One of the main effects of cadmium poisoning is weak and brittle bones. Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the cadmium. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Other complications include coughing, anemia, and kidney failure, leading to death.

A marked prevalence in older, postmenopausal women has been observed. The cause of this phenomenon is not fully understood, and is currently under investigation. Current research has pointed to general malnourishment, as well as poor calcium metabolism relating to the women's age.

Recent animal studies have shown that cadmium poisoning alone is not enough to elicit all of the symptoms of itai-itai disease. These studies are pointing to damage of the mitochondria of kidney cells by cadmium as a key factor of the disease.

Increased concentrations of urinary beta-2 microglobulin can be an early indicator of renal dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for renal damage in workers with long-term exposure to high levels of cadmium. Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained renal damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/g, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases.

Itai-itai disease was caused by cadmium poisoning due to mining in Toyama Prefecture. The earliest records of mining for gold in the area date back to 1710. Regular mining for silver started in 1589, and soon thereafter, mining for lead, copper, and zinc began. Increased demand for raw materials during the Russo-Japanese War and World War I, as well as new mining technologies from Europe, increased the output of the mines, putting the Kamioka Mines in Toyama among the world's top mines. Production increased even more before World War II. Starting in 1910 and continuing through 1945, cadmium was released in significant quantities by mining operations, and the disease first appeared around 1912. Prior to World War II, the mining, controlled by the Mitsui Mining & Smelting Co., Ltd., increased to satisfy the wartime demand. This subsequently increased the pollution of the Jinzū River and its tributaries. The river was used mainly for irrigation of rice fields, but also for drinking water, washing, fishing, and other uses by downstream populations.

Due to the cadmium poisoning, the fish in the river started to die, and the rice irrigated with river water did not grow well. The cadmium and other heavy metals accumulated at the bottom of the river and in the water of the river. This water was then used to irrigate the rice fields. The rice absorbed heavy metals, especially the cadmium. The cadmium accumulated in the people eating contaminated rice.

When the population complained to Mitsui Mining & Smelting Co. about this pollution, the company built a basin to store the mining waste water before leading it into the river. This proved ineffective, and many had already been sickened. The causes of the poisoning were not well understood and, up to 1946, it was thought to be simply a regional disease or a type of bacterial infection.

Medical tests started in the 1940s and 1950s, searching for the cause of the disease. Initially, it was expected to be lead poisoning due to the lead mining upstream. Only in 1955 did Dr. Hagino and his colleagues suspect cadmium as the cause of the disease. Toyama Prefecture also started an investigation in 1961, determining that the Mitsui Mining and Smelting's Kamioka Mining Station caused the cadmium pollution and that the worst-affected areas were 30 km downstream of the mine. In 1968, the Ministry of Health and Welfare issued a statement about the symptoms of "itai-itai" disease caused by the cadmium poisoning.

The reduction of the levels of cadmium in the water supply reduced the number of new disease victims; no new victim has been recorded since 1946. While the victims with the worst symptoms came from Toyama prefecture, the government found victims in five other prefectures.

The mines are still in operation and cadmium pollution levels remain high, although improved nutrition and medical care has reduced the occurrence of itai-itai disease.

, sometimes referred to as , is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.

Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local populace, resulted in mercury poisoning. While cat, dog, pig, and human deaths continued for 36 years, the government and company did little to prevent the pollution. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever".

As of March 2001, 2,265 victims had been officially recognised as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims.

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the four big pollution diseases of Japan.

Cadmium is a naturally occurring toxic heavy metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure to humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. Cadmium is also present in the manufacturing of some types of batteries. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, construction industry, and the agricultural industry.

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

Bright's disease was historically 'treated' with warm baths, blood-letting, squill, digitalis, mercuric compounds, opium, diuretics, laxatives, and dietary therapy, including abstinence from alcoholic drinks, cheese and red meat. Arnold Ehret was diagnosed with Bright's disease and pronounced incurable by 24 of Europe's most respected doctors; he designed "The Mucusless Diet Healing System", which apparently cured his illness. William Howard Hay, MD had the illness and, it is claimed, cured himself using the Hay diet.

It is done through isolation of a bacteria from chickens suspected to have history of coryza and clinical finds from infected chickens also is used in the disease diagnosis. Polymerase chain reaction is a reliable means of diagnosis of the disease

Minamata disease remains an important issue in contemporary Japanese society. Lawsuits against Chisso and the prefectural and national governments are still continuing and many regard the government responses to date as inadequate. The company's "historical overview" in its current website makes no mention of their role in the mass contamination of Minamata and the dreadful aftermath. Their 2004 Annual Report however reports an equivalent of about US$50 million (5,820 million yen) in "Minamata Disease Compensation Liabilities". From 2000 to 2003, the company also reported total compensation liabilities of over US$170 million. Their 2000 accounts also show that the Japanese and Kumamoto prefectural governments waived an enormous US$560 million in related liabilities. Their FY2004 and FY2005 reports refer to Minamata disease as "mad hatter's disease", a term coined from the mercury poisoning experienced by hat-makers of the last few centuries (cf. Erethism).

A memorial service was held at the Minamata Disease Municipal Museum on 1 May 2006 to mark 50 years since the official discovery of the disease. Despite bad weather, the service was attended by over 600 people, including Chisso chairman Shunkichi Goto and Environment Minister Yuriko Koike.

On Monday, March 29, 2010, a group of 2,123 uncertified victims reached a settlement with the government of Japan, the Kumamoto Prefectural government, and Chisso Corporation to receive individual lump-sum payments of 2.1 million yen and monthly medical allowances.

