what are the factors determining infection?
Answers
Explanation:
Factors determining clinical expression after infection
There is sufficient evidence in leprosy that not all people who get infected get the disease. The factors that determine clinical expression after infection appear to be as important as the factors that determine infection after exposure. Of the many possible factors that determine clinical expression of disease, a few are discussed below.
Genetic factors
Genetic factors have been considered for a long time in leprosy. This is largely due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy, while others develop non-lepromatous leprosy. Admittedly, it is the host factors that play a key role. However, what is not clear is the role of genetics vis-a-vis other factors in determining this clinical expression.
Route of Infection
Studies by Shepard et al (1982) in the mouse footpad model suggest that the route of entry of the organism may, to some extent, determine the occurrence of leprosy. This is based on the observation that while intradermal administration of killed M.leprae sensitizes the animal, intravenous administration of killed M.leprae tends to tolerize the animal as studied through skin test reactivity. This also raises the possibility of tuberculoid and lepromatous leprosy being the result of different routes of entry of the organisms.
Re-infection
The occurrence of leprosy, presumably for the first time, in older individuals in endemic areas has raised the possibility of re-infection in these individuals, since it is difficult to believe that they remained uninfected for such a long time in an endemic area. However, this occurrence in the older ages can also be explained by the possibility that the disease in these persons represents reactivation of old undetected primary disease following waning of previously acquired immunity. Since there is no evidence of a distinct primary disease occurring in leprosy as in tuberculosis, the hypothesis of re-infection gains some importance. Further, the occurrence of relapse in lepromatous leprosy also suggests, at least in a proportion of relapsed individuals, the possibility of re-infection. There is nothing to prevent these immune deficient inactive patients living in endemic areas from succumbing to fresh infection. In the absence of a metho for the identification of strain variations of M.leprae, the hypothesis on re-infection will remain untested.
Prior infection with other mycobacteria
There is some evidence that as in tuberculosis, the atypical environmental mycobacteria and possibly M.tuberculosis play a role in the occurrence of leprosy. This is possibly due to antigenic overlap between M.leprae and other mycobacteria. The varying degrees of protection given by BCG against leprosy in different geographic areas, and the limited protection seen among natural tuberculin positive reactor in the BCG study in Uganda (Stanley et al, 1981), support this possibility. Rook et al (1981) have gone further and have suggested that the protective efficacy of BCG in different areas may be enhanced or diminished depending upon the local environmental mycobacteria, some acting synergistically with BCG and some antagonistically.
HIV infection and leprosy
It is now well recognized that the HIV infection has created a serious situation with regard to the incidence of tuberculosis. Case control studies carried out in several parts of Africa have clearly shown that the substantial increase in pulmonary tuberculosis is attributable to HIV infection. This is also true for atypical mycobacteriosis. Although a similar situation is possible with regard to leprosy there is no clear information on this so far. There have been a few anecdotal reports on leprosy and HIV infection occurring together. However, it is not clear whether or not this is a result of coincidence. Only good case control studies can provide an answer to the question of HIV infection s a risk factor for clinical leprosy. In a not-so-well controlled study Meeran (1989) reported the prevalence of HIV infection to be significantly higher among patients with leprosy as compared with blood donors or surgical patients. However, other reports (Leonard et al, 1990; Ponnighaus et al, 1991) suggest it may not be so. One of the problems identified recently in interpreting HIV sero-diagnosis information based on ELISA and/or Western Blot is the possibility of a significantly higher rate of false positive results (Shirai et al, 1988 and Andrade et al, 1991) occurring among sera from lepromatous leprosy patients.