There is currently no effective marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis. Novel, very promising, experimental therapeutic regimens rely on antisense technology: phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome could prevent disease in nonhuman primates. Leading medications from Sarepta and Tekmira both have been successfully used in European humans as well as primates.

There are currently no Food and Drug Administration-approved vaccines for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models. Of those, the most promising ones are DNA vaccines or based on Venezuelan equine encephalitis virus replicons, vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials. Marburgviruses are highly infectious, but not very contagious. Importantly, and contrary to popular belief, marburgviruses do not get transmitted by aerosol during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on behavior modification, proper personal protective equipment, and sterilization/disinfection.

If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within two days of symptoms). Beside antivirals, supportive care at home or in a hospital focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of oseltamivir (Tamiflu) or zanamivir (Relenza) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. The virus isolated in the 2009 outbreak have been found resistant to amantadine and rimantadine.

In the U.S., on April 27, 2009, the FDA issued Emergency Use Authorizations to make available Relenza and Tamiflu antiviral drugs to treat the swine influenza virus in cases for which they are currently unapproved. The agency issued these EUAs to allow treatment of patients younger than the current approval allows and to allow the widespread distribution of the drugs, including by volunteers.

As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead, veterinary efforts are focused on preventing the spread of the virus throughout the farm, or to other farms. Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds.

Marburg virus is a hemorrhagic fever virus of the "Filoviridae" family of viruses and a member of the species "Marburg marburgvirus", genus "Marburgvirus". Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. Considered to be extremely dangerous, the WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.

In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.

Thoroughly cleaning boats, trailers, nets and other equipment when traveling between different lakes and streams also

helps. The only EPA-approved disinfectant proven effective against VHS is Virkon AQUATIC (made by Dupont). Chlorine bleach kills the VHS virus, but in concentrations that are much too caustic for ordinary use. Disinfecting stations can be found at various inland lake boat launches in the Great Lakes region.

MARV is one of two Marburg viruses that causes Marburg virus disease (MVD) in humans (in the literature also often referred to as Marburg hemorrhagic fever, MHF). The other one is Ravn virus (RAVV). Both viruses fulfill the criteria for being a member of the species Marburg marburgvirus because their genomes diverge from the prototype Marburg marburgvirus or the Marburg virus variant Musoke (MARV/Mus) by <10% at the nucleotide level.

Spring viraemia of carp, also known as Swim Bladder Inflammation, is caused by a rhabdovirus called "Rhabdovirus carpio". It is listed as a notifiable disease under the World Organisation for Animal Health.

Viral hemorrhagic septicemia (VHS) is a deadly infectious fish disease caused by viral hemorrhagic septicemia virus (VHSV). It afflicts fish of over 50 species of freshwater

and marine fish in several parts of the northern hemisphere.

VHS is caused by viral hemorrhagic septicemia virus (VHSV), different strains of which occur in different regions, and affect different species. There are no signs that the disease affects human health. VHS is also known as "Egtved disease," and VHSV as "Egtved virus."

Historically, VHS was associated mostly with freshwater salmonids in western Europe,

documented as a pathogenic disease among cultured salmonids since the 1950s. Today it is still a major concern for many fish farms in Europe and is therefore being watched closely by the European Community Reference Laboratory for Fish Diseases.

It was first discovered in the US in 1988 among salmon returning from the Pacific in Washington State. This North American genotype was identified as a distinct, more marine-stable strain than the European genotype. VHS has since been found afflicting marine fish in the northeastern

Pacific Ocean, the North Sea, and the Baltic Sea. Since 2005, massive die-offs have occurred among a wide variety of freshwater species in the Great Lakes region of North America.

Clinical symptoms of viral infection include external hemorrhaging, pale gills, and ascites. In some cases, mortality can occur without any apparent clinical signs of the disease. The virus has been found in high concentrations in the liver and kidney, but lower numbers of virions have been isolated from the spleen. The virus has been shown to persist subclinically in fish populations up to 10 weeks following experimental infection. Currently efforts have been made to prevent infection by the virus through the development of DNA vaccines and immunostimulatory therapeutics.

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.

