Lettuce big-vein disease causes leaf distortion and ruffling in affected lettuce plants.

This disease was first associated in 1983 with a rod-shaped virus named lettuce big-vein associated virus (LBVaV), which is transmitted by the obligately parasitic soil-inhabiting fungus, "Olpidium brassicae". However, in 2000, a second virus, "Mirafiori lettuce virus", was found in lettuce showing big-vein symptoms. Furthermore, since the lettuce infected with this virus alone developed big-vein symptoms, it is considered to be a main agent of the big-vein disease.

The main means of prevention is through the promotion of safe handling, cooking and consumption of food. This includes washing raw vegetables and cooking raw food thoroughly, as well as reheating leftover or ready-to-eat foods like hot dogs until steaming hot.

Another aspect of prevention is advising high-risk groups such as pregnant women and immunocompromised patients to avoid unpasteurized pâtés and foods such as soft cheeses like feta, Brie, Camembert cheese, and bleu. Cream cheeses, yogurt, and cottage cheese are considered safe. In the United Kingdom, advice along these lines from the Chief Medical Officer posted in maternity clinics led to a sharp decline in cases of listeriosis in pregnancy in the late 1980s.

Bacteremia should be treated for 2 weeks, meningitis for 3 weeks, and brain abscess for at least 6 weeks. Ampicillin generally is considered antibiotic of choice; gentamicin is added frequently for its synergistic effects. Overall mortality rate is 20–30%; of all pregnancy-related cases, 22% resulted in fetal loss or neonatal death, but mothers usually survive.

Disease cures are almost always more expensive and less effective than simple prevention measures. Often precautions involve maintaining a stable aquarium that is adjusted for the specific species of fish that are kept and not over-crowding a tank or over-feeding the fish. Common preventive strategies include avoiding the introduction of infected fish, invertebrates or plants by quarantining new additions before adding them to an established tank, and discarding water from external sources rather than mixing it with clean water. Similarly, foods for herbivorous fish such as lettuce or cucumbers should be washed before being placed in the tank. Containers that do not have water filters or pumps to circulate water can also increase stress to fish. Other stresses on fish and tanks can include certain chemicals, soaps and detergents, and impacts to tank walls causing shock waves that can damage fish.

In some cases the causes of an infection or disease will be obvious (such as fin rot), though in other cases it may be due to water conditions, requiring special testing equipment and chemicals to appropriately adjust the water. Isolating diseased fish can help prevent the spread of infection to healthy fish in the tank. This also allows the use of chemicals or drugs which may damage the nitrogen cycle, plants or chemical filtration of a properly-functioning tank. Other alternatives include short baths in a bucket that contains the treated water. Salt baths can be used as an antiseptic and fungicide, and will not damage beneficial bacteria, though ordinary table salt may contain additives which can harm fish. Alternatives include aquarium salt, Kosher salt or rock salt. Gradually raising the temperature of the tank may kill certain parasites, though some diseased fish may be harmed and certain species can not tolerate high temperatures. Aeration is necessary since less oxygen is dissolved in warm water.

There are a number of effective treatments for many stains of bacterial infections. Three of the most common are tetracycline, penicillin and naladixic acid. Salt baths are another effective treatment.

When properly diagnosed, the mortality of Lemierre's syndrome is about 4.6%. Since this disease is not well known and often remains undiagnosed, mortality might be much higher.

Lemierre's syndrome is primarily treated with antibiotics given intravenously. "Fusobacterium necrophorum" is generally highly susceptible to beta-lactam antibiotics, metronidazole, clindamycin and third generation cephalosporins while the other fusobacteria have varying degrees of resistance to beta-lactams and clindamycin. Additionally, there may exist a co-infection by another bacterium. For these reasons is often advised not to use monotherapy in treating Lemierre's syndrome. Penicillin and penicillin-derived antibiotics can thus be combined with a beta-lactamase inhibitor such as clavulanic acid or with metronidazole. Clindamycin can be given as monotherapy.

If antibiotic therapy does not improve the clinical picture, it may prove useful to drain any abscesses and/or perform ligation of the internal jugular vein where the antibiotic can not penetrate.

There is no evidence to opt for or against the use of anticoagulation therapy. The low incidence of Lemierre's syndrome has not made it possible to set up clinical trials to study the disease.

