The symptoms of little cherry disease in sweet and sour cherries varies greatly depending on cultivar, with respect to both the range and the severity of symptoms; some cultivars show signs of tolerance.

In infected trees of the commercially important cultivar Lambert, the fruit develops normally until about ten days before harvest, when maturation stops. At picking time, the cherries are 1/2–2/3 of the regular size, dull in color, with an angular pointed shape. The sugar and acid levels of the cherries are severely impacted, resulting in tasteless fruits, lacking both sweetness and flavor. Other cultivars show symptoms similar to those in Lambert, but usually less severe and more varied. Typically, dark-fruited cultivars show more severe fruit symptoms than cultivars with red or yellow fruit. The ability to recover is also dependent on cultivar, with some able to return to fruit sizes and coloring comparable to uninfected trees. The taste, however, never recovers.

Some sweet cherry cultivars display foliage symptoms, with the fruit crop less hidden by the canopy, and leaf symptoms, varying from a slight marginal up-curl of the leaves to marked reddening of leaf surfaces. The general vigor of infected trees may be impaired, though this is not always apparent. Diagnosis of the disease can be assisted by RT-PCR assays.

Other "Prunus" species may act as symptomless or tolerant carriers of the disease; especially cultivars of Japanese flowering cherry ("Prunus serrulata") have been implicated as such.

Little cherry disease or LChD, sometimes referred to as little cherry, K & S little cherry or sour cherry decline, is a viral infectious disease that affects cherry trees, most notably sweet cherries ("Prunus avium") and sour cherries ("Prunus cerasus").

Little cherry disease should not be confused with cherry buckskin disease, which is caused by Phytoplasma.

Note that both diseases are among the diseases referred to as cherry decline.

The symptoms of Cherry X disease vary greatly depending on the host. On cherry hosts symptoms can usually first be seen on the fruits, causing them to be smaller in size with a leathery skin. Pale fruit is common at harvest time. It is common for symptoms to first be seen in a single branch. The branch may lose its older leaves, and the leaves tend to be smaller with a bronzed complexion.

The rootstock that the cherry is grafted onto can play a significant role in the disease symptoms seen. Rootstocks of Mahaleb cherry exhibit different symptoms from stocks of Colt, Mazzard, or Stockton Morello. When the scion is grafted onto Mahaleb, symptoms consistent with Phytophthora root rot can be seen. To distinguish between root rot and x-disease the wood under the bark at the graft union should be examined. If it is x-disease the wood at the union will have grooves and pits this causes a browning of the phloem and shows the cells in decline. This rapid decline is caused by the rootstock cells near the graft union dying in large quantities. Foliage begins to turn yellow and the curl upward and inward toward the leaf midrib. Trees infected with Mahaleb rootstock die by late summer or early the following year.

When Cherries are grafted onto Colt, Mazzard, or Stockton Morello rootstocks, there is a different range of symptoms. Affected leaves are smaller than normal and the foliage may be sparse. Dieback of shoot tips is common as the disease progresses. Fruit on branches are smaller, lighter, pointed, low sugar content, poor flavor, and a bitter taste.

Peaches are the next most common economic fruit host of the X-disease. Symptoms can be seen after about two months single branches will begin to show symptoms of their individual leaves. These leaves curl up and inward with irregular yellow to reddish-purple spots. These spots can drop out leaving “shotholes”. Leaves that are affected by the disease will fall prematurely. After 2–3 years the entire tree will show symptoms.

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.

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".

The fungal pathogen "Wilsonomyces carpophilus" affects members of the "Prunus" genera. Almond, apricot, nectarine, peach, prune and cherry trees can be affected. Both edible and ornamental varieties are vulnerable to infection. Shot hole disease produces small (1/10-1/4”) reddish or purplish-brown spots. There may be a light green or yellow ring around these spots. Damaged areas become slightly larger and then dry up and fall away, leaving BB-sized holes in leaves. As the fungus spreads, more leaf tissue is damaged until the leaf falls. Significant infections can reduce the amount of photosynthesis that can occur, weakening the plant, and decreasing fruit production. The fungi can also affect fruit, beginning as small purple spots that develop into gray to white lesions. Gummosis may occur. These lesions leave toughened spots on the skin, and in some cases the fruit may be lost. Infected buds may appear darker than normal. Branches may develop concentric lesions when infected. These lesions may girdle a twig and kill it.

