Protective antigens present in whole cells of bovine enterotoxigenic Escherichia coli strains were tested in an infant mouse diarrhea model. Reduction of mortality rates of infant mice suckling vaccinated mothers was measured 1, 2, and 5 days after oral challenge with strain B41 (0101:K99,F41:H-). Vaccines consisted of strains of serogroup 0101, 09, 08, or 020 and of variants bearing or not bearing antigens K99 and F41. K99 and F41 expressions were checked by slide agglutination with K99 and F41 antisera and by mannose-resistant microhemagglutination with horse, sheep, and guinea pig erythrocytes. Absence of production of K99 antibodies following hyperimmunization with K99-negative variants was established in rabbit antisera. Strains bearing K9 alone induced less protection of infant mice 5 days after challenge than strains bearing F41 alone or both K99 and F41. Absence of expression of K99 in the vaccinal strains resulted in either a slight decrease (strains bearing additional F41) or complete abolishment (strains bearing K99 alone) of protection. Failure of F41 synthesis by 0101 strains or variants resulted in no protection 5 days after challenge. F41 probably also supplied most of the protection induced by the 09 strain. When negative for both K99 and F41, strains of serogroup 0101 still provided protection 1 and 2 days after challenge. This protection was also induced by strain H510a, the reference for 0101 antigen. Thus, 0 antigen contributed to the best vaccinal protection, in addition to K99 and F41.Enterotoxigenic Escherichia coli (ETEC) cause diarrhea in humans and other animals by colonizing the small intestine and producing enterotoxins. Colonization of the small intestine by ETEC is facilitated by surface factors, known as pili, which mediate adhesion to the epithelium. In bovine and ovine ETEC strains, K99 pilus has been long considered to be the major adherence factor (27). Vaccination of pregnant cows and ewes with whole cells of K99 ETEC strains (1,2,14,22,23) or with K99 cell-free extracts (2,3,8,24,32,33) conferred protection to their suckling offsprings orally challenged with homologous or heterologous K99 ETEC strains. Concomitantly, anti-K99 antibodies which appeared in colostrum of vaccinated dams have been supposed to supply protection. Therefore, K99 adhesin is generally considered to be greatly involved in the prevention of colibacillosis induced by K99 ETEC strains. More recently, an additional adherence factor, called F41, has been demonstrated in K99-positive bovine strains of serogroups 09 and 0101 (10,19); like K99, F41 is antigenic, hemagglutinating, and probably piluslike. Some porcine ETEC strains, lacking wellknown fimbrial adhesins, namely, K88, K99, and 987P, have also been reported to express F41 adhesin (20). ETEC strains bearing F41 but not K99 colonized small intestine, produced F41 in vivo, and induced diarrhea after inoculation to germfree piglets (19) and lambs (21) or to conventional colostrum-fed calves and piglets (34), but the role of F41 in the virulence of these st...
