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:

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.

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.

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".

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.

Shot hole disease is a major concern of the stone fruit industry. It is estimated that 80% of the California almond crop may be infested with shot hole disease, resulting in a potential yield loss of 50-75%. In the 1930s, it was found that applications of Bordeaux mixture reduces shot hole disease on peaches from 80% to 9%.

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.

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.

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.

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.

The eastern tent caterpillar infestation in the spring of 2001 was extraordinary. It was not uncommon to observe more than a dozen caterpillars per square foot of lawn or pasture. One photograph shows a water bucket completely engulfed with ETCs. The pasture presence of ETCs was thought to be related to the MRLS abortions, leading to ETC epidemiological studies. ETC eggs are preferentially laid in webs on black cherry trees, and the primary food for ETCs is black cherry tree leaves.

By June 2001, Kentucky ETCs were no longer available for research, and would not reappear until the following April/May. MRLS research in the interim focused on the possible role of black cherry tree-related cyanide as the proximal cause of MRLS. The leaves of black cherry trees are known to be toxic due to their production of cyanide. Cyanide conveyed to mares via the caterpillars was initially thought to be the causative agent. Administration of both cyanide and mandelonitrile (a cyanide-containing chemical in cherry leaves) to horses demonstrated cyanide does not cause MRLS.

When the caterpillars returned to central Kentucky in late April 2002, they were readily shown to cause both the early and late fetal losses.

In 2002, investigators' attention was drawn to the highly toxic Brazilian "Lonomia obliqua" caterpillar setae and their enzymatic fibrinolysin toxin. A caterpillar defense mechanism based on specific setal toxins made more biological sense than a defense based on intestinal cyanide content. More importantly, if the ETC abortions were due to an enzyme or toxin, it should be possible to vaccinate horses against the toxin, an approach already explored with reference to the "Lonomia" toxin. In June 2002, conception of this ETC enzymatic setal toxin hypothesis was recorded as an intellectual property (IP) disclosure with the University of Kentucky IP office in which creation of an anti-ETC abortifacient toxin vaccine was proposed.

Following these initiatives, when ETCs again became available in 2002, a number of experiments on pregnant mice seeking to evaluate the use of pregnant mice as a laboratory model of MRLS and to develop experimental support for a filterable protein ETC toxin. These experiments showed intact ETC setae appeared to cause fetal resorption in mice, but frozen ETC setae and ETC setal filtrates failed to produce fetal resorptions in mice.

People with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems. Among the most common organisms that cause disease in CGD patients are:

- bacteria (particularly those that are catalase-positive)

- "Staphylococcus aureus".

- "Serratia marcescens".

- "Listeria" species.

- "E. coli".

- "Klebsiella" species.

- "Pseudomonas cepacia, a.k.a. Burkholderia cepacia.

- "Nocardia".

- fungi

- "Aspergillus" species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, "Aspergillus fumigatus" seems to be most common in CGD.

- "Candida" species.

Patients with CGD can usually resist infections of catalase-negative bacteria but are susceptible to catalase-positive bacteria. Catalase is an enzyme that catalyzes the breakdown of hydrogen peroxide in many organisms. In infections caused by organisms that lack catalase (catalase-negative), the host with CGD is successfully able to "borrow" hydrogen peroxide being made by the organism and use it to fight off the infection. In infections by organisms that have catalase (catalase-positive), this "borrowing mechanism" is unsuccessful because the catalase enzyme first breaks down any hydrogen peroxide that would be borrowed from the organism. Therefore in the CGD patient, hydrogen peroxide cannot be used to make oxygen radicals to fight infection, leaving the patient vulnerable to infection by catalase-positive bacteria.

In most patients, the number and size of cherry angiomas increases with advancing age. They are harmless, having no relation to cancer at all.

