Paravaccinia virus originates from livestock infected with bovine papular stomatitis. When a human makes physical contact with the livestock's muzzle, udders, or an infected area, the area of contact will become infected. Livestock may not show symptoms of bovine papular stomatitis and still be infected and contagious. Paravaccinia can enter the body though all pathways including: skin contact by mechanical means, through the respiratory tract, or orally. Oral or respiratory contraction may be more likely to cause systemic symptoms such as lesions across the whole body

A person who has not previously been infected with paravaccinia virus should avoid contact with infected livestock to prevent contraction of disease. There is no commercially available vaccination for cattle or humans against paravaccinia. However, following infection, immunization has been noted in humans, making re-infection difficult. Unlike other pox viruses, there is no record of contracting paravaccinia virus from another human. Further, cattle only show a short immunization after initial infection, providing opportunity to continue to infect more livestock and new human hosts.

Lesions of paravaccinia virus will clear up with little to no scaring after 4 to 8 weeks. An antibiotic may be prescribed by a physician to help prevent bacterial infection of the lesion area. In rare cases, surgical removal of the lesions can be done to help increase rate of healing, and help minimize risk of bacterial or fungal infection. Upon healing, no long term side effects have been reported.

Currently, there is no proven, safe treatment for monkeypox. The people who have been infected can be vaccinated up to 14 days after exposure.

Although no specific treatment for acute infection with SuHV1 is available, vaccination can alleviate clinical signs in pigs of certain ages. Typically, mass vaccination of all pigs on the farm with a modified live virus vaccine is recommended. Intranasal vaccination of sows and neonatal piglets one to seven days old, followed by intramuscular (IM) vaccination of all other swine on the premises, helps reduce viral shedding and improve survival. The modified live virus replicates at the site of injection and in regional lymph nodes. Vaccine virus is shed in such low levels, mucous transmission to other animals is minimal. In gene-deleted vaccines, the thymidine kinase gene has also been deleted; thus, the virus cannot infect and replicate in neurons. Breeding herds are recommended to be vaccinated quarterly, and finisher pigs should be vaccinated after levels of maternal antibody decrease. Regular vaccination results in excellent control of the disease. Concurrent antibiotic therapy via feed and IM injection is recommended for controlling secondary bacterial pathogens.

SuHV1 can be used to analyze neural circuits in the central nervous system (CNS). For this purpose the attenuated (less virulent) Bartha SuHV1 strain is commonly used and is employed as a retrograde and anterograde transneuronal tracer. In the retrograde direction, SuHV1-Bartha is transported to a neuronal cell body via its axon, where it is replicated and dispersed throughout the cytoplasm and the dendritic tree. SuHV1-Bartha released at the synapse is able to cross the synapse to infect the axon terminals of synaptically connected neurons, thereby propagating the virus; however, the extent to which non-synaptic transneuronal transport may also occur is uncertain. Using temporal studies and/or genetically engineered strains of SuHV1-Bartha, second, third, and higher order neurons may be identified in the neural network of interest.

However, simple husbandry changes and practical midge control measures may help break the livestock infection cycle. Housing livestock during times of maximum midge activity (from dusk to dawn) may lead to significantly reduced biting rates. Similarly, protecting livestock shelters with fine mesh netting or coarser material impregnated with insecticide will reduce contact with the midges. The "Culicoides" midges that carry the virus usually breed on animal dung and moist soils, either bare or covered in short grass. Identifying breeding grounds and breaking the breeding cycle will significantly reduce the local midge population. Turning off taps, mending leaks and filling in or draining damp areas will also help dry up breeding sites. Control by trapping midges and removing their breeding grounds may reduce vector numbers. Dung heaps or slurry pits should be covered or removed, and their perimeters (where most larvae are found) regularly scraped.

Prevention is effected via quarantine, inoculation with live modified virus vaccine and control of the midge vector, including inspection of aircraft.

Vaccination against smallpox is assumed to provide protection against human monkeypox infection considering they are closely related viruses and the vaccine protects animals from experimental lethal monkeypox challenge. This has not been conclusively demonstrated in humans because routine smallpox vaccination was discontinued following the apparent eradication of smallpox and due to safety concerns with the vaccine.

