The treatment is antimalarial chemotherapy, intravenous fluid and sometimes supportive care such as intensive care and dialysis.

Louping ill is caused by RNA virus called Louping ill virus. Louping ill virus belongs to genus Flavivirus, family Flaviviridae.

There are four subtypes: British, Irish, Spanish and Turkish.

According to a ProMED article, disease in sheep has been controlled in the UK by a vaccine (ATCvet code: QI04AA01), originally developed by Scotland's Moredun Research Institute by Prof John Russell Greig. In 2009, however, a shortage of vaccine combined with an increase in the number of ticks found in sheep pasture areas cause an increased risk of this disease.

Blackwater fever is a complication of malaria infection in which red blood cells burst in the bloodstream (hemolysis), releasing hemoglobin directly into the blood vessels and into the urine, frequently leading to kidney failure. The disease was first linked to malaria by the Sierra Leonean physician Dr John Farrell Easmon in his 1884 pamphlet entitled "The Nature and Treatment of Blackwater Fever." Easmon coined the name "blackwater fever" and was the first to successfully treat such cases following the publication of his pamphlet.

This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.

The cause is the most mysterious aspect of the disease. Commentators then and now put much blame on the generally poor sanitation, sewage and contaminated water supplies of the time, which might have harboured the source of infection. The first outbreak at the end of the Wars of the Roses means that it may have been brought over from France by the French mercenaries whom Henry VII used to gain the English throne. However, the "Croyland Chronicle" mentions that Thomas Stanley, 1st Earl of Derby used the "sweating sickness" as an excuse not to join with Richard III's army prior to the Battle of Bosworth.

Relapsing fever has been proposed as a possible cause. This disease, which is spread by ticks and lice, occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash.

Noting symptom overlap with hantavirus pulmonary syndrome, several scientists proposed an unknown hantavirus as the cause. A critique of this hypothesis included the argument that, whereas sweating sickness was thought to be transmitted from human to human, hantaviruses are rarely spread in this way. However, infection via human-to-human contact has been proven in hantavirus outbreaks in Argentina.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition. However, this approach does not always stop reinfection.

The symptoms and signs, as described by physician John Caius and others, were as follows: the disease began very suddenly with a sense of apprehension, followed by cold shivers (sometimes very violent), giddiness, headache, and severe pains in the neck, shoulders and limbs, with great exhaustion. After the cold stage, which might last from half an hour to three hours, the hot and sweating stage followed. The characteristic sweat broke out suddenly without any obvious cause. Accompanying the sweat, or after, was a sense of heat, headache, delirium, rapid pulse, and intense thirst. Palpitation and pain in the heart were frequent symptoms. No skin eruptions were noted by observers including Caius. In the final stages, there was either general exhaustion and collapse, or an irresistible urge to sleep, which Caius thought to be fatal if the patient was permitted to give way to it. One attack did not offer immunity, and some people suffered several bouts before dying. The disease tended to occur in summer and early autumn.

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.

First degree relatives of those with primary haemochromatosis should be screened to determine if they are a carrier or if they could develop the disease. This can allow preventive measures to be taken.

Screening the general population is not recommended.

There are several methods available for diagnosing and monitoring iron loading including:

- Serum ferritin: In males and postmenopausal females, a serum ferritin value of over 300 ng/mL (670 pmol/L) indicates iron overload. In premenopausal females, a serum ferritin value of over 150 or 200 ng/mL (330 or 440 pmol/L) indicates iron overload.

- Liver biopsy

- HFE

- MRI

Serum ferritin testing is a low-cost, readily available, and minimally invasive method for assessing body iron stores. However, the major problem with using it as an indicator of iron overload is that it can be elevated in a range of other medical conditions unrelated to iron levels including infection, inflammation, fever, liver disease, kidney disease, and cancer. Also, total iron binding capacity may be low, but can also be normal.

The standard of practice in diagnosis of haemochromatosis was recently reviewed by Pietrangelo. Positive HFE analysis confirms the clinical diagnosis of haemochromatosis in asymptomatic individuals with blood tests showing increased iron stores, or for predictive testing of individuals with a family history of haemochromatosis. The alleles evaluated by HFE gene analysis are evident in ~80% of patients with haemochromatosis; a negative report for HFE gene does not rule out haemochromatosis. In a patient with negative HFE gene testing, elevated iron status for no other obvious reason, and family history of liver disease, additional evaluation of liver iron concentration is indicated. In this case, diagnosis of haemochromatosis is based on biochemical analysis and histologic examination of a liver biopsy. Assessment of the hepatic iron index (HII) is considered the "gold standard" for diagnosis of haemochromatosis.

Magnetic resonance imaging (MRI) is emerging as a noninvasive alternative to accurately estimate iron deposition levels in the liver as well as heart, joints, and pituitary gland.

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.