Samoyed Hereditary Glomerulopathy is caused by a nonsense mutation in codon 1027 of the COL4A5 gene on the X chromosome (glycine to stop codon), which is similar to Alport's syndrome in humans. The disease is simply inherited, X-linked dominant, with males generally having more severe symptoms than females. Clinically, from the age of three to four months, proteinuria in both sexes is seen. In dogs older than this, renal failure in combination with more or less pronounced hearing loss occurs swiftly, and death at the age of 8 to 15 months is expected. In heterozygous females, whereby only one of the two X chromosomes carry the mutation, the disease develops slowly.

The disease is specific to the Samoyed in that, the Samoyed, is the only breed of dog to show the more rapid progression to renal failure and death, as well as affecting males to a much more severe degree than females. The Samoyed, however is not the only breed of dog to suffer from life-threatening renal diseases. Proteinuria has been found consistently in Samoyeds, Doberman Pinschers, and Cocker spaniels.

There are currently no studies detailing the long term outcome of chronic granulomatous disease with modern treatment. Without treatment, children often die in the first decade of life. The increased severity of X-linked CGD results in a decreased survival rate of patients, as 20% of X-linked patients die of CGD-related causes by the age of 10, whereas 20% of autosomal recessive patients die by the age of 35.

Recent experience from centers specializing in the care of patients with CGD suggests that the current mortality has fallen to under 3% and 1% respectively.

CGD was initially termed "fatal granulomatous disease of childhood" because patients rarely survived past their first decade in the time before routine use of prophylactic antimicrobial agents. The average patient now survives at least 40 years.

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.

To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. "Clostridium difficile" toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human "C. difficile"-associated disease of greater than historical severity. "C. difficile" can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant "C. difficile" colitis is a significant and increasing cause of death.

Horses under stress appear to be more susceptible to developing colitis X. Disease onset is often closely associated with surgery or transport. Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms. A similar condition may be seen after administration of tetracycline or lincomycin to horses. These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,

the Quarter Horse stallion Lightning Bar,

and is one theory for the sudden death of Kentucky Derby winner Swale.

The link to stress suggests the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of Gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.

The causative agent may be "Clostridium perfringens", type A, but the bacteria are recoverable only in the preliminary stages of the disease.

The suspect toxin could also be a form of "Clostridium difficile". In a 2009 study at the University of Arizona, "C. difficile" toxins A and B were detected, large numbers of "C. difficile" were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.

Use of antibiotics may also be associated with some forms of colitis-X. In humans, "C. difficile" is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis. (A classic adverse effect of clindamycin in humans is "C. difficile"-associated diarrhea.) In the experiment, the treated horses died. After necropsy, "Clostridium cadaveris" was present, and is proposed as another possible causative agent in some cases of fatal colitis.

Equine SCID is an autosomal recessive disorder that affects the Arabian horse. Similar to the "bubble boy" condition in humans, an affected foal is born with no immune system, and thus generally dies of an opportunistic infection, usually within the first four to six months of life. There is a DNA test that can detect healthy horses who are carriers of the gene causing SCID, thus testing and careful, planned matings can now eliminate the possibility of an affected foal ever being born.

SCID is one of six genetic diseases known to affect horses of Arabian bloodlines, and the only one of the six for which there is a DNA test to determine if a given horse is a carrier of the allele. There are other genetic diseases that affect other horse breeds, and horses of part-Arabian bloodlines can be carriers of SCID.

Unlike SCID in humans, which can be treated, for horses, to date, the condition remains a fatal disease. When a horse is heterozygous for the gene, it is a carrier, but perfectly healthy and has no symptoms at all. If two carriers are bred together, however, classic Mendelian genetics indicate that there is a 50% chance of any given mating producing a foal that is a carrier heterozygous for the gene, and a 25% risk of producing a foal affected by the disease. If a horse is found to carry the gene, the breeder can choose to geld a male or spay a female horse so that they cannot reproduce, or they can choose to breed the known carrier only to horses that have been tested and found to be "clear" of the gene. In either case, careful breeding practices can avoid ever producing an SCID-affected foal.

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.

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.