The diagnosis by symptoms is not reliable enough so it’s better to do a molecular diagnosis based in test samples. Some of these methods (like Dot-blot hybridisation) allow the scientists to detect the viroid even six months before noticing the first symptoms.

The first step is the purification to obtain the nucleic acids of the plant cells. The leaves of the plant located four or more below the spare leaf are cut. Afterwards, they are blended (homogenize) with sodium sulfite. Then the extract is filtered and clarified by centrifugation (10.000 g during 10 minutes). The next step is to add polyethylene glycol (PEG). Finally, after nearly two hours of incubation at 4 °C, and after another centrifugation (at low speed) the nucleic acids can be extracted by chloroform procedures, for example.

When approximately 1 g of coconut tissue has been purified, the electrophoresis method can be started, which will help to identify the viroid by its relative mobility. The CCCVd is analysed in one or two dimensional polyacrylamide gels with a silver stain.

The viroid can also be detected by a more sensitive method called dot blot molecular hybridization. In this method CCCVd is amplified by the PCR (polymerase chain reaction) and the clones of CCCVd are used as templates to synthesize a complementary DNA or RNA chain. These sequences are radioactively labelled so when they are put over the samples with the intention to analyse (on a supporting membrane) and exposed to x-ray film, then if CCCVd is present it will appear as a dark colour. This dark tonality only appears when nucleic acid hybridisation occurs.

Yellow-band disease has severely affected reef building corals in the Caribbean. This disease have been associated with lower coral fecundity, altered tissue composition and a lower activites of antixenobiotic and antioxidant enzymes. Compared to the late 1990s, current data suggests that the disease remains a severe epidemic. In one study, 10 meter belt transects were taken at various depths, sampling coral colonies in the Lesser Antilles. At a depth of 5 m, yellow band rings and lesions were found on 79% of the colonies per transect, and only 21% of the colonies in this depth range appeared healthy.

Recent research indicates that yellow-band disease continues to be in an infectious phases in the Caribbean. It has been

found to cause infection in Pacific coral as well.

Necrotic ring spot can be managed through chemical and cultural controls. Cultural control includes the use of ammonium sulfate or other acidifying fertilizers to suppress the pathogen by lowering the pH of the soil to between 6.0 and 6.2. The more acidic soil discourages the activity of "O. korrae" (9) When reducing pH to these levels, additional manganese applications should be undertaken to compensate for lower pH. As of now, there are only two resistant cultivars of bluegrass, which are ‘Riviera’, and ‘Patriot’ (9). One component of their resistance could be that they are tolerant to low temperature, because the grass is more susceptible to the pathogen under colder temperatures(8). In addition, reducing watering inputs and growing turf on well drained soils can lessen disease symptoms.

Many different fungicides are used to control the pathogen, Fenarimol, Propiconazole, Myclobutanil, and Azoxystrobin (8). Historically, Fenarimol and Myclobutanil were predominantly used (14). In a study where diluted pesticides were sprayed throughout infested test plots, Fenarimol was found to be the most effective with a 94.6% reduction of the disease. Myclobutanil also decreased the amount of disease, but only by 37.7% (8). Myclobutanil is generally recognized as a very weakly acting demethylation inhibitor (DMI) fungicide and fenarimol is no longer registered for turf so a number of other DMI fungicides have been employed successfully, including Propiconazole, Tebuconazole, Metconazole and others. Pyraclostrobin and Fluoxastrobin have also been used to control the pathogen.

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

Coconut cadang-cadang disease has no treatment yet. However, chemotherapy with antibiotics has been tried with tetracycline solutions; antibiotics failed trying to alter progress of the disease since they had no significant effect on any of the studied parameters. When the treated plants were at the early stage, tetracycline injections failed to prevent the progression of the palms to more advanced stages, nor did they affect significantly the mean number of spathes or nuts. Penicillin treatment had no apparent improvement either.

Control strategies are elimination of reservoir species, vector control, mild strain protection and breeding for host resistance. Eradication of diseased plants is usually performed to minimize spread but is of dubious efficacy due to the difficulties of early diagnosis as the virus etiology remains unknown and the one discovered are the three main stages in the disease development.

