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.

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.

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").

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.

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.

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.

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.

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.

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.

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.

MRLS was initially characterized by four syndromes: (1) EFLs, (2) LFLs and the nonreproductive syndromes, (3) unilateral uveitis, (4) pericarditis, and later (5) "Actinobacillus" encephalitis. MRLS was observed in mares of all breeds and ages. Early and late fetal losses were observed within the first and last trimesters of pregnancy, respectively. For EFLs, clinical signs from the sick mares included pus-like discharge from the vulva and fetal membranes protruding from the vulva, as the fetuses were located in either the vagina or vulva. One to three days prior to the EFLs, several mares showed mild colic symptoms, abdominal straining, or low-grade fever. Within a week of abortion, inspections indicated moderate to severe inflammation within the uterine region. Performing ultrasounds revealed either dead fetuses or live fetuses with slow heart rates and lethargic movements. All the fetuses, both alive and dead, were surrounded by cloudy amniotic fluid.

Clinical signs for LFLs included explosive parturition, dystocia, foaling while standing, premature placenta separation, and foals either stillborn or born weak. Placentas were observed to carry a pale brown hue as opposed to their usual dark reddish-brown color. The umbilical cords were thick, dull, yellowish, and inflamed. The weak foals were often incapable of breathing on their own and required resuscitation. These foals were also observed to be dehydrated and hypothermic, with irregular heartbeat and respiration. The majority of these foals did not survive past four days.

One finding observed exclusively in MRLS was unilateral uveitis; initially, affected horses expressed inflammation around a single eye, along with fluid accumulation on the corneas, anterior and posterior chambers due to the inflammation. The fluid in the anterior chambers exhibited tan to yellow hues, and often was accompanied by hemorrhaging around the surface of the iris.

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.

Classically, patients with chronic granulomatous disease will suffer from recurrent bouts of infection due to the decreased capacity of their immune system to fight off disease-causing organisms. The recurrent infections they acquire are specific and are, in decreasing order of frequency:

- pneumonia

- abscesses of the skin, tissues, and organs

- suppurative arthritis

- osteomyelitis

- bacteremia/fungemia

- superficial skin infections such as cellulitis or impetigo

Most people with CGD are diagnosed in childhood, usually before age 5. Early diagnosis is important since these people can be placed on antibiotics to ward off infections before they occur. Small groups of CGD patients may also be affected by McLeod syndrome because of the proximity of the two genes on the same X-chromosome.

Chronic granulomatous disease (CGD) (also known as Bridges–Good syndrome, chronic granulomatous disorder, and Quie syndrome) is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly the superoxide radical due to defective phagocyte NADPH oxidase) used to kill certain ingested pathogens. This leads to the formation of granulomata in many organs. CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.

This condition was first discovered in 1950 in a series of 4 boys from Minnesota, and in 1957 it was named "a fatal granulomatosus of childhood" in a publication describing their disease. The underlying cellular mechanism that causes chronic granulomatous disease was discovered in 1967, and research since that time has further elucidated the molecular mechanisms underlying the disease. Bernard Babior made key contributions in linking the defect of superoxide production of white blood cells, to the cause of the disease. In 1986, the X-linked form of CGD was the first disease for which positional cloning was used to identify the underlying genetic mutation.

Samoyed hereditary glomerulopathy [glo-mer″u-lop´ah-the] (SHG) is an hereditary noninflammatory disease of the renal glomeruli, occurring in the Samoyed breed of dog. The disease has been shown to be a model for hereditary nephritis (HN) in humans in that the disease resembles that of the human disease. Because of this, it is sometimes referred to by the name given to the disease in humans when referring to the conditions in Samoyed dogs. Alternatively, it may also be known as X-linked hereditary nephritis. Genetically, the trait is inherited as a sex-linked, genetically dominant disease, and thus affects male dogs to a greater degree than female dogs, since males only have one X chromosome.

