Photomutilation and transfusion dependent anemia are common complications. Liver disease is also observed in some cases. It has been reported that early childhood-onset haematological manifestations is a poor prognosis factor.

Gunther disease, also known as congenital erythropoietic porphyria (CEP), uroporphyrinogen III synthase deficiency and UROS deficiency, is a congenital form of erythropoietic porphyria. The word porphyria originated from the Greek word porphura. Porphura actually means "purple pigment", which, in suggestion, the color that the body fluid changes when a person has Gunther's disease. It is a rare, autosomal recessive metabolic disorder affecting heme, caused by deficiency of the enzyme uroporphyrinogen cosynthetase. It is extremely rare, with a prevalence estimated at 1 in 1,000,000 or less. There have been times that prior to birth of a fetus, Gunther's disease has been shown to lead to anemia. In milder cases patients have not presented any symptoms until they have reached adulthood. In Gunther's disease, porphyrins are accumulated in the teeth and bones and an increased amount are seen in the plasma, bone marrow, feces, red blood cells, and urine.

Rates of all types of porphyria taken together have been estimated to be approximately one in 25,000 in the United States. The worldwide prevalence has been estimated to be between one in 500 and one in 50,000 people.

Some liver diseases may cause porphyria even in the absence of genetic predisposition. These include hemochromatosis and hepatitis C. Treatment of iron overload may be required.

Patients with the acute porphyrias (AIP, HCP, VP) are at increased risk over their life for hepatocellular carcinoma (primary liver cancer) and may require monitoring. Other typical risk factors for liver cancer need not be present.

A lethal infection in mink, the Aleutian disease virus lies dormant in ferrets until stress or injury allows it to surface. While the parvovirus itself causes little or no harm to the ferret host, the large number of antibodies produced in response to the presence of the virus results in a systemic vasculitis, resulting in eventual renal failure, bone marrow suppression and death.

The symptoms are chronic, progressive weight loss, lethargy, splenomegaly (enlarged spleen), anemia, rear leg weakness, seizures and black tarry stool. Additional symptoms include poor reproduction and/or oral bleeding/gastrointestinal bleeding. Lesions can also be found within the pelt depending on the severity of the disease. This virus can unfortunately reduce fitness of wild mink especially, by disturbing both the productivity within adult females and the overall survivor rates of both juveniles and adults. Likewise, in the mink kits that survive, it infects the alveolar cells and ultimately causes respiratory distress, possibly leading to death.

Once symptoms show themselves, the disease progresses rapidly, usually to death within a few months.

There is currently no known treatment for Aleutian virus. When evidence of ADV shows in a ferret, it is strongly recommended that a CEP (counterimmunoelectrophoresis) blood test or an IFA (immunoflourescent antibody) test be done. The CEP test is usually faster and less expensive than the IFA test, but the IFA test is more sensitive and can detect the disease in borderline cases.

Additionally modern methods such as Real-Time PCR allow for rapid and accurate detection as well as determination of the amount of viron present.

Prevention is best accomplished by stopping the spread of ADV. Any new ferret, or those who have been confirmed as serum positive for the virus should be perpetually isolated from other ferrets. All items that may have come into contact with the infected ferret should be cleaned with a 10% bleach solution.

This is a growing concern within mink producers as it is the most crucial infectious disease which affects farmed mink worldwide.

Eosinophilic pneumonia is a rare disease. Parasitic causes are most common in geographic areas where each parasite is endemic. AEP can occur at any age, even in previously healthy children, though most patients are between 20 and 40 years of age. Men are affected approximately twice as frequently as women. AEP has been associated with smoking. CEP occurs more frequently in women than men and does not appear to be related to smoking. An association with radiation for breast cancer has been described.

Medications, substance abuse, and environmental exposures may all trigger eosinophil dysfunction. Medications such as NSAIDs (e.g. ibuprofen), nitrofurantoin, phenytoin, L-tryptophan, daptomycin and ampicillin and drugs of abuse such as inhaled heroin and cocaine may trigger an allergic response which results in EP. Chemicals such as sulfites, aluminum silicate, and cigarette smoke can cause EP when inhaled. A New York City firefighter developed EP after inhalation of dust from the World Trade Center on September 11, 2001.

Exercise in middle age may reduce the risk of Parkinson's disease later in life. Caffeine also appears protective with a greater decrease in risk occurring with a larger intake of caffeinated beverages such as coffee. People who smoke cigarettes or use smokeless tobacco are less likely than non-smokers to develop PD, and the more they have used tobacco, the less likely they are to develop PD. It is not known what underlies this effect. Tobacco use may actually protect against PD, or it may be that an unknown factor both increases the risk of PD and causes an aversion to tobacco or makes it easier to quit using tobacco.

Antioxidants, such as vitamins C and E, have been proposed to protect against the disease, but results of studies have been contradictory and no positive effect has been proven. The results regarding fat and fatty acids have been contradictory, with various studies reporting protective effects, risk-increasing effects or no effects. There have been preliminary indications that the use of anti-inflammatory drugs and calcium channel blockers may be protective. A 2010 meta-analysis found that nonsteroidal anti-inflammatory drugs (apart from aspirin), have been associated with at least a 15 percent (higher in long-term and regular users) reduction of incidence of the development of Parkinson's disease.

Exposure to pesticides and a history of head injury have each been linked with Parkinson disease (PD), but the risks are modest. Never having smoked cigarettes, and never drinking caffeinated beverages, are also associated with small increases in risk of developing PD.

Low concentrations of urate in the blood serum is associated with an increased risk of PD.