Black band disease is a coral disease in which corals develop a black band. It is characterized by complete tissue degradation due to a pathogenic microbial consortium. The mat is present between apparently healthy coral tissue and freshly exposed coral skeleton.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

Black band disease was first observed on reefs in Belize in 1973 by A. Antonius, who described the pathogen he found infecting corals as "Oscillatoria membranacea", one of the cyanobacteria. The band color may be blackish brown to red depending on the vertical position of a cyanobacterial population associated with the band. The vertical position is based on a light intensity-dependent photic response of the cyanobacterial filaments, and the color (due to the cyanobacterial pigment phycoerythrin) is dependent on the thickness of the band. The band is approximately thick and ranges in width from to White specks may be present on surface, at times forming dense white patches. The pathogenic microbial mat moves across coral colonies at rates from to a day. Tissue death is caused by exposure to an hypoxic, sulfide-rich microenvironment associated with the base of the band.

Coral diseases, comprising the diseases that affect corals, injure the living tissues and often result in the death of part or the whole of the colony. These diseases have been occurring more frequently in the twenty-first century as conditions become more stressful for many shallow-water corals. The pathogens causing the diseases include bacteria, fungi and protozoa, but it is not always possible to identify the pathogen involved.

Fungicidal agents such as azadirachtin and phytoallexin have been used against some muscardine pathogens. Silkworm breeders dust their cages with slaked lime to discourage fungal growth. In India a dust of chaff soaked in formalin is applied to the larvae.

Breeding resistant varieties is the most cost-effective method to control this rust. Fungicides are available but vary in availability depending on their registration restrictions by national or state governments. Development of varieties resistant to the disease is always an important objective in wheat breeding programs for crop improvement. These resistance genes, however, became ineffective due to the acquisition of virulence to that particular resistance gene rendering the variety susceptible.

Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.

While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.

There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.

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.

Diagnosis of mycetoma is usually established clinically in endemic areas.

X rays and ultrasonography may be employed in evaluating the extent of the disease. X rays findings are extremely variable. The disease is most often observed at an advanced stage that exhibits extensive destruction of all bones of the foot. Rarely, a single lesion may be seen in the tibia where the picture is identical with chronic osteomyelitis. Cytology of fine needle aspirate or pus from the lesion, and tissue biopsy may be undertaken sometimes. Some publications have claimed a "dot in a circle sign" as a characteristic MRI feature for this condition (this feature has also been described on ultrasound).

Skeletal eroding band (SEB) is a disease of corals that appears as a black or dark gray band that slowly advances over corals, leaving a spotted region of dead coral in its wake. It is the most common disease of corals in the Indian and Pacific Oceans, and is also found in the Red Sea.

So far one agent has been clearly identified, the ciliate "Halofolliculina corallasia". This makes SEB the first coral disease known to be caused by a protozoan. When "H. corallasia" divides, the daughter cells move to the leading edge of the dark band and produce a protective shell called a lorica. To do this, they drill into the coral's limestone skeleton, killing coral polyps in the process.

A disease with very similar symptoms has been found in the Caribbean Sea, but has been given a different name as it is caused by a different species in the genus "Halofolliculina" and occurs in a different type of environment.

Necrotic ring spot is a common disease of turf caused by soil borne fungi (Ophiosphaerella korrae) that mainly infects roots (4). It is an important disease as it destroys the appearance of turfgrasses on park, playing fields and golf courses. Necrotic Ring Spot is caused by a fungal pathogen that is an ascomycete that produces ascospores in an ascocarp (6). They survive over winter, or any unfavorable condition as sclerotia. Most infection occurs in spring and fall when the temperature is about 13 to 28°C (5). The primary hosts of this disease are cool-season grasses such as Kentucky bluegrass and annual bluegrass (6). Once turf is infected with "O. korrae", it kills turf roots and crowns. Symptoms of the disease are quite noticeable since they appear as large yellow ring-shaped patches of dead turf. Management of the disease is often uneasy and requires application of multiple controls. The disease can be controlled by many different kind of controls including chemicals and cultural.

