe, and Flame Seedless. Early in the growing season, the disease can delay the growth of the plant and cause leaves to turn yellow and curl. Small, brown spots on the shoots and leaf veins are very common first symptoms of this disease. Soil moisture and temperature can impact the severity of symptoms, leading to a systemic infection in warm, wet conditions. As the name of this disease suggests, it also causes one or more arms of the grapevine to die, often leading to death of the entire vine.

"W. carpophilus" can remain viable for several months and spores are often airborne. Since the fungi thrive in wet conditions, overhead watering should be avoided. Remove and dispose of any infected buds, leaves, fruit and twigs. In fall, fixed copper or Bordeaux mixture can be applied.

Leucostoma canker is a fungal disease that can kill stone fruit ("Prunus" spp.). The disease is caused by the plant pathogens "Leucostoma persoonii" and "Leucostoma cinctum" (teleomorph) and "Cytospora leucostoma" and "Cytospora cincta" (anamorphs). The disease can have a variety of signs and symptoms depending on the part of the tree infected. One of the most lethal symptoms of the disease are the Leucostoma cankers. The severity of the Leucostoma cankers is dependent on the part of the plant infected. The fungus infects through injured, dying or dead tissues of the trees. Disease management can consist of cultural management practices such as pruning, late season fertilizers or chemical management through measures such as insect control. Leucostoma canker of stone fruit can cause significant economic losses due to reduced fruit production or disease management practices. It is one of the most important diseases of stone fruit tree all over the world.

Rabbits helped keep vegetation in their environments short through grazing and short grasses are conducive to habitation by the butterfly, "Plebejus argus""." When the population of rabbits experienced a decline due to Myxomatosis, grass lengths increased, limiting the environments in which "P. argus" could live, thereby contributing to the decline of the butterfly population.

The development of resistance to the disease has taken different courses. In Australia, the virus initially killed rabbits very quickly – about 4 days after infection. This gave little time for the infection to spread. However, a less virulent form of the virus then became prevalent there, which spread more effectively by being less lethal. In Europe, many rabbits are genetically resistant to the original virus that was spread. The survival rate of diseased rabbits has now increased to 35%, while in the 1950s it was near zero.

Hares are not affected by myxomatosis, but can act as vectors.

Hay fever was relatively uncommon in Japan until the early 1960s. Shortly after World War II, reforestation policies resulted in large forests of cryptomeria and Japanese cypress trees, which were an important resource for the construction industry. As these trees matured, they started to produce large amounts of pollen. Peak production of pollen occurs in trees of 30 years and older. As the Japanese economy developed in the 1970s and 1980s, cheaper imported building materials decreased the demand for cryptomeria and Japanese cypress materials. This resulted in increasing forest density and aging trees, further contributing to pollen production and thus, hay fever. In 1970, about 50% of cryptomeria were more than 10 years old, and just 25% were more than 20 years old. By 2000, almost 85% of cryptomeria were over 20 years old, and more than 60% of trees were over 30 years old. This cryptomeria aging trend has continued since then, and though cryptomeria forest acreage has hardly increased since 1980, pollen production has continued to increase. Furthermore, urbanization of land in Japan led to increasing coverage of soft soil and grass land by concrete and asphalt. Pollen settling on such hard surfaces can easily be swept up again by winds to recirculate and contribute to hay fever. As a result, approximately 25 million people (about 20% of the population) currently suffer from this type of seasonal hay fever in Japan.

A sizable industry has developed in Japan around services and products that help people deal with hay fever, including protective wear such as coats with smooth surfaces, masks, and glasses; medication and remedies; household goods such as air-conditioner filters and fine window screens; and even "hay fever relief vacations" to low-pollen areas such as Okinawa and Hokkaido. Some people in Japan use medical laser therapy to desensitize the parts of their nose that are sensitive to pollen.

Manganese (Mn) deficiency is a plant disorder that is often confused with, and occurs with, iron deficiency. Most common in poorly drained soils, also where organic matter levels are high. Manganese may be unavailable to plants where pH is high.

