The disease can be prevented in horses with the use of vaccinations. These vaccinations are usually given together with vaccinations for other diseases, most commonly WEE, VEE, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans there is no vaccine for EEE so prevention involves reducing the risk of exposure. Using repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention

A vaccine is available in the UK and Europe, however in laboratory tests it is not possible to distinguish between antibodies produced as a result of vaccination and those produced in response to infection with the virus. Management also plays an important part in the prevention of EVA.

There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.

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.

People reduce the chance of getting infected with LACV by preventing mosquito bites. There is no vaccine or preventive drug.

Prevention measures against LACV include reducing exposure to mosquito bites. Use repellent such as DEET and picaridin, while spending time outside, especially at during the daytime - from dawn until dusk. "Aedes triseriatus" mosquitoes that transmit (LACV) are most active during the day. Wear long sleeves, pants and socks while outdoors. Ensure all screens are in good condition to prevent mosquitoes from entering your home. "Aedes triseriatus" prefer treeholes to lay eggs in. Also, remove stagnant water such as old tires, birdbaths, flower pots, and barrels.

Marburgviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment, laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.

Equine viral arteritis (EVA) is a disease of horses caused by equine arteritis virus, an RNA virus of the genus "Arterivirus". The virus which causes EVA was first isolated in 1953, but the disease has afflicted equine animals worldwide for centuries. It has been more common in some breeds of horses in the United States, but there is no breed "immunity". In the UK, it is a notifiable disease. There is no known human hazard.

No specific therapy is available at present for La Crosse encephalitis, and management is limited to alleviating the symptoms and balancing fluids and electrolyte levels. Intravenous ribavirin is effective against La Crosse encephalitis virus in the laboratory, and several studies in patients with severe, brain biopsy confirmed, La Crosse encephalitis are ongoing.

In a trial with 15 children being infected with La Crosse viral encephalitis were treated at certain phases with ribavirin (RBV). RBV appeared to be safe at moderate doses. At escalated doses of RBV, adverse events occurred and then the trial was discontinued. Nonetheless, this was the largest study of antiviral treatment for La Crosse encephalitis.

Unfortunately a vaccine for malignant catarrhal fever (MCF) has not yet been developed. Developing a vaccine has been difficult because the virus will not grow in cell culture and until recently it was not known why. Researchers at the Agricultural Research Service (ARS) found that the virus undergoes changes within the animal's body, a process known as "cell tropism switching". In cell tropism switching, the virus targets different cells at different points in its life cycle. This phenomenon explains why it has been impossible to grow the virus on any one particular cell culture.

Because the virus is transmitted from sheep to bison and cattle, researchers are first focusing on the viral life cycle in sheep. The viral life cycle is outlined in three stages: entry, maintenance, and shedding. Entry occurs through the sheep's nasal cavity and enters into the lungs where it replicates. The virus undergoes a tropic change and infects lymphocytes, also known as white blood cells, which play a role in the sheep's immune system. In the maintenance stage the virus remains on the sheep's lymphocytes and circulates the body. Finally, during the shedding stage, the virus undergoes another change and shifts its target cells from lymphocytes to nasal cavity cells, where it is then shed through nasal secretions. This discovery undoubtedly puts scientists on the right track for developing a vaccine – starting with the correct cell culture for each stage of the virus lifecycle – but ARS researchers are also looking into alternative methods to develop a vaccine. Researchers are experimenting with the MCF virus that infects topi (an African antelope) because it will grow in cell culture and does not infect cattle. Researchers hope that inserting genes from the sheep MCF virus into the topi MCF virus will ultimately be an effective MCF vaccine for cattle and bison. While there is much ground left to cover, scientists are getting closer and closer to developing a vaccine.

The term "bovine malignant catarrhal fever" has been applied to three different patterns of disease:

- In Africa, wildebeests carry a lifelong infection of AlHV-1 but are not affected by the disease. The virus is passed from mother to offspring and shed mostly in the nasal secretions of wildebeest calves under one year old. Wildebeest associated MCF is transmitted from wildebeest to cattle normally following the wildebeest calving period. Cattle of all ages are susceptible to the disease, with a higher infection rate in adults, particularly in peripartuent females. Cattle are infected by contact with the secretions, but do not spread the disease to other cattle. Because no commercial treatment or vaccine is available for this disease, livestock management is the only method of control. This involves keeping cattle away from wildebeest during the critical calving period. This results in Massai pastoralists in Tanzania and Kenya being excluded from prime pasture grazing land during the wet season leading to a loss in productivity. In Eastern and Southern Africa MCF is classed as one of the five most important problems affecting pastoralists along with East coast fever, contagious bovine pleuropneumonia, foot and mouth disease and anthrax.Hartebeests and topi also may carry the disease. However, hartebeests and other antelopes are infected by a variant, Alcelaphine herpesvirus 2.