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.

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.

In rabbits of the genus "Sylvilagus" (cottontail rabbits) living in the Americas, myxomatosis causes only localized skin tumors, but the European rabbit ("Oryctolagus cuniculus") is more severely affected. At first, normally the disease is visible by lumps (myxomata) and puffiness around the head and genitals. It may progress to acute conjunctivitis and possibly blindness; however, this also may be the first visible symptom of the disease. The rabbits become listless, lose appetite, and develop a fever. Secondary bacterial infections occur in most cases, which cause pneumonia and purulent inflammation of the lungs. In cases where the rabbit has little or no resistance, death may take place rapidly, often in as little as 48 hours; most cases result in death within 14 days. Often the symptoms like blindness make the infected rabbit more vulnerable to predators.

The hosts for Leucostoma canker include stone fruits such as cultivated peach, plum, prune, cherry ("Prunus spp".), or other wild "Prunus" spp. It can also be found on apple ("Malus domestica"). Stone fruits are referred to as drupe, which are fruits containing a seed encased by a hard endocarp, surrounded by a fleshy outer portion.

Leucostoma canker symptoms differ depending on where on the tree infection takes place. Discoloration occurs in sunken patches on infected twigs. Light and dark concentric circles of narcotic tissue characterize this symptom, occurring near buds killed by cold or on leaf scars. Infections on the nodes are seen 2–4 weeks after bud break. As time passes, darkening occurs within diseased tissues, and eventually, amber gum ooze may seep from infected tissue. Nodal infections are particularly vulnerable in one-year-old shoots that develop within the center of the tree. If fungal growth persists without treatment, scaffold limbs and large branches will likely become invaded within a short time frame. Cankers occurring on branches that are the product of such infections will contain dead twigs or twig stubs at the canker’s center.

The most striking symptom of infection includes cankers located on the main trunk, branch crotches, scaffold limbs, and older branches. A symptom called “flagging” can be found on necrotic scaffold limbs. The cankers are parallel to the long axis of the stem and take on an oval shape. Normally, large-scale production of amber colored gum marks the first external symptom of such cankers. While gum production is the typical plant response to irritation, the gum secretion of Leucostoma occurs in bulk amounts. This gum darkens as time passes, gradually leading to the drying and cracking of bark; thus exposing the blackened tissue below.

As the tree continues to mature in the early growing season, the tree resists additional fungal penetration through the formation of callus rings surrounding the canker. However, the Leucostoma generally reinvades the tissue late in the growing season while the tree switches into dormancy. Due to the alteration of callus production and canker formation, cankers with circular callus rings are usually observed.

Foliar symptoms might develop from branch or twig infections. Symptoms include chlorosis, wilting, and necrosis. Signs include small black structures on dead bark which contain pycnidia.

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.

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.

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.

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".

Paravaccinia virus presents itself with blisters, nodules, or lesions about 4 mm in diameter, typically in the area that has made contact with livestock that is infected with bovine papular stomatitis. Lesions may begin forming as late as three weeks after contact has been made with an infected animal. In rare cases, lesions may be seen systemic. General signs of infection are also common, such as fever and fatigue.

Infected livestock may present with blisters or lesions on their udders or snout. Often, however, infected livestock show little to no symptoms.

Children affected by nodding disease experience a complete and permanent stunting of growth. The growth of the brain is also stunted, leading to mental handicap. The disease is named for the characteristic, pathological nodding seizure, which often begins when the children begin to eat, or sometimes when they feel cold. These seizures are brief and halt after the children stop eating or when they feel warm again. Seizures in nodding disease span a wide range of severity. Neurotoxicologist Peter Spencer, who has investigated the disease, has stated that upon presentation with food, "one or two [children] will start nodding very rapidly in a continuous, pendulous nod. A nearby child may suddenly go into a tonic–clonic seizure, while others will freeze." Severe seizures can cause the child to collapse, leading to further injury. Sub-clinical seizures have been identified in electroencephalograms, and MRI scans have shown brain atrophy and damage to the hippocampus and glia cells.

It has been found that no seizures occur when victims are given an unfamiliar or non-traditional food, such as chocolate.

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.