Smallpox vaccine has been reported to reduce the risk of monkeypox among previously vaccinated persons in Africa. The decrease in immunity to poxviruses in exposed populations is a factor in the prevalence of monkeypox. It is attributed both to waning cross-protective immunity among those vaccinated before 1980 when mass smallpox vaccinations were discontinued, and to the gradually increasing proportion of unvaccinated individuals. The United States Centers for Disease Control and Prevention (CDC) recommends that persons investigating monkeypox outbreaks and involved in caring for infected individuals or animals should receive a smallpox vaccination to protect against monkeypox. Persons who have had close or intimate contact with individuals or animals confirmed to have monkeypox should also be vaccinated.

CDC does not recommend preexposure vaccination for unexposed veterinarians, veterinary staff, or animal control officers, unless such persons are involved in field investigations.

Immunosuppressive therapy has been effective in halting the disease for laboratory animals.

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.

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.

Key measures to prevent outbreaks of the disease are maintaining hygiene standards and using screening to exclude persons with suspicious infections from engaging in contact sports. A skin check performed before practice or competition takes place can identify individuals who should be evaluated, and if necessary treated by a healthcare professional. In certain situations, i.e. participating in wrestling camps, consider placing participants on valacyclovir 1GM daily for the duration of camp. 10-year study has shown 89.5% reduction in outbreaks and probable prevention of contracting the virus. Medication must be started 5 days before participation to ensure proper concentrations exist.

Although the house mouse ("Mus musculus") is the primary reservoir host for LCMV, it is also often found in the wood mouse ("Apodemus sylvaticus") and the yellow-necked mouse ("Apodemus flavicollis"). Hamster populations can act as reservoir hosts. Other rodents including guinea pigs, rats and chinchillas can be infected but do not appear to maintain the virus. LCMV has been shown to cause illness in New World primates such as macaques, marmosets and tamarins. Infections have also been reported in rabbits, dogs and pigs. After experimental inoculation, the incubation period in adult mice is 5 to 6 days. Congenitally or neonatally infected mice and hamsters do not become symptomatic for several months or longer.

Vaccines are available (ATCvet codes: for the inactivated vaccine, for the live vaccine, plus various combinations).

Given that avian reovirus infections are widespread, the viruses are relatively resistant outside the host, and that vertical and horizontal transmission occurs, eradicating avian reovirus infection in commercial chicken flocks is very unlikely. In addition, absence of detectable seroconversion and failure to detect virus in cloacal swabs are unreliable indicators of resisting infection, or transmission via the egg. Thus, the most proactive and successful approach to controlling this disease is through vaccination. Since chicks are more prone to being detrimentally affected by the disease right after hatching, vaccine protocols that use live and killed vaccines are designed to provide protection during the very early stages of life. This approach has been accomplished through active immunity after early vaccination and a live vaccine or passive immunity from maternal antibodies followed with vaccination of the breeder hens. Currently, efforts toward administering inactivated or live vaccines to breeding stock to allow passive immunity to the offspring via the yolk are being taken.

The mainstay of eradication is the identification and removal of persistently infected animals. Re-infection is then prevented by vaccination and high levels of biosecurity, supported by continuing surveillance. PIs act as viral reservoirs and are the principal source of viral infection but transiently infected animals and contaminated fomites also play a significant role in transmission.

Leading the way in BVD eradication, almost 20 years ago, were the Scandinavian countries. Despite different conditions at the start of the projects in terms of legal support, and regardless of initial prevalence of herds with PI animals, it took all countries approximately 10 years to reach their final stages.

Once proven that BVD eradication could be achieved in a cost efficient way, a number of regional programmes followed in Europe, some of which have developed into national schemes.

Vaccination is an essential part of both control and eradication. While BVD virus is still circulating within the national herd, breeding cattle are at risk of producing PI neonates and the economic consequences of BVD are still relevant. Once eradication has been achieved, unvaccinated animals will represent a naïve and susceptible herd. Infection from imported animals or contaminated fomites brought into the farm, or via transiently infected in-contacts will have devastating consequences.

, no approved vaccines are available. A phase-II vaccine trial used a live, attenuated virus, to develop viral resistance in 98% of those tested after 28 days and 85% still showed resistance after one year. However, 8% of people reported transient joint pain, and attenuation was found to be due to only two mutations in the E2 glycoprotein. Alternative vaccine strategies have been developed, and show efficacy in mouse models. In August 2014 researchers at the National Institute of Allergy and Infectious Diseases in the USA were testing an experimental vaccine which uses virus-like particles (VLPs) instead of attenuated virus. All the 25 people participated in this phase 1 trial developed strong immune responses. As of 2015, a phase 2 trial was planned, using 400 adults aged 18 to 60 and to take place at 6 locations in the Caribbean. Even with a vaccine, mosquito population control and bite prevention will be necessary to control chikungunya disease.