Although no treatment has been found it has been shown that affected individuals benefit considerably from rehabilitation and use of adequate walking aids. In the Central African Republic some children have been operated with an elongation of the Achilles tendon which improved the position of the foot but the long term consequence remains uncertain.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

Konzo can be prevented by use of the “wetting method,” which is used to remove residual cyanogens from cassava flour, as an additional processing method. Cassava flour is placed in a bowl and the level marked on the inside of the bowl. Water is added with mixing until the height of the wet flour comes up to the mark. The wet flour is placed in a thin layer on a mat for 2 hours in the sun or 5 hours in the shade to allow the escape of hydrogen cyanide produced by the breakdown of linamarin by the enzyme linamarase. The damp flour is then cooked in boiling water in the traditional way to produce a thick porridge called “fufu” or “ugali”, which is flavoured by some means such as a sauce. The wetting method is accepted by rural women because it requires little extra work or equipment and produces fufu which is not bitter, because the bitter tasting linamarin has gone.

In 2010 the wetting method was taught to the women in Kay Kalenge village, Popokabaka Health Zone, Bandundu Province, DRC, where there were 34 konzo cases. The women used the method and during the intervention there were no new konzo cases and the urinary thiocyanate content of the school children fell to safe levels. Konzo had been prevented for the first time ever in the same health zone in which it had first been discovered by Dr Trolli in 1938. Fourteen months after the intervention ceased the village was visited again. It was found that there were no new cases of konzo, the school children had low urinary thiocyanate levels, the wetting method was still being used and it had spread by word of mouth to three nearby villages. It is important to teach the women that konzo is due to a poison present in their food, to get them to regularly use the wetting method and posters are available in 13 different languages as a teaching aid as an additional method to remove residual cyanogens.

The wetting method has now been used in 13 villages in DRC with nearly 10000 people. The time of the intervention has been reduced from 18 months in the first intervention, to 12 months in the second intervention, to 9 months in the third and fourth interventions. This has reduced the cost per person of the intervention to prevent konzo by removing cyanogens from cassava flour, to $16 per person. This targeted method to reduce cyanide intake is much cheaper and more effective in preventing konzo than broad based interventions.

Chronic cases may be treated with tonsillectomy (surgical removal of tonsils) as a choice for treatment. Children have had only a modest benefit from tonsillectomy for chronic cases of tonsillitis.

If the tonsillitis is caused by group A streptococcus, then antibiotics are useful, with penicillin or amoxicillin being primary choices. Cephalosporins and macrolides are considered good alternatives to penicillin in the acute setting. A macrolide such as erythromycin is used for people allergic to penicillin. Individuals who fail penicillin therapy may respond to treatment effective against beta-lactamase producing bacteria such as clindamycin or amoxicillin-clavulanate. Aerobic and anaerobic beta lactamase producing bacteria that reside in the tonsillar tissues can "shield" group A streptococcus from penicillins.

WAD is typically self-limited, generally resolving without specific treatment. Oral rehydration therapy with rehydration salts is often beneficial to replace lost fluids and electrolytes. Clear, disinfected water or other liquids are routinely recommended.

Hikers who develop three or more loose stools in a 24-hour period – especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools – should be treated by a doctor and may benefit from antibiotics, usually given for 3–5 days. Alternatively, a single dose azithromycin or levofloxacin may be prescribed. If diarrhea persists despite therapy, travelers should be evaluated and treated for possible parasitic infection.

"Cryptosporidium" can be quite dangerous to patients with compromised immune systems. Alinia (nitazoxanide) is approved by the FDA for treatment of "Cryptosporidium".

Since wilderness acquired diarrhea can be caused by insufficient hygiene, contaminated water, and (possibly) increased susceptibility from vitamin deficiency, prevention methods should address these causes.

Tetrabenazine was approved in 2008 for treatment of chorea in Huntington's disease in the US. Other drugs that help to reduce chorea include neuroleptics and benzodiazepines. Compounds such as amantadine or remacemide are still under investigation but have shown preliminary positive results. Hypokinesia and rigidity, especially in juvenile cases, can be treated with antiparkinsonian drugs, and myoclonic hyperkinesia can be treated with valproic acid.

Psychiatric symptoms can be treated with medications similar to those used in the general population. Selective serotonin reuptake inhibitors and mirtazapine have been recommended for depression, while atypical antipsychotic drugs are recommended for psychosis and behavioral problems. Specialist neuropsychiatric input is recommended as people may require long-term treatment with multiple medications in combination.

Crayfish plague, "Aphanomyces astaci", is a water mold that infects crayfish, most notably the European "Astacus" which dies within a few weeks of being infected. When experimentally tested, species from Australia, New Guinea and Japan were also found to be susceptible to the infection.

