In psychiatry, dysaesthesia aethiopica was an alleged mental illness described by American physician Samuel A. Cartwright in 1851, which proposed a theory for the cause of laziness among slaves. Today, dysaesthesia aethiopica is considered an example of pseudoscience, and part of the edifice of scientific racism.

Found exclusively among Blacks, dysaesthesia aethiopica – "called by overseers 'rascality'" – was characterized by partial insensitivity of the skin and "so great a of the intellectual faculties, as to be like a person half asleep." Other symptoms included "lesions of the body discoverable to the medical observer, which are always present and sufficient to account for the symptoms." Cartwright noted that the existence of dysaesthesia aethiopica was "clearly established by the most direct and positive testimony," but other doctors had failed to notice it because their "attention [had] not been sufficiently directed to the maladies of the negro race."

According to Cartwright, dysaesthesia aethiopica was "much more prevalent among free negroes living in clusters by themselves, than among slaves on our plantations, and attacks only such slaves as live like free negroes in regard to diet, drinks, exercise, etc." – indeed, according to Cartwright, "nearly all [free negroes] are more or less afflicted with it, that have not got some white person to direct and to take care of them." He explicitly dismissed the opinion which assigned the causes of the "problematic" behaviour to the social situation of the slaves without further justifications: "[The northern physicians] ignorantly attribute the symptoms to the debasing influence of slavery on the mind."

Cartwright felt that dysaesthesia aethiopica was "easily curable, if treated on sound physiological principles." Insensitivity of the skin was one symptom of the disease, so the skin should be stimulated:

Author Vanessa Jackson has noted that lesions were a symptom of dysaesthesia aethiopica and "the ever-resourceful Dr. Cartwright determined that whipping could ... cure this disorder. Of course, one wonders if the whipping were not the cause of the 'lesions' that confirmed the diagnosis."

According to Cartwright, after the prescribed "course of treatment" the slave will "look grateful and thankful to the white man whose compulsory power ... has restored his sensation and dispelled the mist that clouded his intellect."

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.

Mucocutaneous leishmaniasis is an especially disturbing form of cutaneous leishmaniasis, because it produces destructive and disfiguring lesions of the face. It is most often caused by "Leishmania braziliensis", but cases caused by "L. aethiopica" have also been described.

Mucocutaneous leishmaniasis is very difficult to treat. Treatment involves the use of pentavalent antimonial compounds, which are highly toxic (common side effects include thrombophlebitis, pancreatitis, cardiotoxicity and hepatotoxicity) and not very effective. For example, in one study, despite treatment with high doses of sodium stibogluconate for 28 days, only 30% of patients remained disease-free at 12 months follow-up. Even in those patients who achieve an apparent cure, as many as 19% will relapse. Several drug combinations with immunomodulators have been tested, for example, a combination of pentoxifylline (inhibitor of TNF-α) and a pentavalent antimonial at a high dose for 30 days in a small-scale (23 patients) randomised placebo-controlled study from Brazil achieved cure rates of 90% and reduced time to cure, a result that should be interpreted cautiously in light of inherent limitations of small-scale studies. In an earlier small-scale (12 patients) study, addition of imiquimod showed promising results which need yet to be confirmed in larger trials.