Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs.

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.

Currently, no specific treatment for chikungunya is available. Supportive care is recommended, and symptomatic treatment of fever and joint swelling includes the use of nonsteroidal anti-inflammatory drugs such as naproxen, non-aspirin analgesics such as paracetamol (acetaminophen) and fluids. Aspirin is not recommended due to the increased risk of bleeding. Despite anti-inflammatory effects, corticosteroids are not recommended during the acute phase of disease, as they may cause immunosuppression and worsen infection.

Passive immunotherapy has potential benefit in treatment of chikungunya. Studies in animals using passive immunotherapy have been effective, and clinical studies using passive immunotherapy in those particularly vulnerable to severe infection are currently in progress. Passive immunotherapy involves administration of anti-CHIKV hyperimmune human intravenous antibodies (immunoglobulins) to those exposed to a high risk of chikungunya infection. No antiviral treatment for chikungunya virus is currently available, though testing has shown several medications to be effective "in vitro".

Treatment is primarily supportive in nature. Early supportive care with rehydration and symptomatic treatment improves survival. Rehydration may be via the oral or by intravenous route. These measures may include management of pain, nausea, fever and anxiety. The World Health Organization recommends avoiding the use of aspirin or ibuprofen for pain due to the bleeding risk associated with use of these medications.

Blood products such as packed red blood cells, platelets or fresh frozen plasma may also be used. Other regulators of coagulation have also been tried including heparin in an effort to prevent disseminated intravascular coagulation and clotting factors to decrease bleeding. Antimalarial medications and antibiotics are often used before the diagnosis is confirmed, though there is no evidence to suggest such treatment helps. A number of experimental treatments are being studied.

If hospital care is not possible, the World Health Organization has guidelines for care at home that have been relatively successful. In such situations, recommendations include using towels soaked in bleach solutions when moving infected people or bodies and applying bleach on stains. It is also recommended that the caregivers wash hands with bleach solutions and cover their mouth and nose with a cloth.

No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease.

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

No specific treatment is currently approved. The Food and Drug Administration (FDA) advises people to be careful of advertisements making unverified or fraudulent claims of benefits supposedly gained from various anti-Ebola products.

In those who have more than two weeks of arthritis, ribavirin may be useful. The effect of chloroquine is not clear. It does not appear to help acute disease, but tentative evidence indicates it might help those with chronic arthritis. Steroids do not appear to be an effective treatment. NSAIDs and simple analgesics can be used to provide partial symptom relief in most cases. Methotrexate, a drug used in the treatment of rheumatoid arthritis, has been shown to have benefit in treating inflammatory polyarthritis resulting from chikungunya, though the drug mechanism for improving viral arthritis is unclear.

Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .

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.

As for other flavivirus infections, no cure is known for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Different methods for acute treatment of the disease have been shown not to be very successful; passive immunisation after emergence of symptoms is probably without effect. Ribavirin and other antiviral drugs, as well as treatment with interferons, do not have a positive effect in patients.

A symptomatic treatment includes rehydration and pain relief with drugs such as paracetamol (acetaminophen in the United States). Acetylsalicylic acid (aspirin) should not be given because of its anticoagulant effect, which can be devastating in the case of internal bleeding that can occur with yellow fever.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

Preventative measures require effective personal and community hygiene. Some specific safeguards include the following:

- Purification of drinking water.

- Proper handling of food.

- Careful disposal of human feces.

- Monitoring the contacts of balantidiasis patients.

Bright's disease was historically 'treated' with warm baths, blood-letting, squill, digitalis, mercuric compounds, opium, diuretics, laxatives, and dietary therapy, including abstinence from alcoholic drinks, cheese and red meat. Arnold Ehret was diagnosed with Bright's disease and pronounced incurable by 24 of Europe's most respected doctors; he designed "The Mucusless Diet Healing System", which apparently cured his illness. William Howard Hay, MD had the illness and, it is claimed, cured himself using the Hay diet.

Currently Sandhoff disease does not have any standard treatment and does not have a cure. However, a person suffering from the disease needs proper nutrition, hydration, and maintenance of clear airways. To reduce some symptoms that may occur with Sandhoff disease, the patient may take anticonvulsants to manage seizures or medications to treat respiratory infections, and consume a precise diet consisting of puree foods due to difficulties swallowing. Infants with the disease usually die by the age of 3 due to respiratory infections. The patient must be under constant surveillance because they can suffer from aspiration or lack the ability to change from the passageway to their lungs versus their stomach and their spit travels to the lungs causing bronchopneumonia. The patient also lacks the ability to cough and therefore must undergo a treatment to shake up their body to remove the mucus from the lining of their lungs. Medication is also given to patients to lessen their symptoms including seizures.

Currently the government is testing several treatments including N-butyl-deoxynojirimycin in mice, as well as stem cell treatment in humans and other medical treatments recruiting test patients.

