Because this disease is highly durable in its equine host, it has proved very difficult to develop a vaccine for it. There are four main drugs on the market that are used to treat the clinical signs of dourine: Suramin, Diminazen, Cymerlarsan, and Quinapyramin. However, none of the listed drugs are a cure and even the individual animals that are treated will experience relapses. Although this disease is not fatal in all cases and spontaneous recovery can occur, the death rate is relatively high and listed at a mortality rate of over fifty percent.

This lack of a cure or vaccine is a definite problem in the equine industry, especially in developing countries where equines are highly valuable for both agriculture and transportation. Dourine is considered an endemic problem in developing countries, where over sixty percent of equines in the world are located. The protocol for this disease, as stated by OIE, currently stands at slaughter of seropositive animals. This is not an economically feasible option for many people who depend on horses for their livelihood. Therefore, it is crucial to continue research in this field and develop a viable vaccine.

Subcutaneous cysts may be surgically opened to remove less mature bots. If more matured, cysts may be opened and "cuterebra" may be removed using mosquito forceps. Covering the pore in petroleum jelly may aide in removal. If larvae are discovered within body tissues, rather than subcutaneously, surgical removal is the only means of treatment. Ivermectin may be administered with corticosteroids to halt larval migration in cats presenting with respiratory cuterebriasis, but this is not approved for use in cats. There is not yet a known cure for cerebrospinal cuterebriasis.

When proper treatment is provided for patients with rat-bite fever, the prognosis is positive. Without treatment, the infection usually resolves on its own, although it may take up to a year to do so. A particular strain of rat-bite fever in the United States can progress and cause serious complications that can be potentially fatal. Before antibiotics were used, many cases resulted in death. If left untreated, streptobacillary rat-bite fever can result in infection in the lining of the heart, covering over the spinal cord and brain, or in the lungs. Any tissue or organ throughout the body may develop an abscess.

Macrolides, tetracyclines and quinolones are active against "M. capricolum" subsp." capripneumoniae". Disease incidence is reduced by good hygiene and husbandry practices.

Movement restrictions and slaughtering infected animals are recommended for countries that are newly infected.

Covering sickness, or dourine (French, from the Arabic "darina", meaning mangy (said of a female camel), feminine of "darin", meaning dirty), is a disease of horses and other members of the family Equidae. The disease is caused by "Trypanosoma equiperdum", which belongs to an important genus of parasitic protozoa, and is the only member of the genus that is spread through sexual intercourse. The occurrence of dourine is notifiable in the European Union under legislation from the OIE. There currently is no vaccine and although clinical signs can be treated, there is no cure.

While obviously preventable by staying away from rodents, otherwise hands and face should be washed after contact and any scratches both cleaned and antiseptics applied. The effect of chemoprophylaxis following rodent bites or scratches on the disease is unknown. No vaccines are available for these diseases.

Improved conditions to minimize rodent contact with humans are the best preventive measures. Animal handlers, laboratory workers, and sanitation and sewer workers must take special precautions against exposure. Wild rodents, dead or alive, should not be touched and pets must not be allowed to ingest rodents.

Those living in the inner cities where overcrowding and poor sanitation cause rodent problems are at risk from the disease. Half of all cases reported are children under 12 living in these conditions.

To reduce the itching, an application of anti-itch cream containing hydrocortisone, calamine, or benzyl benzoate is often used (though calamine has been shown not to be effective). Hydrogen peroxide and capsaicin cream has also been effective. Another good way to relieve itching is to apply heat—either by using a hand held shower with water hot as one can stand, or by heating the bite with a hair dryer. The heat method will relieve itching for about four hours and will require repeating.

In some cases, the chigger is still present when the bite appears. A 10× magnifier can be used to see the chigger and it may be removed with fine-tipped tweezers. Once it is gone, covering the bite with nail polish, calamine lotion, vaseline or other petroleum jelly, baby oil, or anything else may help the pain and itching, but will neither suffocate the chigger nor help the bites heal any faster. Medication such as antihistamines or corticosteroid creams may be prescribed by doctors, and might help in some instances.

Treatment options in persons without HIV-infection have not been well studied. Intravenous Amphotericin B combined with flucytosine by mouth is recommended.

Persons living with AIDS often have a greater burden of disease and higher mortality (30-70% at 10-weeks), but recommended therapy is with amphotericin B and flucytosine. Where flucytosine is not available (many low and middle income countries), fluconazole should be used with amphotericin. Amphotericin-based induction therapy has much greater microbiologic activity than fluconazole monotherapy with 30% better survival at 10-weeks. Based on a systematic review of existing data, the most cost-effective induction treatment in resource-limited settings appears to be one week of amphotericin B coupled with high-dose fluconazole. After initial induction treatment as above, typical consolidation therapy is with oral fluconazole for at least 8 weeks used with secondary prophylaxis with fluconazole thereafter.

