The potent effects of HIV infection on the human immune system, the complexity of the host-parasite interaction in leprosy, and the paucity of current information on the natural history of co-infected patients makes this area a fertile ground for clinical and immunologic investigation. Several studies have now validated the prediction that there exists a large cohort of patients, particularly in Africa, who are concurrently infected with HIV and M. leprae. Sparse but tantalizing evidence suggests that infection with HIV may increase the incidence of leprosy among individuals with subclinical infection with M. leprae, either through shortening the incubation period or by increasing disease penetrance. Similarly, active mycobacterial disease may accelerate the course of HIV disease, as has been postulated to occur during concurrent infections with certain other viral and bacterial pathogens in HIV-positive patients. A subtle and complex interplay between HIV and leprosy may thus result which will impact the observed epidemiology of both illnesses in regions where both are prevalent. Possible effects of the HIV epidemic on leprosy control programs have been outlined by the World Health Organization and in an editorial by Turk and Rees. The published experience provides few guidelines for the clinical care of co-infected patients. The initial response to conventional therapeutic regimens appears to be excellent, but no follow-up data have been included. The possible absence of ENL in these patients would simplify care for multibacillary disease, if this observation is confirmed in larger field studies.(ABSTRACT TRUNCATED AT 250 WORDS)
PIP: A literature search of coinfection with HIV and leprosy retrieved 4 case reports, 4 epidemiologic studies, 2 primate studies, and an editorial The 1st case was a 43-year old male with borderline tuberculoid leprosy who was successfully treated with dapsone and clofazimine, but later developed Kaposi's sarcoma and pulmonary tuberculosis. The 2nd case was a 28-year old male from Martinique who had been treated with triple therapy (dapsone, rifampin, and clofazimine) for lepromatous disease with erythema nodosum leprosum for 9 years, but later developed reactive polyarthritis and 1+ bacterial index along with generalized lymphadenopathy with his HIV. A 3rd case was a 27-year old male who had been treated for cutaneous leprosy for 4 years. 5 years later he had polyneuropathy and palpable nerve trunks suggestive of a reversal reaction, and candida esophagitis with a CD4/CD8 ratio of 0.3. The 4th case was a 35-year old woman with BT-BB leprosy on clinical grounds, but apparent BL leprosy by histology. It was also noted that her granulomas had a high CD4+ lymphocyte count, while her circulating CD4/CD8 ratio was 0.6 with a low CD4 count of 300. The 4 epidemiologic series were from Zambia, Haiti, Ethiopia, and a large series of cases from Ivory Coast, Congo, Senegal, and Yemen. Some preliminary conclusions from these data were that HIV infection does not affect the clinical classification of leprosy, that HIV infection may confer anergy to lepromin, that HIV infection may cause relapse of leprosy, and that leprosy may accelerate the progression of HIV. There were 2 cases where leprosy grading reaction reversed or downgraded in coinfected patients. In the primate model, coinfection with SIV and M. leprae increases susceptibility of monkeys to leprosy.