We followed 93 subjects with
amebic liver abscess (ALA) and 963 close associate controls at 3-month intervals for 36 months to characterize intestinal and humoral antibody responses to the amebic
galactose-inhibitable
lectin and to determine whether immunity developed to Entamoeba histolytica or Entamoeba dispar
infection following cure of ALA. We found that ALA subjects had a higher prevalence and level of intestinal antilectin
immunoglobulin A (
IgA) and serum anti-LC3 (
cysteine-rich recombinant
lectin protein)
IgA and
IgG antibodies, P < 0.01 and P < 0.05, respectively, compared to controls. The intestinal antilectin
IgA antibody response was sustained over a longer time period in ALA subjects (71.8% remained positive at 18 months and 52.6% at 36 months, P < 0.001 compared to 17.6% and 10.3% of controls, respectively). ALA subjects were highly immune to E. dispar
infection throughout the study (0% infected at 6 and 36 months, compared to 6.5% and 4.9% of control subjects, respectively, P < 0.05). Upon entry into the study, 6.3% of ALA subjects were infected with E. histolytica; the incidence of new E. histolytica
infections in controls (as determined by culture) was too low (1.4%) to determine whether ALA subjects exhibited immunity to new
infections. We found that stool cultures every 3 months markedly underestimated the occurrence of new E. histolytica
infections, as 15.3% of controls seroconverted after 12 months of follow-up. Unfortunately, under the field conditions present in Durban, South Africa,
enzyme-linked
immunosorbent assay for detection of
lectin antigen in stool yielded unreliable results. In summary, subjects cured of ALA exhibited sustained mucosal
IgA antibody responses to the amebic
galactose-inhibitable
lectin and a high level of immunity to E. dispar
infection. Determination of immunity to E. histolytica following cure of ALA will require the use of more sensitive and reliable diagnostic methods.