Affected plants include onion, apple, peas, French beans, cherry and raspberry, and symptoms include yellowing of leaves with smallest leaf veins remaining green to produce a ‘chequered’ effect. The plant may seem to grow away from the problem so that younger

leaves may appear to be unaffected. Brown spots may appear on leaf surfaces, and severely affected leaves turn brown and wither.

Prevention can be achieved by improving soil structure. Do not over-lime.

Manganese deficiency can be easy to spot in plants because, much like magnesium deficiency, the leaves start to turn yellow and undergo interveinal chlorosis. The difference between these two is that the younger leaves near the top of the plant show symptoms first because manganese is not mobile while in magnesium deficiency show symptoms in older leaves near the bottom of the plant.

Paravaccinia virus originates from livestock infected with bovine papular stomatitis. When a human makes physical contact with the livestock's muzzle, udders, or an infected area, the area of contact will become infected. Livestock may not show symptoms of bovine papular stomatitis and still be infected and contagious. Paravaccinia can enter the body though all pathways including: skin contact by mechanical means, through the respiratory tract, or orally. Oral or respiratory contraction may be more likely to cause systemic symptoms such as lesions across the whole body

A person who has not previously been infected with paravaccinia virus should avoid contact with infected livestock to prevent contraction of disease. There is no commercially available vaccination for cattle or humans against paravaccinia. However, following infection, immunization has been noted in humans, making re-infection difficult. Unlike other pox viruses, there is no record of contracting paravaccinia virus from another human. Further, cattle only show a short immunization after initial infection, providing opportunity to continue to infect more livestock and new human hosts.

Nodding syndrome is debilitating both physically and mentally. In 2004, Peter Spencer stated: "It is, by all reports, a progressive disorder and a fatal disorder, perhaps with a duration of about three years or more." While a few children are said to have recovered from it, many have died from the illness. Seizures can also cause children to collapse, potentially causing injury or death.

"Balamuthia" infection is a cutaneous condition resulting from "Balamuthia" that may result in various skin lesions.

"Balamuthia mandrillarisis" a free-living amoeba (a single-celled living organism) found in the environment. It is one of the causes of granulomatous amoebic encephalitis (GAE), a serious infection of the brain and spinal cord. "Balamuthia" is thought to enter the body when soil containing it comes in contact with skin wounds and cuts, or when dust containing it is breathed in or gets in the mouth. The "Balamuthia" amoebae can then travel to the brain through the blood stream and cause GAE. GAE is a very rare disease that is usually fatal.

Scientists at the Centers for Disease Control and Prevention (CDC) first discovered "Balamuthia mandrillaris" in 1986. The amoeba was found in the brain of a dead mandrill. After extensive research, "B. mandrillaris" was declared a new species in 1993. Since then, more than 200 cases of "Balamuthia" infection have been diagnosed worldwide, with at least 70 cases reported in the United States. Little is known at this time about how a person becomes infected.

It is currently not known what causes the disease, but it is believed to be connected to infestations of the parasitic worm "Onchocerca volvulus", which is prevalent in all outbreak areas, and a possible explanation involves the formation of antibodies against parasite antigen that are cross-reactive to leiomodin-1 in the hippocampus. "O. volvulus", a nematode, is carried by the black fly and causes river blindness. In 2004, most children suffering from nodding disease lived close to the Yei River, a hotbed for river blindness, and 93.7% of nodding disease sufferers were found to harbour the parasite — a far higher percentage than in children without the disease. A link between river blindness and normal cases of epilepsy, as well as retarded growth, had been proposed previously, although the evidence for this link is inconclusive. Of the connection between the worm and the disease, Scott Dowell, the lead investigator into the syndrome for the US Centers for Disease Control and Prevention (CDC), stated: "We know that ["Onchocerca volvulus"] is involved in some way, but it is a little puzzling because [the worm] is fairly common in areas that do not have nodding disease". Andrea Winkler, the first author of a 2008 Tanzanian study, has said of the connection: "We could not establish any hint that "Onchocerca volvulus" is actually going into the brain, but what we cannot exclude is that there is an autoimmune mechanism going on." In the most severely affected region of Uganda, infection with microfilariae in epileptic or nodding children ranged from 70% to 100%.

