The primary route of transmission has not yet been identified, but direct contact may result in its transmission to developing embryos in viviparous species and eggs in oviparous species. Venereal transmission is also indicated as a possibility. The snake mite, "Ophionyssus natricis", has been implicated as a possible vector for the virus, since mite infestations are commonly seen in epizootics of IBD and in captive specimens of these snakes. Mites are sometimes very difficult to eradicate due to their resistance to certain toxins used to eliminate them.

Permethrin is known to be effective against mite infestations, but should be used with great caution and only in small quantities due to their toxic nature. Also, several nonchemical substances may be just as effective. These biological agents are sprayed onto the infested animal and desiccate the mites, rendering them unable to lay their eggs or consume blood beneath the scales of their host. The incubation period for mite eggs is thought to be about 10–14 days, so the treatment should be repeated after 10 days to ensure that any eggs that hatch or larvae that develop into nymphs are also quickly eliminated from the host before reaching sexual maturity and able to repeat their reproduction cycle.

To date, no treatment for IBD is known. Snakes diagnosed with or suspected of having IBD should be euthanized because progression and transmission of the virus is both very rapid and destructive. All newly acquired snakes should, therefore, be quarantined for at least 3 and preferably 6 months before being introduced into established collections. The recommended period of quarantine for any wild-caught boa or python is at least 4–6 months.

Often no treatment is required. However, as porcine cytomegalovirus is a herpes virus it remains latent and sheds at times of stress. Therefore husbandry measures to minimise stress levels should be in place.

Inclusion Body Rhinitis, also known as IBR or Cytomegalic Inclusion Disease, is a pig disease caused by porcine cytomegalovirus, which is a member of the herpesvirus family. It is a notifiable disease that is found worldwide. It is spread both vertically and horizontally and prevalence is high.

It is not a zoonosis but the risk to humans that receive pig organ transplants is currently under investigation.

Tick control is the most effective method of prevention, but tetracycline at a lower dose can be given daily for 200 days during the tick season in endemic regions.

The prognosis is good for dogs with acute ehrlichiosis. For dogs that have reached the chronic stage of the disease, the prognosis is guarded. When bone marrow suppression occurs and there are low levels of blood cells, the animal may not respond to treatment.

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 household disinfectants will inactivate FHV-1. The virus can survive up to 18 hours in a damp environment, but less in a dry environment and only shortly as an aerosol.

Should the viral progression be diagnosed during stage 1 (even during late stage 1 when stage 2 symptoms start to manifest themselves) then treatment to combat the infection can be administered successfully—there is no cure for SSPE but if it is caught early enough then the sufferer can respond to the treatment and prevent symptom recurrence by taking the medication for the rest of their life. The treatment for the SSPE infection is the immunomodulator interferon and specific antiviral medication—ribavirin and inosine pranobex are specifically used to greater effect than antivirals such as amantadine.

For those who have progressed to stage 2 or beyond, the disease is incurable. For patients in the terminal phase of the disease there is a palliative care and treatment scheme—this involves anticonvulsant therapy (to help with the body's progressive loss of control of the nervous system causing gradually more intensive spasms/convulsions) alongside supportive measures to help maintain vital functioning. It is fairly standard as the infection spreads and symptoms intensify that feeding tubes need to be inserted to keep a nutritional balance. As the disease progresses to its most advanced phase, the patient will need constant nursing as normal bodily function declines to the complete collapse of the nervous system.

Combinations of treatment for SSPE include:

- Oral inosine pranobex (oral isoprinosine) combined with intrathecal (injection through a lumbar puncture into the spinal fluid) or intraventricular interferon alpha.

- Oral inosine pranobex (oral isoprinosine) combined with interferon beta.

- Intrathecal interferon alpha combined with intravenous ribavirin.

In the classic presentation of the disease death usually occurs within 3 years, however there are rarely both fast and slower progressions. Faster deterioration in cases of acute fulminant SSPE leads to death within 3 months of diagnosis.

If the diagnosis is made during stage 1 of the SSPE infection then it may be possible to treat the disease with oral isoprinosine (Inosiplex) and intraventricular interferon alfa, but the response to these drugs varies from patient to patient. However, once SSPE progresses to stage 2 then it is universally fatal in all occurrences. The standard rate of decline spans anywhere between 1–3 years after the onset of the infection. The progression of each stage is unique to the sufferer and cannot be predicted although the pattern or symptoms/signs can be.

Although the prognosis is bleak for SSPE past stage 1, there is a 5% spontaneous remission rate—this may be either a full remission that may last many years or an improvement in condition giving a longer progression period or at least a longer period with the less severe symptoms.

In many cases, MHA requires no treatment. However, in extreme cases, blood platelet transfusions may be necessary

Cytomegalic inclusion body disease (CIBD) is a series of signs and symptoms caused by cytomegalovirus infection, toxoplasmosis or other rare infections such as herpes or rubella viruses. It can produce massive calcification of the central nervous system, and often the kidneys.

