Diagnosis is often made by visualization of yeast cells in tissue, or superficial scrapings. Radiography of the chest reveals interstitial infiltrates in the majority of cases.

Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic broad based budding organisms in sputum or tissues by KOH prep, cytology, or histology. Tissue biopsy of skin or other organs may be required in order to diagnose extra-pulmonary disease. Blastomycosis is histologically associated with granulomatous nodules. Commercially available urine antigen testing appears to be quite sensitive in suggesting the diagnosis in cases where the organism is not readily detected. While culture of the organism remains the definitive diagnostic standard, its slow growing nature can lead to delays in treatment of up to several weeks. However, sometimes blood and sputum cultures may not detect blastomycosis.

Mortality rate in treated cases

- 0-2% in treated cases among immunocompetent patients

- 29% in immunocompromised patients

- 40% in the subgroup of patients with AIDS

- 68% in patients presenting as acute respiratory distress syndrome (ARDS)

It is not practical to test or decontaminate most sites that may be contaminated with "H. capsulatum", but the following sources list environments where histoplasmosis is common, and precautions to reduce a person's risk of exposure, in the three parts of the world where the disease is prevalent. Precautions common to all geographical locations would be to avoid accumulations of bird or bat droppings.

The US National Institute for Occupational Safety and Health (NIOSH) provides information on work practices and personal protective equipment that may reduce the risk of infection. This document is available in English and Spanish.

Authors at the University of Nigeria have published a review which includes information on locations in which histoplasmosis has been found in Africa (in chicken runs, bats and the caves bats infest, and in soil), and a thorough reference list including English, French, and Spanish language references.

The diagnosis is confirmed by a skin biopsy and a positive culture for acid-fast bacilli. A PPD test may also result positive.

Sulfonamides are the traditional remedies to paracoccidiodomycosis. They were introduced by Oliveira Ribeiro and used for more than 50 years with good results. The most-used sulfa drugs in this infection are sulfadimethoxime, sulfadiazine, and co-trimoxazole. This treatment is generally safe, but several adverse effects can appear, the most severe of which are the Stevens-Johnson syndrome and agranulocytosis. Similarly to tuberculosis treatment, it must be continued for up to three years to eradicate the fungus, and relapse and treatment failures are not unusual.

Antifungal drugs such as amphotericin B or itraconazole and ketoconazole are more effective in clearing the infection, but are limited by their cost when compared with sulfonamides.During therapy, fibrosis can appear and surgery may be needed to correct this. Another possible complication is Addisonian crisis. The mortality rate in children is around 7-10%.

Surgical excision or cryosurgery is the treatment of choice. Treatment with antifungals has been considered ineffective, but the use of clofazimine and dapsone in patients with leprosy and lobomycosis has been found to improve the latter. This treatment regimen, with concomitant itraconazole, has been used to prevent recurrence after surgery.

Clinically, there is a wide spectrum of disease manifestation, making diagnosis somewhat difficult. More severe forms include: (1) the chronic pulmonary form, often occurring in the presence of underlying pulmonary disease; and (2) a disseminated form, which is characterized by the progressive spread of infection to extra-pulmonary sites. Oral manifestations have been reported as the main complaint of the disseminated forms, leading the patient to seek treatment, whereas pulmonary symptoms in disseminated disease may be mild or even misinterpreted as flu. Histoplasmosis can be diagnosed by samples containing the fungus taken from sputum (via bronchoalveolar lavage), blood, or infected organs. It can also be diagnosed by detection of antigens in blood or urine samples by ELISA or PCR. Antigens can cross-react with antigens of African histoplasmosis (caused by Histoplasma duboisii), blastomycosis, coccidioidomycosis, paracoccidioidomycosis, and Penicillium marneffei infection. Histoplasmosis can also be diagnosed by a test for antibodies against "Histoplasma" in the blood. "Histoplasma" skin tests indicate whether a person has been exposed, but do not indicate whether they have the disease. Formal histoplasmosis diagnoses are often confirmed only by culturing the fungus directly. Sabouraud agar is one type of agar growth media on which the fungus can be cultured. Cutaneous manifestations of disseminated disease are diverse and often present as a nondescript rash with systemic complaints. Diagnosis is best established by urine antigen testing, as blood cultures may take up to 6 weeks for diagnostic growth to occur and serum antigen testing often comes back with a false negative before 4 weeks of disseminated infection.

The disease is often misdiagnosed as "Blastomyces dermatitidis" or "Paracoccidiodes brasiliensis" due to its similar morphology.

Therapy for cutaneous tuberculosis is the same as for systemic tuberculosis, and usually consists of a 4-drug regimen, i.e., isoniazid, rifampin, pyrazinamide, and ethambutol or streptomycin.

CLM can be treated in a number of different ways:

- Systemic (oral) agents include albendazole (trade name "Albenza") and ivermectin (trade name "Stromectol")).

