The Importance of the K1 Capsule in Invasive Infections Caused by Escherichia coli

Abstract

We examined 534 clinical isolates of Escherichia coli for sensitivity to rough lipopolysaccharide-specific and K1-specific phages. Twenty-eight percent of bacteremic isolates were sensitive to rough-specific phages. Forty-two percent of these strains, against only 20% of bacteremic isolates insensitive to rough-specific phages, had K1 capsule (P less than 0.001). K1-positive strains were usually resistant to phagocytic killing, whereas strains lacking the K1 capsule were more likely to be killed regardless of capsular type. Eighty-two percent of strains were typable with O-specific, 57% with K-specific, and 74% with H-specific antisera. Sixty percent of E coli were agglutinated by only 10 O-specific antisera. K1 was the most common capsular type, followed by K5, K2, and K12, whereas four H antigens accounted for nearly half of the H-typable strains. We conclude that (1) the combination of rough-specific and K1-specific phage sensitivity defines functionally similar groups of bacteria and (2) a polyvalent vaccine against invasive E coli is possible given the relatively limited number of invasive O:K:H serotypes.

Escherichia coliin extra-intestinal infections

“…Bortolussi et al (1979) showed that the K 1 antigen protected the K 1 strains against opsonization by the alternative pathway and further that strains with much cell-associated K antigen were more resistant to phagocytosis and more virulent in newborn rats than strains with little capsular polysaccharide. Cross et al (1984) found similarly that the K 1 antigen protected against opsonophagocytosis by normal human serum and neutrophils, and, in contrast to some earlier observations cited above, they found that most other K antigens did not offer any protection against phagocytosis. Thus at the present time more investigation is needed on the role of coli K antigensother than K 1 -in phagocytosis.…”

“…Korhonen et al (1985) found that 018ac:K1 :H7, 07:K1 :H1, 06:K2:H1 and Rough:K1:H33 altogether counted for 33 0 of 63 Finnish strains from infants blood. Cross et al (1984) found 018ac:K1, 01 :K1 and 016:K1 to be the most common 0:K types in the above-mentioned material from a Washington DC hospital. Thus, even 562 E. coli in extra-intestinal infections though complete 0: K: H serotyping has not been published from all studies based on American strains, it is most likely that it really is the same serotypes that are found frequently in blood in USA and in Scandinavia; 016: K 1 may be an exception, being highly prevalent in American blood isolates and not at all represented among the published results based upon Scandinavian strains.…”

“…Antisera corresponding to the most common 0 groups could classify 57 0 of the strains. Cross et al (1984), who examined a large collection of material from Washington D.C., found that 0 groups 06, 04, 01, 018ac, 016, 0 75, 0 8, 0 2, 0 12 and 0 15 were the most frequent ones and made up 59o of all strains. Thus, even though minor differences among these materials from various geographical areas could be found, the uniformity of results is impressing.…”

“…While Olling (1977) and Bj6rksten et al (1976) could find no simple correlation between occurrence or amount of K 1 antigen in clinical isolates, Stevens et al (1978) found that K 1 antigen inhibited complement activation. Cross et al (1984), who examined a large collection of strains from blood, reported that 950% of the strains were serum resistant and related this ability to the presence of K 1 and other K antigens; K 1 was by far the most common K antigen. Many such K 1 strains had a rough lipopolysaccharide at the same time; in this respect K 1 strains were unique, as a common association between a degraded LPS and other K antigens could not be found.…”

Acquisition of genes from an O18:K1:H7 ColV+strain ofEscherichia colirenders intracranially-inoculatedE. coliK12 highly virulent for chickens, ducks and guinea-pigs but not mice

“…KI serum resistance has since been noted and studied more fully by other workers (Gemski, Cross & Sadoff, 1980;Agueero & Cabello, 1984;Pluschke et al 1983;Pluschke & Achtman, 1984), the classical complement pathway being shown to be important in the particular susceptibility of newborns to K1 + infections (Pluschke & Achtman, 1984). The KI antigen, too, has also been found to endow organisms with increased resistance to phagocytic killing (Cross et al 1984). Unlike the position of intramuscularly and intraperitoneally-inoculated MW forms (Smith & Huggins, 1980), the virulence genes of the ColV plasmid, be they those that encode iron transport systems (Williams, 1979;Williams & Warner, 1980;Stuart, Greenwood & Luke, 1980) or complement resistance (Binns, Davis & Hardy, 1979;Binns, Mayden & Levine, 1982;Nilius & Savage, 1984), only slightly increased the virulence of these forms when given intracranially.…”