Antibiotics are commonly used to prevent secondary bacterial infection. There are no specific antiviral drugs in common use at this time for FVR, although one study has shown that ganciclovir, PMEDAP, and cidofovir hold promise for treatment. More recent research has indicated that systemic famciclovir is effective at treating this infection in cats without the side effects reported with other anti-viral agents. More severe cases may require supportive care such as intravenous fluid therapy, oxygen therapy, or even a feeding tube. Conjunctivitis and corneal ulcers are treated with topical antibiotics for secondary bacterial infection.

Lysine is commonly used as a treatment, however in a 2015 systematic review, where the authors investigated all clinical trials with cats as well as "in vitro" studies, concluded that lysine supplementation is not effective for the treatment or prevention of feline herpesvirus 1 infection.

Ribavirin is one medication which has shown good potential for the treatment of HPIV-3 given recent in-vitro tests (in-vivo tests show mixed results). Ribavirin is a broadscale anti-viral and is currently being administered to those who are severely immuno-compromised, despite the lack of conclusive evidence for its use. Protein inhibitors and novel forms of medication have also been proposed to relieve the symptoms of infection.

Furthermore, antibiotics may be used if a secondary bacterial infection develops. Corticosteroid treatment and nebulizers are also a first line choice against croup if breathing difficulties ensue.

There is a vaccine for FHV-1 available (ATCvet code: , plus various combination vaccines), but although it limits or weakens the severity of the disease and may reduce viral shedding, it does not prevent infection with FVR. Studies have shown a duration of immunity of this vaccine to be at least three years. The use of serology to demonstrate circulating antibodies to FHV-1 has been shown to have a positive predictive value for indicating protection from this disease.

Most people recover from West Nile virus without treatment. No specific treatment is available for WNV infection. In mild cases over the counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases treatment consists of supportive care that often involves hospitalization, intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.

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.

No treatment exists for the viral infection. Antibiotics may help prevent secondary infections.

Vaccination is available in different forms, usually for naive flocks.

Good biosecurity measures should be maintained including adequate quarantine, isolation, separation of different age groups and disinfection.

Despite decades of research, no vaccines currently exist.

Recombinant technology has however been used to target the formation of vaccines for HPIV-1, -2 and -3 and has taken the form of several live-attenuated intranasal vaccines. Two vaccines in particular were found to be immunogenic and well tolerated against HPIV-3 in phase I trials. HPIV-1 and -2 vaccine candidates remain less advanced.

Vaccine techniques which have been used against HPIVs are not limited to intranasal forms, but also viruses attenuated by cold passage, host range attenuation, chimeric construct vaccines and also introducing mutations with the help of reverse genetics to achieve attenuation.

Maternal antibodies may offer some degree of protection against HPIVs during the early stages of life via the colostrum in breast milk.

In cases of viral pneumonia where influenza A or B are thought to be causative agents, patients who are seen within 48 hours of symptom onset may benefit from treatment with oseltamivir or zanamivir. Respiratory syncytial virus (RSV) has no direct acting treatments, but ribavirin in indicated for severe cases. Herpes simplex virus and varicella-zoster virus infections are usually treated with aciclovir, whilst ganciclovir is used to treat cytomegalovirus. There is no known efficacious treatment for pneumonia caused by SARS coronavirus, MERS coronavirus, adenovirus, hantavirus, or parainfluenza. Care is largely supportive.

All persons suspected of Lassa fever infection should be admitted to isolation facilities and their body fluids and excreta properly disposed of.

Early and aggressive treatment using ribavirin was pioneered by Joe McCormick in 1979. After extensive testing, early administration was determined to be critical to success. Additionally, ribavirin is almost twice as effective when given intravenously as when taken by mouth. Ribavirin is a prodrug which appears to interfere with viral replication by inhibiting RNA-dependent nucleic acid synthesis, although the precise mechanism of action is disputed. The drug is relatively inexpensive, but the cost of the drug is still very high for many of those in West African states. Fluid replacement, blood transfusion, and fighting hypotension are usually required. Intravenous interferon therapy has also been used.