The decision on when to start treatment for HIV appears to be very different than other opportunistic infections. A large multi-site trial supports deferring ART for 4–6 weeks was overall preferable with 15% better 1-year survival than earlier ART initiation at 1–2 weeks after diagnosis. A Cochrane review also supports the delayed starting of treatment until cryptococcosis starts improving with antifungal treatment.

Definitive diagnosis can only occur with positive identification of the larvae. This involves radiologic imaging (preferably MRI which can reveal larval migration tracks and in some cases the larvae themselves) as well as surgical exploration during which larvae can be removed and examined for identification. Identification of exact species is often impossible as the instars of the various "Cuterebra" and "Trychoderma" spp. exhibit significant resemblance, but identification as a "Cuterebra" bot fly is sufficient for diagnosis as cuterebriasis. Typically, a third larval instar is found and identifiable by its dark, thick, heavily spined body.

Equine venereal diseases are sexually transmitted infections in horses. They include contagious equine metritis (CEM) (caused by "Taylorella equigenitalis") and equine coital exanthema (caused by equine herpesvirus 3).

In an endemic herd, only a minority of the animals develops clinical signs; most animals either eliminate the infection or become asymptomatic carriers. The mortality rate is about 1%, but up to 50% of the animals in the herd can be asymptomatically infected, resulting in losses in production. Once the symptoms appear, paratuberculosis is progressive and affected animals eventually die. The percentage of asymptomatic carriers that develop overt disease is unknown.

MAP is capable of causing Johne's-like symptoms in humans, though difficulty in testing for MAP infection presents a diagnostic hurdle.

Clinical similarities are seen between Johne's disease in ruminants and inflammatory bowel disease in humans, and because of this, some researchers contend the organism is a cause of Crohn's disease. However, epidemiologic studies have provided variable results; in certain studies, the organism (or an immune response directed against it) has been much more frequently found in patients with Crohn's disease than asymptomatic people.

Chiggers are commonly found on the tip of blades of grasses to catch a host, so keeping grass short, and removing brush and wood debris where potential mite hosts may live, can limit their impact on an area. Sunlight that penetrates the grass will make the lawn drier and make it less favorable for chigger survival.

Chiggers seem to affect warm covered areas of the body more than drier areas. Thus, the bites are often clustered behind the knees, or beneath tight undergarments such as socks, underwear, or brassieres. Areas higher in the body (chest, back, waist-band, and under-arms) are affected more easily in small children than in adults, since children are shorter and are more likely than adults to come in contact with low-lying vegetation and dry grass where chiggers thrive. An exceptional case has been described in the eye, producing conjunctivitis.

Application of repellent to the shoes, lower trousers and skin is also useful. Because they are found in grass, staying on trails, roads, or paths can prevent contact. Dusting sulfur is used commercially for mite control and can be used to control chiggers in yards. The dusting of shoes, socks and trouser legs with sulfur can be highly effective in repelling chiggers.

Another good strategy is to recognize the chigger habitat to avoid exposure in the first place. Chiggers in North America thrive late in summer, in dry tall grasses and other thick, unshaded vegetation. Insect repellents containing one of the following active ingredients are recommended: DEET, catnip oil extract (nepetalactone), citronella oil or eucalyptus oil extract. However, in 1993 issue a study reported on tests of two commercial repellents: DEET and citrus oil: "All chiggers exposed on the filter papers treated with DEET died and did not move off the treated papers. None of the chiggers that were placed on papers treated with citrus oil were killed." It was concluded that DEET was more effective than citrus oil.

Chiggers can also be treated using common household vinegar (5% acetic acid).

This disease affects the external genitalia, and is caused by equine herpesvirus 3. This disease remains with the horse for all its life. Equine coital exanthema is believed to only be transmitted during the acute phase of the disease through serous fluid from the blisters during sexual intercourse, and via breeding tools, handlers, etc.

Clinical signs include cute small lesions, no bigger than 2 mm in diameter around the vulva in mares, and on the sheath in stallions. The small bumps blister and then rupture, leaving raw, ulcerated, painful sores. While the majority of the symptoms are external, the presence of the virus can cause small and large plaque variants in tissues.

Contagious caprine pleuropneumonia (CCPP) is a cause of major economic losses to goat producers in Africa, Asia and the Middle East.