Colitis-X is a term used for colitis cases in which no definitive diagnosis can be made and the horse dies. Clinical signs include sudden, watery diarrhea that is usually accompanied by symptoms of hypovolemic shock and usually leads to death in 3 to 48 hours, usually in less than 24 hours. Other clinical signs include tachycardia, tachypnea, and a weak pulse. Marked depression is present. An explosive diarrhea develops, resulting in extreme dehydration. Hypovolemic and endotoxic shock are manifest by increased capillary refill time, congested or cyanotic (purplish) mucous membranes, and cold extremities. While there may initially be a fever, temperature usually returns to normal.

Clinical signs are similar to those of other diarrheal diseases, including toxemia caused by "Clostridium", Potomac horse fever, experimental endotoxic shock, and anaphylaxis.

The severe combined immunodeficiency (SCID) is a severe immunodeficiency genetic disorder that is characterized by the complete inability of the adaptive immune system to mount, coordinate, and sustain an appropriate immune response, usually due to absent or atypical T and B lymphocytes. In humans, SCID is colloquially known as "bubble boy" disease, as victims may require complete clinical isolation to prevent lethal infection from environmental microbes.

Several forms of SCID occur in animal species. Not all forms of SCID have the same cause; different genes and modes of inheritance have been implicated in different species.

Cherry angiomas are made up of clusters of capillaries at the surface of the skin, forming a small round dome ("papule") , which may be flat topped . They range in colour from bright red to purple. When they first develop, they may be only a tenth of a millimeter in diameter and almost flat, appearing as small red dots. However, they then usually grow to about one or two millimeters across, and sometimes to a centimeter or more in diameter . As they grow larger, they tend to expand in thickness, and may take on the raised and rounded shape of a dome. Multiple adjoining angiomas are said to form a "polypoid angioma". Because the blood vessels comprising an angioma are so close to the skin's surface, cherry angiomas may bleed profusely if they are injured.

One study found that the majority of capillaries in cherry hemangiomas are fenestrated because of staining for carbonic anhydrase activity.

Affected male and carrier female dogs generally begin to show signs of the disease at two to three months of age, with proteinuria. By three to four months of age, symptoms include for affected male dogs: bodily wasting and loss of weight, proteinuria & hypoalbuminemia. Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for affected males, symptoms are reported as being renal failure, hearing loss and death. Since the condition is genetically dominant, diagnosis would also include analysis of the health of the sire and dam of the suspected affected progeny if available.

Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be "Clostridium difficile", but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, there also is an association with prior antibiotic use. Immediate and aggressive treatment can sometimes save the horse, but even in such cases, 75% mortality is considered a best-case scenario.

Cherry angiomas, also known as Campbell De Morgan spots or senile angiomas, are cherry red papules on the skin. They are a harmless (benign) tumor, containing an abnormal proliferation of blood vessels, and have no relationship to cancer. They are the most common kind of angioma, and increase with age, occurring in nearly all adults over 30 years.

Campbell de Morgan is the nineteenth-century British surgeon who first described them.

Affected males develop generalized reticular hyper pigmentation in early childhood.

Hair often looks bedraggled or brushed backwards, hanging low on the forehead.

Among the associated extracutaneous manifestations are described:

- Respiratory infections

- Dyskeratosis corneal photophobia

- Hypohidrosis with large deficit of thermoregulation

- Growth retardation

- Gastrointestinal disorders

- Kidney disease

- Kidney stones

- Urinary infections

- Webbed feet or hands

- Electrolyte imbalance

- Retinitis pigmentosa

- Lymphoedema

- Thyroid abnormalities

Each patient shows some of the symptoms listed above. Not every sick person will show all of the listed symptoms.

In females the disease is characterized by skin rashes linear hyper pigmentation following the Blaschko's lines, morphologically similar to stage 3 pigment incontinence. There are no systemic manifestations associated with XLPDR in females.