When Lassa fever infects pregnant women late in their third trimester, induction of delivery is necessary for the mother to have a good chance of survival. This is because the virus has an affinity for the placenta and other highly vascular tissues. The fetus has only a one in ten chance of survival no matter what course of action is taken; hence, the focus is always on saving the life of the mother. Following delivery, women should receive the same treatment as other Lassa fever patients.

Work on a vaccine is continuing, with multiple approaches showing positive results in animal trials.

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.

Treatment is generally supportive. Rest, hydration, antipyretics, and pain or anti-inflammatory medications may be given as needed.

Herpes simplex virus, varicella zoster virus and cytomegalovirus have a specific antiviral therapy. For herpes the treatment of choice is aciclovir.

Surgical management is indicated where there is extremely increased intracranial pressure, infection of an adjacent bony structure (e.g. mastoiditis), skull fracture, or abscess formation.

The majority of people that have viral meningitis get better within 7-10 days.

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.

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.

Modern vaccination programmes aim not only to provide a high level of protection from clinical disease for the dam, but, crucially, to protect against viraemia and prevent the production of PIs. While the immune mechanisms involved are the same, the level of immune protection required for foetal protection is much higher than for prevention of clinical disease.

While challenge studies indicate that killed, as well as live, vaccines prevent foetal infection under experimental conditions, the efficacy of vaccines under field conditions has been questioned. The birth of PI calves into vaccinated herds suggests that killed vaccines do not stand up to the challenge presented by the viral load excreted by a PI in the field.

Treatment is similar to hepatitis B, but due to its high lethality, more aggressive therapeutic approaches are recommended in the acute phase. In absence of a specific vaccine against delta virus, the vaccine against HBV must be given soon after birth in risk groups.

While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover. People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.

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.

Vaccinations exist for several biological BRD precursors, but the multitude of possible precursors complicates the process of choosing a vaccine regime. Additionally, vaccines are not completely effective in stopping the disease, but are merely helpful in mitigation. Many of the problems with vaccine effectiveness rest with improper use, such as failing to time vaccine doses appropriately, or not administering them before shipping.

Vaccines are available for a number of viral/bacterial agents, including IBR, PI3, BVD, BRSV, Pasteurella, and "Haemophilus somnus". Many of these vaccines can be given simultaneously, because of their similar dosing schedule. For example, IBR, PI3, BVD, and BRSV vaccines are often sold in combination with each other.

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

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

Corticosteroids, such as dexamethasone and budesonide, have been shown to improve outcomes in children with all severities of croup. Significant relief is obtained as early as six hours after administration. While effective when given by injection, or by inhalation, giving the medication by mouth is preferred. A single dose is usually all that is required, and is generally considered to be quite safe. Dexamethasone at doses of 0.15, 0.3 and 0.6 mg/kg appear to be all equally effective.

While other treatments for croup have been studied, none have sufficient evidence to support their use. Inhalation of hot steam or humidified air is a traditional self-care treatment, but clinical studies have failed to show effectiveness and currently it is rarely used. The use of cough medicines, which usually contain dextromethorphan or guaifenesin, are also discouraged. There is tentative evidence that breathing heliox (a mixture of helium and oxygen) to decrease the work of breathing is useful in those with severe disease. Since croup is usually a viral disease, antibiotics are not used unless secondary bacterial infection is suspected. In cases of possible secondary bacterial infection, the antibiotics vancomycin and cefotaxime are recommended. In severe cases associated with influenza A or B, the antiviral neuraminidase inhibitors may be administered.

In the absence of vaccination (often because calves are bought unvaccinated), antibiotics can help to stop the bacterial factors of the disease. The Virginia Cooperative Extension recommends Micotil, Nuflor, and Baytril 100 as newer antibiotics that do not need daily dosing, but also notes that Naxcel, Excenel, and Adspec are effective as well.

No specific cure is known. Treatment is largely supportive. Nonsteroidal anti-inflammatory drugs (NSAIDs) are indicated for tender lymph nodes and fever, and corticosteroids are useful in severe extranodal or generalized disease.

Symptomatic measures aimed at relieving the distressing local and systemic complaints have been described as the main line of management of KFD. Analgesics, antipyretics, NSAIDs, and corticosteroids have been used. If the clinical course is more severe, with multiple flares of bulky enlarged cervical lymph nodes and fever, then a low-dose corticosteroid treatment has been suggested.

Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.