Leaf rust is a fungal disease of barley caused by "Puccinia hordei". It is also known as brown rust and it is the most important rust disease on barley.

Pustules of leaf rust are small and circular, producing a mass of orange-brown powdery spores. They appear on the leaf sheaths and predominantly on the upper leaf surfaces. Heavily infected leaves die prematurely.

Citrus Black Spot is a fungal disease caused by Guignardia citricarpa. This Ascomycete fungus affects citrus plants throughout subtropical climates, causing a reduction in both fruit quantity and quality. Symptoms include both fruit and leaf lesions, the latter being critical to inter-tree dispersal. Strict regulation and management is necessary to control this disease since there are currently no citrus varieties that are resistant.

Beet vascular necrosis and rot is a soft rot disease caused by the bacterium Pectobacterium carotovorum" subsp. "betavasculorum, which has also been known as "Pectobacterium betavasculorum" and "Erwinia carotovora" subsp. "betavasculorum". It was classified in the genus "Erwinia" until genetic evidence suggested that it belongs to its own group; however, the name Erwinia is still in use. As such, the disease is sometimes called Erwinia rot today. It is a very destructive disease that has been reported across the United States as well as in Egypt. Symptoms include wilting and black streaks on the leaves and petioles. It is usually not fatal to the plant, but in severe cases the beets will become hollowed and unmarketable. The bacteria is a generalist species which rots beets and other plants by secreting digestive enzymes that break down the cell wall and parenchyma tissues. The bacteria thrive in warm and wet conditions, but cannot survive long in fallow soil. However, it is able to persist for long periods of time in the rhizosphere of weeds and non-host crops. While it is difficult to eradicate, there are cultural practices that can be used to control the spread of the disease, such as avoiding injury to the plants and reducing or eliminating application of nitrogen fertilizer.

False melanose lesions are characterized by many small, tan, slightly raised lesions. The lesions are much smaller than the hard spot variety with an average diameter of less than 1 mm (.04 in).

They are found on unripe fruit and are difficult to observe later in the season. Unlike hard spot lesions, no pycnidia are present.

Wheat yellow rust ("Puccinia striiformis" f.sp. "tritici"), also known as stripe rust, is one of the three wheat rust diseases principally found in wheat grown in cooler environments. Such locations are generally associated with northern latitudes or cooler seasons.

As R.P. Singh, J. Huerta-Espino, and A.P. Roelfs say in their (undated) comprehensive review of literature on the wheat rusts for UN FAO:

"Although Gadd first described stripe rust of wheat in 1777, it was not until 1896 that Eriksson and Henning (1896) showed that stripe rust resulted from a separate pathogen, which they named P. glumarum. In 1953, Hylander et al. (1953) revived the name P. striiformis."

Symptoms can be found on both beet roots and foliage, although foliar symptoms are not always present. If present, foliar symptoms include dark streaking along petioles and viscous froth deposits on the crown which are a by-product of bacterial metabolism. Petioles can also become necrotic and demonstrate vascular necrosis. When roots become severely affected, wilting also occurs. Below ground symptoms include both soft and dry root rot. Affected vascular bundles in roots become necrotic and brown, and tissue adjacent to necrosis becomes pink upon air contact. The plants that do not die completely may have rotted-out, cavernous roots.

Various pathogens can cause root rot in beets; however the black streaking on petioles and necrotic vascular bundles in roots and adjacent pink tissue help to distinguish this disease from others such as Fusarium Yellows. Additionally, sampling from the rhizosphere of infected plants and serological tests can confirm the presence of "Erwinia caratovora" subs.

Velvet disease (also called gold-dust, rust and coral disease) is a fish disease caused by dinoflagellate parasites of the genus "Piscinoodinium", specifically "Amyloodinium" in marine fish, and "Oodinium" in freshwater fish. The disease gives infected organisms a dusty, brownish-gold color. The disease occurs most commonly in tropical fish, and to a lesser extent, marine aquaria.

The single-celled parasite's life cycle can be divided into three major phases. First, as a tomont, the parasite rests at the water's floor and divides into as many as 256 tomites. Second, these juvenile, motile tomites swim about in search of a fish host, meanwhile using photosynthesis to grow, and to fuel their search. Finally, the adolescent tomite finds and enters the slime coat of a host fish, dissolving and consuming the host's cells, and needing only three days to reach full maturity before detaching to become a tomont once more.

Typically the first symptom of starfish wasting disease is white lesions that appear on the surface of the starfish and spread rapidly, followed by decay of tissue surrounding the lesions. Next the animal becomes limp as the water vascular system fails and it is no longer able to maintain its internal hydrostatic balance. The body structure begins to break down, signs of stretching appear between the arms which may twist and fall off, and the animal dies. The arms may continue to crawl around for a while after being shed. Progression of these events can be rapid, leading to death within a few days.

A deflated appearance can precede other morphological signs of the disease. All of these symptoms are also associated with ordinary attributes of unhealthy stars and can arise when an individual is stranded too high in the intertidal zone (for example) and simply desiccates. "True" wasting disease will be present in individuals that are found in suitable habitat, often in the midst of other individuals that might also be affected.