The disease can often be untreatable, especially if other negative factors occur, i.e. various diseases occurring at the same time, such as meningitis, pneumonia.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

"Verticillium" wilt begins as a mild, local infection, which over a few years will grow in strength as more virile strains of the fungus develop. If left unchecked the disease will become so widespread that the crop will need to be replaced with resistant varieties, or a new crop will need to be planted altogether.

Control of "Verticilium" can be achieved by planting disease free plants in uncontaminated soil, planting resistant varieties, and refraining from planting susceptible crops in areas that have been used repeatedly for solanaceous crops. Soil fumigation can also be used, but is generally too expensive over large areas.

In tomato plants, the presence of ethylene during the initial stages of infection inhibits disease development, while in later stages of disease development the same hormone will cause greater wilt. Tomato plants are available that have been engineered with resistant genes that will tolerate the fungus while showing significantly lower signs of wilting.

"Verticillium albo-altrum", "Verticilium dahliae" and "V. longisporum" can overwinter as melanized mycelium or microsclerotia within live vegetation or plant debris. As a result, it can be important to clear plant debris to lower the spread of disease. "Verticilium dahliae" and "V. longisporum" are able to survive as microsclerotia in soil for up to 15 years.

Susceptible tomato seedlings inoculated with arbuscular mycorrhizal fungi and "Trichoderma Harzianum" show increased resistance towards "Verticillium" wilt.

Hughes–Stovin syndrome is a rare autoimmune disorder of unknown cause that is characterized by the combination of multiple pulmonary artery aneurysms and deep vein thrombosis. It is named after the two British physicians, John Patterson Hughes and Peter George Ingle Stovin, who first described it in 1959. It is a rare variant of Behçet's disease, which entails more general problems with the circulatory system. Most patients are young adult males between the age of 20-40.

Common clinical presentations include fever, cough, dyspnea and hemoptysis. Radiological features are similar to those of Behçet's disease. There is no satisfactory treatment for this disease.

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

Phlegmasia alba dolens (also colloquially known as milk leg or white leg) is part of a spectrum of diseases related to deep vein thrombosis. Historically, it was commonly seen during pregnancy and in mothers who have just given birth. In cases of pregnancy, it is most often seen during the third trimester, resulting from a compression of the left common iliac vein against the pelvic rim by the enlarged uterus. Today, this disease is most commonly (40% of the time) related to some form of underlying malignancy. Hypercoagulability (a propensity to clot formation) is a well-known state that occurs in many cancer states. The incidence of this disease is not well reported.

Banti's syndrome (also known as Banti's disease), named for is Guido Banti., is a chronic congestive enlargement of the spleen resulting in premature destruction of the red blood cells by the spleen.

Treatment for Thrombotic Storm may include lifelong anticoagulation therapy and/or thrombolytic therapy, plasmapherisis, and corticosteroids. Studies have shown that when anticoagulant therapy is withheld recurrence of thrombosis usually follows. INR is closely monitored in the course of treatment.

Phlegmasia alba dolens literally means "painful white edema". It received the name "milk leg" because it was once thought to be caused by the metastasis of milk.

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

Surgery to remove the clot is possible, but rarely performed. In the past, surgical removal of the renal vein clot was the primary treatment but it is very invasive and many complications can occur. In the past decades, treatment has shifted its focus from surgical intervention to medical treatments that include intravenous and oral anticoagulants. The use of anticoagulants may improve renal function in RVT cases by removing the clot in the vein and preventing further clots from occurring. Patients already suffering from nephrotic syndrome may not need to take anticoagulants. In this case, patients should keep an eye out and maintain reduced level of proteinuria by reducing salt and excess protein, and intaking diuretics and statins. Depending on the severity of RVT, patients may be on anticoagulants from a year up to a lifetime. As long as the albumen levels in the bloodstream are below 2.5g/L, it is recommended that RVT patients continue taking anticoagulants. Main anticoagulants that can be used to treat RVT include warfarin and low molecular weight heparin. Heparin has become very popular, because of its low risk of complications, its availability and because it can easily be administered. Warfarin is known to interact with many other drugs, so careful monitoring is required. If a nephrotic syndrome patient experiences any of the RVT symptoms (flank or back pain, blood in the urine or decreased renal function), he or she should immediately see a doctor to avoid further complications.