Most congenital patients are now in their forties and fifties and their health is deteriorating. Their parents, who are often their only source of care, are into their seventies or eighties or already deceased. Often these patients find themselves tied to their own homes and the care of their family, effectively isolated from the local community. Some welfare facilities for patients do exist. One notable example is , a vocational training centre for congenital patients as well as other disabled people in the Minamata area. Hot House members are also involved in raising awareness of Minamata disease, often attending conferences and seminars as well as making regular visits to elementary schools throughout Kumamoto Prefecture.

Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

The symptoms and signs of Bright's disease were first described in 1827 by the English physician Richard Bright, after whom the disease was named. In his "Reports of Medical Cases", he described 25 cases of dropsy (edema) which he attributed to kidney disease. Symptoms and signs included: inflammation of serous membranes, hemorrhages, apoplexy, convulsions, blindness and coma. Many of these cases were found to have albumin in their urine (detected by the spoon and candle-heat coagulation), and showed striking morbid changes of the kidneys at autopsy. The triad of dropsy, albumin in the urine and kidney disease came to be regarded as characteristic of Bright's disease. Subsequent work by Bright and others indicated an association with cardiac hypertrophy, which was attributed by Bright to stimulation of the heart. Subsequent work by Mahomed showed that a rise in blood pressure could precede the appearance of albumin in the urine, and the rise in blood pressure and increased resistance to flow was believed to explain the cardiac hypertrophy.

It is now known that Bright's disease is due to a wide range of diverse kidney diseases; thus, the term "Bright's disease" is retained strictly for historical application. The disease was diagnosed frequently in patients with diabetes; at least some of these cases would probably correspond to a modern diagnosis of diabetic nephropathy.

The standard diagnostic workup of suspected kidney disease is history & examination, as well as a urine test strip. Also, renal ultrasonography is essential in the diagnosis and management of kidney-related diseases.

Feline hepatic lipidosis shares similar symptoms to other problems, including liver disease, renal failure, feline leukemia, Feline infectious peritonitis and some cancers. Diagnosis requires tests that target the liver to make an accurate diagnosis. Jaundice is highly indicative of the disease. Blood tests and a liver biopsy will confirm the presence of the disease.

Amniocentesis or chorionic villus sampling can be used to screen for the disease before birth. After birth, urine tests, along with blood tests and skin biopsies can be used to diagnose Schindler disease. Genetic testing is also always an option, since different forms of Schindler disease have been mapped to the same gene on chromosome 22; though different changes (mutations) of this gene are responsible for the infantile- and adult-onset forms of the disease.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Fabry disease is suspected based on the individual's clinical presentation, and can be diagnosed by an enzyme assay (usually done on leukocytes) to measure the level of alpha-galactosidase activity. An enzyme assay is not reliable for the diagnosis of disease in females due to the random nature of X-inactivation. Molecular genetic analysis of the "GLA" gene is the most accurate method of diagnosis in females, particularly if the mutations have already been identified in male family members. Many disease-causing mutations have been noted. Kidney biopsy may also be suggestive of Fabry disease if excessive lipid buildup is noted. Pediatricians, as well as internists, commonly misdiagnose Fabry disease.

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Infants with Schindler disease tend to die within 4 years of birth, therefore, treatment for this form of the disease is mostly palliative. However, Type II Schindler disease, with its late onset of symptoms, is not characterized by neurological degeneration. There is no known cure for Schindler disease, but bone marrow transplants have been trialed, as they have been successful in curing other glycoprotein disorders.

Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of non-destructive seronegative arthritis, often of large joints.

Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing non-acid-fast gram-positive bacilli. Immunohistochemical staining for antibodies against "T. whipplei" has been used to detect the organism in a variety of tissues, and a PCR-based assay is also available. PCR can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual.

Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.

A D-Xylose test can be performed, which is where the patient will consume 4.5g of D-xylose, a sugar, by mouth. The urine excretion of D-Xylose is then measured after 5 hours. The majority of D-Xylose is absorbed normally, and should be found in the urine. If the D-Xylose is found to be low in the urine, this suggests an intestinal malabsorption problem such as bacterial overgrowth of the proximal small intestine, Whipple's Disease, or an autoimmune with diseases such as Celiac's Disease (allergy to gluten) or Crohn's Disease (autoimmune disease affecting the small intestine). With empiric antibiotic treatment after an initial positive D-Xylose test, and if a follow-up D-Xylose test is positive (decreased urine excretion) after antibiotic therapy, then this would signify it is not bacterial overgrowth of the proximal small intestine. Since Whipple's disease is so rare, a follow-up positive D-Xylose test more likely indicates a non-infectious etiology and more likely an autoimmune etiology. Clinical correlation is recommended to rule out Whipple's disease.

The first approach, which is the best approach at an effective management practice would be to eradicate or severely damage the Mountain and Cherry Leafhopper population because the leafhoppers are the number one vectors for this pathogen. To do this, pesticides (i.e. acephate, bifenthrin, cyfluthrin) could be applied or biological control (predators of the leafhopper) could be used. There should be a pre-season application of control measures as well as a post-season application. This is to maximize the effort at controlling both types of leafhoppers (Cherry and Mountain), thus cutting down the starting inoculum at both stages in the life cycle.

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

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Disease mongering is a term for the practice of widening the diagnostic boundaries of illnesses and aggressively promoting their public awareness in order to expand the markets for treatment.

Among the entities benefiting from selling and delivering treatments are pharmaceutical companies, physicians, alternative practitioners and other professional or consumer organizations. It is distinct from the promulgation of bogus or unrecognised diagnoses.