- Another agent which can be applied either topically "or" taken by mouth is thiabendazole (trade name "Mintezol")), an anti-helminthic.

- Topical freezing agents, such as ethylene chloride or liquid nitrogen, applied locally can freeze and kill the larvae, but this method has a high failure rate because the larvae are usually located away from the site of the visible skin trails. Additionally, this is a painful method which can cause blistering and/or ulceration of the skin and it is therefore not recommended.

- It is recommended to use Benadryl or some anti-itch cream (i.e. Cortizone or Calamine lotion). This will help relieve some of the itch.

- Wearing shoes in areas where these parasites are known to be endemic offers protection from infection. In general, avoiding exposure of skin to contaminated soil or sand offers the best protection. In some areas dogs have been banned from beaches in an attempt to control human infection.

Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as "Staphylococcus aureus", in someone who has returned from an endemic area.

The gold standard for diagnosis is PCR (polymerase chain reaction) helps DNA polymerase to create new strands of DNA equivalent to template given.

The best treatment for cutaneous leishmaniasis is not known. Treatments that work for one species of leishmania may not work for another; it is recommended that advice of a tropical medicine or geographical medicine specialist be sought. Ideally, every effort should be made to establish the species of leishmania by molecular techniques (PCR) prior to starting treatment. In the setting of a developing country, there is often only one species present in a particular locality, so it is usually unnecessary to speciate every infection. Unfortunately, leishmaniasis is an orphan disease in developed nations, and almost all the current treatment options are toxic with significant side effects. The most sound treatment for cutaneous leishmaniasis thus far is prevention.

- "Leishmania major" :"L. major" infections are usually considered to heal spontaneously and do not require treatment, but there have been several reports of severe cases caused by "L. major" in Afghanistan. In Saudi Arabia, a six-week course of oral fluconazole 200 mg daily has been reported to speed up healing. In a randomized clinical trial from Iran, fluconazole 400 mg daily was shown to be significantly more effective than fluconazole 200 mg daily in the treatment of cutaneous leishmaniasis.

- "Leishmania braziliensis" :Treatment with pentavalent antimonials or amphotericin is necessary, because of the risk of developing disfiguring mucocutaneous lesions.

- "Leishmania infantum" :"L. infantum" causes cutaneous leishmaniasis in southern France.

New treatment options are arising from the new oral drug miltefosine (Impavido) which has shown in several clinical trials to be very efficient and safe in visceral and cutaneous leishmaniasis. Recent studies from Bolivia show a high cure rate for mucocutaneous leishmaniasis. Comparative studies against pentavalent antimonials in Iran and Pakistan are also beginning to show a high cure rate for "L. major" and "L. tropica". It is registered in many countries of Latin America, as well in Germany. In October 2006 it received orphan drug status from the US Food and Drug administration. The drug is generally better tolerated than other drugs. Main side effects are gastrointestinal disturbances in the 1–2 days of treatment which does not affect the efficacy.

Secondary bacterial infection (especially with "Staphylococcus aureus") is common and may require antibiotics. Clinicians who are unfamiliar with cutaneous leishmaniasis may mistake the lesion for a pure bacterial infection (especially after isolation of "S. aureus" from bacterial skin swabs) and fail to consider the possibility of leishmaniasis.

The number of cases in the US is not known, but a Hampshire veterinary practice reported on 24 March 2015 that there had been 103 suspected cases in the UK, including 52 deaths confirmed by postmortem examination.

The course of ACA is long-standing, from a few to several years, and it leads to extensive atrophy of the skin and, in some patients, to the limitation of upper and lower limb joint mobility.The outlook is good if the acute inflammatory stage of ACA is treated adequately. The therapeutic outcome is difficult to assess in patients with the chronic atrophic phase, in which many changes are only partially reversible.

Physicians should use serologic and histologic examination to confirm the diagnosis of ACA. Treatment consists of antibiotics including doxycycline and penicillin for up to four weeks in the acute case.

Treatment is primarily symptomatic involving wound management of skin lesions and aggressive supportive therapy when renal compromise occurs. Some UK dogs with Alabama rot have been successfully treated since 2013. A webinar on Alabama rot by the Royal Veterinary College on 11 February 2015 was tutored by David Walker of Anderson Moores Veterinary Specialists.

The infection causes a red, intensely pruritic (itchy) eruption. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop. Cutaneous larva migrans usually heals spontaneously over weeks to months and has been known to last as long as one year. However, the severity of the symptoms usually causes those infected to seek medical treatment before spontaneous resolution occurs. Following proper treatment, migration of the larvae within the skin is halted and relief of the associated itching can occur in less than 48 hours (reported for thiabendazole).

This is separate from the similar cutaneous larva currens which is caused by "Strongyloides". Larva currens is also a cause of migratory pruritic eruptions but is marked by 1) migratory speed on the order of inches per hour 2) perianal involvement due to autoinfection from stool and 3) a wide band of urticaria.