There is currently no vaccine available. The primary method of disease prevention is minimizing mosquito bites, as the disease is only transmitted by mosquitoes. Typical advice includes use of mosquito repellent and mosquito screens, wearing light coloured clothing, and minimising standing water around homes (e.g. removing Bromeliads, plant pots, garden ponds). Staying indoors during dusk/dawn hours when mosquitos are most active may also be effective. Bush camping is a common precipitant of infection so particular care is required.

Bovine malignant catarrhal fever (BMCF) is a fatal lymphoproliferative disease caused by a group of ruminant gamma herpes viruses including Alcelaphine gammaherpesvirus 1 (AlHV-1) and Ovine gammaherpesvirus 2 (OvHV-2) These viruses cause unapparent infection in their reservoir hosts (sheep with OvHV-2 and wildebeest with AlHV-1), but are usually fatal in cattle and other ungulates such as deer, antelope, and buffalo.

BMCF is an important disease where reservoir and susceptible animals mix. There is a particular problem with Bali cattle in Indonesia, bison in the US and in pastoralist herds in Eastern and Southern Africa.

Disease outbreaks in cattle are usually sporadic although infection of up to 40% of a herd has been reported. The reasons for this are unknown. Some species appear to be particularly susceptible, for example Pére Davids deer, Bali cattle and bison, with many deer dying within 48 hours of the appearance of the first symptoms and bison within three days. In contrast, post infection cattle will usually survive a week or more.

It has been recorded since the late 19th century and has been reported from most sheep-or goat-raising areas including those in Europe, the Middle East, the United States, Africa, Asia, Alaska, South America, Canada, New Zealand and Australia. Orf is spread by fomites and direct contact. In some environments infection is injected by scratches from thistles of both growing and felled plants. Symptoms include papules and pustules on the lips and muzzle, and less commonly in the mouth of young lambs and on the eyelids, feet, and teats of ewes. The lesions progress to thick crusts which may bleed. Orf in the mouths of lambs may prevent suckling and cause weight loss, and can infect the udder of the mother ewe, thus potentially leading to mastitis. Sheep are prone to reinfection. Occasionally the infection can be extensive and persistent if the animal does not produce an immune response.

A live virus vaccine (ATCvet code: ) is made from scab material and usually given to ewes at the age of two months, but only to lambs when there is an outbreak. The vaccine can cause disease in humans.

In sheep and goats the lesions mostly appear on or near the hairline and elsewhere on the lips and muzzle. In some cases the lesions appear on and in the nostrils, around the eyes, on the thigh, coronet, vulva, udder and axilla. In rare cases, mostly involving young lambs, lesions are found on the tongue, gums, roof of the mouth and the oesophagus. It has also been reported a number of times to cause lesions in the rumen. In one case it was shown that a severe form of orf virus caused an outbreak involving the gastrointestinal tract, lungs, heart, as well as the buccal cavity, cheeks, tongue and lips. Another severe case was reported pharyngitis, genital lesions and infection of the hooves which led to lameness and, in some cases, sloughing of the hoof.

More typically sheep will become free of orf within a week or so as the disease runs its course. Sheep custodians can assist by ensuring infected lambs receive sufficient milk and separating out the infected stock to slow down cross-transmission to healthy animals. It is advisable for those handling infected animals to wear disposable gloves to prevent cross-infection and self-infection. A veterinarian needs to be contacted if there is a risk of misdiagnosis with other, more serious conditions.

The study of RRF has been recently facilitated by the development of a mouse model. Mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice is characterized by an inflammatory infiltrate including macrophages which are immunopathogenic and exacerbate disease. Furthermore, mice deficient in the C3 protein do not suffer from severe disease following infection. This indicates that an aberrant innate immune response is responsible for severe disease following RRV infection.

Primarily, orf is a disease of sheep and goats although it has been reported as a natural disease in the following: humans, steenbok and alpacas, chamois and thar, reindeer, musk ox, dog, cat, mountain goat, bighorn sheep, dall sheep, and the red squirrel .

West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps, carbon dioxide-baited light traps, and gravid traps, testing blood samples drawn from wild birds, dogs, and sentinel monkeys, as well as testing brains of dead birds found by various animal control agencies and the public.