- Throughout the rest of the world, cattle and deer contract BMCF by close contact with sheep or goats during lambing. The natural host reservoir for Ovine herpesvirus 2 is the subfamily Caprinae (sheep and goats) whilst MCF affected animals are from the families Bovidae, Cervidae and suidae. Susceptibility to OHV-2 varies by species, with domestic cattle and zebus somewhat resistant, water buffalo and most deer somewhat susceptible, and bison, Bali cattle, and Pere David's deer very susceptible. OHV-2 viral DNA has been detected in the alimentary, respiratory and urino-genital tracts of sheep all of which could be possible transmission routes. Antibody from sheep and from cattle with BMCF is cross reactive with AlHV-1.

- AHV-1/OHV-2 can also cause problems in zoological collections, where inapparently infected hosts (wildebeest and sheep) and susceptible hosts are often kept in close proximity.

- Feedlot bison in North America not in contact with sheep have also been diagnosed with a form of BMCF. OHV-2 has been recently documented to infect herds of up to 5 km away from the nearest lambs, with the levels of infected animals proportional to the distance away from the closest herds of sheep.

The incubation period of BMCF is not known, however intranasal challenge with AHV-1 induced MCF in one hundred percent of challenged cattle between 2.5 and 6 weeks.

Shedding of the virus is greater from 6–9 month old lambs than from adults. After experimental infection of sheep, there is limited viral replication in nasal cavity in the first 24 hours after infection, followed by later viral replication in other tissues.

A vaccine is available, called "Chinese Live Attenuated EIA vaccine", developed in China and widely used there since 1983. Another attenuated live virus vaccine is in development in the United States.

Reuse of syringes and needles is a risk factor for transfer of the disease. Currently in the United States, all horses that test positive must be reported to federal authorities by the testing laboratory. EIA-positive horses are infected for life. Options for the horse include sending the horse to a recognized research facility, branding the horse and quarantining it at least 200 yards from other horses for the rest of its life, and euthanizing the horse. Very few quarantine facilities exist, which usually leads to the option of euthanizing the horse. The Florida Research Institute for Equine Nurturing, Development and Safety (a.k.a. F.R.I.E.N.D.S.) is one of the largest such quarantine facilities and is located in south Florida.

The horse industry and the veterinary industry strongly suggest that the risks posed by infected horses, even if they are not showing any clinical signs, are enough of a reason to impose such stringent rules. The precise impacts of the disease on the horse industry are unknown.

Zika virus vaccine clinical trials are to be conducted and established. There are efforts being put toward advancing antiviral therapeutics against zika virus for swift control. Present day Zika virus treatment is symptomatic through antipyretics and analgesics. Currently there are no publications regarding viral drug screening. Nevertheless, therapeutics for this infection have been used.

West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, specifically from the genus Flavivirus which also contain the Zika virus, dengue virus, and the yellow fever virus. The West Nile virus is primarily transmitted through mosquitoes, mostly by the Culex species. However, ticks have been found to carry the virus. The primary hosts of WNV are birds, so that the virus remains within a "bird-mosquito-bird" transmission cycle.

The Coggins test (agar immunodiffusion) is a sensitive diagnostic test for equine infectious anemia developed by Dr. Leroy Coggins in the 1970s.

Currently, the US does not have an eradication program due to the low rate of incidence. However, many states require a negative Coggins test for interstate travel. In addition, most horse shows and events require a negative Coggins test. Most countries require a negative test result before allowing an imported horse into the country.

Horse owners should verify that all the horses at a breeding farm and or boarding facility have a negative Coggins test before using the services of the facility. A Coggins test should be done on an annual basis. Tests every 6 months are recommended if there is increased traveling.

The sterile insect technique (SIT) uses irradiation to sterilize insect pests before releasing them in large numbers to mate with wild females. Since they do not produce any offspring, the population, and consequently the disease incidence, is reduced over time. Used successfully for decades to combat fruit flies and livestock pests such as screwworm and tsetse flies, the technique can be adapted also for some disease-transmitting mosquito species. Pilot projects are being initiated or are under way in different parts of the world.

Viral encephalitis is a type of encephalitis caused by a virus.

It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.

Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.