The final result is a white, mushy blob, which no longer seems to be a sea star.

Sea star wasting disease or starfish wasting syndrome is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of affected starfish. There are around 40 different species of sea stars that have been affected by this disease. The disease seems to be associated with raised water temperatures. It starts with the emergence of lesions, followed by body fragmentation and death. In 2014 it was shown that the disease is associated with a densovirus now known as the sea star-associated densovirus (SSaDV).

The lesions are most frequent on the lower limbs, but may occur anywhere on the body, including the hands, arms, torso and even the neck. They may vary in number and erupt in mass numbers.

They consist of irregular patches of orange or brown pigmentation with characteristic "cayenne pepper" spots appearing within and at the edge of old lesions.

There are usually no symptoms, although there may be some slight itching, but there is no pain.

The eruption may persist for many years. The pattern of the eruption changes, with slow extension and often some clearing of the original lesions.

Schamberg's disease, or progressive pigmented purpuric dermatitis, is a chronic discoloration of the skin which usually affects the legs and often spreads slowly. This disease is more common in males and may occur at any age from childhood onward. This condition is observed worldwide and has nothing to do with race or ethnic background.

There are two expressions of this condition, one for long or double coated breeds and one for short coated breeds, both with differing presentations.

- For long- or double-coated breeds such as Poodles, Akitas and Samoyeds, the condition often presents itself with silvery dandruff which adheres to the coat, hair loss (not to be confused with moulting or "blowing coat"), a dull and brittle coat, and later on skin lesions along the back and ears as well as thickened skin and a musty or rancid odour.

- For short-coated breeds such as Vizslas, the condition causes facial swellings, nodular skin lesions, fine dandruff which does not adhere to the coat, and a general "moth-eaten" appearance to the coat.

Schamberg's disease, (also known as "progressive pigmentary dermatosis of Schamberg", "purpura pigmentosa progressiva" (PPP), and "Schamberg's purpura") is a chronic discoloration of the skin found in people of all ages, usually affecting the legs. It slowly spreads throughout the body, and is most common in males. It is named after Jay Frank Schamberg, who described it in 1901. There is no known cure for this disease and it is not a life-threatening condition. The skin lesions may cause itching, which can be treated by applying cortisone cream. The cortisone cream will only help with the itching and the discoloration of the skin will remain, which may cause a cosmetic concern in the future. Schamberg's disease is usually asymptomatic meaning that it shows no signs of this condition, except for the discoloration of the skin. This condition is caused by leaky blood vessels, where red blood cells escape near the surface of skin and release its iron into the surrounding tissue. The cause of the leaky capillaries is unknown.

Sebaceous adenitis in an uncommon skin disease found in some breeds of dog, and more rarely in cats, rabbits and horses. characterised by an inflammatory response against the dog's sebaceous glands (glands found in the hair follicles in the skin dermis), which can lead to the destruction of the gland. It was first described in veterinary literature in the 1980s.

Lichen aureus (also known as "lichen purpuricus") is a skin condition characterized by the sudden appearance of one or several golden or rust-colored, closely packed macules or lichenoid papules.

Gougerot–Blum syndrome (also known as "pigmented purpuric lichenoid dermatitis", and "pigmented purpuric lichenoid dermatitis of Gougerot and Blum") is a variant of pigmented purpuric dermatitis, a skin condition characterized by minute, rust-colored to violaceous, lichenoid papules that tend to fuse into plaques of various hues. Relative to other variants, it is characterized clinically by a male predominance, pruritus, with a predilection for the legs, and histologically, it features a densely cellular lichenoid infiltrate.

It was characterized in 1925.

Gougerot–Blum syndrome is named after the French dermatologists Henri Gougerot (1881–1955) and Paul Blum (1878–1933).

Porphyria cutanea tarda (commonly referred to as PCT) is recognized as the most prevalent subtype of porphyritic diseases.

The disease is characterized by onycholysis and blistering of the skin in areas that receive higher levels of exposure to sunlight. The primary cause of this disorder is a deficiency of uroporphyrinogen decarboxylase (UROD), a cytosolic enzyme that is a step in the enzymatic pathway that leads to the synthesis of heme. While a deficiency in this enzyme is the direct cause leading to this disorder, there are a number of both genetic and environmental risk factors that are associated with PCT.

Typically, patients who are ultimately diagnosed with PCT first seek treatment following the development of photosensitivities in the form of blisters and erosions on commonly exposed areas of the skin. This is usually observed in the face, hands, forearms, and lower legs. It heals slowly and with scarring. Though blisters are the most common skin manifestations of PCT, other skin manifestations like hyperpigmentation (as if they are getting a tan) and hypertrichosis (mainly on top of the cheeks) also occur. PCT is a chronic condition, with external symptoms often subsiding and recurring as a result of a number of factors. In addition to the symptomatic manifestation of the disease in the skin, chronic liver problems are extremely common in patients with the sporadic form of PCT. These include hepatic fibrosis (scarring of the liver), cirrhosis, and inflammation. However, liver problems are less common in patients with the inherited form of the disease. Additionally, patients will often void a wine-red color urine with an increased concentration of uroporphyrin I due to their enzymatic deficiency.

