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."

Post-kala-azar dermal leishmaniasis (PKDL) is a recurrence of kala-azar that may appear on the skin of affected individuals months and up to 20 years after being partially treated, untreated or even in those considered adequately treated. In Sudan, they can be demonstrated in up to 60% of treated cases. They manifest as hypopigmented skin lesions (such as macules, papules, nodules), or facial redness. Though any organism causing kala-azar can lead to PKDL, it is commonly associated with "Leishmania donovani" which gives different disease patterns in India and Sudan. In the Indian variant, nodules enlarge with time and form plaques but rarely ulcerate, but nodules from the African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent. Histology demonstrates a mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma. Parasite concentration is not consistent among studies, perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.

Current approach to diagnosis involves 1. demonstration of parasite by microscopy, "in vitro" culture or animal inoculation; 2. immunodiagnosis of parasite antigen; 3. detection of parasite DNA in tissue. Newer PCR based tools have higher sensitivity and specificity. Emergence of PKDL has been reported in HIV affected individuals and may become a problem in future.

Sodium stibogluconate alone or in combination with rifampicin is used for the treatment of PKDL for a long course of up to 4 months. Compliance can be an issue for such a long course.

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.