Intestinal antilectin immunoglobulin A antibody response and immunity to Entamoeba dispar infection following cure of amebic liver abscess.
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.
Ravdin
Jonathan I
JI
Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA. ravdi0001@umn.edu
Abd-Alla
Mohamed D
MD
Welles
Seth L
SL
Reddy
Selvan
S
Jackson
Terry F H G
TF
D000328:Adult; D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D015331:Cohort Studies; D004747:Entamoeba / Q000276:immunology*; D004748:Entamoeba histolytica / Q000276:immunology; D004749:Entamoebiasis / Q000453:epidemiology / Q000276:immunology* / Q000469:parasitology; D005243:Feces / Q000469:parasitology; D005260:Female; D006801:Humans; D007071:Immunoglobulin A, Secretory / Q000032:analysis* / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007422:Intestines / Q000276:immunology*; D037102:Lectins / Q000276:immunology; D008101:Liver Abscess, Amebic / Q000628:therapy*; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology; D011446:Prospective Studies; D015800:Protozoan Proteins / Q000276:immunology
D000913:Antibodies, Protozoan; D007071:Immunoglobulin A, Secretory; D007074:Immunoglobulin G; D037102:Lectins; D008562:Membrane Glycoproteins; D015800:Protozoan Proteins; C052452:galactose inhibitable adherence protein, Entamoeba histolytica