Dermatitis symptoms vary with all different forms of the condition. They range from skin rashes to bumpy rashes or including blisters. Although every type of dermatitis has different symptoms, there are certain signs that are common for all of them, including redness of the skin, swelling, itching and skin lesions with sometimes oozing and scarring. Also, the area of the skin on which the symptoms appear tends to be different with every type of dermatitis, whether on the neck, wrist, forearm, thigh or ankle. Although the location may vary, the primary symptom of this condition is itchy skin. More rarely, it may appear on the genital area, such as the vulva or scrotum. Symptoms of this type of dermatitis may be very intense and may come and go. Irritant contact dermatitis is usually more painful than itchy.

Although the symptoms of atopic dermatitis vary from person to person, the most common symptoms are dry, itchy, red skin. Typical affected skin areas include the folds of the arms, the back of the knees, wrists, face and hands. Perioral dermatitis refers to a red bumpy rash around the mouth.

Dermatitis herpetiformis symptoms include itching, stinging and a burning sensation. Papules and vesicles are commonly present. The small red bumps experienced in this type of dermatitis are usually about 1 cm in size, red in color and may be found symmetrically grouped or distributed on the upper or lower back, buttocks, elbows, knees, neck, shoulders, and scalp. Less frequently, the rash may appear inside the mouth or near the hairline.

The symptoms of seborrheic dermatitis, on the other hand, tend to appear gradually, from dry or greasy scaling of the scalp (dandruff) to scaling of facial areas, sometimes with itching, but without hair loss. In newborns, the condition causes a thick and yellowish scalp rash, often accompanied by a diaper rash. In severe cases, symptoms may appear along the hairline, behind the ears, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.

Although many people with a defective AMPD gene are asymptomatic, others may have symptoms such as exercise intolerance, muscle pain, and muscle cramping.

- Fatigue

- MADD lowers aerobic power output, so increased anaerobic power is needed to perform the same amount of work.

- Without myoadenlyate deaminase, heavy activity causes adenosine to be released into the cell or perfused into the surrounding tissues. Fatigue and sedation after heavy exertion can be caused by excess adenosine in the cells which signals muscle fiber to feel fatigued. In the brain, excess adenosine decreases alertness and causes sleepiness. In this way, adenosine may play a role in fatigue from MADD.

- Recovery from over-exertion can be hours, days or even months. In cases of rhabdomyolysis, which is the rapid breakdown of muscle fibers, time to recovery is dependent on duration and intensity of original activity plus any excess activity during the recovery period.

- Muscle pain

- Muscle pain from MADD is not well understood, but is partially due to high levels of lactate. Increased levels of free adenosine temporarily decrease pain, allowing over-exertion without awareness. The over exertion can cause mild to severe cases of rhabdomyolysis, which is painful.

- Adenosine mediates pain through adenosine receptors. MADD causes an increase of free adenosine during heavy activity which may cause exercise-induced muscle pain. Over time, excess free adenosine down-regulates primary A1 adenosine receptors, leading to increased muscle pain. Secondary receptors (A3) increase peripheral inflammation, which also increases pain.

- Muscle cramping

- The cause of cramping is unknown, but may be related to elevated lactate, increased calcium signaling across the sarcoplasmic reticulum caused by membrane instability from reduced levels of ATP, or increased levels of free adenosine.

- Muscle weakness

- Muscle weakness is not a major symptom, though the progressive effects of chronic muscle damage from rhabdomyolysis will eventually cause significant weakness. Similarly, the long-term metabolic effects may result in nerve damage.

Venous eczema (gravitational eczema, stasis dermatitis, varicose eczema) occurs in people with impaired circulation, varicose veins, and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin, and itching. The disorder predisposes to leg ulcers. (ICD-10 I83.1)

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate properly during cell division. There are three forms of nondisjunction: failure of a pair of homologous chromosomes to separate in meiosis I, failure of sister chromatids to separate during meiosis II, and failure of sister chromatids to separate during mitosis. Nondisjunction results in daughter cells with abnormal chromosome numbers (aneuploidy).

Calvin Bridges and Thomas Hunt Morgan are credited with discovering nondisjunction in "Drosophila melanogaster" sex chromosomes in the spring of 1910, while working in the Zoological Laboratory of Columbia University.

Porphyria cutanea tarda (PCT) is the most common subtype of porphyria. The disease is named because it is a porphyria that often presents with skin manifestations later in life. The disorder results from low levels of the enzyme responsible for the fifth step in heme production. Heme is a vital molecule for all of the body's organs. It is a component of hemoglobin, the molecule that carries oxygen in the blood.

Hepatoerythropoietic porphyria has been described as a homozygous form of porphyria cutanea tarda, although it can also be caused if two different mutations occur at the same locus.

Adenosine monophosphate deaminase deficiency type 1, also called myoadenylate deaminase deficiency (MADD), is a recessive genetic metabolic disorder that affects approximately 1–2% of populations of European descent. It appears to be considerably rarer in Asian populations. The genetic form is caused by a defect in the gene for AMP deaminase though there is also an acquired form of AMP deficiency.