Cutaneous amoebiasis refers to a form of amoebiasis that presents primarily in the skin.

It can be caused by "Acanthamoeba" or "Entamoeba histolytica". When associated with "Acanthamoeba", it is also known as "cutaneous acanthamoebiasis".

It is also known as "amoebiasis cutis".

"Balamuthia mandrillaris" can cause cutaneous amoebiasis, but can prove fatal if the amoeba enters the bloodstream

If suspected, fungal meningitis is diagnosed by testing blood and CSF samples for pathogens. Identifying the specific pathogen is necessary to determine the proper course of treatment and the prognosis. Measurement of opening pressure, cell count with differential, glucose and protein concentrations, Gram's stain, India ink, and culture tests should be preformed on CSF samples when fungal meningitis is suspected.

Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.

The physical examination of the skin and its appendages, as well as the mucous membranes, forms the cornerstone of an accurate diagnosis of cutaneous conditions. Most of these conditions present with cutaneous surface changes termed "lesions," which have more or less distinct characteristics. Often proper examination will lead the physician to obtain appropriate historical information and/or laboratory tests that are able to confirm the diagnosis. Upon examination, the important clinical observations are the (1) morphology, (2) configuration, and (3) distribution of the lesion(s). With regard to morphology, the initial lesion that characterizes a condition is known as the "primary lesion," and identification of such a lesions is the most important aspect of the cutaneous examination. Over time, these primary lesions may continue to develop or be modified by regression or trauma, producing "secondary lesions." However, with that being stated, the lack of standardization of basic dermatologic terminology has been one of the principal barriers to successful communication among physicians in describing cutaneous findings. Nevertheless, there are some commonly accepted terms used to describe the macroscopic morphology, configuration, and distribution of skin lesions, which are listed below.

Leishmaniasis is diagnosed in the hematology laboratory by direct visualization of the amastigotes (Leishman-Donovan bodies). Buffy-coat preparations of peripheral blood or aspirates from marrow, spleen, lymph nodes, or skin lesions should be spread on a slide to make a thin smear and stained with Leishman stain or Giemsa stain (pH 7.2) for 20 minutes. Amastigotes are seen within blood and spleen monocytes or, less commonly, in circulating neutrophils and in aspirated tissue macrophages. They are small, round bodies 2–4 μm in diameter with indistinct cytoplasm, a nucleus, and a small, rod-shaped kinetoplast. Occasionally, amastigotes may be seen lying free between cells. However, the retrieval of tissue samples is often painful for the patient and identification of the infected cells can be difficult. So, other indirect immunological methods of diagnosis are developed, including enzyme-linked immunosorbent assay, antigen-coated dipsticks, and direct agglutination test. Although these tests are readily available, they are not the standard diagnostic tests due to their insufficient sensitivity and specificity.

Several different polymerase chain reaction tests are available for the detection of "Leishmania" DNA. With this assay, a specific and sensitive diagnostic procedure is finally possible.

Most forms of the disease are transmitted only from nonhuman animals, but some can be spread between humans. Infections in humans are caused by about 21 of 30 species that infect mammals; the different species look the same, but they can be differentiated by isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies.

Treatment consists of antibiotics, elevation of the affected limb, and compression. For persons with elephantiasis nostras who are overweight or obese, weight loss is recommended. Oral retinoids have been used to treat the cutaneous manifestations of the disease.

Lichen planus has a unique microscopic appearance that is similar between cutaneous, mucosal and oral. A Periodic acid-Schiff stain of the biopsy may be used to visualise the specimen. Histological features seen include:

- thickening of the stratum corneum both with nuclei present (parakeratosis) and without (orthokeratosis). Parakeratosis is more common in oral variants of lichen planus.

- thickening of the stratum granulosum

- thickening of the stratum spinosum (acanthosis) with formation of colloid bodies (also known as Civatte bodies, Sabouraud bodies) that may stretch down to the lamina propria.

- liquefactive degeneration of the stratum basale, with separation from the underlying lamina propria, as a result of desmosome loss, creating small spaces (Max Joseph spaces).

- Infiltration of T cells in a band-like pattern into the dermis "hugging" the basal layer.

- Development of a "saw-tooth" appearance of the rete pegs, which is much more common in non-oral forms of lichen planus.

The differential diagnosis for OLP includes:

- Other oral vesiculo-ulcerative conditions such as Pemphigus vulgaris and Benign mucous membrane pemphigoid

- Lupus erythematosus, with lesions more commonly occur on the palate and appear as centrally ulcerated or erythematous with radiating white striae. In contrast, OLP and lichenoid reactions rarely occur on the palate, and the striae are randomly arranged rather than radial.

- Chronic ulcerative stomatitis

- Frictional keratosis and Morsicatio buccarum (chronic cheek biting)

- Oral leukoplakia

- Oral candidiasis