The main side effect of anticoagulants is the risk of excessive bleeding. Other side effects include: blood in the urine or feces, severe bruising, prolonged nosebleeds (lasting longer than 10 minutes), bleeding gum, blood in your vomit or coughing up blood, unusual headaches, sudden severe back pain, difficulty breathing or chest pain, in women, heavy or increased bleeding during the period, or any other bleeding from the vagina. Warfarin can cause rashes, diarrhea, nausea (feeling sick) or vomiting, and hair loss. Heparin can cause hair loss (alopecia) thrombocytopenia – a sudden drop in the number of platelets in the blood.

It has been reported in a case study of 27 patients with nephrotic syndrome caused RVT, there was a 40% mortality rate, mostly due to hemorrhagic complications and sepsis. In 75% of the remaining surviving patients, the RVT was resolved and renal function returned to normal. It has been concluded that age is not a factor on the survival of RVT patients, although older patient (55 and older) are more likely to develop renal failure. Heparin is crucial in returning normal renal function; in patients that did not take heparin, long term renal damage was observed in 100%. In patients that did take heparin, renal damage was observed in about 33%. By quickly treating, and receiving the correct medications, patients should increase their chances of survival and reduce the risk of the renal vein clot from migrating to another part of the body.

Cruveilhier–Baumgarten disease or Pégot-Cruveilhier–Baumgarten disease is a rare medical condition in which the umbilical or paraumbilical veins are distended, with an abdominal wall bruit (the Cruveilhier-Baumgarten bruit) and palpable thrill, portal hypertension with splenomegaly, hypersplenism and oesophageal varices, with a normal or small liver.

It was first described by Pégot in 1833, and then by Jean Cruveilhier (1835) and Paul Clemens von Baumgarten (1907).

Armstrong "et al." (1942) and Steinburg and Galambos (1967) described two different types of the condition:

- Cruveilhier-Baumgarten syndrome: liver cirrhosis or portal hypertension is the cause of the distension of the paraumbilical veins (i.e. an "acquired" condition in which the veins reopen due to high portal pressure).

- Cruveilhier–Baumgarten disease: the distension of the paraumbilical veins is due to failure of umbilical vein closure, with little or no evidence of liver disease found on liver biopsy (i.e. a "congenital" patency of the umbilical vein leading to portal hypertension).

The causes for PWS are either genetic or unknown. Some cases are a direct result of the RASA1 gene mutations. And individuals with RASA1 can be identified because this genetic mutation always causes multiple capillary malformations. PWS displays an autosomal dominant pattern of inheritance. This means that one copy of the damaged or altered gene is sufficient to elicit PWS disorder. In most cases, PWS can occur in people that have no family history of the condition. In such cases the mutation is sporadic. And for patients with PWS with the absence of multiple capillary mutations, the causes are unknown.

According to Boston’s Children Hospital, no known food, medications or drugs can cause PWS during pregnancy. PWS is not transmitted from person to person. But it can run in families and can be inherited. PWS effects both males and females equally and as of now no racial predominance is found

At the moment, there are no known measures that can be taken in order to prevent the onset of the disorder. But Genetic Testing Registry can be great resource for patients with PWS as it provides information of possible genetic tests that could be done to see if the patient has the necessary mutations. If PWS is sporadic or does not have RASA1 mutation then genetic testing will not work and there is not a way to prevent the onset of PWS.

Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm HO or else portal hypertension will ensue. Methods of shunt attenuation should aim to slowly occlude the vessel over several weeks to months in order to avoid complications associated with portal hypertension. These methods include ameroid ring constrictors, cellophane banding, intravascular or percutaneous silicone hydraulic occluders. The most common methods of attenuation used by veterinarians are ameroid ring constrictors and cellophane banding. Both methods have reportedly good outcomes in both cats and dogs, although the true composition of readily sourced cellophane has been found to be made from plastics (inert) and not cellulose (stimulates a fibrous reaction). Recently, a commercial supplier of regenerated cellulose based cellophane for veterinarians has been established for use of cellophane banding for portosystemic shunts in dogs and cats. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. When surgery is not an option, PSS is treated as are other forms of liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.