An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 20 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens. EIDs are caused by newly identified species or strains (e.g. Severe acute respiratory syndrome, HIV/AIDS) that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile fever) or to an area undergoing ecologic transformation (e.g. Lyme disease), or be "reemerging" infections, like drug resistant tuberculosis. Nosocomial (hospital-acquired) infections, such as methicillin-resistant Staphylococcus aureus are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics. Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics. Many emerging diseases are zoonotic - an animal reservoir incubates the organism, with only occasional transmission into human populations.

In June 2009, the United States Department of Agriculture (USDA) Animal and Plant Health Inspection Service (APHIS) approved the first canine influenza vaccine. This vaccine must be given twice initially with a two-week break, then annually thereafter.

Canine influenza (dog flu) is influenza occurring in canine animals. Canine influenza is caused by varieties of influenzavirus A, such as equine influenza virus H3N8, which in 2004 was discovered to cause disease in dogs. Because of the lack of previous exposure to this virus, dogs have no natural immunity to it. Therefore, the disease is rapidly transmitted between individual dogs. Canine influenza may be endemic in some regional dog populations of the United States. It is a disease with a high morbidity (incidence of symptoms) but a low incidence of death.

A newer form was identified in Asia during the 2000s and has since caused outbreaks in the US as well. It is a mutation of H3N2 that adapted from its avian influenza origins. Vaccines have been developed for both strains.

Studies of phylogenetic lineages determined WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages. Lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an African zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

The United States virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, "Macaca sylvanus", was the first nonhuman primate to contract WNV. Both the United States and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.

This condition most commonly occurs after the administration of a horse origin biological agent such as equine-derived antiserum, and usually occurs 4–10 weeks after the event. Diseases that have been vaccinated against using equine-origin antiserum, resulting in subsequent Theiler's disease, include: African horse sickness, Eastern and Western Equine Encephalitis, "Bacillus anthracis", tetanus antitoxin, "Clostridium perfringens", "Clostridium botulinum", "Streptococcus equi" subspecies "equi", Equine influenza, Equine herpesvirus type 1, pregnant mare's serum, and plasma. Although it occurs sporadically, It appears to be spreadable within a premises, and there have been outbreaks occurring on farms involving multiple horses over several months. In the Northern hemisphere it is most common between August to November. It is seen almost exclusively in adult horses, and lactating broodmares given tetanus antitoxin post foaling may be more susceptible.

There is currently no specific therapy. Intravenous fluids and treatment of the hepatic encephalopathy may help. Increasing dietary levels of branched chain amino acids and feeding low protein diets can help signs of hepatic encephalopathy, which is often accomplished by feeding small amounts of grain and/or beet pulp, and removing high-protein feedstuffs such as alfalfa hay. Grazing on non-legume grass may be acceptable if it is late summer or fall, although the horse should only be permitted to eat in the evening so as to avoid photosensitization. Due to the risk of gastric impaction, stomach size should be monitored.

Sedation is minimized and used only to control behavior that could lead to injury of the animal and to allow therapeutic procedures, and should preferably involve a sedative other than a benzodiazepine. Stressing the animal should be avoided if at all possible. Plasma transfusions may be needed if spontaneous bleeding occurs, to replace clotting factors. Antibiotics are sometimes prescribed to prevent bacterial translocation from the intestines. Antioxidants such as vitamin E, B-complex vitamins, and acetylcysteine may be given. High blood ammonia is often treated with oral neomycin, often in conjunction with lactulose, metronidazole and probiotics, to decrease production and absorption of ammonia from the gastrointestinal tract.

Possible complications include the horse becoming a chronic carrier of the disease, asphyxia due to enlarged lymph nodes compressing the larynx or windpipe, bastard strangles (spreading to other areas of the body), pneumonia, guttural pouch filled with pus, abscesses, purpura haemorrhagica, and heart disease. The average length for the course of this disease is 23 days.

Types of encephalitis in humans include:

- Arbovirus encephalitis

- La Crosse encephalitis

- Enterovirus

- California encephalitis virus

- Japanese encephalitis

- St. Louis encephalitis

- Eastern equine encephalitis virus

- Western equine encephalitis virus

- Venezuelan equine encephalitis virus

- Murray Valley encephalitis virus

- Tick-borne meningoencephalitis

- Powassan encephalitis

- West Nile virus

- Herpes simplex

- Human herpesvirus 6

- Varicella zoster virus

- Rabies

- HIV

- H5N1 encephalitis

- Nipah virus encephalitis

- Lymphocytic choriomeningitis, which also causes encephalitis