The first approach, which is the best approach at an effective management practice would be to eradicate or severely damage the Mountain and Cherry Leafhopper population because the leafhoppers are the number one vectors for this pathogen. To do this, pesticides (i.e. acephate, bifenthrin, cyfluthrin) could be applied or biological control (predators of the leafhopper) could be used. There should be a pre-season application of control measures as well as a post-season application. This is to maximize the effort at controlling both types of leafhoppers (Cherry and Mountain), thus cutting down the starting inoculum at both stages in the life cycle.

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

The first treatment for Fabry's disease was approved by the US FDA on April 24, 2003. Fabrazyme (agalsidase beta, or Alpha-galactosidase) was licensed to the Genzyme Corporation. It is an enzyme replacement therapy (ERT) designed to provide the enzyme the patient is missing as a result of a genetic malfunction. The drug is expensive — in 2012, Fabrazyme's annual cost was about US$200,000 per patient, which is unaffordable to many patients around the world without enough insurance. ERT is not a cure, but can allow improved metabolism and partially prevent disease progression, as well as potentially reverse some symptoms.

The pharmaceutical company Shire manufactures agalsidase alpha (which differs in the structure of its oligosaccharide side chains) under the brand name Replagal as a treatment for Fabry's disease, and was granted marketing approval in the EU in 2001. FDA approval was applied for the United States. However, Shire withdrew their application for approval in the United States in 2012, citing that the agency will require additional clinical trials before approval.

Clinically the two products are generally perceived to be similar in effectiveness. Both are available in Europe and in many other parts of the world, but treatment costs remain very high.

Besides these drugs, a gene therapy treatment is also available from the Canadian Institutes of Health. Other treatments (oral chaperone therapy -Amicus-, plant-based ERT -Protalix-, substrate reduction therapy -Sanofi-Genzyme-, bio-better ERT -Codexis-, gene editing solution -Sangamo- are currently being researched.

Pain associated with Fabry disease may be partially alleviated by ERT in some patients, but pain management regimens may also include analgesics, anticonvulsants, and nonsteroidal anti-inflammatory drugs, though the latter are usually best avoided in renal disease.

Cattle infested with bovine pediculosis are generally treated chemically, by drugs like ivermectin and cypermethrin.

Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive, invariably fatal, conditions that affect the brain (encephalopathies) and nervous system of many animals, including humans. According to the most widespread hypothesis, they are transmitted by prions, though some other data suggest an involvement of a "Spiroplasma" infection. Mental and physical abilities deteriorate and myriad tiny holes appear in the cortex causing it to appear like a sponge (hence spongiform) when brain tissue obtained at autopsy is examined under a microscope. The disorders cause impairment of brain function, including memory changes, personality changes and problems with movement that worsen chronically.

Prion diseases of humans include Creutzfeldt–Jakob disease—which has four main forms, the sporadic (sCJD), the hereditary/familiar (fCJD), the iatrogenic (iCJD) and the variant form (vCJD)—Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia, kuru, and the recently discovered variably protease-sensitive prionopathy. These conditions form a spectrum of diseases with overlapping signs and symptoms. TSEs in non-human mammals include scrapie in sheep, bovine spongiform encephalopathy (BSE)—popularly known as 'mad cow's disease'—in cattle and chronic wasting disease (CWD) in deer and elk. The variant form of Creutzfeldt–Jakob disease is caused by exposure to bovine spongiform encephalopathy prions.

Unlike other kinds of infectious disease, which are spread by agents with a DNA or RNA genome (such as virus or bacteria), the infectious agent in TSEs is believed to be a prion, thus being composed solely of protein material. Misshapen prion proteins carry the disease between individuals and cause deterioration of the brain. TSEs are unique diseases in that their aetiology may be genetic, sporadic, or infectious via ingestion of infected foodstuffs and via iatrogenic means (e.g., blood transfusion). Most TSEs are sporadic and occur in an animal with no prion protein mutation. Inherited TSE occurs in animals carrying a rare mutant prion allele, which expresses prion proteins that contort by themselves into the disease-causing conformation. Transmission occurs when healthy animals consume tainted tissues from others with the disease. In the 1980s and 1990s, bovine spongiform encephalopathy (BSE) spread in cattle in an epidemic fashion. This occurred because cattle were fed the processed remains of other cattle, a practice now banned in many countries. In turn, consumption (by humans) of bovine-derived foodstuff which contained prion-contaminated tissues resulted in an outbreak of the variant form of Creutzfeldt–Jakob disease in the 1990s and 2000s.

Prions cannot be transmitted through the air or through touching or most other forms of casual contact. However, they may be transmitted through contact with infected tissue, body fluids, or contaminated medical instruments. Normal sterilization procedures such as boiling or irradiating materials fail to render prions non-infective.

Pacheco's disease is an eponymously named disease; it is named after the Brazilian veterinarian, Genesio Pacheco, who first came across the disease in 1929, in an outbreak affecting the turquoise-fronted amazon parrot, "Amazona aestiva". Initially, Pacheco's disease was thought to be a manifestation of avian psittacosis. The causative agent of the disease, a herpesvirus, was not identified until 1975.