Virulence-Associated Acquisition of Iron in Mammalian Serum by Escherichia coli

Abstract

Effects of iron on the growth of avirulent and virulent strains of Escherichia coli were tested in mice and in mammalian sera. Infection of the animals with iron increased mortality rates in mice infected with the avirulent strain to levels found in mice infected with the virulent strain. In vitro experiments showed that bacteria deprived of iron in bovine or human sera or milk or in chicken egg white stopped miltiplication and died in a very short time. These antibacterial effects were neutralized effectively with the addition of exogenous iron or the iron-binding bacterial product, enterochelin. In contrast to avirulent bacteria, which were effectively inhibited in mammalian serum, virulent bacteria were able to obtain iron and multiply. The ability of virulent bacteria to grow in mammalian serum is being attributed to the presence of iron-binding enterochelin and lipopolysaccharide in large amounts on the cell walls of virulent bacteria.

Iron enhancement of experimental infection of mice by Tritrichomonas foetus

“…The eect of experimentally induced iron overload on certain bacterial infections in mice does not dier substantially from that observed with T. foetus. Treatment of mice with various iron-containing compounds enhanced pathological consequences of infections with strains of low virulence (Sword 1966;Kochan et al 1977;Sawatzki et al 1983) or avirulent mutants (Jackson and Burrows 1956) up to the level exerted by the virulent strains. The eect was accompanied by proliferation of bacteria and dependent on early treatment (Holbein 1980(Holbein , 1981 thus indicating that availability of iron during the early proliferative phase of the infection was the critical factor.…”

Identification of the transferrin- and lactoferrin-binding proteins in Haemophilus influenzae

“…The iron-binding protein lactoferrin is present on mucosal surfaces to sequester iron (Masson et al, 1966) and in the systemic circulation transferrin is largely responsible for reducing the level of available iron (Weinberg, 1978). It has been suggested that the ability to compete with lactoferrin and transferrin for iron is essential for the pathogenesis of a number of bacterial infections (Bullen et al, 1974;Kochan et al, 1977;Miles and Khimji, 1975;Williams and Warner, 1980). Haemophilus influenzae has been shown to utilise transferrin-bound iron for growth and the demonstration of transferrin-iron utilisation in almost all invasive strains but not in most non-typable, avirulent isolates is consistent with an 'important role in ,pathogenesis (Herrington and Sparling, 1985).…”

Fever and survival: the role of serum iron.

“…Iron is known to be necessary for the growth of bacteria in isolated host tissues. Unavailability of iron due to the presence of host iron chelating proteins or the addition of chelating substances such as Desferal (desferrioxamine B methane sulphate) results in the marked decrease in the growth potential of various strains of bacteria (Kochan, 1973: Kochan, Kvach & Wiles, 1977. Conversely, the injection of iron supplements in bacterially infected mammals has been demonstrated to produce increased mortality in those mammals (Bullen, Leigh & Rogers, 1968: Bullen, Rogers & Griffiths, 1974.…”

“…An iron-free broth was prepared by stirring the soy broth with magnesium carbonate (15 g/100 ml. broth) followed by centrifugation to remove the iron/MgCO3 precipitate (Kochan et al 1977). This broth was then supplemented with ferric ammonium citrate to increase the T. A. GRIEGER AND M. J. KLUGER iron concentration to approximately 50,ug iron/100 ml.…”