Cytomegalic inclusion body disease is the most common cause of congenital abnormalities in the United States. It can also cause pneumonia and other diseases in immunocompromised patients, such as those with HIV/AIDS or recipients of organ transplants.

Microvillus inclusion disease is thought to be extremely rare; only approximately 200 cases have been identified in children in Europe.

One patient, a teenage female living in Arizona, suddenly began to grow microvilli after thirteen years of TPN (Total Parenteral Nutrition) and Lipid dependency. She now enjoys a typical teenage diet and is seen regularly by her Gastroenterologist.

One patient from the UK was documented to achieve nutritional independence at age 3.

On 26 June 2009 a six-year-old girl diagnosed with microvillus inclusion disease became the third person in the UK to die of swine flu.

Although no specific treatment exists, the disease can be managed with anticonvulsants, physiotherapy, etc.

There is no specific treatment for Chédiak–Higashi syndrome. Bone marrow transplants appear to have been successful in several patients. Infections are treated with antibiotics and abscesses are surgically drained when appropriate. Antiviral drugs such as acyclovir have been tried during the

terminal phase of the disease. Cyclophosphamide and prednisone have been tried. Vitamin C therapy has improved immune function and clotting in some patients.

It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant. The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients.

PRP is very rare and similar to SSPE but without intracellular inclusion bodies.

Only 20 patients have been identified since first recognized in 1974.

It is named for the Cuban physician and serologist Alejandro Moisés Chédiak (1903–1993) and the Japanese pediatrician Otokata Higashi (1883–1981). It is often spelled without the accent as Chediak–Higashi syndrome.

The methods used differ from country to country (definitions used, type of nosocomial infections covered, health units surveyed, inclusion or exclusion of imported infections, etc.), so the international comparisons of nosocomial infection rates should be made with the utmost care.

There is no standard course of treatment to slow or stop the progression of the disease. sIBM patients do not reliably respond to the anti-inflammatory, immunosuppressant, or immunomodulatory medications. Management is symptomatic. Prevention of falls is an important consideration. Specialized exercise therapy may supplement treatment to enhance quality of life. Physical therapy is recommended to teach the patient a home exercise program, to teach how to compensate during mobility-gait training with an assistive device, transfers and bed mobility.

Isolation is the implementation of isolating precautions designed to prevent transmission of microorganisms by common routes in hospitals. (See Universal precautions and Transmission-based precautions.) Because agent and host factors are more difficult to control, interruption of transfer of microorganisms is directed primarily at transmission for example isolation of infectious cases in special hospitals and isolation of patient with infected wounds in special rooms also isolation of joint transplantation patients on specific rooms.

Various systems are affected.

- CNS abnormalities – microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification

- Eye – choroidoretinitis and optic atrophy

- Ear – sensorineural deafness

- Liver – hepatosplenomegaly and jaundice due to hepatitis

- Lung – pneumonitis (interstitial pneumonitis)

- Heart – myocarditis

- Thrombocytopenic purpura, haemolytic anaemia

- Late sequelae in individuals asymptomatic at birth – hearing defects and reduced intelligence

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

Antivirals such as acyclovir, famciclovir, or valacyclovir may be used. Intravenous acyclovir is reserved for individuals who cannot swallow due to the pain, individuals with other systemic manifestations of herpes or severely immunocompromised individuals.

The disease is named after Gonzalo Rodríguez Lafora (1886–1971), a Spanish neuropathologist who first recognized small inclusion bodies in Lafora patients. Since the discovery of Lafora Disease in early to mid 1900's there has not been too much research into it, until more recent years.

Recent research is looking into how inhibition of glycogen synthesis, since increased glucose uptake causes increased glycogen, could potentially stop the formation of the Lafora Bodies in neurons in laforin-deficient mice models while also reducing the chances of seizures. The adipocyte hormone Leptin is what this research targeted by blocking the leptin signaling to reduce glucose uptake and stop Lafora bodies from forming.

Other researchers are looking into the ways in which Lafora bodies are being regulated at the level of gene expression. There is specific research looking into how Laforin, a glycogen dephosphatase, gene expression is potentially being downregulated or mutations are arising in the DNA in LD allowing more phosphates to be present helping to render glycogen insoluble.

During the past two years (2015-2017), researchers in U.S., Canada, and Europe have formed the (LECI) Lafora Epilepsy Cure Initiative to try and find a cure for Lafora Disease with funding from the National Institutes of Health (NIH) led by Dr. Matthew Gentry at the University of Kentucky. Since researchers have found the two genes that cause LD, they are currently aiming to interrupt the process of how these mutations in those genes interfere with normal carbohydrate metabolism in mice models. They predict they will have one or more drugs ready for human clinical trials within the next few years.