The following clinical conditions may be considered before diagnosing a patient with mycetoma:

1. Tuberculous ulcer

2. Kaposi's sarcoma, a vascular tumour of skin usually seen in AIDS.

3. Leprosy

4. Syphilis

5. Malignant neoplasm

6. Tropical ulcer

7. Botryomycosis, a skin infection usually caused by the bacteria Staphylococcus aureus.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

Corals growing in the Caribbean Sea are particularly affected by disease, perhaps because of the limited water circulation and the density of the human population on the surrounding land masses. Disease is also present in the tropical Indo-Pacific, but it is not so widespread, perhaps because of the more dispersed locations of the reefs.

A survey in the Caribbean Sea conducted in 2004 and published in 2006 reported a disease with very similar symptoms, affecting 25 species of coral within 6 families. Although the authors initially suspected "H.corallasia", more detailed examination showed that the culprit was another species that was previously unknown and has not yet been formally named, although it is clearly a member of the same genus, "Halofolliculina". A follow-up analysis noted that the Caribbean infestations were commonest in oceanic waters, while those in the Indian and Pacific Oceans were more prevalent in coastal waters. Because of these two differences, the authors gave this new manifestation the name "Caribbean ciliate infection". Coral diseases are a relatively new topic of research, and the use of standardized terminology has not yet been fixed.

During the latest outbreak of the disease (2004), several treatment methods were tested. Main treatment involved the administration of antibiotics, in some cases glucose solution or dietary mixtures were additionally supplemented. Outcome of the different treatment methods varied greatly. Especially the success of antibiotic treatment and a widespread use on wild animals remains a matter of debate.

Up until the advent of modern therapies, favid was widespread worldwide; prior to Schönlein's recognition of it as a fungal disease, it was frequently confused with Hansen's disease, better known as leprosy, and European sufferers were sometimes committed to leprosaria. Today, due to this species' high susceptibility to the antifungal drug griseofulvin, it has been eliminated from most parts of the world except rural central Asia and scattered rural areas of Africa. It is mainly a disease connected to demographic poverty and isolation, but is so readily treatable that it is among the diseases most likely to be completely eliminated by modern medicine.

Favid (of "favus" Latin for "honeycomb" or tinea favosa) is a disease usually affecting the scalp, but occurring occasionally on any part of the skin, and even at times on mucous membranes.

The word “Favid” is more used than French word “favus”, which is close to the Latin etymology.

Diphtheritic stomatitis is a recently discovered disease and has thus far been reported only in Yellow-eyed penguins ("Megadyptes antipodes"). Its symptoms are similar to human diphtheria and is characterized by infecteous lesions in the mouth area that impede swallowing and cause respiratory troubles. The infection is caused by "Corynebacterium amycolatum", an aerobic Gram-positive bacterium and mainly affects very young chicks. However, it seems likely that a triggering agent (e.g. a virus) might be involved in which renders the corynebacterium a secondary pathogen.

The disease has been a serious cause of mortality in the 2002 and 2004 Yellow-eyed penguin breeding seasons. It seems that only the New Zealand South Island and Stewart Island/Rakiura were affected.

Currently, no therapeutic drugs are prescribed for the disease. Therefore, prevention is the sole mode of treatment. This disease can only be prevented by quarantining sick birds and preventing migration of birds around the house, causing them to spread the disease. Deworming of birds with anthelmintics can reduce exposure to the cecal nematodes that carry the protozoan. Good management of the farm, including immediate quarantine of infected birds and sanitation, is the main useful strategy for controlling the spread of the parasitic contamination. The only drug used for the control (prophylaxis) in the United States is nitarsone at 0.01875% of feed until 5 days before marketing. Natustat and nitarsone were shown to be effective therapeutic drugs. Nifurtimox, a compound with known antiprotozoal activity, was demonstrated to be significantly effective at 300–400 ppm, and well tolerated by turkeys.