Testing of the mosquito samples requires the use of reverse-transcriptase PCR (RT-PCR) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC) or enzyme-linked immunosorbent assay (ELISA).

Dead birds, after necropsy, or their oral swab samples collected on specific RNA-preserving filter paper card, can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.

West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides.

Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, "Culex pipiens", is a canopy feeder.

Herpes outbreaks should be treated with antiviral medications like Acyclovir, Valacyclovir, or Famcyclovir, each of which is available in tablet form.

Oral antiviral medication is often used as a prophylactic to suppress or prevent outbreaks from occurring. The recommended dosage for suppression therapy for recurrent outbreaks is 1,000 mg of valacyclovir once a day or 400 mg Acyclovir taken twice a day. In addition to preventing outbreaks, these medications greatly reduce the chance of infecting someone while the patient is not having an outbreak.

Often, people have regular outbreaks of anywhere from 1 to 10 times per year, but stress (because the virus lies next to the nerve cells), or a weakened immune system due to a temporary or permanent illness can also spark outbreaks. Some people become infected but fail to ever have a single outbreak, although they remain carriers of the virus and can pass the disease on to an uninfected person through asymptomatic shedding (when the virus is active on the skin but rashes or blisters do not appear).

The use of antiviral medications has been shown to be effective in preventing acquisition of the herpes virus. Specific usage of these agents focus on wrestling camps where intense contact between individuals occur on a daily basis over several weeks. They have also been used for large outbreaks during seasonal competition, but further research needs to be performed to verify efficacy.

Personal protective measures can be taken to greatly reduce the risk of being bitten by an infected mosquito:

- Using insect repellent on exposed skin to repel mosquitoes. EPA-registered repellents include products containing DEET (N,N-diethylmetatoluamide) and picaridin (KBR 3023). DEET concentrations of 30% to 50% are effective for several hours. Picaridin, available at 7% and 15% concentrations, needs more frequent application. DEET formulations as high as 30% are recommended for children over two months of age. Protect infants less than two months of age by using a carrier draped with mosquito netting with an elastic edge for a tight fit.

- When using sunscreen, apply sunscreen first and then repellent. Repellent should be washed off at the end of the day before going to bed.

- Wear long-sleeve shirts, which should be tucked in, long pants, socks, and hats to cover exposed skin. Insect repellents should be applied over top of protective clothing for greater protection. Do not apply insect repellents underneath clothing.

- The application of permethrin-containing ("e.g.", Permanone) or other insect repellents to clothing, shoes, tents, mosquito nets, and other gear for greater protection. Permethrin is not labeled for use directly on skin. Most repellent is generally removed from clothing and gear by a single washing, but permethrin-treated clothing is effective for up to five washings.

- Be aware that most mosquitoes that transmit disease are most active during twilight periods (dawn and dusk or in the evening). A notable exception is the Asian tiger mosquito, which is a daytime feeder and is more apt to be found in, or on the periphery of, shaded areas with heavy vegetation. They are now widespread in the United States, and in Florida they have been found in all 67 counties.

- Staying in air-conditioned or well-screened housing, and/or sleeping under an insecticide-treated bed net. Bed nets should be tucked under mattresses and can be sprayed with a repellent if not already treated with an insecticide.

The virus’s transmission cycle in the wild is similar to the continuous sylvatic cycle of yellow fever and is believed to involve wild primates (monkeys) as the reservoir and the tree-canopy-dwelling "Haemagogus" species mosquito as the vector. Human infections are strongly associated with exposure to humid tropical forest environments. Chikungunya virus is closely related, producing a nearly indistinguishable, highly debilitating arthralgic disease. On February 19, 2011, a Portuguese-language news source reported on a recent survey which revealed Mayaro virus activity in Manaus, Amazonas State, Brazil. The survey studied blood samples from 600 residents of Manaus who had experienced a high fever; Mayaro virus was identified in 33 cases. Four of the cases experienced mild hemorrhagic (bleeding) symptoms, which had not previously been described in Mayaro virus disease. The report stated that this outbreak is the first detected in a metropolitan setting, and expressed concern that the disease might be adapting to urban species of mosquito vectors, which would make it a risk for spreading within the country. A study published in 1991 demonstrated that a colonized strain of Brazilian "Aedes albopictus" was capable of acquiring MAYV from infected hamsters and subsequently transmitting it and a study published in October 2011 demonstrated that "Aedes aegypti" can transmit MAYV, supporting the possibility of wider transmission of Mayaro virus disease in urban settings.