Nodding disease or nodding syndrome is a recent, little-known disease which emerged in Sudan in the 1960s. It is a mentally and physically disabling disease that only affects children, typically between the ages of 5 and 15. It is currently restricted to small regions in South Sudan, Tanzania, and northern Uganda. Prior to the South Sudan outbreaks and subsequent limited spread, the disease was first described in 1962 existing in secluded mountainous regions of Tanzania, although the connection between that disease and nodding syndrome was only made recently.

Infections by "Mansonella perstans", while often asymptomatic, can be associated with angioedema, pruritus, fever, headaches, arthralgias, and neurologic manifestations. "Mansonella streptocerca" can manifest on the skin via pruritus, papular eruptions and pigmentation changes. "Mansonella ozzardi" can cause symptoms that include arthralgias, headaches, fever, pulmonary symptoms, adenopathy, hepatomegaly, and pruritus. Eosinophilia is often prominent in all cases of Mansonelliasis. "M. perstans" can also present with Calabar-like swellings, hives, and a condition known as Kampala, or Ugandan eye worm. This occurs when adult M. perstans invades the conjunctiva or periorbital connective tissues in the eye. "M. perstans" can also present with hydrocele in South America. However, it is often hard to distinguish between the symptoms of Mansonelliasis and other nematode infections endemic to the same areas.

"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.

Paravaccinia virus is a viral infection of the Parapoxvirus genus of viruses. Human can contract the virus from contact with livestock infected with Bovine papular stomatitis and is common with ranchers, milkers, and veterinarians. Infection will present with fever, fatigue, and lesion on the skin.

A contagious disease is a subset category of transmissible diseases, which are transmitted to other persons, either by physical contact with the person suffering the disease, or by casual contact with their secretions or objects touched by them or airborne route among other routes.

Non-contagious infections, by contrast, usually require a special mode of transmission between persons or hosts. These include need for intermediate vector species (mosquitoes that carry malaria) or by non-casual transfer of bodily fluid (such as transfusions, needle sharing or sexual contact).

The boundary between contagious and non-contagious infectious diseases is not perfectly drawn, as illustrated classically by tuberculosis, which is clearly transmissible from person to person, but was not classically considered a contagious disease. In the present day, most sexually transmitted diseases are considered contagious, but only some of them are subject to medical isolation.

Viliuisk Encephalomyelitis (VE) is a fatal progressive neurological disorder found only in the Sakha (Iakut/Yakut) population of central Siberia. About 15 new cases are reported each year. VE is a very rare disease and little research has been conducted. The causative agents, origin of the disease, and involved candidate genes are currently unknown, but much research has been done in pursuit of the answers.

Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma. In all cases the disease is fatal.

As of 2007, fewer than 500 Yakut individuals have been infected with VE. Viliuisk Encephalomyelitis is classified as a progressive neurological disorder that ultimately ends in the death of the infected individual. The disease has three distinguishable phases: The acute form, the progressive form, and the chronic form.

The acute form is the most rapid and most violent of all the stages. It begins with the characteristic rigidity of the muscles, accompanied by slurred speech, severe headaches, and exaggeration of cold-like symptoms. Patients usually die within weeks of the initial symptoms. Routine post-mortem examinations yield: severe inflammation of the brain lining, clusters of dead cells and tissue, and largely increased amounts of macrophages and lymphocytes.

The progressive form is the most common case. Patients initially experience acute-like symptoms which are not as severe, and subside within a few weeks. Following the sub-acute phase, the patients experience a few mild symptoms including some behavioral changes, incoordination, and difficulty in speech. Eventually the disease developed fully and those infected were stricken with the characteristic symptoms of rigidity, slurred speech, and deterioration of cognitive functions. Ultimately, brain function depreciates rapidly resulting in death.

Many patients who undergo the chronic form claim never to have had an acute attack. These patients endure varying measures of impairment and suffer mental deterioration for the remainder of their lives. Usually they live to be very old and succumb to other diseases.

In almost all cases there are changes characteristic of VE. Early onset shows an increased number of lymphocytes and increased protein concentration — which reduces over many years. These factors help neurologists determine the form of VE based on progression. The trademark changes in the brain include: thickened inflamed meninges, necrotic cortical lesions, increased number of lymphocytes, and neuronal death.