The disease prognosis includes:

- Spread of infection to other areas of body can occur through the bloodstream (bacteremia), including septic arthritis. Glomerulonephritis can follow an episode of streptococcal erysipelas or other skin infection, but not rheumatic fever.

- of infection: Erysipelas can recur in 18–30% of cases even after antibiotic treatment. A chronic state of recurrent erysipelas infections can occur with several predisposing factors including alcoholism, diabetes, and tinea pedis (athlete's foot). Another predisposing factor is chronic cutaneous edema, such as can in turn be caused by venous insufficiency or heart failure.

- Lymphatic damage

- Necrotizing fasciitis, commonly known as "flesh-eating" bacterial infection, is a potentially deadly exacerbation of the infection if it spreads to deeper tissue.

Weight loss and eating difficulties due to dysphagia and other muscle discoordination are common, making nutrition management increasingly important as the disease advances. Thickening agents can be added to liquids as thicker fluids are easier and safer to swallow. Reminding the affected person to eat slowly and to take smaller pieces of food into the mouth may also be of use to prevent choking. If eating becomes too hazardous or uncomfortable, the option of using a percutaneous endoscopic gastrostomy is available. This is a feeding tube, permanently attached through the abdomen into the stomach, which reduces the risk of aspirating food and provides better nutritional management. Assessment and management by speech-language pathologists with experience in Huntington's disease is recommended.

People with Huntington's disease may see a physical therapist for non-invasive and non-medication-based ways of managing the physical symptoms. Physical therapists may implement fall risk assessment and prevention, as well as strengthening, stretching, and cardiovascular exercises. Walking aids may be prescribed as appropriate. Physical therapists also prescribe breathing exercises and airway clearance techniques with the development of respiratory problems. Consensus guidelines on physiotherapy in Huntington's disease have been produced by the European HD Network. Goals of early rehabilitation interventions are prevention of loss of function. Participation in rehabilitation programs during early to middle stage of the disease may be beneficial as it translates into long term maintenance of motor and functional performance. Rehabilitation during the late stage aims to compensate for motor and functional losses. For long-term independent management, the therapist may develop home exercise programs for appropriate people.

Additionally, an increasing number of people with Huntington’s disease are turning to palliative care, which aims to improve quality of life through the treatment of the symptoms and stress of serious illness, in addition to their other treatments.

Crayfish plague first arrived in Europe in Italy in 1859, either with imported crayfish from North America, or in ballast water. After its original introduction in Italy in 1860, it spread quickly through Europe and was discovered in Sweden in 1907, in Spain in 1972, in Norway in 1971, in Great Britain in 1981, in Turkey in 1984 and in Ireland in 1987.

In 1959, to bolster dwindling stocks of native crayfish, the signal crayfish was introduced to Sweden. The signal crayfish was known to be resistant, and it was not recognised at that time that it was a carrier of the disease. After 150 years of contact, no resistance has been discovered in native European crayfish.

This species was studied and named by the German Mycologist, Friedrich Schikora (1859–1932), from a type specimen in Germany in 1906.

Desmopressin (DDAVP) may be used in those with mild haemophilia A. Tranexamic acid or epsilon aminocaproic acid may be given along with clotting factors to prevent breakdown of clots.

Pain medicines, steroids, and physical therapy may be used to reduce pain and swelling in an affected joint.

Various strategies targeting the mollusc and avian hosts of schistosomes, have been used by lakeside residents in recreational areas of North America to deal with outbreaks of swimmer's itch. In Michigan, for decades, authorities used copper sulfate as a molluscicide to reduce snail host populations and thereby the incidence of swimmer's itch. The results with this agent have been inconclusive, possibly because:

- Snails become tolerant

- Local water chemistry reduces the molluscicide's efficacy

- Local currents diffuse it

- Adjacent snail populations repopulate a treated area

More importantly, perhaps, copper sulfate is toxic to more than just molluscs, and the effects of its use on aquatic ecosystems are not well understood.

Another method targeting the snail host, mechanical disturbance of snail habitat, has been also tried in some areas of North America and Lake Annecy in France, with promising results. Some work in Michigan suggests that administering praziquantel to hatchling waterfowl can reduce local swimmer's itch rates in humans. Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice. Public education of risk factors, a good alternative to the aforementioned interventionist strategies, can also reduce human exposure to cercariae.