The Dancing Plague (or Dance Epidemic) of 1518 was a case of dancing mania that occurred in Strasbourg, Alsace, (then part of the Holy Roman Empire) in July 1518. Around 400 people took to dancing for days without rest and, over the period of about one month, some of those affected collapsed or even died of heart attack, stroke, or exhaustion.

There exist other causes of excess iron accumulation, which have to be considered before haemochromatosis is diagnosed.

- African iron overload, formerly known as Bantu siderosis, was first observed among people of African descent in Southern Africa. Originally, this was blamed on ungalvanised barrels used to store home-made beer, which led to increased oxidation and increased iron levels in the beer. Further investigation has shown that only some people drinking this sort of beer get an iron overload syndrome, and that a similar syndrome occurred in people of African descent who have had no contact with this kind of beer ("e.g.," African Americans). This led investigators to the discovery of a gene polymorphism in the gene for ferroportin which predisposes some people of African descent to iron overload.

- Transfusion haemosiderosis is the accumulation of iron, mainly in the liver, in patients who receive frequent blood transfusions (such as those with thalassaemia).

- Dyserythropoeisis, also known as myelodysplastic syndrome, is a disorder in the production of red blood cells. This leads to increased iron recycling from the bone marrow and accumulation in the liver.

Blood is generally drawn from the father to help determine fetal antigen status. If he is homozygous for the antigen, there is a 100% chance of all offspring in the pairing to be positive for the antigen and at risk for HDN. If he is heterozygous, there is a 50% chance of offspring to be positive for the antigen. This test can help with knowledge for the current baby, as well as aid in the decision about future pregnancies. With RhD, the test is called the RhD genotype. With RhCE, and Kell antigen it is called an antigen phenotype.

In some cases, the direct coombs will be negative but severe, even fatal HDN can occur. An indirect coombs needs to be run in cases of anti-C, anti-c, and anti-M. Anti-M also recommends antigen testing to rule out the presence of HDN.

- Hgb - the infant’s hemoglobin should be tested from cord blood.

- Reticulocyte count - Reticulocytes are elevated when the infant is producing more blood to combat anemia. A rise in the retic count can mean that an infant may not need additional transfusions. Low retic is observed in infants treated with IUT and in those with HDN from anti-Kell

- Neutrophils - as Neutropenia is one of the complications of HDN, the neutrophil count should be checked.

- Thrombocytes - as thrombocytopenia is one of the complications of HDN, the thrombocyte count should be checked.

- Bilirubin should be tested from cord blood.

- Ferritin - because most infants affected by HDN have iron overload, a ferritin must be run before giving the infant any additional iron.

- Newborn Screening Tests - Transfusion with donor blood during pregnancy or shortly after birth can affect the results of the Newborn Screening Tests. It is recommended to wait and retest 10–12 months after last transfusion. In some cases, DNA testing from saliva can be used to rule out certain conditions.

Liver biopsies involve taking a sample of tissue from the liver, using a thin needle. The amount of iron in the sample is then quantified and compared to normal, and evidence of liver damage, especially cirrhosis, measured microscopically. Formerly, this was the only way to confirm a diagnosis of haemochromatosis but measures of transferrin and ferritin along with a history are considered adequate in determining the presence of the malady. Risks of biopsy include bruising, bleeding and infection. Now, when a history and measures of transferrin or ferritin point to haemochromatosis, it is debatable whether a liver biopsy is still necessary to quantify the amount of accumulated iron.

The outbreak began in July 1518 when a woman, Mrs. Troffea, began to dance fervently in a street in Strasbourg. This lasted somewhere between four and six days. Within a week, 34 others had joined, and within a month, there were around 400 dancers, predominantly female. Some of these people would die from heart attacks, strokes, or exhaustion. One report indicates that for a period, the plague killed around fifteen people per day.

Historical documents, including "physician notes, cathedral sermons, local and regional chronicles, and even notes issued by the Strasbourg city council" are clear that the victims danced. It is not known why these people danced, some even to their deaths.

As the dancing plague worsened, concerned nobles sought the advice of local physicians, who ruled out astrological and supernatural causes, instead announcing that the plague was a "natural disease" caused by "hot blood". However, instead of prescribing bleeding, authorities encouraged more dancing, in part by opening two guildhalls and a grain market, and even constructing a wooden stage. The authorities did this because they believed that the dancers would recover only if they danced continuously night and day. To increase the effectiveness of the cure, authorities even paid for musicians to keep the afflicted moving.

Historian John Waller stated that a marathon runner could not have lasted the intense workout that these men and women did hundreds of years ago.

During any pregnancy a small amount of the baby's blood can enter the mother's circulation. If the mother is Rh negative and the baby is Rh positive, the mother produces antibodies (including IgG) against the rhesus D antigen on her baby's red blood cells. During this and subsequent pregnancies the IgG is able to pass through the placenta into the fetus and if the level of it is sufficient, it will cause destruction of rhesus D positive fetal red blood cells leading to the development of Rh disease. It may thus be regarded as insufficient immune tolerance in pregnancy. Generally rhesus disease becomes worse with each additional rhesus incompatible pregnancy.

