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.

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.

The simplest procedure for 'in field diagnosis' is the detection of antibodies by latex agglutination (LAT) as it is quick and simple to run, and has a long shelf-life. Other procedures used for diagnosis include growth inhibition disc tests (GI), direct and indirect fluorescent antibody tests, complement fixation tests (CFT), indirect haemagglutination test (IHA), ELISA and PCR. These have varying degrees of efficacy.

Isolation of "M. capricolum "subsp. "capripneumoniae" from clinical samples is the only way to definitively diagnose the infection but it is not normally performed as it is time consuming and difficult.

This condition is diagnosed by detecting the bacteria in skin, blood, joint fluid, or lymph nodes. Blood antibody tests may also be used. To get a proper diagnosis for rat-bite fever, different tests are run depending on the symptoms being experienced.

To diagnosis streptobacillary rat-bite fever, blood or joint fluid is extracted and the organisms living in it are cultured. Diagnosis for spirillary rat bite fever is by direct visualization or culture of spirilla from blood smears or tissue from lesions or lymph nodes. Treatment with antibiotics is the same for both types of infection. The condition responds to penicillin, and where allergies to it occur, erythromycin or tetracyclines are used.

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.

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.

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.

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.

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.

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.

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.

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).

Dependent on the infectious syndrome, symptoms include fever, fatigue, dry cough, headache, blurred vision, and confusion. Symptom onset is often subacute, progressively worsened over several weeks. The two most common presentations are meningitis (an infection in and around the brain) and pulmonary (lung) infection.

Detection of cryptococcal antigen (capsular material) by culture of CSF, sputum and urine provides definitive diagnosis. Blood cultures may be positive in heavy infections. India ink of the CSF is a traditional microscopic method of diagnosis, although the sensitivity is poor in early infection, and may miss 15-20% of patients with culture-positive cryptococcal meningitis. Unusual morphological forms are rarely seen. Cryptococcal antigen from cerebrospinal fluid is the best test for diagnosis of cryptococcal meningitis in terms of sensitivity. Apart from conventional methods of detection like direct microscopy and culture, rapid diagnostic methods to detect cryptococcal antigen by latex agglutination test, lateral flow immunochromatographic assay (LFA), or enzyme immunoassay (EIA). A new cryptococcal antigen LFA was FDA approved in July 2011. Polymerase chain reaction (PCR) has been used on tissue specimens.

Cryptococcosis can rarely occur in the non-immunosuppressed people, particularly with "Cryptococcus gattii".

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.

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).

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.

Clinical examination and MRI are often the first steps in a MLD diagnosis. MRI can be indicative of MLD, but is not adequate as a confirming test.

An ARSA-A enzyme level blood test with a confirming urinary sulfatide test is the best biochemical test for MLD. The confirming urinary sulfatide is important to distinguish between MLD and pseudo-MLD blood results.

Genomic sequencing may also confirm MLD, however, there are likely more mutations than the over 200 already known to cause MLD that are not yet ascribed to MLD that cause MLD so in those cases a biochemical test is still warranted.

"For further information, see the MLD Testing page at MLD Foundation."

The diagnosis is based on microscopic criteria. Ideally, phase-contrast microscopy is used with a magnification of 400x (high-power field). For scoring purposes, along with relative number of leucocytes, percentage of toxic leucocytes, background flora and proportion of epitheliocytes, lactobacillary grade must be evaluated:

- grade I

- grade IIa

- grade IIb

- grade III

The "AV score" is calculated according to what is described in the table.

- AV score <3: no signs of AV

- AV score 3 or 4: light AV

- AV score 5 or 6: moderate AV

- AV score ≥6: severe AV.

pH measurement alone is not enough for the diagnosis.

Aerobic vaginitis has been associated with several gynecological and obstetrical complications, including:

- Premature rupture of membranes

- Preterm labour

- Ascending chorioamnionitis.

- Increased risk to acquire sexually transmitted infections (including HIV)

- Abnormal Pap test results

Beech bark disease is a disease that causes mortality and defects in beech trees in the eastern United States and Europe. In North America, the disease occurs after extensive bark invasion by the beech scale insect, "Cryptococcus fagisuga". Through a presently unknown mechanism, excessive feeding by this insect causes two different fungi ("Neonectria faginata" (previously "Nectria coccinea var. faginata") and "Neonectria ditissima" (previously "Nectria galligena")) to produce annual cankers on the bark of the tree. The continuous formation of lesions around the tree eventually girdles it, resulting in canopy death. In Europe, "N. coccinea" is the primary fungus causing the infection. Infection in European trees occurs in the same manner as it does in North American trees. Though the disease still appears in Europe, it is less serious today than it once was.

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%.

The cause of the disease is thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buerger's as primary disease.

A neurological examination would show evidence of muscle rigidity; weakness; and abnormal postures, movements, and tremors. If other family members are also affected, this may help determine the diagnosis. Genetic tests can confirm an abnormal gene causing the disease. However, this test is not yet widely available. Other movement disorders and diseases must be ruled out. Individuals exhibiting any of the above listed symptoms are often tested using MRI (Magnetic Resonance Imaging) for a number of neuro-related disorders. As PKAN is a disease prominently evident in the brain, MRIs are very useful in making a sound diagnosis. An MRI usually shows iron deposits in the basal ganglia. Development of diagnostic criteria continues in the hope of further separating PKAN from other forms of neurodegenerative diseases featuring NBIA.

Microscopic features of PKAN include:

- Iron granules

- Spheroid bodies

- Lewy bodies within neurons

Because it is a rare disease, diagnosis is often complicated and takes a long time. Early in the disease patients may have erosions in the mouth or blisters on the skin. These blisters can be itchy or painful. Theoretically, the blisters should demonstrate a positive Nikolsky's sign, in which the skin sloughs off from slight rubbing, but this is not always reliable. The gold standard for diagnosis is a punch biopsy from the area around the lesion that is examined by direct immunofluorescent staining, in which cells are acantholytic, that is, lacking the normal intercellular connections that hold them together. These can also be seen on a Tzanck smear. These cells are basically rounded, nucleated keratinocytes formed due to antibody mediated damage to cell adhesion protein desmoglein.

Pemphigus vulgaris is easily confused with impetigo and candidiasis. IgG4 is considered pathogenic. The diagnosis can be confirmed by testing for the infections that cause these other conditions, and by a lack of response to antibiotic treatment.