Prospective clinico-pathological study of pregnancy and leprosy in Ethiopia

Abstract

One hundred and fourteen women with leprosy and 33 healthy controls were studied through 120 and 36 pregnancies respectively and followed up with their babies during lactation. Sixty-one mothers showed deterioration of their leprosy status (overt leprosy, relapse in cured cases, and deterioration in those on treatment, 28 with suspected drug resistance); 31 showed relapse during the third trimestre of pregnancy, 21 as a transient phenomenon. Reversal reaction, in contrast, occurred immediately after delivery, while erythema nodosum leprosum showed the highest incidence in the first trimestre; both reactions persisted/recurred well into the second year of lactation. The most serious effect of these reactions was nerve damage. Nearly half of the leprosy patients showed loss of sensory and/or motor nerve function during a single pregnancy/lactation: all mothers were at risk. Silent neuritis seen more frequently than overt neuritis (48 : 37 episodes) was a particularly dangerous and hitherto undescribed risk of pregnancy.

Placental function, normal in healthy controls, showed a falling trend across the leprosy spectrum to lowest in mothers with lepromatous leprosy: babies' birth weights, placental weights and placental coefficients followed the same trend. No morphological abnormality was detected in any of the placentae. Placentae of lepromatous mothers were small because of reduced cytoplasmic mass; very few acid-fast bacilli or debris were found, even in placentae from women with very active lepromatous leprosy. Milk studies showed no DVcobacterium lei e and no significant differences between the different groups of mothers in terms of total protein or defence factors. Babies of mothers with leprosy grew more slowly, were more susceptible to infections and had a higher infant mortality rate than babies of healthy mothers: this was most marked in babies of mothers with lepromatous leprosy. Two children developed overt leprosy, with histological confirmation and spontaneous healing.

Evidence for the transplacental transmission of Mycobacterium lei rae antigen/whole Mycobacterium leprae are: i) increase in IgA in cord sera; ii) increased antibodies against Mycobacterium leprae antigen 7 during the first 18 months of life; and iii) specific IgA, IgG and IgM antibodies against Mycobacterium leprarea e during the first two years of life, in babies of mothers with lepromatous leprosy.