Disease is caused by members of the Mycoplasma genus - usually "Mycoplasma capricolum subsp. capricolum" but sometimes by "M. mycoides" subsp. "capri" or "M. mycoides" subsp. "mycoides". It is extremely contagious with very high morbidity and mortality rates, causing an interstitial fibrinous pleuropneumonia in infected goats. Infection is spread by close-contact aerosol, therefore overcrowding and confinement increases disease incidence. Stress factors such as malnutrition and long transport can also predispose animals to disease.

Goats are the only species affected, therefore the disease is not a zoonosis. There is no age breed or sex predilection, but clinical signs are often worse in younger animals.

Cryptococcosis is a very subacute infection with a prolonged subclinical phase lasting weeks to months in persons with HIV/AIDS before the onset of symptomatic meningitis. In Sub-Saharan Africa, the prevalence rates of detectable cryptococcal antigen in peripheral blood is often 4–12% in persons with CD4 counts lower than 100 cells/mcL.

Cryptococcal antigen screen and preemptive treatment with fluconazole is cost saving to the healthcare system by avoiding cryptococcal meningitis. The World Health Organization recommends cryptococcal antigen screening in HIV-infected persons entering care with CD4<100 cells/μL. This undetected subclinical cryptococcal (if not preemptively treated with anti-fungal therapy) will often go on to develop cryptococcal meningitis, despite receiving HIV therapy. Cryptococcosis accounts for 20-25% of the mortality after initiating HIV therapy in Africa. What is effective preemptive treatment is unknown, with the current recommendations on dose and duration based on expert opinion. Screening in the United States is controversial, with official guidelines not recommending screening, despite cost-effectiveness and a 3% U.S. cryptococcal antigen prevalence in CD4<100 cells/μL.

Smoking cessation has been shown to slow the progression of the disease and decrease the severity of amputation in most patients, but does not halt the progression.

In acute cases, drugs and procedures which cause vasodilation are effective in reducing pain experienced by patient. For example, prostaglandins like Limaprost are vasodilators and give relief of pain, but do not help in changing the course of disease. Epidural anesthesia and hyperbaric oxygen therapy also have vasodilator effect.

In chronic cases, lumbar sympathectomy may be occasionally helpful. It reduces vasoconstriction and increases blood flow to limb. It aids in healing and giving relief from pain of ischemic ulcers. Bypass can sometimes be helpful in treating limbs with poor perfusion secondary to this disease. Use of vascular growth factor and stem cell injections have been showing promise in clinical studies. Debridement is done in necrotic ulcers. In gangrenous digits, amputation is frequently required. Above-knee and below-knee amputation is rarely required.

Streptokinase has been proposed as adjuvant therapy in some cases.

Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as corticosteroids have not been shown to be beneficial in healing, but do have significant anti-inflammatory and pain relief qualities in low dosage intermittent form. Similarly, strategies of anticoagulation have not proven effective.

physical therapy: interferential current therapy to decrease inflammation

No curative treatment against EV has been found yet. Several treatments have been suggested, and acitretin 0.5–1 mg/day for 6 months’ duration is the most effective treatment owing to antiproliferative and differentiation-inducing effects.

Interferons can also be used effectively together with retinoids.

Cimetidine was reported to be effective because of its depressing mitogen-induced lymphocyte proliferation and regulatory T cell activity features. A report by Oliveira "et al." showed that cimetidine was ineffective. Hayashi "et al." applied topical calcipotriol to a patient with a successful result.

As mentioned, various treatment methods are offered against EV; however, most importantly, education of the patient, early diagnosis, and excision of the tumoral lesions take preference to prevent the development of cutaneous tumors.

Treatment is not always easy and aims at correcting the three key changes encountered in aerobic vaginitis: the presence of atrophy, inflammation and abnormal flora. The treatment can include topical steroids to diminish the inflammation and topical estrogen to reduce the atrophy. The use and choice of antibiotics to diminish the load/proportion of aerobic bacteria is still a matter of debate. The use of local antibiotics, preferably local non-absorbed and broad spectrum, covering enteric gram-positive and gram-negative aerobes, like kanamycin can be an option. In some cases, systemic antibiotics can be helpful, such as amoxyclav or moxifloxacin. Vaginal rinsing with povidone iodine can provide rapid relief of symptoms but does not provide long-term reduction of bacterial loads. Dequalinium chloride can also be an option for treatment.

