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.

Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, or possibly contaminated materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, ought to be discouraged or modified, ideally with the help of local traditional healers.

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.

The viral strains fall into two clades — Ravn virus and Marburg virus. The Marburg strains can be divided into two — A and B. The A strains were isolated from Uganda (five from 1967), Kenya (1980) and Angola (2004–2005) while the B strains were from the Democratic Republic of the Congo epidemic (1999–2000) and a group of Ugandan isolates isolated in 2007-2009.

The mean evolutionary rate of the whole genome was 3.3 × 10 substitutions/site/year (credibility interval 2.0–4.8).The Marburg strains had a mean root time of the most recent common ancestor of 177.9 years ago (95% highest posterior density 87–284) suggesting an origin in the mid 1800s. In contrast the Ravn strains origin dated back to a mean 33.8 years ago (early 1980s). The most probable location of the Marburg virus ancestor was Uganda whereas that of the RAVV ancestor was Kenya.

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.

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.

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.

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.

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.

Spring viraemia of carp virus has been shown to infect a wide variety of fish species including silver carp, grass carp, crucian carp, and bighead carp. It has also been shown experimentally to infect other fish species including northern pike, guppies, zebrafish, and pumpkinseed. It is considered to be a major threat to naive fish populations, especially farmed fish including ornamental koi and common carp.

Konzo is an epidemic paralytic disease occurring in outbreaks in remote rural areas of low income African countries. The people of these regions have been associated with several weeks of almost exclusive consumption of insufficiently processed "bitter" (high cyanide) cassava ("Manihot esculenta")—a perennial crop native to Amazonia in South America, but widely cultivated in tropical regions worldwide. It is the third most important food source in the tropics after rice and maize and is the staple food of tropical Africa. Cassava yields well in poor soils, is drought-resistant, and the roots give food security during droughts and famine. Nutritionally, the starchy roots are complemented by consumption of cassava leaves, which are rich in proteins and vitamins. Konzo was first described by Giovanni Trolli in 1938 who compiled the observations from eight doctors working in the Kwango area of the Belgian Congo (now Democratic Republic of the Congo).

The character of the neurological injury is not clear. The disease onset is associated with high intake of cyanide from a monotonous diet of bitter cassava, which is low in protein, particularly sulfur amino acids. These are essential for the detoxification in the body of cyanide to thiocyanate, which is removed in the urine. A number of studies implicate the combination of high cyanide intake from bitter cassava and low intake of sulfur amino acids as the cause. It has now been shown that the month by month incidence of konzo is significantly correlated with the percentage of children with high urinary thiocyanate content, which is a measure of their cyanide intake. The importance of an adequate supply of protein sulfur amino acids is shown from three unrelated konzo epidemics in Mozambique, Tanzania and DRC. People of the same ethnic group living only 5 km away from those with konzo had near zero konzo prevalence, because in Mozambique they lived near the sea, in Tanzania they lived near Lake Victoria and had access to fish and in DRC they lived near the forest and had access to animal protein.

The dose-response relationship between konzo incidence and cyanide intake, together with the prevention of konzo in many villages by reducing cyanide intake from cassava (see below) and the importance of sulfur amino acids in prevention of konzo, shows that konzo is very likely due to high cyanide/low sulfur amino acid intake in a diet of bitter cassava. Konzo does not occur unless these conditions are met, which occurs only in remote villages in six tropical African countries. The total number of reported cases up to 2009 was 6788, but most cases are never reported and there was an estimate of 100,000 cases in DRC alone in 2002. Konzo is spreading geographically as cassava is being grown in new areas where there is little knowledge of processing methods to remove cyanogens. Konzo epidemics occur due to war which causes disruption of life in poor villages and drought, when the plant increases the cyanogen content of roots 2-4 times and the cyanide content of cassava flour also increases greatly. Konzo is also endemic in certain areas.

Traditional methods of processing cassava to remove cyanogens consist of sun drying and heap fermentation in East Africa, which are inadequate in removal of cyanogens even in a year of normal rainfall. In Central Africa soaking (retting) of cassava roots in water for 4–5 days is adequate, but short soaking for 1–2 days leaves large amounts of cyanogens in flour and leads to konzo. In West Africa a roasted product called gari is produced by a different method than that used to produce flour, which reduces the total cyanide content to 10-20 ppm. There are no reported cases of konzo west of Cameroon. However another neurological disease called tropical ataxic neuropathy (TAN), occurs amongst older people in south-west Nigeria, Tanzania, Uganda, Kenya, West Indies and South India, and is probably due to long term intake of cyanogens from cassava at a lower level than that needed to cause konzo.

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.

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.

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 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.

It is named for the neurosurgeon Theodore Rasmussen (1910–2002), who succeeded Wilder Penfield as head of the Montreal Neurological Institute, and served as Neurosurgeon-in-Chief at the Royal Victoria Hospital.

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.

The Tanganyika laughter epidemic of 1962 was an outbreak of mass hysteriaor mass psychogenic illness (MPI)rumored to have occurred in or near the village of Kashasha on the western coast of Lake Victoria in the modern nation of Tanzania (formerly Tanganyika) near the border of Uganda.

One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.

The laughter epidemic began on January 30, 1962, at a mission-run boarding school for girls in Kashasha. The laughter started with three girls and spread haphazardly throughout the school, affecting 95 of the 159 pupils, aged 12–18. Symptoms lasted from a few hours to 16 days in those affected. The teaching staff were not affected but reported that students were unable to concentrate on their lessons. The school was forced to close down on March 18, 1962.

After the school was closed and the students were sent home, the epidemic spread to Nshamba, a village that was home to several of the girls. In April and May, 217 people had laughing attacks in the village, most of them being school children and young adults. The Kashasha school was reopened on May 21, only to be closed again at the end of June. In June, the laughing epidemic spread to Ramashenye girls’ middle school, near Bukoba, affecting 48 girls.

The school from which the epidemic sprang was sued; the children and parents transmitted it to the surrounding area. Other schools, Kashasha itself, and another village, comprising thousands of people, were all affected to some degree. Six to eighteen months after it started, the phenomenon died off. The following symptoms were reported on an equally massive scale as the reports of the laughter itself: pain, fainting, flatulence, respiratory problems, rashes, attacks of crying, and random screaming. In total 14 schools were shut down and 1000 people were affected.

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.

Treatments to reduce the discomfort from tonsillitis include:

- pain and fever reducing medications such as paracetamol (acetaminophen) and ibuprofen

- warm salt water gargle, lozenges, or warm liquids

When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, symptoms may last for up to two weeks.

There is no known treatment for FTS, as the cause is not yet known. There are conflicting reports on whether the paralysis is reversible; some sources claim that moving an elephant away from the area in which it contracted the condition will allow it to recover, while others claim that damage to the trunk is irreversible.

In some extreme cases, wildlife managers have killed affected elephants for humane reasons.

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.