A minority of patients can be treated medically with sodium restriction, diuretics to control ascites, anticoagulants such as heparin and warfarin, and general symptomatic management. The majority of patients require further intervention. Milder forms of Budd–Chiari may be treated with surgical shunts to divert blood flow around the obstruction or the liver itself. Shunts must be placed early after diagnosis for best results. The TIPS is similar to a surgical shunt: it accomplishes the same goal but has a lower procedure-related mortality—a factor that has led to a growth in its popularity. If all the hepatic veins are blocked, the portal vein can be approached via the intrahepatic part of inferior vena cava, a procedure called DIPS (direct intrahepatic portocaval shunt). Patients with stenosis or vena caval obstruction may benefit from angioplasty. Limited studies on thrombolysis with direct infusion of urokinase and tissue plasminogen activator into the obstructed vein have shown moderate success in treating Budd–Chiari syndrome; however, it is not routinely attempted.

Liver transplantation is an effective treatment for Budd–Chiari. It is generally reserved for patients with fulminant liver failure, failure of shunts or progression of cirrhosis that reduces the life expectancy to 1 year. Long-term survival after transplantation ranges from 69–87%. The most common complications of transplant include rejection, arterial or venous thromboses and bleeding due to anticoagulation. Up to 10% of patients may have a recurrence of Budd–Chiari syndrome after the transplant.

There is no specific treatment for thrombophilia, unless it is caused by an underlying medical illness (such as nephrotic syndrome), where the treatment of the underlying disease is needed. In those with unprovoked and/or recurrent thrombosis, or those with a high-risk form of thrombophilia, the most important decision is whether to use anticoagulation medications, such as warfarin, on a long-term basis to reduce the risk of further episodes. This risk needs to weighed against the risk that the treatment will cause significant bleeding, as the reported risk of major bleeding is over 3% per year, and 11% of those with major bleeding may die as a result.

Apart from the abovementioned forms of thrombophilia, the risk of recurrence after an episode of thrombosis is determined by factors such as the extent and severity of the original thrombosis, whether it was provoked (such as by immobilization or pregnancy), the number of previous thrombotic events, male sex, the presence of an inferior vena cava filter, the presence of cancer, symptoms of post-thrombotic syndrome, and obesity. These factors tend to be more important in the decision than the presence or absence of a detectable thrombophilia.

Those with antiphospholipid syndrome may be offered long-term anticoagulation after a first unprovoked episode of thrombosis. The risk is determined by the subtype of antibody detected, by the antibody titer (amount of antibodies), whether multiple antibodies are detected, and whether it is detected repeatedly or only on a single occasion.

Women with a thrombophilia who are contemplating pregnancy or are pregnant usually require alternatives to warfarin during pregnancy, especially in the first 13 weeks, when it may produce abnormalities in the unborn child. Low molecular weight heparin (LMWH, such as enoxaparin) is generally used as an alternative. Warfarin and LMWH may safely be used in breastfeeding.

When women experience recurrent pregnancy loss secondary to thrombophilia, some studies have suggested that low molecular weight heparin reduces the risk of miscarriage. When the results of all studies are analysed together, no statistically signifiant benefit could be demonstrated.

According to NIH clinical trials.gov, research on the port-wine stain and its relation to polymorphisms of RASA1 has commenced in November 2010 and expected to end in November 2019. The purpose of the study is to assess how the port-wine stains can lead to complex syndromes such as PWS. Currently there is little knowledge about the epidemiology of the stains and how they progress with the disease. The research is ongoing and the results are yet to be published.

In an another review published in July 2017 (discussed in treatments and prognosis), Banzic et. al. discussed clinical findings that embolization works really well in patients with PWS. Also, embolization along with surgical resection that targets arteriovenous malformations reliably leads to significant clinical improvements.

In some cases, foot diseases and painful conditions can be treated. Synovium hydrates the cartilage in the heal and can bring pain relief quickly. Synovium gel looks as well as strongly smells like urine, straying some consumers away. However this only occurs after expiration. Blood thinners can also work however are deemed as bad relievers by medical practitioners due to the fact that they can contribute to headaches and in some cases increase foot pain afterwards.

Treatment usually consists of NSAIDs, such as ibuprofen and local compression (e.g., by compression stockings or a compress). If the phlebitis is associated with local bacterial infection, antibiotics may be used.

For acute infusion superficial thrombophlebitis, not enough evidence exists as of 2015 to determine treatment.