There are a few controls for beech bark disease. One important management strategy is prohibiting the movement of nursery stock or other materials that may harbor the beech scale insect. Insecticides, generally not applied under forest conditions, are primarily used on high-value ornamental trees. The use of other organisms as controls is also a possibility. The ladybird beetle is a beetle that preys on the beech scale insect. A fungus that parasitizes the "Neonectria" fungus could also be employed. The problem with using these organisms to control beech bark disease is that their impact on the disease has not been evaluated extensively. In a forest setting, controlling the beech bark disease is too costly. Timely salvage cutting can reduce economic losses of beech in a forest. In stands where beech bark disease is established, silvicultural best practice is to retain large overstory trees which show visual resistance (no scale, cankers or fungus), remove heavily infested/dying trees and then treat sprouts from infested trees with herbicides. The residual, resistant parent trees are future sources of resistant seed/sprouts. Resistance to beech bark disease in a stand may be 1%-5% of trees or more, with significant regional variation. A study of 35 sites in three Canadian provinces found resistance rates ranging from 2.2%-5.7%.

Corticosteroids and other immunosuppressive medications have historically been employed to reduce pemphigus symptoms, yet steroids are associated with serious and long-lasting side effects and their use should be limited as much as possible. Intravenous immunoglobulin, mycophenolate mofetil, methotrexate, azathioprine, and cyclophosphamide have also been used with varying degrees of success.

An established alternative to steroids are monoclonal antibodies such as rituximab, which are increasingly being used as first-line treatment. In numerous case series, many patients achieve remission after one cycle of rituximab. Treatment is more successful if initiated early on in the course of disease, perhaps even at diagnosis. Rituximab treatment combined with monthly IV immunoglobulin infusions has resulted in long-term remission with no recurrence of disease in 10 years after treatment was halted. This was a small trial study of 11 patients with 10 patients followed to completion.

There is currently no therapy or cure for MLD in late infantile patients displaying symptoms, or for juvenile and adult onset with advanced symptoms. These patients typically receive clinical treatment focused on pain and symptom management.

Pre-symptomatic late infantile MLD patients, as well as those with juvenile or adult MLD that are either presymptomatic or displaying mild symptoms, can consider bone marrow transplantation (including stem cell transplantation), which may slow down progression of the disease in the central nervous system. However, results in the peripheral nervous system have been less dramatic, and the long-term results of these therapies have been mixed. Recent success has involved stem cells being taken from the bone marrow of children with the disorder and infecting the cells with a retro-virus, replacing the stem cells' mutated gene with the repaired gene before re-injecting it back into the patient where they multiplied. The children by the age of five were all in good condition and going to kindergarten when normally by this age, children with the disease can not even speak.

Several therapy options are currently being investigated using clinical trials primarily in late infantile patients. These therapies include gene therapy, enzyme replacement therapy (ERT), substrate reduction therapy (SRT), and potentially enzyme enhancement therapy (EET).

A team of international researchers and foundations gathered in 2008 to form an international MLD Registry to create and manage a shared repository of knowledge, including the natural history of MLD. This consortium consisted of scientific, academic and industry resources. This registry never became operational.

Although there is no known cure for Krabbe disease, bone marrow transplantation has been shown to benefit cases early in the course of the disease. Generally, treatment for the disorder is symptomatic and supportive. Physical therapy may help maintain or increase muscle tone and circulation. Cord blood transplants have been successful in stopping the disease as long as they are given before overt symptoms appear.

There have been no major breakthroughs in the treatment of PKAN, with most pharmacologic treatments focusing on the easing or temporary relieving of PKAN’s symptoms. Iron chelating agents have been used somewhat successfully in retarding the disorder, but they have not been a significant success.

Current research focuses on the future use of high dose pantothenate, the PANK2 enzyme substrate, in possibly alleviating symptoms as well as the further development of iron chelating agents that may be better aimed at reaching the central nervous system and working to better remove excess iron from the individual’s system.

Complications may result from the medication used to treat symptoms. Immobility from the disease can also lead to skin breakdown, respiratory infections, and blood clots, among others.

There is no cure for Canavan disease, nor is there a standard course of treatment. Treatment is symptomatic and supportive. There is also an experimental treatment using lithium citrate. When a person has Canavan disease, his or her levels of N-acetyl aspartate are chronically elevated. The lithium citrate has proven in a rat genetic model of Canavan disease to be able to significantly decrease levels of N-acetyl aspartate. When tested on a human, the subject's condition reversed during a two-week wash-out period after withdrawal of lithium.

The investigation revealed both decreased N-acetyl aspartate levels in regions of the brain tested and magnetic resonance spectroscopic values that are more characteristic of normal development and myelination. This evidence suggests that a larger controlled trial of lithium may be warranted as supportive therapy for children with Canavan disease.

Experimental gene therapy trial results, published in 2002, used a healthy gene to take over for the defective one that causes Canavan disease.

In human trials, the results of which were published in 2012, this method appeared to improve the life of the patient without long-term adverse effects during a 5-year follow-up.