The main and most frequent sensitizing event is child birth (about 86% of sensitized cases), but fetal blood may pass into the maternal circulation earlier during the pregnancy (about 14% of sensitized cases). Sensitizing events during pregnancy include c-section, miscarriage, therapeutic abortion, amniocentesis, ectopic pregnancy, abdominal trauma and external cephalic version. However, in many cases there was no apparent sensitizing event.

The incidence of Rh disease in a population depends on the proportion that are rhesus negative. Many non-Caucasian people have a very low proportion who are rhesus negative, so the incidence of Rh disease is very low in these populations. In Caucasian populations about 1 in 10 of all pregnancies are of a rhesus negative woman with a rhesus positive baby. It is very rare for the first rhesus positive baby of a rhesus negative woman to be affected by Rh disease. The first pregnancy with a rhesus positive baby is significant for a rhesus negative woman because she can be sensitized to the Rh positive antigen. In Caucasian populations about 13% of rhesus negative mothers are sensitized by their first pregnancy with a rhesus positive baby. Without modern prevention and treatment, about 5% of the second rhesus positive infants of rhesus negative women would result in stillbirths or extremely sick babies. Many babies who managed to survive would be severely ill. Even higher disease rates would occur in the third and subsequent rhesus positive infants of rhesus negative women. By using anti-RhD immunoglobulin (Rho(D) immune globulin) the incidence is massively reduced.

Rh disease sensitization is about 10 times more likely to occur if the fetus is ABO compatible with the mother than if the mother and fetus are ABO incompatible.

In the presence of suspicious symptoms a number of test are helpful in the diagnosis:

- Muscle enzymes are often elevated, i.e. creatine kinase

- Anti-Jo-1 antibody testing

- Electromyography

- Muscle biopsy

- Pulmonary function testing

- Lung biopsy

In certain situations, testing of other antibodies, specific imaging (MRI, thoracic high resolution computed tomography), and swallowing evaluation may be needed.

Devon colic was a condition that affected people in the English county of Devon during parts of the 17th and 18th centuries, before it was discovered to be lead poisoning.

The first written account of the colic comes from 1655. Symptoms began with severe abdominal pains and the condition was occasionally fatal. Cider is the traditional drink of Devonians, and the connection between the colic and cider drinking had been observed for many years. The condition was commonly attributed to the acidity of the beverage.

William Musgrave's publication "De arthritide symptomatica" (2nd edn, 1715) included the first scientific description of "Devonshire colic" – it was later referred to by John Huxham and Sir George Baker.

However, the precise cause was not discovered until the 1760s when Dr George Baker put forward the hypothesis that poisoning from lead in cider was to blame. He observed that the symptoms of the colic were similar to those of lead poisoning. He pointed out that lead was used in the cider making process both as a component of the cider presses and in the form of lead shot which was used to clean them. He also conducted chemical tests to demonstrate the presence of lead in Devon apple juice.

The publication of his results met with some hostile reaction from cider manufacturers, keen to defend their product. Once Baker's conclusions became accepted and the elimination of lead from the cider presses was undertaken, the colic declined. By 1818, Baker's son reported that it was "hardly known to exist" in Devon.

The diagnosis of retroperitoneal fibrosis cannot be made on the basis of results of laboratory studies. CT is the best diagnostic modality: a confluent mass surrounding the aorta can be seen on a CT scan. Although biopsy is not usually recommended, it is appropriate when malignancy or infection is suspected. Biopsy should also be done if the location of fibrosis is atypical or if there is an inadequate response to initial treatment.

The 1951 Pont-Saint-Esprit mass poisoning, also known as Le Pain Maudit, occurred on 15 August 1951, in the small town of Pont-Saint-Esprit in southern France. More than 250 people were involved, including 50 persons interned in asylums and resulted in 7 deaths. A foodborne illness was suspected, and among these it was originally believed to be a case of "cursed bread" ("pain maudit").

Most academic sources accept ergot poisoning as the cause of the epidemic, while a few theorize other causes such as poisoning by mercury, mycotoxins, or nitrogen trichloride.

A dermatologist or general physician usually administers combination therapy of drugs used for tuberculosis, such as Rifampicin, Isoniazid and Pyrazinamide (possibly with either streptomycin or ethambutol).

In longstanding scarred lesions, squamous cell carcinoma can develop.

Shortly after the incident, in September 1951, scientists writing in the "British Medical Journal" declared that “the outbreak of poisoning” was due to eating bread made from rye grain that was infected with the fungus. The victims appeared to have one common connection. They had eaten bread from the bakery of Roch Briand who was subsequently blamed for using flour made from rye.