Passive immunization during experimental amebic liver-abscess development

The role of antibodies during invasive amebic infection in humans or in experimental animals has not been clearly established. Early investigations by Swartzwelder and Avant (1952) found partial protection in dogs passively immunized with whole blood from animals made resistant to rectal inoculation of Entamoeba histolytica trophozoites. Sepflveda et al. (1971) also induced partial protection against ameba challenge in hamsters injected intraperitoneally with serum from a patient with amebic liver abscess. Virtually no further report appeared until 1992, when Cieslak et al. carried out a passive immunization study in severe combined immunodeficient mice (SCID), suggesting that antiamebic antibodies are protective, in contrast to several clinical findings that tend to support the opposite (Kretschmer 1986). Thus, although specific circulating antibodies can be detected at a relatively early stage of invasive amebiasis and last for months or even years after the completion of treatment (Knobloch and Mannweiler 1983; Krupp and Powell 1971; Osinsaya and Warhust 1980), antibodies neither cure nor prevent the establishment of disease (Krupp 1970). On the other hand, under certain experimental conditions a partial protection can be induced in rodents that have been actively immunized with purified amebic proteins; however, in spite of the presence of circulating antiamebic antibodies, larger liver lesions have developed in immunized animals than in controls (Petri and Ravdin 1991). Recently, Zhang et al. (1994) reported the induction of protective immunity in gerbils immunized with a recombinant E. histolytica protein, although antibody titers and the degree of protection were unrelated. We performed passive immunization studies in hamsters using purified and characterized antiamebic immunoglobulins obtained from rabbits or hamsters.