The CDC is investigating a possible connection with wartime chemical exposure. The team is also investigating whether a deficiency in vitamin B (pyridoxine) could be a cause, noting the seizures of pyridoxine-dependent epilepsy and this common deficiency in disease sufferers. Older theories include a 2002 toxicology report that postulated a connection with tainted monkey meat, as well as the eating of agricultural seeds provided by relief agencies that were covered in toxic chemicals.

Mare reproductive loss syndrome (MRLS) is a syndrome consisting of equine abortions and three related nonreproductive syndromes which occur in horses of all breeds, sexes, and ages. MRLS was first observed in the U.S. state of Kentucky in a three-week period around May 5, 2001, when about 20% to 30% of Kentucky's pregnant mares suffered abortions. A primary infectious cause was rapidly ruled out, and the search began for a candidate toxin. No abortifacient toxins were identified.

In the spring of 2001, Kentucky had experienced an extraordinarily heavy infestation of eastern tent caterpillars (ETCs). An epidemiological study showed ETCs to be associated with MRLS. When ETCs returned to Kentucky in the spring of 2002, equine exposure to caterpillars was immediately shown to produce abortions. Research then focused on how the ETCs produced the abortions. Reviewing the speed with which ETCs produced late-term abortions in 2002 experiments, the nonspecific bacterial infections in the placenta/fetus were assigned a primary driving role. The question then became how exposure to the caterpillars produced these non-specific bacterial infections of the affected placenta/fetus and also the uveitis and pericarditis cases.

Reviewing the barbed nature of ETC hairs (setae), intestinal blood vessel penetration by barbed setal fragments was shown to introduce barbed setal fragments and associated bacterial contaminants into intestinal collecting blood vessels (septic penetrating setae). Distribution of these materials following cardiac output would deliver these materials to all tissues in the body (septic penetrating setal emboli). About 15% of cardiac output goes to the late-term fetus, at which point the septic barbed setal fragments are positioned to penetrate placental tissues which lack an immune response. Bacterial proliferation, therefore, proceeds unchecked and the late-term fetus is rapidly aborted.

Similar events occur with the early-term fetus, but as a much smaller target receiving an equivalently smaller fraction of cardiac output, the early-term fetus is less likely to be "hit" by a randomly distributing setal fragment. Since this MRLS pathogenesis model was first proposed in 2002, other caterpillar-related abortion syndromes have been recognized, most notably equine amnionitis and fetal loss in Australia, and more recently, a long-recognized relationship between pregnant camels eating caterpillars and abortions among the camel pastoralists in the western Sahara.

Mansonelliasis (or mansonellosis) is the condition of infection by the nematode "Mansonella".

The disease exists in Africa and tropical Americas, spread by biting midges or blackflies. It is usually asymptomatic.

Florida keratopathy, also known as Florida spots, is an eye condition characterized by the presence of multiple spots within both corneas. It is most commonly seen in dogs and cats, but is also rarely seen in horses and birds. The disease is found in the southeastern parts of the United States. In other parts of the world it is confined to tropics and subtropics, and it is known as tropical keratopathy.

Florida keratopathy appears as multiple cloudy opacities in the stromal layer of the cornea. The spots appear concentrated at the center and become more diffuse at the periphery. They can range in size from one to eight millimeters. There are no other symptoms, and there is no response to treatment with either anti-inflammatory or antimicrobial drugs. Histological analysis of affected corneas has found acid-fast staining organisms, suggesting Florida keratopathy may be caused by a type of mycobacterium. The disease may be induced by repeated stings to the eyes by the little fire ant, "Wasmannia auropunctata".

Lesions of paravaccinia virus will clear up with little to no scaring after 4 to 8 weeks. An antibiotic may be prescribed by a physician to help prevent bacterial infection of the lesion area. In rare cases, surgical removal of the lesions can be done to help increase rate of healing, and help minimize risk of bacterial or fungal infection. Upon healing, no long term side effects have been reported.

Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.